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Aneuploidy

Aneuploidy is the presence of an abnormal number of chromosomes in a cell, for example a human cell having 45 or 47 chromosomes instead of the usual 46. It does not include a difference of one or more complete sets of chromosomes. A cell with any number of complete chromosome sets is called a euploid cell.An extra or missing chromosome is a common cause of some genetic disorders. Some cancer cells also have abnormal numbers of chromosomes. About 68% of human solid tumors are aneuploid. Aneuploidy originates during cell division when the chromosomes do not separate properly between the two cells (nondisjunction). Most cases of aneuploidy in the autosomes result in miscarriage, and the most common extra autosomal chromosomes among live births are 21, 18 and 13. Chromosome abnormalities are detected in 1 of 160 live human births. Autosomal aneuploidy is more dangerous than sex chromosome aneuploidy, as autosomal aneuploidy is almost always lethal to embryos that cease developing because of it. Chromosomes Most cells in the human body have 23 pairs of chromosomes, or a total of 46 chromosomes. (The sperm and egg, or gametes, each have 23 unpaired chromosomes, and red blood cells at first in bone marrow have nucleus but those red blood cells that are active in blood lose their nucleus and thus they have no nucleus and no chromosomes.)One copy of each pair is inherited from the mother and the other copy is inherited from the father. The first 22 pairs of chromosomes (called autosomes) are numbered from 1 to 22, from largest to smallest. The 23rd pair of chromosomes are the sex chromosomes. Normal females have two X chromosomes, while normal males have one X chromosome and one Y chromosome. The characteristics of the chromosomes in a cell as they are seen under a light microscope are called the karyotype. During meiosis, when germ cells divide to create sperm and egg (gametes), each half should have the same number of chromosomes. But sometimes, the whole pair of chromosomes will end up in one gamete, and the other gamete will not get that chromosome at all. Most embryos cannot survive with a missing or extra autosome (numbered chromosome) and are spontaneously aborted. The most frequent aneuploidy in humans is trisomy 16 and fetuses affected with the full version of this chromosome abnormality do not survive to term, although it is possible for surviving individuals to have the mosaic form, where trisomy 16 exists in some cells but not all. The most common aneuploidy that infants can survive with is trisomy 21, which is found in Down syndrome, affecting 1 in 800 births. Trisomy 18 (Edwards syndrome) affects 1 in 6,000 births, and trisomy 13 (Patau syndrome) affects 1 in 10,000 births. 10% of infants with trisomy 18 or 13 reach 1 year of age.Changes in chromosome number may not necessarily be present in all cells in an individual. When aneuploidy is detected in a fraction of cells in an individual, it is called chromosomal mosaicism. In general, individuals who are mosaic for a chromosomal aneuploidy tend to have a less severe form of the syndrome compared to those with full trisomy. For many of the autosomal trisomies, only mosaic cases survive to term. However, mitotic aneuploidy may be more common than previously recognized in somatic tissues, and aneuploidy is a characteristic of many types of tumorigenesis (see below). Mechanisms Aneuploidy arises from errors in chromosome segregation, which can go wrong in several ways.Nondisjunction usually occurs as the result of a weakened mitotic checkpoint, as these checkpoints tend to arrest or delay cell division until all components of the cell are ready to enter the next phase. For example, if a checkpoint is weakened, the cell may fail to notice that a chromosome pair is not lined with the spindle apparatus. In such a case, most chromosomes would separate normally (with one chromatid ending up in each cell), while others could fail to separate at all. This would generate a daughter cell lacking a copy and a daughter cell with an extra copy.Completely inactive mitotic checkpoints may cause nondisjunction at multiple chromosomes, possibly all. Such a scenario could result in each daughter cell possessing a disjoint set of genetic material.Merotelic attachment occurs when one kinetochore is attached to both mitotic spindle poles. One daughter cell would have a normal complement of chromosomes; the second would lack one. A third daughter cell may end up with the missing chromosome. Multipolar spindles: more than two spindle poles form. Such a mitotic division would result in one daughter cell for each spindle pole; each cell may possess an unpredictable complement of chromosomes. Monopolar spindle: only a single spindle pole forms. This produces a single daughter cell with its copy number doubled. A tetraploid intermediate may be produced as the end-result of the monopolar spindle mechanism. In such a case, the cell has double the copy number of a normal cell, and produces double the number of spindle poles as well. This results in four daughter cells with an unpredictable complement of chromosomes, but in the normal copy number. Somatic mosaicism in the nervous system Mosaicism for aneuploid chromosome content may be part of the constitutional make-up of the mammalian brain. In the normal human brain, brain samples from six individuals ranging from 2–86 years of age had mosaicism for chromosome 21 aneuploidy (average of 4% of neurons analyzed). This low-level aneuploidy appears to arise from chromosomal segregation defects during cell division in neuronal precursor cells, and neurons containing such aneuploid chromosome content reportedly integrate into normal circuits. However, recent research using single-cell sequencing has challenged these findings, and has suggested that aneuploidy in the brain is actually very rare. Somatic mosaicism in cancer Aneuploidy is consistently observed in virtually all cancers. The German biologist Theodor Boveri was first to propose a causative role for aneuploidy in cancer. However, the theory of Boveri was forgotten until the molecular biologist Peter Duesberg reappraised it. Understanding through what mechanisms it can affect tumor evolution is an important topic of current cancer research.Somatic mosaicism occurs in virtually all cancer cells, including trisomy 12 in chronic lymphocytic leukemia (CLL) and trisomy 8 in acute myeloid leukemia (AML). However, these forms of mosaic aneuploidy occur through mechanisms distinct from those typically associated with genetic syndromes involving complete or mosaic aneuploidy, such as chromosomal instability (due to mitotic segregation defects in cancer cells). Therefore, the molecular processes that lead to aneuploidy are targets for the development of cancer drugs. Both resveratrol and aspirin have been found in vivo (in mice) to selectively destroy tetraploid cells that may be precursors of aneuploid cells, and activate AMPK, which may be involved in the process.Alteration of normal mitotic checkpoints are also important tumorigenic events, and these may directly lead to aneuploidy. Loss of tumor suppressor p53 gene often results in genomic instability, which could lead to the aneuploidy genotype.In addition, genetic syndromes in which an individual is predisposed to breakage of chromosomes (chromosome instability syndromes) are frequently associated with increased risk for various types of cancer, thus highlighting the role of somatic aneuploidy in carcinogenesis.The ability to evade the immune system appears to be enhanced in tumoral cells with strong aneuploidy. This has therefore suggested that the presence of an abnormal number of chromosomes might be an effective predictive biomarker for response to precise immunotherapy. For example, in melanoma patients, high somatic copy number alterations are associated with less effective response to immune checkpoint blockade anti–CTLA4 (cytotoxic T lymphocyte–associated protein 4) therapy.A research work published in 2008 focuses on the mechanisms involved in aneuploidy formation, specifically on the epigenetic origin of aneuploid cells. Epigenetic inheritance is defined as cellular information other than the DNA sequence itself, that is still heritable during cell division. DNA methylation and histone modifications comprise two of the main epigenetic modifications important for many physiological and pathological conditions, including cancer. Aberrant DNA methylation is the most common molecular lesion in cancer-cells, even more frequent than gene mutations. Tumor suppressor gene silencing by CpG island promoter hypermethylation is supposed to be the most frequent epigenetic modification in cancer cells. Epigenetic characteristics of cells may be modified by several factors including environmental exposure, deficiencies of certain nutrients, radiation, etc. Some of the alterations have been correlated with the formation of aneuploid cells in vivo. In this study it is suggested on a growing basis of evidence, that not only genetics but also epigenetics, contribute to aneuploid cell formation. Partial aneuploidy The terms "partial monosomy" and "partial trisomy" are used to describe an imbalance of genetic material caused by loss or gain of part of a chromosome. In particular, these terms would be used in the situation of an unbalanced translocation, where an individual carries a derivative chromosome formed through the breakage and fusion of two different chromosomes. In this situation, the individual would have three copies of part of one chromosome (two normal copies and the portion that exists on the derivative chromosome) and only one copy of part of the other chromosome involved in the derivative chromosome. Robertsonian translocations, for example, account for a very small minority of Down syndrome cases (<5%). The formation of one isochromosome results in partial trisomy of the genes present in the isochromosome and partial monosomy of the genes in the lost arm. Aneugens Agents capable of causing aneuploidy are called aneugens. Many mutagenic carcinogens are aneugens. X-rays, for example, may cause aneuploidy by fragmenting the chromosome; it may also target the spindle apparatus. Other chemicals such as colchicine can also produce aneuploidy by affecting microtubule polymerization. Exposure of males to lifestyle, environmental and/or occupational hazards may increase the risk of spermatozoa aneuploidy. Tobacco smoke contains chemicals that cause DNA damage. Smoking also can induce aneuploidy. For instance, smoking increases chromosome 13 disomy in spermatozoa by 3-fold, and YY disomy by 2-fold.Occupational exposure to benzene is associated with a 2.8-fold increase of XX disomy and a 2.6-fold increase of YY disomy in spermatozoa.Pesticides are released to the environment in large quantities so that most individuals have some degree of exposure. The insecticides fenvalerate and carbaryl have been reported to increase spermatozoa aneuploidy. Occupational exposure of pesticide factory workers to fenvalerate is associated with increased spermatozoa DNA damage. Exposure to fenvalerate raised sex chromosome disomy 1.9-fold and disomy of chromosome 18 by 2.6-fold. Exposure of male workers to carbaryl increased DNA fragmentation in spermatozoa, and also increased sex chromosome disomy by 1.7-fold and chromosome 18 disomy by 2.2-fold.Humans are exposed to perfluorinated compounds (PFCs) in many commercial products. Men contaminated with PFCs in whole blood or seminal plasma have spermatozoa with increased levels of DNA fragmentation and chromosomal aneuploidies. Diagnosis Germline aneuploidy is typically detected through karyotyping, a process in which a sample of cells is fixed and stained to create the typical light and dark chromosomal banding pattern and a picture of the chromosomes is analyzed. Other techniques include fluorescence in situ hybridization (FISH), quantitative PCR of short tandem repeats, quantitative fluorescence PCR (QF-PCR), quantitative PCR dosage analysis, Quantitative Mass Spectrometry of Single Nucleotide Polymorphisms, and comparative genomic hybridization (CGH). These tests can also be performed prenatally to detect aneuploidy in a pregnancy, through either amniocentesis or chorionic villus sampling. Pregnant women of 35 years or older are offered prenatal testing because the chance of chromosomal aneuploidy increases as the mothers age increases. Recent advances have allowed for less invasive testing methods based on the presence of fetal genetic material in maternal blood. See Triple test and Cell-free fetal DNA. Types Terminology In the strict sense, a chromosome complement having a number of chromosomes other than 46 (in humans) is considered heteroploid while an exact multiple of the haploid chromosome complement is considered euploid. See also Chromosome abnormality Chromosome segregation Nondisjunction Ploidy Robertsonian translocation References External links Aneuploidy Testing Aneuploidy FAQ Genetics of Aneuploids

Chest pain

Chest pain is pain or discomfort in the chest, typically the front of the chest. It may be described as sharp, dull, pressure, heaviness or squeezing. Associated symptoms may include pain in the shoulder, arm, upper abdomen, or jaw, along with nausea, sweating, or shortness of breath. It can be divided into heart-related and non-heart-related pain. Pain due to insufficient blood flow to the heart is also called angina pectoris. Those with diabetes or the elderly may have less clear symptoms.Serious and relatively common causes include acute coronary syndrome such as a heart attack (31%), pulmonary embolism (2%), pneumothorax, pericarditis (4%), aortic dissection (1%) and esophageal rupture. Other common causes include gastroesophageal reflux disease (30%), muscle or skeletal pain (28%), pneumonia (2%), shingles (0.5%), pleuritis, traumatic and anxiety disorders. Determining the cause of chest pain is based on a persons medical history, a physical exam and other medical tests. About 3% of heart attacks, however, are initially missed.Management of chest pain is based on the underlying cause. Initial treatment often includes the medications aspirin and nitroglycerin. The response to treatment does not usually indicate whether the pain is heart-related. When the cause is unclear, the person may be referred for further evaluation.Chest pain represents about 5% of presenting problems to the emergency room. In the United States, about 8 million people go to the emergency department with chest pain a year. Of these, about 60% are admitted to either the hospital or an observation unit. The cost of emergency visits for chest pain in the United States is more than US$8 billion per year. Chest pain accounts for about 0.5% of visits by children to the emergency department. Signs and symptoms Chest pain may present in different ways depending upon the underlying diagnosis. Chest pain may also vary from person to person based upon age, sex, weight, and other differences. Chest pain may present as a stabbing, burning, aching, sharp, or pressure-like sensation in the chest. Chest pain may also radiate, or move, to several other areas of the body. This may include the neck, left or right arms, cervical spine, back, and upper abdomen. Other associated symptoms with chest pain can include nausea, vomiting, dizziness, shortness of breath, anxiety, and sweating. The type, severity, duration, and associated symptoms of chest pain can help guide diagnosis and further treatment. Differential diagnosis Causes of chest pain range from non-serious to serious to life-threatening.In adults the most common causes of chest pain include: gastrointestinal (42%), coronary artery disease (31%), musculoskeletal (28%), pericarditis (4%) and pulmonary embolism (2%). Other less common causes include: pneumonia, lung cancer, and aortic aneurysms. Psychogenic causes of chest pain can include panic attacks; however, this is a diagnosis of exclusion.In children, the most common causes for chest pain are musculoskeletal (76-89%), exercise-induced asthma (4-12%), gastrointestinal illness (8%), and psychogenic causes (4%). Chest pain in children can also have congenital causes. Cardiovascular Acute coronary syndrome Stable or unstable angina Myocardial infarction ("heart attack"): People usually complained of a pressure or squeezing sensation over the chest. Other associated symptoms are: excessive sweating, nausea, vomiting, and weakness. Chest pain is more commonly associated with anterior infarction because of left ventricular impairment; inferior infarction is more commonly associated with nausea, vomiting, and excessive sweating due to irritation of vagus nerve; lateral infarction is associated with left arm pain. Prinzmetals angina: Chest pain is caused by coronary vasospasm. More common in women younger than 50 years. Person usually complain of chest pain at rest. It may occur early in the morning which awaken person from sleep. Cocaine use: This condition is suspected when a person with few or no risk of arteriosclerosis presented with non-traumatic chest pain. Ingestion of cocaine can cause vasoconstriction of coronary arteries, thus producing chest pain similar to heart attack. Symptoms can appear within one hour of cocaine use. Aortic stenosis: This condition happens when the person has underlying congenital bicuspid valve, aortic sclerosis, or history of rheumatic fever. Chest pain usually happens during physical activity. Syncope is a late symptom. Signs and symptoms of heart failure may also present. On auscultation, loud ejection systolic murmur can be best heard at the right second intercostal space and radiates to the carotid artery in the neck. Splitting of second heart sound is heard in severe stenosis. Hypertrophic cardiomyopathy: It is the hypertrophy of interventricular septum that causes outflow obstruction of left ventricle. Dyspnea and chest pain commonly occurs during daily activities. Sometimes, syncope (fainting) may happen. On physical examination, significant findings include: loud systolic murmur and palpable triple apical impulse due to palpable presystolic fourth heart sound. Aortic dissection is characterized by severe chest pain that radiates the back. It is usually associated with Marfans syndrome and hypertension. On examination, murmur of aortic insufficiency can be heard with unequal radial pulses. Pericarditis: This condition can be the result of viral infection such as coxsackie virus and echovirus, tuberculosis, autoimmune disease, uremia, and after myocardial infarction (Dressler syndrome). The chest pain is often pleuritic in nature (associated with respiration) which is aggravated when lying down and relieved on sitting forward, sometimes, accompanied by fever. On auscultation, pericardial friction rub can be heard. Cardiac tamponade Arrhythmia: Atrial fibrillation and a number of other arrhythmias can cause chest pain. Myocarditis Mitral valve prolapse syndrome: Those affected are usually slim females presented with chest pain which is sharp in quality, localized at the apex, and relieved when lying down. Other symptoms include: shortness of breath, fatigue, and palpitations. On auscultation, midsystolic click followed by late systolic murmur can be heard, louder when person is in standing position. Aortic aneurysm Respiratory Asthma is a common long-term inflammatory disease of the airways of the lungs. It is characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm. Symptoms include episodes of wheezing, coughing, chest tightness, and shortness of breath. Chest pain usually happens during a strenuous activity or heavy exercise. Bronchitis Pulmonary embolism: Common signs and symptoms are shortness of breath, pleuritic chest pain, blood in sputum during cough, and lower limb swelling. Risk factors includes: recent surgery, malignancy, and bedridden state. Source of embolus usually comes from venous thromboembolism. Pneumonia Hemothorax Pneumothorax: Those who are at a higher risk of developing pneumothorax are tall, slim male smokers who have had underlying lung diseases such as emphysema. Those affected can have a sharp chest pain which radiates to the shoulder of the same side. Physical examination revealed absent breath sounds and hyperresonance on the affected side of the chest. Pleurisy Tuberculosis Tracheitis Lung cancer Gastrointestinal Gastroesophageal reflux disease: The pain is aggravated when lying down or after meals. Persons may describe this as a heartburn. Besides, they may also complain of tasting bitter contents from the stomach. Achalasia, nutcracker esophagus, and other motility disorders of the esophagus Diffuse esophageal spasm: Unlike cardiac chest pain, esophageal pain is not related to activity. The pain is usually associated with swallowing of hot or cold water. Esophageal rupture: Those affected usually complain of sudden, severe, and constant pain that starts from the neck to the upper abdomen. The pain is aggravated by swallowing. On examination, neck swelling and crepitations can be felt due to subcutaneous emphysema as free air is entering from esophagus into the subcutaneous tissue. Esophagitis: There are many causes of esophagitis. Esophagitis caused by Candida albicans is usually found in chemotherapy or HIV patients. Medication such as nonsteroidal anti-inflammatory drug and alendronate can induce esophagitis if not swallowed properly. Functional dyspepsia Hiatus hernia Jackhammer esophagus (hypercontractile peristalsis): Intense long-lasting esophageal muscle spasm. Acute cholecystitis: Characterized by positive Murphys sign where the person has a cessation of inhalation when the doctor places his finger at the right subcostal region of the abdomen. Acute pancreatitis: History of excessive alcohol use, cholelithiasis (stones in the gallbladder), and hypertriglyceridemia are risk factors for pancreatitis. It is a constant, boring pain in the upper abdomen. Perforated peptic ulcer: Sudden onset of severe pain in the upper abdomen which later develops into peritonitis (inflammation of tissues that lines the abdominal organs). Acute gastritis Chest wall Costochondritis or Tietzes syndrome: An inflammation of a costochondral junction. Any movements or palpation of the chest can reproduce the symptoms. Spinal nerve problem Fibromyalgia Chest wall problems Radiculopathy Precordial catch syndrome: Another benign and harmless form of a sharp, localized chest pain often mistaken for heart disease. Breast conditions Herpes zoster (shingles): It is usually described as a burning sensation over the chest in a unilateral dermatome distribution. However, diagnosis can be difficult because the pain usually appears before the characteristic rash is visible. Tuberculosis Osteoarthritis Bornholm disease Rib fracture Psychological Panic attack: Chest pain is a common symptom of panic attacks, with as high as 78% of persons describing chest pain with their worst panic attacks. Overall chest pain is a symptom of up to 48% of sudden-onset panic attacks, and 10% of gradual-onset panic attacks. Anxiety Clinical depression Somatization disorder Hypochondria Others Hyperventilation syndrome often presents with chest pain and a tingling sensation of the fingertips and around the mouth. Da costas syndrome Carbon monoxide poisoning Sarcoidosis Lead poisoning Prolapsed intervertebral disc Thoracic outlet syndrome Adverse effect from certain medications Diagnostic approach History taking Knowing a persons risk factors can be extremely useful in ruling in or ruling out serious causes of chest pain. For example, heart attack and thoracic aortic dissection are very rare in healthy individuals under 30 years of age, but significantly more common in individuals with significant risk factors, such as older age, smoking, hypertension, diabetes, history of coronary artery disease or stroke, positive family history (premature atherosclerosis, cholesterol disorders, heart attack at early age), and other risk factors. Chest pain that radiates to one or both shoulders or arms, chest pain that occurs with physical activity, chest pain associated with nausea or vomiting, chest pain accompanied by diaphoresis or sweating, or chest pain described as "pressure," has a higher likelihood of being related to acute coronary syndrome, or inadequate supply of blood to the heart muscle, but even without these symptoms chest pain may be a sign of acute coronary syndrome. Other clues in the history can help lower the suspicion for myocardial infarction. These include chest pain described as "sharp" or "stabbing", chest pain that is positional or pleuritic in nature, and chest pain that can be reproduced with palpation. However, both atypical and typical symptoms of acute coronary syndrome can occur, and in general a history cannot be enough to rule out the diagnosis of acute coronary syndrome. In some cases, chest pain may not even be a symptom of an acute cardiac event. An estimated 33% of persons with myocardial infarction in the United States do not present with chest pain, and carry a significantly higher mortality as a result of delayed treatment. Physical examination Careful medical history and physical examination is essential in separating dangerous from trivial causes of disease, and the management of chest pain may be done on specialized units (termed medical assessment units) to concentrate the investigations. Occasionally, invisible medical signs will direct the diagnosis towards particular causes, such as Levines sign in cardiac ischemia. However, in the case of acute coronary syndrome, a third heart sound, diaphoresis, and hypotension are the most strongly associated physical exam findings. However these signs are limited in their prognostic and diagnostic value. Other physical exam findings suggestive of cardiac chest pain may include hypertension, tachycardia, bradycardia, and new heart murmurs. Chest pain that is reproducible during the physical exam with contact of the chest wall is more indicative of non-cardiac chest pain, but still cannot completely rule out acute coronary syndrome. For this reason, in general, additional tests are required to establish the diagnosis. In the emergency department the typical approach to chest pain involves ruling out the most dangerous causes: heart attack, pulmonary embolism, thoracic aortic dissection, esophageal rupture, tension pneumothorax, and cardiac tamponade. By elimination or confirmation of the most serious causes, a diagnosis of the origin of the pain may be made. Often, no definite cause will be found and reassurance is then provided. Risk scores The Global Registry of Acute Coronary Events score and the Thrombosis in Myocardial Infarction performed at time of admission may help stratify persons into low, intermediate and high risk groups for acute coronary syndrome. However these scores do not provide management guidelines for risk-stratified persons. The HEART score, stratifies persons into low-risk and high-risk groups, and recommends either discharge or admission based upon the score. Cumulative score: 0-3: 2.5% risk of adverse cardiac event. Patients can be discharged with follow-up. 4-6: 20.3% risk of adverse cardiac event. Patients should be admitted to the hospital for trending of troponin and provocative testing. ≥7: 72.7% risk of adverse cardiac event, suggesting early invasive measures with these patients and close coordination with inpatient cardiology.If acute coronary syndrome ("heart attack") is suspected, many people are admitted briefly for observation, sequential ECGs, and measurement of cardiac enzymes in the blood over time. On occasion, further tests on follow up may determine the cause. Medical tests On the basis of the above, a number of tests may be ordered: An electrocardiogram (ECG) Chest radiograph or chest x rays are frequently performed Echocardiography can be useful in patients with known cardiac disease or aortic dissection CT scanning is used in the diagnosis of aortic dissection V/Q scintigraphy or CT pulmonary angiogram (when a pulmonary embolism is suspected) Blood tests: Troponin I or T (to indicate myocardial damage) Complete blood count Electrolytes and renal function (creatinine) Liver enzymes Creatine kinase (and CK-MB fraction in many hospitals) D-dimer (when suspicion for pulmonary embolism is present but low) serum lipase to exclude acute pancreatitis Management Management of chest pain varies with the underlying cause of the pain and the stage of care. Prehospital care Chest pain is a common symptom encountered by emergency medical services. Aspirin increases survival in people with acute coronary syndrome and it is reasonable for EMS dispatchers to recommend it in people with no recent serious bleeding. Supplemental oxygen was used in the past for most people with chest pain but is not needed unless the oxygen saturations are less than 94% or there are signs of respiratory distress. Entonox is frequently used by EMS personnel in the prehospital environment. However, there is little evidence about its effectiveness. Hospital care Hospital care of chest pain begins with initial survey of a persons vital signs, airway and breathing, and level of consciousness. This may also include attachment of ECG leads, cardiac monitors, intravenous lines and other medical devices depending on initial evaluation. After evaluation of a persons history, risk factors, physical examination, laboratory testing and imaging, management begins depending on suspected diagnoses. Depending upon the diagnosis, a person may be placed in the intensive care unit, admitted to the hospital, or be treated outpatient. For persons with suspected cardiac chest pain or acute coronary syndrome, or other emergent diagnoses such as pneumothorax, pulmonary embolism, or aortic dissection, admission to the hospital is most often recommended for further treatment. Outpatient care For people with non-cardiac chest pain, cognitive behavioral therapy might be helpful on an outpatient basis. A 2015 Cochrane review found that cognitive behavioral therapy might reduce the frequency of chest pain episodes the first three months after treatment. For persons with chest pain due to gastroesophageal reflux disease, a proton-pump inhibitor has been shown to be the most effective treatment. However, treatment with proton pump inhibitors has been shown to be no better than placebo in persons with noncardiac chest pain not caused by gastroesophageal reflux disease. For musculoskeletal causes of chest pain, manipulation therapy or chiropractic therapy, acupuncture, or a recommendation for increased exercise are often used as treatment. Studies have shown conflicting results on the efficacy of these treatments. A combination therapy of nonsteroidal anti-inflammatory drugs and manipulation therapy with at-home exercises has been shown to be most effective in treatment of musculoskeletal chest pain. Epidemiology Chest pain is a common presenting problem. Overall chest pain is responsible for an estimated 6% of all emergency department visits in the United States and is the most common reason for hospital admission. Chest pain is also very common in primary care clinics, representing 1-3% of all visits. The rate of emergency department visits in the US for chest pain decreased 10% from 1999 to 2008. but a subsequent increase of 13% was seen from 2006 to 2011. Less than 20% of all cases of chest pain admissions are found to be due to coronary artery disease. The rate of chest pain as a symptom of acute coronary syndrome varies among populations based upon age, sex, and previous medical conditions. In general, women are more likely than men to present without chest pain (49% vs. 38%) in cases of myocardial infarction. References == External links ==

Motion sickness

Motion sickness occurs due to a difference between actual and expected motion. Symptoms commonly include nausea, vomiting, cold sweat, headache, dizziness, tiredness, loss of appetite, and increased salivation. Complications may rarely include dehydration, electrolyte problems, or a lower esophageal tear.The cause of motion sickness is either real or perceived motion. This may include from car travel, air travel, sea travel, space travel, or reality simulation. Risk factors include pregnancy, migraines, and Ménières disease. The diagnosis is based on symptoms.Treatment may include behavioral measures or medications. Behavioral measures include keeping the head still and focusing on the horizon. Three types of medications are useful: antimuscarinics such as scopolamine, H1 antihistamines such as dimenhydrinate, and amphetamines such as dexamphetamine. Side effects, however, may limit the use of medications. A number of medications used for nausea such as ondansetron are not effective for motion sickness.Nearly all people are affected with sufficient motion and most people will experience motion sickness at least once in their lifetime. Susceptibility, however, is variable, with about one-third of the population being highly susceptible while most other people are affected under extreme conditions. Women are more easily affected than men. Motion sickness has been described since at least the time of Homer (c. eighth century BC). Signs and symptoms Symptoms commonly include nausea, vomiting, cold sweat, headache, dizziness, tiredness, loss of appetite, and increased salivation. Occasionally, tiredness can last for hours to days after an episode of motion sickness, known as "sopite syndrome". Rarely severe symptoms such as the inability to walk, ongoing vomiting, or social isolation may occur while rare complications may include dehydration, electrolyte problems, or a lower esophageal tear from severe vomiting. Cause Motion sickness can be divided into three categories: Motion sickness caused by motion that is felt but not seen, as in terrestrial motion sickness; Motion sickness caused by motion that is seen but not felt, as in space motion sickness; Motion sickness caused when both systems detect motion but they do not correspond, as in either terrestrial or space motion sickness. Motion felt but not seen In these cases, motion is sensed by the vestibular system and hence the motion is felt, but no motion or little motion is detected by the visual system, as in terrestrial motion sickness. Carsickness A specific form of terrestrial motion sickness, being carsick is quite common and evidenced by disorientation while reading a map, a book, or a small screen during travel. Carsickness results from the sensory conflict arising in the brain from differing sensory inputs. Motion sickness is caused by a conflict between signals arriving in the brain from the inner ear, which forms the base of the vestibular system, the sensory apparatus that deals with movement and balance, and which detects motion mechanically. If someone is looking at a stationary object within a vehicle, such as a magazine, their eyes will inform their brain that what they are viewing is not moving. Their inner ears, however, will contradict this by sensing the motion of the vehicle.Varying theories exist as to cause. The sensory conflict theory notes that the eyes view motion while riding in the moving vehicle while other body sensors sense stillness, creating conflict between the eyes and inner ear. Another suggests the eyes mostly see the interior of the car which is motionless while the vestibular system of the inner ear senses motion as the vehicle goes around corners or over hills and even small bumps. Therefore, the effect is worse when looking down but may be lessened by looking outside of the vehicle. In the early 20th century, Austro-Hungarian scientist Róbert Bárány observed the back and forth movement of the eyes of railroad passengers as they looked out the side windows at the scenery whipping by. He called it "railway nystagmus". Also called "optokinetic nystagmus". It causes nausea and vomiting. His findings were published in the journal Laeger, 83:1516, Nov.17, 1921. Airsickness Air sickness is a kind of terrestrial motion sickness induced by certain sensations of air travel. It is a specific form of motion sickness and is considered a normal response in healthy individuals. It is essentially the same as carsickness but occurs in an airplane. An airplane may bank and tilt sharply, and unless passengers are sitting by a window, they are likely to see only the stationary interior of the plane due to the small window sizes and during flights at night. Another factor is that while in flight, the view out of windows may be blocked by clouds, preventing passengers from seeing the moving ground or passing clouds. Seasickness Seasickness is a form of terrestrial motion sickness characterized by a feeling of nausea and, in extreme cases, vertigo experienced after spending time on a boat. It is essentially the same as carsickness, though the motion of a watercraft tends to be more regular. It is typically brought on by the rocking motion of the craft or movement while the craft is immersed in water. As with airsickness, it can be difficult to visually detect motion even if one looks outside the boat since water does not offer fixed points with which to visually judge motion. Poor visibility conditions, such as fog, may worsen seasickness. The greatest contributor to seasickness is the tendency for people being affected by the rolling or surging motions of the craft to seek refuge below decks, where they are unable to relate themselves to the boats surroundings and consequent motion. Some people with carsickness are resistant to seasickness and vice versa. Adjusting to the crafts motion at sea is called "gaining ones sea legs"; it can take a significant portion of the time spent at sea after disembarking to regain a sense of stability "post-sea legs". Centrifuge motion sickness Rotating devices such as centrifuges used in astronaut training and amusement park rides such as the Rotor, Mission: Space and the Gravitron can cause motion sickness in many people. While the interior of the centrifuge does not appear to move, one will experience a sense of motion. In addition, centrifugal force can cause the vestibular system to give one the sense that downward is in the direction away from the center of the centrifuge rather than the true downward direction. Dizziness due to spinning When one spins and stops suddenly, fluid in the inner ear continues to rotate causing a sense of continued spinning while ones visual system no longer detects motion. Virtual reality Usually, VR programs would detect the motion of the users head and adjust the rotation of vision to avoid dizziness. However, some cases such as system lagging or software crashing could cause lags in the screen updates. In such cases, even some small head motions could trigger the motion sickness by the defense mechanism mentioned below: the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. Motion seen but not felt In these cases, motion is detected by the visual system and hence the motion is seen, but no motion or little motion is sensed by the vestibular system. Motion sickness arising from such situations has been referred to as "visually induced motion sickness" (VIMS). Space motion sickness Zero gravity interferes with the vestibular systems gravity-dependent operations, so that the two systems, vestibular and visual, no longer provide a unified and coherent sensory representation. This causes unpleasant disorientation sensations often quite distinct from terrestrial motion sickness, but with similar symptoms. The symptoms may be more intense because a condition caused by prolonged weightlessness is usually quite unfamiliar.Space motion sickness was effectively unknown during the earliest spaceflights because the very cramped conditions of the spacecraft allowed for only minimal bodily motion, especially head motion. Space motion sickness seems to be aggravated by being able to freely move around, and so is more common in larger spacecraft. Around 60% of Space Shuttle astronauts experienced it on their first flight; the first case of space motion sickness is now thought to be the Soviet cosmonaut Gherman Titov, in August 1961 onboard Vostok 2, who reported dizziness, nausea, and vomiting. The first severe cases were in early Apollo flights; Frank Borman on Apollo 8 and Rusty Schweickart on Apollo 9. Both experienced identifiable and quite unpleasant symptoms—in the latter case causing the mission plan to be modified. Screen images This type of terrestrial motion sickness is particularly prevalent when susceptible people are watching films presented on very large screens such as IMAX, but may also occur in regular format theaters or even when watching TV or playing games. For the sake of novelty, IMAX and other panoramic type theaters often show dramatic motions such as flying over a landscape or riding a roller coaster. This type of motion sickness can be prevented by closing ones eyes during such scenes.In regular-format theaters, an example of a movie that caused motion sickness in many people is The Blair Witch Project. Theaters warned patrons of its possible nauseating effects, cautioning pregnant women in particular. Blair Witch was filmed with a handheld camcorder, which was subjected to considerably more motion than the average movie camera, and lacks the stabilization mechanisms of steadicams.Home movies, often filmed with a cell phone camera, also tend to cause motion sickness in those who view them. The person holding the cell phone or other camera usually is unaware of this as the recording is being made since the sense of motion seems to match the motion seen through the cameras viewfinder. Those who view the film afterward only see the movement, which may be considerable, without any sense of motion. Using the zoom function seems to contribute to motion sickness as well since zooming is not a normal function of the eye. The use of a tripod or a camera or cell phone with image stabilization while filming can reduce this effect. Virtual reality Motion sickness due to virtual reality is very similar to simulation sickness and motion sickness due to films. In virtual reality the effect is made more acute as all external reference points are blocked from vision, the simulated images are three-dimensional and in some cases stereo sound that may also give a sense of motion. The NADS-1, a simulator located at the National Advanced Driving Simulator, is capable of accurately stimulating the vestibular system with a 360-degree horizontal field of view and 13 degrees of freedom motion base. Studies have shown that exposure to rotational motions in a virtual environment can cause significant increases in nausea and other symptoms of motion sickness.In a study conducted by the U.S. Army Research Institute for the Behavioral and Social Sciences in a report published May 1995 titled "Technical Report 1027 – Simulator Sickness in Virtual Environments", out of 742 pilot exposures from 11 military flight simulators, "approximately half of the pilots (334) reported post-effects of some kind: 250 (34%) reported that symptoms dissipated in less than one hour, 44 (6%) reported that symptoms lasted longer than four hours, and 28 (4%) reported that symptoms lasted longer than six hours. There were also four (1%) reported cases of spontaneously occurring flashbacks." Motion that is seen and felt When moving within a rotating reference frame such as in a centrifuge or environment where gravity is simulated with centrifugal force, the coriolis effect causes a sense of motion in the vestibular system that does not match the motion that is seen. Pathophysiology There are various hypotheses that attempt to explain the cause of the condition. Sensory conflict theory Contemporary sensory conflict theory, referring to "a discontinuity between either visual, proprioceptive, and somatosensory input, or semicircular canal and otolith input", is probably the most thoroughly studied. According to this theory, when the brain presents the mind with two incongruous states of motion; the result is often nausea and other symptoms of disorientation known as motion sickness. Such conditions happen when the vestibular system and the visual system do not present a synchronized and unified representation of ones body and surroundings.According to sensory conflict theory, the cause of terrestrial motion sickness is the opposite of the cause of space motion sickness. The former occurs when one perceives visually that ones surroundings are relatively immobile while the vestibular system reports that ones body is in motion relative to its surroundings. The latter can occur when the visual system perceives that ones surroundings are in motion while the vestibular system reports relative bodily immobility (as in zero gravity.) Neural mismatch A variation of the sensory conflict theory is known as neural mismatch, implying a mismatch occurring between ongoing sensory experience and long-term memory rather than between components of the vestibular and visual systems. This theory emphasizes "the limbic system in the integration of sensory information and long-term memory, in the expression of the symptoms of motion sickness, and the impact of anti-motion-sickness drugs and stress hormones on limbic system function. The limbic system may be the neural mismatch center of the brain." Defense against poisoning It has also been proposed that motion sickness could function as a defense mechanism against neurotoxins. The area postrema in the brain is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling motion but not seeing it (for example, in the cabin of a ship with no portholes), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the incongruity, the brain concludes that the individual is hallucinating and further concludes that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treismans indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis. The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the bodys poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness. Nystagmus hypothesis Yet another theory, known as the nystagmus hypothesis, has been proposed based on stimulation of the vagus nerve resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., semicircular canals and otolith organs, and a change in tonus among various of each eyes six extra-ocular muscles. Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherringtons Law describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherringtons Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally, there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction. Thus, tenth nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine-defective individuals are immune to motion sickness; why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherringtons Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.A recent theory argues that the main reason motion sickness occurs is due to an imbalance in vestibular outputs favoring the semicircular canals (nauseogenic) vs. otolith organs (anti-nauseogenic). This theory attempts to integrate previous theories of motion sickness. For example, there are many sensory conflicts that are associated with motion sickness and many that are not, but those in which canal stimulation occurs in the absence of normal otolith function (e.g., in free fall) are the most provocative. The vestibular imbalance theory is also tied to the different roles of the otoliths and canals in autonomic arousal (otolith output more sympathetic). Diagnosis The diagnosis is based on symptoms. Other conditions that may present similarly include vestibular disorders such as benign paroxysmal positional vertigo and vestibular migraine and stroke. Treatment Treatment may include behavioral measures or medications. Behavioral measures Behavioral measures to decrease motion sickness include holding the head still and lying on the back. Focusing on the horizon may also be useful. Listening to music, mindful breathing, being the driver, and not reading while moving are other techniques.Habituation is the most effective technique but requires significant time. It is often used by the military for pilots. These techniques must be carried out at least every week to retain effectiveness.A head-worn, computer device with a transparent display can be used to mitigate the effects of motion sickness (and spatial disorientation) if visual indicators of the wearers head position are shown. Such a device functions by providing the wearer with digital reference lines in their field of vision that indicate the horizons position relative to the users head. This is accomplished by combining readings from accelerometers and gyroscopes mounted in the device. This technology has been implemented in both standalone devices and Google Glass. One promising looking treatment is to wear LCD shutter glasses that create a stroboscopic vision of 4 Hz with a dwell of 10 milliseconds. Medication Three types of medications are useful: antimuscarinics such as scopolamine, H1 antihistamines such as dimenhydrinate, and amphetamines such as dexamphetamine. Benefits are greater if used before the onset of symptoms or shortly after symptoms begin. Side effects, however, may limit the use of medications. A number of medications used for nausea such as ondansetron and metoclopramide are not effective in motion sickness.Scopolamine is the most effective medication. Evidence is best for when it is used preventatively. It is available as a skin patch. Side effects may include blurry vision.Other effective first generation antihistamines include doxylamine, diphenhydramine, promethazine, meclizine, cyclizine, and cinnarizine. In pregnancy meclizine, dimenhydrinate and doxylamine are generally felt to be safe. Side effects include sleepiness. Second generation antihistamines have not been found to be useful.Dextroamphetamine may be used together with an antihistamine or an antimuscarinic. Concerns include their addictive potential.Those involved in high-risk activities, such as SCUBA diving, should evaluate the risks versus the benefits of medications. Promethazine combined with ephedrine to counteract the sedation is known as "the Coast Guard cocktail". Alternative medicine Alternative treatments include acupuncture and ginger although their effectiveness against motion sickness is variable. Providing smells does not appear to have a significant effect on the rate of motion sickness. Epidemiology Roughly one-third of people are highly susceptible to motion sickness, and most of the rest get motion sick under extreme conditions. Around 80% of the general population is susceptible to cases of medium to high motion sickness. The rates of space motion sickness have been estimated at between forty and eighty percent of those who enter weightless orbit. Several factors influence susceptibility to motion sickness, including sleep deprivation and the cubic footage allocated to each space traveler. Studies indicate that women are more likely to be affected than men, and that the risk decreases with advancing age. There is some evidence that people with Asian ancestry may develop motion sickness more frequently than people of European ancestry, and there are situational and behavioral factors, such as whether a passenger has a view of the road ahead, and diet and eating behaviors. See also Mal de debarquement - disembarkment syndrome, usually follows a cruise or other motion experience References External links Davis, Christopher J.; Lake-Bakaar, Gerry V.; Grahame-Smith, David G. (2012). Nausea and Vomiting: Mechanisms and Treatment. Springer Science & Business Media. p. 123. ISBN 978-3-642-70479-6. Motion Sickness from MedlinePlus

Myelitis

Myelitis is inflammation of the spinal cord which can disrupt the normal responses from the brain to the rest of the body, and from the rest of the body to the brain. Inflammation in the spinal cord, can cause the myelin and axon to be damaged resulting in symptoms such as paralysis and sensory loss. Myelitis is classified to several categories depending on the area or the cause of the lesion; however, any inflammatory attack on the spinal cord is often referred to as transverse myelitis. Types of myelitis Myelitis lesions usually occur in a narrow region but can be spread and affect many areas. Acute flaccid myelitis: a polio-like syndrome that causes muscle weakness and paralysis. Poliomyelitis: disease caused by viral infection in the gray matter with symptoms of muscle paralysis or weakness Transverse myelitis: caused by axonal demyelination encompassing both sides of the spinal cord Leukomyelitis: lesions in the white matter Meningococcal myelitis (or meningomyelitis): lesions occurring in the region of meninges and the spinal cordOsteomyelitis of the vertebral bone surrounding the spinal cord (that is, vertebral osteomyelitis) is a separate condition, although some infections (for example, Staphylococcus aureus infection) can occasionally cause both at once. The similarity of the words reflects that the combining form myel(o)- has multiple (homonymous) senses referring to bone marrow or the spinal cord. Symptoms Depending on the cause of the disease, such clinical conditions manifest different speed in progression of symptoms in a matter of hours to days. Most myelitis manifests fast progression in muscle weakness or paralysis starting with the legs and then arms with varying degrees of severity. Sometimes the dysfunction of arms or legs cause instability of posture and difficulty in walking or any movement. Also symptoms generally include paresthesia which is a sensation of tickling, tingling, burning, pricking, or numbness of a persons skin with no apparent long-term physical effect. Adult patients often report pain in the back, extremities, or abdomen. Patients also present increased urinary urgency, bowel or bladder dysfunctions such as bladder incontinence, difficulty or inability to void, and incomplete evacuation of bowel or constipation. Others also report fever, respiratory problems and intractable vomiting. Diseases associated with myelitis Conditions associated with myelitis include: Acute disseminated encephalomyelitis: autoimmune demyelination of the brain causing severe neurological signs and symptoms Multiple sclerosis: demyelination of the brain and spinal cord Neuromyelitis optica or Devics disease: immune attack on optic nerve and spinal cord Sjögrens syndrome: destruction of the exocrine system of the body Systemic lupus erythematosus: a systemic autoimmune disease featuring a wide variety of neurological signs and symptoms Sarcoidosis: chronic inflammatory cells form as nodules in multiple organs Atopy: an immune disorder of children manifesting as eczema or other allergic conditions. It can include atopic myelitis, which causes weakness. Immune-mediated myelopathies, heterogeneous group of inflammatory spinal cord disorders including autoimmune disorders with known antibodies Cause Myelitis occurs due to various reasons such as infections. Direct infection by viruses, bacteria, mold, or parasites such as human immunodeficiency virus (HIV), human T-lymphotropic virus types I and II (HTLV-I/II), syphilis, lyme disease, and tuberculosis can cause myelitis but it can also be caused due to non-infectious or inflammatory pathway. Myelitis often follows after the infections or after vaccination. These phenomena can be explained by a theory of autoimmune attack which states that the autoimmune bodies attack its spinal cord in response to immune reaction. Mechanism of myelitis The theory of autoimmune attack claims that a person with neuroimmunologic disorders have genetic predisposition to auto-immune disorder, and the environmental factors would trigger the disease. The specific genetics in myelitis is not completely understood. It is believed that the immune system response could be to viral, bacterial, fungal, or parasitic infection; however, it is not known why the immune system attacks itself. Especially, for the immune system to cause inflammatory response anywhere in the central nervous system, the cells from the immune system must pass through the blood brain barrier. In the case of myelitis, not only is the immune system dysfunctional, but the dysfunction also crosses this protective blood brain barrier to affect the spinal cord. Infectious myelitis Viral myelitisMost viral myelitis is acute, but the retroviruses (such as HIV and HTLV) can cause chronic myelitis. Poliomyelitis, or gray matter myelitis, is usually caused by infection of anterior horn of the spinal cord by the enteroviruses (polioviruses, enteroviruses (EV) 70 and 71, echoviruses, coxsackieviruses A and B) and the flaviviruses (West Nile, Japanese encephalitis, tick-borne encephalitis). On the other hand, transverse myelitis or leukomyelitis, or white matter myelitis, are often caused by the herpesviruses and influenza virus. It can be due to direct viral invasion or via immune mediated mechanisms. Bacterial myelitisBacterial myelitis includes Mycoplasma pneumoniae, which is a common agent for respiratory tract. Studies have shown respiratory tract infections within 4–39 days prior to the onset of transverse myelitis. Or, tuberculosis, syphilis, and brucellosis are also known to cause myelitis in immune-compromised individuals. Myelitis is a rare manifestation of bacterial infection. Fungal myelitisFungi have been reported to cause spinal cord disease either by forming abscesses inside the bone or by granuloma. In general, there are two groups of fungi that may infect the CNS and cause myelitis - primary and secondary pathogens. Primary pathogens include the following: Cryptococcus neoformans, Coccidioides immitis, Blastomyces dermatitides, and Hystoplasma capsulatum. Secondary pathogens are opportunistic agents that primarily infect immunocompromised hosts such as Candida species, Aspergillus species, and zygomycetes. Parasitic myelitisParasitic species infect human hosts through larvae that penetrate the skin. Then they enter the lymphatic and circulatory system, and migrate to liver and lung. Some reach the spinal cord. Parasitic infections have been reported with Schistosoma species, Toxocara canis, Echinococcus species, Taenia solium, Trichinella spiralis, and Plasmodium species. Autoimmune myelitis In 2016, it was identified in Mayo clinic an autoimmune form of myelitis due to the presence of anti-GFAP autoantibodies. Immunoglobulins directed against the α-isoform of glial fibrillary acidic protein (GFAP-IgG) predicted a special meningoencephalomyelitis termed autoimmune GFAP Astrocytopathy that later was found also to be able to appear as a myelitis. Diagnosis Myelitis has an extensive differential diagnosis. The type of onset (acute versus subacute/chronic) along with associated symptoms such as the presence of pain, constitutional symptoms that encompass fever, malaise, weight loss or a cutaneous rash may help identify the cause of myelitis. In order to establish a diagnosis of myelitis, one has to localize the spinal cord level, and exclude cerebral and neuromuscular diseases. Also a detailed medical history, a careful neurologic examination, and imaging studies using magnetic resonance imaging (MRI) are needed. In respect to the cause of the process, further work-up would help identify the cause and guide treatment. Full spine MRI is warranted, especially with acute onset myelitis, to evaluate for structural lesions that may require surgical intervention, or disseminated disease. Adding gadolinium further increases diagnostic sensitivity. A brain MRI may be needed to identify the extent of central nervous system (CNS) involvement. Lumbar puncture is important for the diagnosis of acute myelitis when a tumoral process, inflammatory or infectious cause are suspected, or the MRI is normal or non-specific. Complementary blood tests are also of value in establishing a firm diagnosis. Rarely, a biopsy of a mass lesion may become necessary when the cause is uncertain. However, in 15–30% of people with subacute or chronic myelitis, a clear cause is never uncovered. Treatment Since each case is different, the following are possible treatments that patients might receive in the management of myelitis. Intravenous steroidsHigh-dose intravenous methyl-prednisolone for 3–5 days is considered as a standard of care for patients suspected to have acute myelitis, unless there are compelling reasons otherwise. The decision to offer continued steroids or add a new treatment is often based on the clinical course and MRI appearance at the end of five days of steroids. Plasma exchange (PLEX)Patients with moderate to aggressive forms of disease who do not show much improvement after being treated with intravenous and oral steroids will be treated with PLEX. Retrospective studies of patients with TM treated with IV steroids followed by PLEX showed a positive outcome. It also has been shown to be effective with other autoimmune or inflammatory central nervous system disorders. Particular benefit has been shown with patients who are in the acute or subacute stage of the myelitis showing active inflammation on MRI. However, because of the risks implied by the lumbar puncture procedure, this intervention is determined by the treating physician on a case-by-case basis. Immunosuppressants/Immunomodulatory agentsMyelitis with no definite cause seldom recurs, but for others, myelitis may be a manifestation of other diseases that are mentioned above. In these cases, ongoing treatment with medications that modulate or suppress the immune system may be necessary. Sometimes there is no specific treatment. Either way, aggressive rehabilitation and long-term symptom management are an integral part of the healthcare plan. Prospective research direction Central nervous system nerve regeneration would be able to repair or regenerate the damage caused to the spinal cord. It would restore functions lost due to the disease. Engineering endogenous repairCurrently, there exists a hydrogel based scaffold which acts as a channel to deliver nerve growth-enhancing substrates while providing structural support. These factors would promote nerve repairs to the target area. Hydrogels macroporous properties would enable attachment of cells and enhance ion and nutrient exchange. In addition, hydrogels biodegradability or bioresolvability would prevent the need for surgical removal of the hydrogel after drug delivery. It means that it would be dissolved naturally by the bodys enzymatic reaction. Biochemical repairNeurotropic factor therapy and gene therapy Neurotropic growth factors regulate growth, survival, and plasticity of the axon. They benefit nerve regeneration after injury to the nervous system. They are a potent initiator of sensory axon growth and are up-regulated at the lesion site. The continuous delivery of neurotropic growth factor (NGF) would increase the nerve regeneration in the spinal cord. However, the excessive dosing of NGF often leads to undesired plasticity and sprouting of uninjured sensory nerves. Gene therapy would be able to increase the NGF efficacy by the controlled and sustained delivery in a site-specific manner.Stem cell-based therapiesThe possibility for nerve regeneration after injury to the spinal cord was considered to be limited because of the absence of major neurogenesis. However, Joseph Altman showed that cell division does occur in the brain which allowed potential for stem cell therapy for nerve regeneration. The stem cell-based therapies are used in order to replace cells lost and injured due to inflammation, to modulate the immune system, and to enhance regeneration and remyelination of axons. Neural stem cells (NSC) have the potential to integrate with the spinal cord because in the recent past investigations have demonstrated their potential for differentiation into multiple cell types that are crucial to the spinal cord. Studies show that NSCs that were transplanted into a demyelinating spinal cord lesion were found to regenerate oligodendrocytes and Schwann cells, and completely remyelinated axons. See also Encephalomyelitis Myalgic encephalomyelitis – also known as chronic fatigue syndrome Transverse myelitis References == External links ==

Chédiak–Higashi syndrome

Chédiak–Higashi syndrome (CHS) is a rare autosomal recessive disorder that arises from a mutation of a lysosomal trafficking regulator protein, which leads to a decrease in phagocytosis. The decrease in phagocytosis results in recurrent pyogenic infections, albinism, and peripheral neuropathy. In Chédiak–Higashi syndrome, the lysosomal trafficking regulator (LYST) gene is mutated, leading to disruption of protein synthesis as well as the storage and secretory function of lysosomal granules in white blood cells. This results in defective white blood cell function with enlarged vesicles. This syndrome also leads to neutropenia and phagocyte bactericidal dysfunction due to impaired chemotaxis. Deficiency in serotonin and adenosine-phosphate-containing granules in platelets causes impaired platelet aggregation, leading to prolonged bleeding time. Thus, patients are susceptible to infections and often present with oculo-cutaneous albinism and coagulation defects. Patients often present with early-onset aggressive periodontitis associated with advanced alveolar bone loss and tooth mobility due to neutropenia and defective neutrophil function. Recurrent oral ulcerations are also one of the common oral manifestations in patients with this disease. Dental practitioners who notice child patients who present with recurrent unexplained gingivitis and periodontitis along with hypopigmentation of hair, skin and eyes should consider making a referral to medical practitioners to investigate for the possible diagnosis of Chédiak–Higashi syndrome. Signs and symptoms People with CHS have light skin and silvery hair (albinism) and frequently complain of solar sensitivity and photophobia. Other signs and symptoms vary considerably, but frequent infections and neuropathy are common. The infections involve mucous membranes, skin, and the respiratory tract. Affected children are susceptible to infection by Gram-positive and gram-negative bacteria and fungi, with Staphylococcus aureus being the most common infectious cause. Infections in CHS patients tend to be very serious and even life-threatening. Neuropathy often begins in the teenage years and becomes the most prominent problem. Few patients with this condition live to adulthood.Most children with Chédiak–Higashi syndrome ultimately reach a stage known as the "accelerated phase", or the "lymphoma-like syndrome", in which defective white blood cells divide uncontrollably and invade many of the bodys organs. The accelerated phase is associated with fever, episodes of abnormal bleeding, overwhelming infections, and organ failure. These medical problems are usually life-threatening in childhood. Causes Mutations in the CHS1 gene (also called LYST) located on the chromosome 1q42-q43 have been found to be connected with Chédiak–Higashi syndrome. This gene provides instructions for making a protein known as the lysosomal trafficking regulator. Researchers believe that this protein plays a role in the transport (trafficking) of materials into lysosomes. Lysosomes act as recycling centers within cells. They use digestive enzymes to break down toxic substances, digest bacteria that invade the cell and recycle worn-out cell components. Although the lysosomal trafficking regulator protein is involved in the normal function of lysosomes, its exact role is unknown.In melanocytic cells, LYST gene expression may be regulated by MITF. Mutations in MITF are known to cause Waardenburg syndrome type 2 and Tietz syndrome, which result in depigmentation and deafness. Pathophysiology CHS is a disease causing impaired bacteriolysis due to failure of phagolysosome formation. As a result of disordered intracellular trafficking there is impaired lysosome degranulation with phagosomes, so phagocytosed bacteria are not destroyed by the lysosomes enzymes.In addition, secretion of lytic secretory granule by cytotoxic T cells is affected.The disease is characterised by large lysosome vesicles in phagocytes (neutrophils), which thus have poor bactericidal function, leading to susceptibility to infections, abnormalities in nuclear structure of leukocytes, anemia, and hepatomegaly. Döhle bodies (remnants of endoplasmic reticulum) in the neutrophil are also seen. Diagnosis The diagnosis is confirmed by bone marrow smears that show "giant inclusion bodies" in the cells that develop into white blood cells (leukocyte precursor cells). CHS can be diagnosed prenatally by examining a sample of hair from a fetal scalp biopsy or testing leukocytes from a fetal blood sample.Under light microscopy the hairs present evenly distributed, regular melanin granules, larger than those found in normal hairs. Under polarized light microscopy these hairs exhibit a bright and polychromatic refringence pattern. Clinical findings There are several manifestations of Chédiak–Higashi syndrome as mentioned above; however, neutropenia seems to be the most common. The syndrome is associated with oculocutaneous albinism. Patients are prone to infections, especially with Staphylococcus aureus, as well as Streptococci.It is associated with periodontal disease of the deciduous dentition. Associated features include abnormalities in melanocytes (albinism), nerve defects, and bleeding disorders. Treatment There is no specific treatment for Chédiak–Higashi syndrome. Bone marrow transplants appear to have been successful in several patients. Infections are treated with antibiotics and abscesses are surgically drained when appropriate. Antiviral drugs such as acyclovir have been tried during the terminal phase of the disease. Cyclophosphamide and prednisone have been tried. Vitamin C therapy has improved immune function and clotting in some patients. Eponym It is named for the Cuban physician and serologist of Lebanese descent Moisés Chédiak Ahuayda (1903–1993) and the Japanese pediatrician Ototaka Higashi (1883–1981). It is often spelled without the accent as Chediak–Higashi syndrome. Other species It occurs in humans, cattle, blue Persian cats, Australian blue rats, mice, mink, foxes, and the only known captive white orca. See also Griscelli syndrome (also known as "Chédiak–Higashi like syndrome") References == External links ==

Sleep state misperception

Sleep state misperception (SSM) is a term in the International Classification of Sleep Disorders (ICSD) most commonly used for people who mistakenly perceive their sleep as wakefulness, though it has been proposed that it be applied to those who severely overestimate their sleep time as well ("positive" sleep state misperception). While most sleepers with this condition will report not having slept in the previous night at all or having slept very little, clinical recordings generally show normal sleep patterns. Though the sleep patterns found in those with SSM have long been considered indistinguishable from those without, some preliminary research suggest there may be subtle differences (see Symptoms and diagnosis: Spectral analysis).Patients are otherwise generally in good health, and any illnesses—such as depression—appear to be more associated with fear of negative consequences of insomnia ("insomnia phobia") than from any actual loss of sleep.Sleep state misperception was adopted by the ICSD to replace two previous diagnostic terminologies: "subjective insomnia complaint without objective findings" and "subjective sleepiness complaint without objective findings."The validity and reliability of sleep state misperception as a pertinent diagnosis has been questioned, with studies finding poor empirical support. Classification Sleep state misperception is classified as an intrinsic dyssomnia. While SSM is regarded a sub-type of insomnia, it is also established as a separate sleep-condition, with distinct pathophysiology. Nonetheless, the value of distinguishing this type of insomnia from other types is debatable due to the relatively low frequency of SSM being reported.Sleep state misperception can also be further broken down into several types, by patients who: report short sleep (subjective insomnia complaint without objective findings)or no sleep at all (subjective total insomnia) report excessive daytime sleepiness (subjective sleepiness complaint without objective findings) report sleeping too much (subjective hypersomnia without objective findings) Validity The validity and reliability of the sleep state misperception as a pertinent medical entity was questioned. A study found poor empirical support for this diagnostic item. Symptoms and diagnosis This sleep disorder frequently applies when patients report not feeling tired despite their subjective perception of not having slept. Generally, they may describe experiencing several years of no sleep, short sleep, or non-restorative sleep. Otherwise, patients appear healthy, both psychiatrically and medically. (That this condition is often asymptomatic could explain why it is relatively unreported.) However, upon clinical observation, it is found that patients may severely overestimate the time they took to fall asleep—often reporting having slept half the amount of time indicated by polysomnogram or electroencephalography (EEG), which may record normal sleep. Observing such discrepancy between subjective and objective reports, clinicians may conclude that the perception of poor sleep is primarily illusionary. Alternatively, some people may report excessive daytime sleepiness or chronic disabling sleepiness, while no sleep disorder has been found to exist. Methods of diagnosing sleepiness objectively, such as the Multiple Sleep Latency Test, do not confirm the symptom—objective sleepiness is not observed despite the complaint.Finally, on the opposite end of the spectrum, other patients may report feeling that they have slept much longer than is observed. It has been proposed that this experience be subclassified under sleep state misperception as "positive sleep state misperception", "reverse sleep state misperception", and "negative sleep state misperception". Diagnostic criteria The patient has a complaint of insomnia while sleep quality and duration are normal. Polysomnographic monitoring demonstrates normal sleep latency, a normal number of arousals and awakenings, and normal sleep duration with or without a multiple sleep latency test that demonstrates a mean sleep latency of greater than 10 minutes. No medical or mental disorder produces the complaint. Other sleep disorders producing insomnia are not present to a degree that would explain the patient’s complaint. Detection and difficulties Detecting sleep state misperception by objective means has been elusive.A 2011 study published in the journal Psychosomatic Medicine has shown that sleep misperception (i.e., underestimation of sleep duration) is prevalent among chronic insomniacs who sleep objectively more than 6 hours in the sleep lab. The psychological profile of these chronic insomniacs with objective normal sleep duration is characterized by depressive, anxious-ruminative traits and poor coping resources. Thus, it appears that not all chronic insomniacs underestimate their sleep duration, and that sleep misperception is a clinical characteristic of chronic insomniacs with objective normal sleep duration. Furthermore, rumination and poor coping resources may play a significant role in sleep misperception. Spectral analysis According to a May 2014 article published in New Scientist, spectral analysis may help clinicians find objective evidence for sleep state misperception: [...] it uncovered [...] subtle differences in the EEGs of sleeping insomniacs: alpha waves – signatures of wakefulness that are supposed to show up only in early sleep – were intruding into deep sleep. [...] [psychologist and sleep researcher Michael] Perlis. But Andrew Krystal of Duke University in Durham, North Carolina, used spectral analysis to quantify just how much they were intruding. Krystals non-sleepers not only had a greater proportion of these alpha disturbances, but the alpha waves were bigger and the delta waves were correspondingly smaller. That wasnt all. When Perlis and other researchers applied spectral analysis algorithms to the EEGs of their sleeping insomniacs, they found different patterns, fast waves known as beta and gamma (Sleep, vol 24, p 110). Normally, these are indicators of consciousness, alertness and even anxiety [...] Like alpha waves, Perlis calls these beta and gamma waves "intrusions" into normal sleep: "Its as if somebody is playing with the switch – boop, boop – flipping at a mad rate between wake and sleep". Distinction from insomnia What is considered objective insomnia, unlike SSM, can easily be confirmed empirically through clinical testing, such as by polysomnogram. Those who experience SSM may believe that they have not slept for extended periods of time, when they in fact do sleep but without perceiving it. For example, while patients who claim little or no sleep may usually acknowledge impaired job performance and daytime drowsiness, sleep state misperceivers often do not.Cases of objective total insomnia are extremely rare. The few that have been recorded have predominantly been ascribed to a rare incurable genetic disorder called fatal familial insomnia, which patients rarely survive for more than 26 months after the onset of illness—often much less. Treatment Behavioral treatment can be effective in some cases. Sedative hypnotics may also help relieve the symptoms. Additionally, education about normal patterns of the sleep-wake cycle may alleviate anxiety in some patients. For patients with severe depression resulting from the fear of having insomnia, electroconvulsive therapy appears to be a safe and effective treatment. Complications A subject who is not being monitored (by a recording or other observer) may not have a way to tell if a treatment is working properly due to the amnesic nature of SSM. The condition may worsen as a result of persistent attempts to treat the symptoms through conventional methods of dealing with insomnia. The prescription of hypnotics or stimulants may lead to drug dependency as a complication.Nonetheless, chronic SSM may increase risk for depression, anxiety, and substance abuse. It has also been noted that patients with this condition may sometimes opt to take medications over other treatments "for the wrong reasons (e.g. because of euphoriant properties)." Epidemiology SSM is poorly understood. As of 2008, there is little to no information regarding risk factors or prevention, though it is believed to be most prevalent among young to middle aged adults.Distribution among the general population and by gender is unknown. About 5% of the clinical population may be affected, though that figure is subject to sampling bias. See also Second wind (sleep) Somniphobia References == External links ==

