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You are an assistant in medical learning. Your role is to clarify medical terminology, ensuring the information is both accurate and accessible.

I'm not familiar with the medical term 'Potassium iodide.' Could you provide some insights?

Potassium iodide is a chemical compound, medication, and dietary supplement. It is a medication used for treating hyperthyroidism, in radiation emergencies, and for protecting the thyroid gland when certain types of radiopharmaceuticals are used. In the third world it is also used for treating skin sporotrichosis and phycomycosis. It is a supplement used by people with low dietary intake of iodine. It is administered orally.Common side effects include vomiting, diarrhea, abdominal pain, rash, and swelling of the salivary glands. Other side effects include allergic reactions, headache, goitre, and depression. While use during pregnancy may harm the baby, its use is still recommended in radiation emergencies. Potassium iodide has the chemical formula KI. Commercially it is made by mixing potassium hydroxide with iodine.Potassium iodide has been used medically since at least 1820. It is on the World Health Organizations List of Essential Medicines. Potassium iodide is available as a generic medication and over the counter. Potassium iodide is also used for the iodization of salt. Medical uses Dietary supplement Potassium-iodide is a nutritional-supplement in animal feeds and also in the human diet. In humans it is the most common additive used for "iodizing" table salt (a public health measure to prevent iodine deficiency in populations that get little seafood). The oxidation of iodide causes slow loss of iodine content from iodised salts that are exposed to excess air. The alkali metal iodide salt, over time and exposure to excess oxygen and carbon dioxide, slowly oxidizes to metal carbonate and elemental iodine, which then evaporates. Potassium iodate (KIO3) is used to iodize some salts so that the iodine is not lost by oxidation. Dextrose or sodium thiosulfate are often added to iodized table salt to stabilize potassium iodide thus reducing loss of the volatile chemical. Thyroid protection Thyroid iodine uptake blockade with potassium iodide is used in nuclear medicine scintigraphy and therapy with some radioiodinated compounds that are not targeted to the thyroid, such as iobenguane (MIBG), which is used to image or treat neural tissue tumors, or iodinated fibrinogen, which is used in fibrinogen scans to investigate clotting. These compounds contain iodine, but not in the iodide form. However, since they may be ultimately metabolized or break down to radioactive iodide, it is common to administer non-radioactive potassium iodide to ensure that iodide from these radiopharmaceuticals is not sequestered by the normal affinity of the thyroid for iodide. U.S. Food and Drug Administration-approved dosing of potassium iodide for this purpose with iobenguane, is as follows (per 24 hours): infants less than 1 month old, 16 mg; children 1 month to 3 years, 32 mg; children 3 years to 18 years, 65 mg; adults 130 mg. However, some sources recommend alternative dosing regimens.Not all sources are in agreement on the necessary duration of thyroid blockade, although agreement appears to have been reached about the necessity of blockade for both scintigraphic and therapeutic applications of iobenguane. Commercially available iobenguane is labeled with iodine-123, and product labeling recommends administration of potassium iodide 1 hour prior to administration of the radiopharmaceutical for all age groups, while the European Association of Nuclear Medicine recommends (for iobenguane labeled with either isotope), that potassium iodide administration begin one day prior to radiopharmaceutical administration, and continue until the day following the injection, with the exception of new-borns, who do not require potassium iodide doses following radiopharmaceutical injection.Product labeling for diagnostic iodine-131 iobenguane recommends potassium iodide administration one day before injection and continuing 5 to 7 days following administration, in keeping with the much longer half-life of this isotope and its greater danger to the thyroid. Iodine-131 iobenguane used for therapeutic purposes requires a different pre-medication duration, beginning 24–48 hours prior to iobenguane injection and continuing 10–15 days following injection. Nuclear accidents In 1982, the U.S. Food and Drug Administration approved potassium iodide to protect thyroid glands from radioactive iodine involving accidents or fission emergencies. In an accidental event or attack on a nuclear power plant, or in nuclear bomb fallout, volatile fission product radionuclides may be released. Of these products, 131I (Iodine-131) is one of the most common and is particularly dangerous to the thyroid gland because it may lead to thyroid cancer. By saturating the body with a source of stable iodide prior to exposure, inhaled or ingested 131I tends to be excreted, which prevents radioiodine uptake by the thyroid. According to one 2000 study "KI administered up to 48 h before 131I exposure can almost completely block thyroid uptake and therefore greatly reduce the thyroid absorbed dose. However, KI administration 96 h or more before 131I exposure has no significant protective effect. In contrast, KI administration after exposure to radioiodine induces a smaller and rapidly decreasing blockade effect." For optimal prevention, KI must be dosed daily until a risk of significant exposure to radioiodine by either inhalation or ingestion no longer exists.Emergency 130 milligrams potassium iodide doses provide 100 mg iodide (the other 30 mg is the potassium in the compound), which is roughly 700 times larger than the normal nutritional need (see recommended dietary allowance) for iodine, which is 150 micrograms (0.15 mg) of iodine (as iodide) per day for an adult. A typical tablet weighs 160 mg, with 130 mg of potassium iodide and 30 mg of excipients, such as binding agents. Potassium iodide cannot protect against any other mechanisms of radiation poisoning, nor can it provide any degree of protection against dirty bombs that produce radionuclides other than those of iodine. The potassium iodide in iodized salt is insufficient for this use. A likely lethal dose of salt (more than a kilogram) would be needed to equal the potassium iodide in one tablet.The World Health Organization does not recommend KI prophylaxis for adults over 40 years, unless the radiation dose from inhaled radioiodine is expected to threaten thyroid function, because the KI side effects increase with age and may exceed the KI protective effects; "...unless doses to the thyroid from inhalation rise to levels threatening thyroid function, that is of the order of about 5 Gy. Such radiation doses will not occur far away from an accident site."The U.S. Department of Health and Human Services restated these two years later as "The downward KI (potassium iodide) dose adjustment by age group, based on body size considerations, adheres to the principle of minimum effective dose. The recommended standard (daily) dose of KI for all school-age children is the same (65 mg). However, adolescents approaching adult size (i.e., >70 kg [154 lbs]) should receive the full adult dose (130 mg) for maximal block of thyroid radioiodine uptake. Neonates ideally should receive the lowest dose (16 mg) of KI."SSKI (i.e., the "saturated solution of KI" rather than tablets) may be used in radioiodine-contamination emergencies (i.e., nuclear accidents) to "block" the thyroids uptake of radioiodine, at a dose of two drops of SSKI per day for an adult. This is not the same as blocking the thyroids release of thyroid hormone, for which the adult dose is different (and is actually higher by a factor of 7 or 8), and for which KI anti-radiation pills (not a common medical treatment form of KI) are not usually available in pharmacies, or normally used in hospitals, or by physicians. Although the two forms of potassium iodide are completely interchangeable, normally in practice the SSKI solution, which is the historical medical form of high dose iodine, is generally used for all medical purposes save for radioiodine prophylaxis. For protection of the thyroid against radioiodine (iodine-131) contamination, the convenient standard 130 mg KI pill is used, if available. As noted, the equivalent two drops of SSKI (equaling the dose of one KI pill) may be used for this purpose, if the pills are not available. Side effects There is reason for caution with prescribing the ingestion of high doses of potassium iodide and iodate, because their unnecessary use can cause conditions such as the Jod-Basedow phenomena, trigger and/or worsen hyperthyroidism and hypothyroidism, and then cause temporary or even permanent thyroid conditions. It can also cause sialadenitis (an inflammation of the salivary gland), gastrointestinal disturbances, and rashes. Potassium iodide is also not recommended for people with dermatitis herpetiformis and hypocomplementemic vasculitis – conditions that are linked to a risk of iodine sensitivity.There have been some reports of potassium iodide treatment causing swelling of the parotid gland (one of the three glands that secrete saliva), due to its stimulatory effects on saliva production.A saturated solution of KI (SSKI) is typically given orally in adult doses several times a day (5 drops of SSKI assumed to be 1⁄3 mL) for thyroid blockade (to prevent the thyroid from excreting thyroid hormone) and occasionally this dose is also used, when iodide is used as an expectorant (the total dose is about one gram KI per day for an adult). The anti-radioiodine doses used for 131I uptake blockade are lower, and range downward from 100 mg a day for an adult, to less than this for children (see table). All of these doses should be compared with the far lower dose of iodine needed in normal nutrition, which is only 150 μg per day (150 micrograms, not milligrams). At maximal doses, and sometimes at much lower doses, side effects of iodide used for medical reasons, in doses of 1000 times the normal nutritional need, may include: acne, loss of appetite, or upset stomach (especially during the first several days, as the body adjusts to the medication). More severe side effects that require notification of a physician are: fever, weakness, unusual tiredness, swelling in the neck or throat, mouth sores, skin rash, nausea, vomiting, stomach pains, irregular heartbeat, numbness or tingling of the hands or feet, or a metallic taste in the mouth.In the event of a radioiodine release the ingestion of prophylaxis potassium iodide, if available, or even iodate, would rightly take precedence over perchlorate administration, and would be the first line of defence in protecting the population from a radioiodine release. However, in the event of a radioiodine release too massive and widespread to be controlled by the limited stock of iodide and iodate prophylaxis drugs, then the addition of perchlorate ions to the water supply, or distribution of perchlorate tablets would serve as a cheap, efficacious, second line of defense against carcinogenic radioiodine bioaccumulation. The ingestion of goitrogen drugs is, much like potassium iodide also not without its dangers, such as hypothyroidism. In all these cases however, despite the risks, the prophylaxis benefits of intervention with iodide, iodate or perchlorate outweigh the serious cancer risk from radioiodine bioaccumulation in regions where radioiodine has sufficiently contaminated the environment. Potassium iodide in its raw form is a mild irritant and should be handled with gloves. Chronic overexposure can have adverse effects on the thyroid. Potassium iodide is a possible teratogen. Industrial uses KI is used with silver nitrate to make silver iodide (AgI), an important chemical in film photography. KI is a component in some disinfectants and hair treatment chemicals. KI is also used as a fluorescence quenching agent in biomedical research, an application that takes advantage of collisional quenching of fluorescent substances by the iodide ion. However, for several fluorophores addition of KI in μM-mM concentrations results in increase of fluorescence intensity, and iodide acts as fluorescence enhancer.Potassium iodide is a component in the electrolyte of dye sensitised solar cells (DSSC) along with iodine. Potassium iodide finds its most important applications in organic synthesis mainly in the preparation of aryl iodides in the Sandmeyer reaction, starting from aryl amines. Aryl iodides are in turn used to attach aryl groups to other organics by nucleophilic substitution, with iodide ion as the leaving group. Chemistry Potassium iodide is an ionic compound which is made of the following ions: K+I−. It crystallises in the sodium chloride structure. It is produced industrially by treating KOH with iodine.It is a white salt, which is the most commercially significant iodide compound, with approximately 37,000 tons produced in 1985. It absorbs water less readily than sodium iodide, making it easier to work with. Aged and impure samples are yellow because of the slow oxidation of the salt to potassium carbonate and elemental iodine. 