Blizzard

A blizzard is a severe snowstorm characterized by strong sustained winds and low visibility, lasting for a prolonged period of time—typically at least three or four hours. A ground blizzard is a weather condition where snow is not falling but loose snow on the ground is lifted and blown by strong winds. Blizzards can have an immense size and usually stretch to hundreds or thousands of kilometres. Definition and etymology In the United States, the National Weather Service defines a blizzard as a severe snow storm characterized by strong winds causing blowing snow that results in low visibilities. The difference between a blizzard and a snowstorm is the strength of the wind, not the amount of snow. To be a blizzard, a snow storm must have sustained winds or frequent gusts that are greater than or equal to 56 km/h (35 mph) with blowing or drifting snow which reduces visibility to 400 m or 0.25 mi or less and must last for a prolonged period of time—typically three hours or more. Environment Canada defines a blizzard as a storm with wind speeds exceeding 40 km/h (25 mph) accompanied by visibility of 400 metres (0.25 mi) or less, resulting from snowfall, blowing snow, or a combination of the two. These conditions must persist for a period of at least four hours for the storm to be classified as a blizzard, except north of the arctic tree line, where that threshold is raised to six hours. The Australia Bureau of Meteorology describes a blizzard as, "Violent and very cold wind which is laden with snow, some part, at least, of which has been raised from snow covered ground." While severe cold and large amounts of drifting snow may accompany blizzards, they are not required. Blizzards can bring whiteout conditions, and can paralyze regions for days at a time, particularly where snowfall is unusual or rare. A severe blizzard has winds over 72 km/h (45 mph), near zero visibility, and temperatures of −12 °C (10 °F) or lower. In Antarctica, blizzards are associated with winds spilling over the edge of the ice plateau at an average velocity of 160 km/h (99 mph).Ground blizzard refers to a weather condition where loose snow or ice on the ground is lifted and blown by strong winds. The primary difference between a ground blizzard as opposed to a regular blizzard is that in a ground blizzard no precipitation is produced at the time, but rather all the precipitation is already present in the form of snow or ice at the surface. The Oxford English Dictionary concludes the term blizzard is likely onomatopoeic, derived from the same sense as blow, blast, blister, and bluster; the first recorded use of it for weather dates to 1829, when it was defined as a "violent blow". It achieved its modern definition by 1859, when it was in use in the western United States. The term became common in the press during the harsh winter of 1880–81. United States storm systems In the United States, storm systems powerful enough to cause blizzards usually form when the jet stream dips far to the south, allowing cold, dry polar air from the north to clash with warm, humid air moving up from the south.When cold, moist air from the Pacific Ocean moves eastward to the Rocky Mountains and the Great Plains, and warmer, moist air moves north from the Gulf of Mexico, all that is needed is a movement of cold polar air moving south to form potential blizzard conditions that may extend from the Texas Panhandle to the Great Lakes and Midwest. A blizzard also may be formed when a cold front and warm front mix together and a blizzard forms at the border line. Another storm system occurs when a cold core low over the Hudson Bay area in Canada is displaced southward over southeastern Canada, the Great Lakes, and New England. When the rapidly moving cold front collides with warmer air coming north from the Gulf of Mexico, strong surface winds, significant cold air advection, and extensive wintry precipitation occur. Low pressure systems moving out of the Rocky Mountains onto the Great Plains, a broad expanse of flat land, much of it covered in prairie, steppe and grassland, can cause thunderstorms and rain to the south and heavy snows and strong winds to the north. With few trees or other obstructions to reduce wind and blowing, this part of the country is particularly vulnerable to blizzards with very low temperatures and whiteout conditions. In a true whiteout there is no visible horizon. People can become lost in their own front yards, when the door is only 3 m (10 ft) away, and they would have to feel their way back. Motorists have to stop their cars where they are, as the road is impossible to see. Noreaster blizzards A noreaster is a macro-scale storm that occurs off the New England and Atlantic Canada coastlines. It gets its name from the direction the wind is coming from. The usage of the term in North America comes from the wind associated with many different types of storms some of which can form in the North Atlantic Ocean and some of which form as far south as the Gulf of Mexico. The term is most often used in the coastal areas of New England and Atlantic Canada. This type of storm has characteristics similar to a hurricane. More specifically it describes a low-pressure area whose center of rotation is just off the coast and whose leading winds in the left-forward quadrant rotate onto land from the northeast. High storm waves may sink ships at sea and cause coastal flooding and beach erosion. Notable noreasters include The Great Blizzard of 1888, one of the worst blizzards in U.S. history. It dropped 100–130 cm (40–50 in) of snow and had sustained winds of more than 45 miles per hour (72 km/h) that produced snowdrifts in excess of 50 feet (15 m). Railroads were shut down and people were confined to their houses for up to a week. It killed 400 people, mostly in New York. Historic events 1972 Iran blizzard The 1972 Iran blizzard, which caused 4,000 reported deaths, was the deadliest blizzard in recorded history. Dropping as much as 26 feet (7.9 m) of snow, it completely covered 200 villages. After a snowfall lasting nearly a week, an area the size of Wisconsin was entirely buried in snow. 2008 Afghanistan blizzard The 2008 Afghanistan blizzard, was a fierce blizzard that struck Afghanistan on the 10th of January 2008. Temperatures fell to a low of −30 °C (−22 °F), with up to 180 centimetres (71 in) of snow in the more mountainous regions, killing at least 926 people. It was the third deadliest blizzard in history. The weather also claimed more than 100,000 sheep and goats, and nearly 315,000 cattle died. The Snow Winter of 1880–1881 The winter of 1880–1881 is widely considered the most severe winter ever known in parts of the United States. Many children—and their parents—learned of "The Snow Winter" through the childrens book The Long Winter by Laura Ingalls Wilder, in which the author tells of her familys efforts to survive. The snow arrived in October 1880 and blizzard followed blizzard throughout the winter and into March 1881, leaving many areas snowbound throughout the entire winter. Accurate details in Wilders novel include the blizzards frequency and the deep cold, the Chicago and North Western Railway stopping trains until the spring thaw because the snow made the tracks impassable, the near-starvation of the townspeople, and the courage of her future husband Almanzo and another man, who ventured out on the open prairie in search of a cache of wheat that no one was even sure existed. The October blizzard brought snowfalls so deep that two-story homes had snow up to the second floor windows. No one was prepared for the deep snow so early in the season and farmers all over the region were caught before their crops had even been harvested, their grain milled, or with their fuel supplies for the winter in place. By January the train service was almost entirely suspended from the region. Railroads hired scores of men to dig out the tracks but it was a wasted effort: As soon as they had finished shoveling a stretch of line, a new storm arrived, filling up the line and leaving their work useless. There were no winter thaws and on February 2, 1881, a second massive blizzard struck that lasted for nine days. In the towns the streets were filled with solid drifts to the tops of the buildings and tunneling was needed to secure passage about town. Homes and barns were completely covered, compelling farmers to tunnel to reach and feed their stock. When the snow finally melted in late spring of 1881, huge sections of the plains were flooded. Massive ice jams clogged the Missouri River and when they broke the downstream areas were ravaged. Most of the town of Yankton, in what is now South Dakota, was washed away when the river overflowed its banks. The Storm of the Century The Storm of the Century, also known as the Great Blizzard of 1993, was a large cyclonic storm that formed over the Gulf of Mexico on March 12, 1993, and dissipated in the North Atlantic Ocean on March 15. It is unique for its intensity, massive size and wide-reaching effect. At its height, the storm stretched from Canada towards Central America, but its main impact was on the United States and Cuba. The cyclone moved through the Gulf of Mexico, and then through the Eastern United States before moving into Canada. Areas as far south as northern Alabama and Georgia received a dusting of snow and areas such as Birmingham, Alabama, received up to 12 in (30 cm) with hurricane-force wind gusts and record low barometric pressures. Between Louisiana and Cuba, hurricane-force winds produced high storm surges across northwestern Florida, which along with scattered tornadoes killed dozens of people. In the United States, the storm was responsible for the loss of electric power to over 10 million customers. It is purported to have been directly experienced by nearly 40 percent of the countrys population at that time. A total of 310 people, including 10 from Cuba, perished during this storm. The storm cost $6 to $10 billion in damages. List of blizzards North America 1700 to 1799 The Great Snow 1717 series of four snowstorms between February 27 and March 7, 1717. There were reports of about five feet of snow already on the ground when the first of the storms hit. By the end, there were about ten feet of snow and some drifts reaching 25 feet (7.6 m), burying houses entirely. In the colonial era, this storm made travel impossible until the snow simply melted. Blizzard of 1765. March 24, 1765. Affected area from Philadelphia to Massachusetts. High winds and over 2 feet (61 cm) of snowfall recorded in some areas. Blizzard of 1772. "The Washington and Jefferson Snowstorm of 1772". January 26–29, 1772. One of largest D.C. and Virginia area snowstorms ever recorded. Snow accumulations of 3 feet (91 cm) recorded. The "Hessian Storm of 1778". December 26, 1778. Severe blizzard with high winds, heavy snows and bitter cold extending from Pennsylvania to New England. Snow drifts reported to be 15 feet (4.6 m) high in Rhode Island. Storm named for stranded Hessian troops in deep snows stationed in Rhode Island during the Revolutionary War. The Great Snow of 1786. December 4–10, 1786. Blizzard conditions and a succession of three harsh snowstorms produced snow depths of 2 feet (61 cm) to 4 feet (120 cm) from Pennsylvania to New England. Reportedly of similar magnitude of 1717 snowstorms. The Long Storm of 1798. November 19–21, 1798. Heavy snowstorm produced snow from Maryland to Maine. 1800 to 1850 Blizzard of 1805. January 26–28, 1805. Cyclone brought heavy snowstorm to New York City and New England. Snow fell continuously for two days where over 2 feet (61 cm) of snow accumulated. New York City Blizzard of 1811. December 23–24, 1811. Severe blizzard conditions reported on Long Island, in New York City, and southern New England. Strong winds and tides caused damage to shipping in harbor. Luminous Blizzard of 1817. January 17, 1817. In Massachusetts and Vermont, a severe snowstorm was accompanied by frequent lightning and heavy thunder. St. Elmos fire reportedly lit up trees, fence posts, house roofs, and even people. John Farrar professor at Harvard, recorded the event in his memoir in 1821. Great Snowstorm of 1821. January 5–7, 1821. Extensive snowstorm and blizzard spread from Virginia to New England. Winter of Deep Snow in 1830. December 29, 1830. Blizzard storm dumped 36 inches (91 cm) in Kansas City and 30 inches (76 cm) in Illinois. Areas experienced repeated storms thru mid-February 1831. "The Great Snowstorm of 1831" January 14–16, 1831. Produced snowfall over widest geographic area that was only rivaled, or exceeded by, the 1993 Blizzard. Blizzard raged from Georgia, to Ohio Valley, all the way to Maine. "The Big Snow of 1836" January 8–10, 1836. Produced 30 inches (76 cm) to 40 inches (100 cm) of snowfall in interior New York, northern Pennsylvania, and western New England. Philadelphia got a reported 15 inches (38 cm) and New York City 2 feet (61 cm) of snow. 1851 to 1900 Plains Blizzard of 1856. December 3–5, 1856. Severe blizzard-like storm raged for three days in Kansas and Iowa. Early pioneers suffered. "The Cold Storm of 1857" January 18–19, 1857. Produced severe blizzard conditions from North Carolina to Maine. Heavy snowfalls reported in east coast cities. Midwest Blizzard of 1864. January 1, 1864. Gale-force winds, driving snow, and low temperatures all struck simultaneously around Chicago, Wisconsin and Minnesota. Plains Blizzard of 1873. January 7, 1873. Severe blizzard struck the Great Plains. Many pioneers from the east were unprepared for the storm and perished in Minnesota and Iowa. Great Plains Easter Blizzard of 1873. April 13, 1873 Seattle Blizzard of 1880. January 6, 1880. Seattle areas greatest snowstorm to date. An estimated 4 feet (120 cm) fell around the town. Many barns collapsed and all transportation halted. The Snow Winter of 1880–1881. Laura Ingalls Wilders book The Long Winter details the effects of the blizzards in the Dakota Territory in the winter of 1880–1881. In the three year winter period from December 1885 to March 1888, the Great Plains and Eastern United States suffered a series of the worst blizzards in this nations history ending with the Schoolhouse Blizzard and the Great Blizzard of 1888. The massive explosion of the volcano Krakatoa in the South Pacific late in August 1883 is a suspected cause of these huge blizzards during these several years. The clouds of ash it emitted continued to circulate around the world for many years. Weather patterns continued to be chaotic for years, and temperatures did not return to normal until 1888. Record rainfall was experienced in Southern California during July 1883 to June 1884. The Krakatoa eruption injected an unusually large amount of sulfur dioxide (SO2) gas high into the stratosphere which reflects sunlight and helped cool the planet over the next few years until the suspended atmospheric sulfur fell to ground. Plains Blizzard of late 1885. In Kansas, heavy snows of late 1885 had piled drifts 10 feet (3.0 m) high. Kansas Blizzard of 1886. First week of January 1886. Reported that 80 percent of the cattle were frozen to death in that state alone from the cold and snow. January 1886 Blizzard. January 9, 1886. Same system as Kansas 1886 Blizzard that traveled eastward. Great Plains Blizzards of late 1886. On November 13, 1886, it reportedly began to snow and did not stop for a month in the Great Plains region. Great Plains Blizzard of 1887. January 9–11, 1887. Reported 72-hour blizzard that covered parts of the Great Plains in more than 16 inches (41 cm) of snow. Winds whipped and temperatures dropped to around 50 °F (10 °C). So many cows that were not killed by the cold soon died from starvation. When spring arrived, millions of the animals were dead, with around 90 percent of the open ranges cattle rotting where they fell. Those present reported carcasses as far as the eye could see. Dead cattle clogged up rivers and spoiled drinking water. Many ranchers went bankrupt and others simply called it quits and moved back east. The "Great Die-Up" from the blizzard effectively concluded the romantic period of the great Plains cattle drives. Schoolhouse Blizzard of 1888 North American Great Plains. January 12–13, 1888. What made the storm so deadly was the timing (during work and school hours), the suddenness, and the brief spell of warmer weather that preceded it. In addition, the very strong wind fields behind the cold front and the powdery nature of the snow reduced visibilities on the open plains to zero. People ventured from the safety of their homes to do chores, go to town, attend school, or simply enjoy the relative warmth of the day. As a result, thousands of people—including many schoolchildren—got caught in the blizzard. Great Blizzard of March 1888 March 11–14, 1888. One of the most severe recorded blizzards in the history of the United States. On March 12, an unexpected northeaster hit New England and the mid-Atlantic, dropping up to 50 in (130 cm) of snow in the space of three days. New York City experienced its heaviest snowfall recorded to date at that time, all street railcars were stranded, and the storm led to the creation of the NYC subway system. Snowdrifts reached up to the second story of some buildings. Some 400 people died from this blizzard, including many sailors aboard vessels that were beset by gale-force winds and turbulent seas. Great Blizzard of 1899 February 11–14, 1899. An extremely unusual blizzard in that it reached into the far southern states of the US. It hit in February, and the area around Washington, D.C., experienced 51 hours straight of snowfall. The port of New Orleans was totally iced over; revelers participating in the New Orleans Mardi Gras had to wait for the parade routes to be shoveled free of snow. Concurrent with this blizzard was the extremely cold arctic air. Many city and state record low temperatures date back to this event, including all-time records for locations in the Midwest and South. State record lows: Nebraska reached −47 °F (−44 °C), Ohio experienced −39 °F (−39 °C), Louisiana bottomed out at −16 °F (−27 °C), and Florida dipped below zero to −2 °F (−19 °C). 1901 to 1939 Great Lakes Storm of 1913 November 7–10, 1913. “The White Hurricane” of 1913 was the deadliest and most destructive natural disaster ever to hit the Great Lakes Basin in the Midwestern United States and the Canadian province of Ontario. It produced 90 mph (140 km/h) wind gusts, waves over 35 ft (11 m) high, and whiteout snowsqualls. It killed more than 250 people, destroyed 19 ships, and stranded 19 others. Blizzard of 1918. January 11, 1918. Vast blizzard-like storm moved through Great Lakes and Ohio Valley. 1920 North Dakota blizzard March 15–18, 1920 Knickerbocker Storm January 27–28, 1922 1940 to 1949 Armistice Day Blizzard of 1940 November 10–12, 1940. Took place in the Midwest region of the United States on Armistice Day. This "Panhandle hook" winter storm cut a 1,000 mi-wide path (1,600 km) through the middle of the country from Kansas to Michigan. The morning of the storm was unseasonably warm but by mid afternoon conditions quickly deteriorated into a raging blizzard that would last into the next day. A total of 145 deaths were blamed on the storm, almost a third of them duck hunters who had taken time off to take advantage of the ideal hunting conditions. Weather forecasters had not predicted the severity of the oncoming storm, and as a result the hunters were not dressed for cold weather. When the storm began many hunters took shelter on small islands in the Mississippi River, and the 50 mph (80 km/h) winds and 5-foot (1.5 m) waves overcame their encampments. Some became stranded on the islands and then froze to death in the single-digit temperatures that moved in over night. Others tried to make it to shore and drowned. North American blizzard of 1947 December 25–26, 1947. Was a record-breaking snowfall that began on Christmas Day and brought the Northeast United States to a standstill. Central Park in New York City got 26 inches (66 cm) of snowfall in 24 hours with deeper snows in suburbs. It was not accompanied by high winds, but the snow fell steadily with drifts reaching 10 ft (3.0 m). Seventy-seven deaths were attributed to the blizzard. The Blizzard of 1949 - The first blizzard started on Sunday, January 2, 1949; it lasted for three days. It was followed by two more months of blizzard after blizzard with high winds and bitter cold. Deep drifts isolated southeast Wyoming, northern Colorado, western South Dakota and western Nebraska, for weeks. Railroad tracks and roads were all drifted in with drifts of 20 feet (6.1 m) and more. Hundreds of people that had been traveling on trains were stranded. Motorists that had set out on January 2 found their way to private farm homes in rural areas and hotels and other buildings in towns; some dwellings were so crowded that there wasnt enough room for all to sleep at once. It would be weeks before they were plowed out. The Federal government quickly responded with aid, airlifting food and hay for livestock. The total rescue effort involved numerous volunteers and local agencies plus at least ten major state and federal agencies from the U.S. Army to the National Park Service. Private businesses, including railroad and oil companies, also lent manpower and heavy equipment to the work of plowing out. The official death toll was 76 people and one million livestock. Youtube video Storm of the Century - the Blizzard of 49 Storm of the Century - the Blizzard of 49 1950 to 1959 Great Appalachian Storm of November 1950 November 24–30, 1950 March 1958 Noreaster blizzard March 18–21, 1958. The Mount Shasta California Snowstorm of 1959 – The storm dumped 189 inches (480 cm) of snow on Mount Shasta. The bulk of the snow fell on unpopulated mountainous areas, barely disrupting the residents of the Mount Shasta area. The amount of snow recorded is the largest snowfall from a single storm in North America. 1960 to 1969 March 1960 Noreaster blizzard March 2–5, 1960 December 1960 Noreaster blizzard December 12–14, 1960. Wind gusts up to 50 miles per hour (80 km/h). March 1962 Noreaster Great March Storm of 1962 – Ash Wednesday. North Carolina and Virginia blizzards. Struck during Spring high tide season and remained mostly stationary for almost 5 days causing significant damage along eastern coast, Assateague island was under water, and dumped 42 inches (110 cm) of snow in Virginia. North American blizzard of 1966 January 27–31, 1966 Chicago Blizzard of 1967 January 26–27, 1967 February 1969 noreaster February 8–10, 1969 March 1969 Noreaster blizzard March 9, 1969 December 1969 Noreaster blizzard December 25–28, 1969. 1970 to 1979 The Great Storm of 1975 known as the "Super Bowl Blizzard" or "Minnesotas Storm of the Century". January 9–12, 1975. Wind chills of −50 °F (−46 °C) to −80 °F (−62 °C) recorded, deep snowfalls. Groundhog Day gale of 1976 February 2, 1976 Buffalo Blizzard of 1977 January 28 – February 1, 1977. There were several feet of packed snow already on the ground, and the blizzard brought with it enough snow to reach Buffalos record for the most snow in one season – 199.4 inches (506 cm). Great Blizzard of 1978 also called the "Cleveland Superbomb". January 25–27, 1978. Was one of the worst snowstorms the Midwest has ever seen. Wind gusts approached 100 mph (160 km/h), causing snowdrifts to reach heights of 25 ft (7.6 m) in some areas, making roadways impassable. Storm reached maximum intensity over southern Ontario Canada. Northeastern United States Blizzard of 1978 – February 6–7, 1978. Just one week following the Cleveland Superbomb blizzard, New England was hit with its most severe blizzard in 90 years since 1888. Chicago Blizzard of 1979 January 13–14, 1979 1980 to 1989 February 1987 Noreaster blizzard February 22–24, 1987 1990 to 1999 1991 Halloween blizzard Upper Mid-West US, October 31 – November 3, 1991 December 1992 Noreaster blizzard December 10–12, 1992 1993 Storm of the Century March 12–15, 1993. While the southern and eastern U.S. and Cuba received the brunt of this massive blizzard, the Storm of the Century impacted a wider area than any in recorded history. February 1995 Noreaster blizzard February 3–6, 1995 Blizzard of 1996 January 6–10, 1996 April Fools Day Blizzard March 31 – April 1, 1997. US East Coast 1997 Western Plains winter storms October 24–26, 1997 Mid West Blizzard of 1999 January 2–4, 1999 2000 to 2009 January 25, 2000 Southeastern United States winter storm January 25, 2000. North Carolina and Virginia December 2000 Noreaster blizzard December 27–31, 2000 North American blizzard of 2003 February 14–19, 2003 (Presidents Day Storm II) December 2003 Noreaster blizzard December 6–7, 2003 North American blizzard of 2005 January 20–23, 2005 North American blizzard of 2006 February 11–13, 2006 Early winter 2006 North American storm complex Late November 2006 Colorado Holiday Blizzards (2006–07) December 20–29, 2006 Colorado February 2007 North America blizzard February 12–20, 2007 January 2008 North American storm complex January, 2008 West Coast US North American blizzard of 2008 March 6–10, 2008 2009 Midwest Blizzard 6–8 December 2009, a bomb cyclogenesis event that also affected parts of Canada North American blizzard of 2009 December 16–20, 2009 2009 North American Christmas blizzard December 22–28, 2009 2010 to 2019 February 5–6, 2010 North American blizzard February 5–6, 2010 Referred to at the time as Snowmageddon was a Category 3 ("major") noreaster and severe weather event. February 9–10, 2010 North American blizzard February 9–10, 2010 February 25–27, 2010 North American blizzard February 25–27, 2010 October 2010 North American storm complex October 23–28, 2010 December 2010 North American blizzard December 26–29, 2010 January 31 – February 2, 2011 North American blizzard January 31 – February 2, 2011. Groundhog Day Blizzard of 2011 2011 Halloween noreaster October 28 – Nov 1, 2011 Hurricane Sandy October 29–31, 2012. West Virginia, western North Carolina, and southwest Pennsylvania received heavy snowfall and blizzard conditions from this hurricane November 2012 noreaster November 7–10, 2012 December 17–22, 2012 North American blizzard December 17–22, 2012 Late December 2012 North American storm complex December 25–28, 2012 February 2013 noreaster February 7–20, 2013 February 2013 Great Plains blizzard February 19 – March 6, 2013 March 2013 noreaster March 6, 2013 October 2013 North American storm complex October 3–5, 2013 Buffalo, NY blizzard of 2014. Buffalo got over 6 feet (1.8 m) of snow during November 18–20, 2014. January 2015 North American blizzard January 26–27, 2015 Late December 2015 North American storm complex December 26–27, 2015 Was one of the most notorious blizzards in the state of New Mexico and West Texas ever reported. It had sustained winds of over 30 miles per hour (48 km/h) and continuous snow precipitation that lasted over 30 hours. Dozens of vehicles were stranded in small county roads in the areas of Hobbs, Roswell, and Carlsbad New Mexico. Strong sustained winds destroyed various mobile homes. January 2016 United States blizzard January 20–23, 2016 February 2016 North American storm complex February 1–8, 2016 February 2017 North American blizzard February 6–11, 2017 March 2017 North American blizzard March 9–16, 2017 Early January 2018 nor’easter January 3–6, 2018 March 2019 North American blizzard March 8–16, 2019 April 2019 North American blizzard April 10–14, 2019 2020 to present December 5–6, 2020 noreaster December 5–6, 2020 January 31 – February 3, 2021 noreaster January 31 – February 3, 2021 February 13–17, 2021 North American winter storm February 13–17, 2021 March 2021 North American blizzard March 11–14, 2021 January 2022 North American blizzard January 27–30, 2022 Canada The Eastern Canadian Blizzard of 1971 – Dumped a foot and a half (45.7 cm) of snow on Montreal and more than two feet (61 cm) elsewhere in the region. The blizzard caused the cancellation of a Montreal Canadiens hockey game for the first time since 1918. Saskatchewan blizzard of 2007 – January 10, 2007 Canada United Kingdom Great Frost of 1709 Blizzard of January 1881 Winter of 1894–95 in the United Kingdom Winter of 1946–1947 in the United Kingdom Winter of 1962–1963 in the United Kingdom January 1987 Southeast England snowfall Winter of 1990–91 in Western Europe February 2009 Great Britain and Ireland snowfall Winter of 2009–10 in Great Britain and Ireland Winter of 2010–11 in Great Britain and Ireland Early 2012 European cold wave Other locations 1954 Romanian blizzard 1972 Iran blizzard Winter of 1990–1991 in Western Europe 2008 Afghanistan blizzard 2008 Chinese winter storms Winter storms of 2009–2010 in East Asia See also Cold wave Lake-effect snow Noreaster European windstorm Whiteout (weather) Blowing snow advisory Ground blizzard Severe weather terminology (Canada) Snowsquall Blowing snow List of blizzards References External links Digital Snow Museum Photos of historic blizzards and snowstorms. Farmers Almanac List of Worst Blizzards in the United States United States Search and Rescue Task Force: About Blizzards A Historical Review On The Origin and Definition of the Word Blizzard Archived 2012-04-25 at the Wayback Machine Dr Richard Wild

Ophthalmia nodosa

Ophthalmia nodosa is a cutaneous condition characterized by inflammation of the eye due to lodging of (for example) caterpillar hairs in the conjunctiva, cornea, or iris. See also Bristleworm sting List of cutaneous conditions == References ==

Myalgia

Myalgia (also called muscle pain and muscle ache in laymans terms) is the medical term for muscle pain. Myalgia is a symptom of many diseases. The most common cause of acute myalgia is the overuse of a muscle or group of muscles; another likely cause is viral infection, especially when there has been no trauma. Long-lasting myalgia can be caused by metabolic myopathy, some nutritional deficiencies, and chronic fatigue syndrome. Causes The most common causes of myalgia are overuse, injury, and strain. Myalgia might also be caused by allergies, diseases, medications, or as a response to a vaccination. Dehydration at times results in muscle pain as well, especially for people involved in extensive physical activities such as workout. Muscle pain is also a common symptom in a variety of diseases, including infectious diseases, such as influenza, muscle abscesses, Lyme disease, malaria, trichinosis or poliomyelitis; autoimmune diseases, such as celiac disease, systemic lupus erythematosus, Sjögrens syndrome or polymyositis; gastrointestinal diseases, such as non-celiac gluten sensitivity (which can also occur without digestive symptoms) and inflammatory bowel disease (including Crohns disease and ulcerative colitis).The most common causes are: Overuse Overuse of a muscle is using it too much, too soon or too often. One example is repetitive strain injury. See also: Exercise Weight lifting Injury The most common causes of myalgia by injury are: sprains and strains. Autoimmune Multiple sclerosis (neurologic pain interpreted as muscular) Myositis Mixed connective tissue disease Lupus erythematosus Fibromyalgia syndrome Familial Mediterranean fever Polyarteritis nodosa Devics disease Morphea Sarcoidosis Metabolic defect Carnitine palmitoyltransferase II deficiency Conns syndrome Adrenal insufficiency Hyperthyroidism Hypothyroidism Diabetes Hypogonadism Postorgasmic illness syndrome Other Chronic fatigue syndrome (aka myalgic encephalomyelitis) Channelopathy Ehlers Danlos Syndrome Stickler Syndrome Hypokalemia Hypotonia Exercise intolerance Mastocytosis Peripheral neuropathy Eosinophilia myalgia syndrome Barcoo Fever Herpes Hemochromatosis Delayed onset muscle soreness HIV/AIDS Generalized anxiety disorder Tumor-induced osteomalacia Hypovitaminosis D Infarction Withdrawal syndrome from certain drugs Sudden cessation of high-dose corticosteroids, opioids, barbiturates, benzodiazepines, caffeine, or alcohol can induce myalgia. Treatment When the cause of myalgia is unknown, it should be treated symptomatically. Common treatments include heat, rest, paracetamol, NSAIDs, massage, cryotherapy and muscle relaxants. See also Arthralgia Myopathy Myositis References == External links ==

Hyperglycemia

Hyperglycemia is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a blood sugar level higher than 11.1 mmol/L (200 mg/dL), but symptoms may not start to become noticeable until even higher values such as 13.9–16.7 mmol/L (~250–300 mg/dL). A subject with a consistent range between ~5.6 and ~7 mmol/L (100–126 mg/dL) (American Diabetes Association guidelines) is considered slightly hyperglycemic, and above 7 mmol/L (126 mg/dL) is generally held to have diabetes. For diabetics, glucose levels that are considered to be too hyperglycemic can vary from person to person, mainly due to the persons renal threshold of glucose and overall glucose tolerance. On average, however, chronic levels above 10–12 mmol/L (180–216 mg/dL) can produce noticeable organ damage over time. Signs and symptoms The degree of hyperglycemia can change over time depending on the metabolic cause, for example, impaired glucose tolerance or fasting glucose, and it can depend on treatment. Temporary hyperglycemia is often benign and asymptomatic. Blood glucose levels can rise well above normal and cause pathological and functional changes for significant periods without producing any permanent effects or symptoms. During this asymptomatic period, an abnormality in carbohydrate metabolism can occur, which can be tested by measuring plasma glucose. Chronic hyperglycemia at above normal levels can produce a very wide variety of serious complications over a period of years, including kidney damage, neurological damage, cardiovascular damage, damage to the retina or damage to feet and legs. Diabetic neuropathy may be a result of long-term hyperglycemia. Impairment of growth and susceptibility to certain infections can occur as a result of chronic hyperglycemia.Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). It is most often seen in persons who have uncontrolled insulin-dependent diabetes.The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad: Polyphagia – frequent hunger, especially pronounced hunger Polydipsia – frequent thirst, especially excessive thirst Polyuria – increased volume of urination (not an increased frequency, although it is a common consequence) Blurred vision Fatigue Restlessness Weight loss or weight gain Poor wound healing (cuts, scrapes, etc.) Dry mouth Dry or itchy skin Tingling in feet or heels Erectile dysfunction Recurrent infections, external ear infections (swimmers ear) Delayed gastric emptying Cardiac arrhythmia Stupor Coma Seizures Abnormal movements: chorea, choreoathetosis, ballism, dystonia, opsoclonus-myoclonus, parkinsonism, hemifacial spasm, and Holmes tremorFrequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response.Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys, which leads to the presence of glucose in the urine. This produces an osmotic diuresis.Signs and symptoms of diabetic ketoacidosis may include: Ketoacidosis Kussmaul hyperventilation (deep, rapid breathing) Confusion or a decreased level of consciousness Dehydration due to glycosuria and osmotic diuresis Increased thirst Fruity smelling breath odor Nausea and vomiting Abdominal pain Impairment of cognitive function, along with increased sadness and anxiety Weight lossHyperglycemia causes a decrease in cognitive performance, specifically in processing speed, executive function, and performance. Decreased cognitive performance may cause forgetfulness and concentration loss. Complications In untreated hyperglycemia, a condition called ketoacidosis may develop because decreased insulin levels increase the activity of hormone sensitive lipase. The degradation of triacylglycerides by hormone-sensitive lipase produces free fatty acids that are eventually converted to acetyl-coA by beta-oxidation.Ketoacidosis is a life-threatening condition which requires immediate treatment. Symptoms include: shortness of breath, breath that smells fruity (such as pear drops), nausea and vomiting, and very dry mouth. Chronic hyperglycemia (high blood sugar) injures the heart in patients without a history of heart disease or diabetes and is strongly associated with heart attacks and death in subjects with no coronary heart disease or history of heart failure.Also, a life-threatening consequence of hyperglycemia can be nonketotic hyperosmolar syndrome.Perioperative hyperglycemia has been associated with immunosuppression, increased infections, osmotic diuresis, delayed wound healing, delayed gastric emptying, sympatho-adrenergic stimulation, and increased mortality. In addition, it reduces skin graft success, exacerbates brain, spinal cord, and renal damage by ischemia, worsens neurologic outcomes in traumatic head injuries, and is associated with postoperative cognitive dysfunction following CABG. Causes Hyperglycemia may be caused by: diabetes, various (non-diabetic) endocrine disorders (insulin resistance and thyroid, adrenal, pancreatic, and pituitary disorders), sepsis and certain infections, intracranial diseases (e.g. encephalitis, brain tumors (especially if near the pituitary gland), brain haemorrhages, and meningitis) (frequently overlooked), convulsions, end-stage terminal disease, prolonged/major surgeries, excessive eating, severe stress, and physical trauma. Endocrine Chronic, persistent hyperglycaemia is most often a result of diabetes. Several hormones act to increase blood glucose levels and may thus cause hyperglycaemia when present in excess, including: cortisol, catecholamines, growth hormone, glucagon, and thyroid hormones. Hyperglycaemia may thus be seen in: Cushings syndrome, pheochromocytoma, acromegaly, hyperglucagonemia, and hyperthyroidism. Diabetes mellitus Chronic hyperglycemia that persists even in fasting states is most commonly caused by diabetes mellitus. In fact, chronic hyperglycemia is the defining characteristic of the disease. Intermittent hyperglycemia may be present in prediabetic states. Acute episodes of hyperglycemia without an obvious cause may indicate developing diabetes or a predisposition to the disorder.In diabetes mellitus, hyperglycemia is usually caused by low insulin levels (diabetes mellitus type 1) and/or by resistance to insulin at the cellular level (diabetes mellitus type 2), depending on the type and state of the disease. Low insulin levels and/or insulin resistance prevent the body from converting glucose into glycogen (a starch-like source of energy stored mostly in the liver), which in turn makes it difficult or impossible to remove excess glucose from the blood. With normal glucose levels, the total amount of glucose in the blood at any given moment is only enough to provide energy to the body for 20–30 minutes, and so glucose levels must be precisely maintained by the bodys internal control mechanisms. When the mechanisms fail in a way that allows glucose to rise to abnormal levels, hyperglycemia is the result.Ketoacidosis may be the first symptom of immune-mediated diabetes, particularly in children and adolescents. Also, patients with immune-mediated diabetes, can change from modest fasting hyperglycemia to severe hyperglycemia and even ketoacidosis as a result of stress or an infection. Insulin resistance Obesity has been contributing to increased insulin resistance in the global population. Insulin resistance increases hyperglycemia because the body becomes over saturated by glucose. Insulin resistance desensitizes insulin receptors, preventing insulin from lowering blood sugar levels.The leading cause of hyperglycemia in type 2 diabetes is the failure of insulin to suppress glucose production by glycolysis and gluconeogenesis due to insulin resistance. Insulin normally inhibits glycogenolysis, but fails to do so in a condition of insulin resistance, resulting in increased glucose production. In the liver, Fox06 normally promotes gluconeogenesis in the fasted state, but insulin blocks Fox06 upon feeding. In a condition of insulin resistance insulin fails to block Fox06, resulting in continued gluconeogenesis even upon feeding. Medications Certain medications increase the risk of hyperglycemia, including: corticosteroids, octreotide, beta blockers, epinephrine, thiazide diuretics, statins, niacin, pentamidine, protease inhibitors, L-asparaginase, and antipsychotics. The acute administration of stimulants such as amphetamines typically produces hyperglycemia; chronic use, however, produces hypoglycemia. Thiazides are used to treat type 2 diabetes but it also causes severe hyperglycemia. Stress A high proportion of patients with an acute stress such as stroke or myocardial infarction may develop hyperglycemia, even in the absence of a diagnosis of diabetes. (Or perhaps stroke or myocardial infarction was caused by hyperglycemia and undiagnosed diabetes.) Human and animal studies suggest that this is not benign, and that stress-induced hyperglycemia is associated with a high risk of mortality after both stroke and myocardial infarction. Somatostatinomas and aldosteronoma-induced hypokalemia can cause hyperglycemia but usually disappears after the removal of the tumour.Stress causes hyperglycaemia via several mechanisms, including through metabolic and hormonal changes, and via increased proinflammatory cytokines that interrupt carbohydrate metabolism, leading to excessive glucose production and reduced uptake in tissues, can cause hyperglycemia.Hormones such as the growth hormone, glucagon, cortisol and catecholamines, can cause hyperglycemia when they are present in the body in excess amounts. Diagnosis Monitoring It is critical for patients who monitor glucose levels at home to be aware of which units of measurement their glucose meter uses. Glucose levels are measured in either: Millimoles per liter (mmol/L) is the SI standard unit used in most countries around the world. Milligrams per deciliter (mg/dL) is used in some countries such as the United States, Japan, France, Egypt and Colombia.Scientific journals are moving towards using mmol/L; some journals now use mmol/L as the primary unit but quote mg/dL in parentheses.Glucose levels vary before and after meals, and at various times of day; the definition of "normal" varies among medical professionals. In general, the normal range for most people (fasting adults) is about 4 to 6 mmol/L or 80 to 110 mg/dL. (where 4 mmol/L or 80 mg/dL is "optimal".) A subject with a consistent range above 7 mmol/L or 126 mg/dL is generally held to have hyperglycemia, whereas a consistent range below 4 mmol/L or 70 mg/dL is considered hypoglycemic. In fasting adults, blood plasma glucose should not exceed 7 mmol/L or 126 mg/dL. Sustained higher levels of blood sugar cause damage to the blood vessels and to the organs they supply, leading to the complications of diabetes.Chronic hyperglycemia can be measured via the HbA1c test. The definition of acute hyperglycemia varies by study, with mmol/L levels from 8 to 15 (mg/dL levels from 144 to 270).Defects in insulin secretion, insulin action, or both, results in hyperglycemia. Chronic hyperglycemia can be measured by clinical urine tests which can detect sugar in the urine or microalbuminuria which could be a symptom of diabetes. Treatment Treatment of hyperglycemia requires elimination of the underlying cause, such as diabetes. Acute hyperglycemia can be treated by direct administration of insulin in most cases. Severe hyperglycemia can be treated with oral hypoglycemic therapy and lifestyle modification. In diabetes mellitus (by far the most common cause of chronic hyperglycemia), treatment aims at maintaining blood glucose at a level as close to normal as possible, in order to avoid serious long-term complications. This is done by a combination of proper diet, regular exercise, and insulin or other medication such as metformin, etc.Those with hyperglycaemia can be treated using sulphonylureas or metformin or both. These drugs help by improving glycaemic control. Dipeptidyl peptidase-4 inhibitor alone or in combination with basal insulin can be used as a treatment for hyperglycemia with patients still in hospital.Hyperglycemia can also be improved through minor lifestyle changes. Increasing aerobic exercise to at least 30 minutes a day causes the body to make better use of accumulated glucose since the glucose is being converted to energy by the muscles. Calorie monitoring, with restriction as necessary, can reduce over-eating, which contributes to hyperglycemia.Diets higher in healthy unsaturated fats and whole wheat carbohydrates such as the Mediterranean diet can help reduce carbohydrate intake to better control hyperglycemia. Diets such as intermittent fasting and ketogenic diet help reduce calorie consumption which could significantly reduce hyperglycemia. Carbohydrates are the main cause for hyperglycemia—non-whole-wheat items should be substituted for whole-wheat items. Although fruits are a part of a complete nutritious diet, fruit intake should be limited due to high sugar content. Epidemiology Environmental factors Hyperglycemia is lower in higher income groups since there is access to better education, healthcare and resources. Low-middle income groups are more likely to develop hyperglycemia, due in part to a limited access to education and a reduced availability of healthy food options. Living in warmer climates can reduce hyperglycemia due to increased physical activity while people are less active in colder climates. Population Hyperglycemia is one of the main symptoms of diabetes and it has substantially affected the population making it an epidemic due to the populations increased calorie consumption. Healthcare providers are trying to work more closely with people allowing them more freedom with interventions that suit their lifestyle. As physical inactivity and calorie consumption increases it makes individuals more susceptible to developing hyperglycemia. Hyperglycemia is caused by type 1 diabetes and non-whites have a higher susceptibility for it. Etymology The origin of the term is Greek: prefix ὑπέρ- hyper- "over-", γλυκός glycos "sweet wine, must", αἷμα haima "blood", -ία, -εια -ia suffix for abstract nouns of feminine gender. See also Prediabetes Reference ranges for blood tests References External links Hyperglycemia in infants – from MedlinePlus

Laryngocele

A laryngocele is a congenital anomalous air sac communicating with the cavity of the larynx, which may bulge outward on the neck.It may also be acquired, as seen in glassblowers, due to continual forced expiration producing increased pressures in the larynx which leads to dilatation of the laryngeal ventricle (sinus of Morgagni). It is also seen in people with chronic obstructive airway disease. Additional images References == External links ==

Long QT syndrome

Long QT syndrome (LQTS) is a condition affecting repolarization (relaxing) of the heart after a heartbeat, giving rise to an abnormally lengthy QT interval. It results in an increased risk of an irregular heartbeat which can result in fainting, drowning, seizures, or sudden death. These episodes can be triggered by exercise or stress. Some rare forms of LQTS are associated with other symptoms and signs including deafness and periods of muscle weakness.Long QT syndrome may be present at birth or develop later in life. The inherited form may occur by itself or as part of larger genetic disorder. Onset later in life may result from certain medications, low blood potassium, low blood calcium, or heart failure. Medications that are implicated include certain antiarrhythmics, antibiotics, and antipsychotics. LQTS can be diagnosed using an electrocardiogram (EKG) if a corrected QT interval of greater than 480–500 milliseconds is found, but clinical findings, other EKG features, and genetic testing may confirm the diagnosis with shorter QT intervals.Management may include avoiding strenuous exercise, getting sufficient potassium in the diet, the use of beta blockers, or an implantable cardiac defibrillator. For people with LQTS who survive cardiac arrest and remain untreated, the risk of death within 15 years is greater than 50%. With proper treatment this decreases to less than 1% over 20 years.Long QT syndrome is estimated to affect 1 in 7,000 people. Females are affected more often than males. Most people with the condition develop symptoms before they are 40 years old. It is a relatively common cause of sudden death along with Brugada syndrome and arrhythmogenic right ventricular dysplasia. In the United States it results in about 3,500 deaths a year. The condition was first clearly described in 1957. Signs and symptoms Many people with long QT syndrome have no signs or symptoms. When symptoms occur, they are generally caused by abnormal heart rhythms (arrhythmias), most commonly a form of ventricular tachycardia called Torsades de pointes (TdP). If the arrhythmia reverts to a normal rhythm spontaneously the affected person may experience lightheadedness (known as presyncope) or faint which may be preceded by a fluttering sensation in the chest. If the arrhythmia continues, the affected person may experience a cardiac arrest, which if untreated may lead to sudden death. Those with LQTS may also experience seizure-like activity (non-epileptic seizure) as a result of reduced blood flow to the brain during an arrhythmia. Epilepsy is also associated with certain types of long QT syndrome.The arrhythmias that lead to faints and sudden death are more likely to occur in specific circumstances, in part determined by which genetic variant is present. While arrhythmias can occur at any time, in some forms of LQTS arrhythmias are more commonly seen in response to exercise or mental stress (LQT1), in other forms following a sudden loud noise (LQT2), and in some forms during sleep or immediately upon waking (LQT3).Some rare forms of long QT syndrome affect other parts of the body, leading to deafness in the Jervell and Lange-Nielsen form of the condition, and periodic paralysis in the Andersen–Tawil (LQT7) form. Risk for arrhythmias While those with long QT syndrome have an increased risk of developing abnormal heart rhythms the absolute risk of arrhythmias is very variable. The strongest predictor of whether someone will develop TdP is whether they have experienced this arrhythmia or another form of cardiac arrest in the past. Those with LQTS who have experienced syncope without an ECG having been recorded at the time are also at higher risk, as syncope in these cases is frequently due to an undocumented self-terminating arrhythmia.In addition to a history of arrhythmias, the extent to which the QT is prolonged predicts risk. While some have QT intervals that are very prolonged, others have only slight QT prolongation, or even a normal QT interval at rest (concealed LQTS). Those with the longest QT intervals are more likely to experience TdP, and a corrected QT interval of greater than 500 ms is thought to represent those at higher risk. Despite this, those with only subtle QT prolongation or concealed LQTS still have some risk of arrhythmias. Overall, every 10 ms increase in the corrected QT interval is associated with a 15% increase in arrhythmic risk.As the QT prolonging effects of both genetic variants and acquired causes of LQTS are additive, those with inherited LQTS are more likely to experience TdP if given QT prolonging drugs or if they experience electrolyte problems such as low blood levels of low potassium (hypokalaemia). Similarly, those taking QT prolonging medications are more likely to experience TdP if they have a genetic tendency to a prolonged QT interval, even it this tendency is concealed. Arrhythmias occur more commonly in drug-induced LQTS if the medication in question has been rapidly given intravenously, or if high concentrations of the drug are present in the persons blood. The risk of arrhythmias is also higher if the person receiving the drug has heart failure, is taking digitalis, or has recently been cardioverted from atrial fibrillation. Other risk factors for developing torsades de pointes among those with LQTS include female sex, increasing age, pre-existing cardiovascular disease, and abnormal liver or kidney function. Causes There are several subtypes of long QT syndrome. These can be broadly split into those caused by genetic mutations which those affected are born with, carry throughout their lives, and can pass on to their children (inherited or congenital long QT syndrome), and those caused by other factors which cannot be passed on and are often reversible (acquired long QT syndrome). Inherited Inherited, or congenital long QT syndrome, is caused by genetic abnormalities. LQTS can arise from variants in several genes, leading in some cases to quite different features. The common thread linking these variants is that they affect one or more ion currents leading to prolongation of the ventricular action potential, thus lengthening the QT interval. Classification systems have been proposed to distinguish between subtypes of the condition based on the clinical features (and named after those who first described the condition) and subdivided by the underlying genetic variant. The commonest of these, accounting for 99% of cases, is Romano–Ward syndrome (genetically LQT1-6 and LQT9-16), an autosomal dominant form in which the electrical activity of the heart is affected without involving other organs. A less commonly seen form is Jervell and Lange-Nielsen syndrome, an autosomal recessive form of LQTS combining a prolonged QT interval with congenital deafness. Other rare forms include Anderson–Tawil syndrome (LQT7) with features including a prolonged QT interval, periodic paralysis, and abnormalities of the face and skeleton; and Timothy syndrome (LQT8) in which a prolonged QT interval is associated with abnormalities in the structure of the heart and autism spectrum disorder. Romano–Ward syndrome LQT1 is the most common subtype of Romano–Ward syndrome, responsible for 30 to 35% of all cases. The gene responsible, KCNQ1, has been isolated to chromosome 11p15.5 and encodes the alpha subunit of the KvLQT1 potassium channel. This subunit interacts with other proteins (in particular, the minK beta subunit) to create the channel, which carries the delayed potassium rectifier current IKs responsible for the repolarisation phase of the cardiac action potential. Variants in KCNQ1 that decrease IKs (loss of function variants) slow the repolarisation of the action potential. This causes the LQT1 subtype of Romano–Ward syndrome when a single copy of the variant is inherited (heterozygous, autosomal dominant inheritance). Inheriting two copies of the variant (homozygous, autosomal recessive inheritance) leads to the more severe Jervell and Lange–Nielsen syndrome. Conversely, variants in KCNQ1 that increase IKs lead to more rapid repolarisation and the short QT syndrome.The LQT2 subtype is the second-most common form of Romano–Ward syndrome, responsible for 25 to 30% of all cases. It is caused by variants in the KCNH2 gene (also known as hERG) on chromosome 7 which encodes the potassium channel that carries the rapid inward rectifier current IKr. This current contributes to the terminal repolarisation phase of the cardiac action potential, and therefore the length of the QT interval.The LQT3 subtype of Romano–Ward syndrome is caused by variants in the SCN5A gene located on chromosome 3p21–24. SCN5A encodes the alpha subunit of the cardiac sodium channel, NaV1.5, responsible for the sodium current INa which depolarises cardiac cells at the start of the action potential. Cardiac sodium channels normally inactivate rapidly, but the mutations involved in LQT3 slow their inactivation leading to a small sustained late sodium current. This continued inward current prolongs the action potential and thereby the QT interval. While some variants in SCN5A cause LQT3, other variants can cause quite different conditions. Variants causing a reduction in the early peak current can cause Brugada syndrome and cardiac conduction disease, while other variants have been associated with dilated cardiomyopathy. Some variants which affect both the early and late sodium current can cause overlap syndromes which combine aspects of both LQT3 and Brugada syndrome. Rare Romano–Ward subtypes (LQT4-6 and LQT9-16) LQT5 is caused by variants in the KCNE1 gene responsible for the potassium channel beta subunit MinK. This subunit, in conjunction with the alpha subunit encoded by KCNQ1, is responsible for the potassium current IKs which is decreased in LQTS. LQT6 is caused by variants in the KCNE2 gene responsible for the potassium channel beta subunit MiRP1 which generates the potassium current IKr. Variants that decrease this current have been associated with prolongation of the QT interval. However, subsequent evidence such as the relatively common finding of variants in the gene in those without long QT syndrome, and the general need for a second stressor such as hypokalaemia to be present to reveal the QT prolongation, has suggested that this gene instead represents a modifier to susceptibility to QT prolongation. Some therefore dispute whether variants in KCNE2 are sufficient to cause Romano-Ward syndrome by themselves.LQT9 is caused by variants in the membrane structural protein, caveolin-3. Caveolins form specific membrane domains called caveolae in which voltage-gated sodium channels sit. Similar to LQT3, these caveolin variants increase the late sustained sodium current, which impairs cellular repolarization.LQT10 is an extremely rare subtype, caused by variants in the SCN4B gene. The product of this gene is an auxiliary beta-subunit (NaVβ4) forming cardiac sodium channels, variants in which increase the late sustained sodium current. LQT13 is caused by variants in GIRK4, a protein involved in the parasympathetic modulation of the heart. Clinically, the patients are characterized by only modest QT prolongation, but an increased propensity for atrial arrhythmias. LQT14, LQT15 and LQT16 are caused by variants in the genes responsible for calmodulin (CALM1, CALM2, and CALM3 respectively). Calmodulin interacts with several ion channels and its roles include modulation of the L-type calcium current in response to calcium concentrations, and trafficking the proteins produced by KCNQ1 and thereby influencing potassium currents. The precise mechanisms by which means these genetic variants prolong the QT interval remain uncertain. Jervell and Lange–Nielsen syndrome Jervell and Lange–Nielsen syndrome (JLNS) is a rare form of LQTS inherited in an autosomal recessive manner. In addition to severe prolongation of the QT interval, those affected are born with severe sensorineural deafness affecting both ears. The syndrome is caused by inheriting two copies of certain variant in the KCNE1 or KCNQ1 genes. The same genetic variants lead to the LQT1 and LQT5 forms of Romano-Ward syndrome if only a single copy of the variant is inherited. JLNS is generally associated with a higher risk of arrhythmias than most other forms of LQTS. Andersen–Tawil syndrome (LQT7) LQT7, also known as Andersen–Tawil syndrome, is characterised by a triad of features – in addition to a prolonged QT interval, those affected may experience intermittent weakness often occurring at times when blood potassium concentrations are low (hypokalaemic periodic paralysis), and characteristic facial and skeletal abnormalities such as a small lower jaw (micrognathia), low set ears, and fused or abnormally angled fingers and toes (syndactyly and clinodactyly). The condition is inherited in an autosomal-dominant manner and is caused by mutations in the KCNJ2 gene which encodes the potassium channel protein Kir2.1. Timothy syndrome (LQT8) LQT8, also known as Timothy syndrome combines a prolonged QT interval with fused fingers or toes (syndactyly). Abnormalities of the structure of the heart are commonly seen including ventricular septal defect, tetralogy of Fallot, and hypertrophic cardiomyopathy. The condition presents early in life and the average life expectancy is 2.5 years with death most commonly caused by ventricular arrhythmias. Many children with Timothy syndrome who survive longer than this have features of autism spectrum disorder. Timothy syndrome is caused by variants in the calcium channel Cav1.2 encoded by the gene CACNA1c. Table of associated genes The following is a list of genes associated with Long QT syndrome: Acquired Although long QT syndrome is often a genetic condition, a prolonged QT interval associated with an increased risk of abnormal heart rhythms can also occur in people without a genetic abnormality, commonly due to a side effect of medications. Drug-induced QT prolongation is often a result of treatment by antiarrhythmic drugs such as amiodarone and sotalol, antibiotics such as erythromycin, or antihistamines such as terfenadine. Other drugs which prolong the QT interval include some antipsychotics such as haloperidol and ziprasidone, and the antidepressant citalopram. Lists of medications associated with prolongation of the QT interval such as the CredibleMeds database can be found online.Other causes of acquired LQTS include abnormally low levels of potassium (hypokalaemia) or magnesium (hypomagnesaemia) within the blood. This can be exacerbated following a sudden reduction in the blood supply to the heart (myocardial infarction), low levels of thyroid hormone (hypothyroidism), and a slow heart rate (bradycardia).Anorexia nervosa has been associated with sudden death, possibly due to QT prolongation. The malnutrition seen in this condition can sometimes affect the blood concentration of salts such as potassium, potentially leading to acquired long QT syndrome, in turn causing sudden cardiac death. The malnutrition and associated changes in salt balance develop over a prolonged period of time, and rapid refeeding may further disturb the salt imbalances, increasing the risk of arrhythmias. Care must therefore be taken to monitor electrolyte levels to avoid the complications of refeeding syndrome.Factors which prolong the QT interval are additive, meaning that a combination of factors (such as taking a QT-prolonging drug and having low levels of potassium) can cause a greater degree of QT prolongation than each factor alone. This also applies to some genetic variants which by themselves only minimally prolong the QT interval but can make people more susceptible to significant drug-induced QT prolongation. Mechanisms The various forms of long QT syndrome, both congenital and acquired, produce abnormal heart rhythms (arrhythmias) by influencing the electrical signals used to coordinate individual heart cells. The common theme is a prolongation of the cardiac action potential – the characteristic pattern of voltage changes across the cell membrane that occur with each heart beat. Heart cells when relaxed normally have fewer positively charged ions on the inner side of their cell membrane than on the outer side, referred to as the membrane being polarised. When heart cells contract, positively charged ions such as sodium and calcium enter the cell, equalising or reversing this polarity, or depolarising the cell. After a contraction has taken place, the cell restores its polarity (or repolarises) by allowing positively charged ions such as potassium to leave the cell, restoring the membrane to its relaxed, polarised state. In long QT syndrome it takes longer for this repolarisation to occur, shown in individual cells as a longer action potential while being marked on the surface ECG as a long QT interval.The prolonged action potentials can lead to arrhythmias through several mechanisms. The arrhythmia characteristic of long QT syndrome, Torsades de Pointes, starts when an initial action potential triggers further abnormal action potentials in the form of afterdepolarisations. Early afterdepolarisations, occurring before the cell has fully repolarised, are particularly likely to be seen when action potentials are prolonged, and arise due to reactivation of calcium and sodium channels that would normally switch off until the next heartbeat is due. Under the right conditions, reactivation of these currents, facilitated by the sodium-calcium exchanger, can cause further depolarisation of the cell. The early afterdepolarisations triggering arrhythmias in long QT syndrome tend to arise from the Purkinje fibres of the cardiac conduction system. Early afterdepolarisations may occur as single events, but may occur repeatedly leading to multiple rapid activations of the cell.Some research suggests that delayed afterdepolarisations, occurring after repolarisation has completed, may also play a role in long QT syndrome. This form of afterdepolarisation originates from the spontaneous release of calcium from the intracellular calcium store known as the sarcoplasmic reticulum, forcing calcium out of cell through the sodium calcium exchanger in exchange for sodium, generating a net inward current.While there is strong evidence that the trigger for Torsades de Pointes comes from afterdepolarisations, it is less certain what sustains this arrhythmia. Some lines of evidence suggest that repeated afterdepolarisations from many sources contribute to the continuing arrhythmia. However, some suggest that the arrhythmia sustains through a mechanism known as re-entry. According to this model, the action potential prolongation occurs to a variable extent in different layers of the heart muscle with longer action potentials in some layers than others. In response to a triggering impulse, the waves of depolarisation will spread through regions with shorter action potentials but block in regions with longer action potentials. This allows the depolarising wavefront to bend around areas of block, potentially forming a complete loop and self-perpetuating. The twisting pattern on the ECG can be explained by movement of the core of the re-entrant circuit in the form of a meandering spiral wave. Diagnosis Diagnosing long QT syndrome is challenging. Whilst the hallmark of LQTS is prolongation of the QT interval, the QT interval is highly variable among both those who are healthy and those who have LQTS. This leads to overlap between the QT intervals of those with and without LQTS. 2.5% of those with genetically proven LQTS have a QT interval within the normal range. Conversely, given the normal distribution of QT intervals, a proportion of healthy people will have a longer QT interval than any arbitrary cutoff. Other factors beyond the QT interval should therefore be taken into account when making a diagnosis, some of which have been incorporated into scoring systems. Electrocardiogram Long QT syndrome is principally diagnosed by measuring the QT interval corrected for heart rate (QTc) on a 12-lead electrocardiogram (ECG). Long QT syndrome is associated with a prolonged QTc, although in some genetically proven cases of LQTS this prolongation can be hidden, known as concealed LQTS. The QTc is less than 450 ms in 95% of normal males, and less than 460 ms in 95% of normal females. LQTS is suggested if the QTc is longer than these cutoffs. However, as 5% of normal people also fall into this category, some suggest cutoffs of 470 and 480 ms for males and females respectively, corresponding with the 99th centiles of normal values.The major subtypes of inherited LQTS are associated with specific ECG features. LQT1 is typically associated with broad-based T-waves, whereas the T-waves in LQT2 are notched and of lower amplitude, whilst in LQT3 the T-waves are often late onset, being preceded by a long isoelectric segment. Schwartz score The Schwartz score has been proposed as a method of combining clinical and ECG factors to assess how likely an individual is to have an inherited form of LQTS. The table below lists the criteria used to calculate the score. Other investigations In cases of diagnostic uncertainty, other investigations may be helpful to unmask a prolonged QT. In addition to prolonging the resting QT interval, LQTS may affect how the QT changes in response to exercise and stimulation by catecholamines such as adrenaline. Provocation tests, in the form of exercise tolerance tests or direct infusion of adrenaline, can be used to detect these abnormal responses. These investigations are most useful for identifying those with concealed congenital Type 1 LQTS 1 (LQT1) who have a normal QT interval at rest. While in healthy persons the QT interval shortens during exercise, in those with concealed LQT1 exercise or adrenaline infusion may lead to paradoxical prolongation of the QT interval, revealing the underlying condition. Guideline cutoffs International consensus guidelines differ on the degree of QT prolongation required to diagnose LQTS. The European Society of Cardiology recommends that, with or without symptoms or other investigations, LQTS can be diagnosed if the corrected QT interval is longer than 480ms. They recommend that a diagnosis can be considered in the presence of a QTc of greater than 460 ms if unexplained syncope has occurred. The Heart Rhythm Society guidelines are more stringent, recommending QTc cutoff of greater than 500 ms in the absence of other factors that prolong the QT, or greater than 480 ms with syncope. Both sets of guidelines agree that LQTS can also be diagnosed if an individual has a Schwartz score of greater than 3 or if a pathogenic genetic variant associated with LQTS is identified, regardless of QT interval. Treatment Those diagnosed with LQTS are usually advised to avoid drugs that can prolong the QT interval further or lower the threshold for TDP, lists of which can be found in public access online databases. In addition to this, two intervention options are known for individuals with LQTS: arrhythmia prevention and arrhythmia termination. Arrhythmia prevention Arrhythmia suppression involves the use of medications or surgical procedures that attack the underlying cause of the arrhythmias associated with LQTS. Since the cause of arrhythmias in LQTS is early afterdepolarizations (EADs), and they are increased in states of adrenergic stimulation, steps can be taken to blunt adrenergic stimulation in these individuals. These include administration of beta receptor blocking agents, which decreases the risk of stress-induced arrhythmias. Nadolol, a powerful non-selective beta blocker, has been shown to reduce the arrhythmic risk in all three main genotypes (LQT1, LQT2, and LQT3).Genotype and QT interval duration are independent predictors of recurrence of life-threatening events during beta-blocker therapy. To be specific, the presence of QTc >500 ms and LQT2 and LQT3 genotype are associated with the highest incidence of recurrence. In these patients, primary prevention with use of implantable cardioverter-defibrillators can be considered. Potassium supplementation: If the potassium content in the blood rises, the action potential shortens, so increasing potassium concentration could minimize the occurrence of arrhythmias. It should work best in LQT2, since the hERG channel is especially sensitive to potassium concentration, but the use is experimental and not evidence-based. Sodium channel blocking drugs such as mexiletine have been used to prevent arrhythmias in long QT syndrome. While the most compelling indication is for those whose long QT syndrome is caused by defective sodium channels producing a sustained late current (LQT3), mexiletine also shortens the QT interval in other forms of long QT syndrome including LQT1, LQT2 and LQT8. As the predominant action of mexiletine is on the early peak sodium current, there are theoretical reasons why drugs which preferentially suppress the late sodium current such as ranolazine may be more effective, although evidence that this is the case in practice is limited. Amputation of the cervical sympathetic chain (left stellectomy). This therapy is typically reserved for LQTS caused by JLNS, but may be used as an add-on therapy to beta blockers in certain cases. In most cases, modern therapy favors ICD implantation if beta blocker therapy fails. In patients considered at high risk of life-threatening arrhythmic events, ICD implantation may be considered as a preventive step. Arrhythmia termination Arrhythmia termination involves stopping a life-threatening arrhythmia once it has already occurred. One effective form of arrhythmia termination in individuals with LQTS is placement of an implantable cardioverter-defibrillator (ICD). Also, external defibrillation can be used to restore sinus rhythm. ICDs are commonly used in patients with fainting episodes despite beta blocker therapy, and in patients having experienced a cardiac arrest. As mentioned earlier, ICDs may be used also in patients considered at high risk of life-threatening arrhythmic events.With better knowledge of the genetics underlying LQTS, more precise treatments hopefully will become available. Outcomes Genotype and QT interval duration are the strongest predictors of outcome for patients with LQTS. These have been combined to create an externally validated risk score calculator, estimating a 5-year risk for each individual patient, which can help physicians to identify patients at the highest risk of life-threatening arrhythmic events.For people who experience cardiac arrest or fainting caused by LQTS and who are untreated, the risk of death within 15 years is around 50%. With careful treatment this decreases to less than 1% over 20 years. Those who exhibit symptoms before the age of 18 are more likely to experience a cardiac arrest. Epidemiology Inherited LQTS is estimated to affect between one in 2,500 and 7,000 people. History The first documented case of LQTS was described in Leipzig by Meissner in 1856, when a deaf girl died after her teacher yelled at her. Soon after being notified, the girls parents reported that her older brother, also deaf, had previously died after a terrible fright. This was several decades before the ECG was invented, but is likely the first described case of Jervell and Lange-Nielsen syndrome. In 1957, the first case documented by ECG was described by Anton Jervell and Fred Lange-Nielsen, working in Tønsberg, Norway. Italian pediatrician Cesarino Romano, in 1963, and Irish pediatrician Owen Conor Ward, in 1964, separately described the more common variant of LQTS with normal hearing, later called Romano-Ward syndrome. The establishment of the International Long-QT Syndrome Registry in 1979 allowed numerous pedigrees to be evaluated in a comprehensive manner. This helped in detecting many of the numerous genes involved. Transgenic animal models of the LQTS helped define the roles of various genes and hormones involved, and recently experimental pharmacological therapies to normalize the abnormal repolarization in animals were published. References NotesGoldman L (2011). Goldmans Cecil Medicine (24th ed.). Philadelphia: Elsevier Saunders. p. 1196. ISBN 978-1437727883.

Nausea

Nausea is a diffuse sensation of unease and discomfort, sometimes perceived as an urge to vomit. While not painful, it can be a debilitating symptom if prolonged and has been described as placing discomfort on the chest, abdomen, or back of the throat.Over 30 definitions of nausea were proposed in a 2011 book on the topic.Nausea is a non-specific symptom, which means that it has many possible causes. Some common causes of nausea are gastroenteritis and other gastrointestinal disorders, food poisoning, motion sickness, dizziness, migraine, fainting, low blood sugar, anxiety, and lack of sleep. Nausea is a side effect of many medications including chemotherapy, or morning sickness in early pregnancy. Nausea may also be caused by disgust and depression.Medications taken to prevent and treat nausea and vomiting are called antiemetics. The most commonly prescribed antiemetics in the US are promethazine, metoclopramide, and the newer ondansetron. The word nausea is from Latin nausea, from Greek ναυσία – nausia, "ναυτία" – nautia, motion sickness, "feeling sick or queasy". Causes Gastrointestinal infections (37%) and food poisoning are the two most common causes of acute nausea and vomiting. Side effects from medications (3%) and pregnancy are also relatively frequent. There are many causes of chronic nausea. Nausea and vomiting remain undiagnosed in 10% of the cases. Aside from morning sickness, there are no sex differences in complaints of nausea. After childhood, doctor consultations decrease steadily with age. Only a fraction of one percent of doctor visits by those over 65 are due to nausea. Gastrointestinal Gastrointestinal infection is one of the most common causes of acute nausea and vomiting. Chronic nausea may be the presentation of many gastrointestinal disorders, occasionally as the major symptom, such as gastroesophageal reflux disease, functional dyspepsia, gastritis, biliary reflux, gastroparesis, peptic ulcer, celiac disease, non-celiac gluten sensitivity, Crohns disease, hepatitis, upper gastrointestinal malignancy, and pancreatic cancer. Uncomplicated Helicobacter pylori infection does not cause chronic nausea. Food poisoning Food poisoning usually causes an abrupt onset of nausea and vomiting one to six hours after ingestion of contaminated food and lasts for one to two days. It is due to toxins produced by bacteria in food. Medications Many medications can potentially cause nausea. Some of the most frequently associated include cytotoxic chemotherapy regimens for cancer and other diseases, and general anaesthetic agents. An old cure for migraine, ergotamine, is well known to cause devastating nausea in some patients; a person using it for the first time will be prescribed an antiemetic for relief if needed. Pregnancy Nausea or "morning sickness" is common during early pregnancy but may occasionally continue into the second and third trimesters. In the first trimester nearly 80% of women have some degree of nausea. Pregnancy should therefore be considered as a possible cause of nausea in any sexually active woman of child-bearing age. While usually it is mild and self-limiting, severe cases known as hyperemesis gravidarum may require treatment. Disequilibrium A number of conditions involving balance such as motion sickness and vertigo can lead to nausea and vomiting. Gynecologic Dysmenorrhea can cause nausea. Psychiatric Nausea may be caused by depression, anxiety disorders and eating disorders. Potentially serious While most causes of nausea are not serious, some serious conditions are associated with nausea. These include pancreatitis, small bowel obstruction, appendicitis, cholecystitis, hepatitis, Addisonian crisis, diabetic ketoacidosis, increased intracranial pressure, spontaneous intracranial hypotension, brain tumors, meningitis, heart attack, rabies carbon monoxide poisoning and many others. Comprehensive list Inside the abdomen Obstructing disorders Gastric outlet obstruction Small bowel obstruction Colonic obstruction Superior mesenteric artery syndromeEnteric infections Viral infection Bacterial infectionInflammatory diseases Celiac disease Cholecystitis Pancreatitis Appendicitis HepatitisSensorimotor dysfunction Gastroparesis Intestinal pseudo-obstruction Gastroesophageal reflux disease Irritable bowel syndrome Cyclic vomiting syndromeOther Non-celiac gluten sensitivity Biliary colic Kidney stone Cirrhosis Abdominal irradiation Outside the abdomen Cardiopulmonary Cardiomyopathy Myocardial infarction (heart attack) Paroxysmal coughInner-ear diseases Motion sickness Labyrinthitis MalignancyIntracerebral disorders Malignancy Hemorrhage Abscess Hydrocephalus Meningitis Encephalitis RabiesPsychiatric illnesses Anorexia and bulimia nervosa DepressionOther Post-operative vomiting Nociception Medications and metabolic disorders Drugs Chemotherapy Antibiotics Antiarrhythmics Digoxin Oral hypoglycemic medications Oral contraceptivesEndocrine/metabolic disease Pregnancy Uremia Ketoacidosis Thyroid and parathyroid disease Adrenal insufficiencyToxins Liver failure Alcohol Pathophysiology Research on nausea and vomiting has relied on using animal models to mimic the anatomy and neuropharmacologic features of the human body. The physiologic mechanism of nausea is a complex process that has yet to be fully elucidated. There are four general pathways that are activated by specific triggers in the human body that go on to create the sensation of nausea and vomiting. Central nervous system (CNS): Stimuli can affect areas of the CNS including the cerebral cortex and the limbic system. These areas are activated by elevated intracranial pressure, irritation of the meninges (i.e. blood or infection), and extreme emotional triggers such as anxiety. The supratentorial region is also responsible for the sensation of nausea. Chemoreceptor trigger zone (CTZ): The CTZ is located in the area postrema in the floor of the fourth ventricle within the brain. This area is outside the blood brain barrier, and is therefore readily exposed to substances circulating through the blood and cerebral spinal fluid. Common triggers of the CTZ include metabolic abnormalities, toxins, and medications. Activation of the CTZ is mediated by dopamine (D2) receptors, serotonin (5HT3) receptors, and neurokinin receptors (NK1). Vestibular system: This system is activated by disturbances to the vestibular apparatus in the inner ear. These include movements that cause motion sickness and dizziness. This pathway is triggered via histamine (H1) receptors and acetylcholine (ACh) receptors. Peripheral Pathways: These pathways are triggered via chemoreceptors and mechanoreceptors in the gastrointestinal tract, as well as other organs such as the heart and kidneys. Common activators of these pathways include toxins present in the gastrointestinal lumen and distension of the gastrointestinal lumen from blockage or dysmotility of the bowels. Signals from these pathways travel via multiple neural tracts including the vagus, glossopharyngeal, splanchnic, and sympathetic nerves.Signals from any of these pathways then travel to the brainstem, activating several structures including the nucleus of the solitary tract, the dorsal motor nucleus of the vagus, and central pattern generator. These structures go on to signal various downstream effects of nausea and vomiting. The bodys motor muscle responses involve halting the muscles of the gastrointestinal tract, and in fact causing reversed propulsion of gastric contents towards the mouth while increasing abdominal muscle contraction. Autonomic effects involve increased salivation and the sensation of feeling faint that often occurs with nausea and vomiting. Pre-nausea pathophysiology It has been described that alterations in heart rate can occur as well as the release of vasopressin from the posterior pituitary. Diagnosis Patient history Taking a thorough patient history may reveal important clues to the cause of nausea and vomiting. If the patients symptoms have an acute onset, then drugs, toxins, and infections are likely. In contrast, a long-standing history of nausea will point towards a chronic illness as the culprit. The timing of nausea and vomiting after eating food is an important factor to pay attention to. Symptoms that occur within an hour of eating may indicate an obstruction proximal to the small intestine, such as gastroparesis or pyloric stenosis. An obstruction further down in the intestine or colon will cause delayed vomiting. An infectious cause of nausea and vomiting such as gastroenteritis may present several hours to days after the food was ingested. The contents of the emesis is a valuable clue towards determining the cause. Bits of fecal matter in the emesis indicate obstruction in the distal intestine or the colon. Emesis that is of a bilious nature (greenish in color) localizes the obstruction to a point past the stomach. Emesis of undigested food points to an obstruction prior to the gastric outlet, such as achalasia or Zenkers diverticulum. If patient experiences reduced abdominal pain after vomiting, then obstruction is a likely etiology. However, vomiting does not relieve the pain brought on by pancreatitis or cholecystitis. Physical exam It is important to watch out for signs of dehydration, such as orthostatic hypotension and loss of skin turgor. Auscultation of the abdomen can produce several clues to the cause of nausea and vomiting. A high-pitched tinkling sound indicates possible bowel obstruction, while a splashing "succussion" sound is more indicative of gastric outlet obstruction. Eliciting pain on the abdominal exam when pressing on the patient may indicate an inflammatory process. Signs such as papilledema, visual field losses, or focal neurological deficits are red flag signs for elevated intracranial pressure. Diagnostic testing When a history and physical exam are not enough to determine the cause of nausea and vomiting, certain diagnostic tests may prove useful. A chemistry panel would be useful for electrolyte and metabolic abnormalities. Liver function tests and lipase would identify pancreaticobiliary diseases. Abdominal X-rays showing air-fluid levels indicate bowel obstruction, while an X-ray showing air-filled bowel loops are more indicative of ileus. More advanced imaging and procedures may be necessary, such as a CT scan, upper endoscopy, colonoscopy, barium enema, or MRI. Abnormal GI motility can be assessed using specific tests like gastric scintigraphy, wireless motility capsules, and small-intestinal manometry. Treatment If dehydration is present due to loss of fluids from severe vomiting, rehydration with oral electrolyte solutions is preferred. If this is not effective or possible, intravenous rehydration may be required. Medical care is recommended if: a person cannot keep any liquids down, has symptoms more than 2 days, is weak, has a fever, has stomach pain, vomits more than two times in a day or does not urinate for more than 8 hours. Medications Many pharmacologic medications are available for the treatment of nausea. There is no medication that is clearly superior to other medications for all cases of nausea. The choice of antiemetic medication may be based on the situation during which the person experiences nausea. For people with motion sickness and vertigo, antihistamines and anticholinergics such as meclizine and scopolamine are particularly effective. Nausea and vomiting associated with migraine headaches respond best to dopamine antagonists such as metoclopramide, prochlorperazine, and chlorpromazine. In cases of gastroenteritis, serotonin antagonists such as ondansetron were found to suppress nausea and vomiting, as well as reduce the need for IV fluid resuscitation. The combination of pyridoxine and doxylamine is the first line treatment for pregnancy-related nausea and vomiting. Dimenhydrinate is an inexpensive and effective over the counter medication for preventing postoperative nausea and vomiting. Other factors to consider when choosing an antiemetic medication include the persons preference, side-effect profile, and cost. Nabilone is also indicated for this purpose. Alternative medicine In certain people, cannabinoids may be effective in reducing chemotherapy associated nausea and vomiting. Several studies have demonstrated the therapeutic effects of cannabinoids for nausea and vomiting in the advanced stages of illnesses such as cancer and AIDS.In hospital settings topical anti-nausea gels are not indicated because of lack of research backing their efficacy. Topical gels containing lorazepam, diphenhydramine, and haloperidol are sometimes used for nausea but are not equivalent to more established therapies.Ginger has also been shown to be potentially effective in treating several types of nausea. Prognosis The outlook depends on the cause. Most people recover within few hours or a day. While short-term nausea and vomiting are generally harmless, they may sometimes indicate a more serious condition. When associated with prolonged vomiting, it may lead to dehydration or dangerous electrolyte imbalances or both. Repeated intentional vomiting, characteristic of bulimia, can cause stomach acid to wear away at the enamel in teeth. Epidemiology Nausea and or vomiting is the main complaint in 1.6% of visits to family physicians in Australia. However, only 25% of people with nausea visit their family physician. In Australia, nausea, as opposed to vomiting, occurs most frequently in persons aged 15–24 years, and is less common in other age groups. See also Cancer and nausea Vasodilation References External links The dictionary definition of nausea at Wiktionary

Polyarthritis

Polyarthritis is any type of arthritis that involves 5 or more joints simultaneously. It is usually associated with autoimmune conditions and may be experienced at any age and is not sex specific. Causes Polyarthritis is most often caused by an auto-immune disorder such as rheumatoid arthritis, amyloidosis, psoriatic arthritis, and lupus erythematosus but can also be caused by infection with an alphavirus such as chikungunya virus and Ross River virus. This condition is termed alphavirus polyarthritis syndrome. Sindbis virus, which is endemic in Northern Europe, Africa, the Middle East, and Australia, is the most widely distributed of the alphaviruses causing polyarthritis, though infection is usually mild or asymptomatic. Associated conditions It may be associated with bilateral edema in lower limbs, pain and joint swelling. Sometimes there is previous history of inflammatory joint problems and bilateral edema of lower limbs. Alphavirus Polyarthritis Syndrome has an incubation period of 3–21 days, depending on the specific virus, with either a gradual or sudden onset of fever, arthralgias, headache, and lymphadenitis and conjunctivitis in some forms. A maculopapular rash may present 4–8 days post symptom onset and may be accompanied by an increase in fever. Joint pains associated with this condition may recur for many months after initial illness for up to a year. See also Polyarteritis nodosa == External links ==

Persistent pupillary membrane

Persistent pupillary membrane (PPM) is a condition of the eye involving remnants of a fetal membrane that persist as strands of tissue crossing the pupil. The pupillary membrane in mammals exists in the fetus as a source of blood supply for the lens. It normally atrophies from the time of birth to the age of four to eight weeks. PPM occurs when this atrophy is incomplete. It generally does not cause any symptoms. The strands can connect to the cornea or lens, but most commonly to other parts of the iris. Attachment to the cornea can cause small corneal opacities, while attachment to the lens can cause small cataracts. Using topical atropine to dilate the pupil may help break down PPMs. In dogs, PPM is inherited in the Basenji but can occur in other breeds such as the Pembroke Welsh Corgi, Chow Chow, Mastiff, and English Cocker Spaniel. It can also be observed in cats, horses, and cattle. References == External links ==

Synovial bursa

A synovial bursa (plural bursae or bursas) is a small fluid-filled sac lined by synovial membrane with an inner capillary layer of viscous synovial fluid (similar in consistency to that of a raw egg white). It provides a cushion between bones and tendons and/or muscles around a joint. This helps to reduce friction between the bones and allows free movement. Bursae are found around most major joints of the body. Structure There are four types of bursa: adventitious, subcutaneous, synovial, and sub-muscular. Among these, only adventitious is non-native. When any surface of the body is subjected to repeated stress, an adventitious bursa develops under it. Examples are Students elbow and bunion. Clinical significance Infection or irritation of a bursa leads to bursitis (inflammation of a bursa). The general term for disease of bursae is "bursopathy." History Etymology Bursa is Medieval Latin for "purse", so named for the resemblance of an anatomical bursa to a purse. Bursae or bursas is its plural form. See also Bursa of Fabricius (a lymphatic organ in birds) Bursectomy Knee bursae Shoulder joint#Bursae External links Hirji, Zameer; Hunjun, Jaspal S; Choudur, Hema N (2 May 2011). "Imaging of the Bursae". Journal of Clinical Imaging Science. 1: 22. doi:10.4103/2156-7514.80374. PMC 3177464. PMID 21966619. Bursa Diagram of elbow with olecranon bursa

Trimester

Trimester or Trimestre may refer to: Academic term, a trimester system divides the academic year into three terms Pregnancy § Trimesters in humans, where the time of pregnancy is divided into three terms of 13 weeks to refer to the fetuss development The trimester framework in Roe v. Wade, which organized constitutional issues in abortion law according to trimesters A period of three months (Latin tri +mensis=month or moon) In Europe, where financial years start on 1 January each year, often Jan+Feb+Mar etc. See also Semester Term (disambiguation)

Hypermagnesemia

Hypermagnesemia is an electrolyte disorder in which there is a high level of magnesium in the blood. Symptoms include weakness, confusion, decreased breathing rate, and decreased reflexes. Complications may include low blood pressure and cardiac arrest.It is typically caused by kidney failure or is treatment-induced such as from antacids that contain magnesium. Less common causes include tumor lysis syndrome, seizures, and prolonged ischemia. Diagnosis is based on a blood level of magnesium greater than 1.1 mmol/L (2.6 mg/dL). It is severe if levels are greater than 2.9 mmol/L (7 mg/dL). Specific electrocardiogram (ECG) changes may be present.Treatment involves stopping the magnesium a person is getting. Treatment when levels are very high include calcium chloride, intravenous normal saline with furosemide, and hemodialysis. Hypermagnesemia is uncommon. Rates among hospitalized patients in renal failure may be as high as 10%. Signs and symptoms Symptoms include weakness, confusion, decreased breathing rate, and decreased reflexes. As well as nausea, low blood pressure, low blood calcium, abnormal heart rhythms and asystole, dizziness, and sleepiness. Abnormal heart rhythms and asystole are possible complications of hypermagnesemia related to the heart. Magnesium acts as a physiologic calcium blocker, which results in abnormalities of the electrical conduction system of the heart. Consequences related to serum concentration: 4.0 mEq/L – Decreased reflexes >5.0 mEq/L – Prolonged atrioventricular conduction >10.0 mEq/L – Complete heart block >13.0 mEq/L – Cardiac arrestThe therapeutic range for the prevention of the pre-eclamptic uterine contractions is: 4.0–7.0 mEq/L. As per Lu and Nightingale, serum magnesium concentrations associated with maternal toxicity (also neonate depression, hypotonia and low Apgar scores) are: 7.0–10.0 mEq/L – Loss of patellar reflex 10.0-13.0 mEq/L – Respiratory depression 15.0-25.0 mEq/L – Altered atrioventricular conduction and (further) complete heart block >25.0 mEq/L – Cardiac arrest Complications Severe hypermagnesemia (levels greater than 12 mg/dL) can lead to cardiovascular complications (hypotension and arrhythmias) and neurological disorder (confusion and lethargy). Higher values of serum magnesium (exceeding 15 mg/dL) can induce cardiac arrest and coma. Causes Magnesium status depends on three organs: uptake in the intestine, storage in the bone, and excretion in the kidneys. Hypermagnesemia is therefore often due to problems in these organs, mostly the intestine or kidney. Predisposing conditions Hemolysis, magnesium concentration in red blood cells is approximately three times greater than in serum, therefore hemolysis can increase plasma magnesium. Hypermagnesemia is expected only in massive hemolysis. Chronic kidney disease, excretion of magnesium becomes impaired when creatinine clearance falls below 30 ml/min. However, hypermagnesemia is not a prominent feature of chronic kidney disease unless magnesium intake is increased. Magnesium toxicity from emergency pre-eclampsia treatment during labor and delivery. Other conditions that can predispose to mild hypermagnesemia are diabetic ketoacidosis, adrenal insufficiency, hypothyroidism, hyperparathyroidism, and lithium intoxication. Metabolism For a detailed description of magnesium homeostasis and metabolism see hypomagnesemia. Diagnosis Hypermagnesemia is diagnosed by measuring the concentration of magnesium in the blood. Concentrations of magnesium greater than 1.1 mmol/L are considered diagnostic. Treatment People with normal kidney function (glomerular filtration rate (GFR) over 60 ml/min) and mild asymptomatic hypermagnesemia require no treatment except for the removal of all sources of exogenous magnesium. One must consider that the half-time of elimination of magnesium is approximately 28 hours. In more severe cases, close monitoring of the ECG, blood pressure, and neuromuscular function and early treatment are necessary: Intravenous calcium gluconate or calcium chloride since the actions of magnesium in neuromuscular and cardiac function become antagonized by calcium. Severe clinical conditions require increasing renal magnesium excretion through: Intravenous loop diuretics (e.g., furosemide), or hemodialysis, when kidney function is impaired, or the patient is symptomatic from severe hypermagnesemia. This approach usually removes magnesium efficiently (up to 50% reduction after a 3- to 4-hour treatment). Dialysis can, however, increase the excretion of calcium by developing hypocalcemia, thus possibly worsening the symptoms and signs of hypermagnesemia. The use of diuretics must be associated with infusions of saline solutions to avoid further electrolyte disturbances (e.g., hypokalemia) and metabolic alkalosis. The clinician must perform serial measurements of calcium and magnesium. In association with electrolytic correction, it is often necessary to support cardiorespiratory activity. As a consequence, the treatment of this electrolyte disorder can frequently require intensive care unit (ICU) admission. Particular clinical conditions require a specific approach. For instance, during the management of eclampsia, the magnesium infusion is stopped if urine output drops to less than 80 mL (in 4 hours), deep tendon reflexes are absent, or the respiratory rate is below 12 breaths/minute. A 10% calcium gluconate or chloride solution can serve as an antidote. Prognosis The prognosis of hypermagnesemia depends on magnesium values and on the clinical condition that induced hypermagnesemia. Values that are not excessively high (mild hypermagnesemia) and in the absence of triggering and aggravating conditions (e.g., chronic kidney disease) are benign conditions. On the contrary, high values (severe hypermagnesemia) expose the patient to high risks and high mortality. Epidemiology Hypermagnesemia is an uncommon electrolyte disorder. It occurs in approximately 10 to 15% of hospitalized patients with renal failure. Furthermore, epidemiological data suggest that there is a significant prevalence of high levels of serum magnesium in selected healthy populations. For instance the overall prevalence of hypermagnesemia was 3.0%, especially in males in Iran. High magnesium concentrations were typical in people with cardiovascular disease, and 2.3 mg/dL or higher values were associated with worse hospital mortality. References == External links ==

Lymphocytosis

Lymphocytosis is an increase in the number or proportion of lymphocytes in the blood. Absolute lymphocytosis is the condition where there is an increase in the lymphocyte count beyond the normal range while relative lymphocytosis refers to the condition where the proportion of lymphocytes relative to white blood cell count is above the normal range. In adults, absolute lymphocytosis is present when the lymphocyte count is greater than 5000 per microliter (5.0 x 109/L), in older children greater than 7000 per microliter and in infants greater than 9000 per microliter. Lymphocytes normally represent 20% to 40% of circulating white blood cells. When the percentage of lymphocytes exceeds 40%, it is recognized as relative lymphocytosis. Causes Lymphocytosis is a feature of infection, particularly in children. In the elderly, lymphoproliferative disorders, including chronic lymphocytic leukemia and lymphomas, often present with lymphadenopathy and a lymphocytosis.Causes of absolute lymphocytosis include: acute viral infections, such as infectious mononucleosis (glandular fever), hepatitis and Cytomegalovirus infection other acute infections such as pertussis some protozoal infections, such as toxoplasmosis and American trypanosomiasis (Chagas disease) chronic intracellular bacterial infections such as tuberculosis or brucellosis chronic lymphocytic leukemia acute lymphoblastic leukemia lymphoma post-splenectomy state CARD11-related congenital B cell lymphocytosis (rare, also known as BENTA disease)Causes of relative lymphocytosis include: age less than 2 years; acute viral infections; connective tissue diseases, thyrotoxicosis, Addisons disease, splenomegaly with splenic sequestration of granulocytes. Diagnosis Lymphocytosis is usually detected when a complete blood count is obtained. If not provided the lymphocyte count can be calculated by multiplying the total white blood cell (WBC) count by the percentage of lymphocytes found in the differential count. The lymphocyte count can also be directly measured by flow cytometry. See also Lymphocytopenia References == External links ==

Thrombosis

Thrombosis (from Ancient Greek θρόμβωσις thrómbōsis "clotting") is the formation of a blood clot inside a blood vessel, obstructing the flow of blood through the circulatory system. When a blood vessel (a vein or an artery) is injured, the body uses platelets (thrombocytes) and fibrin to form a blood clot to prevent blood loss. Even when a blood vessel is not injured, blood clots may form in the body under certain conditions. A clot, or a piece of the clot, that breaks free and begins to travel around the body is known as an embolus.Thrombosis may occur in veins (venous thrombosis) or in arteries (arterial thrombosis). Venous thrombosis (sometimes called DVT, deep vein thrombosis) leads to a blood clot in the affected part of the body, while arterial thrombosis (and, rarely, severe venous thrombosis) affects the blood supply and leads to damage of the tissue supplied by that artery (ischemia and necrosis). A piece of either an arterial or a venous thrombus can break off as an embolus, which could then travel through the circulation and lodge somewhere else as an embolism. This type of embolism is known as a thromboembolism. Complications can arise when a venous thromboembolism (commonly called a VTE) lodges in the lung as a pulmonary embolism. An arterial embolus may travel further down the affected blood vessel, where it can lodge as an embolism. Signs and symptoms Thrombosis is generally defined by the type of blood vessel affected (arterial or venous thrombosis) and the precise location of the blood vessel or the organ supplied by it. Venous thrombosis Deep vein thrombosis Deep vein thrombosis (DVT) is the formation of a blood clot within a deep vein. It most commonly affects leg veins, such as the femoral vein. Three factors are important in the formation of a blood clot within a deep vein—these are the rate of blood flow, the thickness of the blood and qualities of the vessel wall. Classical signs of DVT include swelling, pain and redness of the affected area. Paget-Schroetter disease Paget-Schroetter disease or upper extremity DVT (UEDVT) is the obstruction of an arm vein (such as the axillary vein or subclavian vein) by a thrombus. The condition usually comes to light after vigorous exercise and usually presents in younger, otherwise healthy people. Men are affected more than women. Budd-Chiari syndrome Budd-Chiari syndrome is the blockage of a hepatic vein or of the hepatic part of the inferior vena cava. This form of thrombosis presents with abdominal pain, ascites and enlarged liver. Treatment varies between therapy and surgical intervention by the use of shunts. Portal vein thrombosis Portal vein thrombosis affects the hepatic portal vein, which can lead to portal hypertension and reduction of the blood supply to the liver. It usually happens in the setting of another disease such as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma. Renal vein thrombosis Renal vein thrombosis is the obstruction of the renal vein by a thrombus. This tends to lead to reduced drainage from the kidney."Renal vein thrombosis: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 27 May 2019.</ref> Cerebral venous sinus thrombosis Cerebral venous sinus thrombosis (CVST) is a rare form of stroke which results from the blockage of the dural venous sinuses by a thrombus. Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body and seizures. The diagnosis is usually made with a CT or MRI scan. The majority of persons affected make a full recovery. The mortality rate is 4.3%. Jugular vein thrombosis Jugular vein thrombosis is a condition that may occur due to infection, intravenous drug use or malignancy. Jugular vein thrombosis can have a varying list of complications, including: systemic sepsis, pulmonary embolism, and papilledema. Though characterized by a sharp pain at the site of the vein, it can prove difficult to diagnose, because it can occur at random. Cavernous sinus thrombosis Cavernous sinus thrombosis is a specialised form of cerebral venous sinus thrombosis, where there is thrombosis of the cavernous sinus of the basal skull dura, due to the retrograde spread of infection and endothelial damage from the danger triangle of the face. The facial veins in this area anastomose with the superior and inferior ophthalmic veins of the orbit, which drain directly posteriorly into the cavernous sinus through the superior orbital fissure. Staphyloccoal or Streptococcal infections of the face, for example nasal or upper lip pustules may thus spread directly into the cavernous sinus, causing stroke-like symptoms of double vision, squint, as well as spread of infection to cause meningitis."Guidelines Cavernous sinus thrombosis" (PDF).</ref> Arterial thrombosis Arterial thrombosis is the formation of a thrombus within an artery. In most cases, arterial thrombosis follows rupture of atheroma (a fat-rich deposit in the blood vessel wall), and is therefore referred to as atherothrombosis. Arterial embolism occurs when clots then migrate downstream and can affect any organ.Alternatively, arterial occlusion occurs as a consequence of embolism of blood clots originating from the heart ("cardiogenic" emboli). The most common cause is atrial fibrillation, which causes a blood stasis within the atria with easy thrombus formation, but blood clots can develop inside the heart for other reasons too as infective endocarditis. Stroke A stroke is the rapid decline of brain function due to a disturbance in the supply of blood to the brain. This can be due to ischemia, thrombus, embolus (a lodged particle) or hemorrhage (a bleed). In thrombotic stroke, a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, the onset of symptomatic thrombotic strokes is slower. Thrombotic stroke can be divided into two categories — large vessel disease or small vessel disease. The former affects vessels such as the internal carotids, vertebral and the circle of Willis. The latter can affect smaller vessels, such as the branches of the circle of Willis. Myocardial infarction Myocardial infarction (MI), or heart attack, is caused by ischemia (restriction in the blood supply), which is often due to the obstruction of a coronary artery by a thrombus. This restriction gives an insufficient supply of oxygen to the heart muscle which then results in tissue death (infarction). A lesion is then formed which is the infarct. MI can quickly become fatal if emergency medical treatment is not received promptly. If diagnosed within 12 hours of the initial episode (attack) then thrombolytic therapy is initiated. Limb ischemia An arterial thrombus or embolus can also form in the limbs, which can lead to acute limb ischemia. Other sites Hepatic artery thrombosis usually occurs as a devastating complication after liver transplantation. Causes Thrombosis prevention is initiated with assessing the risk for its development. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism. Some of these risk factors are related to inflammation. "Virchows triad" has been suggested to describe the three factors necessary for the formation of thrombosis: stasis of blood, vessel wall injury, and altered blood coagulation. Some risk factors predispose for venous thrombosis while others increase the risk of arterial thrombosis. Newborn babies in the neonatal period are also at risk of a thromboembolism. Mechanism Pathogenesis The main causes of thrombosis are given in Virchows triad which lists thrombophilia, endothelial cell injury, and disturbed blood flow. Generally speaking the risk for thrombosis increases over the life course of individuals, depending on life style factors like smoking, diet, and physical activity, the presence of other diseases like cancer or autoimmune disease, while also platelet properties change in aging individuals which is an important consideration as well. Hypercoagulability Hypercoagulability or thrombophilia, is caused by, for example, genetic deficiencies or autoimmune disorders. Recent studies indicate that white blood cells play a pivotal role in deep vein thrombosis, mediating numerous pro-thrombotic actions. Endothelial cell injury Any inflammatory process, such as trauma, surgery or infection, can cause damage to the endothelial lining of the vessels wall. The main mechanism is exposure of tissue factor to the blood coagulation system. Inflammatory and other stimuli (such as hypercholesterolemia) can lead to changes in gene expression in endothelium producing to a pro-thrombotic state. When this occurs, endothelial cells downregulate substances such as thrombomodulin, which is a key modulator of thrombin activity. The result is a sustained activation of thrombin and reduced production of protein C and tissue factor inhibitor, which furthers the pro-thrombotic state.Endothelial injury is almost invariably involved in the formation of thrombi in arteries, as high rates of blood flow normally hinder clot formation. In addition, arterial and cardiac clots are normally rich in platelets–which are required for clot formation in areas under high stress due to blood flow. Disturbed blood flow Causes of disturbed blood flow include stagnation of blood flow past the point of injury, or venous stasis which may occur in heart failure, or after long periods of sedentary behaviour, such as sitting on a long airplane flight. Also, atrial fibrillation, causes stagnant blood in the left atrium (LA), or left atrial appendage (LAA), and can lead to a thromboembolism. Cancers or malignancies such as leukemia may cause increased risk of thrombosis by possible activation of the coagulation system by cancer cells or secretion of procoagulant substances (paraneoplastic syndrome), by external compression on a blood vessel when a solid tumor is present, or (more rarely) extension into the vasculature (for example, renal cell cancers extending into the renal veins). Also, treatments for cancer (radiation, chemotherapy) often cause additional hypercoagulability. There are scores that correlate different aspects of patient data (comorbidities, vital signs, and others) to risk of thrombosis, such as the POMPE-C, which stratifies risk of mortality due to pulmonary embolism in patients with cancer, who typically have higher rates of thrombosis. Also, there are several predictive scores for thromboembolic events, such as Padua, Khorana, and ThroLy score. Pathophysiology Natural history Fibrinolysis is the physiological breakdown of blood clots by enzymes such as plasmin. Organisation: following the thrombotic event, residual vascular thrombus will be re-organised histologically with several possible outcomes. For an occlusive thrombus (defined as thrombosis within a small vessel that leads to complete occlusion), wound healing will reorganise the occlusive thrombus into collagenous scar tissue, where the scar tissue will either permanently obstruct the vessel, or contract down with myofibroblastic activity to unblock the lumen. For a mural thrombus (defined as a thrombus in a large vessel that restricts the blood flow but does not occlude completely), histological reorganisation of the thrombus does not occur via the classic wound healing mechanism. Instead, the platelet-derived growth factor degranulated by the clotted platelets will attract a layer of smooth muscle cells to cover the clot, and this layer of mural smooth muscle will be vascularised by the blood inside the vessel lumen rather than by the vasa vasorum.Ischemia/infarction: if an arterial thrombus cannot be lysed by the body and it does not embolise, and if the thrombus is large enough to impair or occlude blood flow in the involved artery, then local ischemia or infarction will result. A venous thrombus may or may not be ischemic, since veins distribute deoxygenated blood that is less vital for cellular metabolism. Nevertheless, non-ischemic venous thrombosis may still be problematic, due to the swelling caused by blockage to venous drainage. In deep vein thrombosis this manifests as pain, redness, and swelling; in retinal vein occlusion this may result in macular oedema and visual acuity impairment, which if severe enough can lead to blindness. Embolization A thrombus may become detached and enter circulation as an embolus, finally lodging in and completely obstructing a blood vessel, which unless treated very quickly will lead to tissue necrosis (an infarction) in the area past the occlusion. Venous thrombosis can lead to pulmonary embolism when the migrated embolus becomes lodged in the lung. In people with a "shunt" (a connection between the pulmonary and systemic circulation), either in the heart or in the lung, a venous clot can also end up in the arteries and cause arterial embolism.Arterial embolism can lead to obstruction of blood flow through the blood vessel that is obstructed by it, and a lack of oxygen and nutrients (ischemia) of the downstream tissue. The tissue can become irreversibly damaged, a process known as necrosis. This can affect any organ; for instance, arterial embolism of the brain is one of the causes of stroke. Prevention The use of heparin following surgery is common if there are no issues with bleeding. Generally, a risk-benefit analysis is required, as all anticoagulants lead to an increased risk of bleeding. In people admitted to hospital, thrombosis is a major cause for complications and occasionally death. In the UK, for instance, the Parliamentary Health Select Committee heard in 2005 that the annual rate of death due to thrombosis was 25,000, with at least 50% of these being hospital-acquired. Hence thromboprophylaxis (prevention of thrombosis) is increasingly emphasized. In patients admitted for surgery, graded compression stockings are widely used, and in severe illness, prolonged immobility and in all orthopedic surgery, professional guidelines recommend low molecular weight heparin (LMWH) administration, mechanical calf compression or (if all else is contraindicated and the patient has recently developed deep vein thrombosis) the insertion of a vena cava filter. In patients with medical rather than surgical illness, LMWH too is known to prevent thrombosis, and in the United Kingdom the Chief Medical Officer has issued guidance to the effect that preventative measures should be used in medical patients, in anticipation of formal guidelines. Treatment The treatment for thrombosis depends on whether it is in a vein or an artery, the impact on the person, and the risk of complications from treatment. Anticoagulation Warfarin and vitamin K antagonists are anticoagulants that can be taken orally to reduce thromboembolic occurrence. Where a more effective response is required, heparin can be given (by injection) concomitantly. As a side effect of any anticoagulant, the risk of bleeding is increased, so the international normalized ratio of blood is monitored. Self-monitoring and self-management are safe options for competent patients, though their practice varies. In Germany, about 20% of patients were self-managed while only 1% of U.S. patients did home self-testing (according to one 2012 study). Other medications such as direct thrombin inhibitors and direct Xa inhibitors are increasingly being used instead of warfarin. Thrombolysis Thrombolysis is the pharmacological destruction of blood clots by administering thrombolytic drugs including recombinant tissue plasminogen activator, which enhances the normal destruction of blood clots by the bodys enzymes. This carries an increased risk of bleeding so is generally only used for specific situations (such as severe stroke or a massive pulmonary embolism). Surgery Arterial thrombosis may require surgery if it causes acute limb ischemia. Endovascular treatment Mechanical clot retrieval and catheter-guided thrombolysis are used in certain situations. Antiplatelet agents Arterial thrombosis is platelet-rich, and inhibition of platelet aggregation with antiplatelet drugs such as aspirin may reduce the risk of recurrence or progression. Targeting ischemia/reperfusion injury With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes cell death in reperfused tissue and contributes significantly to post-reperfusion mortality and morbidity. For example, in a feline model of intestinal ischemia, four hours of ischemia resulted in less injury than three hours of ischemia followed by one hour of reperfusion. In ST-elevation myocardial infarction (STEMI), IRI contributes up to 50% of final infarct size despite timely primary percutaneous coronary intervention. This is a key reason for the continued high mortality and morbidity in these conditions, despite endovascular reperfusion treatments and continuous efforts to improve timeliness and access to these treatments. Hence, protective therapies are required to attenuate IRI alongside reperfusion in acute ischemic conditions to improve clinical outcomes. Therapeutic strategies that have potential to improve clinical outcomes in reperfused STEMI patients include remote ischemic conditioning (RIC), exenatide, and metoprolol. These have emerged amongst a multitude of cardioprotective interventions investigated with largely neutral clinical data. Of these, RIC has the most robust clinical evidence, especially in the context of STEMI, but also emerging for other indications such as acute ischemic stroke and aneurysmal subarachnoid hemorrhage. Neonatal thrombosis Treatment options for full-term and preterm babies who develop thromboembolism include expectant management (with careful observation), nitroglycerin ointment, pharmacological therapy (thrombolytics and/or anticoagulants), and surgery. The evidence supporting these treatment approaches is weak. For anticoagulant treatment, t is not clear if unfractionated and/or low molecular weight heparin treatment is effective at decreasing mortality and serious adverse events in this population. There is also insufficient evidence to understand the risk of adverse effects associated with these treatment approaches in term or preterm infants. See also Blood clotting tests Disseminated intravascular coagulation Hepatic artery thrombosis Thrombotic microangiopathy References Bibliography Brunner, Lillian (2010). Brunner & Suddarths textbook of medical-surgical nursing. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-0781785907. Copstead, Lee (2013). Pathophysiology. St. Louis, Mo: Elsevier. ISBN 978-1455726509. Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 978-0071716727. Moliterno, David (2013). Therapeutic advances in thrombosis. Chichester, West Sussex: Wiley-Blackwell. ISBN 978-1405196253. Abele, H (2014). Atlas of gynecologic surgery. Stuttgart: Thieme. ISBN 978-3136507049; Access provided by the University of Pittsburgh{{cite book}}: CS1 maint: postscript (link) External links Media related to Thrombosis at Wikimedia Commons Thrombosis at Curlie

Nasal fracture

A nasal fracture, commonly referred to as a broken nose, is a fracture of one of the bones of the nose. Symptoms may include bleeding, swelling, bruising, and an inability to breathe through the nose. They may be complicated by other facial fractures or a septal hematoma.The most common causes include assault, trauma during sports, falls, and motor vehicle collisions. Diagnosis is typically based on the signs and symptoms and may occasionally be confirmed by plain X-ray.Treatment is typically with pain medication and cold compresses. Reduction, if needed, can typically occur after the swelling has come down. Depending on the type of fracture reduction may be closed or open. Outcomes are generally good. Nasal fractures are common, comprising about 40% of facial fractures. Males in their 20s are most commonly affected. Signs and symptoms Symptoms of a broken nose include bruising, swelling, tenderness, pain, deformity, and/or bleeding of the nose and nasal region of the face. The patient may have difficulty breathing, or excessive nosebleeds (if the nasal mucosa are damaged). The patient may also have bruising around one or both eyes. Cause Nasal fractures are caused by physical trauma to the face. Common sources of nasal fractures include sports injuries, fighting, falls, and car accidents in the younger age groups, and falls from syncope or impaired balance in the elderly. Diagnosis Nasal fractures are usually identified visually and through physical examination. Medical imaging is generally not recommended. A priority is to distinguish simple fractures limited to the nasal bones (Type 1) from fractures that also involve other facial bones and/or the nasal septum (Types 2 and 3). In simple Type 1 fractures X-Rays supply surprisingly little information beyond clinical examination. However, diagnosis may be confirmed with X-rays or CT scans, and these are required if other facial injuries are suspected.A fracture that runs horizontally across the septum is sometimes called a "Jarjavay fracture", and a vertical one, a "Chevallet fracture".Although treatment of an uncomplicated fracture of nasal bones is not urgent—a referral for specific treatment in five to seven days usually suffices—an associated injury, nasal septal hematoma, occurs in about 5% of cases and does require urgent treatment and should be looked for during the assessment of nasal injuries. Treatment Minor nasal fractures may be allowed to heal on their own provided there is not significant cosmetic deformity. Ice and pain medication may be prescribed to ease discomfort during the healing process. For nasal fractures where the nose has been deformed, manual alignment may be attempted, usually with good results. Injuries involving other structures (Types 2 and 3) must be recognized and treated surgically. Prognosis Bone stability after a fracture occurs between 3 and 5 weeks. Full bone fusion occurs between 4 and 8 weeks. References == External links ==

Diffuse idiopathic skeletal hyperostosis

Diffuse idiopathic skeletal hyperostosis (DISH) is a condition characterized by abnormal calcification/bone formation (hyperostosis) of the soft tissues surrounding the joints of the spine, and also of the peripheral or appendicular skeleton. In the spine, there is bone formation along the anterior longitudinal ligament and sometimes the posterior longitudinal ligament, which may lead to partial or complete fusion of adjacent vertebrae. The facet and sacroiliac joints tend to be uninvolved. The thoracic spine is the most common level involved. In the peripheral skeleton, DISH manifests as a calcific enthesopathy, with pathologic bone formation at sites where ligaments and tendons attach to bone. Signs and symptoms The majority of people with DISH are not symptomatic, and the findings are an incidental imaging abnormality. In some, the x-ray findings may correspond to symptoms of back stiffness with flexion/extension or with mild back pain. Back pain or stiffness may be worse in the morning. Rarely, large anterior cervical spine osteophytes may affect the esophagus or the larynx and cause pain, difficulty swallowing or even dyspnea. Similar calcification and ossification may be seen at peripheral entheseal sites, including the shoulder, iliac crest, ischial tuberosity, trochanters of the hip, tibial tuberosities, patellae, and bones of the hands and/or feet.DISH can be a complicating factor when suffering from trauma involving the spine. It increases the risk of unstable fractures involving the intervertebral disc and the calcified/ossified ligaments which influences the need for surgical treatment. Cause The exact cause is unknown. Mechanical, dietary factors and use of some medications (e.g. isotretinoin, etretinate, acitretin and other vitamin A derivatives) may be of significance. There is a correlation between these factors but not a cause or effect. The distinctive radiological feature of DISH is the continuous linear calcification along the antero-medial aspect of the thoracic spine. DISH is usually found in people in their 60s and above, and is extremely rare in people in their 30s and 40s. The disease can spread to any joint of the body, affecting the neck, shoulders, ribs, hips, pelvis, knees, ankles, and hands. The disease is not fatal; however, some associated complications can lead to death. Complications may include paralysis, dysphagia (difficulty swallowing), and lung infections. Although DISH manifests in a similar manner to ankylosing spondylitis, they are separate diseases. Ankylosing spondylitis is a genetic disease with identifiable marks, tends to start showing signs in adolescence or young adulthood, is more likely to affect the lumbar spine, and affects organs. DISH has no indication of a genetic link, is primarily thoracic and does not affect organs other than the lungs, and only indirectly due to the fusion of the rib cage.Long-term treatment of acne with vitamin derived retinoids, such as etretinate and acitretin, have been associated with extraspinal hyperostosis. Diagnosis DISH is diagnosed by findings on x-ray studies. Radiographs of the spine will show abnormal bone formation (ossification) along the anterior spinal ligament. The disc spaces, facet and sacroiliac joints remain unaffected. Diagnosis requires confluent ossification of at least four contiguous vertebral bodies. Classically, advanced disease may have "melted candle wax" appearance along the spine on radiographic studies. In some cases, DISH may be manifested as ossification, or enthesis, in other parts of the skeleton. The calcification and ossification is most common on the right side of the spine. In people with dextrocardia and situs inversus this calcification occurs on the left side. Examples of DISH Treatment There is limited scientific evidence for the treatment for symptomatic DISH. Symptoms of pain and stiffness may be treated with conservative measures, analgesic medications (such as non-steroidal anti-inflammatory drugs), and physical therapy.In extraordinary cases where calcification or osteophyte formation is causing severe and focal symptoms, such as difficulty swallowing or nerve impingement, surgical intervention may be pursued. See also Ankylosing spondylitis Enthesitis Osteoarthritis Retinoids References == External links ==

Premature ejaculation

Premature ejaculation (PE) occurs when a man expels semen (and most likely experiences orgasm) soon after beginning sexual activity, and with minimal penile stimulation. It has also been called early ejaculation, rapid ejaculation, rapid climax, premature climax and (historically) ejaculatio praecox. There is no uniform cut-off defining "premature", but a consensus of experts at the International Society for Sexual Medicine endorsed a definition of around one minute after penetration. The International Classification of Diseases (ICD-10) applies a cut-off of 15 seconds from the beginning of sexual intercourse.Although men with premature ejaculation describe feeling that they have less control over ejaculating, it is not clear if that is true, and many or most average men also report that they wish they could last longer. Mens typical ejaculatory latency is approximately 4–8 minutes. The opposite condition is delayed ejaculation.Men with PE often report emotional and relationship distress, and some avoid pursuing sexual relationships because of PE-related embarrassment. Compared with men, women consider PE less of a problem, but several studies show that the condition also causes female partners distress. Cause The causes of premature ejaculation are unclear. Many theories have been suggested, including that PE was the result of masturbating quickly during adolescence to avoid being caught, performance anxiety, passive-aggressiveness or having too little sex; but there is little evidence to support any of these theories.Several physiological mechanisms have been hypothesized to contribute to causing premature ejaculation, including serotonin receptors, a genetic predisposition, elevated penile sensitivity and nerve conduction atypicalities. Scientists have long suspected a genetic link to certain forms of premature ejaculation. However, studies have been inconclusive in isolating the gene responsible for lifelong PE. The nucleus paragigantocellularis of the brain has been identified as having involvement in ejaculatory control. Other researchers have noted that men who have premature ejaculation have a faster neurological response in the pelvic muscles.PE may be caused by prostatitis or as a medication side effect. PE has been classified into four subtypes - lifelong, acquired, variable and subjective PE. The pathophysiology of lifelong PE is mediated by a complex interplay of central and peripheral serotonergic, dopaminergic, oxytocinergic, endocrinological, genetic and epigenetic factors. Acquired PE may occur due to psychological problems - such as sexual performance anxiety, and psychological or relationship problems - and/or co-morbidity, including Erectile dysfunction, prostatitis and hyperthyroidism. Mechanism The physical process of ejaculation requires two actions: emission and expulsion. The emission is the first phase. It involves deposition of fluid from the ampullary vas deferens, seminal vesicles and prostate gland into the posterior urethra. The second phase is the expulsion phase. It involves closure of bladder neck, followed by the rhythmic contractions of the urethra by pelvic-perineal and bulbospongiosus muscle and intermittent relaxation of external urethral sphincters.Sympathetic motor neurons control the emission phase of ejaculation reflex, and expulsion phase is executed by somatic and autonomic motor neurons. These motor neurons are located in the thoracolumbar and lumbosacral spinal cord and are activated in a coordinated manner when sufficient sensory input to reach the ejaculatory threshold has entered the central nervous system. Intromission time The 1948 Kinsey Report suggested that three-quarters of men ejaculate within two minutes of penetration in over half of their sexual encounters.Current evidence supports an average intravaginal ejaculation latency time (IELT) of six and a half minutes in 18- to 30-year-olds. If the disorder is defined as an IELT percentile below 2.5, then premature ejaculation could be suggested by an IELT of less than about two minutes. Nevertheless, it is possible that men with abnormally low IELTs could be satisfied with their performance and do not report a lack of control. Likewise, those with higher IELTs may consider themselves premature ejaculators, have detrimental side effects normally associated with premature ejaculation, and even benefit from treatment. Diagnosis The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) defines premature ejaculation as "A persistent or recurrent pattern of ejaculation occurring during partnered sexual activity within approximately 1 minute following vaginal penetration and before the person wishes it," with the additional requirements that the condition occurs for a duration longer than 6 months, causes clinically significant distress, and cannot be better explained by relationship distress, another mental disorder, or the use of medications. These factors are identified by talking with the person, not through any diagnostic test. The DSM-5 allows for specifiers whether the condition is lifelong or acquired, applying in general or only to certain situations, and severity based on the time under one minute, however these subtypes have been criticised as lacking validity due to insufficient evidence.The 2007 ICD-10 defined PE as ejaculating without control, and within around 15 seconds. Treatments Several treatments have been tested for treating premature ejaculation. A combination of medication and non-medication treatments is often the most effective method. Self-treatment Many men attempt to treat themselves for premature ejaculation by trying to distract themselves, such as by trying to focus their attention away from the sexual stimulation. There is little evidence to indicate that it is effective and it tends to detract from the sexual fulfilment of both partners. Other self-treatments include thrusting more slowly, withdrawing the penis altogether, purposefully ejaculating before sexual intercourse, and using more than one condom. Using more than one condom is not recommended as the friction will often lead to breakage. Some men report these to have been helpful.A qualitative clinical trial, conducted by Kings College London medical school teaching hospitals, compared use of the Prolong device with cognitive behavioural therapy. Using the Climax Control Training program in 58 subjects was found to delay time to ejaculation from 48 seconds (0.8 minutes) to 8 minutes and 48 seconds (8.8 minutes) on average in 61% of men, compared to 2 minutes and 36 seconds (2.6 minutes) in 40% of men having cognitive behavioural therapy, with a difference on average of 6 minutes and 12 seconds (6.2 minutes) between the two groups. Sex therapy Several techniques have been developed and applied by sex therapists, including Kegel exercises (to strengthen the muscles of the pelvic floor) and Masters and Johnsons "stop-start technique" (to desensitize the mans responses) and "squeeze technique" (to reduce excessive arousal).: 27 To treat premature ejaculation, Masters and Johnson developed the "squeeze technique", based on the Semans technique developed by James Semans in 1956. Men were instructed to pay close attention to their arousal pattern and learn to recognize how they felt shortly before their "point of no return", the moment ejaculation felt imminent and inevitable. Sensing it, they were to signal their partner, who squeezed the head of the penis between thumb and index finger, suppressing the ejaculatory reflex and allowing the man to last longer.The squeeze technique worked, but many couples found it cumbersome. From the 1970s to the 1990s, sex therapists refined the Masters and Johnson approach, largely abandoning the squeeze technique and focused on a simpler and more effective technique called the "stop-start" technique. During intercourse, as the man senses he is approaching climax, both partners stop moving and remain still until the mans feelings of ejaculatory inevitability subside, at which point, they are free to resume active intercourse.These techniques appear to work for around half of people, in the short-term studies that had been done as of 2017.: 27 Medications As of 2019, there are no drugs specifically approved for the treatment of PE. Selective serotonin reuptake inhibitors (SSRIs) are used to treat PE, including fluoxetine, paroxetine, citalopram, escitalopram or dapoxetine and clomipramine. The opioid tramadol, an atypical oral analgesic is also used. Results have found PDE5 inhibitors to be effective in combination treatment with SSRIs. The full effects of these medications typically emerge after 2-3 weeks, with results indicating about ejaculatory delay varying between 6–20 times greater than before medication. Premature ejaculation can return upon discontinuation, and the side effects of these SSRIs can also include anorgasmia, erectile dysfunction, and diminished libido.Topical anesthetics such as lidocaine and benzocaine that are applied to the tip and shaft of the penis have also been used. They are applied 10–15 minutes before sexual activity and have fewer potential side effects as compared to SSRIs. However, this is sometimes disliked due to the reduction of sensation in the penis as well as for the partner (due to the medication rubbing onto the partner). Surgical treatments Two different surgeries, both developed in South Korea, are available to permanently treat premature ejaculation: selective dorsal neurectomy (SDN) and glans penis augmentation using a hyaluronan gel. Circumcision has shown no effect on PE. The International Society for Sexual Medicine guidelines do not recommend either surgical treatment due to the risk of permanent loss of sexual function and insufficient reliable data and on the basis of violating the medical principle of non-maleficence as the surgery can lead to complications, of which some might not yet be known. The most common complication of surgery is the recurrence of PE, reported to occur in about 10% of surgeries. Other sources consider SDN as a safe and efficient treatment and these surgeries are popular in Asian countries. Epidemiology Premature ejaculation is a prevalent sexual dysfunction in men; however, because of the variability in time required to ejaculate and in partners desired duration of sex, exact prevalence rates of PE are difficult to determine. In the "Sex in America" surveys (1999 and 2008), University of Chicago researchers found that between adolescence and age 59, approximately 30% of men reported having experienced PE at least once during the previous 12 months, whereas about 10 percent reported erectile dysfunction (ED). Although ED is mens most prevalent sex problem after age 60, and may be more prevalent than PE overall according to some estimates, premature ejaculation remains a significant issue that, according to the survey, affects 28 percent of men age 65–74, and 22 percent of men age 75–85. Other studies report PE prevalence ranging from 3 percent to 41 percent of men over 18, but the great majority estimate a prevalence of 20 to 30 percent—making PE a very common sex problem.There is a common misconception that younger men are more likely to develop premature ejaculation and that its frequency decreases with age. Prevalence studies have indicated, however, that rates of PE are constant across age groups. History Male mammals ejaculate quickly during intercourse, prompting some biologists to speculate that rapid ejaculation had evolved into mens genetic makeup to increase their chances of passing their genes.Ejaculatory control issues have been documented for more than 1,500 years. The Kamasutra, the 4th century BCE Indian marriage handbook, declares: "Women love the man whose sexual energy lasts a long time, but they resent a man whose energy ends quickly because he stops before they reach a climax." Waldinger summarizes professional perspectives from early in the twentieth century.Sex researcher Alfred Kinsey did not consider rapid ejaculation a problem, but viewed it as a sign of "masculine vigor" that could not always be cured. The belief that it should be considered a disease rather than a normal variation, has also been disputed by some modern researchers. Psychoanalysis Freudian theory postulated that rapid ejaculation was a symptom of underlying neurosis. It stated that the man has unconscious hostility toward women, so he ejaculates rapidly, which satisfies him but frustrates his lover, who is unlikely to experience orgasm that quickly. Freudians claimed that premature ejaculation could be cured using psychoanalysis. But even years of psychoanalysis accomplished little, if anything, in curing premature ejaculation.In 1974, there was no evidence found to suggest that men with premature ejaculation harbor unusual hostility toward women. See also Anorgasmia Delayed ejaculation Edging (sexual practice) Pre-ejaculate Retrograde ejaculation Erectile dysfunction Blue balls Pull out method Foreplay References Cited sources Kaplan, Helen S. (1974). The New Sex Therapy. Psychology Press. ISBN 9780876300831. Kaplan, Helen S. (1989). How to Overcome Premature Ejaculation. Routledge. ISBN 978-0876305423. Further reading Hamblin, James (2012). "When Is Ejaculation Premature, and When Should a Penis Be Made Numb?". The Atlantic. Retrieved 6 March 2017. According to [Dr. John Mulhall], when we talk casually about premature ejaculation ... were usually talking about what the medical community would consider premature-ejaculatory-like syndrome, or simply rapid ejaculation. ... Mulhall says it comes down to whether the guy lasts long enough. If his partner is made wholly replete in 90 seconds, then a man who lasts 95 seconds can be fine. But if another guy lasts 15 minutes, and thats not cutting it, then its a problem and can be considered rapid. == External links ==

Incidents

Incidents is a 1987 collection of four essays by Roland Barthes. It was published posthumously by François Wahl, Barthes literary executor. Summary In the first essay, La Lumiere du Sud-Ouest, first published in LHumanité in 1977, Roland Barthes reflects on the South West of France, the Adour and Bayonne. The second essay, Incidents, written in 1969, details Barthess holiday in Morocco, where he pays men and boys for sex. In Au Palace Ce Soir, the third essay, first published in issue 10 of Vogue-Hommes in May 1978, Barthes describes Le Palace, a fashionable theatre-house in Paris. The fourth essay, Soirées de Paris, is a diary from August to September 1979, where Roland Barthes admits to using male escorts as all his relationships have been disappointing to him. Literary significance and criticism Although critics have questioned whether Roland Barthes intended to publish Incidents and Soirées de Paris, it has been argued that they have informed our reading of Barthess oeuvre because of their explicit revelations of his homosexuality. Drawing upon these essays, D.A. Miller, in Bringing Out Roland Barthes, re-reads Barthess oeuvre through a gay lens.The essay Incidents has been compared to André Gides Amyntas with its pastoral theme, although Gide writes about Tunisia and Algeria rather than Morocco. It has also been compared to Jean-Jacques Rousseaus Confessions. References External links Barthes, Roland. Incidents. Berkeley: University of California Press, 1992. Free Online - UC Press E-Books Collection

Ketonuria

Ketonuria is a medical condition in which ketone bodies are present in the urine. It is seen in conditions in which the body produces excess ketones as an indication that it is using an alternative source of energy. It is seen during starvation or more commonly in type 1 diabetes mellitus. Production of ketone bodies is a normal response to a shortage of glucose, meant to provide an alternate source of fuel from fatty acids. Pathophysiology Ketones are metabolic end-products of fatty acid metabolism. In healthy individuals, ketones are formed in the liver and are completely metabolized so that only negligible amounts appear in the urine. However, when carbohydrates are unavailable or unable to be used as an energy source, fat becomes the predominant body fuel instead of carbohydrates and excessive amounts of ketones are formed as a metabolic byproduct. Higher levels of ketones in the urine indicate that the body is using fat as the major source of energy. Ketone bodies that commonly appear in the urine when fats are burned for energy are acetoacetate and beta-hydroxybutyric acid. Acetone is also produced and is expired by the lungs. Normally, the urine should not contain a noticeable concentration of ketones to give a positive reading. As with tests for glucose, acetoacetate can be tested by a dipstick or by a lab. The results are reported as small, moderate, or large amounts of acetoacetate. A small amount of acetoacetate is a value under 20 mg/dL; a moderate amount is a value of 30–40 mg/dL, and a finding of 80 mg/dL or greater is reported as a large amount. One 2010 study admits that though ketonurias relation to general metabolic health is ill-understood, there is a positive relationship between the presence of ketonuria after fasting and positive metabolic health. Causes Metabolic abnormalities such as diabetes, renal glycosuria, or glycogen storage disease. Dietary conditions such as starvation, fasting, low-carbohydrate diets, prolonged vomiting, and anorexia including caused by hyperemesis gravidarum. Conditions in which metabolism is increased, such as hyperthyroidism, fever, pregnancy or lactation.In non-diabetic persons, ketonuria may occur during acute illness or severe stress. Approximately 15% of hospitalized patients may have ketonuria, even though they do not have diabetes. In a diabetic patient, ketone bodies in the urine suggest that the patient is not adequately controlled and that adjustments of medication, diet, or both should be made promptly. In the non diabetic patient, ketonuria reflects a reduced carbohydrate metabolism and an increased fat metabolism. Diagnosis A wide variety of companies manufacture ketone screening strips. A strip consists of a thin piece of plastic film slightly larger than a matchstick, with a reagent pad on one end that is either dipped into a urine sample or passed through the stream while the user is voiding. The pad is allowed to react for an exact, specified amount of time (it is recommended to use a stopwatch to time this exactly and disregard any resultant colour change after the specified time); its resulting colour is then compared to a graded shade chart indicating a detection range from negative presence of ketones up to a significant quantity. In severe diabetic ketoacidosis, the dipstix reaction based on sodium nitroprusside may underestimate the level of ketone bodies in the blood. It is sensitive to acetoacetate only, and the ratio of beta-hydroxybutyric to acetoacetate is shifted from a normal value of around 1:1 up to around 10:1 under severely ketoacetotic conditions, due to a changing redox milieu in the liver. Measuring acetoacetate alone will thus underestimate the accompanying beta-hydroxybutyrate if the standard conversion factor is applied. Screening Screening for ketonuria is done frequently for acutely ill patients, presurgical patients, and pregnant women. Any diabetic patient who has elevated levels of blood and urine glucose should be tested for urinary ketones. In addition, when diabetic treatment is being switched from insulin to oral hypoglycemic agents, the patients urine should be monitored for ketonuria. The development of ketonuria within 24 hours after insulin withdrawal usually indicates a poor response to the oral hypoglycemic agents. Diabetic patients should have their urine tested regularly for glucose and ketones, particularly when acute infection or other illness develops. In conditions associated with acidosis, urinary ketones are tested to assess the severity of acidosis and to monitor treatment response. Urine ketones appear before there is any significant increase in blood ketones; therefore, urine ketone measurement is especially helpful in emergency situations. References External links National Institute of Health (NIH) webpage on Ketonuria

Hereditary fructose intolerance

Hereditary fructose intolerance (HFI) is an inborn error of fructose metabolism caused by a deficiency of the enzyme aldolase B. Individuals affected with HFI are asymptomatic until they ingest fructose, sucrose, or sorbitol. If fructose is ingested, the enzymatic block at aldolase B causes an accumulation of fructose-1-phosphate which, over time, results in the death of liver cells. This accumulation has downstream effects on gluconeogenesis and regeneration of adenosine triphosphate (ATP). Symptoms of HFI include vomiting, convulsions, irritability, poor feeding as a baby, hypoglycemia, jaundice, hemorrhage, hepatomegaly, hyperuricemia and potentially kidney failure. While HFI is not clinically a devastating condition, there are reported deaths in infants and children as a result of the metabolic consequences of HFI. Death in HFI is always associated with problems in diagnosis.HFI is an autosomal recessive condition caused by mutations in the ALDOB gene, located at 9q31.1. HFI is typically suspected based on dietary history, especially in infants who become symptomatic after breast feeding. This suspicion is typically confirmed by molecular analysis Treatment of HFI involves strict avoidance of fructose in the diet. Older patients with HFI typically self-select a diet low in fructose, even before being diagnosed. Presentation The key identifying feature of HFI is the appearance of symptoms with the introduction of fructose to the diet. Affected individuals are asymptomatic and healthy, provided they do not ingest foods containing fructose or any of its common precursors, sucrose and sorbitol. In the past, infants often became symptomatic when they were introduced to formulas that were sweetened with fructose or sucrose. These sweeteners are not common in formulas used today. Symptoms such as vomiting, nausea, restlessness, pallor, sweating, trembling and lethargy can also first present in infants when they are introduced to fruits and vegetables. These can progress to apathy, coma and convulsions if the source is not recognized early.When patients are diagnosed with HFI, a dietary history will often reveal an aversion to fruit and other foods that contain large amounts of fructose. Most adult patients do not have any dental caries. Fructose metabolism After ingestion, fructose is converted to fructose-1-phosphate in the liver by fructokinase. Deficiencies of fructokinase cause essential fructosuria, a clinically benign condition characterized by the excretion of unmetabolized fructose in the urine. Fructose-1-phosphate is metabolized by aldolase B into dihydroxyacetone phosphate and glyceraldehyde. HFI is caused by a deficiency of aldolase B.A deficiency of aldolase B results in an accumulation of fructose-1-phosphate, and trapping of phosphate (fructokinase requires adenosine triphosphate (ATP)). The downstream effects of this enzyme block are the inhibition of glucose production and reduced regeneration of ATP. Diagnosis Because of the ease of therapy (dietary exclusion of fructose), HFI can be effectively managed if properly diagnosed. In HFI, the diagnosis of homozygotes is difficult, requiring a genomic DNA screening with allele-specific probes or an enzyme assay from a liver biopsy. Once identified, parents of infants who carry mutant aldolase B alleles leading to HFI, or older individuals who have clinical histories compatible with HFI can be identified and counselled with regard to preventive therapy: dietary exclusion of foods containing fructose, sucrose, or sorbitol. If possible, individuals who suspect they might have HFI should avoid testing via fructose challenge as the results are non-conclusive for individuals with HFI, and even if the diagnostic administration of fructose is properly controlled, profound hypoglycemia and its sequelae can threaten the patients well-being. Treatment Treatment of HFI depends on the stage of the disease, and the severity of the symptoms. Stable patients without acute intoxication events are treated by careful dietary planning that avoids fructose and its metabolic precursors. Fructose is replaced in the diet by glucose, maltose or other sugars. Management of patients with HFI often involves dietitians who have a thorough knowledge of what foods are acceptable. See also Fructose malabsorption References == External links ==