4 KI + 2 CO 2 + O 2 ⟶ 2 K 2 CO 3 + 2 I 2 {\displaystyle {\ce {4 KI + 2 CO2 + O2 -> 2 K2CO3 + 2 I2}}} Inorganic chemistry Since the iodide ion is a mild reducing agent, I− is easily oxidised to iodine (I2) by powerful oxidising agents such as chlorine: 2 KI ( aq ) + Cl 2 ( aq ) ⟶ 2 KCl ( aq ) + I 2 ( aq ) {\displaystyle {\ce {2 KI_{(aq)}{}+ Cl2_{(aq)}-> 2 KCl_{(aq)}{}+ I2_{(aq)}}}} This reaction is employed in the isolation of iodine from natural sources. Air will oxidize iodide, as evidenced by the observation of a purple extract when aged samples of KI are rinsed with dichloromethane. As formed under acidic conditions, hydriodic acid (HI) is a stronger reducing agent.Like other iodide salts, KI forms triiodide (I−3) when combined with elemental iodine. KI ( aq ) + I 2 ( s ) ⟶ KI 3 ( aq ) {\displaystyle {\ce {KI_{(aq)}{}+ I2_{(s)}-> KI3_{(aq)}}}} Unlike I2, I−3 salts can be highly water-soluble. Through this reaction, iodine is used in redox titrations. Aqueous KI3, "Lugols solution", is used as a disinfectant and as an etchant for gold surfaces. Potassium iodide and silver nitrate are used to make silver(I) iodide, which is used for high speed photographic film and for cloud seeding: KI ( aq ) + 9 AgNO 3 ( aq ) ⟶ AgI ( s ) + KNO 3 ( aq ) {\displaystyle {\ce {KI_{(aq)}{}+ 9AgNO3_{(aq)}-> AgI_{(s)}{}+ KNO3_{(aq)}}}} Organic chemistry KI serves as a source of iodide in organic synthesis. A useful application is in the preparation of aryl iodides from arenediazonium salts. KI, acting as a source of iodide, may also act as a nucleophilic catalyst for the alkylation of alkyl chlorides, bromides, or mesylates. History Potassium iodide has been used medically since at least 1820. Some of the earliest uses included for syphilis. Chernobyl Potassium iodides (KI) value as a radiation protective (thyroid blocking) agent was demonstrated following the Chernobyl nuclear reactor disaster in April, 1986. A saturated solution of potassium iodide (SSKI) was administered to 10.5 million children and 7 million adults in Poland as a preventative measure against accumulation of radioactive 131I in the thyroid gland. Reports differ concerning whether people in the areas immediately surrounding Chernobyl itself were given the supplement. However the US Nuclear Regulatory Commission (NRC) reported, "thousands of measurements of I-131 (radioactive iodine) activity...suggest that the observed levels were lower than would have been expected had this prophylactic measure not been taken. The use of KI...was credited with permissible iodine content in 97% of the evacuees tested."With the passage of time, people living in irradiated areas where KI was not available have developed thyroid cancer at epidemic levels, which is why the US Food and Drug Administration (FDA) reported "The data clearly demonstrate the risks of thyroid radiation... KI can be used [to] provide safe and effective protection against thyroid cancer caused by irradiation."Chernobyl also demonstrated that the need to protect the thyroid from radiation was greater than expected. Within ten years of the accident, it became clear that thyroid damage caused by released radioactive iodine was virtually the only adverse health effect that could be measured. As reported by the NRC, studies after the accident showed that "As of 1996, except for thyroid cancer, there has been no confirmed increase in the rates of other cancers, including leukemia, among the... public, that have been attributed to releases from the accident."But equally important to the question of KI is the fact that radioactivity releases are not "local" events. Researchers at the World Health Organization accurately located and counted the residents with cancer from Chernobyl and were startled to find that "the increase in incidence [of thyroid cancer] has been documented up to 500 km from the accident site... significant doses from radioactive iodine can occur hundreds of kilometers from the site, beyond emergency planning zones." Consequently, far more people than anticipated were affected by the radiation, which caused the United Nations to report in 2002 that "The number of people with thyroid cancer... has exceeded expectations. Over 11,000 cases have already been reported." Nagasaki These findings were consistent with studies of the effects of previous radioactivity releases. In 1945, millions of Japanese were exposed to radiation from nuclear weapons, and the effects can still be measured. Today, nearly half (44.8%) the survivors of Nagasaki studied have identifiable thyroid disease, with an editorial in The Journal of the American Medical Association reporting "it is remarkable that a biological effect from a single brief environmental exposure nearly 60 years in the past is still present and can be detected." Nuclear weapons testing The development of thyroid cancer among residents in the North Pacific from radioactive fallout following the United States nuclear weapons testing in the 1950s (on islands nearly 200 miles downwind of the tests) were instrumental in the 1978 decision by the FDA to issue a request for the availability of KI for thyroid protection in the event of a release from a commercial nuclear power plant or weapons-related nuclear incident. Noting that KIs effectiveness was "virtually complete" and finding that iodine in the form of KI was substantially superior to other forms including iodate (KIO3) in terms of safety, effectiveness, lack of side effects, and speed of onset, the FDA invited manufacturers to submit applications to produce and market KI. Fukushima It was reported on March 16, 2011, that potassium iodide tablets were given preventively to U.S. Naval air crew members flying within 70 nautical miles of the Fukushima Daiichi Nuclear Power Plant damaged in the earthquake (8.9/9.0 magnitude) and ensuing tsunami on March 11, 2011. The measures were seen as precautions, and the Pentagon said no U.S. forces have shown signs of radiation poisoning. By March 20, the US Navy instructed personnel coming within 100 miles of the reactor to take the pills. The Netherlands In the Netherlands, the central storage of iodine-pills is located in Zoetermeer, near The Hague. In 2017, the Dutch government distributed pills to hundreds of thousands of residents who lived within a certain distance of nuclear power plants and met some other criteria. Belgium By 2020, potassium iodide tablets are made available free of charge for all residents in all pharmacies throughout the country. Formulations Three companies (Anbex, Inc., Fleming Co, and Recipharm of Sweden) have met the strict FDA requirements for manufacturing and testing of KI, and they offer products (IOSAT, ThyroShield, and ThyroSafe, respectively) which are available for purchase. In 2012, Fleming Co. sold all its product rights and manufacturing facility to other companies and no longer exists. ThyroShield is currently not in production. The Swedish manufacturing facility for Thyrosafe, a half-strength potassium iodide tablet for thyroid protection from radiation, was mentioned on the secret US 2008 Critical Foreign Dependencies Initiative leaked by Wikileaks in 2010.Tablets of potassium iodide are supplied for emergency purposes related to blockade of radioiodine uptake, a common form of radiation poisoning due to environmental contamination by the short-lived fission product 131I. Potassium iodide may also be administered pharmaceutically for thyroid storm. For reasons noted above, therapeutic drops of SSKI, or 130 mg tablets of KI as used for nuclear fission accidents, are not used as nutritional supplements, since an SSKI drop or nuclear-emergency tablet provides 300 to 700 times more iodine than the daily adult nutritional requirement. Dedicated nutritional iodide tablets containing 0.15 mg (150 micrograms (μg)) of iodide, from KI or from various other sources (such as kelp extract) are marketed as supplements, but they are not to be confused with the much higher pharmaceutical dose preparations. Potassium iodide can be conveniently prepared in a saturated solution, abbreviated SSKI. This method of delivering potassium iodide doesnt require a method to weigh out the potassium iodide, thus allowing it to be used in an emergency situation. KI crystals are simply added to water until no more KI will dissolve and instead sits at the bottom of the container. With pure water, the concentration of KI in the solution depends only on the temperature. Potassium iodide is highly soluble in water thus SSKI is a concentrated source of KI. At 20 degrees Celsius the solubility of KI is 140-148 grams per 100 grams of water. Because the volumes of KI and water are approximately additive, the resulting SSKI solution will contain about 1.00 gram (1000 mg) KI per milliliter (mL) of solution. This is 100% weight/volume (note units of mass concentration) of KI (one gram KI per mL solution), which is possible because SSKI is significantly more dense than pure water—about 1.67 g/mL. Because KI is about 76.4% iodide by weight, SSKI contains about 764 mg iodide per mL. This concentration of iodide allows the calculation of the iodide dose per drop, if one knows the number of drops per milliliter. For SSKI, a solution more viscous than water, there are assumed to be 15 drops per mL; the iodide dose is therefore approximately 51 mg per drop. It is conventionally rounded to 50 mg per drop. The term SSKI is also used, especially by pharmacists, to refer to a U.S.P. pre-prepared solution formula, made by adding KI to water to prepare a solution containing 1000 mg KI per mL solution (100% wt/volume KI solution), to closely approximate the concentration of SSKI made by saturation. This is essentially interchangeable with SSKI made by saturation, and also contains about 50 mg iodide per drop. Saturated solutions of potassium iodide can be an emergency treatment for hyperthyroidism (so-called thyroid storm), as high amounts of iodide temporarily suppress secretion of thyroxine from the thyroid gland. The dose typically begins with a loading dose, then 1⁄3 mL SSKI (5 drops or 250 mg iodine as iodide), three times per day. Iodide solutions made from a few drops of SSKI added to drinks have also been used as expectorants to increase the water content of respiratory secretions and encourage effective coughing. SSKI has been proposed as a topical treatment for sporotrichosis, but no trials have been conducted to determine the efficacy or side effects of such treatment. Potassium iodide has been used for symptomatic treatment of erythema nodosum patients for persistent lesions whose cause remains unknown. It has been used in cases of erythema nodosum associated with Crohns disease. Due to its high potassium content, SSKI is extremely bitter, and if possible it is administered in a sugar cube or small ball of bread. It may also be mixed into much larger volumes of juices. Neither SSKI or KI tablets form nutritional supplements, since the nutritional requirement for iodine is only 150 micrograms (0.15 mg) of iodide per day. Thus, a drop of SSKI provides 50/0.15 = 333 times the daily iodine requirement, and a standard KI tablet provides twice this much. See also Elephant toothpaste References External links "Potassium iodide". Drug Information Portal. U.S. National Library of Medicine. World Health Organizations guidelines for iodine prophylaxis following a nuclear accident