Aphasia

Aphasia is an inability to comprehend or formulate language because of damage to specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine but aphasia due to stroke is estimated to be 0.1–0.4% in the Global North. Aphasia can also be the result of brain tumors, brain infections, or neurodegenerative diseases (such as dementias).To be diagnosed with aphasia, a persons speech or language must be significantly impaired in one (or more) of the four aspects of communication following acquired brain injury. Alternatively, in the case of progressive aphasia, it must have significantly declined over a short period of time. The four aspects of communication are auditory comprehension, verbal expression, reading and writing, and functional communication. The difficulties of people with aphasia can range from occasional trouble finding words, to losing the ability to speak, read, or write; intelligence, however, is unaffected. Expressive language and receptive language can both be affected as well. Aphasia also affects visual language such as sign language. In contrast, the use of formulaic expressions in everyday communication is often preserved. For example, while a person with aphasia, particularly expressive aphasia (Brocas aphasia), may not be able to ask a loved one when their birthday is, they may still be able to sing "Happy Birthday". One prevalent deficit in the aphasias is anomia, which is a difficulty in finding the correct word.: 72 With aphasia, one or more modes of communication in the brain have been damaged and are therefore functioning incorrectly. Aphasia is not caused by damage to the brain that results in motor or sensory deficits, which produces abnormal speech; that is, aphasia is not related to the mechanics of speech but rather the individuals language cognition (although a person can have both problems, as an example, if they have a haemorrhage that damaged a large area of the brain). An individuals language is the socially shared set of rules, as well as the thought processes that go behind communication (as it affects both verbal and nonverbal language). It is not a result of a more peripheral motor or sensory difficulty, such as paralysis affecting the speech muscles or a general hearing impairment. Neurodevelopmental forms of auditory processing disorder are differentiable from aphasia in that aphasia is by definition caused by acquired brain injury, but acquired epileptic aphasia has been viewed as a form of APD. Prevalence Aphasia affects about two million people in the U.S. and 250,000 people in Great Britain. Nearly 180,000 people acquire the disorder every year in the U.S., 170,000 due to stroke. Any person of any age can develop aphasia, given that it is often caused by a traumatic injury. However, people who are middle aged and older are the most likely to acquire aphasia, as the other etiologies are more likely at older ages. For example, approximately 75% of all strokes occur in individuals over the age of 65. Strokes account for most documented cases of aphasia: 25% to 40% of people who survive a stroke develop aphasia as a result of damage to the language-processing regions of the brain. Aphasia and dysphasia Technically, dysphasia means impaired language and aphasia means lack of language. There have been calls to use the term aphasia regardless of severity. Reasons for doing so include dysphasia being easily confused with the swallowing disorder dysphagia, consumers and speech pathologists preferring the term aphasia, and many languages other than English using a word similar to aphasia. The term "aphasia" is more commonly used in North America, while "dysphasia" is more frequently used elsewhere. Signs and symptoms People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems, such as dysarthria or apraxia, and not primarily due to aphasia. Aphasia symptoms can vary based on the location of damage in the brain. Signs and symptoms may or may not be present in individuals with aphasia and may vary in severity and level of disruption to communication. Often those with aphasia may have a difficulty with naming objects, so they might use words such as thing or point at the objects. When asked to name a pencil they may say it is a “thing used to write”. Related behaviors Given the previously stated signs and symptoms, the following behaviors are often seen in people with aphasia as a result of attempted compensation for incurred speech and language deficits: Self-repairs: Further disruptions in fluent speech as a result of mis-attempts to repair erred speech production. Struggle in non-fluent aphasias: A severe increase in expelled effort to speak after a life where talking and communicating was an ability that came so easily can cause visible frustration. Preserved and automatic language: A behavior in which some language or language sequences that were used so frequently prior to onset are still produced with more ease than other language post onset. Subcortical Subcortical aphasias characteristics and symptoms depend upon the site and size of subcortical lesion. Possible sites of lesions include the thalamus, internal capsule, and basal ganglia. Causes Aphasia is most often caused by stroke, where about a quarter of patients who experience an acute stroke develop aphasia. However, any disease or damage to the parts of the brain that control language can cause aphasia. Some of these can include brain tumors, traumatic brain injury, and progressive neurological disorders. In rare cases, aphasia may also result from herpesviral encephalitis. The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia. In acute disorders, such as head injury or stroke, aphasia usually develops quickly. When caused by brain tumor, infection, or dementia, it develops more slowly.Substantial damage to tissue anywhere within the region shown in blue (on the figure in the infobox above) can potentially result in aphasia. Aphasia can also sometimes be caused by damage to subcortical structures deep within the left hemisphere, including the thalamus, the internal and external capsules, and the caudate nucleus of the basal ganglia. The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms. A very small number of people can experience aphasia after damage to the right hemisphere only. It has been suggested that these individuals may have had an unusual brain organization prior to their illness or injury, with perhaps greater overall reliance on the right hemisphere for language skills than in the general population.Primary progressive aphasia (PPA), while its name can be misleading, is actually a form of dementia that has some symptoms closely related to several forms of aphasia. It is characterized by a gradual loss in language functioning while other cognitive domains are mostly preserved, such as memory and personality. PPA usually initiates with sudden word-finding difficulties in an individual and progresses to a reduced ability to formulate grammatically correct sentences (syntax) and impaired comprehension. The etiology of PPA is not due to a stroke, traumatic brain injury (TBI), or infectious disease; it is still uncertain what initiates the onset of PPA in those affected by it.Epilepsy can also include transient aphasia as a prodromal or episodic symptom. Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain. Classification Aphasia is best thought of as a collection of different disorders, rather than a single problem. Each individual with aphasia will present with their own particular combination of language strengths and weaknesses. Consequently, it is a major challenge just to document the various difficulties that can occur in different people, let alone decide how they might best be treated. Most classifications of the aphasias tend to divide the various symptoms into broad classes. A common approach is to distinguish between the fluent aphasias (where speech remains fluent, but content may be lacking, and the person may have difficulties understanding others), and the nonfluent aphasias (where speech is very halting and effortful, and may consist of just one or two words at a time).However, no such broad-based grouping has proven fully adequate. There is wide variation among people even within the same broad grouping, and aphasias can be highly selective. For instance, people with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors.It is important to note that there are typical difficulties with speech and language that come with normal aging as well. As we age, language can become more difficult to process resulting in a slowing of verbal comprehension, reading abilities and more likely word finding difficulties. With each of these though, unlike some aphasias, functionality within daily life remains intact.: 7 Boston classification Individuals with receptive aphasia (Wernickes aphasia), also referred to as fluent aphasia, may speak in long sentences that have no meaning, add unnecessary words, and even create new "words" (neologisms). For example, someone with receptive aphasia may say, "delicious taco", meaning "The dog needs to go out so I will take him for a walk". They have poor auditory and reading comprehension, and fluent, but nonsensical, oral and written expression. Individuals with receptive aphasia usually have great difficulty understanding the speech of both themselves and others and are, therefore, often unaware of their mistakes. Receptive language deficits usually arise from lesions in the posterior portion of the left hemisphere at or near Wernickes area.: 71  It is often the result of trauma to the temporal region of the brain, specifically damage to Wernickes area. Trauma can be the result from an array of problems, however it is most commonly seen as a result of stroke Individuals with expressive aphasia (Brocas aphasia) frequently speak short, meaningful phrases that are produced with great effort. It is thus characterized as a nonfluent aphasia. Affected people often omit small words such as "is", "and", and "the". For example, a person with expressive aphasia may say, "walk dog", which could mean "I will take the dog for a walk", "you take the dog for a walk" or even "the dog walked out of the yard." Individuals with expressive aphasia are able to understand the speech of others to varying degrees. Because of this, they are often aware of their difficulties and can become easily frustrated by their speaking problems. While Brocas aphasia may appear to be solely an issue with language production, evidence suggests that it may be rooted in an inability to process syntactical information. Individuals with expressive aphasia may have a speech automatism (also called recurring or recurrent utterance). These speech automatisms can be repeated lexical speech automatisms; e.g., modalisations (I cant..., I cant...), expletives/swearwords, numbers (one two, one two) or non-lexical utterances made up of repeated, legal but meaningless, consonant-vowel syllables (e.g.., /tan tan/, /bi bi/). In severe cases, the individual may be able to utter only the same speech automatism each time they attempt speech. Individuals with anomic aphasia have difficulty with naming. People with this aphasia may have difficulties naming certain words, linked by their grammatical type (e.g., difficulty naming verbs and not nouns) or by their semantic category (e.g., difficulty naming words relating to photography but nothing else) or a more general naming difficulty. People tend to produce grammatic, yet empty, speech. Auditory comprehension tends to be preserved. Anomic aphasia is the aphasial presentation of tumors in the language zone; it is the aphasial presentation of Alzheimers disease. Anomic aphasia is the mildest form of aphasia, indicating a likely possibility for better recovery. Individuals with transcortical sensory aphasia, in principle the most general and potentially among the most complex forms of aphasia, may have similar deficits as in receptive aphasia, but their repetition ability may remain intact. Global aphasia is considered a severe impairment in many language aspects since it impacts expressive and receptive language, reading, and writing. Despite these many deficits, there is evidence that has shown individuals benefited from speech language therapy. Even though individuals with global aphasia will not become competent speakers, listeners, writers, or readers, goals can be created to improve the individuals quality of life. Individuals with global aphasia usually respond well to treatment that includes personally relevant information, which is also important to consider for therapy. Individuals with conduction aphasia have deficits in the connections between the speech-comprehension and speech-production areas. This might be caused by damage to the arcuate fasciculus, the structure that transmits information between Wernickes area and Brocas area. Similar symptoms, however, can be present after damage to the insula or to the auditory cortex. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Paraphasic errors include phonemic/literal or semantic/verbal. Repetition ability is poor. Conduction and transcortical aphasias are caused by damage to the white matter tracts. These aphasias spare the cortex of the language centers but instead create a disconnection between them. Conduction aphasia is caused by damage to the arcuate fasciculus. The arcuate fasciculus is a white matter tract that connects Brocas and Wernickes areas. People with conduction aphasia typically have good language comprehension, but poor speech repetition and mild difficulty with word retrieval and speech production. People with conduction aphasia are typically aware of their errors. Two forms of conduction aphasia have been described: reproduction conduction aphasia (repetition of a single relatively unfamiliar multisyllabic word) and repetition conduction aphasia (repetition of unconnected short familiar words. Transcortical aphasias include transcortical motor aphasia, transcortical sensory aphasia, and mixed transcortical aphasia. People with transcortical motor aphasia typically have intact comprehension and awareness of their errors, but poor word finding and speech production. People with transcortical sensory and mixed transcortical aphasia have poor comprehension and unawareness of their errors. Despite poor comprehension and more severe deficits in some transcortical aphasias, small studies have indicated that full recovery is possible for all types of transcortical aphasia. Classical-localizationist approaches Localizationist approaches aim to classify the aphasias according to their major presenting characteristics and the regions of the brain that most probably gave rise to them. Inspired by the early work of nineteenth-century neurologists Paul Broca and Carl Wernicke, these approaches identify two major subtypes of aphasia and several more minor subtypes: Expressive aphasia (also known as "motor aphasia" or "Brocas aphasia"), which is characterized by halted, fragmented, effortful speech, but well-preserved comprehension relative to expression. Damage is typically in the anterior portion of the left hemisphere, most notably Brocas area. Individuals with Brocas aphasia often have right-sided weakness or paralysis of the arm and leg, because the left frontal lobe is also important for body movement, particularly on the right side. Receptive aphasia (also known as "sensory aphasia" or "Wernickes aphasia"), which is characterized by fluent speech, but marked difficulties understanding words and sentences. Although fluent, the speech may lack in key substantive words (nouns, verbs, adjectives), and may contain incorrect words or even nonsense words. This subtype has been associated with damage to the posterior left temporal cortex, most notably Wernickes area. These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement. Conduction aphasia, where speech remains fluent, and comprehension is preserved, but the person may have disproportionate difficulty repeating words or sentences. Damage typically involves the arcuate fasciculus and the left parietal region. Transcortical motor aphasia and transcortical sensory aphasia, which are similar to Brocas and Wernickes aphasia respectively, but the ability to repeat words and sentences is disproportionately preserved.Recent classification schemes adopting this approach, such as the Boston-Neoclassical Model, also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Brocas aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernickes aphasia, conduction aphasia and transcortical sensory aphasia). These schemes also identify several further aphasia subtypes, including: anomic aphasia, which is characterized by a selective difficulty finding the names for things; and global aphasia, where both expression and comprehension of speech are severely compromised. Many localizationist approaches also recognize the existence of additional, more "pure" forms of language disorder that may affect only a single language skill. For example, in pure alexia, a person may be able to write but not read, and in pure word deafness, they may be able to produce speech and to read, but not understand speech when it is spoken to them. Cognitive neuropsychological approaches Although localizationist approaches provide a useful way of classifying the different patterns of language difficulty into broad groups, one problem is that a sizeable number of individuals do not fit neatly into one category or another. Another problem is that the categories, particularly the major ones such as Brocas and Wernickes aphasia, still remain quite broad. Consequently, even amongst those who meet the criteria for classification into a subtype, there can be enormous variability in the types of difficulties they experience.Instead of categorizing every individual into a specific subtype, cognitive neuropsychological approaches aim to identify the key language skills or "modules" that are not functioning properly in each individual. A person could potentially have difficulty with just one module, or with a number of modules. This type of approach requires a framework or theory as to what skills/modules are needed to perform different kinds of language tasks. For example, the model of Max Coltheart identifies a module that recognizes phonemes as they are spoken, which is essential for any task involving recognition of words. Similarly, there is a module that stores phonemes that the person is planning to produce in speech, and this module is critical for any task involving the production of long words or long strings of speech. Once a theoretical framework has been established, the functioning of each module can then be assessed using a specific test or set of tests. In the clinical setting, use of this model usually involves conducting a battery of assessments, each of which tests one or a number of these modules. Once a diagnosis is reached as to the skills/modules where the most significant impairment lies, therapy can proceed to treat these skills. Progressive aphasias Primary progressive aphasia (PPA) is a neurodegenerative focal dementia that can be associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimers disease, which is the gradual process of progressively losing the ability to think. Gradual loss of language function occurs in the context of relatively well-preserved memory, visual processing, and personality until the advanced stages. Symptoms usually begin with word-finding problems (naming) and progress to impaired grammar (syntax) and comprehension (sentence processing and semantics). The loss of language before the loss of memory differentiates PPA from typical dementias. People with PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence. There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA).Progressive Jargon Aphasia is a fluent or receptive aphasia in which the persons speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the person has problems with the selection of nouns. Either they will replace the desired word with another that sounds or looks like the original one or has some other connection or they will replace it with sounds. As such, people with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they cannot find with sounds. Substitutions commonly involve picking another (actual) word starting with the same sound (e.g., clocktower – colander), picking another semantically related to the first (e.g., letter – scroll), or picking one phonetically similar to the intended one (e.g., lane – late). Deaf aphasia There have been many instances showing that there is a form of aphasia among deaf individuals. Sign languages are, after all, forms of language that have been shown to use the same areas of the brain as verbal forms of language. Mirror neurons become activated when an animal is acting in a particular way or watching another individual act in the same manner. These mirror neurons are important in giving an individual the ability to mimic movements of hands. Brocas area of speech production has been shown to contain several of these mirror neurons resulting in significant similarities of brain activity between sign language and vocal speech communication. Facial communication is a significant portion of how animals interact with each other. Humans use facial movements to create, what other humans perceive, to be faces of emotions. While combining these facial movements with speech, a more full form of language is created which enables the species to interact with a much more complex and detailed form of communication. Sign language also uses these facial movements and emotions along with the primary hand movement way of communicating. These facial movement forms of communication come from the same areas of the brain. When dealing with damages to certain areas of the brain, vocal forms of communication are in jeopardy of severe forms of aphasia. Since these same areas of the brain are being used for sign language, these same, at least very similar, forms of aphasia can show in the Deaf community. Individuals can show a form of Wernickes aphasia with sign language and they show deficits in their abilities in being able to produce any form of expressions. Brocas aphasia shows up in some people, as well. These individuals find tremendous difficulty in being able to actually sign the linguistic concepts they are trying to express. Severity The severity of the type of aphasia varies depending on the size of the stroke. However, there is much variance between how often one type of severity occurs in certain types of aphasia. For instance, any type of aphasia can range from mild to profound. Regardless of the severity of aphasia, people can make improvements due to spontaneous recovery and treatment in the acute stages of recovery. Additionally, while most studies propose that the greatest outcomes occur in people with severe aphasia when treatment is provided in the acute stages of recovery, Robey (1998) also found that those with severe aphasia are capable of making strong language gains in the chronic stage of recovery as well. This finding implies that persons with aphasia have the potential to have functional outcomes regardless of how severe their aphasia may be. While there is no distinct pattern of the outcomes of aphasia based on severity alone, global aphasia typically makes functional language gains, but may be gradual since global aphasia affects many language areas. Cognitive deficits in aphasia While aphasia has traditionally been described in terms of language deficits, there is increasing evidence that many people with aphasia commonly experience co-occurring non-linguistic cognitive deficits in areas such as attention, memory, executive functions and learning. By some accounts, cognitive deficits, such as attention and working memory constitute the underlying cause of language impairment in people with aphasia. Others suggest that cognitive deficits often co-occur but are comparable to cognitive deficits in stroke patients without aphasia and reflect general brain dysfunction following injury. The degree to which deficits in attention and other cognitive domains underlie language deficits in aphasia is still unclear.In particular, people with aphasia often demonstrate short-term and working memory deficits. These deficits can occur in both the verbal domain as well as the visuospatial domain. Furthermore, these deficits are often associated with performance on language specific tasks such as naming, lexical processing, and sentence comprehension, and discourse production. Other studies have found that most, but not all people with aphasia demonstrate performance deficits on tasks of attention, and their performance on these tasks correlate with language performance and cognitive ability in other domains. Even patients with mild aphasia, who score near the ceiling on tests of language often demonstrate slower response times and interference effects in non-verbal attention abilities.In addition to deficits in short-term memory, working memory, and attention, people with aphasia can also demonstrate deficits in executive function. For instance, people with aphasia may demonstrate deficits in initiation, planning, self-monitoring, and cognitive flexibility. Other studies have found that people with aphasia demonstrate reduced speed and efficiency during completion executive function assessments.Regardless of their role in the underlying nature of aphasia, cognitive deficits have a clear role in the study and rehabilitation of aphasia. For instance, the severity of cognitive deficits in people with aphasia has been associated with lower quality of life, even more so than the severity of language deficits. Furthermore, cognitive deficits may influence the learning process of rehabilitation and language treatment outcomes in aphasia. Non-linguistic cognitive deficits have also been the target of interventions directed at improving language ability, though outcomes are not definitive. While some studies have demonstrated language improvement secondary to cognitively-focused treatment, others have found little evidence that the treatment of cognitive deficits in people with aphasia has an influence on language outcomes.One important caveat in the measurement and treatment of cognitive deficits in people with aphasia is the degree to which assessments of cognition rely on language abilities for successful performance. Most studies have attempted to circumvent this challenge by utilizing non-verbal cognitive assessments to evaluate cognitive ability in people with aphasia. However, the degree to which these tasks are truly non-verbal and not mediated by language in unclear. For instance, Wall et al. found that language and non-linguistic performance was related, except when non-linguistic performance was measured by real life cognitive tasks. Prevention of aphasia Aphasia is largely caused by unavoidable instances. However, some precautions can be taken to decrease risk for experiencing one of the two major causes of aphasia: stroke and traumatic brain injury (TBI). To decrease the probability of having an ischemic or hemorrhagic stroke, one should take the following precautions: Exercising regularly Eating a healthy diet, avoiding cholesterol in particular Keeping alcohol consumption low and avoiding tobacco use Controlling blood pressure Going to the emergency room immediately if you begin to experience unilateral extremity (especially leg) swelling, warmth, redness, and/or tenderness as these are symptoms of a deep vein thrombosis which can lead to a strokeTo prevent aphasia due to traumatic injury, one should take precautionary measures when engaging in dangerous activities such as: Wearing a helmet when operating a bicycle, motor cycle, ATV, or any other moving vehicle that could potentially be involved in an accident Wearing a seatbelt when driving or riding in a car Wearing proper protective gear when playing contact sports, especially American football, rugby, and hockey, or refraining from such activities Minimizing anticoagulant use (including aspirin) if at all possible as they increase the risk of hemorrhage after a head injuryAdditionally, one should always seek medical attention after sustaining head trauma due to a fall or accident. The sooner that one receives medical attention for a traumatic brain injury, the less likely one is to experience long-term or severe effects. Management When addressing Wernickes aphasia, according to Bakheit et al. (2007), the lack of awareness of the language impairments, a common characteristic of Wernickes aphasia, may affect the rate and extent of therapy outcomes. Robey (1998) determined that at least 2 hours of treatment per week is recommended for making significant language gains. Spontaneous recovery may cause some language gains, but without speech-language therapy, the outcomes can be half as strong as those with therapy.When addressing Brocas aphasia, better outcomes occur when the person participates in therapy, and treatment is more effective than no treatment for people in the acute period. Two or more hours of therapy per week in acute and post-acute stages produced the greatest results. High-intensity therapy was most effective, and low-intensity therapy was almost equivalent to no therapy.People with global aphasia are sometimes referred to as having irreversible aphasic syndrome, often making limited gains in auditory comprehension, and recovering no functional language modality with therapy. With this said, people with global aphasia may retain gestural communication skills that may enable success when communicating with conversational partners within familiar conditions. Process-oriented treatment options are limited, and people may not become competent language users as readers, listeners, writers, or speakers no matter how extensive therapy is. However, peoples daily routines and quality of life can be enhanced with reasonable and modest goals. After the first month, there is limited to no healing to language abilities of most people. There is a grim prognosis leaving 83% who were globally aphasic after the first month they will remain globally aphasic at the first year. Some people are so severely impaired that their existing process-oriented treatment approaches offer no signs of progress, and therefore cannot justify the cost of therapy.Perhaps due to the relative rareness of conduction aphasia, few studies have specifically studied the effectiveness of therapy for people with this type of aphasia. From the studies performed, results showed that therapy can help to improve specific language outcomes. One intervention that has had positive results is auditory repetition training. Kohn et al. (1990) reported that drilled auditory repetition training related to improvements in spontaneous speech, Francis et al. (2003) reported improvements in sentence comprehension, and Kalinyak-Fliszar et al. (2011) reported improvements in auditory-visual short-term memory.Most acute cases of aphasia recover some or most skills by working with a speech-language pathologist. Recovery and improvement can continue for years after the stroke. After the onset of Aphasia, there is approximately a six-month period of spontaneous recovery; during this time, the brain is attempting to recover and repair the damaged neurons. Improvement varies widely, depending on the aphasias cause, type, and severity. Recovery also depends on the persons age, health, motivation, handedness, and educational level.There is no one treatment proven to be effective for all types of aphasias. The reason that there is no universal treatment for aphasia is because of the nature of the disorder and the various ways it is presented, as explained in the above sections. Aphasia is rarely exhibited identically, implying that treatment needs to be catered specifically to the individual. Studies have shown that, although there is no consistency on treatment methodology in literature, there is a strong indication that treatment, in general, has positive outcomes. Therapy for aphasia ranges from increasing functional communication to improving speech accuracy, depending on the persons severity, needs and support of family and friends. Group therapy allows individuals to work on their pragmatic and communication skills with other individuals with aphasia, which are skills that may not often be addressed in individual one-on-one therapy sessions. It can also help increase confidence and social skills in a comfortable setting.: 97 Evidence does not support the use of transcranial direct current stimulation (tDCS) for improving aphasia after stroke. Moderate quality evidence does indicate naming performance improvements for nouns but not verbs using tDCSSpecific treatment techniques include the following: Copy and recall therapy (CART) – repetition and recall of targeted words within therapy may strengthen orthographic representations and improve single word reading, writing, and naming Visual communication therapy (VIC) – the use of index cards with symbols to represent various components of speech Visual action therapy (VAT) – typically treats individuals with global aphasia to train the use of hand gestures for specific items Functional communication treatment (FCT) – focuses on improving activities specific to functional tasks, social interaction, and self-expression Promoting aphasics communicative effectiveness (PACE) – a means of encouraging normal interaction between people with aphasia and clinicians. In this kind of therapy, the focus is on pragmatic communication rather than treatment itself. People are asked to communicate a given message to their therapists by means of drawing, making hand gestures or even pointing to an object Melodic intonation therapy (MIT) – aims to use the intact melodic/prosodic processing skills of the right hemisphere to help cue retrieval of words and expressive language: 93  Other – i.e. drawing as a way of communicating, trained conversation partnersSemantic feature analysis (SFA) – a type of aphasia treatment that targets word-finding deficits. It is based on the theory that neural connections can be strengthened by using related words and phrases that are similar to the target word, to eventually activate the target word in the brain. SFA can be implemented in multiple forms such as verbally, written, using picture cards, etc. The SLP provides prompting questions to the individual with aphasia in order for the person to name the picture provided. Studies show that SFA is an effective intervention for improving confrontational naming.Melodic intonation therapy is used to treat non-fluent aphasia and has proved to be effective in some cases. However, there is still no evidence from randomized controlled trials confirming the efficacy of MIT in chronic aphasia. MIT is used to help people with aphasia vocalize themselves through speech song, which is then transferred as a spoken word. Good candidates for this therapy include people who have had left hemisphere strokes, non-fluent aphasias such as Brocas, good auditory comprehension, poor repetition and articulation, and good emotional stability and memory. An alternative explanation is that the efficacy of MIT depends on neural circuits involved in the processing of rhythmicity and formulaic expressions (examples taken from the MIT manual: "I am fine," "how are you?" or "thank you"); while rhythmic features associated with melodic intonation may engage primarily left-hemisphere subcortical areas of the brain, the use of formulaic expressions is known to be supported by right-hemisphere cortical and bilateral subcortical neural networks.Systematic reviews support the effectiveness and importance of partner training. According to the National Institute on Deafness and Other Communication Disorders (NIDCD), involving family with the treatment of an aphasic loved one is ideal for all involved, because while it will no doubt assist in their recovery, it will also make it easier for members of the family to learn how best to communicate with them.When a persons speech is insufficient, different kinds of augmentative and alternative communication could be considered such as alphabet boards, pictorial communication books, specialized software for computers or apps for tablets or smartphones. Intensity of treatment The intensity of aphasia therapy is determined by the length of each session, total hours of therapy per week, and total weeks of therapy provided. There is no consensus about what "intense" aphasia therapy entails, or how intense therapy should be to yield the best outcomes. A 2016 Cochrane review of speech and language therapy for people with aphasia found that treatments that are higher intensity, higher dose or over a long duration of time led to significantly better functional communication but people were more likely to drop out of high intensity treatment (up to 15 hours per week).Intensity of therapy is also dependent on the recency of stroke. People with aphasia react differently to intense treatment in the acute phase (0–3 months post stroke), sub-acute phase (3–6 months post stroke), or chronic phase (6+ months post stroke). Intensive therapy has been found to be effective for people with nonfluent and fluent chronic aphasia, but less effective for people with acute aphasia. People with sub-acute aphasia also respond well to intensive therapy of 100 hours over 62 weeks. This suggests people in the sub-acute phase can improve greatly in language and functional communication measures with intensive therapy compared to regular therapy. Individualized service delivery Intensity of treatment should be individualized based on the recency of stroke, therapy goals, and other specific characteristics such as age, size of lesion, overall health status, and motivation. Each individual reacts differently to treatment intensity and is able to tolerate treatment at different times post-stroke. Intensity of treatment after a stroke should be dependent on the persons motivation, stamina, and tolerance for therapy. Outcomes If the symptoms of aphasia last longer than two or three months after a stroke, a complete recovery is unlikely. However, it is important to note that some people continue to improve over a period of years and even decades. Improvement is a slow process that usually involves both helping the individual and family understand the nature of aphasia and learning compensatory strategies for communicating.After a traumatic brain injury (TBI) or cerebrovascular accident (CVA), the brain undergoes several healing and re-organization processes, which may result in improved language function. This is referred to as spontaneous recovery. Spontaneous recovery is the natural recovery the brain makes without treatment, and the brain begins to reorganize and change in order to recover. There are several factors that contribute to a persons chance of recovery caused by stroke, including stroke size and location. Age, sex, and education have not been found to be very predictive. There is also research pointing to damage in the left hemisphere healing more effectively than the right.Specific to aphasia, spontaneous recovery varies among affected people and may not look the same in everyone, making it difficult to predict recovery.Though some cases of Wernickes aphasia have shown greater improvements than more mild forms of aphasia, people with Wernickes aphasia may not reach as high a level of speech abilities as those with mild forms of aphasia. History The first recorded case of aphasia is from an Egyptian papyrus, the Edwin Smith Papyrus, which details speech problems in a person with a traumatic brain injury to the temporal lobe.During the second half of the 19th century, aphasia was a major focus for scientists and philosophers who were working in the beginning stages of the field of psychology. In medical research, speechlessness was described as an incorrect prognosis, and there was no assumption that underlying language complications existed. Broca and his colleagues were some of the first to write about aphasia, but Wernicke was the first credited to have written extensively about aphasia being a disorder that contained comprehension difficulties. Despite claims of who reported on aphasia first, it was F.J. Gall that gave the first full description of aphasia after studying wounds to the brain, as well as his observation of speech difficulties resulting from vascular lesions. A recent book on the entire history of aphasia is available (Reference: Tesak, J. & Code, C. (2008) Milestones in the History of Aphasia: Theories and Protagonists. Hove, East Sussex: Psychology Press). Etymology Aphasia is from Greek a- ("without", negative prefix) + phásis (φάσις, "speech"). The word aphasia comes from the word ἀφασία aphasia, in Ancient Greek, which means "speechlessness", derived from ἄφατος aphatos, "speechless" from ἀ- a-, "not, un" and φημί phemi, "I speak". Neuroimaging Methods Magnetic resonance imaging (MRI) and functional magnetic resonance imaging (fMRI) are the most common neuroimaging tools used in identifying aphasia and studying the extent of damage in the loss of language abilities. This is done by doing MRI scans and locating the extent of lesions or damage within brain tissue, particularly within areas of the left frontal and temporal regions- where a lot of language related areas lie. In fMRI studies a language related task is often completed and then the BOLD image is analyzed. If there are lower than normal BOLD responses that indicate a lessening of blood flow to the affected area and can show quantitatively that the cognitive task is not being completed. There are limitations to the use of fMRI in aphasic patients particularly. Because a high percentage of aphasic patients develop it because of stroke there can be infarcts present which is the total loss of blood flow. This can be due to the thinning of blood vessels or the complete blockage of it. This is important in fMRI as it relies on the BOLD response (the oxygen levels of the blood vessels), and this can create a false hyporesponse upon fMRI study. Due to the limitations of fMRI such as a lower spatial resolution, it can show that some areas of the brain are not active during a task when they in reality are. Additionally, with stroke being the cause of many cases of aphasia the extent of damage to brain tissue can be difficult to quantify therefore the effects of stroke brain damage on the functionality of the patient can vary. Neural Substrates of Aphasia Subtypes MRI is often used to predict or confirm the subtype of aphasia present. Researchers compared 3 subtypes of aphasia- nonfluent-variant primary progressive aphasia (nfPPA), logopenic-variant primary progressive aphasia (lvPPA), and semantic-variant primary progressive aphasia (svPPA), with primary progressive aphasia (PPA) and Alzheimer’s disease. This was done by analyzing the MRIs of patients with each of the subsets of PPA. Images which compare subtypes of aphasia as well as for finding the extent of lesions are generated by overlapping images of different participants brains (if applicable) and isolating areas of lesions or damage using third party software such as MRIcron. MRI has also been used to study the relationship between the type of aphasia developed and the age of the person with aphasia. It was found that patients with fluent aphasia are on average older than people with non-fluent aphasia. It was also found that among patients with lesions confined to the anterior portion of the brain an unexpected portion of them presented with fluent aphasia and were remarkably older than those with non-fluent aphasia. This effect was not found when the posterior portion of the brain was studied.Associated Conditions In a study on the features associated with different disease trajectories in Alzheimers disease (AD)-related primary progressive aphasia (PPA), it was found that metabolic patterns via PET SPM analysis can help predict progression of total loss of speech and functional autonomy in AD and PPA patients. This was done by comparing an MRI or CT image of the brain and presence of a radioactive biomarker with normal levels in patients without Alzheimer’s Disease. Apraxia is another disorder often correlated with aphasia. This is due to a subset of apraxia which affects speech. Specifically, this subset affects the movement of muscles associated with speech production, apraxia and aphasia are often correlated due to the proximity of neural substrates associated with each of the disorders. Researchers concluded that there were 2 areas of lesion overlap between patients with apraxia and aphasia, the anterior temporal lobe and the left inferior parietal lobe.Treatment and Neuroimaging Evidence for positive treatment outcomes can also be quantified using neuroimaging tools. The use of fMRI and an automatic classifier can help predict language recovery outcomes in stroke patients with 86% accuracy when coupled with age and language test scores. The stimuli tested were sentences both correct and incorrect and the subject had to press a button whenever the sentence was incorrect. The fMRI data collected focused on responses in regions of interest identified by healthy subjects. Recovery from aphasia can also be quantified using diffusion tensor imaging. The accurate fasciculus (AF) connects the right and left superior temporal lobe, premotor regions/posterior inferior frontal gyrus. and the primary motor cortex. In a study which enrolled patients in a speech therapy program, an increase in AF fibers and volume was found in patients after 6-weeks in the program which correlated with long-term improvement in those patients. The results of the experiment are pictured in Figure 2. This implies that DTI can be used to quantify the improvement in patients after speech and language treatment programs are applied. Conclusion Neuroimaging tools serve as a useful method for determining disorder progression, quantification of cortical damage, aphasia subtype, treatment effectiveness, and differentiating diagnosis with correlated disorders. Utilization of neuroimaging tools is necessary for the progression of knowledge of aphasia and its subtypes. Further research Research is currently being done using functional magnetic resonance imaging (fMRI) to witness the difference in how language is processed in normal brains vs aphasic brains. This will help researchers to understand exactly what the brain must go through in order to recover from Traumatic Brain Injury (TBI) and how different areas of the brain respond after such an injury.Another intriguing approach being tested is that of drug therapy. Research is in progress that will hopefully uncover whether or not certain drugs might be used in addition to speech-language therapy in order to facilitate recovery of proper language function. Its possible that the best treatment for Aphasia might involve combining drug treatment with therapy, instead of relying on one over the other.One other method being researched as a potential therapeutic combination with speech-language therapy is brain stimulation. One particular method, Transcranial Magnetic Stimulation (TMS), alters brain activity in whatever area it happens to stimulate, which has recently led scientists to wonder if this shift in brain function caused by TMS might help people re-learn languages. The research being put into Aphasia has only just begun. Researchers appear to have multiple ideas on how Aphasia could be more effectively treated in the future. See also References External links National Aphasia Association Aphasia at Curlie

Thigh

In human anatomy, the thigh is the area between the hip (pelvis) and the knee. Anatomically, it is part of the lower limb.The single bone in the thigh is called the femur. This bone is very thick and strong (due to the high proportion of bone tissue), and forms a ball and socket joint at the hip, and a modified hinge joint at the knee. Structure Bones The femur is the only bone in the thigh and serves as an attachment site for all muscles in the thigh. The head of the femur articulates with the acetabulum in the pelvic bone forming the hip joint, while the distal part of the femur articulates with the tibia and patella forming the knee. By most measures, the femur is the strongest bone in the body. The femur is also the longest bone in the body.The femur is categorised as a long bone and comprises a diaphysis, the shaft (or body) and two epiphysis or extremities that articulate with adjacent bones in the hip and knee. Muscular compartments In cross-section, the thigh is divided up into three separate compartments, divided by fascia, each containing muscles. These compartments use the femur as an axis and are separated by tough connective tissue membranes (or septa). Each of these compartments has its own blood and nerve supply, and contains a different group of muscles. Medial fascial compartment of thigh, adductor Posterior fascial compartment of thigh, flexion, hamstring Anterior fascial compartment of thigh, extensionAnterior compartment muscles of the thigh include sartorius, and the four muscles that comprise the quadriceps muscles- rectus femoris, vastus medialis, vastus intermedius and vastus lateralis. Posterior compartment muscles of the thigh are the hamstring muscles, which include semimembranosus, semitendinosus, and biceps femoris. Medial compartment muscles are pectineus, adductor magnus, adductor longus and adductor brevis, and also gracilis. Because the major muscles of the thigh are the largest muscles of the body, resistance exercises (strength training) of them stimulate blood flow more than any other localized activity. Blood supply The arterial supply is by the femoral artery and the obturator artery. The lymphatic drainage closely follows the arterial supply and drains to the lumbar lymphatic trunks on the corresponding side, which in turn drains to the cisterna chyli. The deep venous system of the thigh consists of the femoral vein, the proximal part of the popliteal vein, and various smaller vessels; these are the site of proximal deep venous thrombosis. The venae perfortantes connect the deep and the superficial system, which consists of the saphenous veins (the site of varicose veins). Clinical significance Thigh weakness can result in a positive Gowers sign on physical examination.Regarding Sports injury, whether acute or from overuse, a thigh injury can mean significant incapacity to perform. Soft tissue injury can encompass sprains, strains, bruising and tendinitis. Runners knee (Patellofemoral pain): is a direct consequence of the kneecap rubbing against the end of the thigh bone (”femur”). Tight hamstrings and weak thigh muscles, required to stabilize the knee, risk development of runners knee. Food The thigh meat of some animals such as chicken and cow is consumed as food in many parts of the world. Society and culture Western societies generally tolerate clothing that displays thighs, such as short shorts and miniskirts. Beachwear and many athleisure styles often display thighs as well. Professional dress codes may require covering up bare thighs. Many Islamic countries disapprove of or prohibit the display of thighs, especially by women. Strategic covering or display of thighs is used in popular fashion around the world, such as thigh-high boots and zettai ryoiki. Additional images == References ==

Rheumatism

Rheumatism or rheumatic disorders are conditions causing chronic, often intermittent pain affecting the joints or connective tissue. Rheumatism does not designate any specific disorder, but covers at least 200 different conditions, including arthritis and "non-articular rheumatism", also known as "regional pain syndrome" or "soft tissue rheumatism". There is a close overlap between the term soft tissue disorder and rheumatism. Sometimes the term "soft tissue rheumatic disorders" is used to describe these conditions.The term "Rheumatic Diseases" is used in MeSH to refer to connective tissue disorders. The branch of medicine devoted to the diagnosis and therapy of rheumatism is called rheumatology. Types Many rheumatic disorders of chronic, intermittent pain (including joint pain, neck pain or back pain) have historically been caused by infectious diseases. Their etiology was unknown until the 20th century and not treatable. Postinfectious arthritis, also known as reactive arthritis, and rheumatic fever are other examples. In the United States, major rheumatic disorders are divided into 10 major categories based on the nomenclature and classification proposed by the American College of Rheumatology (ACR) in 1983. Diffuse connective tissue diseases Rheumatoid arthritis Juvenile arthritis Systemic lupus erythematosus Sjögren syndrome Scleroderma Polymyositis Dermatomyositis Behçets disease Relapsing polychondritis Arthritis associated with spondylitis (i.e. spondarthritis) Ankylosing spondylitis Reactive arthritis Psoriatic arthritis Osteoarthritis (i.e. osteoarthrosis, degenerative joint disease) Rheumatic syndromes associated with infectious agents (direct and indirect or reactive) Metabolic and endocrine diseases associated with rheumatic states Gout, pseudogout Neoplasms Neurovascular disorders Bone and cartilage disorders Extraarticular disorders Bursitis/Tendinitis of the shoulder, wrist, biceps, leg, knee cap (patella), ankle, hip, and Achilles tendon Capsulitis Miscellaneous disorders associated with articular manifestations Palindromic rheumatism is thought to be a form of rheumatoid arthritis. Diagnosis Blood and urine tests will measure levels of creatinine and uric acid to determine kidney function, an elevation of the ESR and CRP is possible. After a purine-restricted diet, another urine test will help determine whether the body is producing too much uric acid or the body isnt excreting enough uric acid. Rheumatoid factor may be present, especially in the group that is likely to develop rheumatoid arthritis. A fine needle is used to draw fluid from a joint to determine if there is any build up of fluid. The presence of uric acid crystals in the fluid would indicate gout. In many cases there may be no specific test, and it is often a case of eliminating other conditions before getting a correct diagnosis. Management Initial therapy of the major rheumatological diseases is with analgesics, such as paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs). Steroids, especially glucocorticoids, and stronger analgesics are often required for more severe cases. History The term rheumatism stems from the Late Latin rheumatismus, ultimately from Greek ῥευματίζομαι "to suffer from a flux", with rheum meaning bodily fluids, i.e. any discharge of blood or bodily fluid. Before the 17th century, the joint pain which was thought to be caused by viscous humours seeping into the joints was always referred to as gout, a word adopted in Middle English from Old French gote "a drop; the gout, rheumatism", not to be confused with the present day specific term referring to excess of uric acid.The English term rheumatism in the current sense has been in use since the late 17th century, as it was believed that chronic joint pain was caused by excessive flow of rheum which means bodily fluids into a joint. See also Corbetts electrostatic machine References Further reading Callan, Margaret (2011). The Rheumatology Handbook. 15th World Congress of Pain Clinicians, (WSPC 2012) (Illustrated ed.). World Scientific. ISBN 978-1-84816-320-1. External links American College of Rheumatology National Institute of Arthritis and Musculoskeletal and Skin Diseases - US National Institute of Arthritis and Musculoskeletal and Skin Diseases

Bandemia

Bandemia refers to an excess or increased levels of band cells (immature white blood cells) released by the bone marrow into the blood. It thus overlaps with the concept of left shift—bandemia is a principal type of left shift and many (perhaps most) clinical mentions of the latter refer to instances of this type.It is a signifier of infection (or sepsis) or inflammation. Measurement of it can play a role in the approach to appendicitis. See also Granulocytosis References == External links ==

Peritoneal cavity

The peritoneal cavity is a potential space between the parietal peritoneum (the peritoneum that surrounds the abdominal wall) and visceral peritoneum (the peritoneum that surrounds the internal organs). The parietal and visceral peritonea are layers of the peritoneum named depending on their function/location. It is one of the spaces derived from the coelomic cavity of the embryo, the others being the pleural cavities around the lungs and the pericardial cavity around the heart. It is the largest serosal sac, and the largest fluid-filled cavity, in the body and secretes approximately 50 ml of fluid per day. This fluid acts as a lubricant and has anti-inflammatory properties. The peritoneal cavity is divided into two compartments – one above, and one below the transverse colon. Compartments The peritoneal cavity is divided by the transverse colon (and its mesocolon) into an upper supracolic compartment, and a lower infracolic compartment. The liver, spleen, stomach, and lesser omentum are contained within the supracolic compartment. The small intestine surrounded by the ascending, transverse, and descending colon, and the paracolic gutters are contained within the infracolic compartment. Clinical significance The peritoneal cavity is a common injection site, used in intraperitoneal injection. An increase in the capillary pressure in the abdominal viscera can cause fluid to leave the interstitial space and enter the peritoneal cavity, a condition called ascites. In cases where cerebrospinal fluid builds up, such as in hydrocephalus, the fluid is commonly diverted to the peritoneal cavity by use of a shunt placed by surgery.Body fluid sampling from the peritoneal cavity is called peritoneocentesis. The peritoneal cavity is involved in peritoneal dialysis. See also Lesser sac Greater sac References External links peritoneum at The Anatomy Lesson by Wesley Norman (Georgetown University)

Polyphagia

Polyphagia or hyperphagia is an abnormally strong, incessant sensation of hunger or desire to eat often leading to overeating. In contrast to an increase in appetite following exercise, polyphagia does not subside after eating and often leads to rapid intake of excessive quantities of food. Polyphagia is not a disorder by itself; rather, it is a symptom indicating an underlying medical condition. It is frequently a result of abnormal blood glucose levels (both hyperglycemia and hypoglycemia), and, along with polydipsia and polyuria, it is one of the "3 Ps" commonly associated with uncontrolled diabetes mellitus. Etymology and pronunciation The word polyphagia () uses combining forms of poly- + -phagia, from the Greek words πολύς (polys), "very much" or "many", and φαγῶ (phago), "eating" or "devouring". Underlying conditions and possible causes Polyphagia is one of the most common symptoms of diabetes mellitus. It is associated with hyperthyroidism and endocrine diseases, e.g., Graves disease, and it has also been noted in Prader-Willi syndrome and other genetic conditions caused by chromosomal anomalies. It is only one of several diagnostic criteria for bulimia and is not by itself classified as an eating disorder. As a symptom of Kleine–Levin syndrome, it is sometimes termed megaphagia.Knocking out vagal nerve receptors has been shown to cause hyperphagia.Changes in hormones associated with the female menstrual cycle can lead to extreme hunger right before the period. Spikes in estrogen and progesterone and decreased serotonin can lead to cravings for carbohydrates and fats. These can be all part of premenstrual syndrome (PMS).According to the National Center for Biomedical Information, polyphagia is found in the following conditions: Chromosome 22q13 duplication syndrome Chromosome 2p25.3 deletion (MYT1L Syndrome) Chromosome Xq26.3 duplication syndrome Congenital generalized lipodystrophy type 1 Congenital generalized lipodystrophy type 2 Diabetes mellitus type 1 Familial renal glucosuria Frontotemporal dementia Frontotemporal dementia, ubiquitin-positive Graves disease Hypotonia-cystinuria syndrome Kleine-Levin syndrome Leptin deficiency or dysfunction Leptin receptor deficiency Luscan-lumish syndrome Macrosomia adiposa congenita Mental retardation, autosomal dominant 1 Obesity, hyperphagia, and developmental delay (OBHD) Picks disease Prader-Willi syndrome Proopiomelanocortin deficiency Schaaf-yang syndrome Polyphagia in diabetes Diabetes mellitus causes a disruption in the bodys ability to transfer glucose from food into energy. Intake of food causes glucose levels to rise without a corresponding increase in energy, which leads to a persistent sensation of hunger. Polyphagia usually occurs early in the course of diabetic ketoacidosis. However, once insulin deficiency becomes more severe and ketoacidosis develops, appetite is suppressed. See also References External links Diseases and conditions associated with Polyphagia

Arteriovenous fistula

An arteriovenous fistula is an abnormal connection or passageway between an artery and a vein. It may be congenital, surgically created for hemodialysis treatments, or acquired due to pathologic process, such as trauma or erosion of an arterial aneurysm. Clinical features Pathological Hereditary hemorrhagic telangiectasia is a condition where there is direct connection between arterioles and venules without intervening capillary beds, at the mucocutaneous region and internal bodily organs. Those who are affected by this conditions usually do not experience any symptoms. Difficulty in breathing is the most common symptom for those who experience symptoms.Just like berry aneurysm, a cerebral arteriovenous malformation can rupture causing subarachnoid hemorrhage. Causes The cause of this condition include Congenital (developmental defect) Rupture of arterial aneurysm into an adjacent vein Penetrating injuries Inflammatory necrosis of adjacent vessels Complication of catheter insertion rarely causes arteriovenous fistula. It is usually caused by brachial artery puncture because brachial artery is located between two brachial veins.Surgically created Cimino fistula is used as a vascular access for hemodialysis. Blood must be aspirated from the body of the patient, and since arteries are not easy to reach compared to the veins, blood may be aspirated from veins. The problem is that the walls of the veins are thin compared to those of the arteries. The AV fistula is the solution for this problem because, after 4–6 weeks, the walls of the veins become thicker due to the high arterial pressure. Thus, this vein can now tolerate needles during hemodialysis sessions. Mechanism When an arteriovenous fistula is formed involving a major artery like the abdominal aorta, it can lead to a large decrease in peripheral resistance. This lowered peripheral resistance causes the heart to increase cardiac output to maintain proper blood flow to all tissues. The physical manifestations of this typically consist of a relatively normal systolic blood pressure accompanied by decreased diastolic blood pressure, resulting in a wider pulse pressure.Normal blood flow in the brachial artery is 85 to 110 milliliters per minute (mL/min). After the creation of a fistula, the blood flow increases to 400–500 mL/min immediately, and 700–1,000 mL/min within 1 month. A brachiocephalic fistula above the elbow has a greater flow rate than a radiocephalic fistula at the wrist. Both the artery and the vein dilate and elongate in response to the greater blood flow and shear stress, but the vein dilates more and becomes "arterialized". In one study, the cephalic vein increased from 2.3 mm to 6.3 mm diameter after 2 months. When the vein is large enough to allow cannulation, the fistula is defined as "mature".An arteriovenous fistula can increase preload. AV shunts also decrease the afterload of the heart. This is because the blood bypasses the arterioles which results in a decrease in the total peripheral resistance (TPR). AV shunts increase both the rate and volume of blood returning to the heart. Diagnosis The diagnosis of this condition can be done via ultrasound See also References == External links ==

Smear

Smear may refer to: A smear test, wherein a sample is smeared over a microscope slide to be studied for any pathology A smear test usually refers to a pap test, that is, a cervical smear Smear (card game) Smear Lake, a lake in Wisconsin Smear campaign, or smear job, an attack on the reputation of an individual or group making use of disinformation tactics Smear Campaign (album), an album by Napalm Death Pat Smear, the guitarist and actor Smear (optics), motion that degrades sharpness, which is generally linear over the integration time Colloquial name for a glissando, a glide from one musical pitch to anotherSmearing may refer to: Smearing of an image taken by an astronomical interferometer: Bandwidth smearing, a chromatic aberration; Time smearing, a consequence of Earth rotation during the observation; Smearing (climbing), a technique of rock climbing Electron smearing, a tool for improving convergence in DFT calculations See also Smeared, the debut studio album by Canadian rock band Sloan

Avalanche

An avalanche is a rapid flow of snow down a slope, such as a hill or mountain.Avalanches can be set off spontaneously, by such factors as increased precipitation or snowpack weakening, or by external means such as humans, animals, and earthquakes. Primarily composed of flowing snow and air, large avalanches have the capability to capture and move ice, rocks, and trees. Avalanches occur in two general forms, or combinations thereof: slab avalanches made of tightly packed snow, triggered by a collapse of an underlying weak snow layer, and loose snow avalanches made of looser snow. After being set off, avalanches usually accelerate rapidly and grow in mass and volume as they capture more snow. If an avalanche moves fast enough, some of the snow may mix with the air, forming a powder snow avalanche. Though they appear to share similarities, avalanches are distinct from slush flows, mudslides, rock slides, and serac collapses. They are also different from large scale movements of ice. Avalanches can happen in any mountain range that has an enduring snowpack. They are most frequent in winter or spring, but may occur at any time of year. In mountainous areas, avalanches are among the most serious natural hazards to life and property, so great efforts are made in avalanche control. There are many classification systems for the different forms of avalanches, which vary according to their users needs. Avalanches can be described by their size, destructive potential, initiation mechanism, composition, and dynamics. Formation Most avalanches occur spontaneously during storms under increased load due to snowfall and/or erosion. The second largest cause of natural avalanches is metamorphic changes in the snowpack such as melting due to solar radiation. Other natural causes include rain, earthquakes, rockfall and icefall. Artificial triggers of avalanches include skiers, snowmobiles, and controlled explosive work. Contrary to popular belief, avalanches are not triggered by loud sound; the pressure from sound is orders of magnitude too small to trigger an avalanche.Avalanche initiation can start at a point with only a small amount of snow moving initially; this is typical of wet snow avalanches or avalanches in dry unconsolidated snow. However, if the snow has sintered into a stiff slab overlying a weak layer then fractures can propagate very rapidly, so that a large volume of snow, that may be thousands of cubic metres, can start moving almost simultaneously. A snowpack will fail when the load exceeds the strength. The load is straightforward; it is the weight of the snow. However, the strength of the snowpack is much more difficult to determine and is extremely heterogeneous. It varies in detail with properties of the snow grains, size, density, morphology, temperature, water content; and the properties of the bonds between the grains. These properties may all metamorphose in time according to the local humidity, water vapour flux, temperature and heat flux. The top of the snowpack is also extensively influenced by incoming radiation and the local air flow. One of the aims of avalanche research is to develop and validate computer models that can describe the evolution of the seasonal snowpack over time. A complicating factor is the complex interaction of terrain and weather, which causes significant spatial and temporal variability of the depths, crystal forms, and layering of the seasonal snowpack. Slab avalanches Slab avalanches form frequently in snow that has been deposited, or redeposited by wind. They have the characteristic appearance of a block (slab) of snow cut out from its surroundings by fractures. Elements of slab avalanches include the following: a crown fracture at the top of the start zone, flank fractures on the sides of the start zones, and a fracture at the bottom called the stauchwall. The crown and flank fractures are vertical walls in the snow delineating the snow that was entrained in the avalanche from the snow that remained on the slope. Slabs can vary in thickness from a few centimetres to three metres. Slab avalanches account for around 90% of avalanche-related fatalities in backcountry users. Powder snow avalanches The largest avalanches form turbulent suspension currents known as powder snow avalanches or mixed avalanches, a kind of gravity current. These consist of a powder cloud, which overlies a dense avalanche. They can form from any type of snow or initiation mechanism, but usually occur with fresh dry powder. They can exceed speeds of 300 km/h (190 mph), and masses of 10,000,000 tonnes; their flows can travel long distances along flat valley bottoms and even uphill for short distances. Wet snow avalanches In contrast to powder snow avalanches, wet snow avalanches are a low velocity suspension of snow and water, with the flow confined to the track surface (McClung, first edition 1999, page 108). The low speed of travel is due to the friction between the sliding surface of the track and the water saturated flow. Despite the low speed of travel (≈10–40 km/h), wet snow avalanches are capable of generating powerful destructive forces, due to the large mass and density. The body of the flow of a wet snow avalanche can plough through soft snow, and can scour boulders, earth, trees, and other vegetation; leaving exposed and often scored ground in the avalanche track. Wet snow avalanches can be initiated from either loose snow releases, or slab releases, and only occur in snowpacks that are water saturated and isothermally equilibrated to the melting point of water. The isothermal characteristic of wet snow avalanches has led to the secondary term of isothermal slides found in the literature (for example in Daffern, 1999, page 93). At temperate latitudes wet snow avalanches are frequently associated with climatic avalanche cycles at the end of the winter season, when there is significant daytime warming. Ice avalanche An ice avalanche occurs when a large piece of ice, such as from a serac or calving glacier, falls onto ice (such as the Khumbu Icefall), triggering a movement of broken ice chunks. The resulting movement is more analogous to a rockfall or a landslide than a snow avalanche. They are typically very difficult to predict and almost impossible to mitigate. Avalanche pathway As an avalanche moves down a slope it follows a certain pathway that is dependent on the slopes degree of steepness and the volume of snow/ice involved in the mass movement. The origin of an avalanche is called the Starting Point and typically occurs on a 30–45 degree slope. The body of the pathway is called the Track of the avalanche and usually occurs on a 20–30 degree slope. When the avalanche loses its momentum and eventually stops it reaches the Runout Zone. This usually occurs when the slope has reached a steepness that is less than 20 degrees. These degrees are not consistently true due to the fact that each avalanche is unique depending on the stability of the snowpack that it was derived from as well as the environmental or human influences that triggered the mass movement. Injuries and deaths People caught in avalanches can die from suffocation, trauma, or hypothermia. From "1950 - 1951 to 2020 - 2021" there were 1,169 people who died in avalanches in the United states. For the 11-year period ending April 2006 445 people died in avalanches throughout North America. On average, 28 people die in avalanches every winter in the United States.In 2001 it was reported that globally an average of 150 people die each year from avalanches. Three of the deadliest recorded avalanches have killed over a thousand people each. Terrain, snowpack, weather Doug Fesler and Jill Fredston developed a conceptual model of the three primary elements of avalanches: terrain, weather, and snowpack. Terrain describes the places where avalanches occur, weather describes the meteorological conditions that create the snowpack, and snowpack describes the structural characteristics of snow that make avalanche formation possible. Terrain Avalanche formation requires a slope shallow enough for snow to accumulate but steep enough for the snow to accelerate once set in motion by the combination of mechanical failure (of the snowpack) and gravity. The angle of the slope that can hold snow, called the angle of repose, depends on a variety of factors such as crystal form and moisture content. Some forms of drier and colder snow will only stick to shallower slopes, while wet and warm snow can bond to very steep surfaces. In particular, in coastal mountains, such as the Cordillera del Paine region of Patagonia, deep snowpacks collect on vertical and even overhanging rock faces. The slope angle that can allow moving snow to accelerate depends on a variety of factors such as the snows shear strength (which is itself dependent upon crystal form) and the configuration of layers and inter-layer interfaces. The snowpack on slopes with sunny exposures is strongly influenced by sunshine. Diurnal cycles of thawing and refreezing can stabilize the snowpack by promoting settlement. Strong freeze-thaw cycles result in the formation of surface crusts during the night and of unstable surface snow during the day. Slopes in the lee of a ridge or of another wind obstacle accumulate more snow and are more likely to include pockets of deep snow, wind slabs, and cornices, all of which, when disturbed, may result in avalanche formation. Conversely, the snowpack on a windward slope is often much shallower than on a lee slope. Avalanches and avalanche paths share common elements: a start zone where the avalanche originates, a track along which the avalanche flows, and a runout zone where the avalanche comes to rest. The debris deposit is the accumulated mass of the avalanched snow once it has come to rest in the run-out zone. For the image at left, many small avalanches form in this avalanche path every year, but most of these avalanches do not run the full vertical or horizontal length of the path. The frequency with which avalanches form in a given area is known as the return period. The start zone of an avalanche must be steep enough to allow snow to accelerate once set in motion, additionally convex slopes are less stable than concave slopes, because of the disparity between the tensile strength of snow layers and their compressive strength. The composition and structure of the ground surface beneath the snowpack influences the stability of the snowpack, either being a source of strength or weakness. Avalanches are unlikely to form in very thick forests, but boulders and sparsely distributed vegetation can create weak areas deep within the snowpack through the formation of strong temperature gradients. Full-depth avalanches (avalanches that sweep a slope virtually clean of snow cover) are more common on slopes with smooth ground, such as grass or rock slabs. Generally speaking, avalanches follow drainages down-slope, frequently sharing drainage features with summertime watersheds. At and below tree line, avalanche paths through drainages are well defined by vegetation boundaries called trim lines, which occur where avalanches have removed trees and prevented regrowth of large vegetation. Engineered drainages, such as the avalanche dam on Mount Stephen in Kicking Horse Pass, have been constructed to protect people and property by redirecting the flow of avalanches. Deep debris deposits from avalanches will collect in catchments at the terminus of a run out, such as gullies and river beds. Slopes flatter than 25 degrees or steeper than 60 degrees typically have a lower incidence of avalanches. Human-triggered avalanches have the greatest incidence when the snows angle of repose is between 35 and 45 degrees; the critical angle, the angle at which human-triggered avalanches are most frequent, is 38 degrees. When the incidence of human triggered avalanches is normalized by the rates of recreational use, however, hazard increases uniformly with slope angle, and no significant difference in hazard for a given exposure direction can be found. The rule of thumb is: A slope that is flat enough to hold snow but steep enough to ski has the potential to generate an avalanche, regardless of the angle. Snowpack structure and characteristics The snowpack is composed of ground-parallel layers that accumulate over the winter. Each layer contains ice grains that are representative of the distinct meteorological conditions during which the snow formed and was deposited. Once deposited, a snow layer continues to evolve under the influence of the meteorological conditions that prevail after deposition. For an avalanche to occur, it is necessary that a snowpack have a weak layer (or instability) below a slab of cohesive snow. In practice the formal mechanical and structural factors related to snowpack instability are not directly observable outside of laboratories, thus the more easily observed properties of the snow layers (e.g. penetration resistance, grain size, grain type, temperature) are used as index measurements of the mechanical properties of the snow (e.g. tensile strength, friction coefficients, shear strength, and ductile strength). This results in two principal sources of uncertainty in determining snowpack stability based on snow structure: First, both the factors influencing snow stability and the specific characteristics of the snowpack vary widely within small areas and time scales, resulting in significant difficulty extrapolating point observations of snow layers across different scales of space and time. Second, the relationship between readily observable snowpack characteristics and the snowpacks critical mechanical properties has not been completely developed. While the deterministic relationship between snowpack characteristics and snowpack stability is still a matter of ongoing scientific study, there is a growing empirical understanding of the snow composition and deposition characteristics that influence the likelihood of an avalanche. Observation and experience has shown that newly fallen snow requires time to bond with the snow layers beneath it, especially if the new snow falls during very cold and dry conditions. If ambient air temperatures are cold enough, shallow snow above or around boulders, plants, and other discontinuities in the slope, weakens from rapid crystal growth that occurs in the presence of a critical temperature gradient. Large, angular snow crystals are indicators of weak snow, because such crystals have fewer bonds per unit volume than small, rounded crystals that pack tightly together. Consolidated snow is less likely to slough than loose powdery layers or wet isothermal snow; however, consolidated snow is a necessary condition for the occurrence of slab avalanches, and persistent instabilities within the snowpack can hide below well-consolidated surface layers. Uncertainty associated with the empirical understanding of the factors influencing snow stability leads most professional avalanche workers to recommend conservative use of avalanche terrain relative to current snowpack instability. Weather Avalanches only occur in a standing diksnowpack. Typically winter seasons at high latitudes, high altitudes, or both have weather that is sufficiently unsettled and cold enough for precipitated snow to accumulate into a seasonal snowpack. Continentality, through its potentiating influence on the meteorological extremes experienced by snowpacks, is an important factor in the evolution of instabilities, and consequential occurrence of avalanches faster stabilization of the snowpack after storm cycles. The evolution of the snowpack is critically sensitive to small variations within the narrow range of meteorological conditions that allow for the accumulation of snow into a snowpack. Among the critical factors controlling snowpack evolution are: heating by the sun, radiational cooling, vertical temperature gradients in standing snow, snowfall amounts, and snow types. Generally, mild winter weather will promote the settlement and stabilization of the snowpack; conversely, very cold, windy, or hot weather will weaken the snowpack. At temperatures close to the freezing point of water, or during times of moderate solar radiation, a gentle freeze-thaw cycle will take place. The melting and refreezing of water in the snow strengthens the snowpack during the freezing phase and weakens it during the thawing phase. A rapid rise in temperature, to a point significantly above the freezing point of water, may cause avalanche formation at any time of year. Persistent cold temperatures can either prevent new snow from stabilizing or destabilize the existing snowpack. Cold air temperatures on the snow surface produce a temperature gradient in the snow, because the ground temperature at the base of the snowpack is usually around 0 °C, and the ambient air temperature can be much colder. When a temperature gradient greater than 10 °C change per vertical meter of snow is sustained for more than a day, angular crystals called depth hoar or facets begin forming in the snowpack because of rapid moisture transport along the temperature gradient. These angular crystals, which bond poorly to one another and the surrounding snow, often become a persistent weakness in the snowpack. When a slab lying on top of a persistent weakness is loaded by a force greater than the strength of the slab and persistent weak layer, the persistent weak layer can fail and generate an avalanche. Any wind stronger than a light breeze can contribute to a rapid accumulation of snow on sheltered slopes downwind. Wind slabs form quickly and, if present, weaker snow below the slab may not have time to adjust to the new load. Even on a clear day, wind can quickly load a slope with snow by blowing snow from one place to another. Top-loading occurs when wind deposits snow from the top of a slope; cross-loading occurs when wind deposits snow parallel to the slope. When a wind blows over the top of a mountain, the leeward, or downwind, side of the mountain experiences top-loading, from the top to the bottom of that lee slope. When the wind blows across a ridge that leads up the mountain, the leeward side of the ridge is subject to cross-loading. Cross-loaded wind-slabs are usually difficult to identify visually. Snowstorms and rainstorms are important contributors to avalanche danger. Heavy snowfall will cause instability in the existing snowpack, both because of the additional weight and because the new snow has insufficient time to bond to underlying snow layers. Rain has a similar effect. In the short-term, rain causes instability because, like a heavy snowfall, it imposes an additional load on the snowpack; and, once rainwater seeps down through the snow, it acts as a lubricant, reducing the natural friction between snow layers that holds the snowpack together. Most avalanches happen during or soon after a storm. Daytime exposure to sunlight will rapidly destabilize the upper layers of the snowpack if the sunlight is strong enough to melt the snow, thereby reducing its hardness. During clear nights, the snowpack can re-freeze when ambient air temperatures fall below freezing, through the process of long-wave radiative cooling, or both. Radiative heat loss occurs when the night air is significantly cooler than the snowpack, and the heat stored in the snow is re-radiated into the atmosphere. Dynamics When a slab avalanche forms, the slab disintegrates into increasingly smaller fragments as the snow travels downhill. If the fragments become small enough the outer layer of the avalanche, called a saltation layer, takes on the characteristics of a fluid. When sufficiently fine particles are present they can become airborne and, given a sufficient quantity of airborne snow, this portion of the avalanche can become separated from the bulk of the avalanche and travel a greater distance as a powder snow avalanche. Scientific studies using radar, following the 1999 Galtür avalanche disaster, confirmed the hypothesis that a saltation layer forms between the surface and the airborne components of an avalanche, which can also separate from the bulk of the avalanche.Driving an avalanche is the component of the avalanches weight parallel to the slope; as the avalanche progresses any unstable snow in its path will tend to become incorporated, so increasing the overall weight. This force will increase as the steepness of the slope increases, and diminish as the slope flattens. Resisting this are a number of components that are thought to interact with each other: the friction between the avalanche and the surface beneath; friction between the air and snow within the fluid; fluid-dynamic drag at the leading edge of the avalanche; shear resistance between the avalanche and the air through which it is passing, and shear resistance between the fragments within the avalanche itself. An avalanche will continue to accelerate until the resistance exceeds the forward force. Modelling Attempts to model avalanche behaviour date from the early 20th century, notably the work of Professor Lagotala in preparation for the 1924 Winter Olympics in Chamonix. His method was developed by A. Voellmy and popularised following the publication in 1955 of his Ueber die Zerstoerungskraft von Lawinen (On the Destructive Force of Avalanches).Voellmy used a simple empirical formula, treating an avalanche as a sliding block of snow moving with a drag force that was proportional to the square of the speed of its flow: Pref = 1 2 ρ v 2 {\displaystyle {\textrm {Pref}}={\frac {1}{2}}\,{\rho }\,{v^{2}}\,\!} He and others subsequently derived other formulae that take other factors into account, with the Voellmy-Salm-Gubler and the Perla-Cheng-McClung models becoming most widely used as simple tools to model flowing (as opposed to powder snow) avalanches.Since the 1990s many more sophisticated models have been developed. In Europe much of the recent work was carried out as part of the SATSIE (Avalanche Studies and Model Validation in Europe) research project supported by the European Commission which produced the leading-edge MN2L model, now in use with the Service Restauration des Terrains en Montagne (Mountain Rescue Service) in France, and D2FRAM (Dynamical Two-Flow-Regime Avalanche Model), which was still undergoing validation as of 2007. Other known models are the SAMOS-AT avalanche simulation software and the RAMMS software. Human involvement Prevention Preventative measures are employed in areas where avalanches pose a significant threat to people, such as ski resorts, mountain towns, roads, and railways. There are several ways to prevent avalanches and lessen their power and develop preventative measures to reduce the likelihood and size of avalanches by disrupting the structure of the snowpack, while passive measures reinforce and stabilize the snowpack in situ. The simplest active measure is repeatedly traveling on a snowpack as snow accumulates; this can be by means of boot-packing, ski-cutting, or machine grooming. Explosives are used extensively to prevent avalanches, by triggering smaller avalanches that break down instabilities in the snowpack, and removing overburden that can result in larger avalanches. Explosive charges are delivered by a number of methods including hand-tossed charges, helicopter-dropped bombs, Gazex concussion lines, and ballistic projectiles launched by air cannons and artillery. Passive preventive systems such as snow fences and light walls can be used to direct the placement of snow. Snow builds up around the fence, especially the side that faces the prevailing winds. Downwind of the fence, snow build-up is lessened. This is caused by the loss of snow at the fence that would have been deposited and the pickup of the snow that is already there by the wind, which was depleted of snow at the fence. When there is a sufficient density of trees, they can greatly reduce the strength of avalanches. They hold snow in place and when there is an avalanche, the impact of the snow against the trees slows it down. Trees can either be planted or they can be conserved, such as in the building of a ski resort, to reduce the strength of avalanches. In turn, socio-environmental changes can influence the occurrence of damaging avalanches: some studies linking changes in land-use/land-cover patterns and the evolution of snow avalanche damage in mid latitude mountains show the importance of the role played by vegetation cover, that is at the root of the increase of damage when the protective forest is deforested (because of demographic growth, intensive grazing and industrial or legal causes), and at the root of the decrease of damage because of the transformation of a traditional land-management system based on overexploitation into a system based on land marginalization and reforestation, something that has happened mainly since the mid-20th century in mountain environments of developed countries Mitigation In many areas, regular avalanche tracks can be identified and precautions can be taken to minimize damage, such as the prevention of development in these areas. To mitigate the effect of avalanches the construction of artificial barriers can be very effective in reducing avalanche damage. There are several types: One kind of barrier (snow net) uses a net strung between poles that are anchored by guy wires in addition to their foundations. These barriers are similar to those used for rockslides. Another type of barrier is a rigid fence-like structure (snow fence) and may be constructed of steel, wood or pre-stressed concrete. They usually have gaps between the beams and are built perpendicular to the slope, with reinforcing beams on the downhill side. Rigid barriers are often considered unsightly, especially when many rows must be built. They are also expensive and vulnerable to damage from falling rocks in the warmer months. In addition to industrially manufactured barriers, landscaped barriers, called avalanche dams stop or deflect avalanches with their weight and strength. These barriers are made out of concrete, rocks, or earth. They are usually placed right above the structure, road, or railway that they are trying to protect, although they can also be used to channel avalanches into other barriers. Occasionally, earth mounds are placed in the avalanches path to slow it down. Finally, along transportation corridors, large shelters, called snow sheds, can be built directly in the slide path of an avalanche to protect traffic from avalanches. Early warning systems Warning systems can detect avalanches which develop slowly, such as ice avalanches caused by icefalls from glaciers. Interferometric radars, high-resolution cameras, or motion sensors can monitor instable areas over a long term, lasting from days to years. Experts interpret the recorded data and are able to recognize upcoming ruptures in order to initiate appropriate measures. Such systems (e.g. the monitoring of the Weissmies glacier in Switzerland) can recognize events several days in advance. Alarm systems Modern radar technology enables the monitoring of large areas and the localization of avalanches at any weather condition, by day and by night. Complex alarm systems are able to detect avalanches within a short time in order to close (e.g. roads and rails) or evacuate (e.g. construction sites) endangered areas. An example of such a system is installed on the only access road of Zermatt in Switzerland. Two radars monitor the slope of a mountain above the road. The system automatically closes the road by activating several barriers and traffic lights within seconds such that no people are harmed. Survival, rescue, and recovery Avalanche accidents are broadly differentiated into 2 categories: accidents in recreational settings, and accidents in residential, industrial, and transportation settings. This distinction is motivated by the observed difference in the causes of avalanche accidents in the two settings. In the recreational setting most accidents are caused by the people involved in the avalanche. In a 1996 study, Jamieson et al. (pages 7–20) found that 83% of all avalanches in the recreational setting were caused by those who were involved in the accident. In contrast, all of the accidents in the residential, industrial, and transportation settings were due to spontaneous natural avalanches. Because of the difference in the causes of avalanche accidents, and the activities pursued in the two settings, avalanche and disaster management professionals have developed two related preparedness, rescue, and recovery strategies for each of the settings. Notable avalanches Two avalanches occurred in March 1910 in the Cascade and Selkirk Mountain ranges; On 1 March the Wellington avalanche killed 96 in Washington state, United States. Three days later 62 railroad workers were killed in the Rogers Pass avalanche in British Columbia, Canada. During World War I, an estimated 40,000 to 80,000 soldiers died as a result of avalanches during the mountain campaign in the Alps at the Austrian-Italian front, many of which were caused by artillery fire. Some 10,000 men, from both sides, lost their lives in avalanches in December 1916.In the northern hemisphere winter of 1950–1951 approximately 649 avalanches were recorded in a three-month period throughout the Alps in Austria, France, Switzerland, Italy and Germany. This series of avalanches killed around 265 people and was termed the Winter of Terror. A mountain climbing camp on Lenin Peak, in what is now Kyrgyzstan, was wiped out in 1990 when an earthquake triggered a large avalanche that overran the camp. Forty-three climbers were killed.In 1993, the Bayburt Üzengili avalanche killed 60 individuals in Üzengili in the province of Bayburt, Turkey. A large avalanche in Montroc, France, in 1999, 300,000 cubic metres of snow slid on a 30° slope, achieving a speed in the region of 100 km/h (62 mph). It killed 12 people in their chalets under 100,000 tons of snow, 5 meters (16 feet) deep. The mayor of Chamonix was convicted of second-degree murder for not evacuating the area, but received a suspended sentence.The small Austrian village of Galtür was hit by the Galtür avalanche in 1999. The village was thought to be in a safe zone but the avalanche was exceptionally large and flowed into the village. Thirty-one people died. On 1 December 2000, the Glory Bowl Avalanche formed on Mt. Glory which is located within the Teton Mountain Range in Wyoming, United States. Joel Roof was snowboarding recreationally in this backcountry, bowl-shaped run and triggered the avalanche. He was carried nearly 2,000 feet to the base of the mountain and was not successfully rescued. Classification European avalanche risk In Europe, the avalanche risk is widely rated on the following scale, which was adopted in April 1993 to replace the earlier non-standard national schemes. Descriptions were last updated in May 2003 to enhance uniformity.In France, most avalanche deaths occur at risk levels 3 and 4. In Switzerland most occur at levels 2 and 3. It is thought that this may be due to national differences of interpretation when assessing the risks. [1] Stability: Generally described in more detail in the avalanche bulletin (regarding the altitude, aspect, type of terrain etc.)[2] additional load: heavy: two or more skiers or boarders without spacing between them, a single hiker or climber, a grooming machine, avalanche blasting light: a single skier or snowboarder smoothly linking turns and without falling, a group of skiers or snowboarders with a minimum 10 m gap between each person, a single person on snowshoesGradient: gentle slopes: with an incline below about 30° steep slopes: with an incline over 30° very steep slopes: with an incline over 35° extremely steep slopes: extreme in terms of the incline (over 40°), the terrain profile, proximity of the ridge, smoothness of underlying ground European avalanche size table Avalanche size: North American Avalanche Danger Scale In the United States and Canada, the following avalanche danger scale is used. Descriptors vary depending on country. Avalanche Problems There are nine different types of avalanche problems: Storm slab Wind slab Wet slab avalanches Persistent slab Deep persistent slab Loose dry avalanches Loose wet avalanches Glide avalanches Cornice fall Canadian classification for avalanche size The Canadian classification for avalanche size is based upon the consequences of the avalanche. Half sizes are commonly used. United States classification for avalanche size The size of avalanches are classified using two scales; size relative to destructive force or D-scale and size relative to the avalanche path or R-scale. Both size scales range from 1 to 5 with the D size scale half sizes can be used. Rutschblock Test Slab avalanche hazard analysis can be done using the Rutschblock Test. A 2 m wide block of snow is isolated from the rest of the slope and progressively loaded. The result is a rating of slope stability on a seven step scale. (Rutsch means slide in German). Avalanches and climate change Avalanche formation and frequency is highly affected by weather patterns and the local climate. Snowpack layers will form differently depending on whether snow is falling in very cold or very warm conditions, and very dry or very humid conditions. Thus, climate change may affect when, where, and how often avalanches occur, and may also change the type of avalanches that are occurring. Impacts on avalanche type and frequency Overall, a rising seasonal snow line and a decrease in the number of days with snow cover are predicted. Climate change-caused temperature increases and changes in precipitation patterns will likely differ between the different mountain regions, and the impacts of these changes on avalanches will change at different elevations. In the long term, avalanche frequency at lower elevations is expected to decline corresponding to a decrease in snow cover and depth, and a short-term increase in the number of wet avalanches are predicted.Precipitation is expected to increase, meaning more snow or rain depending on the elevation. Higher elevations predicted to remain above the seasonal snow line will likely see an increase in avalanche activity due to the increases in precipitation during the winter season. Storm precipitation intensity is also expected to increase, which is likely to lead to more days with enough snowfall to cause the snowpack to become unstable. Moderate and high elevations may see an increase in volatile swings from one weather extreme to the other. Predictions also show an increase in the number of rain on snow events, and wet avalanche cycles occurring earlier in the spring during the remainder of this century. Impacts on burial survival rate The warm, wet snowpacks that are likely to increase in frequency due to climate change may also make avalanche burials more deadly. Warm snow has a higher moisture content and is therefore denser than colder snow. Denser avalanche debris decreases the ability for a buried person to breath and the amount of time they have before they run out of oxygen. This increases the likelihood of death by asphyxia in the event of a burial. Additionally, the predicted thinner snowpacks may increase the frequency of injuries due to trauma, such as a buried skier striking a rock or tree. Avalanches on the planet Mars See also Related flows Avalanche disasters 1999 Galtür avalanche Montroc 2012 Gayari Sector avalanche References Bibliography McClung, David. Snow Avalanches as a Non-critical, Punctuated Equilibrium System: Chapter 24 in Nonlinear Dynamics in Geosciences, A.A. Tsonsis and J.B. Elsner (Eds.), Springer, 2007 Daffern, Tony: Avalanche Safety for Skiers, Climbers and Snowboarders, Rocky Mountain Books, 1999, ISBN 0-921102-72-0 Billman, John: Mike Elggren on Surviving an Avalanche. Skiing magazine February 2007: 26. McClung, David and Shaerer, Peter: The Avalanche Handbook, The Mountaineers: 2006. 978-0-89886-809-8 Tremper, Bruce: Staying Alive in Avalanche Terrain, The Mountaineers: 2001. ISBN 0-89886-834-3 Munter, Werner: Drei mal drei (3x3) Lawinen. Risikomanagement im Wintersport, Bergverlag Rother, 2002. ISBN 3-7633-2060-1 (in German) (partial English translation included in PowderGuide: Managing Avalanche Risk ISBN 0-9724827-3-3) Michael Falser: Historische Lawinenschutzlandschaften: eine Aufgabe für die Kulturlandschafts- und Denkmalpflege In: kunsttexte 3/2010, unter: Historische Lawinenschutzlandschaften: eine Aufgabe für die Kulturlandschafts- und Denkmalpflege Notes External links Media related to Avalanche chute at Wikimedia Commons The Avalanche Education Project Surviving an Avalanche – A guide for children and youth Avalanche Defense Photographs Avalanche Canada Canadian Avalanche Association Archived 21 October 2020 at the Wayback Machine Colorado Avalanche Information Center Center for Snow and Avalanche Studies EAWS – European Avalanche Warning Services Directory of European avalanche services Avalanches collected news and commentary at The New York Times Swiss Federal Institute for Snow and Avalanche Research Scottish Avalanche Information Service Chisholm, Hugh, ed. (1911). "Avalanche" . Encyclopædia Britannica (11th ed.). Cambridge University Press. But note the myths cited above Utah Avalanche Center New Zealand Avalanche Advisory Gulmarg Avalanche Center US Avalanche.org Sierra Avalanche Center (Tahoe National Forest)

Sacroiliitis

Sacroiliitis is inflammation within the sacroiliac joint. It is a feature of spondyloarthropathies, such as axial spondyloarthritis (including ankylosing spondylitis), psoriatic arthritis, reactive arthritis or arthritis related to inflammatory bowel diseases, including ulcerative colitis or Crohns disease. It is also the most common presentation of arthritis from brucellosis. Symptoms and signs People suffering from sacroiliitis can often experience symptoms in a number of different ways, however it is commonly related to the amount of pressure that is put onto the sacroiliac joint. Sacroiliitis pain is typically axial, meaning that the location of the condition is also where the pain is occurring. Symptoms commonly include prolonged, inflammatory pain in the lower back region, hips or buttocks.However, in more severe cases, pain can become more radicular and manifest itself in seemingly unrelated areas of the body including the legs, groin and feet.Symptoms are typically aggravated by: Transitioning from sitting to standing Walking or standing for extended periods of time Running Climbing stairs Taking long strides Rolling over in bed Bearing more weight on one leg Cause Sacroiliitis is a condition caused by inflammation within the sacroiliac joint. This joint is located where the base of the spine, known as the sacrum, and the pelvis, known as the ilium, intersect. "Itis" is a Latin term denoting inflammation.Since sacroiliitis can describe any type of inflammation found within the sacroiliac joint, there can be a number of issues that cause it. These include: Degenerative arthritis, or osteoarthritis of the spine, can cause degeneration within the sacroiliac joints and lead to inflammation and joint pain. Any form of spondyloarthropathies, which includes ankylosing spondylitis, psoriatic arthritis, reactive arthritis or arthritis related to inflammatory bowel diseases, including ulcerative colitis or Crohns disease. Pregnancy can cause inflammation as a result of the widening and stretching of the sacroiliac joints to prepare for childbirth. Additionally, the added weight carried during childbearing can put an extra amount of stress on the SI joints, leading to abnormal wear. Traumatic injury such as a fall or car crash that affects the lower back, hips, buttocks or legs. Though rare, infection within the sacroiliac joints or another part of the body, such as a urinary tract infection, can cause inflammation. Diagnosis Sacroiliitis can be somewhat difficult to diagnose because the symptoms it manifests can also be caused by other, more common, conditions. If a physician suspects sacroiliitis, they will typically begin their diagnosis by performing a physical exam. Since the condition is axial, they can often pinpoint the affected joint by putting pressure on different places within the legs, hips, spine and buttocks. They may also ask a patient to perform some stretches that will put gentle stress on the sacroiliac joints.X-rays, MRIs and other medical imaging tests can be used to show signs of inflammation and damage within the SI joints. Typically, a spine specialist will order a medical imaging test if they suspect ankylosing spondylitis or another form of arthritis to be the primary cause of inflammation and pain. Treatment Treatment of sacroiliitis can vary depending on the severity of the condition and the amount of pain the patient is currently experiencing. However, it typically falls into one of two categories non-surgical and surgical: Non-surgical In most cases sacroiliitis can be treated without surgery. Often patients will find relief through a combination of rest, heat / ice therapy, physical therapy and anti-inflammatory medication, like ibuprofen. Together these simple treatments help reduce inflammation in the affected SI joints.For more severe forms of sacroiliitis, sacroiliac joint injections might be recommended to help combat symptoms. If chosen, a physician will inject a numbing agent, usually lidocaine, and a steroid containing powerful anti-inflammatory medication into the joint using fluoroscopic guidance. These steroid injections can be delivered up to three or four times a year and should be accompanied with physical therapy to help rehabilitate the affected joint. Surgical Surgery is often the last resort when dealing with sacroiliitis and is rarely required. However, it may be a viable option for patients who are suffering from severe pain that is unresponsive to nonsurgical treatments and is significantly impacting their quality of life. In these cases, a minimally invasive procedure known as Sacroiliac Joint Fusion can effectively stabilize the joint and increase its load-bearing capacity by fusing it together. See also Sacroiliac joint dysfunction Surgery for the dysfunctional sacroiliac joint References == External links ==

Cerebral atherosclerosis

Cerebral atherosclerosis is a type of atherosclerosis where build-up of plaque in the blood vessels of the brain occurs. Some of the main components of the plaques are connective tissue, extracellular matrix, including collagen, proteoglycans, fibronectin, and elastic fibers; crystalline cholesterol, cholesteryl esters, and phospholipids; cells such as monocyte derived macrophages, T-lymphocytes, and smooth muscle cells. The plaque that builds up can lead to further complications such as stroke, as the plaque disrupts blood flow within the intracranial arterioles. This causes the downstream sections of the brain that would normally be supplied by the blocked artery to suffer from ischemia. Diagnosis of the disease is normally done through imaging technology such as angiograms or magnetic resonance imaging. The risk of cerebral atherosclerosis and its associated diseases appears to increase with increasing age; however there are numerous factors that can be controlled in attempt to lessen risk. Diagnosis Diagnostic methods include: AngiogramDue to positive remodeling the plaque build-up shown on angiogram may appear further downstream on the x-ray where the luminal diameter would look normal even though there is severe narrowing at the real site. Because angiograms require x-rays to be visualized the number of times an individual can have it done over a year is limited by the guidelines for the amount of radiation they can be exposed to in a one-year period. Magnetic resonance imaging (MRI)Magnetic resonance imaging has the ability to quantify the plaque anatomy and composition. This allows physicians to determine certain characteristics of the plaque such as how likely it is to break away from the wall and become an embolus. MRI does not use ionizing radiation, so the number of times that it is used on a single person is not a concern; however since it uses strong magnetic fields those who have metal implants cannot use this technique. Computed tomography (CT)In the context of imaging cerebral atherosclerosis, multidirectional computed tomography (MDCT) is often superior to regular CT scans, because it can provide a higher spatial resolution and it has a shorter acquisition time. MDCT uses x-rays to obtain the image; however it can identify the composition of the plaque. Thus it can be determined whether the plaque is calcified plaque and lipid-rich plaque, so the inherent risks can be determined. Subjects are exposed to a substantial amount of radiation with this procedure, so their use is limited. Treatment Asymptomatic individuals with intracranial stenosis are typically told to take over the counter platelet inhibitors like aspirin whereas those with symptomatic presentation are prescribed anti-coagulation medications. For asymptomatic persons the idea is to stop the buildup of plaque from continuing. They are not experiencing symptoms; however if more build up occurs it is likely they will. For symptomatic individuals it is necessary to try and reduce the amount of stenosis. The anti-coagulation medications reduce the likelihood of further buildup while also trying to break down the current build up on the surface without an embolism forming. For those with severe stenosis that are at risk for impending stroke endovascular treatment is used. Depending on the individual and the location of the stenosis there are multiple treatments that can be undertaken. These include angioplasty, stent insertion, or bypass the blocked area. Related diseases Diseases associated with cerebral atherosclerosis include: Hypertensive arteriopathyThis pathological process involves the thickening and damage of arteriole walls. It mainly affects the ends of the arterioles which are located in the deep gray nuclei and deep white matter of the brain. It is thought that this is what causes cerebral microbleeds in deep brain regions. This small vessel damage can also reduce the clearance of amyloid-β, thereby increasing the likelihood of CAA.Diseases cerebral atherosclerosis and associated diseases can cause are: Alzheimers diseaseAlzheimers disease is a form of dementia that entails brain atrophy. Cerebral amyloid angiopathy is found in 90% of the cases at autopsy, with 25% being severe CAA. Cerebral microbleeds (CMB)Cerebral microbleeds have been observed during recent studies on people with dementia using MRI. StrokeStrokes occur from the sudden loss of blood flow to an area of the brain. The loss of flow is generally either from a blockage or hemorrhage. Studies of postmortem stroke cases have shown that intracranial atherosclerotic plaque build up occurred in over half of the individuals and over one third of the overall cases had stenotic build up. == References ==

Pressure

Pressure (symbol: p or P) is the force applied perpendicular to the surface of an object per unit area over which that force is distributed.: 445  Gauge pressure (also spelled gage pressure) is the pressure relative to the ambient pressure. Pressure is a standard mechanical quantity. Various units are used to express pressure. Some of these derive from a unit of force divided by a unit of area; the SI unit of pressure, the pascal (Pa), for example, is one newton per square metre (N/m2); similarly, the pound-force per square inch (psi) is the traditional unit of pressure in the imperial and U.S. customary systems. Pressure may also be expressed in terms of standard atmospheric pressure; the atmosphere (atm) is equal to this pressure, and the torr is defined as 1⁄760 of this. Manometric units such as the centimetre of water, millimetre of mercury, and inch of mercury are used to express pressures in terms of the height of column of a particular fluid in a manometer. Definition Pressure is the amount of force applied perpendicular to the surface of an object per unit area. The symbol for it is "p" or P. The IUPAC recommendation for pressure is a lower-case p. However, upper-case P is widely used. The usage of P vs p depends upon the field in which one is working, on the nearby presence of other symbols for quantities such as power and momentum, and on writing style. Formula Mathematically: p = F A , {\displaystyle p={\frac {F}{A}},} where: p {\displaystyle p} is the pressure, F {\displaystyle F} is the magnitude of the normal force, A {\displaystyle A} is the area of the surface on contact.Pressure is a scalar quantity. It relates the vector area element (a vector normal to the surface) with the normal force acting on it. The pressure is the scalar proportionality constant that relates the two normal vectors: d F n = − p d A = − p n d A . {\displaystyle d\mathbf {F} _{n}=-p\,d\mathbf {A} =-p\,\mathbf {n} \,dA.} The minus sign comes from the convention that the force is considered towards the surface element, while the normal vector points outward. The equation has meaning in that, for any surface S in contact with the fluid, the total force exerted by the fluid on that surface is the surface integral over S of the right-hand side of the above equation. It is incorrect (although rather usual) to say "the pressure is directed in such or such direction". The pressure, as a scalar, has no direction. The force given by the previous relationship to the quantity has a direction, but the pressure does not. If we change the orientation of the surface element, the direction of the normal force changes accordingly, but the pressure remains the same.Pressure is distributed to solid boundaries or across arbitrary sections of fluid normal to these boundaries or sections at every point. It is a fundamental parameter in thermodynamics, and it is conjugate to volume. Units The SI unit for pressure is the pascal (Pa), equal to one newton per square metre (N/m2, or kg·m−1·s−2). This name for the unit was added in 1971; before that, pressure in SI was expressed simply in newtons per square metre. Other units of pressure, such as pounds per square inch (lbf/in2) and bar, are also in common use. The CGS unit of pressure is the barye (Ba), equal to 1 dyn·cm−2, or 0.1 Pa. Pressure is sometimes expressed in grams-force or kilograms-force per square centimetre (g/cm2 or kg/cm2) and the like without properly identifying the force units. But using the names kilogram, gram, kilogram-force, or gram-force (or their symbols) as units of force is expressly forbidden in SI. The technical atmosphere (symbol: at) is 1 kgf/cm2 (98.0665 kPa, or 14.223 psi). Since a system under pressure has the potential to perform work on its surroundings, pressure is a measure of potential energy stored per unit volume. It is therefore related to energy density and may be expressed in units such as joules per cubic metre (J/m3, which is equal to Pa). Mathematically: p = F ⋅ distance A ⋅ distance = Work Volume = Energy (J) Volume ( m 3 ) . {\displaystyle p={\frac {F\cdot {\text{distance}}}{A\cdot {\text{distance}}}}={\frac {\text{Work}}{\text{Volume}}}={\frac {\text{Energy (J)}}{{\text{Volume }}({\text{m}}^{3})}}.} Some meteorologists prefer the hectopascal (hPa) for atmospheric air pressure, which is equivalent to the older unit millibar (mbar). Similar pressures are given in kilopascals (kPa) in most other fields, except aviation where the hecto- prefix is commonly used. The inch of mercury is still used in the United States. Oceanographers usually measure underwater pressure in decibars (dbar) because pressure in the ocean increases by approximately one decibar per metre depth. The standard atmosphere (atm) is an established constant. It is approximately equal to typical air pressure at Earth mean sea level and is defined as 101325 Pa. Because pressure is commonly measured by its ability to displace a column of liquid in a manometer, pressures are often expressed as a depth of a particular fluid (e.g., centimetres of water, millimetres of mercury or inches of mercury). The most common choices are mercury (Hg) and water; water is nontoxic and readily available, while mercurys high density allows a shorter column (and so a smaller manometer) to be used to measure a given pressure. The pressure exerted by a column of liquid of height h and density ρ is given by the hydrostatic pressure equation p = ρgh, where g is the gravitational acceleration. Fluid density and local gravity can vary from one reading to another depending on local factors, so the height of a fluid column does not define pressure precisely. When millimetres of mercury (or inches of mercury) are quoted today, these units are not based on a physical column of mercury; rather, they have been given precise definitions that can be expressed in terms of SI units. One millimetre of mercury is approximately equal to one torr. The water-based units still depend on the density of water, a measured, rather than defined, quantity. These manometric units are still encountered in many fields. Blood pressure is measured in millimetres of mercury in most of the world, and lung pressures in centimetres of water are still common.Underwater divers use the metre sea water (msw or MSW) and foot sea water (fsw or FSW) units of pressure, and these are the standard units for pressure gauges used to measure pressure exposure in diving chambers and personal decompression computers. A msw is defined as 0.1 bar (= 100000 Pa = 10000 Pa), is not the same as a linear metre of depth. 33.066 fsw = 1 atm (1 atm = 101325 Pa / 33.066 = 3064.326 Pa). Note that the pressure conversion from msw to fsw is different from the length conversion: 10 msw = 32.6336 fsw, while 10 m = 32.8083 ft.Gauge pressure is often given in units with "g" appended, e.g. "kPag", "barg" or "psig", and units for measurements of absolute pressure are sometimes given a suffix of "a", to avoid confusion, for example "kPaa", "psia". However, the US National Institute of Standards and Technology recommends that, to avoid confusion, any modifiers be instead applied to the quantity being measured rather than the unit of measure. For example, "pg = 100 psi" rather than "p = 100 psig". Differential pressure is expressed in units with "d" appended; this type of measurement is useful when considering sealing performance or whether a valve will open or close. Presently or formerly popular pressure units include the following: atmosphere (atm) manometric units: centimetre, inch, millimetre (torr) and micrometre (mTorr, micron) of mercury, height of equivalent column of water, including millimetre (mm H2O), centimetre (cm H2O), metre, inch, and foot of water; imperial and customary units: kip, short ton-force, long ton-force, pound-force, ounce-force, and poundal per square inch, short ton-force and long ton-force per square inch, fsw (feet sea water) used in underwater diving, particularly in connection with diving pressure exposure and decompression; non-SI metric units: bar, decibar, millibar, msw (metres sea water), used in underwater diving, particularly in connection with diving pressure exposure and decompression, kilogram-force, or kilopond, per square centimetre (technical atmosphere), gram-force and tonne-force (metric ton-force) per square centimetre, barye (dyne per square centimetre), kilogram-force and tonne-force per square metre, sthene per square metre (pieze). Examples As an example of varying pressures, a finger can be pressed against a wall without making any lasting impression; however, the same finger pushing a thumbtack can easily damage the wall. Although the force applied to the surface is the same, the thumbtack applies more pressure because the point concentrates that force into a smaller area. Pressure is transmitted to solid boundaries or across arbitrary sections of fluid normal to these boundaries or sections at every point. Unlike stress, pressure is defined as a scalar quantity. The negative gradient of pressure is called the force density.Another example is a knife. If we try to cut with the flat edge, force is distributed over a larger surface area resulting in less pressure, and it will not cut. Whereas using the sharp edge, which has less surface area, results in greater pressure, and so the knife cuts smoothly. This is one example of a practical application of pressureFor gases, pressure is sometimes measured not as an absolute pressure, but relative to atmospheric pressure; such measurements are called gauge pressure. An example of this is the air pressure in an automobile tire, which might be said to be "220 kPa (32 psi)", but is actually 220 kPa (32 psi) above atmospheric pressure. Since atmospheric pressure at sea level is about 100 kPa (14.7 psi), the absolute pressure in the tire is therefore about 320 kPa (46 psi). In technical work, this is written "a gauge pressure of 220 kPa (32 psi)". Where space is limited, such as on pressure gauges, name plates, graph labels, and table headings, the use of a modifier in parentheses, such as "kPa (gauge)" or "kPa (absolute)", is permitted. In non-SI technical work, a gauge pressure of 32 psi (220 kPa) is sometimes written as "32 psig", and an absolute pressure as "32 psia", though the other methods explained above that avoid attaching characters to the unit of pressure are preferred.Gauge pressure is the relevant measure of pressure wherever one is interested in the stress on storage vessels and the plumbing components of fluidics systems. However, whenever equation-of-state properties, such as densities or changes in densities, must be calculated, pressures must be expressed in terms of their absolute values. For instance, if the atmospheric pressure is 100 kPa (15 psi), a gas (such as helium) at 200 kPa (29 psi) (gauge) (300 kPa or 44 psi [absolute]) is 50% denser than the same gas at 100 kPa (15 psi) (gauge) (200 kPa or 29 psi [absolute]). Focusing on gauge values, one might erroneously conclude the first sample had twice the density of the second one. Scalar nature In a static gas, the gas as a whole does not appear to move. The individual molecules of the gas, however, are in constant random motion. Because we are dealing with an extremely large number of molecules and because the motion of the individual molecules is random in every direction, we do not detect any motion. If we enclose the gas within a container, we detect a pressure in the gas from the molecules colliding with the walls of our container. We can put the walls of our container anywhere inside the gas, and the force per unit area (the pressure) is the same. We can shrink the size of our "container" down to a very small point (becoming less true as we approach the atomic scale), and the pressure will still have a single value at that point. Therefore, pressure is a scalar quantity, not a vector quantity. It has magnitude but no direction sense associated with it. Pressure force acts in all directions at a point inside a gas. At the surface of a gas, the pressure force acts perpendicular (at right angle) to the surface.A closely related quantity is the stress tensor σ, which relates the vector force F {\displaystyle \mathbf {F} } to the vector area A {\displaystyle \mathbf {A} } via the linear relation F = σ A {\displaystyle \mathbf {F} =\sigma \mathbf {A} } . This tensor may be expressed as the sum of the viscous stress tensor minus the hydrostatic pressure. The negative of the stress tensor is sometimes called the pressure tensor, but in the following, the term "pressure" will refer only to the scalar pressure.According to the theory of general relativity, pressure increases the strength of a gravitational field (see stress–energy tensor) and so adds to the mass-energy cause of gravity. This effect is unnoticeable at everyday pressures but is significant in neutron stars, although it has not been experimentally tested. Types Fluid pressure Fluid pressure is most often the compressive stress at some point within a fluid. (The term fluid refers to both liquids and gases – for more information specifically about liquid pressure, see section below.) Fluid pressure occurs in one of two situations: An open condition, called "open channel flow", e.g. the ocean, a swimming pool, or the atmosphere. A closed condition, called "closed conduit", e.g. a water line or gas line.Pressure in open conditions usually can be approximated as the pressure in "static" or non-moving conditions (even in the ocean where there are waves and currents), because the motions create only negligible changes in the pressure. Such conditions conform with principles of fluid statics. The pressure at any given point of a non-moving (static) fluid is called the hydrostatic pressure. Closed bodies of fluid are either "static", when the fluid is not moving, or "dynamic", when the fluid can move as in either a pipe or by compressing an air gap in a closed container. The pressure in closed conditions conforms with the principles of fluid dynamics. The concepts of fluid pressure are predominantly attributed to the discoveries of Blaise Pascal and Daniel Bernoulli. Bernoullis equation can be used in almost any situation to determine the pressure at any point in a fluid. The equation makes some assumptions about the fluid, such as the fluid being ideal and incompressible. An ideal fluid is a fluid in which there is no friction, it is inviscid (zero viscosity). The equation for all points of a system filled with a constant-density fluid is p γ + v 2 2 g + z = c o n s t , {\displaystyle {\frac {p}{\gamma }}+{\frac {v^{2}}{2g}}+z=\mathrm {const} ,} where: p, pressure of the fluid, γ {\displaystyle {\gamma }} = ρg, density × acceleration of gravity is the (volume-) specific weight of the fluid, v, velocity of the fluid, g, acceleration of gravity, z, elevation, p γ {\displaystyle {\frac {p}{\gamma }}} , pressure head, v 2 2 g {\displaystyle {\frac {v^{2}}{2g}}} , velocity head. Applications Hydraulic brakes Artesian well Blood pressure Hydraulic head Plant cell turgidity Pythagorean cup Pressure washing Explosion or deflagration pressures Explosion or deflagration pressures are the result of the ignition of explosive gases, mists, dust/air suspensions, in unconfined and confined spaces. Negative pressures While pressures are, in general, positive, there are several situations in which negative pressures may be encountered: When dealing in relative (gauge) pressures. For instance, an absolute pressure of 80 kPa may be described as a gauge pressure of −21 kPa (i.e., 21 kPa below an atmospheric pressure of 101 kPa). For example, abdominal decompression is an obstetric procedure during which negative gauge pressure is applied intermittently to a pregnant womans abdomen. Negative absolute pressures are possible. They are effectively tension, and both bulk solids and bulk liquids can be put under negative absolute pressure by pulling on them. Microscopically, the molecules in solids and liquids have attractive interactions that overpower the thermal kinetic energy, so some tension can be sustained. Thermodynamically, however, a bulk material under negative pressure is in a metastable state, and it is especially fragile in the case of liquids where the negative pressure state is similar to superheating and is easily susceptible to cavitation. In certain situations, the cavitation can be avoided and negative pressures sustained indefinitely, for example, liquid mercury has been observed to sustain up to −425 atm in clean glass containers. Negative liquid pressures are thought to be involved in the ascent of sap in plants taller than 10 m (the atmospheric pressure head of water). The Casimir effect can create a small attractive force due to interactions with vacuum energy; this force is sometimes termed "vacuum pressure" (not to be confused with the negative gauge pressure of a vacuum). For non-isotropic stresses in rigid bodies, depending on how the orientation of a surface is chosen, the same distribution of forces may have a component of positive pressure along one surface normal, with a component of negative pressure acting along another surface normal. The stresses in an electromagnetic field are generally non-isotropic, with the pressure normal to one surface element (the normal stress) being negative, and positive for surface elements perpendicular to this. In cosmology, dark energy creates a very small yet cosmically significant amount of negative pressure, which accelerates the expansion of the universe. Stagnation pressure Stagnation pressure is the pressure a fluid exerts when it is forced to stop moving. Consequently, although a fluid moving at higher speed will have a lower static pressure, it may have a higher stagnation pressure when forced to a standstill. Static pressure and stagnation pressure are related by: p 0 = 1 2 ρ v 2 + p {\displaystyle p_{0}={\frac {1}{2}}\rho v^{2}+p} where p 0 {\displaystyle p_{0}} is the stagnation pressure, ρ {\displaystyle \rho } is the density, v {\displaystyle v} is the flow velocity, p {\displaystyle p} is the static pressure.The pressure of a moving fluid can be measured using a Pitot tube, or one of its variations such as a Kiel probe or Cobra probe, connected to a manometer. Depending on where the inlet holes are located on the probe, it can measure static pressures or stagnation pressures. Surface pressure and surface tension There is a two-dimensional analog of pressure – the lateral force per unit length applied on a line perpendicular to the force. Surface pressure is denoted by π: π = F l {\displaystyle \pi ={\frac {F}{l}}} and shares many similar properties with three-dimensional pressure. Properties of surface chemicals can be investigated by measuring pressure/area isotherms, as the two-dimensional analog of Boyles law, πA = k, at constant temperature. Surface tension is another example of surface pressure, but with a reversed sign, because "tension" is the opposite to "pressure". Pressure of an ideal gas In an ideal gas, molecules have no volume and do not interact. According to the ideal gas law, pressure varies linearly with temperature and quantity, and inversely with volume: p = n R T V , {\displaystyle p={\frac {nRT}{V}},} where: p is the absolute pressure of the gas, n is the amount of substance, T is the absolute temperature, V is the volume, R is the ideal gas constant.Real gases exhibit a more complex dependence on the variables of state. Vapour pressure Vapour pressure is the pressure of a vapour in thermodynamic equilibrium with its condensed phases in a closed system. All liquids and solids have a tendency to evaporate into a gaseous form, and all gases have a tendency to condense back to their liquid or solid form. The atmospheric pressure boiling point of a liquid (also known as the normal boiling point) is the temperature at which the vapor pressure equals the ambient atmospheric pressure. With any incremental increase in that temperature, the vapor pressure becomes sufficient to overcome atmospheric pressure and lift the liquid to form vapour bubbles inside the bulk of the substance. Bubble formation deeper in the liquid requires a higher pressure, and therefore higher temperature, because the fluid pressure increases above the atmospheric pressure as the depth increases. The vapor pressure that a single component in a mixture contributes to the total pressure in the system is called partial vapor pressure. Liquid pressure When a person swims under the water, water pressure is felt acting on the persons eardrums. The deeper that person swims, the greater the pressure. The pressure felt is due to the weight of the water above the person. As someone swims deeper, there is more water above the person and therefore greater pressure. The pressure a liquid exerts depends on its depth. Liquid pressure also depends on the density of the liquid. If someone was submerged in a liquid more dense than water, the pressure would be correspondingly greater. Thus, we can say that the depth, density and liquid pressure are directly proportionate. The pressure due to a liquid in liquid columns of constant density or at a depth within a substance is represented by the following formula: p = ρ g h , {\displaystyle p=\rho gh,} where: p is liquid pressure, g is gravity at the surface of overlaying material, ρ is density of liquid, h is height of liquid column or depth within a substance.Another way of saying the same formula is the following: p = weight density × depth . {\displaystyle p={\text{weight density}}\times {\text{depth}}.} The pressure a liquid exerts against the sides and bottom of a container depends on the density and the depth of the liquid. If atmospheric pressure is neglected, liquid pressure against the bottom is twice as great at twice the depth; at three times the depth, the liquid pressure is threefold; etc. Or, if the liquid is two or three times as dense, the liquid pressure is correspondingly two or three times as great for any given depth. Liquids are practically incompressible – that is, their volume can hardly be changed by pressure (water volume decreases by only 50 millionths of its original volume for each atmospheric increase in pressure). Thus, except for small changes produced by temperature, the density of a particular liquid is practically the same at all depths. Atmospheric pressure pressing on the surface of a liquid must be taken into account when trying to discover the total pressure acting on a liquid. The total pressure of a liquid, then, is ρgh plus the pressure of the atmosphere. When this distinction is important, the term total pressure is used. Otherwise, discussions of liquid pressure refer to pressure without regard to the normally ever-present atmospheric pressure. The pressure does not depend on the amount of liquid present. Volume is not the important factor – depth is. The average water pressure acting against a dam depends on the average depth of the water and not on the volume of water held back. For example, a wide but shallow lake with a depth of 3 m (10 ft) exerts only half the average pressure that a small 6 m (20 ft) deep pond does. (The total force applied to the longer dam will be greater, due to the greater total surface area for the pressure to act upon. But for a given 5-foot (1.5 m)-wide section of each dam, the 10 ft (3.0 m) deep water will apply one quarter the force of 20 ft (6.1 m) deep water). A person will feel the same pressure whether their head is dunked a metre beneath the surface of the water in a small pool or to the same depth in the middle of a large lake. If four vases contain different amounts of water but are all filled to equal depths, then a fish with its head dunked a few centimetres under the surface will be acted on by water pressure that is the same in any of the vases. If the fish swims a few centimetres deeper, the pressure on the fish will increase with depth and be the same no matter which vase the fish is in. If the fish swims to the bottom, the pressure will be greater, but it makes no difference what vase it is in. All vases are filled to equal depths, so the water pressure is the same at the bottom of each vase, regardless of its shape or volume. If water pressure at the bottom of a vase were greater than water pressure at the bottom of a neighboring vase, the greater pressure would force water sideways and then up the narrower vase to a higher level until the pressures at the bottom were equalized. Pressure is depth dependent, not volume dependent, so there is a reason that water seeks its own level. Restating this as energy equation, the energy per unit volume in an ideal, incompressible liquid is constant throughout its vessel. At the surface, gravitational potential energy is large but liquid pressure energy is low. At the bottom of the vessel, all the gravitational potential energy is converted to pressure energy. The sum of pressure energy and gravitational potential energy per unit volume is constant throughout the volume of the fluid and the two energy components change linearly with the depth. Mathematically, it is described by Bernoullis equation, where velocity head is zero and comparisons per unit volume in the vessel are p γ + z = c o n s t . {\displaystyle {\frac {p}{\gamma }}+z=\mathrm {const} .} Terms have the same meaning as in section Fluid pressure. Direction of liquid pressure An experimentally determined fact about liquid pressure is that it is exerted equally in all directions. If someone is submerged in water, no matter which way that person tilts their head, the person will feel the same amount of water pressure on their ears. Because a liquid can flow, this pressure isnt only downward. Pressure is seen acting sideways when water spurts sideways from a leak in the side of an upright can. Pressure also acts upward, as demonstrated when someone tries to push a beach ball beneath the surface of the water. The bottom of a boat is pushed upward by water pressure (buoyancy). When a liquid presses against a surface, there is a net force that is perpendicular to the surface. Although pressure doesnt have a specific direction, force does. A submerged triangular block has water forced against each point from many directions, but components of the force that are not perpendicular to the surface cancel each other out, leaving only a net perpendicular point. This is why water spurting from a hole in a bucket initially exits the bucket in a direction at right angles to the surface of the bucket in which the hole is located. Then it curves downward due to gravity. If there are three holes in a bucket (top, bottom, and middle), then the force vectors perpendicular to the inner container surface will increase with increasing depth – that is, a greater pressure at the bottom makes it so that the bottom hole will shoot water out the farthest. The force exerted by a fluid on a smooth surface is always at right angles to the surface. The speed of liquid out of the hole is 2 g h {\displaystyle \scriptstyle {\sqrt {2gh}}} , where h is the depth below the free surface. This is the same speed the water (or anything else) would have if freely falling the same vertical distance h. Kinematic pressure P = p / ρ 0 {\displaystyle P=p/\rho _{0}} is the kinematic pressure, where p {\displaystyle p} is the pressure and ρ 0 {\displaystyle \rho _{0}} constant mass density. The SI unit of P is m2/s2. Kinematic pressure is used in the same manner as kinematic viscosity ν {\displaystyle \nu } in order to compute the Navier–Stokes equation without explicitly showing the density ρ 0 {\displaystyle \rho _{0}} . Navier–Stokes equation with kinematic quantities ∂ u ∂ t + ( u ∇ ) u = − ∇ P + ν ∇ 2 u . {\displaystyle {\frac {\partial u}{\partial t}}+(u\nabla )u=-\nabla P+\nu \nabla ^{2}u.} See also Notes References External links Introduction to Fluid Statics and Dynamics on Project PHYSNET Pressure being a scalar quantity wikiUnits.org - Convert units of pressure

Hypertensive crisis

Severely elevated blood pressure (equal to or greater than a systolic 180 or diastolic of 120—sometimes termed malignant or accelerated hypertension) is referred to as a hypertensive crisis, as blood pressure at this level confers a high risk of complications. People with blood pressures in this range may have no symptoms, but are more likely to report headaches (22% of cases) and dizziness than the general population. Other symptoms accompanying a hypertensive crisis may include visual deterioration due to retinopathy, breathlessness due to heart failure, or a general feeling of malaise due to kidney failure. Most people with a hypertensive crisis are known to have elevated blood pressure, but additional triggers may have led to a sudden rise.A "hypertensive emergency" is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic. This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilledema and/or fundal bleeds and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the coughing up of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system. Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur. In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage. In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks. Use of oral medications to lower the BP gradually over 24 to 48h is advocated in hypertensive urgencies.There are several etiologies of a hypertensive crisis, including a tumor. A rare, neuroendocrine tumor called a pheochromocytoma can cause a hypertensive crisis due to elevated levels of catecholamines. == References ==

Aphagia

Aphagia is the inability or refusal to swallow. The word is derived from the Ancient Greek prefix α, meaning "not" or "without," and the suffix φαγία, derived from the verb φαγεῖν, meaning "to eat." It is related to dysphagia which is difficulty swallowing (Greek prefix δυσ, dys, meaning difficult, or defective), and odynophagia, painful swallowing (from ὀδύνη, odyn(o), meaning "pain"). Aphagia may be temporary or long term, depending on the affected organ. It is an extreme, life-threatening case of dysphagia. Depending on the cause, untreated dysphagia may develop into aphagia. Behavioural classification The following behavioural classifications result from studies performed on rats, in which lesions were made on the lateral hypothalamus region in the brain. Passive aphagia: An animal with passive aphagia will not respond to food if it is presented. However, if food is inserted into the mouth, the animal will chew. Active aphagia: Active aphagia is a complete rejection of food. The animal will physically push food away or move its head from it. One might first sample the food by smelling or tasting, then spit out anything in the mouth. Afterwards the animal will show a complete repulsion to the food. The animal reacts to food as if it is bitter or foul. Mixed aphagia: When presented with food, the animal initially does not react positively or negatively. However, when food is placed in the mouth, the animal demonstrates active aphagia, spitting out the food and refusing to eat thereafter.These studies point to the function of the hypothalamus in regulating food intake. Animals in this study also demonstrated several other types of eating behaviour: "weak eating," in which the animal slowly approaches, chews, and swallows small observable amounts of food for a brief period; "good eating," in which the animal reaches normally for the food and eats reliably; and "vigorous eating," in which the animal gluttonously reaches for and devours the food. In these cases, there was either minor or no damage to the lateral hypothalamus.Aphagia not classified under behavioral aphagia typically has a structural cause, see causes. Causes Aphagia is usually the result of many different diseases as well as different medical treatments. The most common causes of aphagia are: Aesophageal cancer – there are two types of aesophageal cancer. The squamous cell cancer from the squamous cells of the tongue or the adenocarcinoma from glandular cells present at the junction of the esophagus and stomach. This leads to a local tumour growth with spreading later. This spreading may lead to larger tumors that would result in the inability to swallow. Aesophageal webs – thin membranes located in the esophagus. Abnormalities can cause constrictions within the esophagus. Globus pharyngis – commonly referred to as lumps in ones throat Myasthenia gravis – the thymus gland is thought to be necessary for the deletion of auto-reactive T cells, and seems to have an important role in the pathogenesis of myasthenia gravis. In patients the thymus is typically enlarged, and contains many germinal centres with T and B cell areas very similar to those seen in lymph nodes. The tumour in thymoma associated disease is typically epithelial in nature. Facioscapulohumeral muscular dystrophy – even though there is not a clear correlation between the facioscapulohumeral muscular dystrophy and the pharyngeal and upper aesophageal striated muscle. Minor, and nonspecific, primary aesophageal dysmotility was present as seen in the 2008 study by Joerg-patrick Stübgen. Multiple sclerosis – may lead to aesophageal dysmotility Chemotherapy – radiation from cancer therapy may cause a stricture of the throat leading to the inability to swallow. Stroke – swallowing problems can cause stroke victims to aspirate food or liquid into the lungs and cause pneumonia mostly in elderly people. Parkinsons disease – the mechanism of swallowing disorders in Parkinsons disease may be related to extrapyramidal and autonomic system disorders. The cardinal symptoms of Parkinsons disease: tremor, bradykinesia, and rigidity are initially responsible for swallowing, which is mainly observed in the advanced stages of the disease Damage to the lateral hypothalamus can also lead to aphagia, as seen in the 1978 study by Timothy Schallert and Ian Whishaw. Other causes might be due to depression, cervical spine disease and conversion disorders.It is important to note that all these causes (except due to the damage of the lateral hypothalamus) are indirect. Diagnosis Modified barium swallow – videofluoroscopic swallow (fluoroscopy). A lateral video X-ray that provides objective information on bolus transport, safest consistency of bolus, and possible head positioning and maneuvers that may facilitate swallow function depending on each individuals anatomy and physiology. Esophagogastroduodenoscopy – a diagnostic endoscopic procedure that visualizes the upper part of the gastrointestinal tract. Esophageal motility study – a test to assess motor function of the upper and lower esophageal sphincter as well as the esophageal body. Treatment and compensatory techniques During the treatment of aphagia (or dysphagia), it is important to provide adequate nutrition and hydration. If a person is not able to tolerate a regular diet, diet modifications and alternative means of nutrition may be considered. These include thickening liquids (typical thickening hierarchy is nectar/syrup thick, honey thick, and pudding thick) or by changing the texture of the solid foods to reduce the required amount of mastication (chewing) needed or to reduce other symptoms of oral dysphagia (such as buccal pocketing or anterior loss). Alternative means of nutrition may also be needed in more severe cases (such as when a person is deemed NPO and is not safe to eat anything orally). In these cases, nasogastric (NG) or percutaneous endoscopic gastronomy (PEG) tubes may be placed. Other compensatory measures may include reducing the bolus size (small bites/sips) or postural strategies (such as tucking the chin, turning the head to one side or the other). A speech-language pathologist is one professional who evaluates and treats aphagia and dysphagia and can recommend these strategies depending on the etiology of the deficit and the location of the breakdown within the swallowing mechanism. True treatment of aphagia/dysphagia comes from neuromuscular re-education and strengthening/coordination in most cases. This can be achieved by use of pharyngeal strengthening exercises, thermal stimulation of the swallowing trigger and oral motor exercises. In some cases, it is also appropriate to complete therapeutic exercises in conjunction with neuromuscular electrical stimulation (NMES) which utilizes low-level electrical currents to target muscle fibers from an external source (electrodes placed on the surface of the skin in strategic places to target muscles and nerves needed during the swallowing process). == References ==

Sealpox

Sealpox is a cutaneous (skin) condition caused by a Parapoxvirus, usually affecting seal handlers who have been bitten by infected harbor or grey seals.: 394  First identified in 1969, it wasnt unequivocally proven to be transmissible to humans until 2005, though such transmission had been reported at least as early as 1987. It causes lesions that closely resemble those caused by orf. As many as 2% of seals in marine mammal rehabilitation facilities in North America may have it. See also Farmyard pox Tanapox Skin lesion References == External links ==

Tachypnea

Tachypnea, also spelt tachypnoea, is a respiratory rate greater than normal, resulting in abnormally rapid and shallow breathing.In adult humans at rest, any respiratory rate of 12–20 per minute is considered clinically normal, with tachypnea being any rate above that. Children have significantly higher resting ventilatory rates, which decline rapidly during the first three years of life and then steadily until around 18 years. Tachypnea can be an early indicator of pneumonia and other lung diseases in children, and is often an outcome of a brain injury. Distinction from other breathing terms Different sources produce different classifications for breathing terms. Some of the public describe tachypnea as any rapid breathing. Hyperventilation is then described as increased ventilation of the alveoli (which can occur through increased rate or depth of breathing, or a mix of both) where there is a smaller rise in metabolic carbon dioxide relative to this increase in ventilation. Hyperpnea, on the other hand, is defined as breathing an increased volume of air, with or without an increase in respiration rate.Others give another classification: tachypnea is as any rapid breathing, hyperventilation is increased rate of breathing at rest, hyperpnea is an increase in breathing that is appropriately proportional to an increase in metabolic rate.A third paradigm is: tachypnea is abnormally rapid and shallow respiration (though some may argue this is inaccurate as breathing differs from respiration), hyperventilation is increased rate or depth of respiration to abnormal levels causing decreased levels of blood carbon dioxide and hyperpnea is any increase in breathing rate or depth that is not normal. Threshold definition As normal respiratory rate varies with age, the definition of tachypnea also varies with age. Causes Tachypnea may have physiological or pathological causes. Both of these categories would include large lists of individual causes. Physiological causes Physiological causes of tachypnea include exercise. This type is usually not a cause of concern unless its excessive. Pathological causes Pathological causes of tachypnea include sepsis, compensation for diabetic ketoacidosis or other metabolic acidosis, pneumonia, pleural effusion, carbon monoxide poisoning, pulmonary embolism, asthma, COPD, laryngospasm, allergic reaction causing airway edema, foreign body aspiration, tracheobronchomalacia, congestive heart failure, anxiety states, haemorrhage, or many other medical issues. Etymology and pronunciation The word tachypnea () uses combining forms of tachy- + -pnea, yielding "fast breathing". See pronunciation information at dyspnea. See also Control of respiration Hypoventilation List of terms of lung size and activity Bradypnea References External links The dictionary definition of tachypnea at Wiktionary

Bloating

Abdominal bloating (or simply bloating) is a short-term disease that affects the gastrointestinal tract. Bloating is generally characterized by an excess buildup of gas, air or fluids in the stomach. A person may have feelings of tightness, pressure or fullness in the stomach; it may or may not be accompanied by a visibly distended abdomen. Bloating can affect anyone of any age range and is usually self-diagnosed, in most cases does not require serious medical attention or treatment. Although this term is usually used interchangeably with abdominal distension, these symptoms probably have different pathophysiological processes, which are not fully understood.The first step for the management is to find a treatment for the underlying causes that produce it through a detailed medical history and a physical examination. The discomfort can be alleviated by the use of certain drugs and dietary modifications.Bloating can also be caused by chronic conditions and in rare cases can be a reoccurring life-threatening problem. Symptoms and signs The most common symptom associated with bloating is a sensation that the abdomen is full or distended. Rarely, bloating may be painful or cause shortness of breath.Pains that are due to bloating will feel sharp and cause the stomach to cramp. These pains may occur anywhere in the body and can change locations quickly. They are so painful that they are sometimes mistaken for heart pains when they develop on the upper left side of the chest. Pains on the right side are often confused with problems in the appendix or the gallbladder. One symptom of gas that is not normally associated with it is the hiccup. Hiccups are harmless and will diminish on their own; they also help to release gas that is in the digestive tract before it moves down to the intestines and causes bloating. Important but uncommon causes of abdominal bloating include ascites and tumors. Causes There are many causes of bloating, including: diet, irritable bowel syndrome, lactose intolerance, reflux, and constipation. Specific medical conditions like Crohns disease or bowel obstruction can also contribute to the amount of stomach bloating experienced. Common causes of abdominal bloating are: Overeating Gastric distension Lactose intolerance, fructose intolerance and other food intolerances Premenstrual syndrome Food allergy Aerophagia (air swallowing, a nervous habit) Irritable bowel syndrome Celiac disease Non-celiac gluten sensitivity Partial bowel obstruction Gastric dumping syndrome or rapid gastric emptying Gas-producing foods Constipation Visceral fat Splenic-flexure syndrome Menstruation, dysmenorrhea Polycystic ovary syndrome and ovarian cysts Alvarez syndrome, bloating of unknown or psychogenic origin without excess gas in the digestive tract Massive infestation with intestinal parasites (e.g., Ascaris lumbricoides) Diverticulosis Certain medications, such as phentermine Occurs in some due to salivary hypersecretion and dehydration. Ovarian cancerImportant but uncommon causes of abdominal bloating include: Large cancerous intra-abdominal tumors of the ovary, liver, uterus and stomach Megacolon, an abnormal dilation of the colon caused by some diseases, such as Chagas disease, a parasitic infection Cardiopulmonary resuscitation procedures, due to the artificial mouth-to-mouth insufflation of air.In animals, causes of abdominal bloating include: Gastric dilatation volvulus, a condition of dogs which occurs when gas is trapped inside the stomach and gastric torsion prevents it from escaping Ruminal tympany, a condition of ruminant animals which occurs when gas cannot escape from the rumen.All the factors mentioned contribute to bloated stomach abdominal pain. Every person produces gases in their body during the digestion of food, such as methane, hydrogen, carbon dioxide, and nitrogen. And some of them are released outside the body, sometimes in small quantities that one does not notice and sometimes in larger quantities that may affect the normal course of life. Fiber Most cases of stomach bloating are due to improper diet. Gas occurs because of the bacteria in the colon and is a by-product of soluble fiber digestion. Inadequate or irregular intake of fiber and water will cause a person to experience bloating or constipation. The most common natural sources of fiber include fruits and vegetables as well as wheat or oat bran. These fibers are most likely to cause flatulence. Fiber is made by plants and is not easily digested by the human gastrointestinal tract. There are two main types of dietary fiber: soluble and insoluble fiber. Soluble fiber is prebiotic and readily fermented in the colon into gases, while insoluble fiber is metabolically inert and absorbs water as it moves through the digestive system, aiding in defecation. Most types of fiber (insoluble) are attached to body water in the intestine and increase the volume of stools. Bowel gas Gas in the gastrointestinal tract has only two sources. It is either swallowed air or is produced by bacteria that normally inhabit the intestines, primarily the colon.Belching or burping is a universal ability that works by removing gas from the stomach through the mouth. The stomach can become bloated when too much air is swallowed during eating and drinking too quickly. As the stomach swells, belching removes the gas and alleviates the pain associated with it. Burping can also be used as a form of relief from abdominal discomfort other than too much gas in the stomach.Flatulence, or farting, provides relief of much the same kind as burping, but involves the passage of gas from the body via the anus, not the mouth. Bacteria present in the intestinal tract cause gas that is expelled from the anus. They produce the gas as food is digested and moved from the small intestine. This gas builds up and causes swelling or bloating in the abdominal area before it is released. Constipation A common gastrointestinal problem is constipation—infrequent bowel movements, hard stools, or strain during the movements—which causes serious cases of bloating. Since most cases of constipation are temporary, simple lifestyle changes, such as getting more exercise and increasing ones intake of fiber, can contribute to alleviating constipation. Some cases of constipation will continue to worsen and require unconventional methods to release the feces and reduce the amount of stomach bloating. Blood in the stool, intense pain in the abdomen, rectal pain, unexplained weight loss, and continued bloating and constipation not relieved by the above lifestyle changes should be reported to a doctor. Bloating consistently accompanies constipation, and they will not develop without an underlying cause. Heartburn and acid reflux Painful burning sensations in the chest that are caused by gastroesophageal reflux is known as heartburn. Reflux is the backflow of gastric acid juices from the stomach into the oesophagus. Heartburn has different triggers, including certain foods, medications, obesity, and stress. These triggers are different for each individual. Gastroesophageal reflux disease or GERD is a chronic condition that can lead to more serious complications like esophageal cancer. Treatment options are available to treat the symptoms and the condition, but there is no cure for the disease. Symptoms include burping, abdominal and stomach bloating, along with pain and discomfort. Heavy meals, lying down or bending over after eating should be avoided to help prevent reflux from occurring. The stomach bloating experienced with reflux is intense and will remain until the food is digested all the way. Postmortem bloating occurs in cadavers, due to the formation of gases by bacterial action and putrefaction of the internal tissues of the abdomen and the inside of the intestines. Related conditions Conditions that are related to bloating include constipation, lactose intolerance, and acid reflux disease. All of these conditions share the same symptoms and can share the same causative agents. These causes include unhealthy diet, smoking, alcohol consumption, low amount of exercise, and overall health. Each of these conditions can be experienced as a symptom of the others and is also a cause for each of them. In most cases where one of the conditions is present, there is at least one if not two of the others. Treatment for each condition is performed using the same medications and recommended dietary changes like increased fiber intake and reduced fat intake. If the conditions develop into diseases such as gastroesophageal reflux disease or chronic constipation, additional medications will be required. Bloating and flatulence are sometimes related to constipation, and treating the underlying condition may be helpful. Treatment Diets Promising evidence on the potential efficacy of the low-FODMAP diet in functional abdominal bloating is provided by the reduction of the bloating which has been observed in some studies on patients with irritable bowel syndrome. Regarding the gluten-free diet, there is insufficient scientific evidence to recommend it to reduce bloating and abdominal distension. As regards the FODMAP diet, this should be provided by experts in nutrition to reduce the risks associated with elimination diets. Medications There are many over-the-counter (OTC) medications that can be used to treat bloating. Food enzymes can be found in some products that will help break down the sugars found in grains, vegetables and dairy products. They can be taken before food is consumed or added to the food that causes the gas and bloating. The most common treatment is antacids. These medications have no effect on the gas that is present in the intestines but enable gas build-up to be belched away more easily, reducing the amount of bloating that develops. Another treatment is simethicone, an oral anti-foaming agent that helps the body to expel the gas more quickly. Combinations of prokinetics, such as domperidone + metoclopramide + diphenhydramine (the latter for the prevention of extrapyramidal reactions, especially acute dystonic reactions) + proton pump inhibitors (PPIs), have dramatic effects on bloaters and belchers especially. See also Tympany References Notes Bibliography Partly based on Abdominal bloating. MedlinePlus (US public domain Medical Encyclopedia). Update Date: 10 November 2004. Updated by: Christian Stone, M.D., Division of Gastroenterology, Washington University in St. Louis School of Medicine, St. Louis, MO. Review provided by VeriMed Healthcare Network. Ahmed Shazly. Van Vorous, Heather. Eating for IBS. 2000. ISBN 1-56924-600-9. Excerpted with authors permission at Help for Irritable Bowel Syndrome (see IBS Diet Section) (2021, January 16) Lower back pain and bloated tummy: causes and best treatments - Everything to Know about Back Muscles.

Ultralight aviation

Ultralight aviation (called microlight aviation in some countries) is the flying of lightweight, 1- or 2-seat fixed-wing aircraft. Some countries differentiate between weight-shift control and conventional three-axis control aircraft with ailerons, elevator and rudder, calling the former "microlight" and the latter "ultralight". During the late 1970s and early 1980s, mostly stimulated by the hang gliding movement, many people sought affordable powered flight. As a result, many aviation authorities set up definitions of lightweight, slow-flying aeroplanes that could be subject to minimum regulations. The resulting aeroplanes are commonly called "ultralight aircraft" or "microlights", although the weight and speed limits differ from country to country. In Europe, the sporting (FAI) definition limits the maximum stalling speed to 65 km/h (40 mph) and the maximum take-off weight to 450 kg (992 lb), or 472.5 kg (1,042 lb) if a ballistic parachute is installed. The definition means that the aircraft has a slow landing speed and short landing roll in the event of an engine failure.In most affluent countries, microlights or ultralight aircraft now account for a significant percentage of the global civilian-owned aircraft. For instance in Canada in February 2018, the ultralight aircraft fleet made up to 20.4% of the total civilian aircraft registered. In other countries that do not register ultralight aircraft, like the United States, it is unknown what proportion of the total fleet they make up. In countries where there is no specific extra regulation, ultralights are considered regular aircraft and subject to certification requirements for both aircraft and pilot. Definitions Australia In Australia, ultralight aircraft and their pilots can either be registered with the Hang Gliding Federation of Australia (HGFA) or Recreational Aviation Australia (RA Aus). In all cases, except for privately built single seat ultralight aeroplanes, microlight aircraft or trikes are regulated by the Civil Aviation Regulations. Canada United Kingdom Pilots of a powered, fixed wing aircraft or paramotors do not need a licence, provided its weight with a full fuel tank is not more than 75 kg (165 lb), but they must obey the rules of the air.For heavier microlights the current UK regulations are similar to the European ones, but helicopters and gyroplanes are not included.Other than the very earliest aircraft, all two-seat UK microlights (and until 2007 all single-seaters) have been required to meet an airworthiness standard; BCAR Section S. In 2007, Single Seat DeRegulated (SSDR), a sub-category of single seat aircraft was introduced, allowing owners more freedom for modification and experiments. By 2017 the airworthiness of all single seat microlights became solely the responsibility of the user, but pilots must hold a microlight licence; currently NPPL(M) (National Private Pilots Licence). New Zealand Ultralights in New Zealand are subject to NZCAA General Aviation regulations with microlight specific variations as described in Part 103 and AC103-1. United States The United States FAAs definition of an ultralight is significantly different from that in most other countries and can lead to some confusion when discussing the topic. The governing regulation in the United States is FAR 103 Ultralight Vehicles. In 2004, the FAA introduced the "Light-sport aircraft" category, which resembles some other countries microlight categories. Ultralight aviation is represented by the United States Ultralight Association (USUA), which acts as the US aeroclub representative to the Fédération Aéronautique Internationale. Types There are several categories of aircraft which qualify as ultralights in some countries: Fixed-wing aircraft: traditional airplane-style designs. Weight-shift control trike: use a hang glider-style wing, below which is suspended a three-wheeled carriage which carries the engine and aviators. These aircraft are controlled by pushing against a horizontal control bar in roughly the same way as a hang glider pilot flies. Powered parachute: fuselage-mounted engines with parafoil wings, which are wheeled aircraft. Powered paraglider: backpack engines with parafoil wings, which are foot-launched. Powered hang glider: motorized foot-launched hang glider harness. Autogyro: rotary wing with fuselage-mounted engine, a gyrocopter is different from a helicopter in that the rotating wing is not powered, the engine provides forward thrust and the airflow through the rotary blades causes them to autorotate or "spin up" thereby creating lift. Helicopter: there are a number of single-seat and two-place helicopters which fall under the microlight categories in countries such as New Zealand. However, few helicopter designs fall within the more restrictive ultralight category defined in the United States of America. Hot air balloon: there are numerous ultralight hot air balloons in the US, and several more have been built and flown in France and Australia in recent years. Some ultralight hot air balloons are hopper balloons, while others are regular hot air balloons that carry passengers in a basket. Electric Advancements in batteries, motors, and motor controllers has led to some practical production electric propulsion systems for some ultralight applications. In many ways, ultralights are a good application for electric power as some models are capable of flying with low power, which allows longer duration flights on battery power.In 2007, the first pioneering company in this field, the Electric Aircraft Corporation, began offering engine kits to convert ultralight weight shift trikes to electric power. The 18 hp motor weighs 26 lb (12 kg) and an efficiency of 90% is claimed by designer Randall Fishman. The battery consists of a lithium-polymer battery pack of 5.6kWh which provides 1.5 hours of flying in the trike application. The company claimed a flight recharge cost of 60 cents in 2007.A significant obstacle to the adoption of electric propulsion for ultralights in the U.S. is the weight of the battery, which is considered part of the empty weight of the aircraft despite efforts to have it considered as fuel. As battery energy density improves lighter batteries can be used. See also Aerosport (airshow) Backpack helicopter Jetpack Nanolight Experimental Aircraft Association Recreational Aviation Australia United States Ultralight Association United States Powered Paragliding Association Volksflugzeug References External links Media related to Ultralight aircraft at Wikimedia Commons

Apraxia

Apraxia is a motor disorder caused by damage to the brain (specifically the posterior parietal cortex or corpus callosum), which causes difficulty with motor planning to perform tasks or movements. The nature of the damage determines the disorders severity, and the absence of sensory loss or paralysis helps to explain the level of difficulty. Children may be born with apraxia; its cause is unknown, and symptoms are usually noticed in the early stages of development. Apraxia occurring later in life, known as acquired apraxia, is typically caused by traumatic brain injury, stroke, dementia, Alzheimers disease, brain tumor, or other neurodegenerative disorders. The multiple types of apraxia are categorized by the specific ability and/or body part affected. The term "apraxia" comes from the Greek ἀ- a- ("without") and πρᾶξις praxis ("action"). Types The several types of apraxia include: Apraxia of speech (AOS) is having difficulty planning and coordinating the movements necessary for speech (e.g. potato=totapo, topato). AOS can independently occur without issues in areas such as verbal comprehension, reading comprehension, writing, articulation, or prosody. Buccofacial or orofacial apraxia, the most common type of apraxia, is the inability to carry out facial movements on demand. For example, an inability to lick ones lips, wink, or whistle when requested to do so. This suggests an inability to carry out volitional movements of the tongue, cheeks, lips, pharynx, or larynx on command. Constructional apraxia is the inability to draw, construct, or copy simple configurations, such as intersecting shapes. These patients have difficulty copying a simple diagram or drawing basic shapes. Gait apraxia is the loss of ability to have normal function of the lower limbs such as walking. This is not due to loss of motor or sensory functions. Ideational/conceptual apraxia is having an inability to conceptualize a task and impaired ability to complete multistep actions. This form of apraxia consists of an inability to select and carry out an appropriate motor program. For example, the patient may complete actions in incorrect orders, such as buttering bread before putting it in the toaster, or putting on shoes before putting on socks. Also, a loss occurs in the ability to voluntarily perform a learned task when given the necessary objects or tools. For instance, if given a screwdriver, these patients may try to write with it as if it were a pen, or try to comb their hair with a toothbrush. Ideomotor apraxia is having deficits in the ability to plan or complete motor actions that rely on semantic memory. These patients are able to explain how to perform an action, but unable to "imagine" or act out a movement such as "pretend to brush your teeth" or "pucker as though you bit into a sour lemon." When the ability to perform an action automatically when cued remains intact, though, this is known as automatic-voluntary dissociation. For example, they may not be able to pick up a phone when asked to do so, but can perform the action without thinking when the phone rings. Limb-kinetic apraxia is having the inability to perform precise, voluntary movements of extremities. For example, a person affected by limb apraxia may have difficulty waving hello, tying shoes, or typing on a computer. This type is common in patients who have experienced a stroke, some type of brain trauma, or have Alzheimers disease. Oculomotor apraxia is having difficulty moving the eye on command, especially with saccade movements that direct the gaze to targets. This is one of the three major components of Balints syndrome. Causes Apraxia is most often due to a lesion located in the dominant (usually left) hemisphere of the brain, typically in the frontal and parietal lobes. Lesions may be due to stroke, acquired brain injuries, or neurodegenerative diseases such as Alzheimers disease or other dementias, Parkinsons disease, or Huntingtons disease. Also, apraxia possibly may be caused by lesions in other areas of the brain.Ideomotor apraxia is typically due to a decrease in blood flow to the dominant hemisphere of the brain and particularly the parietal and premotor areas. It is frequently seen in patients with corticobasal degeneration.Ideational apraxia has been observed in patients with lesions in the dominant hemisphere near areas associated with aphasia, but more research is needed on ideational apraxia due to brain lesions. The localization of lesions in areas of the frontal and temporal lobes would provide explanation for the difficulty in motor planning seen in ideational apraxia, as well as its difficulty to distinguish it from certain aphasias.Constructional apraxia is often caused by lesions of the inferior nondominant parietal lobe, and can be caused by brain injury, illness, tumor, or other condition that can result in a brain lesion. Diagnosis Although qualitative and quantitative studies exist, little consensus exists on the proper method to assess for apraxia. The criticisms of past methods include failure to meet standard psychometric properties and research-specific designs that translate poorly to nonresearch use.The Test to Measure Upper Limb Apraxia (TULIA) is one method of determining upper limb apraxia through the qualitative and quantitative assessment of gesture production. In contrast to previous publications on apraxic assessment, the reliability and validity of TULIA was thoroughly investigated. The TULIA consists of subtests for the imitation and pantomime of nonsymbolic ("put your index finger on top of your nose"), intransitive ("wave goodbye"), and transitive ("show me how to use a hammer") gestures. Discrimination (differentiating between well- and poorly performed tasks) and recognition (indicating which object corresponds to a pantomimed gesture) tasks are also often tested for a full apraxia evaluation.However, a strong correlation may not be seen between formal test results and actual performance in everyday functioning or activities of daily living (ADLs). A comprehensive assessment of apraxia should include formal testing, standardized measurements of ADLs, observation of daily routines, self-report questionnaires, and targeted interviews with the patients and their relatives.As stated above, apraxia should not be confused with aphasia (the inability to understand language); however, they frequently occur together. Apraxia is so often accompanied by aphasia that many believe that if a person displays AOS, then the patient also having some level of aphasia should be assumed. Treatment Treatment for individuals with apraxia includes speech therapy, occupational therapy, and physical therapy. Currently, no medications are indicated for the treatment of apraxia, only therapy treatments. Generally, treatments for apraxia have received little attention for several reasons, including the tendency for the condition to resolve spontaneously in acute cases. Additionally, the very nature of the automatic-voluntary dissociation of motor abilities that defines apraxia means that patients may still be able to automatically perform activities if cued to do so in daily life. Nevertheless, patients experiencing apraxia have less functional independence in their daily lives, and that evidence for the treatment of apraxia is scarce. However, a literature review of apraxia treatment to date reveals that although the field is in its early stages of treatment design, certain aspects can be included to treat apraxia.One method is through rehabilitative treatment, which has been found to positively impact apraxia, as well as ADLs. In this review, rehabilitative treatment consisted of 12 different contextual cues, which were used to teach patients how to produce the same gesture under different contextual situations. Additional studies have also recommended varying forms of gesture therapy, whereby the patient is instructed to make gestures (either using objects or symbolically meaningful and nonmeaningful gestures) with progressively less cuing from the therapist. Patients with apraxia may need to use a form of alternative and augmentative communication depending on the severity of the disorder. In addition to using gestures as mentioned, patients can also use communication boards or more sophisticated electronic devices if needed.No single type of therapy or approach has been proven as the best way to treat a patient with apraxia, since each patients case varies. One-on-one sessions usually work the best, though, with the support of family members and friends. Since everyone responds to therapy differently, some patients will make significant improvements, while others will make less progress. The overall goal for treatment of apraxia is to treat the motor plans for speech, not treating at the phoneme (sound) level. Individuals with apraxia of speech should receive treatment that focuses on the repetition of target words and rate of speech. The overall goal for treatment of apraxia should be to improve speech intelligibility, rate of speech, and articulation of targeted words. Prognosis The prognosis for individuals with apraxia varies. With therapy, some patients improve significantly, while others may show very little improvement. Some individuals with apraxia may benefit from the use of a communication aid. However, many people with apraxia are no longer able to be independent. Those with limb-kinetic and/or gait apraxia should avoid activities in which they might injure themselves or others.Occupational therapy, physical therapy, and play therapy may be considered as other references to support patients with apraxia. These treatments could work along with the SLP to provide the best therapy for people with apraxia. Because people with limb apraxia may have trouble directing their motor movements, however, occupational therapy for stroke or other brain injury can be difficult. See also Praxis (process) Ataxia Aging movement control Developmental coordination disorder Lists of language disorders References Further reading External links Acquired Apraxia of Speech: A Treatment Overview Apraxia: Symptoms, Causes, Tests, Treatments ApraxiaKids GettingTheWordOutOnApraxia.com: A Community for Parents of Children with Apraxia