You are a medical knowledge base. Your task is to elucidate medical terminology, offering insights into their meanings, origins, and applications.

I'm seeking clarification on the medical term 'Pulmonary contusion.' Could you explain it?

A pulmonary contusion, also known as lung contusion, is a bruise of the lung, caused by chest trauma. As a result of damage to capillaries, blood and other fluids accumulate in the lung tissue. The excess fluid interferes with gas exchange, potentially leading to inadequate oxygen levels (hypoxia). Unlike pulmonary laceration, another type of lung injury, pulmonary contusion does not involve a cut or tear of the lung tissue. A pulmonary contusion is usually caused directly by blunt trauma but can also result from explosion injuries or a shock wave associated with penetrating trauma. With the use of explosives during World Wars I and II, pulmonary contusion resulting from blasts gained recognition. In the 1960s its occurrence in civilians began to receive wider recognition, in which cases it is usually caused by traffic accidents. The use of seat belts and airbags reduces the risk to vehicle occupants. Diagnosis is made by studying the cause of the injury, physical examination and chest radiography. Typical signs and symptoms include direct effects of the physical trauma, such as chest pain and coughing up blood, as well as signs that the body is not receiving enough oxygen, such as cyanosis. The contusion frequently heals on its own with supportive care. Often nothing more than supplemental oxygen and close monitoring is needed; however, intensive care may be required. For example, if breathing is severely compromised, mechanical ventilation may be necessary. Fluid replacement may be required to ensure adequate blood volume, but fluids are given carefully since fluid overload can worsen pulmonary edema, which may be lethal. The severity ranges from mild to severe: small contusions may have little or no impact on health, yet pulmonary contusion is the most common type of potentially lethal chest trauma. It occurs in 30–75% of severe chest injuries. The risk of death following a pulmonary contusion is between 14 and 40%. Pulmonary contusion is usually accompanied by other injuries. Although associated injuries are often the cause of death, pulmonary contusion is thought to cause death directly in a quarter to half of cases. Children are at especially high risk for the injury because the relative flexibility of their bones prevents the chest wall from absorbing force from an impact, causing it to be transmitted instead to the lung. Pulmonary contusion is associated with complications including pneumonia and acute respiratory distress syndrome, and it can cause long-term respiratory disability. Classification Pulmonary contusion and laceration are injuries to the lung tissue. Pulmonary laceration, in which lung tissue is torn or cut, differs from pulmonary contusion in that the former involves disruption of the macroscopic architecture of the lung, while the latter does not. When lacerations fill with blood, the result is pulmonary hematoma, a collection of blood within the lung tissue. Contusion involves hemorrhage in the alveoli (tiny air-filled sacs responsible for absorbing oxygen), but a hematoma is a discrete clot of blood not interspersed with lung tissue. A collapsed lung can result when the pleural cavity (the space outside the lung) accumulates blood (hemothorax) or air (pneumothorax) or both (hemopneumothorax). These conditions do not inherently involve damage to the lung tissue itself, but they may be associated with it. Injuries to the chest wall are also distinct from but may be associated with lung injuries. Chest wall injuries include rib fractures and flail chest, in which multiple ribs are broken so that a segment of the ribcage is detached from the rest of the chest wall and moves independently. Signs and symptoms Presentation may be subtle; people with mild contusion may have no symptoms at all. However, pulmonary contusion is frequently associated with signs (objective indications) and symptoms (subjective states), including those indicative of the lung injury itself and of accompanying injuries. Because gas exchange is impaired, signs of low blood oxygen saturation, such as low concentrations of oxygen in arterial blood gas and cyanosis (bluish color of the skin and mucous membranes) are commonly associated. Dyspnea (painful breathing or difficulty breathing) is commonly seen, and tolerance for exercise may be lowered. Rapid breathing and a rapid heart rate are other signs. With more severe contusions, breath sounds heard through a stethoscope may be decreased, or rales (an abnormal crackling sound in the chest accompanying breathing) may be present. People with severe contusions may have bronchorrhea (the production of watery sputum). Wheezing and coughing are other signs. Coughing up blood or bloody sputum is present in up to half of cases. Cardiac output (the volume of blood pumped by the heart) may be reduced, and hypotension (low blood pressure) is frequently present. The area of the chest wall near the contusion may be tender or painful due to associated chest wall injury. Signs and symptoms take time to develop, and as many as half of cases are asymptomatic at the initial presentation. The more severe the injury, the more quickly symptoms become apparent. In severe cases, symptoms may occur as quickly as three or four hours after the trauma. Hypoxemia (low oxygen concentration in the arterial blood) typically becomes progressively worse over 24–48 hours after injury. In general, pulmonary contusion tends to worsen slowly over a few days, but it may also cause rapid deterioration or death if untreated. Causes Pulmonary contusion is the most common injury found in blunt chest trauma, occurring in 25–35% of cases. It is usually caused by the rapid deceleration that results when the moving chest strikes a fixed object. About 70% of cases result from motor vehicle collisions, most often when the chest strikes the inside of the car. Falls, assaults, and sports injuries are other causes. Pulmonary contusion can also be caused by explosions; the organs most vulnerable to blast injuries are those that contain gas, such as the lungs. Blast lung is severe pulmonary contusion, bleeding, or edema with damage to alveoli and blood vessels, or a combination of these. This is the primary cause of death among people who initially survive an explosion. Unlike other mechanisms of injury in which pulmonary contusion is often found alongside other injuries, explosions can cause pulmonary contusion without damage to the chest wall.In addition to blunt trauma, penetrating trauma can cause pulmonary contusion. Contusion resulting from penetration by a rapidly moving projectile usually surrounds the path along which the projectile traveled through the tissue. The pressure wave forces tissue out of the way, creating a temporary cavity; the tissue readily moves back into place, but it is damaged. Pulmonary contusions that accompany gun and knife wounds are not usually severe enough to have a major effect on outcome; penetrating trauma causes less widespread lung damage than does blunt trauma. An exception is shotgun wounds, which can seriously damage large areas of lung tissue through a blast injury mechanism. Mechanism The physical processes behind pulmonary contusion are poorly understood. However, it is known that lung tissue can be crushed when the chest wall bends inward on impact. Three other possible mechanisms have been suggested: the inertial effect, the spalling effect, and the implosion effect. In the inertial effect, the lighter alveolar tissue is sheared from the heavier hilar structures, an effect similar to diffuse axonal injury in head injury. It results from the fact that different tissues have different densities, and therefore different rates of acceleration or deceleration. In the spalling effect, lung tissue bursts or is sheared where a shock wave meets the lung tissue, at interfaces between gas and liquid. The alveolar walls form such a gas-liquid interface with the air in the alveoli. The spalling effect occurs in areas with large differences in density; particles of the denser tissue are spalled (thrown) into the less dense particles. The implosion effect occurs when a pressure wave passes through a tissue containing bubbles of gas: the bubbles first implode, then rebound and expand beyond their original volume. The air bubbles cause many tiny explosions, resulting in tissue damage; the overexpansion of gas bubbles stretches and tears alveoli. This effect is thought to occur microscopically when the pressure in the airways increases sharply.Contusion usually occurs on the lung directly under the site of impact, but, as with traumatic brain injury, a contrecoup contusion may occur at the site opposite the impact as well. A blow to the front of the chest may cause contusion on the back of the lungs because a shock wave travels through the chest and hits the curved back of the chest wall; this reflects the energy onto the back of the lungs, concentrating it. (A similar mechanism may occur at the front of the lungs when the back is struck.)The amount of energy transferred to the lung is determined in a large part by the compliance (flexibility) of the chest wall. Childrens chests are more flexible because their ribs are more elastic and there is less ossification of their intercostal cartilage. Therefore, their chest walls bend, absorbing less of the force and transmitting more of it to the underlying organs. An adults more bony chest wall absorbs more of the force itself rather than transmitting it. Thus children commonly get pulmonary contusions without fractures overlying them, while elderly people are more likely to develop fractures than contusions. One study found that pulmonary contusions were accompanied by fractures 62% of the time in children and 80% of the time in adults. Pathophysiology Pulmonary contusion results in bleeding and fluid leakage into lung tissue, which can become stiffened and lose its normal elasticity. The water content of the lung increases over the first 72 hours after injury, potentially leading to frank pulmonary edema in more serious cases. As a result of these and other pathological processes, pulmonary contusion progresses over time and can cause hypoxia (insufficient oxygen). Bleeding and edema In contusions, torn capillaries leak fluid into the tissues around them. The membrane between alveoli and capillaries is torn; damage to this capillary–alveolar membrane and small blood vessels causes blood and fluids to leak into the alveoli and the interstitial space (the space surrounding cells) of the lung. With more severe trauma, there is a greater amount of edema, bleeding, and tearing of the alveoli. Pulmonary contusion is characterized by microhemorrhages (tiny bleeds) that occur when the alveoli are traumatically separated from airway structures and blood vessels. Blood initially collects in the interstitial space, and then edema occurs by an hour or two after injury. An area of bleeding in the contused lung is commonly surrounded by an area of edema. In normal gas exchange, carbon dioxide diffuses across the endothelium of the capillaries, the interstitial space, and across the alveolar epithelium; oxygen diffuses in the other direction. Fluid accumulation interferes with gas exchange, and can cause the alveoli to fill with proteins and collapse due to edema and bleeding. The larger the area of the injury, the more severe respiratory compromise will be. Consolidation and collapse Pulmonary contusion can cause parts of the lung to consolidate, alveoli to collapse, and atelectasis (partial or total lung collapse) to occur. Consolidation occurs when the parts of the lung that are normally filled with air fill with material from the pathological condition, such as blood. Over a period of hours after the injury, the alveoli in the injured area thicken and may become consolidated. A decrease in the amount of surfactant produced also contributes to the collapse and consolidation of alveoli; inactivation of surfactant increases their surface tension. Reduced production of surfactant can also occur in surrounding tissue that was not originally injured.Inflammation of the lungs, which can result when components of blood enter the tissue due to contusion, can also cause parts of the lung to collapse. Macrophages, neutrophils, and other inflammatory cells and blood components can enter the lung tissue and release factors that lead to inflammation, increasing the likelihood of respiratory failure. In response to inflammation, excess mucus is produced, potentially plugging parts of the lung and leading to their collapse. Even when only one side of the chest is injured, inflammation may also affect the other lung. Uninjured lung tissue may develop edema, thickening of the septa of the alveoli, and other changes. If this inflammation is severe enough, it can lead to dysfunction of the lungs like that seen in acute respiratory distress syndrome. Ventilation/perfusion mismatch Normally, the ratio of ventilation to perfusion is about one-to-one; the volume of air entering the alveoli (ventilation) is about equal to that of blood in the capillaries around them (perfusion). This ratio is reduced in pulmonary contusion; fluid-filled alveoli cannot fill with air, oxygen does not fully saturate the hemoglobin, and the blood leaves the lung without being fully oxygenated. Insufficient inflation of the lungs, which can result from inadequate mechanical ventilation or an associated injury such as flail chest, can also contribute to the ventilation/perfusion mismatch. As the mismatch between ventilation and perfusion grows, blood oxygen saturation is reduced. Pulmonary hypoxic vasoconstriction, in which blood vessels near the hypoxic alveoli constrict (narrow their diameter) in response to the lowered oxygen levels, can occur in pulmonary contusion. The vascular resistance increases in the contused part of the lung, leading to a decrease in the amount of blood that flows into it, directing blood to better-ventilated areas. Although reducing blood flow to the unventilated alveoli is a way to compensate for the fact that blood passing unventilated alveoli is not oxygenated, the oxygenation of the blood remains lower than normal. If it is severe enough, the hypoxemia resulting from fluid in the alveoli cannot be corrected just by giving supplemental oxygen; this problem is the cause of a large portion of the fatalities that result from trauma. Diagnosis To diagnose pulmonary contusion, health professionals use clues from a physical examination, information about the event that caused the injury, and radiography. Laboratory findings may also be used; for example, arterial blood gasses may show insufficient oxygen and excessive carbon dioxide even in someone receiving supplemental oxygen. However, blood gas levels may show no abnormality early in the course of pulmonary contusion. X-ray Chest X-ray is the most common method used for diagnosis, and may be used to confirm a diagnosis already made using clinical signs. Consolidated areas appear white on an X-ray film. Contusion is not typically restricted by the anatomical boundaries of the lobes or segments of the lung. The X-ray appearance of pulmonary contusion is similar to that of aspiration, and the presence of hemothorax or pneumothorax may obscure the contusion on a radiograph. Signs of contusion that progress after 48 hours post-injury are likely to be actually due to aspiration, pneumonia, or ARDS.Although chest radiography is an important part of the diagnosis, it is often not sensitive enough to detect the condition early after the injury. In a third of cases, pulmonary contusion is not visible on the first chest radiograph performed. It takes an average of six hours for the characteristic white regions to show up on a chest X-ray, and the contusion may not become apparent for 48 hours. When a pulmonary contusion is apparent in an X-ray, it suggests that the trauma to the chest was severe and that a CT scan might reveal other injuries that were missed with X-ray. Computed tomography Computed tomography (CT scanning) is a more sensitive test for pulmonary contusion, and it can identify abdominal, chest, or other injuries that accompany the contusion. In one study, chest X-ray detected pulmonary contusions in 16.3% of people with serious blunt trauma, while CT detected them in 31.2% of the same people. Unlike X-ray, CT scanning can detect the contusion almost immediately after the injury. However, in both X-ray and CT a contusion may become more visible over the first 24–48 hours after trauma as bleeding and edema into lung tissues progress. CT scanning also helps determine the size of a contusion, which is useful in determining whether a patient needs mechanical ventilation; a larger volume of contused lung on CT scan is associated with an increased likelihood that ventilation will be needed. CT scans also help differentiate between contusion and pulmonary hematoma, which may be difficult to tell apart otherwise. However, pulmonary contusions that are visible on CT but not chest X-ray are usually not severe enough to affect outcome or treatment. Ultrasound Pulmonary ultrasound, performed at the bedside or on the accident scene, is being explored as a diagnosis for pulmonary contusion. Its use is still not widespread, being limited to facilities which are comfortable with its use for other applications, like pneumothorax, airway management, and hemothorax. Accuracy has been found to be comparable to CT scanning. Prevention Prevention of pulmonary contusion is similar to that of other chest trauma. Airbags in combination with seat belts can protect vehicle occupants by preventing the chest from striking the interior of the vehicle during a collision, and by distributing forces involved in the crash more evenly across the body. However, in rare cases, an airbag causes pulmonary contusion in a person who is not properly positioned when it deploys. Child restraints such as carseats protect children in vehicle collisions from pulmonary contusion. Equipment exists for use in some sports to prevent chest and lung injury; for example, in softball the catcher is equipped with a chest protector. Athletes who do not wear such equipment, such as basketball players, can be trained to protect their chests from impacts. Protective garments can also prevent pulmonary contusion in explosions. Although traditional body armor made from rigid plates or other heavy materials protects from projectiles generated by a blast, it does not protect against pulmonary contusion, because it does not prevent the blasts shock wave from being transferred to the lung. Special body armor has been designed for military personnel at high risk for blast injuries; these garments can prevent a shock wave from being propagated across the chest wall to the lung, and thus protect wearers from blast lung injuries. These garments alternate layers of materials with high and low acoustic impedance (the product of a materials density and a waves velocity through it) in order to "decouple" the blast wave, preventing its propagation into the tissues. Treatment No treatment is known to speed the healing of a pulmonary contusion; the main care is supportive. Attempts are made to discover injuries accompanying the contusion, to prevent additional injury, and to provide supportive care while waiting for the contusion to heal. Monitoring, including keeping track of fluid balance, respiratory function, and oxygen saturation using pulse oximetry is also required as the patients condition may progressively worsen. Monitoring for complications such as pneumonia and acute respiratory distress syndrome is of critical importance. Treatment aims to prevent respiratory failure and to ensure adequate blood oxygenation. Supplemental oxygen can be given and it may be warmed and humidified. When the contusion does not respond to other treatments, extracorporeal membranous oxygenation may be used, pumping blood from the body into a machine that oxygenates it and removes carbon dioxide prior to pumping it back in. Ventilation Positive pressure ventilation, in which air is forced into the lungs, is needed when oxygenation is significantly impaired. Noninvasive positive pressure ventilation including continuous positive airway pressure (CPAP) and bi-level positive airway pressure (BiPAP), may be used to improve oxygenation and treat atelectasis: air is blown into the airways at a prescribed pressure via a face mask. Noninvasive ventilation has advantages over invasive methods because it does not carry the risk of infection that intubation does, and it allows normal coughing, swallowing, and speech. However, the technique may cause complications; it may force air into the stomach or cause aspiration of stomach contents, especially when level of consciousness is decreased.People with signs of inadequate respiration or oxygenation may need to be intubated and mechanically ventilated. Mechanical ventilation aims to reduce pulmonary edema and increase oxygenation. Ventilation can reopen collapsed alveoli, but it is harmful for them to be repeatedly opened, and positive pressure ventilation can also damage the lung by overinflating it. Intubation is normally reserved for when respiratory problems occur, but most significant contusions do require intubation, and it may be done early in anticipation of this need. People with pulmonary contusion who are especially likely to need ventilation include those with prior severe lung disease or kidney problems; the elderly; those with a lowered level of consciousness; those with low blood oxygen or high carbon dioxide levels; and those who will undergo operations with anesthesia. Larger contusions have been correlated with a need for ventilation for longer periods of time.Pulmonary contusion or its complications such as acute respiratory distress syndrome may cause lungs to lose compliance (stiffen), so higher pressures may be needed to give normal amounts of air and oxygenate the blood adequately. Positive end-expiratory pressure (PEEP), which delivers air at a given pressure at the end of the expiratory cycle, can reduce edema and keep alveoli from collapsing. PEEP is considered necessary with mechanical ventilation; however, if the pressure is too great it can expand the size of the contusion and injure the lung. When the compliance of the injured lung differs significantly from that of the uninjured one, the lungs can be ventilated independently with two ventilators in order to deliver air at different pressures; this helps avoid injury from overinflation while providing adequate ventilation. Fluid therapy The administration of fluid therapy in individuals with pulmonary contusion is controversial. Excessive fluid in the circulatory system (hypervolemia) can worsen hypoxia because it can cause fluid leakage from injured capillaries (pulmonary edema), which are more permeable than normal. However, low blood volume (hypovolemia) resulting from insufficient fluid has an even worse impact, potentially causing hypovolemic shock; for people who have lost large amounts of blood, fluid resuscitation is necessary. A lot of the evidence supporting the idea that fluids should be withheld from people with pulmonary contusion came from animal studies, not clinical trials with humans; human studies have had conflicting findings on whether fluid resuscitation worsens the condition. Current recommendations suggest giving enough fluid to ensure sufficient blood flow but not giving any more fluid than necessary. For people who do require large amounts of intravenous fluid, a catheter may be placed in the pulmonary artery to measure the pressure within it. Measuring pulmonary artery pressure allows the clinician to give enough fluids to prevent shock without exacerbating edema. Diuretics, drugs that increase urine output to reduce excessive fluid in the system, can be used when fluid overload does occur, as long as there is not a significant risk of shock. Furosemide, a diuretic used in the treatment of pulmonary contusion, also relaxes the smooth muscle in the veins of the lungs, thereby decreasing pulmonary venous resistance and reducing the pressure in the pulmonary capillaries. Supportive care Retaining secretions in the airways can worsen hypoxia and lead to infections. Thus, an important part of treatment is pulmonary toilet, the use of suction, deep breathing, coughing, and other methods to remove material such as mucus and blood from the airways. Chest physical therapy makes use of techniques such