4

4 (four) is a number, numeral and digit. It is the natural number following 3 and preceding 5. It is the smallest semiprime and composite number, and is considered unlucky in many East Asian cultures. In mathematics Four is the smallest composite number, its proper divisors being 1 and 2. Four is the sum and product of two with itself: 2 {\displaystyle 2} + 2 {\displaystyle 2} = 4 {\displaystyle 4} = 2 {\displaystyle 2} x 2 {\displaystyle 2} , the only number b {\displaystyle b} such that a {\displaystyle a} + a {\displaystyle a} = b {\displaystyle b} = a {\displaystyle a} x a {\displaystyle a} , which also makes four the smallest squared prime number p 2 {\displaystyle p^{2}} . In Knuths up-arrow notation, 2 ↑↑ 2 = 2 ↑↑↑ 2 = 4, and so forth, for any number of up arrows. By consequence, four is the only square one more than a prime number, specifically three. The sum of the first four prime numbers two + three + five + seven is the only sum of four consecutive prime numbers that yields an odd prime number, seventeen, which is the fourth super-prime. Four lies between the first proper pair of twin primes, three and five, which are the first two Fermat primes, like seventeen, which is the third. On the other hand, the square of four 42, equivalently the fourth power of two 24, is sixteen; the only number that has a b {\displaystyle a^{b}} = b a {\displaystyle b^{a}} as a form of factorization. Holistically, there are four elementary arithmetic operations in mathematics: addition (+), subtraction (−), multiplication (×), and division (÷); and four basic number systems, the real numbers R {\displaystyle \mathbb {R} } , rational numbers Q {\displaystyle \mathbb {Q} } , integers Z {\displaystyle \mathbb {Z} } , and natural numbers N {\displaystyle \mathbb {N} } . Each natural number divisible by 4 is a difference of squares of two natural numbers, i.e. 4 x {\displaystyle 4x} = y 2 {\displaystyle y^{2}} − z 2 {\displaystyle z^{2}} . A number is a multiple of 4 if its last two digits are a multiple of 4. For example, 1092 is a multiple of 4 because 92 = 4 × 23. Lagranges four-square theorem states that every positive integer can be written as the sum of at most four square numbers. Three are not always sufficient; 7 for instance cannot be written as the sum of three squares.There are four all-Harshad numbers: 1, 2, 4, and 6. 12, which is divisible by four thrice over, is a Harshad number in all bases except octal. A four-sided plane figure is a quadrilateral or quadrangle, sometimes also called a tetragon. It can be further classified as a rectangle or oblong, kite, rhombus, and square. Four is the highest degree general polynomial equation for which there is a solution in radicals.The four-color theorem states that a planar graph (or, equivalently, a flat map of two-dimensional regions such as countries) can be colored using four colors, so that adjacent vertices (or regions) are always different colors. Three colors are not, in general, sufficient to guarantee this. The largest planar complete graph has four vertices.A solid figure with four faces as well as four vertices is a tetrahedron, which is the smallest possible number of faces and vertices a polyhedron can have. The regular tetrahedron, also called a 3-simplex, is the simplest Platonic solid. It has four regular triangles as faces that are themselves at dual positions with the vertices of another tetrahedron. Tetrahedra can be inscribed inside all other four Platonic solids, and tessellate space alongside the regular octahedron in the alternated cubic honeycomb. Four-dimensional space is the highest-dimensional space featuring more than three regular convex figures: Two-dimensional: infinitely many regular polygons. Three-dimensional: five regular polyhedra; the five Platonic solids which are the tetrahedron, cube, octahedron, dodecahedron, and icosahedron. Four-dimensional: six regular polychora; the 5-cell, 8-cell or tesseract, 16-cell, 24-cell, 120-cell, and 600-cell. The 24-cell, made of regular octahedra, has no analogue in any other dimension; it is self-dual, with its 24-cell honeycomb dual to the 16-cell honeycomb. Five-dimensional and every higher dimension: three regular convex n {\displaystyle n} -polytopes, all within the infinite family of regular n {\displaystyle n} -simplexes, n {\displaystyle n} -hypercubes, and n {\displaystyle n} -orthoplexes.The fourth dimension is also the highest dimension where regular self-intersecting figures exist: Two-dimensional: infinitaly many regular star polygons. Three-dimensional: four regular star polyhedra, the regular Kepler-Poinsot star polyhedra. Four-dimensional: ten regular star polychora, the Schläfli–Hess star polychora. They contain cells of Kepler-Poinsot polyhedra alongside regular tetrahedra, icosahedra and dodecahedra. Five-dimensional and every higher dimension: zero regular star-polytopes; uniform star polytopes in dimensions n {\displaystyle n} > 4 {\displaystyle 4} are the most symmetric, which mainly originate from stellations of regular n {\displaystyle n} -polytopes.Altogether, sixteen (or 16 = 42) regular convex and star polychora are generated from symmetries of four (4) Coxeter Weyl groups and point groups in the fourth dimension: the A 4 {\displaystyle \mathrm {A} _{4}} simplex, B 4 {\displaystyle \mathrm {B} _{4}} hypercube, F 4 {\displaystyle \mathrm {F} _{4}} icositetrachoric, and H 4 {\displaystyle \mathrm {H} _{4}} hexacosichoric groups; with the D 4 {\displaystyle \mathrm {D} _{4}} demihypercube group generating two alternative constructions. There are also sixty-four (or 64 = 43) four-dimensional Bravais lattices, and sixty-four uniform polychora in the fourth dimension based on the same A 4 {\displaystyle \mathrm {A} _{4}} , B 4 {\displaystyle \mathrm {B} _{4}} , F 4 {\displaystyle \mathrm {F} _{4}} and H 4 {\displaystyle \mathrm {H} _{4}} Coxeter groups, and extending to prismatic groups of uniform polyhedra, including one special non-Wythoffian form, the grand antiprism. There are also two infinite families of duoprisms and antiprismatic prisms in the fourth dimension. Four-dimensional differential manifolds have some unique properties. There is only one differential structure on R n {\displaystyle \mathbb {R} ^{n}} except when n {\displaystyle n} = 4 {\displaystyle 4} , in which case there are uncountably many. The smallest non-cyclic group has four elements; it is the Klein four-group. An alternating groups are not simple for values n {\displaystyle n} ≤ 4 {\displaystyle 4} . Further extensions of the real numbers under Hurwitzs theorem states that there are four normed division algebras: the real numbers R {\displaystyle \mathbb {R} } , the complex numbers C {\displaystyle \mathbb {C} } , the quaternions H {\displaystyle \mathbb {H} } , and the octonions O {\displaystyle \mathbb {O} } . Under Cayley–Dickson constructions, the sedenions S {\displaystyle \mathbb {S} } constitute a further fourth extension over R {\displaystyle \mathbb {R} } . The real numbers are ordered, commutative and associative algebras, as well as alternative algebras with power-associativity. The complex numbers C {\displaystyle \mathbb {C} } share all four multiplicative algebraic properties of the reals R {\displaystyle \mathbb {R} } , without being ordered. The quaternions loose a further commutative algebraic property, while holding associative, alternative, and power-associative properties. The octonions are alternative and power-associative, while the sedenions are only power-associative. The sedenions and all further extensions of these four normed division algebras are solely power-associative with non-trivial zero divisors, which makes them non-division algebras. R {\displaystyle \mathbb {R} } has a vector space of dimension 1, while C {\displaystyle \mathbb {C} } , H {\displaystyle \mathbb {H} } , O {\displaystyle \mathbb {O} } and S {\displaystyle \mathbb {S} } work in algebraic number fields of dimensions 2, 4, 8, and 16, respectively. List of basic calculations Evolution of the Hindu-Arabic digit Brahmic numerals represented 1, 2, and 3 with as many lines. 4 was simplified by joining its four lines into a cross that looks like the modern plus sign. The Shunga would add a horizontal line on top of the digit, and the Kshatrapa and Pallava evolved the digit to a point where the speed of writing was a secondary concern. The Arabs 4 still had the early concept of the cross, but for the sake of efficiency, was made in one stroke by connecting the "western" end to the "northern" end; the "eastern" end was finished off with a curve. The Europeans dropped the finishing curve and gradually made the digit less cursive, ending up with a digit very close to the original Brahmin cross.While the shape of the character for the digit 4 has an ascender in most modern typefaces, in typefaces with text figures the glyph usually has a descender, as, for example, in . On the seven-segment displays of pocket calculators and digital watches, as well as certain optical character recognition fonts, 4 is seen with an open top.Television stations that operate on channel 4 have occasionally made use of another variation of the "open 4", with the open portion being on the side, rather than the top. This version resembles the Canadian Aboriginal syllabics letter ᔦ. The magnetic ink character recognition "CMC-7" font also uses this variety of "4". In religion Buddhism Four Noble Truths – Dukkha, Samudaya, Nirodha, Magga Four sights – observations which affected Prince Siddhartha deeply and made him realize the sufferings of all beings, and compelled him to begin his spiritual journey—an old man, a sick man, a dead man, and an ascetic Four Great Elements – earth, water, fire, and wind Four Heavenly Kings Four Foundations of Mindfulness – contemplation of the body, contemplation of feelings, contemplation of mind, contemplation of mental objects Four Right Exertions Four Bases of Power Four jhānas Four arūpajhānas Four Divine Abidings – loving-kindness, compassion, sympathetic joy, and equanimity Four stages of enlightenment – stream-enterer, once-returner, non-returner, and arahant Four main pilgrimage sites – Lumbini, Bodh Gaya, Sarnath, and Kusinara Judeo-Christian symbolism The Tetragrammaton is the four-letter name of God. Ezekiel has a vision of four living creatures: a man, a lion, an ox, and an eagle. The four Matriarchs (foremothers) of Judaism are Sarah, Rebekah, Leah, and Rachel. The Four Species (lulav, hadass, aravah and etrog) are taken as one of the mitzvot on the Jewish holiday of Sukkot. (Judaism) The Four Cups of Wine to drink on the Jewish holiday of Passover. (Judaism) The Four Questions to be asked on the Jewish holiday of Passover. (Judaism) The Four Sons to be dealt with on the Jewish holiday of Passover. (Judaism) The Four Expressions of Redemption to be said on the Jewish holiday of Passover. (Judaism) The four Gospels: Matthew, Mark, Luke, and John. (Christianity) The Four Horsemen of the Apocalypse ride in the Book of Revelation. (Christianity) The four holy cities of Judaism: Jerusalem, Hebron, Safed, and Tiberius Hinduism There are four Vedas: Rigveda, Samaveda, Yajurveda and Atharvaveda. In Puruṣārtha, there are four aims of human life: Dharma, Artha, Kāma, Moksha. The four stages of life Brahmacharya (student life), Grihastha (household life), Vanaprastha (retired life) and Sannyasa (renunciation). The four primary castes or strata of society: Brahmana (priest/teacher), Kshatriya (warrior/politician), Vaishya (landowner/entrepreneur) and Shudra (servant/manual laborer). The swastika symbol is traditionally used in Hindu religions as a sign of good luck and signifies good from all four directions. The god Brahma has four faces. There are four yugas: Satya, Dvapara, Treta and Kali Islam Eid al-Adha lasts for four days, from the 10th to the 14th of Dhul Hijja. The four holy cities of Islam: Mecca, Medina, Jerusalem and Damascus. The four tombs in the Green Dome: Muhammad, Abu Bakr, Umar ibn Khattab and Isa ibn Maryam (Jesus). There are four Rashidun or Rightly Guided Caliphs: Abu Bakr, Umar ibn al-Khattab, Uthman ibn Affan and Ali ibn Abi Talib. The Four Arch Angels in Islam are: Jibraeel (Gabriel), Mikaeel (Michael), Izraeel (Azrael), and Israfil (Raphael) There are four months in which war is not permitted: Muharram, Rajab, Dhu al-Qidah and Dhu al-Hijjah. There are four Sunni schools of fiqh: Hanafi, Shafi`i, Maliki and Hanbali. There are four major Sunni Imams: Abū Ḥanīfa, Muhammad ibn Idris ash-Shafi`i, Malik ibn Anas and Ahmad ibn Hanbal. There are four books in Islam: Taurait, Zaboor, Injeel, Quran. Waiting for four months is ordained for those who take an oath for abstention from their wives. The waiting period of the woman whose husband dies is four months and ten days. When Abraham said: "My Lord, show me how You give life to the dead," Allah said: "Why! Do you have no faith?" Abraham replied: "Yes, but in order that my heart be at rest." He said: "Then take four birds, and tame them to yourself, then put a part of them on every hill, and summon them; they will come to you flying. [Al-Baqara 2:260] The respite of four months was granted to give time to the mushriks in Surah At-Tawba so that they should consider their position carefully and decide whether to make preparation for war or to emigrate from the country or to accept Islam. Those who accuse honorable women (of unchastity) but do not produce four witnesses, flog them with eighty lashes, and do not admit their testimony ever after. They are indeed transgressors. [An-Noor 24:4] Taoism Four Symbols of I Ching Other In a more general sense, numerous mythological and cosmogonical systems consider Four corners of the world as essentially corresponding to the four points of the compass. Four is the sacred number of the Zia, an indigenous tribe located in the U.S. state of New Mexico. The Chinese, the Koreans, and the Japanese are superstitious about the number four because it is a homonym for "death" in their languages. In Slavic mythology, the god Svetovid has four heads. In politics Four Freedoms: four fundamental freedoms that Franklin D. Roosevelt declared ought to be enjoyed by everyone in the world: Freedom of Speech, Freedom of Religion, Freedom from Want, Freedom from Fear. Gang of Four: Popular name for four Chinese Communist Party leaders who rose to prominence during Chinas Cultural Revolution, but were ousted in 1976 following the death of Chairman Mao Zedong. Among the four was Maos widow, Jiang Qing. Since then, many other political factions headed by four people have been called "Gangs of Four". In computing Four bits (half a byte) are sometimes called a nibble. In science A tetramer is an oligomer formed out of four sub-units. In astronomy Four terrestrial (or rocky) planets in the Solar System: Mercury, Venus, Earth, and Mars. Four giant gas/ice planets in the Solar System: Jupiter, Saturn, Uranus, and Neptune. Four of Jupiters moons (the Galilean moons) are readily visible from Earth with a hobby telescope. Messier object M4, a magnitude 7.5 globular cluster in the constellation Scorpius. The Roman numeral IV stands for subgiant in the Yerkes spectral classification scheme. In biology Four is the number of nucleobase types in DNA and RNA – adenine, guanine, cytosine, thymine (uracil in RNA). Many chordates have four feet, legs or leglike appendages (tetrapods). The mammalian heart consists of four chambers. Many mammals (Carnivora, Ungulata) use four fingers for movement. All insects with wings except flies and some others have four wings. Insects of the superorder Endopterygota, also known as Holometabola, such as butterflies, ants, bees, beetles, fleas, flies, moths, and wasps, undergo holometabolism—complete metamorphism in four stages—from (1) embryo (ovum, egg), to (2) larva (such as grub, caterpillar), then (3) pupa (such as the chrysalis), and finally (4) the imago. In the common ABO blood group system, there are four blood types (A, B, O, AB). Humans have four canines and four wisdom teeth. The cows stomach is divided in four digestive compartments: reticulum, rumen, omasum and abomasum. In chemistry Valency of carbon (that is basis of life on the Earth) is four. Also because of its tetrahedral crystal bond structure, diamond (one of the natural allotropes of carbon) is the hardest known naturally occurring material. It is also the valence of silicon, whose compounds form the majority of the mass of the Earths crust. The atomic number of beryllium There are four basic states of matter: solid, liquid, gas, and plasma. In physics Special relativity and general relativity treat nature as four-dimensional: 3D regular space and one-dimensional time are treated together and called spacetime. Also, any event E has a light cone composed of four zones of possible communication and cause and effect (outside the light cone is strictly incommunicado). There are four fundamental forces (electromagnetism, gravitation, the weak nuclear force, and the strong nuclear force). In statistical mechanics, the four functions inequality is an inequality for four functions on a finite distributive lattice. In logic and philosophy The symbolic meanings of the number four are linked to those of the cross and the square. "Almost from prehistoric times, the number four was employed to signify what was solid, what could be touched and felt. Its relationship to the cross (four points) made it an outstanding symbol of wholeness and universality, a symbol which drew all to itself". Where lines of latitude and longitude intersect, they divide the earth into four proportions. Throughout the world kings and chieftains have been called "lord of the four suns" or "lord of the four quarters of the earth", which is understood to refer to the extent of their powers both territorially and in terms of total control of their subjects doings. The Square of Opposition, in both its Aristotelian version and its Boolean version, consists of four forms: A ("All S is R"), I ("Some S is R"), E ("No S is R"), and O ("Some S is not R"). In regard to whether two given propositions can have the same truth value, there are four separate logical possibilities: the propositions are subalterns (possibly both are true, and possibly both are false); subcontraries (both may be true, but not that both are false); contraries (both may be false, but not that both are true); or contradictories (it is not possible that both are true, and it is not possible that both are false). Aristotle held that there are basically four causes in nature: the material, the formal, the efficient, and the final. The Stoics held with four basic categories, all viewed as bodies (substantial and insubstantial): (1) substance in the sense of substrate, primary formless matter; (2) quality, matters organization to differentiate and individualize something, and coming down to a physical ingredient such as pneuma, breath; (3) somehow holding (or disposed), as in a posture, state, shape, size, action, and (4) somehow holding (or disposed) toward something, as in relative location, familial relation, and so forth. Immanuel Kant expounded a table of judgments involving four three-way alternatives, in regard to (1) Quantity, (2) Quality, (3) Relation, (4) Modality, and, based thereupon, a table of four categories, named by the terms just listed, and each with three subcategories. Arthur Schopenhauers doctoral thesis was On the Fourfold Root of the Principle of Sufficient Reason. Franz Brentano held that any major philosophical period has four phases: (1) Creative and rapidly progressing with scientific interest and results; then declining through the remaining phases, (2) practical, (3) increasingly skeptical, and (4) literary, mystical, and scientifically worthless—until philosophy is renewed through a new periods first phase. (See Brentanos essay "The Four Phases of Philosophy and Its Current State" 1895, tr. by Mezei and Smith 1998.) C. S. Peirce, usually a trichotomist, discussed four methods for overcoming troublesome uncertainties and achieving secure beliefs: (1) the method of tenacity (policy of sticking to initial belief), (2) the method of authority, (3) the method of congruity (following a fashionable paradigm), and (4) the fallibilistic, self-correcting method of science (see "The Fixation of Belief", 1877); and four barriers to inquiry, barriers refused by the fallibilist: (1) assertion of absolute certainty; (2) maintaining that something is unknowable; (3) maintaining that something is inexplicable because absolutely basic or ultimate; (4) holding that perfect exactitude is possible, especially such as to quite preclude unusual and anomalous phenomena (see "F.R.L." [First Rule of Logic], 1899). Paul Weiss built a system involving four modes of being: Actualities (substances in the sense of substantial, spatiotemporally finite beings), Ideality or Possibility (pure normative form), Existence (the dynamic field), and God (unity). (See Weisss Modes of Being, 1958). Karl Popper outlined a tetradic schema to describe the growth of theories and, via generalization, also the emergence of new behaviors and living organisms: (1) problem, (2) tentative theory, (3) (attempted) error-elimination (especially by way of critical discussion), and (4) new problem(s). (See Poppers Objective Knowledge, 1972, revised 1979.) John Boyd (military strategist) made his key concept the decision cycle or OODA loop, consisting of four stages: (1) observation (data intake through the senses), (2) orientation (analysis and synthesis of data), (3) decision, and (4) action. Boyd held that his decision cycle has philosophical generality, though for strategists the point remains that, through swift decisions, one can disrupt an opponents decision cycle. Richard McKeon outlined four classes (each with four subclasses) of modes of philosophical inquiry: (1) Modes of Being (Being); (2) Modes of Thought (That which is); (3) Modes of Fact (Existence); (4) Modes of Simplicity (Experience)—and, corresponding to them, four classes (each with four subclasses) of philosophical semantics: Principles, Methods, Interpretations, and Selections. (See McKeons "Philosophic Semantics and Philosophic Inquiry" in Freedom and History and Other Essays, 1989.) Jonathan Lowe (E.J. Lowe) argues in The Four-Category Ontology, 2006, for four categories: kinds (substantial universals), attributes (relational universals and property-universals), objects (substantial particulars), and modes (relational particulars and property-particulars, also known as "tropes"). (See Lowes "Recent Advances in Metaphysics," 2001, Eprint) Four opposed camps of the morality and nature of evil: moral absolutism, amoralism, moral relativism, and moral universalism. In technology The resin identification code used in recycling to identify low-density polyethylene. Most furniture has four legs – tables, chairs, etc. The four color process (CMYK) is used for printing. Wide use of rectangles (with four angles and four sides) because they have effective form and capability for close adjacency to each other (houses, rooms, tables, bricks, sheets of paper, screens, film frames). In the Rich Text Format specification, language code 4 is for the Chinese language. Codes for regional variants of Chinese are congruent to 4 mod 256. Credit card machines have four-twelve function keys. On most phones, the 4 key is associated with the letters G, H, and I, but on the BlackBerry Pearl, it is the key for D and F. On many computer keyboards, the "4" key may also be used to type the dollar sign ($) if the shift key is held down. It is the number of bits in a nibble, equivalent to half a byte In internet slang, "4" can replace the word "for" (as "four" and "for" are pronounced similarly). For example, typing "4u" instead of "for you". In Leetspeak, "4" may be used to replace the letter "A". The TCP/IP stack consists of four layers. In transport Many internal combustion engines are called four-stroke engines because they complete one thermodynamic cycle in four distinct steps: Intake, compression, power, and exhaust. Most vehicles, including motor vehicles, and particularly cars/automobiles and light commercial vehicles have four road wheels. "Quattro", meaning four in the Italian language, is used by Audi as a trademark to indicate that all-wheel drive (AWD) technologies are used on Audi-branded cars. The word "Quattro" was initially used by Audi in 1980 in its original 4WD coupé, the Audi Quattro. Audi also has a privately held subsidiary company called quattro GmbH. List of highways numbered 4 In sports In the Australian Football League, the top level of Australian rules football, each team is allowed 4 "interchanges" (substitute players), who can be freely substituted at any time, subject to a limit on the total number of substitutions. In baseball: There are four bases in the game: first base, second base, third base, and home plate; to score a run, an offensive player must complete, in the sequence shown, a circuit of those four bases. When a batter receives four pitches that the umpire declares to be "balls" in a single at-bat, a base on balls, informally known as a "walk", is awarded, with the batter sent to first base. For scoring, number 4 is assigned to the second baseman. Four is the most runs that can be scored on any single at bat, whereby all three baserunners and the batter score (the most common being via a grand slam). The fourth batter in the batting lineup is called the cleanup hitter. In basketball, the number four is used to designate the power forward position, often referred to as "the four spot" or "the four". In cricket, a four is a specific type of scoring event, whereby the ball crosses the boundary after touching the ground at least one time, scoring four runs. Taking four wickets in four consecutive balls is typically referred to as a double hat trick (two consecutive, overlapping hat tricks). In American Football teams get four downs to reach the line of gain. In rowing, a four refers to a boat for four rowers, with or without coxswain. In rowing nomenclature, 4− represents a coxless four and 4+ represents a coxed four. In rugby league: A try is worth 4 points. One of the two starting centres wears the jersey number 4. (An exception to this rule is the Super League, which uses static squad numbering.) In rugby union: One of the two starting locks wears the jersey number 4. In the standard bonus points system, a point is awarded in the league standings to a team that scores at least 4 tries in a match, regardless of the match result. In other fields The phrase "four-letter word" is used to describe many swear words in the English language. Four is the only number whose name in English has the same number of letters as its value. Four (四, formal writing: 肆, pinyin sì) is considered an unlucky number in Chinese, Korean, Vietnamese and Japanese cultures mostly in Eastern Asia because it sounds like the word "death" (死, pinyin sǐ). To avoid complaints from people with tetraphobia, many numbered product lines skip the "four": e.g. Nokia cell phones (there was no series beginning with a 4 until the Nokia 4.2), Palm PDAs, etc. Some buildings skip floor 4 or replace the number with the letter "F", particularly in heavily Asian areas. See tetraphobia and Numbers in Chinese culture. In Pythagorean numerology (a pseudocience) the number 4 represents security and stability. The number of characters in a canonical four-character idiom. In the NATO phonetic alphabet, the digit 4 is called "fower". In astrology, Cancer is the 4th astrological sign of the Zodiac. In Tarot, The Emperor is the fourth trump or Major Arcana card. In Tetris, a game named for the Greek word for 4, every shape in the game is formed of 4 blocks each. 4 represents the number of Justices on the Supreme Court of the United States necessary to grant a writ of certiorari (i.e., agree to hear a case; it is one less than the number necessary to render a majority decision) at the courts current size. Number Four is a character in the book series Lorien Legacies. In the performing arts, the fourth wall is an imaginary barrier which separates the audience from the performers, and is "broken" when performers communicate directly to the audience. In music In written music, common time is constructed of four beats per measure and a quarter note receives one beat. In popular or modern music, the most common time signature is also founded on four beats, i.e., 4/4 having four quarter note beats. The common major scale is built on two sets of four notes (e.g., CDEF, GABC), where the first and last notes create an octave interval (a pair-of-four relationship). The interval of a perfect fourth is a foundational element of many genres of music, represented in music theory as the tonic and subdominant relationship. Four is also embodied within the circle of fifths (also known as circle of fourths), which reveals the interval of four in more active harmonic contexts. The typical number of movements in a symphony. The number of completed, numbered symphonies by Johannes Brahms. The number of strings on a violin, a viola, a cello, double bass, a cuatro, a typical bass guitar, and a ukulele, and the number of string pairs on a mandolin. "Four calling birds" is the gift on the fourth day of Christmas in the carol "The Twelve Days of Christmas". Groups of four Big Four (disambiguation) Four basic operations of arithmetic: addition, subtraction, multiplication, division. Greek classical elements (fire, air, water, earth). Four seasons: spring, summer, autumn, winter. The Four Seasons (disambiguation) A leap year generally occurs every four years. Approximately four weeks (4 times 7 days) to a lunar month (synodic month = 29.53 days). Thus the number four is universally an integral part of primitive sacred calendars. Four weeks of Advent (and four Advent candles on the Advent wreath). Four cardinal directions: north, south, east, west. Four Temperaments: sanguine, choleric, melancholic, phlegmatic. Four Humors: blood, yellow bile, black bile, phlegm. Four Great Ancient Capitals of China. Four-corner method. Four Asian Tigers, referring to the economies of Hong Kong, Taiwan, South Korea, and Singapore Cardinal principles. Four cardinal virtues: justice, prudence, temperance, fortitude. Four suits of playing cards: hearts, diamonds, clubs, spades. Four nations of the United Kingdom: England, Wales, Scotland, Northern Ireland. Four provinces of Ireland: Munster, Ulster, Leinster, Connacht. Four estates: politics, administration, judiciary, journalism. Especially in the expression "Fourth Estate", which means journalism. Four Corners is the only location in the United States where four states come together at a single point: Colorado, Utah, New Mexico, and Arizona. Four Evangelists – Matthew, Mark, Luke, and John Four Doctors of Western Church – Saint Gregory the Great, Saint Ambrose, Saint Augustine, and Saint Jerome Four Doctors of Eastern Church – Saint John Chrysostom, Saint Basil the Great, and Gregory of Nazianzus and Saint Athanasius Four Galilean moons of Jupiter – Io, Europa, Ganymede, and Callisto The Gang of Four was a Chinese communist political faction. The Fantastic Four: Mr. Fantastic, The Invisible Woman, The Human Torch, The Thing. The Teenage Mutant Ninja Turtles: Leonardo, Michelangelo, Donatello, Raphael The Beatles were also known as the "Fab Four": John Lennon, Paul McCartney, George Harrison, Ringo Starr. Gang of Four is a British post-punk rock band formed in the late 1970s. Four rivers in the Garden of Eden (Genesis 2:10–14): Pishon (perhaps the Jaxartes or Syr Darya), Gihon (perhaps the Oxus or Amu Darya), Hiddekel (Tigris), and Prat (Euphrates). There are also four years in a single Olympiad (duration between the Olympic Games). Many major international sports competitions follow this cycle, among them the FIFA World Cup and its womens version, the FIBA World Championships for men and women, and the Rugby World Cup. There are four limbs on the human body. Four Houses of Hogwarts in the Harry Potter series: Gryffindor, Hufflepuff, Ravenclaw, Slytherin. Four known continents of the world in the A Song of Ice and Fire series: Westeros, Essos, Sothoryos, Ulthos. Each Grand Prix in Nintendos Mario Kart series is divided into four cups and each cup is divided into four courses. The Mushroom Cup, Flower Cup, Star Cup, and Special Cup make up the Nitro Grand Prix, while the Shell Cup, Banana Cup, Leaf Cup, and the Lightning Cup make up the Retro Grand Prix. See also List of highways numbered 4 References Wells, D. The Penguin Dictionary of Curious and Interesting Numbers London: Penguin Group. (1987): 55–58 External links Marijn.Org on Why is everything four? A few thoughts on the number four, by Penelope Merritt at samuel-beckett.net The Number 4 The Positive Integer 4 Prime curiosities: 4

Intractability

Intractable may refer to: Intractable conflict, a form of complex, severe, and enduring conflict Intractable pain, pain which cannot be controlled/cured by any known treatment Intractability (complexity), in computational complexity theory

Ear pain

Ear pain, also known as earache or otalgia, is pain in the ear. Primary ear pain is pain that originates from the ear. Secondary ear pain is a type of referred pain, meaning that the source of the pain differs from the location where the pain is felt. Most causes of ear pain are non-life-threatening. Primary ear pain is more common than secondary ear pain, and it is often due to infection or injury. The conditions that cause secondary (referred) ear pain are broad and range from temporomandibular joint syndrome to inflammation of the throat.In general, the reason for ear pain can be discovered by taking a thorough history of all symptoms and performing a physical examination, without need for imaging tools like a CT scan. However, further testing may be needed if red flags are present like hearing loss, dizziness, ringing in the ear or unexpected weight loss.Management of ear pain depends on the cause. If there is a bacterial infection, antibiotics are sometimes recommended and over the counter pain medications can help control discomfort. Some causes of ear pain require a procedure or surgery.83 percent of children have at least one episode of a middle ear infection by three years of age. Signs and symptoms Ear pain can present in one or both ears. It may or may not be accompanied by other symptoms such as fever, sensation of the world spinning, ear itchiness, or a sense of fullness in the ear. The pain may or may not worsen with chewing. The pain may also be continuous or intermittent.Ear pain due to an infection is the most common in children and can occur in babies. Adults may need further evaluation if they have hearing loss, dizziness or ringing in the ear. Additional red flags include diabetes, a weakened immune system, swelling seen on the outer ear, or swelling along the jaw. Causes Ear pain has a variety of causes, the majority of which are not life-threatening. Ear pain can originate from a part of the ear itself, known as primary ear pain, or from an anatomic structure outside the ear that is perceived as pain within the ear, known as secondary ear pain. Secondary ear pain is a type of referred pain, meaning that the source of the pain differs from the location where the pain is felt. Primary ear pain is more common in children, whereas secondary (referred) pain is more common in adults.Primary ear pain is most commonly caused by infection or injury to one of the parts of the ear. External ear Many conditions involving the external ear will be visible to the naked eye. Because the external ear is the most exposed portion of the ear, it is vulnerable to trauma or environmental exposures. Blunt trauma, such as a blow to the ear, can result in a hematoma, or collection of blood between the cartilage and perichondrium of the ear. This type of injury is particularly common in contact sports such as wrestling and boxing. Environmental injuries include sunburn, frostbite, or contact dermatitis.Less common causes of external ear pain include: Auricular Cellulitis: a superficial infection of the ear that may be precipitated by trauma, an insect bite, or ear piercing Perichondritis: infection of the perichondrium, or fascia surrounding the ear cartilage, which can develop as a complication of untreated auricular cellulitis. It is important to identify and treat perichondritis with antibiotics to avoid permanent ear deformities. Relapsing polychondritis: a systemic inflammatory condition involving cartilage in many parts of the body, but often including the cartilage of both ears. The severity and prognosis of the disease varies widely. Otitis externa Otitis externa, also known as "swimmers ear", is a cellulitis of the external ear canal. In North America, 98% of cases are caused by bacteria, and the most common causative organisms are Pseudomonas and Staph aureus. Risk factors include exposure to excessive moisture (e.g. from swimming or a warm climate) and disruption of the protective cerumen barrier, which can result from aggressive ear cleaning or placing objects in the ear.Malignant otitis externa is a rare and potentially life-threatening complication of otitis externa in which the infection spreads from the ear canal into the surrounding skull base, hence becoming an osteomyelitis. It occurs largely in diabetic patients. It is very rare in children, though can be seen in immunocompromised children and adults. Pseudomonas is the most common causative organism. The pain tends to be more severe than in uncomplicated otitis externa, and laboratory studies often reveal elevated inflammatory markers (ESR and/or CRP). The infection may extend to cranial nerves, or rarely to the meninges or brain. Examination of the ear canal may reveal granulation tissue in the inferior canal. It is treated with several weeks of IV and oral antibiotics, usually fluoroquinolones. Mechanical obstruction Earwax impaction: results in 12 million medical visits annually in the United States. Cerumen impaction may cause ear pain, but it can also prevent thorough examination of the ear and identification of an alternate source of pain. Foreign body: commonly include insects or small objects like beads Less common Herpes zoster: varicella zoster virus can reactivate in an area that includes the ear. Reactivation can produce pain and visible vesicles within the ear canal and, when combined with facial paralysis due to facial nerve involvement, is called Ramsay Hunt syndrome. Tumors: the most common ear canal tumor is squamous cell carcinoma. Symptoms can resemble those of otitis externa, and cancer should be considered if the symptoms are not improving on appropriate treatment. Middle and inner ear Acute otitis media Acute otitis media is an infection of the middle ear. More than 80% of children experience at least one episode of otitis media by age 3 years. Acute otitis media is also most common in these first 3 years of life, though older children may also experience it. The most common causative bacteria are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Otitis media often occurs with or following cold symptoms. The diagnosis is made by the combination of symptoms and examination of the tympanic membrane for redness, bulging, and/or a middle ear effusion (collection of fluid within the middle ear).Complications of otitis media include hearing loss, facial nerve paralysis, or extension of infection to surrounding anatomic structures, including: Mastoiditis: infection of the air cells in the mastoid process, the area of the skull located right behind the ear Petrositis: infection of the petrous portion of the temporal bone Labyrinthitis Meningitis Subdural abscess Brain abscess Cerebral venous sinus thrombosis Trauma Barotrauma: results from changes in atmospheric pressure that occur when descending in a plane or deep diving. As atmospheric pressure increases with descent, the eustachian tube collapses due to pressure within the middle ear being less than the external pressure, which causes pain. In severe cases, middle ear hemorrhage or tympanic membrane rupture can result. Tympanic membrane rupture: disruption of the eardrum. This can be caused by a blow to the ear, blast injury, barotrauma, or direct penetration of the tympanic membrane by an object entering the ear. Referred ear pain A variety of conditions can cause irritation of one of the nerves that provides sensation to the ear. Conditions causing irritation the trigeminal nerve (cranial nerve V): Temporomandibular joint syndrome: inflammation or abnormal movements of the joint between the jaw and skull. These disorders are most common in women of childbearing age, and are uncommon in children younger than 10 years old. Myofascial pain syndrome: pain in the muscles involved in chewing. There may be certain parts of the muscles or tendons (connective tissue connecting the muscles to bones) that are especially painful when pressed Trigeminal neuralgia: attacks of shooting pain down the face that may be triggered by touching the face or temperature changes Dental pain from cavities or an abscess Oral cavity carcinomaConditions causing irritation of the facial nerve (cranial nerve VII) or glossopharyngeal nerve (cranial nerve IX): Tonsillitis: infection/inflammation of the tonsils Post-tonsillectomy: pain following surgical removal of the tonsils Pharyngitis: infection/inflammation of the throat Sinusitis Parotitis: inflammation of the parotid gland, the salivary gland right in front of the ear Carcinoma of the oropharynx (base of tongue, soft palate, pharyngeal wall, tonsils)Conditions causing irritation of the vagus nerve (cranial nerve X): GERD Myocardial ischemia (inadequate oxygen supply to the heart muscle)Conditions causing irritation of cervical nerves C2-C3: Cervical spine trauma, arthritis (joint inflammation), or tumor Temporal arteritis: an autoimmune disorder leading to inflammation of the temporal artery, a large artery in the head. This condition tends to occur in adults older than 50. Pathophysiology Primary ear pain The ear can be anatomically divided into the external ear, the external auditory canal, the middle ear, and the inner ear. These three are indistinguishable in terms of the pain experienced. Secondary ear pain Many different nerves provide sensation to the various parts of the ear, including cranial nerves V (trigeminal), VII (facial), IX (glossopharyngeal), and X (vagus), and the great auricular nerve (cervical nerves C2-C3). These nerves also supply other parts of the body, from the mouth to the chest and abdomen. Irritation of these nerves in another part of the body has the potential to produce pain in the ear. This is called referred pain. Irritation of the trigeminal nerve (cranial nerve V) is the most common cause of referred ear pain. Diagnostic While some disorders may require specific imaging or testing, most etiologies of ear pain are diagnosed clinically. Because the differential for ear pain is so broad, there is no consensus on the best diagnostic framework to use. One approach is to differentiate by time course, as primary causes of ear pain are typically more acute in nature, while secondary causes of ear pain are more chronic. Acute causes may be further distinguished by the presence of fever (indicating an underlying infection) or the absence of fever (suggesting a structural problem, such as such as trauma or other injury to the ear). Etiologies leading to chronic pain may be broken down by the presence or absence of worrisome clinical features, also known as red flags. One red flag is the presence of one or multiple risk factors including smoking, heavy alcohol use (greater than 3.5 drinks per day), diabetes, coronary artery disease, and older age (greater than 50). These factors increase the risk of having a serious cause of ear pain, like cancer or a serious infection. In particular, second hand smoke may increase risk of acute otitis media in children. In addition, swimming is the most significant risk factor for otitis externae, though other risk factors include high humidity in the ear canal, eczema and/or ear trauma.If red flags are present it may be necessary to do additional workup such as a CT scan or biopsy to rule out a more dangerous diagnosis. Such diagnoses include malignant (or necrotizing) otitis externa, mastoiditis, temporal arteritis, and cancer. It is important to note that while the presence of a red flag does raise suspicion for one of these four disease, it does not guarantee a diagnosis as any one symptom can be seen in a variety of situations. For example, jaw claudication can be seen in temporal arteritis, but also in TMJ dysfunction.If there are no red flags, other sources of referred ear pain become more likely and are reasonable to pursue. *Indicates a "Cant Miss" diagnosis or a red flag. Management Management of ear pain depends on the underlying cause. Antibiotics While not all causes of ear pain are treated with antibiotics, those caused by bacterial infections of the ear are usually treated with antibiotics known to cover the common bacterial organisms for that type of infection. Many bacterial ear infections are treated with cleaning of the area, topical or systemic antibiotics, and oral analgesics for comfort. Some types of bacterial ear infections can benefit from warm compresses included in the treatment. Some of the causes of ear pain that are typically treated with either a topical or systemic antibiotic include: Uncomplicated acute bacterial otitis externa (AOE). For symptoms that are not responsive to treatment within 10 days, a physician should evaluate for necrotizing external otitis. Acute otitis media (AOM) self-resolves within 24–48 hours in 80% of cases. If it does not self-resolve, AOM thought to be caused by bacteria is treated with systemic antibiotics. If symptoms do not respond to a week of treatment, a physician should evaluate for mastoiditis. Acute folliculitis. Auricular cellulitis. Suppurative otitis media. There is also a risk for tympanic membrane rupture. Perichondritis. An otorhinolaryngologist should also evaluate it and if a foreign body is present in the cartilage, this foreign body should be removed. If there is cartilage involvement, then more advance care with hospitalization is needed. Sinusitis can cause secondary ear pain. Treating the underlying sinusitis will treat the ear pain. (See sinusitis.)Some bacterial infections may require a more advanced treatment with evaluation by otorhinolaryngology, IV antibiotics, and hospital admission. Necrotizing external otitis is potentially fatal and should be evaluated by an otorhinolaryngologist with admission to the hospital and IV antibiotics.(See otitis externa.) Acute mastoiditis is treated with admission to the hospital, otorhinolaryngology consultation and empiric IV antibiotics. Cases with intracranial involvement are treated with a mastoidectomy with myringotomy. Chondritis. Procedures Some causes of ear pain require procedural management alone, by a health professional, or in addition to antibiotic therapy. Keratosis obturans is treated with removal of impacted desquamated keratin debris in the ear canal. Chronic perichondritis and chondritis that continues to be symptomatic despite appropriate antibiotic management may require surgical debridement. Surgical drainage could be required. Bullous myringitis leads to the development of bullae on the tympanic membrane that can be punctured to give pain relief. Foreign body in the ear canal can cause pain and be treated with careful removal. Infected sebaceous cyst is treated with incision and drainage of the cysts, oral antibiotics and otorhinolaryngology assessment. Other Given the variety of causes of ear pain, some causes require treatment other than antibiotics and procedures. Relapsing polychondritis is an autoimmune disease treated with immunomodulating medications (medications that help modulate the immune system). Temporomandibular joint dysfunction can lead to secondary ear pain and can be initially treated with a soft food diet, NSAIDs, application of a heat pack, massage of local area, and a referral to a dentist. Myofascial pain syndromes are initially treated with NSAIDs and physical therapy. Local anesthetic injection into the muscle trigger point can be considered in severe cases. Glossopharyngeal neuralgia is treated with carbamazepine. Epidemiology 2/3 of people presenting with ear pain were diagnosed with some sort of primary otalgia and 1/3 were diagnosed with some sort secondary otalgia.A common cause of primary otalgia is ear infection called otitis media, meaning an infection behind the eardrum. The peak age for children to get acute otitis media is ages 6–24 months. One review paper wrote that 83% of children had at least one episode of acute otitis media by 3 years of age. Worldwide, there are 709 millions cases of acute otitis media every year. Hearing loss globally due to ear infection is estimated to be 30 people in every 10,000. Around the world there is around 21,000 to 28,000 deaths due to complications from ear infections. These complications include brain abscesses and meningitis. Otitis externae peaks at age 7–12 years of age and around 10% of people has had it at least once in their lives.Cerumen impaction occurs in 1 out of every 10 children, 1 in every 20 adults and 1 in every 3 elderly citizens.Barotrauma occurs around 1 in every 1000 people.Of people presenting with ear pain, only 3% was diagnosed with eustachian tube dysfunction. History Not much was known about ear pain and acute otitis media before the 17th century. It was a common phenomenon with no treatment. That changed when the otoscope was invented in the 1840s by Anton von Troeltsh in Germany. Another shift came with the invention of antibiotics. Before antibiotics was introduced there use to be a high rate of ear infections spreading to the bone around the ear, but that is now considered a rare complication. Society and culture There was previously a strong tradition of treating acute otitis media with amoxicillin. One quote from the 1980s shows this sentiment by saying "any child with an earache has an acute amoxicillin deficiency". However, people started realizing that using antibiotics too much can cause bacteria to gain resistance. Increasing resistance makes antibiotics less effective. The term antibiotic stewardship is then used to describe the systematic effort to educate antibiotic prescribers to only give these medications when they are warranted. In particular to children, most ear pain resolves by itself with no complications. There are guidelines in place to help determine when antibiotics for ear pain are needed in children. The ear itself played a role in treatment via acupuncture, also known as auriculotherapy. It was believed that acupuncture of the ear could be used to correct other pain or disorders in the body. Such practices may have started as far back as the Stone Age. The first documentation of auriculotherapy in Europe was in the 1600s. One physician described stimulating the ear by burning or scarring to treat sciatic pain, while another physician applied this treatment for toothache. Paul Nogier is known as the father of ear acupuncture for his theory that parts of the ear corresponds to other areas of the body in a reliable fashion. Research There are currently studies going on delivering antibiotics directly into the middle ear. References == External links ==

Central retinal vein occlusion

Central retinal vein occlusion, also CRVO, is when the central retinal vein becomes occluded, usually through thrombosis. The central retinal vein is the venous equivalent of the central retinal artery and both may become occluded. Since the central retinal artery and vein are the sole source of blood supply and drainage for the retina, such occlusion can lead to severe damage to the retina and blindness, due to ischemia (restriction in blood supply) and edema (swelling).CRVO can cause ocular ischemic syndrome. Nonischemic CRVO is the milder form of the disease. It may progress to the more severe ischemic type. CRVO can also cause glaucoma. Diagnosis Despite the role of thrombosis in the development of CRVO, a systematic review found no increased prevalence of thrombophilia (an inherent propensity to thrombosis) in patients with retinal vascular occlusion. Treatment Treatment consists of Anti-VEGF drugs like Lucentis or intravitreal steroid implant (Ozurdex) and Pan-Retinal Laser Photocoagulation usually. Underlying conditions also require treatment. CRVO without ischemia has better visual prognosis than ischemic CRVO. A systematic review studied the effectiveness of the anti-VEGF drugs ranibizumab and pagatanib sodium for patients with non-ischemic CRVO. Though there was a limited sample size, participants in both treatment groups showed improved visual acuity over 6 month periods, with no safety concerns. See also Central retinal artery occlusion Branch retinal artery occlusion Branch retinal vein occlusionEylea Iridodialysis Ischemic optic neuropathy References == External links ==

Denasalization

In phonetics, denasalization is the loss of nasal airflow in a nasal sound, such as a nasal consonant or a nasal vowel. That may be due to speech pathology but also occurs when the sinuses are blocked from a common cold, when it is called a nasal voice, which is not a linguistic term. Acoustically, it is the "absence of the expected nasal resonance." The symbol in the Extended IPA is ⟨◌͊⟩. When one speaks with a cold, the nasal passages still function as a resonant cavity so a denasalized nasal [m͊] does not sound like a voiced oral stop [b], and a denasalized vowel [a͊] does not sound like an oral vowel [a]. However, there are cases of historical or allophonic denasalization that have produced oral stops. In some languages with nasal vowels, such as Paicĩ, nasal consonants may occur only before nasal vowels; before oral vowels, prenasalized stops are found. That allophonic variation is likely to be from a historical process of partial denasalization. Similarly, several languages around Puget Sound underwent a process of denasalization about 100 years ago. Except in special speech registers, such as baby talk, the nasals [m, n] became the voiced stops [b, d]. It appears from historical records that there was an intermediate stage in which the stops were prenasalized stops [ᵐb, ⁿd] or poststopped nasals [mᵇ, nᵈ]. Something similar has occurred with word-initial nasals in Korean; in some contexts, /m/, /n/ are denasalized to [b, d]. The process is sometimes represented with the IPA [m͊] and [n͊], which simply places the IPA ◌͊ denasalization diacritic on [m] and [n] to show the underlying phoneme.In speech pathology, practice varies in whether ⟨m͊⟩ is a partially denasalized /m/, with ⟨b⟩ for full denasalization, or is a target /m/ whether partially denasalized or a fully denasalized [b]. See also Nasalization Hypernasal speech == References ==

Stress

Stress may refer to: Science and medicine Stress (biology), an organisms response to a stressor such as an environmental condition Stress (linguistics), relative emphasis or prominence given to a syllable in a word, or to a word in a phrase or sentence Stress (mechanics), the internal forces that neighboring particles of a continuous material exert on each other Occupational stress, stress related to ones job Psychological stress, a feeling of strain and pressure Surgical stress, systemic response to surgical injury Arts, entertainment, and media Music Groups and musicians Stress (Brazilian band), a Brazilian heavy metal band Stress (British band), a British rock band Stress (pop rock band), an early 1980s melodic rock band from San Diego Stress (musician) (born 1977), hip hop singer from Switzerland Stress (record producer) (born 1979), artistic name of Can Canatan, Swedish musician and record producer Albums Stress (Anonymus album), 1997 Stress (Daddy Freddy album), 1991 Stress (Stress album), self-titled album by Brazilian band Stress Stress: The Extinction Agenda, 1994 album by Organized Konfusion Songs "Stress" (Justice song), 2007 song by Justice "Stress" (Odd Børre song), 1968 song by Odd Børre "Stress", a song by Godsmack from Godsmack "Stress", a 2000 song by Jims Big Ego "The Stress", a 1989 song by Chisato Moritaka Other music Stress (music), a type of emphasis placed on a particular note or set of notes Other arts, entertainment, and media Stress (card game), a card game Stress (journal), a medical journal "Stress" (The Unit), an episode of the television series The Unit Other uses Stress (font), varying stroke widths of a font See also All pages with titles containing Stress Emphasis (disambiguation) Stress cracking (disambiguation) Stress intensity (disambiguation) Stress tensor (disambiguation) Stress test (disambiguation) Tension (disambiguation)

Acute infectious thyroiditis

Acute infectious thyroiditis (AIT) also known as suppurative thyroiditis, microbial inflammatory thyroiditis, pyrogenic thyroiditis and bacterial thyroiditis.The thyroid is normally very resistant to infection. Due to a relatively high amount of iodine in the tissue, as well as high vascularity and lymphatic drainage to the region, it is difficult for pathogens to infect the thyroid tissue. Despite all this, a persistent fistula from the piriform sinus may make the left lobe of the thyroid susceptible to infection and abscess formation. AIT is most often caused by a bacterial infection but can also be caused by a fungal or parasitic infection, most commonly in an immunocompromised host. Signs and symptoms In most cases AIT is characterized by onset of pain, firmness, tenderness, redness or swelling in the anterior aspect of the neck. Patients will also present with a sudden fever, difficulty swallowing and difficulty controlling the voice. Symptoms may be present from 1 to 180 days, with most symptoms lasting an average of about 18 days. The main issue associated with the diagnosis of AIT is differentiating it from other more commonly seen forms of thyroid conditions. Pain, fever and swelling are often much more severe and continue to get worse in people who have AIT compared to those with other thyroid conditions. Causes Despite the thyroid gland being extremely resistant to infection, it is still susceptible to infection by various bacteria. The cause can be almost any bacterium. Staphylococcus aureus, Streptococcus pyogenes, Staphylococcus epidermidis, and Streptococcus pneumoniae in descending order are the organisms most commonly isolated from acute thyroiditis cases in children. Other aerobic organisms are Klebsiella sp, Haemophilus influenza, Streptococcus viridans, Eikenella corrodens, Enterobacteriaceae, and salmonella sp. Occurrences of AIT are most common in patients with prior thyroid disease such as Hashimotos thyroiditis or thyroid cancer. The most common cause of infection in children is a congenital abnormality such as pyriform sinus fistula. In most cases, the infection originates in the piriform sinus and spreads to the thyroid via the fistula. In many reported cases of AIT the infection occurs following an upper respiratory tract infection. One study found that of the reported cases of AIT, 66% occurred after an acute illness involving the upper respiratory tract. Although the rates of infection are still very low, cases of AIT have been on the rise in recent years due to the higher occurrence of immune-compromised patients. Other causes of AIT are commonly due to contamination from an outside source and are included below. Repeated fine needle aspirates Perforation of esophagus Regional infection Diagnosis Patients who are suspected of having AIT often undergo tests to detect for elevated levels of white blood cells as well as an ultrasound to reveal unilobular swelling. Depending on the age and immune status of the patient more invasive procedures may be performed such as fine needle aspiration of the neck mass to facilitate a diagnosis. In cases where the infection is thought to be associated with a sinus fistula it is often necessary to confirm the presence of the fistula through surgery or laryngoscopic examination. While invasive procedures can often tell definitively whether or not a fistula is present, new studies are working on the use of computed tomography as a useful method to visualize and detect the presence of a sinus fistula. Diagnostic tests Fever, redness, swelling Pain Blood tests of thyroid functions including TSH, T4 and T3 are usually normal Ultrasonographic examination often shows the abscess or swelling in thyroid Gallium scan will be positive Barium swallow will show fistula connection to the piriform sinus and left lobe Elevated white blood cell count Elevated erythrocyte sedimentation rate Fine-needle aspiration Subtypes of thyroiditis Treatment Treatment of AIT involves antibiotic treatment. Based on the offending organism found on microscopic examination of the stained fine needle aspirate, the appropriate antibiotic treatment is determined. In the case of a severe infection, systemic antibiotics are necessary. Empirical broad spectrum antimicrobial treatment provides preliminary coverage for a variety of bacteria, including S. aureus and S. pyogenes. Antimicrobial options include penicillinase-resistant penicillins (ex: cloxacillin, dicloxacillin) or a combination of a penicillin and a beta-lactamase inhibitor. However, in patients with a penicillin allergy, clindamycin or a macrolide can be prescribed. The majority of anaerobic organisms involved with AIT are susceptible to penicillin. Certain Gram-negative bacilli (ex: Prevotella, Fusobacteriota, and Porphyromonas) are exhibiting an increased resistance based on the production of beta-lactamase. Patients who have undergone recent penicillin therapy have demonstrated an increase in beta-lactamase-producing (anaerobic and aerobic) bacteria. Clindamycin, or a combination of metronidazole and a macrolide, or a penicillin combined with a beta-lactamase inhibitor is recommended in these cases. Fungal thyroiditis can be treated with amphotericin B and fluconazole. Early treatment of AIT prevents further complications. However, if antibiotic treatment does not manage the infection, surgical drainage is required. Symptoms or indications requiring drainage include continued fever, high white blood cell count, and continuing signs of localized inflammation. The draining procedure is also based on clinical examination or ultrasound/CT scan results that indicate an abscess or gas formation. Another treatment of AIT involves surgically removing the fistula. This treatment is often the option recommended for children. However, in cases of an antibiotic resistant infection or necrotic tissue, a lobectomy is recommended. If diagnosis and/or treatment is delayed, the disease could prove fatal. Epidemiology Acute infectious thyroiditis is very rare, with it only accounting for about 0.1–0.7% of all thyroiditis. Large hospitals tend to only see two cases of AIT annually. For the few cases of AIT that are seen the statistics seem to show a pattern. AIT is found in children and young adults between the ages of 20 and 40. The occurrence of the disease in people between 20 and 40 is only about 8% with the other 92% being in children. Men and women are each just as likely to get the disease. If left untreated, there is a 12% mortality rate. References == External links ==

Influenza

Influenza, commonly known as "the flu", is an infectious disease caused by influenza viruses. Symptoms range from mild to severe and often include fever, runny nose, sore throat, muscle pain, headache, coughing, and fatigue. These symptoms begin from one to four days after exposure to the virus (typically two days) and last for about 2–8 days. Diarrhea and vomiting can occur, particularly in children. Influenza may progress to pneumonia, which can be caused by the virus or by a subsequent bacterial infection. Other complications of infection include acute respiratory distress syndrome, meningitis, encephalitis, and worsening of pre-existing health problems such as asthma and cardiovascular disease. There are four types of influenza virus, termed influenza viruses A, B, C, and D. Aquatic birds are the primary source of Influenza A virus (IAV), which is also widespread in various mammals, including humans and pigs. Influenza B virus (IBV) and Influenza C virus (ICV) primarily infect humans, and Influenza D virus (IDV) is found in cattle and pigs. IAV and IBV circulate in humans and cause seasonal epidemics, and ICV causes a mild infection, primarily in children. IDV can infect humans but is not known to cause illness. In humans, influenza viruses are primarily transmitted through respiratory droplets produced from coughing and sneezing. Transmission through aerosols and intermediate objects and surfaces contaminated by the virus also occur. Frequent hand washing and covering ones mouth and nose when coughing and sneezing reduce transmission. Annual vaccination can help to provide protection against influenza. Influenza viruses, particularly IAV, evolve quickly, so flu vaccines are updated regularly to match which influenza strains are in circulation. Vaccines currently in use provide protection against IAV subtypes H1N1 and H3N2 and one or two IBV subtypes. Influenza infection is diagnosed with laboratory methods such as antibody or antigen tests and a polymerase chain reaction (PCR) to identify viral nucleic acid. The disease can be treated with supportive measures and, in severe cases, with antiviral drugs such as oseltamivir. In healthy individuals, influenza is typically self-limiting and rarely fatal, but it can be deadly in high-risk groups. In a typical year, 5–15% of the population contracts influenza. There are 3–5 million severe cases annually, with up to 650,000 respiratory-related deaths globally each year. Deaths most commonly occur in high-risk groups, including young children, the elderly, and people with chronic health conditions. In temperate regions of the world, the number of influenza cases peaks during winter, whereas in the tropics influenza can occur year-round. Since the late 1800s, large outbreaks of novel influenza strains that spread globally, called pandemics, have occurred every 10–50 years. Five flu pandemics have occurred since 1900: the Spanish flu in 1918–1920, which was the most severe flu pandemic, the Asian flu in 1957, the Hong Kong flu in 1968, the Russian flu in 1977, and the swine flu pandemic in 2009. Signs and symptoms The time between exposure to the virus and development of symptoms, called the incubation period, is 1–4 days, most commonly 1–2 days. Many infections, however, are asymptomatic. The onset of symptoms is sudden, and initial symptoms are predominately non-specific, including fever, chills, headaches, muscle pain or aching, a feeling of discomfort, loss of appetite, lack of energy/fatigue, and confusion. These symptoms are usually accompanied by respiratory symptoms such as a dry cough, sore or dry throat, hoarse voice, and a stuffy or runny nose. Coughing is the most common symptom. Gastrointestinal symptoms may also occur, including nausea, vomiting, diarrhea, and gastroenteritis, especially in children. The standard influenza symptoms typically last for 2–8 days. A 2021 study suggests influenza can cause long lasting symptoms in a similar way to long COVID.Symptomatic infections are usually mild and limited to the upper respiratory tract, but progression to pneumonia is relatively common. Pneumonia may be caused by the primary viral infection or by a secondary bacterial infection. Primary pneumonia is characterized by rapid progression of fever, cough, labored breathing, and low oxygen levels that cause bluish skin. It is especially common among those who have an underlying cardiovascular disease such as rheumatic heart disease. Secondary pneumonia typically has a period of improvement in symptoms for 1–3 weeks followed by recurrent fever, sputum production, and fluid buildup in the lungs, but can also occur just a few days after influenza symptoms appear. About a third of primary pneumonia cases are followed by secondary pneumonia, which is most frequently caused by the bacteria Streptococcus pneumoniae and Staphylococcus aureus. Virology Types of virus Influenza viruses comprise four species. Each of the four species is the sole member of its own genus, and the four influenza genera comprise four of the seven genera in the family Orthomyxoviridae. They are: Influenza A virus (IAV), genus Alphainfluenzavirus Influenza B virus (IBV), genus Betainfluenzavirus Influenza C virus (ICV), genus Gammainfluenzavirus Influenza D virus (IDV), genus DeltainfluenzavirusIAV is responsible for most cases of severe illness as well as seasonal epidemics and occasional pandemics. It infects people of all ages but tends to disproportionately cause severe illness in the elderly, the very young, and those who have chronic health issues. Birds are the primary reservoir of IAV, especially aquatic birds such as ducks, geese, shorebirds, and gulls, but the virus also circulates among mammals, including pigs, horses, and marine mammals. IAV is classified into subtypes based on the viral proteins haemagglutinin (H) and neuraminidase (N). As of 2019, 18 H subtypes and 11 N subtypes have been identified. Most potential combinations have been reported in birds, but H17-18 and N10-11 have only been found in bats. Only H subtypes H1-3 and N subtypes N1-2 are known to have circulated in humans, the current IAV subtypes in circulation being H1N1 and H3N2. IAVs can be classified more specifically to also include natural host species, geographical origin, year of isolation, and strain number, such as H1N1/A/duck/Alberta/35/76.IBV mainly infects humans but has been identified in seals, horses, dogs, and pigs. IBV does not have subtypes like IAV but has two antigenically distinct lineages, termed the B/Victoria/2/1987-like and B/Yamagata/16/1988-like lineages, or simply (B/)Victoria(-like) and (B/)Yamagata(-like). Both lineages are in circulation in humans, disproportionately affecting children. IBVs contribute to seasonal epidemics alongside IAVs but have never been associated with a pandemic.ICV, like IBV, is primarily found in humans, though it also has been detected in pigs, feral dogs, dromedary camels, cattle, and dogs. ICV infection primarily affects children and is usually asymptomatic or has mild cold-like symptoms, though more severe symptoms such as gastroenteritis and pneumonia can occur. Unlike IAV and IBV, ICV has not been a major focus of research pertaining to antiviral drugs, vaccines, and other measures against influenza. ICV is subclassified into six genetic/antigenic lineages.IDV has been isolated from pigs and cattle, the latter being the natural reservoir. Infection has also been observed in humans, horses, dromedary camels, and small ruminants such as goats and sheep. IDV is distantly related to ICV. While cattle workers have occasionally tested positive to prior IDV infection, it is not known to cause disease in humans. ICV and IDV experience a slower rate of antigenic evolution than IAV and IBV. Because of this antigenic stability, relatively few novel lineages emerge. Genome and structure Influenza viruses have a negative-sense, single-stranded RNA genome that is segmented. The negative sense of the genome means it can be used as a template to synthesize messenger RNA (mRNA). IAV and IBV have eight genome segments that encode 10 major proteins. ICV and IDV have seven genome segments that encode nine major proteins. Three segments encode three subunits of an RNA-dependent RNA polymerase (RdRp) complex: PB1, a transcriptase, PB2, which recognizes 5 caps, and PA (P3 for ICV and IDV), an endonuclease. The matrix protein (M1) and membrane protein (M2) share a segment, as do the non-structural protein (NS1) and the nuclear export protein (NEP). For IAV and IBV, hemagglutinin (HA) and neuraminidase (NA) are encoded on one segment each, whereas ICV and IDV encode a hemagglutinin-esterase fusion (HEF) protein on one segment that merges the functions of HA and NA. The final genome segment encodes the viral nucleoprotein (NP). Influenza viruses also encode various accessory proteins, such as PB1-F2 and PA-X, that are expressed through alternative open reading frames and which are important in host defense suppression, virulence, and pathogenicity.The virus particle, called a virion, is pleomorphic and varies between being filamentous, bacilliform, or spherical in shape. Clinical isolates tend to be pleomorphic, whereas strains adapted to laboratory growth typically produce spherical virions. Filamentous virions are about 250 nanometers (nm) by 80 nm, bacilliform 120–250 by 95 nm, and spherical 120 nm in diameter. The virion consists of each segment of the genome bound to nucleoproteins in separate ribonucleoprotein (RNP) complexes for each segment, all of which are surrounded by a lipid bilayer membrane called the viral envelope. There is a copy of the RdRp, all subunits included, bound to each RNP. The envelope is reinforced structurally by matrix proteins on the interior that enclose the RNPs, and the envelope contains HA and NA (or HEF) proteins extending outward from the exterior surface of the envelope. HA and HEF proteins have a distinct "head" and "stalk" structure. M2 proteins form proton ion channels through the viral envelope that are required for viral entry and exit. IBVs contain a surface protein named NB that is anchored in the envelope, but its function is unknown. Life cycle The viral life cycle begins by binding to a target cell. Binding is mediated by the viral HA proteins on the surface of the evelope, which bind to cells that contain sialic acid receptors on the surface of the cell membrane. For N1 subtypes with the "G147R" mutation and N2 subtypes, the NA protein can initiate entry. Prior to binding, NA proteins promote access to target cells by degrading mucous, which helps to remove extracellular decoy receptors that would impede access to target cells. After binding, the virus is internalized into the cell by an endosome that contains the virion inside it. The endosome is acidified by cellular vATPase to have lower pH, which triggers a conformational change in HA that allows fusion of the viral envelope with the endosomal membrane. At the same time, hydrogen ions diffuse into the virion through M2 ion channels, disrupting internal protein-protein interactions to release RNPs into the host cells cytosol. The M1 protein shell surrounding RNPs is degraded, fully uncoating RNPs in the cytosol.RNPs are then imported into the nucleus with the help of viral localization signals. There, the viral RNA polymerase transcribes mRNA using the genomic negative-sense strand as a template. The polymerase snatches 5 caps for viral mRNA from cellular RNA to prime mRNA synthesis and the 3-end of mRNA is polyadenylated at the end of transcription. Once viral mRNA is transcribed, it is exported out of the nucleus and translated by host ribosomes in a cap-dependent manner to synthesize viral proteins. RdRp also synthesizes complementary positive-sense strands of the viral genome in a complementary RNP complex which are then used as templates by viral polymerases to synthesize copies of the negative-sense genome. During these processes, RdRps of avian influenza viruses (AIVs) function optimally at a higher temperature than mammalian influenza viruses.Newly synthesized viral polymerase subunits and NP proteins are imported to the nucleus to further increase the rate of viral replication and form RNPs. HA, NA, and M2 proteins are trafficked with the aid of M1 and NEP proteins to the cell membrane through the Golgi apparatus and inserted into the cells membrane. Viral non-structural proteins including NS1, PB1-F2, and PA-X regulate host cellular processes to disable antiviral responses. PB1-F2 aso interacts with PB1 to keep polymerases in the nucleus longer. M1 and NEP proteins localize to the nucleus during the later stages of infection, bind to viral RNPs and mediate their export to the cytoplasm where they migrate to the cell membrane with the aid of recycled endosomes and are bundled into the segments of the genome.Progenic viruses leave the cell by budding from the cell membrane, which is initiated by the accumulation of M1 proteins at the cytoplasmic side of the membrane. The viral genome is incorporated inside a viral envelope derived from portions of the cell membrane that have HA, NA, and M2 proteins. At the end of budding, HA proteins remain attached to cellular sialic acid until they are cleaved by the sialidase activity of NA proteins. The virion is then released from the cell. The sialidase activity of NA also cleaves any sialic acid residues from the viral surface, which helps prevent newly assembled viruses from aggregating near the cell surface and improving infectivity. Similar to other aspects of influenza replication, optimal NA activity is temperature- and pH-dependent. Ultimately, presence of large quantities of viral RNA in the cell triggers apoptosis, i.e. programmed cell death, which is initiated by cellular factors to restrict viral replication. Antigenic drift and shift Two key processes that influenza viruses evolve through are antigenic drift and antigenic shift. Antigenic drift is when an influenza viruss antigens change due to the gradual accumulation of mutations in the antigens (HA or NA) gene. This can occur in response to evolutionary pressure exerted by the host immune response. Antigenic drift is especially common for the HA protein, in which just a few amino acid changes in the head region can constitute antigenic drift. The result is the production of novel strains that can evade pre-existing antibody-mediated immunity. Antigenic drift occurs in all influenza species but is slower in B than A and slowest in C and D. Antigenic drift is a major cause of seasonal influenza, and requires that flu vaccines be updated annually. HA is the main component of inactivated vaccines, so surveillance monitors antigenic drift of this antigen among circulating strains. Antigenic evolution of influenza viruses of humans appears to be faster than influenza viruses in swine and equines. In wild birds, within-subtype antigenic variation appears to be limited but has been observed in poultry.Antigenic shift is a sudden, drastic change in an influenza viruss antigen, usually HA. During antigenic shift, antigenically different strains that infect the same cell can reassort genome segments with each other, producing hybrid progeny. Since all influenza viruses have segmented genomes, all are capable of reassortment. Antigenic shift, however, only occurs among influenza viruses of the same genus and most commonly occurs among IAVs. In particular, reassortment is very common in AIVs, creating a large diversity of influenza viruses in birds, but is uncommon in human, equine, and canine lineages. Pigs, bats, and quails have receptors for both mammalian and avian IAVs, so they are potential "mixing vessels" for reassortment. If an animal strain reassorts with a human strain, then a novel strain can emerge that is capable of human-to-human transmission. This has caused pandemics, but only a limited number have occurred, so it is difficult to predict when the next will happen. Mechanism Transmission People who are infected can transmit influenza viruses through breathing, talking, coughing, and sneezing, which spread respiratory droplets and aerosols that contain virus particles into the air. A person susceptible to infection can then contract influenza by coming into contact with these particles. Respiratory droplets are relatively large and travel less than two meters before falling onto nearby surfaces. Aerosols are smaller and remain suspended in the air longer, so they take longer to settle and can travel further than respiratory droplets. Inhalation of aerosols can lead to infection, but most transmission is in the area about two meters around an infected person via respiratory droplets that come into contact with mucosa of the upper respiratory tract. Transmission through contact with a person, bodily fluids, or intermediate objects (fomites) can also occur, such as through contaminated hands and surfaces since influenza viruses can survive for hours on non-porous surfaces. If ones hands are contaminated, then touching ones face can cause infection.Influenza is usually transmissible from one day before the onset of symptoms to 5–7 days after. In healthy adults, the virus is shed for up to 3–5 days. In children and the immunocompromised, the virus may be transmissible for several weeks. Children ages 2–17 are considered to be the primary and most efficient spreaders of influenza. Children who have not had multiple prior exposures to influenza viruses shed the virus at greater quantities and for a longer duration than other children. People who are at risk of exposure to influenza include health care workers, social care workers, and those who live with or care for people vulnerable to influenza. In long-term care facilities, the flu can spread rapidly after it is introduced. A variety of factors likely encourage influenza transmission, including lower temperature, lower absolute and relative humidity, less ultraviolet radiation from the Sun, and crowding. Influenza viruses that infect the upper respiratory tract like H1N1 tend to be more mild but more transmissible, whereas those that infect the lower respiratory tract like H5N1 tend to cause more severe illness but are less contagious. Pathophysiology In humans, influenza viruses first cause infection by infecting epithelial cells in the respiratory tract. Illness during infection is primarily the result of lung inflammation and compromise caused by epithelial cell infection and death, combined with inflammation caused by the immune systems response to infection. Non-respiratory organs can become involved, but the mechanisms by which influenza is involved in these cases are unknown. Severe respiratory illness can be caused by multiple, non-exclusive mechanisms, including obstruction of the airways, loss of alveolar structure, loss of lung epithelial integrity due to epithelial cell infection and death, and degradation of the extracellular matrix that maintains lung structure. In particular, alveolar cell infection appears to drive severe symptoms since this results in impaired gas exchange and enables viruses to infect endothelial cells, which produce large quantities of pro-inflammatory cytokines.Pneumonia caused by influenza viruses is characterized by high levels of viral replication in the lower respiratory tract, accompanied by a strong pro-inflammatory response called a cytokine storm. Infection with H5N1 or H7N9 especially produces high levels of pro-inflammatory cytokines. In bacterial infections, early depletion of macrophages during influenza creates a favorable environment in the lungs for bacterial growth since these white blood cells are important in responding to bacterial infection. Host mechanisms to encourage tissue repair may inadvertently allow bacterial infection. Infection also induces production of systemic glucocorticoids that can reduce inflammation to preserve tissue integrity but allow increased bacterial growth.The pathophysiology of influenza is significantly influenced by which receptors influenza viruses bind to during entry into cells. Mammalian influenza viruses preferentially bind to sialic acids connected to the rest of the oligosaccharide by an α-2,6 link, most commonly found in various respiratory cells, such as respiratory and retinal epithelial cells. AIVs prefer sialic acids with an α-2,3 linkage, which are most common in birds in gastrointestinal epithelial cells and in humans in the lower respiratory tract. Furthermore, cleavage of the HA protein into HA1, the binding subunit, and HA2, the fusion subunit, is performed by different proteases, affecting which cells can be infected. For mammalian influenza viruses and low pathogenic AIVs, cleavage is extracellular, which limits infection to cells that have the appropriate proteases, whereas for highly pathogenic AIVs, cleavage is intracellular and performed by ubiquitous proteases, which allows for infection of a greater variety of cells, thereby contributing to more severe disease. Immunology Cells possess sensors to detect viral RNA, which can then induce interferon production. Interferons mediate expression of antiviral proteins and proteins that recruit immune cells to the infection site, and they also notify nearby uninfected cells of infection. Some infected cells release pro-inflammatory cytokines that recruit immune cells to the site of infection. Immune cells control viral infection by killing infected cells and phagocytizing viral particles and apoptotic cells. An exacerbated immune response, however, can harm the host organism through a cytokine storm. To counter the immune response, influenza viruses encode various non-structural proteins, including NS1, NEP, PB1-F2, and PA-X, that are involved in curtailing the host immune response by suppressing interferon production and host gene expression.B cells, a type of white blood cell, produce antibodies that bind to influenza antigens HA and NA (or HEF) and other proteins to a lesser degree. Once bound to these proteins, antibodies block virions from binding to cellular receptors, neutralizing the virus. In humans, a sizeable antibody response occurs ~1 week after viral exposure. This antibody response is typically robust and long-lasting, especially for ICV and IDV. In other words, people exposed to a certain strain in childhood still possess antibodies to that strain at a reasonable level later in life, which can provide some protection to related strains. There is, however, an "original antigenic sin", in which the first HA subtype a person is exposed to influences the antibody-based immune response to future infections and vaccines. Prevention Vaccination Annual vaccination is the primary and most effective way to prevent influenza and influenza-associated complications, especially for high-risk groups. Vaccines against the flu are trivalent or quadrivalent, providing protection against an H1N1 strain, an H3N2 strain, and one or two IBV strains corresponding to the two IBV lineages. Two types of vaccines are in use: inactivated vaccines that contain "killed" (i.e. inactivated) viruses and live attenuated influenza vaccines (LAIVs) that contain weakened viruses. There are three types of inactivated vaccines: whole virus, split virus, in which the virus is disrupted by a detergent, and subunit, which only contains the viral antigens HA and NA. Most flu vaccines are inactivated and administered via intramuscular injection. LAIVs are sprayed into the nasal cavity.Vaccination recommendations vary by country. Some recommend vaccination for all people above a certain age, such as 6 months, whereas other countries recommendation is limited for high at risk groups, such as pregnant women, young children (excluding newborns), the elderly, people with chronic medical conditions, health care workers, people who come into contact with high-risk people, and people who transmit the virus easily. Young infants cannot receive flu vaccines for safety reasons, but they can inherit passive immunity from their mother if inactivated vaccines are administered to the mother during pregnancy. Influenza vaccination also helps to reduce the probability of reassortment.In general, influenza vaccines are only effective if there is an antigenic match between vaccine strains and circulating strains. Additionally, most commercially available flu vaccines are manufactured by propagation of influenza viruses in embryonated chicken eggs, taking 6–8 months. Flu seasons are different in the northern and southern hemisphere, so the WHO meets twice a year, one for each hemisphere, to discuss which strains should be included in flu vaccines based on observation from HA inhibition assays. Other manufacturing methods include an MDCK cell culture-based inactivated vaccine and a recombinant subunit vaccine manufactured from baculovirus overexpression in insect cells. Antiviral chemoprophylaxis Influenza can be prevented or reduced in severity by post-exposure prophylaxis with the antiviral drugs oseltamivir, which can be taken orally by those at least three months old, and zanamivir, which can be inhaled by those above seven years of age. Chemoprophylaxis is most useful for individuals at high-risk of developing complications and those who cannot receive the flu vaccine due to contraindications or lack of effectiveness. Post-exposure chemoprophylaxis is only recommended if oseltamivir is taken within 48 hours of contact with a confirmed or suspected influenza case and zanamivir within 36 hours. It is recommended that it be offered to people who have yet to receive a vaccine for the current flu season, who have been vaccinated less than two week since contact, if there is a significant mismatch between vaccine and circulating strains, or during an outbreak in a closed setting regardless of vaccination history. Infection control Hand hygiene is important in reducing the spread of influenza. This includes frequent hand washing with soap and water, using alcohol-based hand sanitizers, and not touching ones eyes, nose, and mouth with ones hands. Covering ones nose and mouth when coughing or sneezing is important. Other methods to limit influenza transmission include staying home when sick, avoiding contact with others until one day after symptoms end, and disinfecting surfaces likely to be contaminated by the virus, such as doorknobs. Health education through media and posters is often used to remind people of the aforementioned etiquette and hygiene.There is uncertainty about the use of masks since research thus far has not shown a significant reduction in seasonal influenza with mask usage. Likewise, the effectiveness of screening at points of entry into countries is not well researched. Social distancing measures such as school closures, avoiding contact with infected people via isolation or quarantine, and limiting mass gatherings may reduce transmission, but these measures are often expensive, unpopular, and difficult to implement. Consequently, the commonly recommended methods of infection control are respiratory etiquette, hand hygiene, and mask wearing, which are inexpensive and easy to perform. Pharmaceutical measures are effective but may not be available in the early stages of an outbreak.In health care settings, infected individuals may be cohorted or assigned to individual rooms. Protective clothing such as masks, gloves, and gowns is recommended when coming into contact with infected individuals if there is a risk of exposure to infected bodily fluids. Keeping patients in negative pressure rooms and avoiding aerosol-producing activities may help, but special air handling and ventilation systems are not considered necessary to prevent the spread of influenza in the air. In residential homes, new admissions may need to be closed until the spread of influenza is controlled. When discharging patients to care homes, it is important to take care if there is a known influenza outbreak.Since influenza viruses circulate in animals such as birds and pigs, prevention of transmission from these animals is important. Water treatment, indoor raising of animals, quarantining sick animals, vaccination, and biosecurity are the primary measures used. Placing poultry houses and piggeries on high ground away from high-density farms, backyard farms, live poultry markets, and bodies of water helps to minimize contact with wild birds. Closure of live poultry markets appears to the most effective measure and has shown to be effective at controlling the spread of H5N1, H7N9, and H9N2. Other biosecurity measures include cleaning and disinfecting facilities and vehicles, banning visits to poultry farms, not bringing birds intended for slaughter back to farms, changing clothes, disinfecting foot baths, and treating food and water.If live poultry markets are not closed, then "clean days" when unsold poultry is removed and facilities are disinfected and "no carry-over" policies to eliminate infectious material before new poultry arrive can be used to reduce the spread of influenza viruses. If a novel influenza viruses has breached the aforementioned biosecurity measures, then rapid detection to stamp it out via quarantining, decontamination, and culling may be necessary to prevent the virus from becoming endemic. Vaccines exist for avian H5, H7, and H9 subtypes that are used in some countries. In China, for example, vaccination of domestic birds against H7N9 successfully limited its spread, indicating that vaccination may be an effective strategy if used in combination with other measures to limit transmission. In pigs and horses, management of influenza is dependent on vaccination with biosecurity. Diagnosis Diagnosis based on symptoms is fairly accurate in otherwise healthy people during seasonal epidemics and should be suspected in cases of pneumonia, acute respiratory distress syndrome (ARDS), sepsis, or if encephalitis, myocarditis, or breaking down of muscle tissue occur. Because influenza is similar to other viral respiratory tract illnesses, laboratory diagnosis is necessary for confirmation. Common ways of collecting samples for testing include nasal and throat swabs. Samples may be taken from the lower respiratory tract if infection has cleared the upper but not lower respiratory tract. Influenza testing is recommended for anyone hospitalized with symptoms resembling influenza during flu season or who is connected to an influenza case. For severe cases, earlier diagnosis improves patient outcome. Diagnostic methods that can identify influenza include viral cultures, antibody- and antigen-detecting tests, and nucleic acid-based tests.Viruses can be grown in a culture of mammalian cells or embryonated eggs for 3–10 days to monitor cytopathic effect. Final confirmation can then be done via antibody staining, hemadsorption using red blood cells, or immunofluorescence microscopy. Shell vial cultures, which can identify infection via immunostaining before a cytopathic effect appears, are more sensitive than traditional cultures with results in 1–3 days. Cultures can be used to characterize novel viruses, observe sensitivity to antiviral drugs, and monitor antigenic drift, but they are relatively slow and require specialized skills and equipment.Serological assays can be used to detect an antibody response to influenza after natural infection or vaccination. Common serological assays include hemagglutination inhibition assays that detect HA-specific antibodies, virus neutralization assays that check whether antibodies have neutralized the virus, and enzyme-linked immunoabsorbant assays. These methods tend to be relatively inexpensive and fast but are less reliable than nucleic-acid based tests.Direct fluorescent or immunofluorescent antibody (DFA/IFA) tests involve staining respiratory epithelial cells in samples with fluorescently-labeled influenza-specific antibodies, followed by examination under a fluorescent microscope. They can differentiate between IAV and IBV but cant subtype IAV. Rapid influenza diagnostic tests (RIDTs) are a simple way of obtaining assay results, are low cost, and produce results quickly, at less than 30 minutes, so they are commonly used, but they cant distinguish between IAV and IBV or between IAV subtypes and are not as sensitive as nucleic-acid based tests.Nucleic acid-based tests (NATs) amplify and detect viral nucleic acid. Most of these tests take a few hours, but rapid molecular assays are as fast as RIDTs. Among NATs, reverse transcription polymerase chain reaction (RT-PCR) is the most traditional and considered the gold standard for diagnosing influenza because it is fast and can subtype IAV, but it is relatively expensive and more prone to false-positives than cultures. Other NATs that have been used include loop-mediated isothermal amplification-based assays, simple amplification-based assays, and nucleic acid sequence-based amplification. Nucleic acid sequencing methods can identify infection by obtaining the nucleic acid sequence of viral samples to identify the virus and antiviral drug resistance. The traditional method is Sanger sequencing, but it has been largely replaced by next-generation methods that have greater sequencing speed and throughput. Treatment Treatment of influenza in cases of mild or moderate illness is supportive and includes anti-fever medications such as acetaminophen and ibuprofen, adequate fluid intake to avoid dehydration, and resting at home. Cough drops and throat sprays may be beneficial for sore throat. It is recommended to avoid alcohol and tobacco use while sick with the flu. Aspirin is not recommended to treat influenza in children due to an elevated risk of developing Reye syndrome. Corticosteroids likewise are not recommended except when treating septic shock or an underlying medical condition, such as chronic obstructive pulmonary disease or asthma exacerbation, since they are associated with increased mortality. If a secondary bacterial infection occurs, then treatment with antibiotics may be necessary. Antivirals Antiviral drugs are primarily used to treat severely ill patients, especially those with compromised immune systems. Antivirals are most effective when started in the first 48 hours after symptoms appear. Later administration may still be beneficial for those who have underlying immune defects, those with more severe symptoms, or those who have a higher risk of developing complications if these individuals are still shedding the virus. Antiviral treatment is also recommended if a person is hospitalized with suspected influenza instead of waiting for test results to return and if symptoms are worsening. Most antiviral drugs against influenza fall into two categories: neuraminidase (NA) inhibitors and M2 inhibitors. Baloxavir marboxil is a notable exception, which targets the endonuclease activity of the viral RNA polymerase and can be used as an alternative to NA and M2 inhibitors for IAV and IBV.NA inhibitors target the enzymatic activity of NA receptors, mimicking the binding of sialic acid in the active site of NA on IAV and IBV virions so that viral release from infected cells and the rate of viral replication are impaired. NA inhibitors include oseltamivir, which is consumed orally in a prodrug form and converted to its active form in the liver, and zanamivir, which is a powder that is inhaled nasally. Oseltamivir and zanamivir are effective for prophylaxis and post-exposure prophylaxis, and research overall indicates that NA inhibitors are effective at reducing rates of complications, hospitalization, and mortality and the duration of illness. Additionally, the earlier NA inhibitors are provided, the better the outcome, though late administration can still be beneficial in severe cases. Other NA inhibitors include laninamivir and peramivir, the latter of which can be used as an alternative to oseltamivir for people who cannot tolerate or absorb it.The adamantanes amantadine and rimantadine are orally administered drugs that block the influenza viruss M2 ion channel, preventing viral uncoating. These drugs are only functional against IAV but are no longer recommended for use because of widespread resistance to them among IAVs. Adamantane resistance first emerged in H3N2 in 2003, becoming worldwide by 2008. Oseltamivir resistance is no longer widespread because the 2009 pandemic H1N1 strain (H1N1 pdm09), which is resistant to adamantanes, seemingly replaced resistant strains in circulation. Since the 2009 pandemic, oseltamivir resistance has mainly been observed in patients undergoing therapy, especially the immunocompromised and young children. Oseltamivir resistance is usually reported in H1N1, but has been reported in H3N2 and IBVs less commonly. Because of this, oseltamivir is recommended as the first drug of choice for immunocompetent people, whereas for the immunocompromised, oseltamivir is recommended against H3N2 and IBV and zanamivir against H1N1 pdm09. Zanamivir resistance is observed less frequently, and resistance to peramivir and baloxavir marboxil is possible. Prognosis In healthy individuals, influenza infection is usually self-limiting and rarely fatal. Symptoms usually last for 2–8 days. Influenza can cause people to miss work or school, and it is associated with decreased job performance and, in older adults, reduced independence. Fatigue and malaise may last for several weeks after recovery, and healthy adults may experience pulmonary abnormalities that can take several weeks to resolve. Complications and mortality primarily occur in high-risk populations and those who are hospitalized. Severe disease and mortality are usually attributable to pneumonia from the primary viral infection or a secondary bacterial infection, which can progress to ARDS.Other respiratory complications that may occur include sinusitis, bronchitis, bronchiolitis, excess fluid buildup in the lungs, and exacerbation of chronic bronchitis and asthma. Middle ear infection and croup may occur, most commonly in children. Secondary S. aureus infection has been observed, primarily in children, to cause toxic shock syndrome after influenza, with hypotension, fever, and reddening and peeling of the skin. Complications affecting the cardiovascular system are rare and include pericarditis, fulminant myocarditis with a fast, slow, or irregular heartbeat, and exacerbation of pre-existing cardiovascular disease. Inflammation or swelling of muscles accompanied by muscle tissue breaking down occurs rarely, usually in children, which presents as extreme tenderness and muscle pain in the legs and a reluctance to walk for 2–3 days.Influenza can affect pregnancy, including causing smaller neonatal size, increased risk of premature birth, and an increased risk of child death shortly before or after birth. Neurological complications have been associated with influenza on rare occasions, including aseptic meningitis, encephalitis, disseminated encephalomyelitis, transverse myelitis, and Guillain–Barré syndrome. Additionally, febrile seizures and Reye syndrome can occur, most commonly in children. Influenza-associated encephalopathy can occur directly from central nervous system infection from the presence of the virus in blood and presents as suddent onset of fever with convulsions, followed by rapid progression to coma. An atypical form of encephalitis called encephalitis lethargica, characterized by headache, drowsiness, and coma, may rarely occur sometime after infection. In survivors of influenza-associated encephalopathy, neurological defects may occur. Primarily in children, in severe cases the immune system may rarely dramatically overproduce white blood cells that release cytokines, causing severe inflammation.People who are at least 65 years of age, due to a weakened immune system from aging or a chronic illness, are a high-risk group for developing complications, as are children less than one year of age and children who have not been previously exposed to influenza viruses multiple times. Pregnant women are at an elevated risk, which increases by trimester and lasts up to two weeks after childbirth. Obesity, in particular a body mass index greater than 35–40, is associated with greater amounts of viral replication, increased severity of secondary bacterial infection, and reduced vaccination efficacy. People who have underlying health conditions are also considered at-risk, including those who have congenital or chronic heart problems or lung (e.g. asthma), kidney, liver, blood, neurological, or metabolic (e.g. diabetes) disorders, as are people who are immunocompromised from chemotherapy, asplenia, prolonged steroid treatment, splenic dysfunction, or HIV infection. Current or past tobacco use also places a person at risk. The role of genetics in influenza is not well researched, but it may be a factor in influenza mortality. Epidemiology Influenza is typically characterized by seasonal epidemics and sporadic pandemics. Most of the burden of influenza is a result of flu seasons caused by IAV and IBV. Among IAV subtypes, H1N1 and H3N2 currently circulate in humans and are responsible for seasonal influenza. Cases disproportionately occur in children, but most severe causes are among the elderly, the very young, and the immunocompromised. In a typical year, influenza viruses infect 5–15% of the global population, causing 3–5 million cases of severe illness annually and accounting for 290,000–650,000 deaths each year due to respiratory illness. 5–10% of adults and 20–30% of children contract influenza each year. The reported number of influenza cases is usually much lower than the actual number of cases.During seasonal epidemics, it is estimated that about 80% of otherwise healthy people who have a cough or sore throat have the flu. Approximately 30–40% of people hospitalized for influenza develop pneumonia, and about 5% of all severe pneumonia cases in hospitals are due to influenza, which is also the most common cause of ARDS in adults. In children, influenza is one of the two most common causes of ARDS, the other being the respiratory syncytial virus. About 3–5% of children each year develop otitis media due to influenza. Adults who develop organ failure from influenza and children who have PIM scores and acute renal failure have higher rates of mortality. During seasonal influenza, mortality is concentrated in the very young and the elderly, whereas during flu pandemics, young adults are often affected at a high rate. In temperate regions, the number of influenza cases varies from season to season. Lower vitamin D levels, presumably due to less sunlight, lower humidity, lower temperature, and minor changes in virus proteins caused by antigenic drift contribute to annual epidemics that peak during the winter season. In the northern hemisphere, this is from October to May (more narrowly December to April), and in the southern hemisphere, this is from May to October (more narrowly June to September). There are therefore two distinct influenza seasons every year in temperate regions, one in the northern hemisphere and one in the southern hemisphere. In tropical and subtropical regions, seasonality is more complex and appears to be affected by various climatic factors such as minimum temperature, hours of sunshine, maximum rainfall, and high humidity. Influenza may therefore occur year-round in these regions. Influenza epidemics in modern times have the tendency to start in the eastern or southern hemisphere, with Asia being a key reservoir of influenza viruses.IAV and IBV co-circulate, so the two have the same patterns of transmission. The seasonality of ICV, however, is poorly understood. ICV infection is most common in children under the age of 2, and by adulthood most people have been exposed to it. ICV-associated hospitalization most commonly occurs in children under the age of 3 and is frequently accompanied by co-infection with another virus or a bacterium, which may increase the severity of disease. When considering all hospitalizations for respiratory illness among young children, ICV appears to account for only a small percentage of such cases. Large outbreaks of ICV infection can occur, so incidence varies significantly.Outbreaks of influenza caused by novel influenza viruses are common. Depending on the level of pre-existing immunity in the population, novel influenza viruses can spread rapidly and cause pandemics with millions of deaths. These pandemics, in contrast to seasonal influenza, are caused by antigenic shifts involving animal influenza viruses. To date, all known flu pandemics have been caused by IAVs, and they follow the same pattern of spreading from an origin point to the rest of the world over the course of multiple waves in a year. Pandemic strains tend to be associated with higher rates of pneumonia in otherwise healthy individuals. Generally after each influenza pandemic, the pandemic strain continues to circulate as the cause of seasonal influenza, replacing prior strains. From 1700 to 1889, influenza pandemics occurred about once every 50–60 years. Since then, pandemics have occurred about once every 10–50 years, so they may be getting more frequent over time. History It is impossible to know when an influenza virus first infected humans or when the first influenza pandemic occurred. Possibly the first influenza epidemic occurred around 6,000 BC in China, and possible descriptions of influenza exist in Greek writings from the 5th century BC. In both 1173–1174 AD and 1387 AD, epidemics occurred across Europe that were named "influenza". Whether these epidemics and others were caused by influenza is unclear since there was no consistent naming pattern for epidemic respiratory diseases at that time, and "influenza" didnt become completely attached to respiratory disease until centuries later. Influenza may have been brought to the Americas as early as 1493, when an epidemic disease resembling influenza killed most of the population of the Antilles.The first convincing record of an influenza pandemic was chronicled in 1510; it began in East Asia before spreading to North Africa and then Europe. Following the pandemic, seasonal influenza occurred, with subsequent pandemics in 1557 and 1580. The flu pandemic in 1557 was potentially the first time influenza was connected to miscarriage and death of pregnant women. The 1580 flu pandemic originated in Asia during summer, spread to Africa, then Europe, and finally America. By the end of the 16th century, influenza was likely beginning to become understood as a specific, recognizable disease with epidemic and endemic forms. In 1648, it was discovered that horses also experience influenza.Influenza data after 1700 is more informative, so it is easier to identify flu pandemics after this point, each of which incrementally increased understanding of influenza. The first flu pandemic of the 18th century started in 1729 in Russia in spring, spreading worldwide over the course of three years with distinct waves, the later ones being more lethal. The second flu pandemic of the 18th century was in 1781–1782, starting in China in autumn. From this pandemic, influenza became associated with sudden outbreaks of febrile illness. The next flu pandemic was from 1830 to 1833, beginning in China in winter. This pandemic had a high attack rate, but the mortality rate was low.A minor influenza pandemic occurred from 1847 to 1851 at the same time as the third cholera pandemic and was the first flu pandemic to occur with vital statistics being recorded, so influenza mortality was clearly recorded for the first time. Highly pathogenic avian influenza was recognized in 1878 and was soon linked to transmission to humans. By the time of the 1889 pandemic, which may have been caused by an H2N2 strain, the flu had become an easily recognizable disease.Initially, the microbial agent responsible for influenza was incorrently identified in 1892 by R. F. J. Pfeiffer as the bacteria species Haemophilus influenzae, which retains "influenza" in its name. In the following years, the field of virology began to form as viruses were identified as the cause of many diseases. From 1901 to 1903, Italian and Austrian researchers were able to show that avian influenza, then called "fowl plague", was caused by a microscopic agent smaller than bacteria by using filters with pores too small for bacteria to pass through. The fundamental differences between viruses and bacteria, however, were not yet fully understood. From 1918 to 1920, the Spanish flu pandemic became the most devastating influenza pandemic and one of the deadliest pandemics in history. The pandemic, probably caused by H1N1, likely began in the USA before spreading worldwide by soldiers during and after the First World War. The initial wave in the first half of 1918 was relatively minor and resembled past flu pandemics, but the second wave later that year had a much higher mortality rate, accounting for most deaths. A third wave with lower mortality occurred in many places a few months after the second. By the end of 1920, it is estimated that about a third to half of all people in the world had been infected, with tens of millions of deaths, disproportionately young adults. During the 1918 pandemic, the respiratory route of transmission was clearly identified and influenza was shown to be caused by a "filter passer", not a bacterium, but there remained a lack of agreement about influenzas cause for another decade and research on influenza declined. After the pandemic, H1N1 circulated in humans in seasonal form up until the next pandemic.In 1931, Richard Shope published three papers identifying a virus as the cause of swine influenza, a then newly recognized disease among pigs that was first characterized during the second wave of the 1918 pandemic. Shopes research reinvigorated research on human influenza, and many advances in virology, serology, immunology, experimental animal models, vaccinology, and immunotherapy have since arisen from influenza research. Just two years after influenza viruses were discovered, in 1933, IAV was identified as the agent responsible for human influenza. Subtypes of IAV were discovered throughout the 1930s, and IBV was discovered in 1940.During the Second World War, the US government worked on developing inactivated vaccines for influenza, resulting in the first influenza vaccine being licensed in 1945 in the United States. ICV was discovered two years later in 1947. In 1955, avian influenza was confirmed to be caused by IAV. Four influenza pandemics have occurred since WWII, each less severe than the 1918 pandemic. The first of these was the Asian flu from 1957 to 1958, caused by an H2N2 strain and beginning in Chinas Yunnan province. The number of deaths probably exceeded one million, mostly among the very young and very old. Notably, the 1957 pandemic was the first flu pandemic to occur in the presence of a global surveillance system and laboratories able to study the novel influenza virus. After the pandemic, H2N2 was the IAV subtype responsible for seasonal influenza. The first antiviral drug against influenza, amantadine, was approved for use in 1966, with additional antiviral drugs being used since the 1990s.In 1968, H3N2 was introduced into humans as a result of a reassortment between an avian H3N2 strain and an H2N2 strain that was circulating in humans. The novel H3N2 strain first emerged in Hong Kong and spread worldwide, causing the Hong Kong flu pandemic, which resulted in 500,000–2,000,000 deaths. This was the first pandemic to spread significantly by air travel. H2N2 and H3N2 co-circulated after the pandemic until 1971 when H2N2 waned in prevalence and was completely replaced by H3N2. In 1977, H1N1 reemerged in humans, possibly after it was released from a freezer in a laboratory accident, and caused a pseudo-pandemic. Whether the 1977 "pandemic" deserves to be included in the natural history of flu pandemics is debatable. This H1N1 strain was antigenically similar to the H1N1 strains that circulated prior to 1957. Since 1977, both H1N1 and H3N2 have circulated in humans as part of seasonal influenza. In 1980, the current classification system used to subtype influenza viruses was introduced. At some point, IBV diverged into two lineages, named the B/Victoria-like and B/Yamagata-like lineages, both of which have been circulating in humans since 1983. In 1996, HPAI H5N1 was detected in Guangdong, China and a year later emerged in poultry in Hong Kong, gradually spreading worldwide from there. A small H5N1 outbreak in humans in Hong Kong occurred then, and sporadic human cases have occurred since 1997, carrying a high case fatality rate. The most recent flu pandemic was the 2009 swine flu pandemic, which originated in Mexico and resulted in hundreds of thousands of deaths. It was caused by a novel H1N1 strain that was a reassortment of human, swine, and avian influenza viruses. The 2009 pandemic had the effect of replacing prior H1N1 strains in circulation with the novel strain but not any other influenza viruses. Consequently, H1N1, H3N2, and both IBV lineages have been in circulation in seasonal form since the 2009 pandemic.In 2011, IDV was discovered in pigs in Oklahoma, USA, and cattle were later identified as the primary reservoir of IDV. In the same year, avian H7N9 was detected in China and began to cause human infections in 2013, starting in Shanghai and Anhui and remaining mostly in China. HPAI H7N9 emerged sometime in 2016 and has occasionally infected humans incidentally. Other AIVs have less commonly infected humans since the 1990s, including H5N6, H6N1, H7N2-4, H7N7, and H10N7-8, and HPAI H subtypes such as H5N1-3, H5N5-6, and H5N8 have begun to spread throughout much of the world since the 2010s. Future flu pandemics, which may be caused by an influenza virus of avian origin, are viewed as almost inevitable, and increased globalization has made it easier for novel viruses to spread, so there are continual efforts to prepare for future pandemics and improve the prevention and treatment of influenza. Etymology The word influenza comes from the Italian word influenza, from medieval Latin influentia, originally meaning "visitation" or "influence". Terms such as influenza di freddo, meaning "influence of the cold", and influenza di stelle, meaning "influence of the stars" are attested from the 14th century. The latter referred to the diseases cause, which at the time was ascribed by some to unfavorable astrological conditions. As early as 1504, influenza began to mean a "visitation" or "outbreak" of any disease affecting many people in a single place at once. During an outbreak of influenza in 1743 that started in Italy and spread throughout Europe, the word reached the English language and was anglicized in pronunciation. Since the mid-1800s, influenza has also been used to refer to severe colds. The shortened form of the word, "(the) flu", is first attested in 1839 as flue with the spelling flu first attested in 1893. Other names that have been used for influenza include epidemic catarrh, la grippe from French, sweating sickness, and, especially when referring to the 1918 pandemic strain, Spanish fever. Research Influenza research is wide-ranging and includes efforts to understand how influenza viruses enter hosts, the relationship between influenza viruses and bacteria, how influenza symptoms progress, and what make some influenza viruses deadlier than others. Non-structural proteins encoded by influenza viruses are periodically discovered and their functions are continually under research. Past pandemics, and especially the 1918 pandemic, are the subject of much research to understand flu pandemics. As part of pandemic preparedness, the Global Influenza Surveillance and Response System is a global network of laboratories that monitors influenza transmission and epidemiology. Additional areas of research include ways to improve the diagnosis, treatment, and prevention of influenza. Existing diagnostic methods have a variety of limitations coupled with their advantages. For example, NATs have high sensitivity and specificity but are impractical in under-resourced regions due to their high cost, complexity, maintenance, and training required. Low-cost, portable RIDTs can rapidly diagnose influenza but have highly variable sensitivity and are unable to subtype IAV. As a result of these limitations and others, research into new diagnostic methods revolves around producing new methods that are cost-effective, less labor-intensive, and less complex than existing methods while also being able to differentiate influenza species and IAV subtypes. One approach in development are lab-on-a-chips, which are diagnostic devices that make use of a variety of diagnostic tests, such as RT-PCR and serological assays, in microchip form. These chips have many potential advantages, including high reaction efficiency, low energy consumption, and low waste generation.New antiviral drugs are also in development due to the elimination of adamantines as viable drugs and concerns over oseltamivir resistance. These include: NA inhibitors that can be injected intravenously, such as intravenous formulations of zanamivir; favipiravir, which is a polymerase inhibitor used against several RNA viruses; pimodivir, which prevents cap-binding required during viral transcription; and nitazoxanide, which inhibits HA maturation. Reducing excess inflammation in the respiratory tract is also subject to much research since this is one of the primary mechanisms of influenza pathology. Other forms of therapy in development include monoclonal and polyclonal antibodies that target viral proteins, convalescent plasma, different approaches to modify the host antiviral response, and stem cell-based therapies to repair lung damage.Much research on LAIVs focuses on identifying genome sequences that can be deleted to create harmless influenza viruses in vaccines that still confer immunity. The high variability and rapid evolution of influenza virus antigens, however, is a major obstacle in developing effective vaccines. Furthermore, it is hard to predict which strains will be in circulation during the next flu season, manufacturing a sufficient quantity of flu vaccines for the next season is difficult, LAIVs have limited efficacy, and repeated annual vaccination potentially has diminished efficacy. For these reasons, "broadly-reactive" or "universal" flu vaccines are being researched that can provide protection against many or all influenza viruses. Approaches to develop such a vaccine include HA stalk-based methods such as chimeras that have the same stalk but different heads, HA head-based methods such as computationally optimized broadly neutralizing antigens, anti-idiotypic antibodies, and vaccines to elicit immune responses to highly conserved viral proteins. mRNA vaccines to provide protection against influenza are also under research. In animals Birds Aquatic birds such as ducks, geese, shorebirds, and gulls are the primary reservoir of IAVs. In birds, AIVs may be either low pathogenic avian influenza (LPAI) viruses that produce little to no symptoms or highly pathogenic avian influenza (HPAI) viruses that cause severe illness. Symptoms of HPAI infection include lack of energy and appetite, decreased egg production, soft-shelled or misshapen eggs, swelling of the head, comb, wattles, and hocks, purple discoloration of wattles, combs, and legs, nasal discharge, coughing, sneezing, incoordination, and diarrhea. Birds infected with an HPAI virus may also die suddenly without any signs of infection.The distinction between LPAI and HPAI can generally be made based on how lethal an AIV is to chickens. At the genetic level, an AIV can be usually be identified as an HPAI virus if it has a multibasic cleavage site in the HA protein, which contains additional residues in the HA gene. Most AIVs are LPAI. Notable HPAI viruses include HPAI H5N1 and HPAI H7N9. HPAI viruses have been a major disease burden in the 21st century, resulting in the death of large numbers of birds. In H7N9s case, some circulating strains were originally LPAI but became HPAI by acquiring the HA multibasic cleavage site. Avian H9N2 is also of concern because although it is LPAI, it is a common donor of genes to H5N1 and H7N9 during reassortment.Migratory birds can spread influenza across long distances. An example of this was when an H5N1 strain in 2005 infected birds at Qinghai Lake, China, which is a stopover and breeding site for many migratory birds, subsequently spreading the virus to more than 20 countries across Asia, Europe, and the Middle East. AIVs can be transmitted from wild birds to domestic free-range ducks and in turn to poultry through contaminated water, aerosols, and fomites. Ducks therefore act as key intermediates between wild and domestic birds. Transmission to poultry typically occurs in backyard farming and live animal markets where multiple species interact with each other. From there, AIVs can spread to poultry farms in the absence of adequate biosecurity. Among poultry, HPAI transmission occurs through aerosols and contaminated feces, cages, feed, and dead animals. Back-transmission of HPAI viruses from poultry to wild birds has occurred and is implicated in mass die-offs and intercontinental spread.AIVs have occasionally infected humans through aerosols, fomites, and contaminated water. Direction transmission from wild birds is rare. Instead, most transmission involves domestic poultry, mainly chickens, ducks, and geese but also a variety of other birds such as guinea fowl, partridge, pheasants, and quails. The primary risk factor for infection with AIVs is exposure to birds in farms and live poultry markets. Typically, infection with an AIV has an incubation period of 3–5 days but can be up to 9 days. H5N1 and H7N9 cause severe lower respiratory tract illness, whereas other AIVs such as H9N2 cause a more mild upper respiratory tract illness, commonly with conjunctivitis. Limited transmission of avian H2, H5-7, H9, and H10 subtypes from one person to another through respiratory droplets, aerosols, and fomites has occurred, but sustained human-to-human transmission of AIVs has not occurred. Before 2013, H5N1 was the most common AIV to infect humans. Since then, H7N9 has been responsible for most human cases. Pigs Influenza in pigs is a respiratory disease similar to influenza in humans and is found worldwide. Asymptomatic infections are common. Symptoms typically appear 1–3 days after infection and include fever, lethargy, anorexia, weight loss, labored breathing, coughing, sneezing, and nasal discharge. In sows, pregnancy may be aborted. Complications include secondary infections and potentially fatal bronchopneumonia. Pigs become contagious within a day of infection and typically spread the virus for 7–10 days, which can spread rapidly within a herd. Pigs usually recover from infection within 3–7 days after symptoms appear. Prevention and control measures include inactivated vaccines and culling infected herds. The influenza viruses usually responsible for swine flu are IAV subtypes H1N1, H1N2, and H3N2.Some IAVs can be transmitted via aerosols from pigs to humans and vice versa. Furthermore, pigs, along with bats and quails, are recognized as a mixing vessel of influenza viruses because they have both α-2,3 and α-2,6 sialic acid receptors in their respiratory tract. Because of that, both avian and mammalian influenza viruses can infect pigs. If co-infection occurs, then reassortment is possible. A notable example of this was the reassortment of a swine, avian, and human influenza virus in 2009, resulting in a novel H1N1 strain that caused the 2009 flu pandemic. Spillover events from humans to pigs, however, appear to be more common than from pigs to humans. Other animals Influenza viruses have been found in many other animals, including cattle, horses, dogs, cats, and marine mammals. Nearly all IAVs are apparently descended from ancestral viruses in birds. The exception are bat influenza-like viruses, which have an uncertain origin. These bat viruses have HA and NA subtypes H17, H18, N10, and N11. H17N10 and H18N11 are unable to reassort with other IAVs, but they are still able to replicate in other mammals. AIVs sometimes crossover into mammals. For example, in late 2016 to early 2017, an avian H7N2 strain was found to be infecting cats in New York.Equine IAVs include H7N7 and two lineages of H3N8. H7N7, however, has not been detected in horses since the late 1970s, so it may have become extinct in horses. H3N8 in equines spreads via aerosols and causes respiratory illness. Equine H3N8 perferentially binds to α-2,3 sialic acids, so horses are usually considered dead-end hosts, but transmission to dogs and camels has occurred, raising concerns that horses may be mixing vessels for reassortment. In canines, the only IAVs in circulation are equine-derived H3N8 and avian-derived H3N2. Canine H3N8 has not been observed to reassort with other subtypes. H3N2 has a much broader host range and can reassort with H1N1 and H5N1. An isolated case of H6N1 likely from a chicken was found infecting a dog, so other AIVs may emerge in canines.Other mammals to be infected by IAVs include H7N7 and H4N5 in seals, H1N3 in whales, and H10N4 and H3N2 in minks. Various mutations have been identified that are associated with AIVs adapting to mammals. Since HA proteins vary in which sialic acids they bind to, mutations in the HA receptor binding site can allow AIVs to infect mammals. Other mutations include mutations affecting which sialic acids NA proteins cleave and a mutation in the PB2 polymerase subunit that improves tolerance of lower temperatures in mammalian respiratory tracts and enhances RNP assembly by stabilizing NP and PB2 binding.IBV is mainly found in humans but has also been detected in pigs, dogs, horses, and seals. Likewise, ICV primarily infects humans but has been observed in pigs, dogs, cattle, and dromedary camels. IDV causes an influenza-like illness in pigs but its impact in its natural reservoir, cattle, is relatively unknown. It may cause respiratory disease resembling human influenza on its own, or it may be part of a bovine respiratory disease (BRD) complex with other pathogens during co-infection. BRD is a concern for the cattle industry, so IDVs possible involvement in BRD has led to research on vaccines for cattle that can provide protection against IDV. Two antigenic lineages are in circulation: D/swine/Oklahoma/1334/2011 (D/OK) and D/bovine/Oklahoma/660/2013 (D/660). == References ==