as breathing exercises, stimulation of coughing, suctioning, percussion, movement, vibration, and drainage to rid the lungs of secretions, increase oxygenation, and expand collapsed parts of the lungs. People with pulmonary contusion, especially those who do not respond well to other treatments, may be positioned with the uninjured lung lower than the injured one to improve oxygenation. Inadequate pulmonary toilet can result in pneumonia. People who do develop infections are given antibiotics. No studies have yet shown a benefit of using antibiotics as a preventative measure before infection occurs, although some doctors do recommend prophylactic antibiotic use even without scientific evidence of its benefit. However, this can cause the development of antibiotic resistant strains of bacteria, so giving antibiotics without a clear need is normally discouraged. For people who are at especially high risk of developing infections, the sputum can be cultured to test for the presence of infection-causing bacteria; when they are present, antibiotics are used.Pain control is another means to facilitate the elimination of secretions. A chest wall injury can make coughing painful, increasing the likelihood that secretions will accumulate in the airways. Chest injuries also contribute to hypoventilation (inadequate breathing) because the chest wall movement involved in breathing adequately is painful. Insufficient expansion of the chest may lead to atelectasis, further reducing oxygenation of the blood. Analgesics (pain medications) can be given to reduce pain. Injection of anesthetics into nerves in the chest wall, called nerve blockade, is another approach to pain management; this does not depress respiration the way some pain medications can. Prognosis Pulmonary contusion usually resolves itself without causing permanent complications; however it may also have long-term ill effects on respiratory function. Most contusions resolve in five to seven days after the injury. Signs detectable by radiography are usually gone within 10 days after the injury—when they are not, other conditions, such as pneumonia, are the likely cause. Chronic lung disease correlates with the size of the contusion and can interfere with an individuals ability to return to work. Fibrosis of the lungs can occur, resulting in dyspnea (shortness of breath), low blood oxygenation, and reduced functional residual capacity for as long as six years after the injury. As late as four years post-injury, decreased functional residual capacity has been found in most pulmonary contusion patients studied. During the six months after pulmonary contusion, up to 90% of people have difficulty breathing. In some cases, dyspnea persists for an indefinite period. Contusion can also permanently reduce the compliance of the lungs. Complications Pulmonary contusion can result in respiratory failure—about half of such cases occur within a few hours of the initial trauma. Other severe complications, including infections and acute respiratory distress syndrome (ARDS) occur in up to half of cases. Elderly people and those who have heart, lung, or kidney disease prior to the injury are more likely to stay longer in hospital and have complications from the injury. Complications occur in 55% of people with heart or lung disease and 13% of those without. Of people with pulmonary contusion alone, 17% develop ARDS, while 78% of people with at least two additional injuries develop the condition. A larger contusion is associated with an increased risk. In one study, 82% of people with 20% or more of the lung volume affected developed ARDS, while only 22% of people with less than 20% did so.Pneumonia, another potential complication, develops in as many as 20% of people with pulmonary contusion. Contused lungs are less able to remove bacteria than uninjured lungs, predisposing them to infection. Intubation and mechanical ventilation further increase the risk of developing pneumonia; the tube is passed through the nose or mouth into the airways, potentially tracking bacteria from the mouth or sinuses into them. Also, intubation prevents coughing, which would clear bacteria-laden secretions from the airways, and secretions pool near the tubes cuff and allow bacteria to grow. The sooner the endotracheal tube is removed, the lower the risk of pneumonia, but if it is removed too early and has to be put back in, the risk of pneumonia rises. People who are at risk for pulmonary aspiration (e.g. those with lowered level of consciousness due to head injuries) are especially likely to get pneumonia. As with ARDS, the chances of developing pneumonia increase with the size of the contusion. Children and adults have been found to have similar rates of complication with pneumonia and ARDS. Associated injuries A large amount of force is required to cause pulmonary contusion; a person injured with such force is likely to have other types of injuries as well. In fact, pulmonary contusion can be used to gauge the severity of trauma. Up to three quarters of cases are accompanied by other chest injuries, the most common of these being hemothorax and pneumothorax. Flail chest is usually associated with significant pulmonary contusion, and the contusion, rather than the chest wall injury, is often the main cause of respiratory failure in people with these injuries. Other indications of thoracic trauma may be associated, including fracture of the sternum and bruising of the chest wall. Over half of fractures of the scapula are associated with pulmonary contusion. The contusion is frequently found underlying fracture sites. When accompanied by a fracture, it is usually concentrated into a specific location—the contusion is more diffuse when there is no fracture. Pulmonary lacerations may result from the same blunt or penetrating forces that cause contusion. Lacerations can result in pulmonary hematomas; these are reported to develop in 4–11% of pulmonary contusions. Epidemiology Pulmonary contusion is found in 30–75% of severe cases of chest injury, making it the most common serious injury to occur in association with thoracic trauma. Of people who have multiple injuries with an injury severity score of over 15, pulmonary contusion occurs in about 17%. It is difficult to determine the death rate (mortality) because pulmonary contusion rarely occurs by itself. Usually, deaths of people with pulmonary contusion result from other injuries, commonly traumatic brain injury. It is controversial whether pulmonary contusion with flail chest is a major factor in mortality on its own or whether it merely contributes to mortality in people with multiple injuries. The estimated mortality rate of pulmonary contusion ranges from 14 to 40%, depending on the severity of the contusion itself and on associated injuries. When the contusions are small, they do not normally increase the chance of death or poor outcome for people with blunt chest trauma; however, these chances increase with the size of the contusion. One study found that 35% of people with multiple significant injuries including pulmonary contusion die. In another study, 11% of people with pulmonary contusion alone died, while the number rose to 22% in those with additional injuries. Pulmonary contusion is thought to be the direct cause of death in a quarter to a half of people with multiple injuries (polytrauma) who die. An accompanying flail chest increases the morbidity and mortality to more than twice that of pulmonary contusion alone.Pulmonary contusion is the most common cause of death among vehicle occupants involved in accidents, and it is thought to contribute significantly in about a quarter of deaths resulting from vehicle collisions. As vehicle use has increased, so has the number of auto accidents, and with it the number of chest injuries. However an increase in the number of airbags installed in modern cars may be decreasing the incidence of pulmonary contusion. Use of child restraint systems has brought the approximate incidence of pulmonary contusion in children in vehicle accidents from 22% to 10%.Differences in the bodies of children and adults lead to different manifestations of pulmonary contusion and associated injuries; for example, children have less body mass, so the same force is more likely to lead to trauma in multiple body systems. Since their chest walls are more flexible, children are more vulnerable to pulmonary contusion than adults are, and thus suffer from the injury more commonly. Pulmonary contusion has been found in 53% of children with chest injuries requiring hospitalization. Children in forceful impacts suffer twice as many pulmonary contusions as adults with similar injury mechanisms, yet have proportionately fewer rib fractures. The rates of certain types of injury mechanisms differ between children and adults; for example, children are more often hit by cars as pedestrians. Some differences in childrens physiology might be advantageous (for example they are less likely to have other medical conditions), and thus they have been predicted to have a better outcome. However, despite these differences, children with pulmonary contusion have similar mortality rates to adults. History In 1761, the Italian anatomist Giovanni Battista Morgagni was first to describe a lung injury that was not accompanied by injury to the chest wall overlying it. Nonetheless, it was the French military surgeon Guillaume Dupuytren who is thought to have coined the term pulmonary contusion in the 19th century. It still was not until the early 20th century that pulmonary contusion and its clinical significance began to receive wide recognition. With the use of explosives during World War I came many casualties with no external signs of chest injury but with significant bleeding in the lungs. Studies of World War I injuries by D.R. Hooker showed that pulmonary contusion was an important part of the concussive injury that results from explosions.Pulmonary contusion received further attention during World War II, when the bombings of Britain caused blast injuries and associated respiratory problems in both soldiers and civilians. Also during this time, studies with animals placed at varying distances from a blast showed that protective gear could prevent lung injuries. These findings suggested that an impact to the outside of the chest wall was responsible for the internal lesions. In 1945, studies identified a phenomenon termed "wet lung", in which the lungs accumulated fluid and were simultaneously less able to remove it. They attributed the respiratory failure often seen in blunt chest trauma in part to excessive fluid resuscitation, and the question of whether and how much to administer fluids has remained controversial ever since.During the Vietnam War, combat again provided the opportunity for study of pulmonary contusion; research during this conflict played an important role in the development of the modern understanding of its treatment. The condition also began to be more widely recognized in a non-combat context in the 1960s, and symptoms and typical findings with imaging techniques such as X-ray were described. Before the 1960s, it was believed that the respiratory insufficiency seen in flail chest was due to "paradoxical motion" of the flail segment of the chest wall (the flail segment moves in the opposite direction as the chest wall during respiration), so treatment was aimed at managing the chest wall injury, not the pulmonary contusion. For example, positive pressure ventilation was used to stabilize the flail segment from within the chest. It was first proposed in 1965 that this respiratory insufficiency is most often due to injury of the lung rather than to the chest wall, and a group led by J.K. Trinkle confirmed this hypothesis in 1975. Hence the modern treatment prioritizes the management of pulmonary contusion. Animal studies performed in the late 1960s and 1970s shed light on the pathophysiological processes involved in pulmonary contusion. Studies in the 1990s revealed a link between pulmonary contusion and persistent respiratory difficulty for years after the injury in people in whom the injury coexisted with flail chest. In the next decade studies demonstrated that function in contused lungs improves for years after the injury. References External links Chest Trauma - pulmonary contusion, trauma.org

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

What is the significance of the term 'Urinary retention' in the medical field?

Urinary retention is an inability to completely empty the bladder. Onset can be sudden or gradual. When of sudden onset, symptoms include an inability to urinate and lower abdominal pain. When of gradual onset, symptoms may include loss of bladder control, mild lower abdominal pain, and a weak urine stream. Those with long-term problems are at risk of urinary tract infections.Causes include blockage of the urethra, nerve problems, certain medications, and weak bladder muscles. Blockage can be caused by benign prostatic hyperplasia (BPH), urethral strictures, bladder stones, a cystocele, constipation, or tumors. Nerve problems can occur from diabetes, trauma, spinal cord problems, stroke, or heavy metal poisoning. Medications that can cause problems include anticholinergics, antihistamines, tricyclic antidepressants, cyclobenzaprine, diazepam, nonsteroidal anti-inflammatory drugs (NSAID), amphetamines, and opioids. Diagnosis is typically based on measuring the amount of urine in the bladder after urinating.Treatment is typically with a catheter either through the urethra or lower abdomen. Other treatments may include medication to decrease the size of the prostate, urethral dilation, a urethral stent, or surgery. Males are more often affected than females. In males over the age of 40 about 6 per 1,000 are affected a year. Among males over 80 this increases 30%. Signs and symptoms Onset can be sudden or gradual. When the onset is sudden, symptoms include an inability to urinate and lower abdominal pain. When of gradual onset, symptoms may include loss of bladder control, mild lower abdominal pain, and a weak urine stream. Those with long-term problems are at risk of urinary tract infections. Causes Bladder Infection Detrusor sphincter dyssynergia Neurogenic bladder (commonly spinal cord damage, pelvic splanchic nerve damage, cauda equina syndrome, pontine micturition or storage center lesions, demyelinating diseases or Parkinsons disease) Iatrogenic (caused by medical treatment/procedure) scarring of the bladder neck (commonly from removal of indwelling catheters or cystoscopy operations) Damage to the bladder Prostate Benign prostatic hyperplasia (BPH) Prostate cancer and other pelvic malignancies Prostatitis Penile urethra Congenital urethral valves Phimosis or pinhole meatus Circumcision Obstruction in the urethra, for example a stricture (usually caused either by injury or STD), a metastasis or a precipitated pseudogout crystal in the urine Pseudodyssynergia STD lesions (gonorrhoea causes numerous strictures, leading to a "rosary bead" appearance, whereas chlamydia usually causes a single stricture) Emasculation Postoperative Risk factors include Age: Older people may have degeneration of neural pathways involved with bladder function and it can lead to an increased risk of postoperative urinary retention. The risk of postoperative urinary retention increases up to 2.11 fold for people older than 60 years. Medications: Anticholinergics and medications with anticholinergic properties, alpha-adrenergic agonists, opiates, nonsteroidal anti-inflammatories (NSAIDs), calcium-channel blockers and beta-adrenergic agonists, may increase the risk. Anesthesia: General anesthetics during surgery may cause bladder atony by acting as a smooth muscle relaxant. General anesthetics can directly interfere with autonomic regulation of detrusor tone and predispose people to bladder overdistention and subsequent retention. Spinal anesthesia results in a blockade of the micturition reflex. Spinal anesthesia shows a higher risk of postoperative urinary retention compared to general anesthesia. Benign prostatic hyperplasia: Men with benign prostatic hyperplasia are at an increased risk of acute urinary retention. Surgery related: Operative times longer than 2 hours may lead to an increased risk of postoperative urinary retention 3-fold. Postoperative pain. Chronic Chronic urinary retention that is due to bladder blockage which can either be as a result of muscle damage or neurological damage. If the retention is due to neurological damage, there is a disconnect between the brain to muscle communication, which can make it impossible to completely empty the bladder. If the retention is due to muscle damage, it is likely that the muscles are not able to contract enough to completely empty the bladder.The most common cause of chronic urinary retention is BPH. BPH is a result of the ongoing process of testosterone being converted to dihydrotestosterone which stimulates prostate growth. Over a persons lifetime, the prostate experiences constant growth due to the conversion of testosterone to dihydrotestosterone. This can cause the prostate to push on the urethra and block it, which can lead to urinary retention. Other Tethered spinal cord syndrome. Psychogenic causes – psychosocial stresses, fear associated with urination, paruresis ("shy bladder syndrome") – in extreme cases, urinary retention can result. Consumption of some psychoactive substances, mainly stimulants, such as MDMA or amphetamine. Use of NSAIDs, or drugs with anticholinergic properties. Stones or metastases, which can theoretically appear anywhere along the urinary tract, but vary in frequency depending on anatomy. Muscarinic antagonists such as atropine and scopolamine. Malfunctioning artificial urinary sphincter. Diagnosis Analysis of urine flow may aid in establishing the type of micturition (urination) abnormality. Common findings, determined by ultrasound of the bladder, include a slow rate of flow, intermittent flow, and a large amount of urine retained in the bladder after urination. A normal test result should be 20-25 mL/s peak flow rate. A post-void residual urine greater than 50 ml is a significant amount of urine and increases the potential for recurring urinary tract infections. In adults older than 60 years, 50-100 ml of residual urine may remain after each voiding because of the decreased contractility of the detrusor muscle. In chronic retention, ultrasound of the bladder may show massive increase in bladder capacity (normal capacity is 400-600 ml).Non-neurogenic chronic urinary retention does not have a standardized definition; however, urine volumes >300mL can be used as an informal indicator. Diagnosis of urinary retention is conducted over a period of 6 months, with 2 separate measurements of urine volume 6 months apart. Measurements should have a PVR (post-void residual) volume of >300mL.Determining the serum prostate-specific antigen (PSA) may help diagnose or rule out prostate cancer, though this is also raised in BPH and prostatitis. A TRUS biopsy of the prostate (trans-rectal ultra-sound guided) can distinguish between these prostate conditions. Serum urea and creatinine determinations may be necessary to rule out backflow kidney damage. Cystoscopy may be needed to explore the urinary passage and rule out blockages.In acute cases of urinary retention where associated symptoms in the lumbar spine are present such as pain, numbness (saddle anesthesia), parasthesias, decreased anal sphincter tone, or altered deep tendon reflexes, an MRI of the lumbar spine should be considered to further assess cauda equina syndrome. Complications Acute urinary retention is a medical emergency and requires prompt treatment. The pain can be excruciating when urine is not able to flow out. Moreover, one can develop severe sweating, chest pain, anxiety and high blood pressure. Other patients may develop a shock-like condition and may require admission to a hospital. Serious complications of untreated urinary retention include bladder damage and chronic kidney failure. Urinary retention is a disorder treated in a hospital, and the quicker one seeks treatment, the fewer the complications.In the longer term, obstruction of the urinary tract may cause: Bladder stones Atrophy of the detrusor muscle (atonic bladder is an extreme form) Hydronephrosis (congestion of the kidneys) Hypertrophy of the detrusor muscle (the muscle that squeezes the bladder to empty it during urination) Diverticula (formation of pouches) in the bladder wall (which can lead to stones and infection) Treatment In acute urinary retention, urinary catheterization, placement of a prostatic stent, or suprapubic cystostomy relieves the retention. In the longer term, treatment depends on the cause. BPH may respond to alpha blocker and 5-alpha-reductase inhibitor therapy, or surgically with