Meningism

Meningism is a set of symptoms similar to those of meningitis but not caused by meningitis. Whereas meningitis is inflammation of the meninges (membranes that cover the central nervous system), meningism is caused by nonmeningitic irritation of the meninges, usually associated with acute febrile illness, especially in children and adolescents. Meningism involves the triad (3-symptom syndrome) of nuchal rigidity (neck stiffness), photophobia (intolerance of bright light) and headache. It therefore requires differentiating from other CNS problems with similar symptoms, including meningitis and some types of intracranial hemorrhage. Related clinical signs include Kernigs sign and three signs all named Brudzinskis sign. Although nosologic coding systems, such as ICD-10 and MeSH, define meningism/meningismus as meningitis-like but in fact not meningitis, many physicians use the term meningism in a loose sense clinically to refer to any meningitis-like set of symptoms before the cause is definitively known. In this sense, the word implies "suspected meningitis". The words meningeal symptoms can be used instead to avoid ambiguity, thus reserving the term meningism for its strict sense. Signs and symptoms The main clinical signs that indicate meningism are nuchal rigidity, Kernigs sign and Brudzinskis signs. None of the signs are particularly sensitive; in adults with meningitis, nuchal rigidity was present in 30% and Kernigs or Brudzinskis sign only in 5%. Nuchal rigidity Nuchal rigidity is the inability to flex the neck forward due to rigidity of the neck muscles; if flexion of the neck is painful but full range of motion is present, nuchal rigidity is absent. Kernigs sign Kernigs sign (after Waldemar Kernig (1840–1917), a Russian neurologist) is positive when the thigh is flexed at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance). This may indicate subarachnoid hemorrhage or meningitis. Patients may also show opisthotonus—spasm of the whole body that leads to legs and head being bent back and body bowed forward. Brudzinskis signs Jozef Brudzinski (1874–1917), a Polish pediatrician, is credited with several signs in meningitis. The most commonly used sign (Brudzinskis neck sign) is positive when the forced flexion of the neck elicits a reflex flexion of the hips, with the patient lying supine.Other signs attributed to Brudzinski: The symphyseal sign, in which pressure on the pubic symphysis leads to abduction of the leg and reflexive hip and knee flexion. The cheek sign, in which pressure on the cheek below the zygoma leads to rising and flexion in the forearm. Brudzinskis reflex, in which passive flexion of one knee into the abdomen leads to involuntary flexion in the opposite leg, and stretching of a limb that was flexed leads to contralateral extension. See also Meningitis Meningoencephalitis References External links FPnotebook page on meningeal signs Image of Kernigs sign

Unstable angina

Unstable angina (UA), also called crescendo angina, is a type of angina pectoris that is irregular. It is also classified as a type of acute coronary syndrome (ACS).It can be difficult to distinguish unstable angina from non-ST elevation (non-Q wave) myocardial infarction (NSTEMI). They differ primarily in whether the ischemia is severe enough to cause sufficient damage to the hearts muscular cells to release detectable quantities of a marker of injury (typically troponin T or troponin I). Unstable angina is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponin, with or without ECG changes indicative of ischemia (e.g., ST segment depression or transient elevation or new T wave inversion). Since an elevation in troponin may not be detectable for up to 12 hours after presentation, UA and NSTEMI are frequently indistinguishable at initial evaluation. Signs and symptoms Pathophysiology The pathophysiology of unstable angina is controversial. Until recently, unstable angina was assumed to be angina pectoris caused by disruption of an atherosclerotic plaque with partial thrombosis and possibly embolization or vasospasm leading to myocardial ischemia. However, sensitive troponin assays reveal rise of cardiac troponin in the bloodstream with episodes of even mild myocardial ischemia. Since unstable angina is assumed to occur in the setting of acute myocardial ischemia without troponin release, the concept of unstable angina is being questioned with some calling for retiring the term altogether. Diagnosis Unstable angina is characterized by at least one of the following: Occurs at rest or minimal exertion and usually lasts more than 20 minutes (if nitroglycerin is not administered) Being severe (at least Canadian Cardiovascular Society Classification 3) and of new onset (i.e. within 1 month) Occurs with a crescendo pattern (brought on by less activity, more severe, more prolonged or increased frequency than previously).Fifty percent of people with unstable angina will have evidence of necrosis of the hearts muscular cells based on elevated cardiac serum markers such as creatine kinase isoenzyme (CK)-MB and troponin T or I, and thus have a diagnosis of non-ST elevation myocardial infarction. Management Nitroglycerin can be used immediately to dilate the venous system and reduce the circulating blood volume, therefore reducing the work and oxygen demand of the heart. In addition, nitroglycerin causes peripheral venous and artery dilation reducing cardiac preload and afterload. These reductions allow for decreased stress on the heart and therefore lower the oxygen demand of the hearts muscle cells.Antiplatelet drugs such as aspirin and clopidogrel can reduce platelet aggregation at the unstable atherosclerotic plaque, as well as combining these with an anticoagulant such as a low molecular weight heparin, can reduce clot formation. See also Variant angina References == External links ==

Sclera

The sclera, also known as the white of the eye or, in older literature, as the tunica albuginea oculi, is the opaque, fibrous, protective, outer layer of the human eye containing mainly collagen and some crucial elastic fiber. In humans, and some other vertebrates, the whole sclera is white, contrasting with the coloured iris, but in most mammals, the visible part of the sclera matches the colour of the iris, so the white part does not normally show while other vertebrates have distinct colors for both of them. In the development of the embryo, the sclera is derived from the neural crest. In children, it is thinner and shows some of the underlying pigment, appearing slightly blue. In the elderly, fatty deposits on the sclera can make it appear slightly yellow. People with dark skin can have naturally darkened sclerae, the result of melanin pigmentation.The human eye is relatively rare for having a pale sclera (relative to the iris). This makes it easier for one individual to identify where another individual is looking, and the cooperative eye hypothesis suggests this has evolved as a method of nonverbal communication. Structure The sclera forms the posterior five-sixths of the connective tissue coat of the globe. It is continuous with the dura mater and the cornea, and maintains the shape of the globe, offering resistance to internal and external forces, and provides an attachment for the extraocular muscle insertions. The sclera is perforated by many nerves and vessels passing through the posterior scleral foramen, the hole that is formed by the optic nerve. At the optic disc the outer two-thirds of the sclera continues with the dura mater (outer coat of the brain) via the dural sheath of the optic nerve. The inner third joins with some choroidal tissue to form a plate (lamina cribrosa) across the optic nerve with perforations through which the optic fibers (fasciculi) pass. The thickness of the sclera varies from 1 mm at the posterior pole to 0.3 mm just behind the rectus muscle insertions. The scleras blood vessels are mainly on the surface. Along with the vessels of the conjunctiva (which is a thin layer covering the sclera), those in the episclera render the inflamed eye bright red.In many vertebrates, the sclera is reinforced with plates of cartilage or bone, together forming a circular structure called the sclerotic ring. In primitive fish, this ring consists of four plates, but the number is lower in many living ray-finned fishes, and much higher in lobe-finned fishes, various reptiles, and birds. The ring has disappeared in many groups, including living amphibians, some reptiles and fish, and all mammals.The eyes of all non-human primates are dark with small, barely visible sclera. Histology The collagen of the sclera is continuous with the cornea. From outer to innermost, the four layers of the sclera are: episclera stroma lamina fusca endotheliumThe sclera is opaque due to the irregularity of the Type I collagen fibers, as opposed to the near-uniform thickness and parallel arrangement of the corneal collagen. Moreover, the cornea bears more mucopolysaccharide (a carbohydrate that has among its repeating units a nitrogenous sugar, hexosamine) to embed the fibrils. The cornea, unlike the sclera, has five layers. The middle, thickest layer is also called the stroma. The sclera, like the cornea, contains a basal endothelium, above which there is the lamina fusca, containing a high count of pigment cells.Sometimes, very small gray-blue spots can appear on the sclera, a harmless condition called scleral melanocytosis. Function Human eyes are somewhat distinctive in the animal kingdom in that the sclera is very plainly visible whenever the eye is open. This is not just due to the white color of the human sclera, which many other species share, but also to the fact that the human iris is relatively small and comprises a significantly smaller portion of the exposed eye surface compared to other animals. It is theorized that this adaptation evolved because of our social nature as the eye became a useful communication tool in addition to a sensory organ. It is believed that the conspicuous sclera of the human eye makes it easier for one individual to identify where another individual is looking, increasing the efficacy of this particular form of nonverbal communication, called cooperative eye hypothesis. Animal researchers have also found that, in the course of their domestication, dogs have also developed the ability to pick up visual cues from the eyes of humans. Dogs do not seem to use this form of communication with one another and only look for visual information from the eyes of humans. Injury Trauma The bony area that makes up the human eye socket provides exceptional protection to the sclera. However, if the sclera is ruptured by a blunt force or is penetrated by a sharp object, the recovery of full former vision is usually rare. If pressure is applied slowly, the eye is actually very elastic. However, most ruptures involve objects moving at some velocity. The cushion of orbital fat protects the sclera from head-on blunt forces, but damage from oblique forces striking the eye from the side is not prevented by this cushion. Hemorrhaging and a dramatic drop in intraocular pressure are common, along with a reduction in visual perception to only broad hand movements and the presence or absence of light. However, a low-velocity injury which does not puncture and penetrate the sclera requires only superficial treatment and the removal of the object. Sufficiently small objects which become embedded and which are subsequently left untreated may eventually become surrounded by a benign cyst, causing no other damage or discomfort. Thermal trauma The sclera is rarely damaged by brief exposure to heat: the eyelids provide exceptional protection, and the fact that the sclera is covered in layers of moist tissue means that these tissues are able to cause much of the offending heat to become dissipated as steam before the sclera itself is damaged. Even relatively low-temperature molten metals when splashed against an open eye have been shown to cause very little damage to the sclera, even while creating detailed casts of the surrounding eyelashes. Prolonged exposure, however—on the order of 30 seconds—at temperatures above 45 °C (113 °F) will begin to cause scarring, and above 55 °C (131 °F) will cause extreme changes in the sclera and surrounding tissue. Such long exposures even in industrial settings are virtually nonexistent. Chemical injury The sclera is highly resistant to injury from brief exposure to toxic chemicals. The reflexive production of tears at the onset of chemical exposure tends to quickly wash away such irritants, preventing further harm. Acids with a pH below 2.5 are the source of greatest acidic burn risk, with sulfuric acid, the kind present in car batteries and therefore commonly available, being among the most dangerous in this regard. However, acid burns, even severe ones, seldom result in loss of the eye.Alkali burns, on the other hand, such as those resulting from exposure to ammonium hydroxide or ammonium chloride or other chemicals with a pH above 11.5, will cause cellular tissue in the sclera to saponify and should be considered medical emergencies requiring immediate treatment. Abnormal coloring Redness of the sclera is typically caused by eye irritation causing blood vessels to expand, such as in conjunctivitis ("pink eye"). Episcleritis is a generally benign condition of the episclera causing eye redness. Scleritis is a serious inflammatory disease of the sclera causing redness of the sclera often progressing to purple. Yellowing or a light green color of the sclera is a visual symptom of jaundice. In cases of osteogenesis imperfecta, the sclera may appear to have a blue tint, more pronounced than the slight blue tint seen in children. The blue tint is caused by the showing of the underlying uveal tract (choroid and retinal pigment epithelium). In very rare but severe cases of kidney failure and liver failure, the sclera may turn black. See also Extraocular implant Scleral tattooing Sclerotomy Notes References External links Histology image: 08008loa – Histology Learning System at Boston University Atlas image: eye_1 at the University of Michigan Health System—"Sagittal Section Through the Eyeball" MedlinePlus Encyclopedia: 002295

Gephyrophobia

Gephyrophobia is the anxiety disorder or specific phobia characterized by the fear of bridges and tunnels. As a result, sufferers of gephyrophobia may avoid routes that will take them over bridges, or if they are a passenger, will act very apprehensively when passing over a bridge. The term gephyrophobia comes from the Greek γέφυρα (gephura), meaning "bridge", and φόβος (phobos), meaning "fear".Some possible manifestations of gephyrophobia may be fear of driving off the bridge, fear of a gust of wind blowing one off the bridge, or fear that the bridge will collapse when crossing it (e.g., fear that the bridge lacks structural integrity). The fear overlaps with acrophobia (the fear of heights) as gephyrophobia tends to be exacerbated in taller bridges as compared to those closer to the water or ground beneath. Dr. Michael Liebowitz, founder of the Anxiety Disorders Clinic at the New York State Psychiatric Institute, says, "Its not an isolated phobia, but usually part of a larger constellation ... Its people who get panic attacks. You get light-headed, dizzy; your heart races. You become afraid that youll feel trapped." It is a situational phobia.As of 2008, the New York State Thruway Authority would lead gephyrophobiacs over the Tappan Zee Bridge. A driver could call the authority in advance and arrange for someone to drive their car over the bridge for them. The authority performed the service about six times a year.The Maryland Transportation Authority previously offered a similar service for crossing the Chesapeake Bay Bridge, but that role is now filled by private companies.The Mackinac Bridge Authority, which oversees the Mackinac Bridge connecting Michigans Upper and Lower peninsulas, will drive needy gephyrophobiacs cars across the bridge for a nominal fee. Some one thousand drivers take advantage of this program annually. Leslie Ann Pluhar had her Yugo blown off the bridge in 1989. Later investigation concluded she had stopped her car over the open steel grating on the bridges span and that a gust of wind blowing through the grating pushed her vehicle off the bridge, but this assertion is not supported by recorded wind speed measurements taken on and around the bridge at the time of the accident. In media Gephyrophobia is the main plot in "The Bridge" episode of The Middle. The character Brick is plagued by the phobia. In 1965s A Charlie Brown Christmas, Lucy references gephyrophobia (albeit with a slight mispronunciation) when attempting to diagnose Charlie Browns problems at her psychiatric help stand. See also Galloping Gertie List of bridge disasters List of structural failures and collapses List of phobias == References ==

Coronary artery bypass surgery

Coronary artery bypass surgery, also known as coronary artery bypass graft (CABG, pronounced "cabbage") is a surgical procedure to treat coronary artery disease (CAD), the buildup of plaques in the arteries of the heart. It can relieve chest pain caused by CAD, slow the progression of CAD, and increase life expectancy. It aims to bypass narrowings in heart arteries by using arteries or veins harvested from other parts of the body, thus restoring adequate blood supply to the previously ischemic (deprived of blood) heart. There are two main approaches. The first uses a cardiopulmonary bypass machine, a machine which takes over the functions of the heart and lungs during surgery by circulating blood and oxygen. With the heart in arrest, harvested arteries and veins are used to connect across problematic regions—a construction known as surgical anastomosis. In the second approach, called the off-pump coronary artery bypass graft (OPCABG), these anastomoses are constructed while the heart is still beating. The anastomosis supplying the left anterior descending branch is the most significant one and usually, the left internal mammary artery is harvested for use. Other commonly employed sources are the right internal mammary artery, the radial artery, and the great saphenous vein. Doctors were searching for an effective way to treat chest pain (specifically, angina, a common symptom of CAD) since the beginning of the 20th century. In the 1960s, CABG was introduced in its modern form and has since become the main treatment for significant CAD. Significant complications of the operation include bleeding, heart problems (heart attack, arrhythmias), stroke, infections (often pneumonia) and injury to the kidneys. Uses Coronary artery bypass surgery aims to prevent death from coronary artery disease and improve quality of life by relieving angina. Indications for surgery are based on studies examining the pros and cons of CABG in various subgroups of patients (depending on the anatomy of the lesions or how well heart is functioning) with CAD and comparing it with other therapeutic strategies, most importantly percutaneous coronary intervention (PCI). Coronary artery disease Coronary artery disease is caused when coronary arteries of the heart accumulate atheromatic plaques, causing stenosis in one or more arteries and place myocardium at risk of myocardial infarction. CAD can occurs in any of the major vessels of coronary circulation, which are Left Main Stem, Left Ascending Artery, Circumflex artery, and Right Coronary Artery and their branches. CAD can be asymptomatic for some time- causing no trouble, can produce chest pain when patient is exercising, or can produce angina even at rest. The former is called stable angina, while the latter unstable angina. Worse, it can manifest as a myocardial infarction, in (which the blood flow to a part of myocardium is blocked. If the blood flow is not restored within a few hours, either spontaneously or by medical intervention, the specific part of the myocardium becomes necrotic (dies) and is replaced by a scar. It might even lead to other complications such as arrhythmias, rupture of the papillary muscles of the heart, or sudden death.Medical community has various modalities to detect CAD and examine its extent. Apart from history and clinical examination, noninvasive methods include Electrocardiography (ECG) (at rest or during exercise) and chest X-ray. Echocardiography can provide useful information on the functioning of myocardium, as the enlargement of Left Ventricle , the Ejection Fraction and the situation of heart valves. The best modalities to accurately detect CAD though are the coronary angiogram and the Coronary CT angiography. Angiogram can provide detailed anatomy of coronary circulation and lesions albeit not perfect. Significance of each lesions is determined by the diameter loss. Diameter loss of 50% translates to a 75% cross-sectional area loss which is considered moderate, by most groups. Severe stenosis is considered when the diameter loss is 2/3 of original diameter or more, that is 90% loss of cross-sectional area loss or more. To determine the severity of stenosis more accurately, interventional cardiologists might also employ Intravascular ultrasound. Intravascular ultrasound utilizes ultrasound technology to determine the severity of stenosis and provide information on the composition of the atheromatic plaque. Fractional flow reserve also can be of use. With FFR, the post-stenotic pressure is compared to mean aortic pressure. If the value is <0,80, then the stenosis is deemed significant. Indications for CABG Stable patients People suffering from angina during exercise are usually first treated with medical therapy. Noninvasive tests (as stress test, nuclear imaging, dobutamine stress echocardiography) help estimate which patients might benefit from undergoing coronary angiography. Many factors are taken into account but generally, people whose tests reviled that portions of cardiac wall receive less blood that normally should proceed with coronary angiography. There, lesions are identified and a decision is taken whether patient should undergo PCI or GABG.Generally, CABG is preferred over PCI when there is significant atheromatic burden on the coronaries, that is extensive and complex. According to current literature, decreased LV function, LM disease, complex triple system disease (including LAD, Cx and RCA) especially when the lesion at LAD is at its proximal part and diabetes, are factors that point patients will benefit more from CABG rather than PCI. Acute coronary syndrome During an acute heart event, named acute coronary syndrome, it is of vital importance to restore blood flow to the myocardium as fast as possible. Typically, patients arrive at hospital with chest pain. Initially they are treated with medical drugs, particularly the strongest drugs that prevent clots within vessels (dual antiplatelet therapy: aspirin and a P2Y12 inhibitor-like clopidogrel). Patients at risk of ongoing ischemia, undergo PCI and restore blood flow and thus oxygen delivery to the struggling myocardium. In cases where PCI failed to restore blood flow because of anatomic considerations or other technical problems, urgent CABG is indicated to save myocardium. It has also been noted that the timing of the operation, plays a role in survival, it is preferable to delay the surgery if possible (6 hours in cases of nontransmural MI, 3 days in cases of transmural MI)CABG of coronary lesions is also indicated in mechanical complications of an infarction (ventricular septal defect, papillary muscle rupture or myocardial rupture) should be addressed There are no absolute contraindications of CABG but severe disease of other organs such as liver or brain, limited life expectancy, fragility should be taken into consideration when planning the treatment path of a patient. Other cardiac surgery CABG is also performed when a patient is to undergo another cardiac surgical procedure, most commonly for valve disease, and at angiography a significant lesion of the coronaries is found. CABG can be employed in other situations other than atheromatic disease of native heart arteries, like for the dissection of coronary arteries (where a rupture of the coronary layers creates a pseudo-lumen and diminishes blood delivery to the heart) caused e.g. by pregnancy, tissue diseases as Enhler-Danlos, Marfan Syndrome, cocaine abuse or Percutaneous Coronary Intervention). A coronary aneurysm is another reason for CABG, for a thrombus might develop within the vessel, and possibly travel further. CABG vs PCI CABG and percutaneous coronary intervention (PCI) are the two modalities the medical community has to revascularize stenotic lesions of the cardiac arteries. Which one is preferable for each patient is still a matter of debate, but it is clear that in the presence of complex lesions, significant Left Main Disease and in diabetic patients, CABG seems to offer better results to patients than PCI. Strong indications for CABG also include symptomatic patients and in cases where LV function is impaired., CABG offers better results that PCI in left main disease and in multivessel CAD, because of the protection arterial conduits offer to the native arteries of the heart, by producing vasodilator factors and preventing advancement of atherotic plaques. The question which modality has been studied in various trials. Patients with unprotected LM Disease (runoff of LM is not protected by a patent graft since previous CABG operation) were studied in NOBLE and EXCEL trials. NOBLE, which was published in 2016 is a multi-European country that found that CABG outperforms PCI in the long run (5 years). EXCEL, also published in 2016, found that PCI has similar results to CABG at 3 years, but this similarity fades at 4th year and later (CABG is better to PCI).Diabetic patients were studied in the FREEDOM trial, first published in 2012 and a follow up. It demonstrated a significant advantage in this group of patients when treated with CABG (vs PCI). The superiority was evident in a 3.8 year follow up and, an even further followup at 7.5 years, of the same patients documented again the superiority of CABG, enphasazing the benefits in smokers and younger patients. BEST trial was published in 2015, comparing CABG and the latest technological advancement of PCI, second generation Drug-eluting stents in multivessel disease. Their results were indicative of CABG being a better option for patients with CAD. A trial published in 2021 (Fractional Flow Reserve versus Angiography for Multivessel Evaluation, FAME 3), also concluded that CABG is a safer option than PCI, when comparing results after one year from intervention. Complications The most common complications of CABG are postoperative bleeding, heart failure, Atrial fibrillation (a form of arrhythmia), stroke, renal dysfunction, and sternal wound infections.Postoperative bleeding occurs in 2-5% of cases and might force the cardiac team to take the patient back to operating theatre to control the bleeding The most common criterion for that is the amount blood drained by chest tubes, left after the operation. Re-operation addresses surgical causes of that bleeding, which might originate from the aorta, the anastomosis or a branch of the conduit insufficiently sealed or from the sternum. Medical causes of bleeding include platelet abnormalities or coagulopathy due to bypass or the rebound heparin effect (heparin administered at the beginning of CPB reappears at blood after its neutralization by protamine).As for heart failure, low cardiac output syndrome (LCOS) can occur up to 14% of CABG cases and is according to its severity, is treated with inotropes, IABP, optimization of pre- and afterload, or correction of blood gauzes and electrolytes. The aim is to keep a systolic blood pressure above 90mmHg and cardiac index (CI) more than 2.2 L/min/m2. LCOS is often transient. Postoperative Myocardial infarction can occur because of either technical or patients factors- its incidence is hard to estimate though due to various definitions, but most studies place it between 2 and 10%. New ECG features as Q waves and/or US documented alternation of cardiac wall motions are indicative. Ongoing ischemia might prompt emergency angiography or re-operation. Arrhythmias can also occur, most commonly atrial fibrillation (20-40%) that is treated with correcting electrolyte balance, rate and rhythm control.Various neurological adverse effects can occur after CABG, with total incidence about 1,5% they can manifest as type 1-focal deficits (such as stroke or coma) or type 2- global ones (such as delirium) . Inflammation caused by CPB, hypoperfusion or cerebral embolism. Cognitive impairment has been reported in up to 80% cases after CABG at discharge and lasting up to 40% for a year. The causes are rather unclear, it seems CPB is not a suspect since even in CABG cases not including CPB (as in Off-Pump CABG), the incidence is the same, whilst PCI has the same incidence of cognitive decline as well.Infections are also a problem of the postoperative period. Sternal would infections (superficial or deep), most commonly caused by Staphylococcus aureus, can add to mortality. Harvesting of two mammary arteries is a risk factor since the perfusion of sternum is significantly impaired. Pneumonia can also occur. Complications from the GI track have been described, most commonly are caused by peri-operative medications. Procedure Preoperative workup and strategy Routine preoperative workup aims to check the baseline status of systems and organs other than heart. Thus a chest x-ray to check lungs, complete blood count, renal and liver function tests are done to screen for abnormalities. Physical examination to determine the quality of the grafts or the safety of removing them, such as varicosities in the legs, or the Allen test in the arm is performed to be sure that blood supply to the arm wont be disturbed critically.Administration of anticoagulants such as aspirin, clopidogrel, ticagrelol and others, is stopped serval days before the operation, to prevent excessive bleeding during the operation and in the following period. Warfarin is also stopped for the same reason and the patient starts being administered heparin products after INR falls below 2.0.After the angiogram is reviewed by the surgical team, targets are selected (that is, which native arteries will be bypassed and where the anastomosis should be placed). Ideally, all major lesions in significant vessels should be addressed. Most commonly, left internal thoracic artery (LITA; formerly, left internal mammary artery, LIMA) is anastomosed to left anterior descending artery (LAD) because the LAD is the most significant artery of the heart, since it supplies a larger portion of myocardium than other arteries.A conduit can be used to graft one or more native arteries. In the latter case, an end-to-side anastomosis is performed. In the former, utilizing a sequential anastomosis, a graft can then deliver blood to two or more native vessels of the heart. Also, the proximal part of a conduit can be anastomosed to the side of another conduit (by a Y or a T anastomose) adding to the versality of options for the architecture of CABG. It is preferred not to harvest too much length of conduits since it might cause some patients to need re-operation. With CBP (on-pump) The patient is brought to the operating theatre, intubated and lines (e.g., peripheral IV cannulae; central lines such as internal jugular cannulae) are inserted for drug administration and monitoring. The traditional way of a CABG follows: HarvestingA sternotomy is made, while conduits are being harvested (either from the arm or the leg). Then LITA (formerly, LIMA) is harvested through the sternotomy. There are two common ways of mobilizing the LITA, the pedicle (i.e., a pedicle consisting of the artery plus surrounding fat and veins) and the skeletonized (i.e., freed of other tissues). Before being divided in its more distal part, heparin is administered to the patient via a peripheral line (for clot prevention). Catheterization and establishment of cardiopulmonary bypass (on-pump)After harvesting, the pericardium is opened and stay sutures are placed to keep it open. Purse string sutures are placed in aorta to prepare the insertions of the aortic cannula and the catheter for cardioplegia (a solution high in potassium that serves to arrest the heart). Another purse string is placed in right atrium for the venous cannula. Then the cannulas and the catheter are placed, cardiopulmonary bypass is commenced (venous deoxygenated blood arriving to the heart is forwarded to the CBP machine to get oxygenated and delivered to aorta to keep rest of the body saturated, and often cooled to 32 - 34 degrees celsius in order to slow down the metabolism and minimize as much as possible the demand for oxygen. A clamp is placed on the Aorta between the cardioplegic catheter and aortic cannula, so the cardioplegic solution that the flow is controlled by the surgeon that clamps Aorta. Within minutes, heart stops beating. Anastomosis (grafting)With the heart still, the tip of the heart is taken out of pericardium, so the native arteries lying in the posterior side of the heart are accessible. Usually, distal anastomosis are constructed first (first to right coronary system, then to the circumflex) and then the sequential anastomosis if necessary. Surgeons check the anastomosis for patency or leaking and if everything is as it should be, surgeons insert the graft within the pericardium, sometimes attached to the cardioplegic catheter. The anastomosis of LIMA to LAD is usually the last one of the distal anastomoses to be constructed, while it is being constructed the rewarming process starts (by the CPB).. After the anastomosis is completed and checked for leaks, the proximal anastomoses of the conduits, if any, are next. They can be done either with the clamp still on or after removing the aortic clamp and isolating a small segment of the aorta by placing a partial clamp (but atheromatic aortas might be damaged by overhandling them; atheromatic derbis might get detached and cause embolization in end organs) Weaning from cardiopulmonary bypass and closureAfter the proximal anastomoses are done, the clamp is removed, aorta and conduits deaired, pacing wires might be placed if indicated and if the heart and other systems are functioning well CBP is discontinued, cannulas removed and protamine is administered to reverse the effect of heparin . After possible bleeding sites are checked, chest tubes are placed and sternum is closed. Off-pump (OPCABG) Off-pump coronary artery bypass graft (OPCABG) surgery avoids using CPB machine by stabilizing small segments of the heart. It takes great care and coordination among the surgical team and anesthesiologists to not manipulate the heart too much so hemodynamic stability will not be compromised; however, if it is compromised, it should be detected immediately and appropriate action should be taken. To keep heart beating effectively, some maneuvers can take place like placing atrial wires to protect from bradycardia, placing stitches or incisions to pericardium to help exposure. Snares and tapes are used to facilitate exposure. the aim is to avoid distal ischemia by occluding the vessel supplying distal portions of the left ventricle, so usually LIMA to LAD is the first to be anastomosed and others follow. For the anastomosis, a fine tube blowing humidified CO2 is used to keep the surgical field clean of blood. Also, a shunt might be used so the blood can travel pass the anastomotic site. After the distal anastomosis are completed, proximal anastomosis to the aorta are constructed with a partially aortic clamp and rest is similar with on-pump CABG. Alternative approaches and special situations When CABG is performed as an emergency because of hemodynamic compromise after an infraction, priority is to salvage the struggling myocardium. Pre-operatively, an intra-aortic balloon pump (IABP) might be inserted to relieve some of the burden of pumping blood, effectively reducing the amount of oxygen needed by myocardium. Operatively, the standard practice is to place the patient on CPB as soon as possible and revascularize the heart with three saphenous veins. Calcified aorta also poses a problem since it is very dangerous to clamp. In this case, the operation can be done as off-pump CAB utilizing both IMAs or Y, T and sequential grafts, or in deep hypothermic arrest, that is lower the temperature of the body to little above 20 Celsius, can also force the heart stop moving. In cases were a significant artery is totally occluded, theres a possibility to remove the atheroma, and using the same hole in the artery to perform an anastomosis ·this technique is called endarterectomy and is usually performed at the Right Coronary System.Reoperations of CABG (another CABG operation after a previous one), poses some difficulties: Heart may be too close to the sternum and thus at risk when cutting the sternum again, so an oscillating saw is used. Heart may be covered with strong adhesions to adjusting structures, adding to the difficulty of the procedure. Also, aging grafts pose a dilemma, whether they should be replaced with new ones or not. Manipulation of vein grafts risks dislodgement of atheromatic debris and is avoided."Minimally Invasive revascularization" (commonly MIDCAB form minimally invasive direct coronary artery bypass) is a technique that strives to avoid a large sternotomy. It utilizes off pump techniques to place a graft, usually LIMA at LAD. LIMA is monilized through a left thoracotomy, or even endoscopically through a thoracoscope placed in the left chest. Robotic Coronary revascularization avoids the sternotomy to prevent infections and bleeding. Both conduit harvesting and the anastomosis are performed with the aid of a robot, through a thoracotomy. There is still no widespread use of the technique though. Usually it is combined with Hybrid Coronary Revascularization, which is the strategy where combined methods of CABG and PCI are employed. LIMA to LAD is performed in the operating theatre and other lesions are treated with PCI, either at the operating room, right after the anastomosis or serval days later. After the procedure After the procedure, the patient is usually transferred to the intensive care unit, where they are extubated if it hasnt been done already in the operating theatre. The following day they exit the ICU, and 4 days later, if no complications occur, the patient is discharged from the hospital.A series of drugs are commonly used in the early postoperative period. Dobutamine, a beta agent, can be used to increase the cardiac output that sometimes occurs some hours after the operation. Beta blockers are used to prevent atrial fibrillation and other supraventricular arrhythmias. Biatrial pacing through the pacing wires inserted at operation might help towards preventing atrial fibrillation. Aspirin 80mg is used to prevent graft failure. Angiotensin-converting enzyme (ACE) inhibitors and Angiotensin receptor blockers (ARBs) are used to control blood pressure, especially in patients with low cardiac function (<40%). Amlodipine, a calcium channel blocker, is used for patients that radial artery was used as a graft.After the discharge, patients might suffer from insomnia, low appetite, decreased sex drive, and memory problems. This effect is usually transient and lasts 6 to 8 weeks. A tailored exercise plan usually benefits the patient. Results CABG is the best procedure to reduce mortality from severe CAD and improve quality of life. Operative mortality relates strongly to age of patient. According to a study by Eagle et al, for patients 50-59 years old theres an operative mortality rate of 1.8% while patients older than 80, the risk is 8.3%. Other factors which increase mortality are: female gender, re-operation, dysfunction of Left ventricle and left main disease. In most cases, CABG relieves angina, but in some patients it reoccurs in a later stage of their lives. Around 60% of patient will be angina free, 10 years after their operation. Myocardial infarction is rare 5 years after a CABG, but its prevalence increases with time. Also, the risk of sudden death is low for CABG patients. Quality of life is also high for at least 5 years, then starts to decline.The beneficial effects of CABG are clear at cardiac level. LV function is improved and malfunctioning segments of the heart (dyskinetic-moving inefficiently or even akinetic-not moving) can show signs of improvement. Both systolic and diastolic functions are improved and keep improving for up to 5 years in some cases. LV function, and myocardial perfusion, during exercise also improves after CABG. But when the LV function is severely impaired before operation (EF<30%), the benefits at the heart are less impressive in terms of segmental wall movement, but still significant since other parameters might improve as LV functions improves, the pulmonary hypertension might be relieved and survival is prolonged.It is hard to determine the total risk of the procedure since the group of patients undergoing CABG is a heterogeneous one, hence various subgroups have different risk, but it seems like the results for younger patients are better. Also, a CABG with two rather one internal mammary arteries seems to offer greater protection from CAD but results are not yet conclusive. Grafts Various conduits can be utilized for CABG- they fall into two main categories, arteries and veins. Arteries have a superior long term patency, but veins are still largely in use due to practicality. Arterial grafts that can be used originate from the part of the Internal Mammary Artery (IMA) that runs near the edge of sternum and can easily be mobilized and anastomosed to the native target vessel of the heart. Left is most often used as it is closer to heart but Right IMA is utilized depending on patient and surgeon preferences. ITAs advantages are mostly due to their endothelial cells that produce factors (Endothelium-derived relaxing factor and prostacyclin) that protect the artery from atherosclerosis and thus stenosis or occlusion. But using two ITAs has drawbacks, high rate of specific complications (deep sternal wound infections) in some subgroups of patients, mainly in obese and diabetic ones. Left radial artery and left Gastroepiploic artery can be used as well. Long term patency is influenced by the type of artery used, as well as intrinsic factors of the cardiac arterial circulation.Venous grafts used are mostly great saphenous veins and in some cases lesser saphenous vein. Their patency rate is lower than arteries. Aspirin protects grafts from occlusion; adding clopidogrel does not improve rates. CABG vs PCI CABG and percutaneous coronary intervention (PCI) are the two modalities the medical community has to revascularize stenotic lesions of the cardiac arteries. Which one is preferable for each patient is still a matter of debate, but it is clear that in the presence of complex lesions, significant Left Main Disease and in diabetic patients, CABG seems to offer better results to patients than PCI. Strong indications for CABG also include symptomatic patients and in cases where LV function is impaired. History Pre-CABG Surgical interventions aiming relieve angina and prevent death in the early 20th century, were either sympatheticectomy (a cut on the sympathetic chain that supplies the heart, with disappointing and inconsistent results) or pericardial abrasion (with the hope that adhesions would create significant collateral circulation).French Surgeon Alexis Carrel was the first to anastomose a vessel (a branch of carotid artery) to a native artery in the Heart, in a canine model- but because of technical difficulties the operation could not be reproduced. In mid 20th century, revascularization efforts continued. Beck CS, used a carotid conduit to connect descending aorta to coronary sinus -the biggest vein of the heart, while Arthur Vineberg used skeletonized LIMA, placing it in a small tunnel he created next to LAD (known "Vineberg Procedure"), with the hope of spontaneous collateral circulation would form, and it did in canine experiments but was not successful in humans. Goetz RH was the first to perform an anastomosis of the IMA to LAD in the 1960 utilizing a sutureless technique.The development of coronary angiography in 1962 by Mason Sones, helped medical doctors to identify both patients that are in need of operation, but also which native heart vessels should be bypassed. In 1964, Soviet cardiac surgeon, Vasilii Kolesov, performed the first successful internal mammary artery–coronary artery anastomosis, followed by Michael DeBakey in the USA. But it was René Favaloro that standarized the procedure. Their advances made CABG as the standard of care of CAD patients. The CABG era The "modern" era of the CABG begun in 1964 when the Soviet cardiac surgeon Vasilii Kolesov performed the first successful internal mammary artery–coronary artery anastomosis in 1964, while Michael DeBakey used a saphenous vein to create an aorta-coronary artery bypass. The Argentinean surgeon Rene Favaloro advanced and standardized the CABG technique using the patients saphenous vein.Introduction of cardioplegia led to CABG becoming a much less risky operation. A major obstacle of CABG during those times were ischemia and infarction, occurring while the heart was stopped to allow surgeons to construct the distal anastomosis. In the 1970s potassium cardioplegia was utilized. Cardioplegia minimized the oxygen demands of the heart, thus the effects of ischemia were also minimized. Refinement of cardioplegia in the 1980s made CABG less risky (lowering perioperative mortality) and thus a more attractive option when dealing with CAD.In the late 1960s, after the work of Rene Favaloro, the operation was still performed in a few centers of excellence, but was anticipated to change the landscape of Coronary Artery Disease, a significant killer in the developed world. More and more centers began performing CABG, resulting in 114,000 procedures/year in the USA by 1979. The introduction of PCI did not lead to the abandonment of CABG; the number of both procedures continued to increase, albeit PCIs grew more rapidly. In the following decades CABG was extensively studied and compared to PCI. The absence of a clear advantage of CABG over PCI led to a small decrease in numbers of CABGs in some countries (like the USA) at the turn of the millennium, but in European countries CABG was increasingly performed (mainly in Germany). Research is still ongoing on CABG vs PCI.In the history of graft selection, again the work of Favaloro was fundamental. He established that the use of bilateral IMAs was superior to vein grafts. The following years, surgeons examined the use of other arterial grafts (splenic, gastroepiploic mesenteric, subscapular and others) but none of these matched the patency rates of IMA. Carpentier in 1971 introduced the us of the radial artery, which was initially prone to failure, but the evolution of harvesting techniques in the next two decades improved patency significantly. See also Angioplasty Cardiothoracic surgery Cleveland Clinic Dresslers syndrome Hybrid coronary revascularization Totally endoscopic coronary artery bypass surgery Chest tube References Sources Al-Atassi, Talal; Toeg, Hadi D.; Chan, Vincent; Ruel, Marc (2016). "Coronary Artery Bypass Grafting". In Frank Sellke; Pedro J. del Nido (eds.). Sabiston and Spencer Surgery of the Chest. ISBN 978-0-323-24126-7. Bojar, R.M. (2021). Manual of Perioperative Care in Adult Cardiac Surgery. Wiley. ISBN 978-1-119-58255-7. Retrieved 2022-10-26. Farina, Piero; Gaudino, Mario Fulvio Luigi; Taggart, David Paul (2020). "The Eternal Debate With a Consistent Answer: CABG vs PCI". Seminars in Thoracic and Cardiovascular Surgery. Elsevier BV. 32 (1): 14–20. doi:10.1053/j.semtcvs.2019.08.009. ISSN 1043-0679. S2CID 201632303. Fearon, William F.; Zimmermann, Frederik M.; De Bruyne, Bernard; Piroth, Zsolt; van Straten, Albert H.M.; Szekely, Laszlo; Davidavičius, Giedrius; Kalinauskas, Gintaras; Mansour, Samer; Kharbanda, Rajesh; Östlund-Papadogeorgos, Nikolaos; Aminian, Adel; Oldroyd, Keith G.; Al-Attar, Nawwar; Jagic, Nikola; Dambrink, Jan-Henk E.; Kala, Petr; Angerås, Oskar; MacCarthy, Philip; Wendler, Olaf; Casselman, Filip; Witt, Nils; Mavromatis, Kreton; Miner, Steven E.S.; Sarma, Jaydeep; Engstrøm, Thomas; Christiansen, Evald H.; Tonino, Pim A.L.; Reardon, Michael J.; Lu, Di; Ding, Victoria Y.; Kobayashi, Yuhei; Hlatky, Mark A.; Mahaffey, Kenneth W.; Desai, Manisha; Woo, Y. Joseph; Yeung, Alan C.; Pijls, Nico H.J. (2022-01-13). "Fractional Flow Reserve–Guided PCI as Compared with Coronary Bypass Surgery". New England Journal of Medicine. Massachusetts Medical Society. 386 (2): 128–137. doi:10.1056/nejmoa2112299. ISSN 0028-4793. PMID 34735046. S2CID 242940936. Head, S. J.; Kieser, T. M.; Falk, V.; Huysmans, H. A.; Kappetein, A. P. (2013-10-01). "Coronary artery bypass grafting: Part 1--the evolution over the first 50 years". European Heart Journal. Oxford University Press (OUP). 34 (37): 2862–2872. doi:10.1093/eurheartj/eht330. ISSN 0195-668X. PMID 24086085. Smith, Peter K.; Schroder, Jacob N. (2016). "On-Pump Coronary Artery Bypass Grafting". In Josef E. Fischer (ed.). Master Techniques in Surgery CARDIAC SURGERY. ISBN 9781451193534. Kouchoukos, Nicholas; Blackstone, E. H.; Hanley, F. L.; Kirklin, J. K. (2013). Kirklin/Barratt-Boyes Cardiac Surgery E-Book (4th ed.). Elsevier. ISBN 978-1-4160-6391-9. Mick, Stephanie; Keshavamurthy, Suresh; Mihaljevicl, Tomislav; Bonatti, Johannes (2016). "Robotic and Alternative Approaches to Coronary Artery Bypass Grafting". In Frank Sellke; Pedro J. del Nido (eds.). Sabiston and Spencer Surgery of the Chest. pp. 1603–1615. ISBN 978-0-323-24126-7. Ngu, Janet M. C.; Sun, Louise Y.; Ruel, Marc (2018). "Pivotal contemporary trials of percutaneous coronary intervention vs. coronary artery bypass grafting: a surgical perspective". Annals of Cardiothoracic Surgery. AME Publishing Company. 7 (4): 527–532. doi:10.21037/acs.2018.05.12. ISSN 2225-319X. PMC 6082775. PMID 30094218. Welt, Frederick G.P. (2022-01-13). "CABG versus PCI — End of the Debate?". New England Journal of Medicine. Massachusetts Medical Society. 386 (2): 185–187. doi:10.1056/nejme2117325. ISSN 0028-4793. PMID 35020989. External links Lawton JS, Tamis-Holland JE, Bangalore S, Bates ER, Beckie TM, Bischoff JM, Bittl JA, Cohen MG, DiMaio JM, Don CW, Fremes SE, Gaudino MF, Goldberger ZD, Grant MC, Jaswal JB, Kurlansky PA, Mehran R, Metkus TS Jr, Nnacheta LC, Rao SV, Sellke FW, Sharma G, Yong CM, Zwischenberger BA. 2021 ACC/AHA/SCAI guideline for coronary artery revascularization: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2022;79:e21-e129

Unemployment

Unemployment, according to the OECD (Organisation for Economic Co-operation and Development), is people above a specified age (usually 15) not being in paid employment or self-employment but currently available for work during the reference period.Unemployment is measured by the unemployment rate, which is the number of people who are unemployed as a percentage of the labour force (the total number of people employed added to those unemployed).Unemployment can have many sources, such as the following: new technologies and inventions the status of the economy, which can be influenced by a recession competition caused by globalization and international trade policies of the government regulation and marketUnemployment and the status of the economy can be influenced by a country through, for example, fiscal policy. Furthermore, the monetary authority of a country, such as the central bank, can influence the availability and cost for money through its monetary policy. In addition to theories of unemployment, a few categorisations of unemployment are used for more precisely modelling the effects of unemployment within the economic system. Some of the main types of unemployment include structural unemployment, frictional unemployment, cyclical unemployment, involuntary unemployment and classical unemployment. Structural unemployment focuses on foundational problems in the economy and inefficiencies inherent in labor markets, including a mismatch between the supply and demand of laborers with necessary skill sets. Structural arguments emphasize causes and solutions related to disruptive technologies and globalization. Discussions of frictional unemployment focus on voluntary decisions to work based on individuals valuation of their own work and how that compares to current wage rates added to the time and effort required to find a job. Causes and solutions for frictional unemployment often address job entry threshold and wage rates. According to the UNs International Labour Organization (ILO), there were 172 million people worldwide (or 5% of the reported global workforce) without work in 2018.Because of the difficulty in measuring the unemployment rate by, for example, using surveys (as in the United States) or through registered unemployed citizens (as in some European countries), statistical figures such as the employment-to-population ratio might be more suitable for evaluating the status of the workforce and the economy if they were based on people who are registered, for example, as taxpayers. Definitions, types, and theories The state of being without any work yet looking for work is called unemployment. Economists distinguish between various overlapping types of and theories of unemployment, including cyclical or Keynesian unemployment, frictional unemployment, structural unemployment and classical unemployment. Some additional types of unemployment that are occasionally mentioned are seasonal unemployment, hardcore unemployment, and hidden unemployment. Though there have been several definitions of "voluntary" and "involuntary unemployment" in the economics literature, a simple distinction is often applied. Voluntary unemployment is attributed to the individuals decisions, but involuntary unemployment exists because of the socio-economic environment (including the market structure, government intervention, and the level of aggregate demand) in which individuals operate. In these terms, much or most of frictional unemployment is voluntary since it reflects individual search behavior. Voluntary unemployment includes workers who reject low-wage jobs, but involuntary unemployment includes workers fired because of an economic crisis, industrial decline, company bankruptcy, or organizational restructuring. On the other hand, cyclical unemployment, structural unemployment, and classical unemployment are largely involuntary in nature. However, the existence of structural unemployment may reflect choices made by the unemployed in the past, and classical (natural) unemployment may result from the legislative and economic choices made by labour unions or political parties. The clearest cases of involuntary unemployment are those with fewer job vacancies than unemployed workers even when wages are allowed to adjust and so even if all vacancies were to be filled, some unemployed workers would still remain. That happens with cyclical unemployment, as macroeconomic forces cause microeconomic unemployment, which can boomerang back and exacerbate those macroeconomic forces. Real wage unemployment Classical, natural, or real-wage unemployment, occurs when real wages for a job are set above the market-clearing level, causing the number of job-seekers to exceed the number of vacancies. On the other hand, most economists argue that as wages fall below a livable wage, many choose to drop out of the labour market and no longer seek employment. That is especially true in countries in which low-income families are supported through public welfare systems. In such cases, wages would have to be high enough to motivate people to choose employment over what they receive through public welfare. Wages below a livable wage are likely to result in lower labor market participation in the above-stated scenario. In addition, consumption of goods and services is the primary driver of increased demand for labor. Higher wages lead to workers having more income available to consume goods and services. Therefore, higher wages increase general consumption and as a result demand for labor increases and unemployment decreases. Many economists have argued that unemployment increases with increased governmental regulation. For example, minimum wage laws raise the cost of some low-skill laborers above market equilibrium, resulting in increased unemployment as people who wish to work at the going rate cannot (as the new and higher enforced wage is now greater than the value of their labour). Laws restricting layoffs may make businesses less likely to hire in the first place, as hiring becomes more risky.However, that argument overly simplifies the relationship between wage rates and unemployment by ignoring numerous factors that contribute to unemployment. Some, such as Murray Rothbard, suggest that even social taboos can prevent wages from falling to the market-clearing level.In Out of Work: Unemployment and Government in the Twentieth-Century America, economists Richard Vedder and Lowell Gallaway argue that the empirical record of wages rates, productivity, and unemployment in America validates classical unemployment theory. Their data shows a strong correlation between adjusted real wage and unemployment in the United States from 1900 to 1990. However, they maintain that their data does not take into account exogenous events. Cyclical unemployment Cyclical, deficient-demand, or Keynesian unemployment occurs when there is not enough aggregate demand in the economy to provide jobs for everyone who wants to work. Demand for most goods and services falls, less production is needed and consequently, fewer workers are needed, wages are sticky and do not fall to meet the equilibrium level, and unemployment results. Its name is derived from the frequent ups and downs in the business cycle, but unemployment can also be persistent, such as during the Great Depression. With cyclical unemployment, the number of unemployed workers exceeds the number of job vacancies and so even if all open jobs were filled, some workers would still remain unemployed. Some associate cyclical unemployment with frictional unemployment because the factors that cause the friction are partially caused by cyclical variables. For example, a surprise decrease in the money supply may suddenly inhibit aggregate demand and thus inhibit labor demand. Keynesian economists, on the other hand, see the lack of supply of jobs as potentially resolvable by government intervention. One suggested intervention involves deficit spending to boost employment and goods demand. Another intervention involves an expansionary monetary policy to increase the supply of money, which should reduce interest rates, which, in turn, should lead to an increase in non-governmental spending. Unemployment under "full employment" In demands based theory, it is possible to abolish cyclical unemployment by increasing the aggregate demand for products and workers. However, the economy eventually hits an "inflation barrier" that is imposed by the four other kinds of unemployment to the extent that they exist. Historical experience suggests that low unemployment affects inflation in the short term but not the long term. In the long term, the velocity of money supply measures such as the MZM ("money zero maturity", representing cash and equivalent demand deposits) velocity is far more predictive of inflation than low unemployment.Some demand theory economists see the inflation barrier as corresponding to the natural rate of unemployment. The "natural" rate of unemployment is defined as the rate of unemployment that exists when the labour market is in equilibrium, and there is pressure for neither rising inflation rates nor falling inflation rates. An alternative technical term for that rate is the NAIRU, the Non-Accelerating Inflation Rate of Unemployment. Whatever its name, demand theory holds that if the unemployment rate gets "too low," inflation will accelerate in the absence of wage and price controls (incomes policies). One of the major problems with the NAIRU theory is that no one knows exactly what the NAIRU is, and it clearly changes over time. The margin of error can be quite high relative to the actual unemployment rate, making it hard to use the NAIRU in policy-making.Another, normative, definition of full employment might be called the ideal unemployment rate. It would exclude all types of unemployment that represent forms of inefficiency. This type of "full employment" unemployment would correspond to only frictional unemployment (excluding that part encouraging the McJobs management strategy) and so would be very low. However, it would be impossible to attain this full-employment target using only demand-side Keynesian stimulus without getting below the NAIRU and causing accelerating inflation (absent incomes policies). Training programs aimed at fighting structural unemployment would help here. To the extent that hidden unemployment exists, it implies that official unemployment statistics provide a poor guide to what unemployment rate coincides with "full employment." Structural unemployment Structural unemployment occurs when a labour market is unable to provide jobs for everyone who wants one because there is a mismatch between the skills of the unemployed workers and the skills needed for the available jobs. Structural unemployment is hard to separate empirically from frictional unemployment except that it lasts longer. As with frictional unemployment, simple demand-side stimulus will not work to abolish this type of unemployment easily. Structural unemployment may also be encouraged to rise by persistent cyclical unemployment: if an economy suffers from longlasting low aggregate demand, it means that many of the unemployed become disheartened, and their skills (including job-searching skills) become "rusty" and obsolete. Problems with debt may lead to homelessness and a fall into the vicious circle of poverty. That means that they may not fit the job vacancies that are created when the economy recovers. The implication is that sustained high demand may lower structural unemployment. This theory of persistence in structural unemployment has been referred to as an example of path dependence or "hysteresis." Much technological unemployment, caused by the replacement of workers by machines might be counted as structural unemployment. Alternatively, technological unemployment might refer to the way in which steady increases in labour productivity mean that fewer workers are needed to produce the same level of output every year. The fact that aggregate demand can be raised to deal with the problem suggests that the problem is instead one of cyclical unemployment. As indicated by Okuns law, the demand side must grow sufficiently quickly to absorb not only the growing labour force but also the workers who are made redundant by the increased labour productivity. Seasonal unemployment may be seen as a kind of structural unemployment since it is linked to certain kinds of jobs (construction and migratory farm work). The most-cited official unemployment measures erase this kind of unemployment from the statistics using "seasonal adjustment" techniques. That results in substantial and permanent structural unemployment. Frictional unemployment Frictional unemployment is the time period between jobs in which a worker searches for or transitions from one job to another. It is sometimes called search unemployment and can be voluntary, based on the circumstances of the unemployed individual. Frictional unemployment exists because both jobs and workers are heterogeneous, and a mismatch can result between the characteristics of supply and demand. Such a mismatch can be related to skills, payment, work-time, location, seasonal industries, attitude, taste, and a multitude of other factors. New entrants (such as graduating students) and re-entrants (such as former homemakers) can also suffer a spell of frictional unemployment. Workers and employers accept a certain level of imperfection, risk or compromise, but usually not right away. They will invest some time and effort to find a better match. That is, in fact, beneficial to the economy since it results in a better allocation of resources. However, if the search takes too long and mismatches are too frequent, the economy suffers since some work will not get done. Therefore, governments will seek ways to reduce unnecessary frictional unemployment by multiple means including providing education, advice, training, and assistance such as daycare centers. The frictions in the labour market are sometimes illustrated graphically with a Beveridge curve, a downward-sloping, convex curve that shows a correlation between the unemployment rate on one axis and the vacancy rate on the other. Changes in the supply of or demand for labour cause movements along the curve. An increase or decrease in labour market frictions will shift the curve outwards or inwards. Hidden unemployment Official statistics often underestimate unemployment rates because of hidden, or covered, unemployment. That is the unemployment of potential workers that are not reflected in official unemployment statistics because of how the statistics are collected. In many countries, only those who have no work but are actively looking for work and/or qualifying for social security benefits are counted as unemployed. Those who have given up looking for work and sometimes those who are on government "retraining" programs are not officially counted among the unemployed even though they are not employed. The statistic also does not count the "underemployed", those working fewer hours than they would prefer or in a job that fails to make good use of their capabilities. In addition, those who are of working age but are currently in full-time education are usually not considered unemployed in government statistics. Traditional unemployed native societies who survive by gathering, hunting, herding, and farming in wilderness areas may or may not be counted in unemployment statistics. Long-term unemployment Long-term unemployment (LTU) is defined in European Union statistics as unemployment lasting for longer than one year (while unemployment lasting over two years is defined as very long-term unemployment). The United States Bureau of Labor Statistics (BLS), which reports current long-term unemployment rate at 1.9 percent, defines this as unemployment lasting 27 weeks or longer. Long-term unemployment is a component of structural unemployment, which results in long-term unemployment existing in every social group, industry, occupation, and all levels of education.In 2015 the European Commission published recommendations on how to reduce long-term unemployment. These advised governments to: encourage long-term unemployed people to register with an employment service; provide each registered long-term unemployed person with an individual in-depth assessment to identify their needs and potential within 18 months; offer a tailor-made job integration agreement (JIA) to all registered long-term unemployed within 18 months. These might include measures such as mentoring, help with job search, further education and training, support for housing, transport, child and care services and rehabilitation. Each person would have a single point of contact to access this support, which would be implemented in partnership with employers.In 2017–2019 it implemented the Long-Term Unemployment project to research solutions implemented by EU member states and produce a toolkit to guide government action. Progress was evaluated in 2019. Marxian theory of unemployment It is in the very nature of the capitalist mode of production to overwork some workers while keeping the rest as a reserve army of unemployed paupers. Marxists share the Keynesian viewpoint of the relationship between economic demand and employment, but with the caveat that the market systems propensity to slash wages and reduce labor participation on an enterprise level causes a requisite decrease in aggregate demand in the economy as a whole, causing crises of unemployment and periods of low economic activity before the capital accumulation (investment) phase of economic growth can continue. According to Karl Marx, unemployment is inherent within the unstable capitalist system and periodic crises of mass unemployment are to be expected. He theorized that unemployment was inevitable and even a necessary part of the capitalist system, with recovery and regrowth also part of the process. The function of the proletariat within the capitalist system is to provide a "reserve army of labour" that creates downward pressure on wages. This is accomplished by dividing the proletariat into surplus labour (employees) and under-employment (unemployed). This reserve army of labour fight among themselves for scarce jobs at lower and lower wages. At first glance, unemployment seems inefficient since unemployed workers do not increase profits, but unemployment is profitable within the global capitalist system because unemployment lowers wages which are costs from the perspective of the owners. From this perspective low wages benefit the system by reducing economic rents. Yet, it does not benefit workers; according to Karl Marx, the workers (proletariat) work to benefit the bourgeoisie through their production of capital. Capitalist systems unfairly manipulate the market for labour by perpetuating unemployment which lowers laborers demands for fair wages. Workers are pitted against one another at the service of increasing profits for owners. As a result of the capitalist mode of production, Marx argued that workers experienced alienation and estrangement through their economic identity. According to Marx, the only way to permanently eliminate unemployment would be to abolish capitalism and the system of forced competition for wages and then shift to a socialist or communist economic system. For contemporary Marxists, the existence of persistent unemployment is proof of the inability of capitalism to ensure full employment. Measurement There are also different ways national statistical agencies measure unemployment. The differences may limit the validity of international comparisons of unemployment data. To some degree, the differences remain despite national statistical agencies increasingly adopting the definition of unemployment of the International Labour Organization. To facilitate international comparisons, some organizations, such as the OECD, Eurostat, and International Labor Comparisons Program, adjust data on unemployment for comparability across countries. Though many people care about the number of unemployed individuals, economists typically focus on the unemployment rate, which corrects for the normal increase in the number of people employed caused by increases in population and increases in the labour force relative to the population. The unemployment rate is expressed as a percentage and calculated as follows: Unemployment rate = Unemployed workers Total labor force × 100 {\displaystyle {\text{Unemployment rate}}={\frac {\text{Unemployed workers}}{\text{Total labor force}}}\times 100} As defined by the International Labour Organization, "unemployed workers" are those who are currently not working but are willing and able to work for pay, currently available to work, and have actively searched for work. Individuals who are actively seeking job placement must make the effort to be in contact with an employer, have job interviews, contact job placement agencies, send out resumes, submit applications, respond to advertisements, or some other means of active job searching within the prior four weeks. Simply looking at advertisements and not responding will not count as actively seeking job placement. Since not all unemployment may be "open" and counted by government agencies, official statistics on unemployment may not be accurate. In the United States, for example, the unemployment rate does not take into consideration those individuals who are not actively looking for employment, such as those who are still attending college.According to the OECD, Eurostat, and the US Bureau of Labor Statistics the unemployment rate is the number of unemployed people as a percentage of the labour force. "An unemployed person is defined by Eurostat, according to the guidelines of the International Labour Organization, as: someone aged 15 to 74 (in Italy, Spain, the United Kingdom, Iceland, Norway: 16 to 74 years); without work during the reference week; available to start work within the next two weeks (or has already found a job to start within the next three months); actively having sought employment at some time during the last four weeks."The labour force, or workforce, includes both employed (employees and self-employed) and unemployed people but not the economically inactive, such as pre-school children, school children, students and pensioners.The unemployment rate of an individual country is usually calculated and reported on a monthly, quarterly, and yearly basis by the National Agency of Statistics. Organisations like the OECD report statistics for all of its member states.Certain countries provide unemployment compensation for a certain period of time for unemployed citizens who are registered as unemployed at the government employment agency. Furthermore, pension receivables or claims could depend on the registration at the government employment agency.In many countries like in Germany, the unemployment rate is based on the number of people who are registered as unemployed. Other countries like the United States use a labour force survey to calculate the unemployment rate.The ILO describes four different methods to calculate the unemployment rate: Labour Force Sample Surveys are the most preferred method of unemployment rate calculation since they give the most comprehensive results and enables calculation of unemployment by different group categories such as race and gender. This method is the most internationally comparable. Official Estimates are determined by a combination of information from one or more of the other three methods. The use of this method has been declining in favor of labour surveys. Social Insurance Statistics, such as unemployment benefits, are computed base on the number of persons insured representing the total labour force and the number of persons who are insured that are collecting benefits. This method has been heavily criticized because if the expiration of benefits before the person finds work. Employment Office Statistics are the least effective since they include only a monthly tally of unemployed persons who enter employment offices. This method also includes those who are not unemployed by the ILO definition.The primary measure of unemployment, U3, allows for comparisons between countries. Unemployment differs from country to country and across different time periods. For example, in the 1990s and 2000s, the United States had lower unemployment levels than many countries in the European Union, which had significant internal variation, with countries like the United Kingdom and Denmark outperforming Italy and France. However, large economic events like the Great Depression can lead to similar unemployment rates across the globe. In 2013, the ILO adopted a resolution to introduce new indicators to measure the unemployment rate. LU1: Unemployment rate: [persons in unemployment / labour force] × 100 LU2: Combined rate of time-related underemployment and unemployment: [(persons in time-related underemployment + persons in unemployment) / labour force]x 100 LU3: Combined rate of unemployment and potential labour force: [(persons in unemployment + potential labour force) / (extended labour force)] × 100 LU4: Composite measure of labour underutilization: [(persons in time-related underemployment + persons in unemployment + potentiallabour force) / (extended labour force)] × 100 European Union (Eurostat) Eurostat, the statistical office of the European Union, defines unemployed as those persons between age 15 and 74 who are not working, have looked for work in the last four weeks, and are ready to start work within two weeks; this definition conforms to ILO standards. Both the actual count and the unemployment rate are reported. Statistical data are available by member state for the European Union as a whole (EU28) as well as for the eurozone (EA19). Eurostat also includes a long-term unemployment rate, which is defined as part of the unemployed who have been unemployed for more than one year.The main source used is the European Union Labour Force Survey (EU-LFS). It collects data on all member states each quarter. For monthly calculations, national surveys or national registers from employment offices are used in conjunction with quarterly EU-LFS data. The exact calculation for individual countries, resulting in harmonized monthly data, depends on the availability of the data. United States Bureau of Labor statistics The Bureau of Labor Statistics measures employment and unemployment (of those over 17 years of age) by using two different labor force surveys conducted by the United States Census Bureau (within the United States Department of Commerce) and/or the Bureau of Labor Statistics (within the United States Department of Labor) that gather employment statistics monthly. The Current Population Survey (CPS), or "Household Survey," conducts a survey based on a sample of 60,000 households. The survey measures the unemployment rate based on the ILO definition.The Current Employment Statistics survey (CES), or "Payroll Survey," conducts a survey based on a sample of 160,000 businesses and government agencies, which represent 400,000 individual employers. Since the survey measures only civilian nonagricultural employment, it does not calculate an unemployment rate, and it differs from the ILO unemployment rate definition. Both sources have different classification criteria and usually produce differing results. Additional data are also available from the government, such as the unemployment insurance weekly claims report available from the Office of Workforce Security, within the U.S. Department of Labors Employment and Training Administration. The Bureau of Labor Statistics provides up-to-date numbers via a PDF linked here. The BLS also provides a readable concise current Employment Situation Summary, updated monthly. The Bureau of Labor Statistics also calculates six alternate measures of unemployment, U1 to U6, which measure different aspects of unemployment: U1: Percentage of labor force unemployed 15 weeks or longer. U2: Percentage of labor force who lost jobs or completed temporary work. U3: Official unemployment rate, per the ILO definition, occurs when people are without jobs and they have actively looked for work within the past four weeks. U4: U3 + "discouraged workers", or those who have stopped looking for work because current economic conditions make them believe that no work is available for them. U5: U4 + other "marginally attached workers," or "loosely attached workers," or those who "would like" and are able to work but have not looked for work recently. U6: U5 + Part-time workers who want to work full-time, but cannot for economic reasons (underemployment).Note: "Marginally attached workers" are added to the total labour force for unemployment rate calculation for U4, U5, and U6. The BLS revised the CPS in 1994 and among the changes the measure representing the official unemployment rate was renamed U3 instead of U5. In 2013, Representative Hunter proposed that the Bureau of Labor Statistics use the U5 rate instead of the current U3 rate.Statistics for the US economy as a whole hide variations among groups. For example, in January 2008, the US unemployment rates were 4.4% for adult men, 4.2% for adult women, 4.4% for Caucasians, 6.3% for Hispanics or Latinos (all races), 9.2% for African Americans, 3.2% for Asian Americans, and 18.0% for teenagers. Also, the US unemployment rate would be at least 2% higher if prisoners and jail inmates were counted.The unemployment rate is included in a number of major economic indices including the US Conference Boards Index of Leading Indicators a macroeconomic measure of the state of the economy. Alternatives Limitations of definition Some critics believe that current methods of measuring unemployment are inaccurate in terms of the impact of unemployment on people as these methods do not take into account the 1.5% of the available working population incarcerated in US prisons (who may or may not be working while they are incarcerated); those who have lost their jobs and have become discouraged over time from actively looking for work; those who are self-employed or wish to become self-employed, such as tradesmen or building contractors or information technology consultants; those who have retired before the official retirement age but would still like to work (involuntary early retirees); those on disability pensions who do not possess full health but still wish to work in occupations that suitable for their medical conditions; or those who work for payment for as little as one hour per week but would like to work full time.The last people are "involuntary part-time" workers, those who are underemployed, such as a computer programmer who is working in a retail store until he can find a permanent job, involuntary stay-at-home mothers who would prefer to work, and graduate and professional school students who are unable to find worthwhile jobs after they graduated with their bachelors degrees. Internationally, some nations unemployment rates are sometimes muted or appear less severe because of the number of self-employed individuals working in agriculture. Small independent farmers are often considered self-employed and so cannot be unemployed. That can impact non-industrialized economies, such as the United States and Europe in the early 19th century, since overall unemployment was approximately 3% because so many individuals were self-employed, independent farmers; however, non-agricultural unemployment was as high as 80%.Many economies industrialize and so experience increasing numbers of non-agricultural workers. For example, the United States non-agricultural labour force increased from 20% in 1800 to 50% in 1850 and 97% in 2000. The shift away from self-employment increases the percentage of the population that is included in unemployment rates. When unemployment rates between countries or time periods are compared, it is best to consider differences in their levels of industrialization and self-employment. Additionally, the measures of employment and unemployment may be "too high." In some countries, the availability of unemployment benefits can inflate statistics by giving an incentive to register as unemployed. People who do not seek work may choose to declare themselves unemployed to get benefits; people with undeclared paid occupations may try to get unemployment benefits in addition to the money that they earn from their work.However, in the United States, Canada, Mexico, Australia, Japan, and the European Union, unemployment is measured using a sample survey (akin to a Gallup poll). According to the BLS, a number of Eastern European nations have instituted labour force surveys as well. The sample survey has its own problems because the total number of workers in the economy is calculated based on a sample, rather than a census. It is possible to be neither employed nor unemployed by ILO definitions by being outside of the "labour force." Such people have no job and are not looking for one. Many of them go to school or are retired. Family responsibilities keep others out of the labour force. Still others have a physical or mental disability that prevents them from participating in the labour force. Some people simply elect not to work and prefer to be dependent on others for sustenance. Typically, employment and the labour force include only work that is done for monetary gain. Hence, a homemaker is neither part of the labour force nor unemployed. Also, full-time students and prisoners are considered to be neither part of the labour force nor unemployed. The number of prisoners can be important. In 1999, economists Lawrence F. Katz and Alan B. Krueger estimated that increased incarceration lowered measured unemployment in the United States by 0.17% between 1985 and the late 1990s.In particular, as of 2005, roughly 0.7% of the US population is incarcerated (1.5% of the available working population). Additionally, children, the elderly, and some individuals with disabilities are typically not counted as part of the labour force and so are not included in the unemployment statistics. However, some elderly and many disabled individuals are active in the labour market. In the early stages of an economic boom, unemployment often rises. That is because people join the labour market (give up studying, start a job hunt, etc.) as a result of the improving job market, but until they have actually found a position, they are counted as unemployed. Similarly, during a recession, the increase in the unemployment rate is moderated by people leaving the labour force or being otherwise discounted from the labour force, such as with the self-employed. For the fourth quarter of 2004, according to OECD (Employment Outlook 2005 ISBN 92-64-01045-9), normalized unemployment for men aged 25 to 54 was 4.6% in the US and 7.4% in France. At the same time and for the same population, the employment rate (number of workers divided by population) was 86.3% in the US and 86.7% in France. That example shows that the unemployment rate was 60% higher in France than in the US, but more people in that demographic were working in France than in the US, which is counterintuitive if it is expected that the unemployment rate reflects the health of the labour market.Those deficiencies make many labour market economists prefer to look at a range of economic statistics such as labour market participation rate, the percentage of people between 15 and 64 who are currently employed or searching for employment, the total number of full-time jobs in an economy, the number of people seeking work as a raw number and not a percentage, and the total number of person-hours worked in a month compared to the total number of person-hours people would like to work. In particular, the National Bureau of Economic Research does not use the unemployment rate but prefers various employment rates to date recessions. Labor force participation rate The labor force participation rate is the ratio between the labor force and the overall size of their cohort (national population of the same age range). In the West, during the later half of the 20th century, the labor force participation rate increased significantly because of an increase in the number of women entering the workplace. In the United States, there have been four significant stages of womens participation in the labour force: increases in the 20th century and decreases in the 21st century. Male labor force participation decreased from 1953 to 2013. Since October 2013, men have been increasingly joining the labour force. From the late 19th century to the 1920s, very few women worked outside the home. They were young single women who typically withdrew from the labor force at marriage unless family needed two incomes. Such women worked primarily in the textile manufacturing industry or as domestic workers. That profession empowered women and allowed them to earn a living wage. At times, they were a financial help to their families. Between 1930 and 1950, female labor force participation increased primarily because of the increased demand for office workers, womens participation in the high school movement, and electrification, which reduced the time that was spent on household chores. From the 1950s to the early 1970s, most women were secondary earners working mainly as secretaries, teachers, nurses, and librarians (pink-collar jobs). From the mid-1970s to the late 1990s, there was a period of revolution of women in the labor force brought on by various factors, many of which arose from the second-wave feminism movement. Women more accurately planned for their future in the work force by investing in more applicable majors in college that prepared them to enter and compete in the labor market. In the United States, the female labor force participation rate rose from approximately 33% in 1948 to a peak of 60.3% in 2000. As of April 2015, the female labor force participation is at 56.6%, the male labor force participation rate is at 69.4%, and the total is 62.8%.A common theory in modern economics claims that the rise of women participating in the US labor force in the 1950s to the 1990s was caused by the introduction of a new contraceptive technology, birth control pills, as well as the adjustment of age of majority laws. The use of birth control gave women the flexibility of opting to invest and to advance their career while they maintained a relationship. By having control over the timing of their fertility, they were not running a risk of thwarting their career choices. However, only 40% of the population actually used the birth control pill. That implies that other factors may have contributed to women choosing to invest in advancing their careers. One factor may be that an increasing number of men delayed the age of marriage, which allowed women to marry later in life without them worrying about the quality of older men. Other factors include the changing nature of work, with machines replacing physical labor, thus eliminating many traditional male occupations, and the rise of the service sector in which many jobs are gender neutral. Another factor that may have contributed to the trend was the Equal Pay Act of 1963, which aimed at abolishing wage disparity based on sex. Such legislation diminished sexual discrimination and encouraged more women to enter the labor market by receiving fair remuneration to help raising families and children. At the turn of the 21st century, the labor force participation began to reverse its long period of increase. Reasons for the change include a rising share of older workers, an increase in school enrollment rates among young workers, and a decrease in female labor force participation.The labor force participation rate can decrease when the rate of growth of the population outweighs that of the employed and the unemployed together. The labor force participation rate is a key component in long-term economic growth, almost as important as productivity. A historic shift began around the end of the Great Recession as women began leaving the labor force in the United States and other developed countries. The female labor force participation rate in the United States has steadily decreased since 2009, and as of April 2015, the female labor force participation rate has gone back down to 1988 levels of 56.6%.Participation rates are defined as follows: The labor force participation rate explains how an increase in the unemployment rate can occur simultaneously with an increase in employment. If a large number of new workers enter the labor force but only a small fraction become employed, then the increase in the number of unemployed workers can outpace the growth in employment. Unemployment-to-population ratio The unemployment-to-population ratio calculates the share of unemployed for the whole population. This is in contrast to the unemployment rate, which calculates the percentage of unemployed persons in relation to the active population. Particularly, many young people between 15 and 24 are studying full-time and so are neither working nor looking for a job. That means that they are not part of the labor force, which is used as the denominator when the unemployment rate is calculated.The youth unemployment ratios in the European Union range from 5.2 (Austria) to 20.6 percent (Spain). They are considerably lower than the standard youth unemployment rates, ranging from 7.9 (Germany) to 57.9 percent (Greece). Effects High and the persistent unemployment, in which economic inequality increases, has a negative effect on subsequent long-run economic growth. Unemployment can harm growth because it is a waste of resources; generates redistributive pressures and subsequent distortions; drives people to poverty; constrains liquidity limiting labor mobility; and erodes self-esteem promoting social dislocation, unrest, and conflict. The 2013 winner of the Nobel Prize in Economics, Robert J. Shiller, said that rising inequality in the United States and elsewhere is the most important problem. Costs Individual Unemployed individuals are unable to earn money to meet financial obligations. Failure to pay mortgage payments or to pay rent may lead to homelessness through foreclosure or eviction. Across the United States the growing ranks of people made homeless in the foreclosure crisis are generating tent cities.Unemployment increases susceptibility to cardiovascular disease, somatization, anxiety disorders, depression, and suicide. In addition, unemployed people have higher rates of medication use, poor diet, physician visits, tobacco smoking, alcoholic beverage consumption, drug use, and lower rates of exercise. According to a study published in Social Indicator Research, even those who tend to be optimistic find it difficult to look on the bright side of things when unemployed. Using interviews and data from German participants aged 16 to 94, including individuals coping with the stresses of real life and not just a volunteering student population, the researchers determined that even optimists struggled with being unemployed.In 1979, M. Harvey Brenner found that for every 10% increase in the number of unemployed, there is an increase of 1.2% in total mortality, a 1.7% increase in cardiovascular disease, 1.3% more cirrhosis cases, 1.7% more suicides, 4.0% more arrests, and 0.8% more assaults reported to the police.A study by Christopher Ruhm in 2000 on the effect of recessions on health found that several measures of health actually improve during recessions. As for the impact of an economic downturn on crime, during the Great Depression, the crime rate did not decrease. The unemployed in the US often use welfare programs such as food stamps or accumulating debt because unemployment insurance in the US generally does not replace most of the income that was received on the job, and one cannot receive such aid indefinitely. Not everyone suffers equally from unemployment. In a prospective study of 9,570 individuals over four years, highly-conscientious people suffered more than twice as much if they became unemployed. The authors suggested that may because of conscientious people making different attributions about why they became unemployed or through experiencing stronger reactions following failure. There is also the possibility of reverse causality from poor health to unemployment.Some researchers hold that many of the low-income jobs are not really a better option than unemployment with a welfare state, with its unemployment insurance benefits. However, since it is difficult or impossible to get unemployment insurance benefits without having worked in the past, those jobs and unemployment are more complementary than they are substitutes. (They are often held short-term, either by students or by those trying to gain experience; turnover in most low-paying jobs is high.) Another cost for the unemployed is that the combination of unemployment, lack of financial resources, and social responsibilities may push unemployed workers to take jobs that do not fit their skills or allow them to use their talents. Unemployment can cause underemployment, and fear of job loss can spur psychological anxiety. As well as anxiety, it can cause depression, lack of confidence, and huge amounts of stress, which is increased when the unemployed are faced with health issues, poverty, and lack of relational support.Another personal cost of unemployment is its impact on relationships. A 2008 study from Covizzi, which examined the relationship between unemployment and divorce, found that the rate of divorce is greater for couples when one partner is unemployed. However, a more recent study has found that some couples often stick together in "unhappy" or "unhealthy" marriages when they are unemployed to buffer financial costs. A 2014 study by Van der Meer found that the stigma that comes from being unemployed affects personal well-being, especially for men, who often feel as though their masculine identities are threatened by unemployment.Unemployment can also bring personal costs in relation to gender. One study found that women are more likely to experience unemployment than men and that they are less likely to move from temporary positions to permanent positions. Another study on gender and unemployment found that men, however, are more likely to experience greater stress, depression, and adverse effects from unemployment, largely stemming from the perceived threat to their role as breadwinner. The study found that men expect themselves to be viewed as "less manly" after a job loss than they actually are and so they engage in compensating behaviors, such as financial risk-taking and increased assertiveness. Unemployment has been linked to extremely adverse effects on mens mental health. Professor Ian Hickie of the University of Sydney said that evidence showed that men have more restricted social networks than women and that men have are heavily work-based. Therefore, the loss of a job for men means the loss of a whole set of social connections as well. That loss can then lead to men becoming socially isolated very quickly. An Australian study on the mental health impacts of graduating during an economic downturn found that the negative mental health outcomes are greater and more scarring for men than women. The effect was particularly pronounced for those with vocational or secondary education.Costs of unemployment also vary depending on age. The young and the old are the two largest age groups currently experiencing unemployment. A 2007 study from Jacob and Kleinert found that young people (ages 18 to 24) who have fewer resources and limited work experiences are more likely to be unemployed. Other researchers have found that todays high school seniors place a lower value on work than those in the past, which is likely because they recognize the limited availability of jobs. At the other end of the age spectrum, studies have found that older individuals have more barriers than younger workers to employment, require stronger social networks to acquire work, and are also less likely to move from temporary to permanent positions. Additionally, some older people see age discrimination as the reason for them not getting hired. Social An economy with high unemployment is not using all of the resources, specifically labour, available to it. Since it is operating below its production possibility frontier, it could have higher output if all of the workforce were usefully employed. However, there is a tradeoff between economic efficiency and unemployment: if all frictionally unemployed accepted the first job that they were offered, they would be likely to be operating at below their skill level, reducing the economys efficiency.During a long period of unemployment, workers can lose their skills, causing a loss of human capital. Being unemployed can also reduce the life expectancy of workers by about seven years.High unemployment can encourage xenophobia and protectionism since workers fear that foreigners are stealing their jobs. Efforts to preserve existing jobs of domestic and native workers include legal barriers against "outsiders" who want jobs, obstacles to immigration, and/or tariffs and similar trade barriers against foreign competitors. High unemployment can also cause social problems such as crime. If people have less disposable income than before, it is very likely that crime levels within the economy will increase. A 2015 study published in The Lancet, estimates that unemployment causes 45,000 suicides a year globally. Sociopolitical High levels of unemployment can be causes of civil unrest, in some cases leading to revolution, particularly totalitarianism. The fall of the Weimar Republic in 1933 and Adolf Hitlers rise to power, which culminated in World War II and the deaths of tens of millions and the destruction of much of the physical capital of Europe, is attributed to the poor economic conditions in Germany at the time, notably a high unemployment rate of above 20%; see Great Depression in Central Europe for details. However the hyperinflation in the Weimar Republic is not directly blamed for the Nazi rise. Hyperinflation occurred primarily in 1921 to 1923, the year of Hitlers Beer Hall Putsch. Although hyperinflation has been blamed for damaging the credibility of democratic institutions, the Nazis did not assume government until 1933, ten years after the hyperinflation but in the midst of high unemployment. Rising unemployment has traditionally been regarded by the public and the media in any country as a key guarantor of electoral defeat for any government that oversees it. That was very much the consensus in the United Kingdom until 1983, when Thatchers Conservative government won a landslide in the general election, despite overseeing a rise in unemployment from 1.5 million to 3.2 million since the 1979 election. Benefits The primary benefit of unemployment is that people are available for hire, without being headhunted away from their existing employers. That permits both new and old businesses to take on staff. Unemployment is argued to be "beneficial" to the people who are not unemployed in the sense that it averts inflation, which itself has damaging effects, by providing (in Marxian terms) a reserve army of labour, which keeps wages in check. However, the direct connection between full local employment and local inflation has been disputed by some because of the recent increase in international trade that supplies low-priced goods even while local employment rates rise to full employment. Full employment cannot be achieved because workers would shirk if they were not threatened with the possibility of unemployment. The curve for the no-shirking condition (labelled NSC) thus goes to infinity at full employment. The inflation-fighting benefits to the entire economy arising from a presumed optimum level of unemployment have been studied extensively. The Shapiro–Stiglitz model suggests that wages never bid down sufficiently to reach 0% unemployment. That occurs because employers know that when wages decrease, workers will shirk and expend less effort. Employers avoid shirking by preventing wages from decreasing so low that workers give up and become unproductive. The higher wages perpetuate unemployment, but the threat of unemployment reduces shirking. Before current levels of world trade were developed, unemployment was shown to reduce inflation, following the Phillips curve, or to decelerate inflation, following the NAIRU/natural rate of unemployment theory since it is relatively easy to seek a new job without losing a current job. When more jobs are available for fewer workers (lower unemployment), that may allow workers to find the jobs that better fit their tastes, talents and needs. As in the Marxian theory of unemployment, special interests may also benefit. Some employers may expect that employees with no fear of losing their jobs will not work as hard or will demand increased wages and benefit. According to that theory, unemployment may promote general labour productivity and profitability by increasing employers rationale for their monopsony-like power (and profits).Optimal unemployment has also been defended as an environmental tool to brake the constantly-accelerated growth of the GDP to maintain levels that are sustainable in the context of resource constraints and environmental impacts. However, the tool of denying jobs to willing workers seems a blunt instrument for conserving resources and the environment. It reduces the consumption of the unemployed across the board and only in the short term. Full employment of the unemployed workforce, all focused toward the goal of developing more environmentally-efficient methods for production and consumption, might provide a more significant and lasting cumulative environmental benefit and reduced resource consumption.Some critics of the "culture of work" such as the anarchist Bob Black see employment as culturally overemphasized in modern countries. Such critics often propose quitting jobs when possible, working less, reassessing the cost of living to that end, creation of jobs that are "fun" as opposed to "work," and creating cultural norms in which work is seen as unhealthy. These people advocate an "anti-work" ethic for life. Decline in work hours As a result of productivity, the work week declined considerably during the 19th century. By the 1920s, the average workweek in the US was 49 hours, but it was reduced to 40 hours (after which overtime premium was applied) as part of the 1933 National Industrial Recovery Act. During the Great Depression, the enormous productivity gains caused by electrification, mass production, and agricultural mechanization were believed to have ended the need for a large number of previously-employed workers. Remedies Societies try a number of different measures to get as many people as possible into work, and various societies have experienced close to full employment for extended periods, particularly during the post-World War II economic expansion. The United Kingdom in the 1950s and 1960s averaged 1.6% unemployment, and in Australia, the 1945 White Paper on Full Employment in Australia established a government policy of full employment, which lasted until the 1970s.However, mainstream economic discussions of full employment since the 1970s suggest that attempts to reduce the level of unemployment below the natural rate of unemployment will fail but result only in less output and more inflation. Demand-side solutions Increases in the demand for labour move the economy along the demand curve, increasing wages and employment. The demand for labour in an economy is derived from the demand for goods and services. As such, if the demand for goods and services in the economy increases, the demand for labour will increase, increasing employment and wages. There are many ways to stimulate demand for goods and services. Increasing wages to the working class (those more likely to spend the increased funds on goods and services, rather than various types of savings or commodity purchases) is one theory that is proposed. Increased wages are believed to be more effective in boosting demand for goods and services than central banking strategies, which put the increased money supply mostly into the hands of wealthy persons and institutions. Monetarists suggest that increasing money supply in general increases short-term demand. As for the long-term demand, the increased demand is negated by inflation. A rise in fiscal expenditures is another strategy for boosting aggregate demand. Providing aid to the unemployed is a strategy that is used to prevent cutbacks in consumption of goods and services, which can lead to a vicious cycle of further job losses and further decreases in consumption and demand. Many countries aid the unemployed through social welfare programs. Such unemployment benefits include unemployment insurance, unemployment compensation, welfare, and subsidies to aid in retraining. The main goal of such programs is to alleviate short-term hardships and, more importantly, to allow workers more time to search for a job. A direct demand-side solution to unemployment is government-funded employment of the able-bodied poor. This was notably implemented in Britain from the 17th century until 1948 in the institution of the workhouse, which provided jobs for the unemployed with harsh conditions and poor wages to dissuade their use. A modern alternative is a job guarantee in which the government guarantees work at a living wage. Temporary measures can include public works programs such as the Works Progress Administration. Government-funded employment is not widely advocated as a solution to unemployment except in times of crisis. That is attributed to the public sector jobs existence depending directly on the tax receipts from private sector employment. In the US, the unemployment insurance allowance is based solely on previous income (not time worked, family size, etc.) and usually compensates for one third of previous income. To qualify, people must reside in their respective state for at least a year and work. The system was established by the Social Security Act of 1935. Although 90% of citizens are covered by unemployment insurance, less than 40% apply for and receive benefits. However, the number applying for and receiving benefits increases during recessions. For highly-seasonal industries, the system provides income to workers during the off-season, thus encouraging them to stay attached to the industry. According to classical economic theory, markets reach equilibrium where supply equals demand; everyone who wants to sell at the market price can do so. Those who do not want to sell at that price do not; in the labour market, this is classical unemployment. Monetary policy and fiscal policy can both be used to increase short-term growth in the economy, increasing the demand for labour and decreasing unemployment. Supply-side solutions However, the labor market is not 100% efficient although it may be more efficient than the bureaucracy. Some argue that minimum wages and union activity keep wages from falling, which means that too many people want to sell their labour at the going price but cannot. That assumes perfect competition exists in the labour market, specifically that no single entity is large enough to affect wage levels and that employees are similar in ability. Advocates of supply-side policies believe those policies can solve the problem by making the labour market more flexible. These include removing the minimum wage and reducing the power of unions. Supply-siders argue that their reforms increase long-term growth by reducing labour costs. The increased supply of goods and services requires more workers, increasing employment. It is argued that supply-side policies, which include cutting taxes on businesses and reducing regulation, create jobs, reduce unemployment, and decrease labors share of national income. Other supply-side policies include education to make workers more attractive to employers. History There are relatively limited historical records on unemployment because it has not always been acknowledged or measured systematically. Industrialization involves economies of scale, which often prevent individuals from having the capital to create their own jobs to be self-employed. An individual who cannot join an enterprise or create a job is unemployed. As individual farmers, ranchers, spinners, doctors and merchants are organized into large enterprises, those who cannot join or compete become unemployed. Recognition of unemployment occurred slowly as economies across the world industrialized and bureaucratized. Before that, traditional self-sufficient native societies had no concept of unemployment. The recognition of the concept of "unemployment" is best exemplified through the well documented historical records in England. For example, in 16th-century, England no distinction was made between vagrants and the jobless; both were simply categorized as "sturdy beggars", who were to be punished and moved on. 16th century The closing of the monasteries in the 1530s increased poverty, as the Roman Catholic Church had helped the poor. In addition, there was a significant rise in enclosures during the Tudor period. Also, the population was rising. Those unable to find work had a stark choice: starve or break the law. In 1535, a bill was drawn up calling for the creation of a system of public works to deal with the problem of unemployment, which were to be funded by a tax on income and capital. A law that was passed a year later allowed vagabonds to be whipped and hanged.In 1547, a bill was passed that subjected vagrants to some of the more extreme provisions of the criminal law: two years servitude and branding with a "V" as the penalty for the first offense and death for the second. During the reign of Henry VIII, as many as 72,000 people are estimated to have been executed. In the 1576 Act, each town was required to provide work for the unemployed.The Elizabethan Poor Law of 1601, one of the worlds first government-sponsored welfare programs, made a clear distinction between those who were unable to work and those able-bodied people who refused employment. Under the Poor Law systems of England and Wales, Scotland and Ireland, a workhouse was a place people unable to support themselves could go to live and work. Industrial Revolution to late 19th century Poverty was a highly visible problem in the eighteenth century, both in cities and in the countryside. In France and Britain by the end of the century, an estimated 10 percent of the people depended on charity or begging for their food. By 1776, some 1,912 parish and corporation workhouses had been established in England and Wales and housed almost 100,000 paupers. A description of the miserable living standards of the mill workers in England in 1844 was given by Fredrick Engels in The Condition of the Working Class in England in 1844. In the preface to the 1892 edition, Engels noted that the extreme poverty he had written about in 1844 had largely disappeared. David Ames Wells also noted that living conditions in England had improved near the end of the 19th century and that unemployment was low. The scarcity and the high price of labor in the US in the 19th century was well documented by contemporary accounts, as in the following: "The laboring classes are comparatively few in number, but this is counterbalanced by, and indeed, may be one of the causes of the eagerness by which they call in the use of machinery in almost every department of industry. Wherever it can be applied as a substitute for manual labor, it is universally and willingly resorted to.... It is this condition of the labor market, and this eager resort to machinery wherever it can be applied, to which, under the guidance of superior education and intelligence, the remarkable prosperity of the United States is due." Scarcity of labor was a factor in the economics of slavery in the United States. As new territories were opened and federal land sales were conducted, land had to be cleared and new homesteads established. Hundreds of thousands of immigrants annually came to the US and found jobs digging canals and building railroads. Almost all work during most of the 19th century was done by hand or with horses, mules, or oxen since there was very little mechanization. The workweek during most of the 19th century was 60 hours. Unemployment at times was between one and two percent. The tight labor market was a factor in productivity gains by allowing workers to maintain or to increase their nominal wages during the secular deflation that caused real wages to rise at various times in the 19th century, especially in its final decades. 20th century There were labor shortages during World War I. Ford Motor Co. doubled wages to reduce turnover. After 1925, unemployment gradually began to rise.The 1930s saw the Great Depression impact unemployment across the globe. In Germany and the United States, the unemployment rate reached about 25% in 1932.In some towns and cities in the northeast of England, unemployment reached as high as 70%; the national unemployment level peaked at more than 22% in 1932. Unemployment in Canada reached 27% at the depth of the Depression in 1933. In 1929, the U.S. unemployment rate averaged 3%. In the US, the Works Progress Administration (1935–43) was the largest make-work program. It hired men (and some women) off the relief roles ("dole") typically for unskilled labor. During the New Deal, over three million unemployed young men were taken out of their homes and placed for six months into more than 2600 work camps managed by the Civilian Conservation Corps.Unemployment in the United Kingdom fell later in the 1930s as the Depression eased, and it remained low (in single figures) after World War II. Fredrick Mills found that in the US, 51% of the decline in work hours was due to the fall in production and 49% was from increased productivity.By 1972, unemployment in the United Kingdom had crept back up above 1,000,000, and it was even higher by the end of the decade, with inflation also being high. Although the monetarist economic policies of Margaret Thatchers Conservative government saw inflation reduced after 1979, unemployment soared in the early 1980s and in 1982, it exceeded 3,000,000, a level that had not been seen for some 50 years. That represented one in eight of the workforce, with unemployment exceeding 20% in some places that had relied on declining industries such as coal mining.However, it was a time of high unemployment in all other major industrialised nations as well. By the spring of 1983, unemployment had risen by 6% in the previous 12 months, compared to 10% in Japan, 23% in the US, and 34% in West Germany (seven years before Reunification).Unemployment in the United Kingdom remained above 3,000,000 until the spring of 1987, when the economy enjoyed a boom. By the end of 1989, unemployment had fallen to 1,600,000. However, inflation had reached 7.8%, and the following year, it reached a nine-year high of 9.5%; leading to increased interest rates.Another recession occurred from 1990 to 1992. Unemployment began to increase, and by the end of 1992, nearly 3,000,000 in the United Kingdom were unemployed, a number that was soon lowered by a strong economic recovery. With inflation down to 1.6% by 1993, unemployment then began to fall rapidly and stood at 1,800,000 by early 1997. 21st century The official unemployment rate in the 16 European Union (EU) countries that use the euro rose to 10% in December 2009 as a result of another recession. Latvia had the highest unemployment rate in the EU, at 22.3% for November 2009. Europes young workers have been especially hard hit. In November 2009, the unemployment rate in the EU27 for those aged 15–24 was 18.3%. For those under 25, the unemployment rate in Spain was 43.8%. Unemployment has risen in two thirds of European countries since 2010.Into the 21st century, unemployment in the United Kingdom remained low and the economy remaining strong, and several other European economies, such as France and Germany, experienced a minor recession and a substantial rise in unemployment.In 2008, when the recession brought on another increase in the United Kingdom, after 15 years of economic growth and no major rises in unemployment. In early 2009, unemployment passed the 2 million mark, and economists were predicting it would soon reach 3 million. However, the end of the recession was declared in January 2010 and unemployment peaked at nearly 2.7 million in 2011, appearing to ease fears of unemployment reaching 3 million. The unemployment rate of Britains young black people was 47.4% in 2011. 2013/2014 has seen the employment rate increase from 1,935,836 to 2,173,012 as supported by showing the UK is creating more job opportunities and forecasts the rate of increase in 2014/2015 will be another 7.2%.The 2008–2012 global recession has been called a "mancession" because of the disproportionate number of men who lost their jobs as compared to women. The gender gap became wide in the United States in 2009, when 10.5% of men in the labor force were unemployed, compared with 8% of women. Three quarters of the jobs that were lost in the recession in the US were held by men.A 26 April 2005 Asia Times article noted, "In regional giant South Africa, some 300,000 textile workers have lost their jobs in the past two years due to the influx of Chinese goods". The increasing US trade deficit with China cost 2.4 million American jobs between 2001–2008, according to a study by the Economic Policy Institute (EPI). From 2000–2007, the United States lost a total of 3.2 million manufacturing jobs. 12.1% of US military veterans who had served after the September 11 attacks in 2001 were unemployed as of 2011; 29.1% of male veterans aged 18–24 were unemployed. As of September 2016, the total veteran unemployment rate was 4.3 percent. By September 2017, that figure had dropped to 3 percent.About 25,000,000 people in the worlds 30 richest countries lost their jobs between the end of 2007 and the end of 2010, as the economic downturn pushed most countries into recession. In April 2010, the US unemployment rate was 9.9%, but the governments broader U-6 unemployment rate was 17.1%. In April 2012, the unemployment rate was 4.6% in Japan. In a 2012 story, the Financial Post reported, "Nearly 75 million youth are unemployed around the world, an increase of more than 4 million since 2007. In the European Union, where a debt crisis followed the financial crisis, the youth unemployment rate rose to 18% last year from 12.5% in 2007, the ILO report shows." In March 2018, according to US Unemployment Rate Statistics, the unemployment rate was 4.1%, below the 4.5–5.0% norm. See also Notes References Farmer, Roger E. A. (2001). "Unemployment". Macroeconomics (Second ed.). Cincinnati: South-Western Publishing. pp. 173–192. ISBN 978-0-324-14964-7. Kalecki, Michał (1943). "Political aspects of full employment" (PDF). The Political Quarterly. 14 (4): 322–331. doi:10.1111/j.1467-923X.1943.tb01016.x. McGaughey, Ewan (10 January 2018). "Will Robots Automate Your Job Away? Full Employment, Basic Income, and Economic Democracy". Centre for Business Research, University of Cambridge, Working Paper No. 496. doi:10.2139/ssrn.3044448. S2CID 219336439. SSRN 3044448. Reich, Robert B. (2010). Aftershock: The Next Economy and Americas Future (1st ed.). Alfred A. Knopf. ISBN 978-0-307-59281-1. Romer, David (2011). "Unemployment". Advanced Macroeconomics (Fourth ed.). New York: McGraw-Hill Education. pp. 456–512. ISBN 978-0-07-351137-5. Simonazzi, Annamaria; Vianello, Fernando (2001). "Financial Liberalization, the European Single Currency and the Problem of Unemployment". In Franzini, M.; Pizzuti, F. R. (eds.). Globalization, Institutions and Social Cohesion. Heidelberg: Springer. ISBN 978-3-540-67741-3. Historical: Europe and Japan Beveridge, William H. (1944). Full Employment in a Free Society (1st ed.). Allen & Unwin., in Great Britain. Broadberry, Stephen N., and Albrecht Ritschl. "Real Wages, Productivity, and Unemployment in Britain and Germany during the 1920s." Explorations in Economic History 32.3 (1995): 327-349. Dimsdale, Nicholas H., Nicholas Horsewood, and Arthur Van Riel. "Unemployment in interwar Germany: an analysis of the labor market, 1927-1936." Journal of Economic History (2006): 778-808. online Heimberger, Philipp, Jakob Kapeller, and Bernhard Schütz. "The NAIRU determinants: What’s structural about unemployment in Europe?." Journal of Policy Modeling 39.5 (2017): 883-908. online Kato, Michiya. "Unemployment and Public Works Policy in Interwar Britain and Japan: An International Comparison." (2010): 69-101. online Kaufman, Roger T. "Patterns of Unemployment in North America, Western Europe and Japan." Unemployment in Western countries (Palgrave Macmillan, 1980). 3-35. Nickell, Stephen, Luca Nunziata, and Wolfgang Ochel. "Unemployment in the OECD since the 1960s. What do we know?." Economic Journal 115.500 (2005): 1-27 online. Stachura, Peter D., ed. Unemployment and the great depression in Weimar Germany (Springer, 1986). Topp, Niels-Henrik. "Unemployment and Economic Policy in Denmark in the 1930s." Scandinavian Economic History Review 56.1 (2008): 71-90. Webb, Sidney (1912). How the Government Can Prevent Unemployment. The National Committee for the Prevention of Destitution. (First ed.). Letchworth, Herts.: Garden City Press Ltd., in Great Britain Historical: United States Jensen, Richard J. "The causes and cures of unemployment in the Great Depression." Journal of Interdisciplinary History 19.4 (1989): 553-583 online. Keyssar, Alexander (1986). Out of Work: The First Century of Unemployment in Massachusetts. Cambridge University Press. ISBN 978-0-521-23016-2. Margo, Robert A. "Employment and Unemployment in the 1930s." Journal of Economic Perspectives 7.2 (1993): 41-59. online Stricker, Frank. American Unemployment: Past, Present, and Future (University of Illinois Press, 2020) online review Sundstrom, William A. "Last hired, first fired? Unemployment and urban black workers during the Great Depression." Journal of Economic History (1992): 415-429. online Temin, Peter. "Socialism and Wages in the Recovery from the Great Depression in the United States and Germany." Journal of Economic History (1990): 297-307 online. External links Quotations related to unemployment at Wikiquote The dictionary definition of unemployment at Wiktionary Media related to Unemployment at Wikimedia Commons Economic Policy Institute Current unemployment figures, CEIC Data Current unemployment rates by country OECD Unemployment statistics Unemployment statistics by Lebanese-economy-forum, World Bank data JobCity is Right Platform for Govt Jobs Thermal maps of the worlds unemployment percentage rates – by country, 2007–2010

Surgical instrument

A surgical instrument is a tool or device for performing specific actions or carrying out desired effects during a surgery or operation, such as modifying biological tissue, or to provide access for viewing it. Over time, many different kinds of surgical instruments and tools have been invented. Some surgical instruments are designed for general use in all sorts of surgeries, while others are designed for only certain specialties or specific procedures. Classification of surgical instruments helps surgeons to understand the functions and purposes of the instruments. With the goal of optimizing surgical results and performing more difficult operations, more instruments continue to be invented in the modern era. History Many different kinds of surgical instruments and tools have been invented and some have been repurposed as medical knowledge and surgical practices have developed. As surgery practice diversified, some tools are advanced for higher accuracy and stability while some are invented with the completion of medical and scientific knowledge. Two waves in history contributed significantly to the development of surgical tools. In the 1900s, inventions of aseptic surgeries (maintenance of sterile conditions through good hygiene procedures) on the basis of existing antiseptic surgeries (sterilization of tools before, during, and after surgery) led to the manifestations of sale and use of instrument sterilizers, sterile gauze, and cotton. Most importantly, instruments were advanced to be readily and effectively sterilized by replacing wooden and ivory handles with metals. For safety and comfort concerns, the tools are made with as few pieces as possible.Hand surgery emerged as a specialty during World War II, and the tools used by early hand surgeons remain in common use today, and many are identified by the names of those who created them.Individual tools have diverse history development. Below is a brief history of the inventors and tools created for five commonly used surgical tools. Scissors Mayo scissors, created by one of the mayo brothers, was one of the inventions of the Mayo clinic (established by Dr.William Worrall Mayo and his two sons, Dr. William James Mayo and Dr. Charles Horace Mayo in the 1880s). Mayo scissors have semi-blunt ends and they are either straight or curve-bladed. The straight blades are used for cutting tissue near wounds, and curves are used for cutting thick tissue. Metzenbaum scissors were invented by Myron Metzenbaum (1876-1944). This tool was widely used for tonsillectomy (the surgical removal of the tonsils). The lighter and longer handle allows it to be used in tighter operating fields. Knife to Scalpel to Electrocautery Primitive knives were made of perishable materials such as sharp leaf margins or bamboo. After the Dark Ages, Muslims, and later European countries started to develop surgical instruments, scalpels, for cutting. In 1904, King Gillette developed a double-edged safety razor blade with a disposable blade. After 10 years, Morgan Parker, an engineer, developed and patented another type of disposable scalpel, consisting of an overlapping blade locked into a metal handle that allows for easily replacing dull and used blades with fresh sterile blades. Compared to the Gillette ones, this new blade provides stability whilst still being able to exchange blades between uses. Despite the knowledge that heat can control bleeding since the sixth-century BC, it was not until the 18th-century that people started to use electricity to generate heat for cautery. William Stewart Halsted was the pioneer of the technique, which later was called Diathermy. In 1900, physician Joseph Rivière used electrical current to treat a benign carcinomatous ulcer on the dorsum of his patients hand. Then in 1907, Physician Karl Franz Nagelschmidt used diathermy to treat lesions as well as the coagulation of vascular tumors and hemorrhoids. In the early 1900s, William T. Bovie proposed the use of different current (flow of electrical charge of the carrier) for cutting and coagulation. Bovie collaborated with Dr. Harvey Cushing, which led to the birth of “Bovie”, a diathermy apparatus. It allows for careful dissection of tissue while maintaining hemostasis. Retractors During the Renaissance, retractors were lacking so the surgeons uses their fingers to supply the necessary retraction of tissue exploration. Albucasis, a pioneer of modern medicine, devised numerous hooks for surgical retraction including circumcisions, tracheostomies, hemorrhoidectomies, and central extractions in his famous book Al Tasreef Liman ‘Ajaz ‘Aan Al-Taleef around 1000 AD. In the 19th century, Doyen abdominal retractors were invented by French surgeon Eugène-Louis Doyen. The doyen retractors are auto-static, self-retaining retractors that are used primarily in abdominal OB/GYN procedures. It facilitates the completion of difficult surgeries by providing improved exposure. In the late 19th century, Nicholas Senn, an early adopter of Listerism, felt that having a smooth surface on a surgical instrument was important to help to prevent infection. Thus, he developed what is now called the Senn retractor, a double-ended retractor with an end of three bent prongs that may be dull or sharp, and it was often used in plastic or vascular surgery procedures. The Weitlaner retractor, invented by Franz Weitlaner in 1905, is a self-retaining, finger ring retractor with a cam ratchet lock used for holding back tissue and exposing a surgical site that allows the surgeon to activate using a single hand. His invention inspired the invention of more retractors, such as Adson-Beckman retractors for general surgery and Chung retractors for orthopedic surgery. Forceps Back in the 6th century BC, laboring caused a high mortality rate for both mothers and newborns due to the hours or days of the lasting delivery process. This problem led to the establishment of forceps-assisted delivery in the 16th century by the Chamberlen family. Forceps were later developed over several centuries by leading obstetricians of the time including James Simpson, Neville Barnes, and Christian Kielland. Michael Ellis DeBakey invented one of the most common and well-known DeBkey biceps. The vascular atraumatic forceps (DeBakey)were widely used for grasping vascular tissue and causing minimal damage to the vessels. This invention led to the development of the Dacron aortic graft for the repair of aortic aneurysms. Around the mid 1900s, Alfred Washington Adson, a pioneer in neuroscience at Mayo Clinic, invented Adson forceps that allows the lifting and removal of neural tissue. Hemostat/clamp Hemostats are forceps that aim to obliterate the lumen of vessels and to obtain adherence to the crushed surfaces and vascular hemostasis. Originally, this notion of crushing did not exist and arterial catch forceps simply clamped vessels temporarily prior to ligature or cautery. In 1867, Eugene Koeberle, who accidentally found arterial forceps with a catch closure came away spontaneously without the need for ligature, and invented “pince hémostatique,” which have pin and hole catches. In 1882, the Kocher clamp was created by Emil Theodor Kocher, who significantly contributed to thyroidectomies (removal of all or a part of the thyroid gland) and decompressive craniotomy. This invention decreases the risk of contamination while cutting dense tissue. Later, Dr. William Henry Welch and William Stewart Halsted contributed to the invention of clamps and Halsted-Mosquito Hemostats, which were used to clamp small blood vessels. Kelly clamp, invented by Howard Kelly, has similar functions but it can clamp larger vessels due to the slightly larger jaw.Accordingly, the nomenclature of surgical instruments follows certain patterns, such as a description of the action it performs (for example, scalpel, hemostat), the name of its inventor(s) (for example, the Kocher forceps), or a compound scientific name related to the kind of surgery (for example, a tracheotomy is a tool used to perform a tracheotomy). Classification There are several classes of surgical instruments: Graspers, such as forceps (non-locking forceps/ grasping forceps, thumb forceps, pick-ups) Used for tissue or object grasping. Forceps are categorized into toothed or non-toothed at the tip. (e.g.,Tissue forceps, Adson forceps, Bonney forceps, DeBakey forceps, Russian forceps) Clamps (locking forceps) Clamps stabilize or hold tissue and objects in place. They can be used for traumatic or atraumatic purposes. (e.g., Crile hemostat, Kelly clamp, Kocher clamp) Surgical scissors Tool for tissue cutting, dissection, and suture. Straight and curved scissors are used for cutting different structures. (e.g. Mayo scissors, Metzenbaum scissors, Pott’s scissors, Iris Scissors). Bone cutters: unpowered or powered saws, drills and pliers-like devices Needles/Sutures Tools used for suturing dissection sites or closing cuts. Needles have different shapes (e.g. j shape, ½ circle, straight) and cutting edges (tapered - round, conventional cutting - triangular) depending on the application and areas of the suture. Sutures can be categorized based on different sizes (e.g.#5-#11, higher numbers represent larger suture diameter) and types (absorbable and nonabsorbable and braided and non-braided) as well. Needle drivers(needle holders) Tools used to hold suture needle while it is passed through tissue and to grasp suture while instrument knot tying. Retractors, used to spread open skin, ribs and other tissue Tools for various purposes depending on the condition. Retractors can be used to expose incision openings, hold tissue back, or maintain operating areas. They can be categorized into either hand-held retractors or self-retaining ones (via a ratcheting mechanism) (e.g., Deaver retractor, Weitlaner retractor, Malleable Retractor). Distractors, positioners and stereotactic devices Mechanical cutters (scalpels, lancets, trocars, Harmonic scalpel, rongeurs etc.) Dilators and specula, for access to narrow passages or incisions Suction tips and tubes, for removal of bodily fluids Tools used to remove secretion, debris, or any fluid in the surgical area. (e.g. Yankauer Suction Tube, Poole Suction Tube, Frazier Suction Tip) Sealing devices, such as surgical staplers Tools used for resection (Removing part of an organ), transaction (Cutting through and sealing organs and tissues), and anastomoses (Creating connections between structures). (e.g. linear stapler, linear cutter, clips) Irrigation and injection needles, tips and tubes, for introducing fluid Powered devices, such as cranial drills and dermatomes Scopes and probes, including fiber optic endoscopes and tactile probes Carriers and appliers for optical, electronic, and mechanical devices Ultrasound tissue disruptors, cryotomes and cutting laser guides Measurement devices, such as rulers and calipers Energy systems tools are used to cut tissues or seal vesselsElectrosurgery is a modern technology that uses high frequency electrical current to cut or coagulate blood. Argon plasma coagulation involves the application of gas discharges in argon. Ultrasound surgery uses high frequency and high energy sound waves to target and destroy tissue. LigaSure fuses vessels up to 7mm in diameter in an efficient manner. Terminology The expression surgical instrumentation is somewhat interchangeably used with surgical instruments, but its meaning in medical jargon is the activity of providing assistance to a surgeon with the proper handling of surgical instruments during an operation, by a specialized professional, usually a surgical technologist or sometimes a nurse or radiographer.An important relative distinction regarding surgical instruments is the amount of bodily disruption or tissue trauma that their use might cause the patient. Terms relating to this issue are atraumatic and minimally invasive. See also Instruments used in general surgery Medical instruments and implants Gallery References External links Edgar R. McGuire Historical Medical Instrument Collection from the University at Buffalo Libraries Bibliography Wells, MP, Bradley, M: Surgical Instruments A Pocket Guide. W.B. Saunders, 1998.

Occipital neuralgia

Occipital neuralgia (ON) is a painful condition affecting the posterior head in the distributions of the greater occipital nerve (GON), lesser occipital nerve (LON), third occipital nerve (TON), or a combination of the three. It is paroxysmal, lasting from seconds to minutes, and often consists of lancinating pain that directly results from the pathology of one of these nerves. It is paramount that physicians understand the differential diagnosis for this condition and specific diagnostic criteria. There are multiple treatment modalities, several of which have well-established efficacy in treating this condition. Signs and symptoms Patients presenting with a headache originating at the posterior skull base should be evaluated for ON. This condition typically presents as a paroxysmal, lancinating or stabbing pain lasting from seconds to minutes, and therefore a continuous, aching pain likely indicates a different diagnosis. Bilateral symptoms are present in one-third of cases. Causes Occipital neuralgia is caused by damage to the occipital nerves, which can arise from trauma (usually concussive or cervical), physical stress on the nerve, repetitive neck contraction, flexion or extension, and/or as a result of medical complications (such as osteochondroma, a benign bone tumour). A rare cause is a cerebrospinal fluid leak. Rarely, occipital neuralgia may be a symptom of metastasis of certain cancers to the spine. Among other cranial neuropathies, occipital neuralgia is also known to occur in patients with multiple sclerosis. Differential diagnosis The conditions most easily mistaken with ON for other headache and facial pain disorders include migraine, cluster headache, tension headache, and hemicrania continua. Mechanical neck pain from an upper disc, facet, or musculoligamentous sources may refer to the occiput, but is not classically lancinating or otherwise neuropathic and should not be confused with ON. A crucial step in differentiating ON from other disorders is relief with an occipital nerve block. Epidemiology In one study investigating the incidence of facial pain in a Dutch population, ON comprised 8.3% of facial pain cases. The total incidence of ON was 3.2 per 100,000 people, with a mean age of diagnosis of 54.1 years. Treatment There are multiple treatment options for ON. The most conservative treatments, such as immobilization of the neck by the cervical collar, physiotherapy, and cryotherapy have not been shown to perform better than placebo. Non-steroidal anti-inflammatory drugs, tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and anticonvulsants may help to alleviate symptoms. Following diagnostic nerve blocks, therapeutic blocks may be attempted. Typically, a steroid is added to the local anesthetic with variable results. Botulinum Toxin A injection has emerged as a treatment with a conceptually lower side effect profile than many other techniques described here, with most recent trials demonstrating 50% or more improvement.It remains a common practice to utilize a landmark-only approach when performing greater and lesser occipital nerve blocks. For blockade of both nerves, medication is infiltrated along the nuchal ridge. This technique, while easy to perform and relatively safe if done correctly, may not be particularly accurate and as a result, could theoretically increase the risk of a false-positive result. To improve accuracy, ultrasound-guided techniques were developed. The original ultrasound-guided technique for injection of the GON was described by Greher and colleagues in 2010; it targets the nerve as it courses superficial to the obliquus capitis inferior muscle at the C1-C2 level.There are several advanced interventional procedures in clinical use: Pulsed or thermal radiofrequency ablation (RFA) may be considered for longer-lasting relief after a local anesthetic blockade confirms the diagnosis. Thermal RFA aimed at destroying the nerve architecture can render long-term analgesia but also comes with the potential risks of hypesthesia, dysesthesia, anesthesia dolorosa, and painful neuroma formation. Chemical neurolysis with alcohol or phenol carries the same risks as thermal RFA. There is no such risk with pulsed RF, however, some question its efficacy as compared to other procedures. Neuromodulation of the occipital nerve(s) involves the placement of nerve stimulator leads in a horizontal or oblique orientation at the base of the skull across where the greater occipital nerve emerges. Patients should be trialed with temporary leads first, and greater than 50% pain relief for several days is considered a successful trial after which permanent implantation may be considered. Risks include surgical site infection and lead or generator displacement or fracture after the operation. Ultrasound-guided percutaneous cryoablation of the GON is sometimes performed. At the correct temperature, there should be stunning but not permanent damage of the nerve, but at temperatures below negative 70 degrees Celsius, nerve injury is possible. Most recently in the literature, a 2018 article by Kastler and colleagues described 7 patients who underwent cryoneurolysis in a non-blinded fashion to good effect, but the follow-up was limited to 3 months. Surgical decompression is often considered to be the last resort. In one study of 11 patients, only two patients did not experience significant pain relief postoperatively and mean pain episodes per month decreased from 17.1 to 4.1, with mean pain intensity scores also decreasing from 7.18 to 1.73. Resection of part of the obliquus capitis inferior muscle has shown success in patients who have an exacerbation of their pain with flexion of the cervical spine. Another popular surgical technique is C2 gangliotomy, even though patients are left with several days of intermittent nausea and dizziness. As with any large nerve resection, there is a theoretical risk of developing a deafferentation syndrome, though arguably the risk is lower if the resection is pre-ganglionic. References External links Occipital Neuralgia - National Institute of Neurological Disorders and Stroke