prostatectomy or transurethral resection of the prostate (TURP).Use of alpha-blockers can provide relief of urinary retention following de-catheterization for both men and women. In case, if catheter cant be negotiated, suprapubic puncture can be done with lumbar puncture needle. Medication Some people with BPH are treated with medications. These include tamsulosin to relax smooth muscles in the bladder neck, and finasteride and dutasteride to decrease prostate enlargement. The drugs only work for mild cases of BPH but also have mild side effects. Some of the medications decrease libido and may cause dizziness, fatigue and lightheadedness. Catheter Acute urinary retention is treated by placement of a urinary catheter (small thin flexible tube) into the bladder. This can be either an intermittent catheter or a Foley catheter that is placed with a small inflatable bulb that holds the catheter in place.Intermittent catheterization can be done by a health care professional or by the person themselves (clean intermittent self catheterization). Intermittent catheterization performed at the hospital is a sterile technique. Patients can be taught to use a self catheterization technique in one simple demonstration, and that reduces the rate of infection from long-term Foley catheters. Self catheterization requires doing the procedure periodically during the day, the frequency depending on fluid intake and bladder capacity. If fluid intake/outflow is around 1.5 litres per day, this would typically be performed roughly three times per day, i.e. roughly every six to eight hours during the day, more frequently when fluid intake is higher and/or bladder capacity lower. For acute urinary retention, treatment requires urgent placement of a urinary catheter. A permanent urinary catheter may cause discomfort and pain that can last several days. Older people with ongoing problems may require continued intermittent self catheterization (CISC). CISC has a lower infection risk compared to catheterization techniques that stay within the body. Challenges with CISC include compliance issues as some people may not be able to place the catheter themselves. Surgery The chronic form of urinary retention may require some type of surgical procedure. While both procedures are relatively safe, complications can occur. In most patients with benign prostate hyperplasia (BPH), a procedure known as transurethral resection of the prostate (TURP) may be performed to relieve bladder obstruction. Surgical complications from TURP include a bladder infection, bleeding from the prostate, scar formation, inability to hold urine, and inability to have an erection. The majority of these complications are short lived, and most individuals recover fully within 6–12 months. Sitting voiding position A meta-analysis on the influence of voiding position on urodynamics in males with lower urinary tract symptoms showed that in the sitting position, the residual urine in the bladder was significantly reduced, the maximum urinary flow was increased, and the voiding time was decreased. For healthy males, no influence was found on these parameters, meaning that they can urinate in either position. Epidemiology Urinary retention is a common disorder in elderly males. The most common cause of urinary retention is BPH. This disorder starts around age 50 and symptoms may appear after 10–15 years. BPH is a progressive disorder and narrows the neck of the bladder leading to urinary retention. By the age of 70, almost 10 percent of males have some degree of BPH and 33% have it by the eighth decade of life. While BPH rarely causes sudden urinary retention, the condition can become acute in the presence of certain medications including antihypertensives, antihistamines, and antiparkinson medications, and after spinal anaesthesia or stroke.In young males, the most common cause of urinary retention is infection of the prostate (acute prostatitis). The infection is acquired during sexual intercourse and presents with low back pain, penile discharge, low grade fever and an inability to pass urine. The exact number of individuals with acute prostatitis is unknown, because many do not seek treatment. In the US, at least 1–3 percent of males under the age of 40 develop urinary difficulty as a result of acute prostatitis. Most physicians and other health care professionals are aware of these disorders. Worldwide, both BPH and acute prostatitis have been found in males of all races and ethnic backgrounds. Cancers of the urinary tract can cause urinary obstruction but the process is more gradual. Cancer of the bladder, prostate or ureters can gradually obstruct urine output. Cancers often present with blood in the urine, weight loss, lower back pain or gradual distension in the flanks.Urinary retention in females is uncommon, occurring 1 in 100,000 every year, with a female-to-male incidence rate of 1:13. It is usually transient. The causes of UR in women can be multi-factorial, and can be postoperative and postpartum. Prompt urethral catheterization usually resolves the problem. References == External links ==

You act as a bridge between medical jargon and everyday language. Explain medical terms in a manner that is comprehensive yet approachable for non-experts.

Can you demystify the medical term 'Trimalleolar fracture' for me?

A trimalleolar fracture is a fracture of the ankle that involves the lateral malleolus, the medial malleolus, and the distal posterior aspect of the tibia, which can be termed the posterior malleolus. The trauma is sometimes accompanied by ligament damage and dislocation.The three aforementioned parts of bone articulate with the talus bone of the foot. Strictly speaking, there are only two malleoli (medial and lateral), but the term trimalleolar is used nevertheless and as such is a misnomer. The trimalleolar fracture is also known as cotton fracture. Treatment Surgical repair using open reduction and internal fixation is generally required, and because there is no lateral restraint of the foot, the ankle cannot bear any weight while the bone knits. This typically takes six weeks in an otherwise healthy person, but can take as much as twelve weeks. Non-surgical treatment may sometimes be considered in cases where the patient has significant health problems or where the risk of surgery may be too great. References Further reading Weber, Martin (2004). "Trimalleolar Fractures with Impaction of the Posteromedial Tibial Plafond: Implications for Talar Stability". Foot & Ankle International. 25 (10): 716–27. doi:10.1177/107110070402501005. PMID 15566703. S2CID 43182738. Weber, Martin; Ganz, Reinhold (2003). "Malunion following Trimalleolar Fracture with Posterolateral Subluxation of the Talus — Reconstruction Including the Posterior Malleolus". Foot & Ankle International. 24 (4): 338–44. doi:10.1177/107110070302400406. PMID 12735377. S2CID 20888046. Bucholz, R. W.; Henry, S; Henley, M. B. (1994). "Fixation with bioabsorbable screws for the treatment of fractures of the ankle". The Journal of Bone and Joint Surgery. 76 (3): 319–24. doi:10.2106/00004623-199403000-00001. PMID 8126036. Haraguchi, Naoki; Haruyama, H; Toga, H; Kato, F (2006). "Pathoanatomy of Posterior Malleolar Fractures of the Ankle". The Journal of Bone and Joint Surgery. 88 (5): 1085–92. doi:10.2106/JBJS.E.00856. PMID 16651584. Langenhuijsen, Johan F.; Heetveld, Martin J.; Ultee, Jan M.; Steller, E. Philip; Butzelaar, Rudi M. J. M. (2002). "Results of Ankle Fractures with Involvement of the Posterior Tibial Margin". The Journal of Trauma: Injury, Infection, and Critical Care. 53 (1): 55–60. doi:10.1097/00005373-200207000-00012. PMID 12131390. Van Den Bekerom, Michel P. J.; Haverkamp, Daniel; Kloen, Peter (2009). "Biomechanical and Clinical Evaluation of Posterior Malleolar Fractures. A Systematic Review of the Literature". The Journal of Trauma: Injury, Infection, and Critical Care. 66 (1): 279–84. doi:10.1097/TA.0b013e318187eb16. PMID 19131839. Helmy, Naeder; Meyer, Dominik C.; Vienne, Patrick; Espinosa, Norman (2012). "The Posterolateral Approach for the Treatment of Trimalleolar Fractures". Techniques in Foot & Ankle Surgery. 11 (4): 189–93. doi:10.1097/BTF.0b013e3182743f11. Forberger, Jens; Sabandal, Philipp V.; Dietrich, Michael; Gralla, Jan; Lattmann, Thomas; Platz, Andreas (2009). "Posterolateral Approach to the Displaced Posterior Malleolus: Functional Outcome and Local Morbidity". Foot & Ankle International. 30 (4): 309–14. doi:10.3113/FAI.2009.0309. PMID 19356354. S2CID 34963028. == External links ==

You serve as an encyclopedia of medical terms. Deliver clear, detailed explanations, making medical language understandable to a diverse audience.

Could you offer a clear explanation of the term 'Pyometra' as used in the medical field?

Pyometra or pyometritis is a uterine infection. Though it is most commonly known as a disease of the unaltered female dog, it is also a notable human disease. It is also seen in female cattle, horses, goats, sheep, swine, cats, rabbits, hamsters, ferrets, rats and guinea pigs. Pyometra is an important disease to be aware of for any dog or cat owner because of the sudden nature of the disease and the deadly consequences if left untreated. It has been compared to acute appendicitis in humans, because both are essentially empyemas within an abdominal organ. Signs and symptoms The most obvious symptom of open pyometra is a discharge of pus from the vulva in a female that has recently been in heat. However, symptoms of closed pyometra are less obvious. Symptoms of both types include vomiting, loss of appetite, depression, and increased drinking and urinating. Fever is seen in less than a third of female dogs with pyometra. Closed pyometra is a more serious condition than open pyometra not only because there is no outlet for the infection, but also because a diagnosis of closed pyometra can easily be missed due to its insidious nature. Bloodwork may show dehydration and/or increased white blood cell count. X-rays will show an enlarged uterus, and ultrasound will confirm the presence of a fluid filled uterus. Cause The risk of developing pyometra differs between dog breeds. Pyometra is a result of hormonal and structural changes in the uterus lining. This can happen at any age, whether she has bred or not, and whether it is her 1st or 10th heat, although it becomes more common as the dog gets older. The main risk period for a female is for eight weeks after her peak standing heat has ended. Normally during this period, the cervix, which was open during her heat, begins to close, and the inner lining begins to adapt back to normal. However, cystic hyperplasia of the endometrium (inner lining of the uterus) – known as cystic endometrial hyperplasia (CEH) – may occur at this time for some animals, as an inappropriate response to progesterone. Under these circumstances, bacteria (especially E. coli) that have migrated from the vagina into the uterus find the environment favorable to growth, especially since progesterone also causes mucus secretion, closes the cervix (preventing uterine drainage), and decreases uterine contractility. The condition of the cervix is a major factor in the severity of the condition. If the cervix is open, the infected material can leave the body, and this is far easier and safer to treat. This is known as open pyometra. If the cervix is fully closed, there is no discharge from the vulva, and like in appendicitis, the uterus may rupture and pus escapes into the abdomen, causing peritonitis and possible rapid death. This is known as closed pyometra. Hormonal influences and mis-mating shots Females that have received estradiol as a mismating shot in diestrus are at risk for more severe disease because estrogen increases the number of progesterone receptors in the endometrium. 25 percent of females receiving estradiol in diestrus develop pyometra. Pyometra is less common in female cats because progesterone is only released by the ovaries after mating. Also in cats, the risk of developing the disease differs depending on breed. Treatment The most important aspect of treatment of pyometra is quick action to provide supportive care. Female dogs are often septic and in shock (see septic shock). Intravenous fluids and antibiotics should be given immediately. Once the female dog has been stabilized, then the treatment of choice is an emergency spay. In livestock the treatment of choice for minor cases is dinoprost tremethamine (lutalyse). Supportive antibiotic treatment may be recommended also. Severe cases require surgery. References External links Pyometra from The Pet Health Library Pyometra Surgery Photos and Description from The Pet Center

You function as a medical explainer. Your task is to convey the meanings of medical terms in a detailed, yet easy-to-understand manner.

I'm encountering the term 'Alirocumab' in medical literature. What's its definition?

Alirocumab, sold under the brand name Praluent, is a medication used as a second-line treatment for high cholesterol for adults whose cholesterol is not controlled by diet and statin treatment. It is a human monoclonal antibody that belongs to a novel class of anti-cholesterol drugs, known as PCSK9 inhibitors, and it was the first such agent to receive FDA approval. The FDA approval was contingent on the completion of further clinical trials to better determine efficacy and safety.Common side effects include nasopharyngitis (cold), injection site reactions, and influenza.It was approved for medical use in the United States and in the European Union in 2015. Medical uses Alirocumab is used as a second-line treatment to lower LDL cholesterol for adults who have a severe form of hereditary high cholesterol and people with atherosclerosis who require additional lowering of LDL cholesterol when diet and statin treatment have not worked. It is administered by subcutaneous injection. As of July 2015, it is not known whether alirocumab prevents early death from cardiovascular disease or prevents heart attacks; a clinical trial to determine outcomes was ongoing at that time, the results of which were expected in 2017. In November 2018, The New England Journal of Medicine published positive results from a clinical trial with alirocumab. According to the study, alirocumab significantly reduced major adverse cardiovascular events by 15% and it was associated with a 15% lower risk of death from any cause (hazard ratio [HR] 0.85; 95% confidence interval [CI], 0.73 to 0.98).In 2021, the U.S. Food and Drug Administration (FDA) added an indication for alirocumab to treat adults with homozygous familial hypercholesterolemia (HoFH), a genetic condition that causes severely high cholesterol. It is not intended to be used alone but instead added to other treatments for HoFH. Side effects Side effects that occurred in more than 2% of people treated with alirocumab in clinical trials and that occurred more frequently than with placebo, included nose and throat irritation, injection site reactions and bruising, flu-like symptoms, urinary tract infection, diarrhea, bronchitis and cough, and muscle pain, soreness, and spasms.There are no available data on use of alirocumab in pregnant women to assess risks to the fetus, nor is there data on use in children. Pharmacology Alirocumab works by inhibiting the PCSK9 protein. PCSK9 binds to the low-density lipoprotein receptor (LDLR) (which takes cholesterol out of circulation), and that binding leads to the receptor being degraded, and less LDL cholesterol being removed from circulation. Inhibiting PCSK9 prevents the receptor from being degraded, and promotes removal of LDL cholesterol from circulation.After subcutaneous administration of alirocumab, maximal suppression of free PCSK9 occurs within 4 to 8 hours and has an apparent half-life of 17 to 20 days. Inhibition is dose-dependent. The antibody is distributed through the circulation, and it is eliminated at low concentrations by binding to its target, and at higher concentrations through a proteolytic pathway. Chemistry Alirocumab is a human monoclonal antibody of the IgG1 isotype. It is made of two disulfide-linked human heavy chains, each disulfide-linked to a human light chain. It has an approximate molecular weight of 146 kDa.It is produced using Chinese hamster ovary cells transfected with recombinant DNA, that are grown in tanks. History The importance of PCSK9 as a biological target for drug discovery emerged in 2003, when a series of discoveries led to identification of the protein and its gene, its role in causing some cases of familial hypercholesterolaemia when some mutations are present, and its role in causing very low levels of LDL cholesterol when other mutations are present.The discovery and validation of the target set off a race among pharmaceutical and biotech companies.Alirocumab was discovered by Regeneron Pharmaceuticals using its "VelocImmune" mouse, in which many of the genes coding for antibodies have been replaced with human genes.: 255–258  In an investor presentation, Regeneron claimed that with their system, it took only about 19 months from when they first immunized mice with PCSK9 until they filed their IND.: Slide 26  Alirocumab was co-developed with Sanofi under a deal made in 2007. Before it received its international nonproprietary name it was known as REGN727 and SAR236553.Phase 1 trial results were reported in 2012 in The New England Journal of Medicine. A phase 3 trial of statin intolerant patients called ODYSSEY ran for 65 weeks. Results were presented at the 2014 European Society of Cardiology meeting. A 78-week study of alirocumab in 2341 people taking statins who were at high risk for cardiovascular events and had high LDL cholesterol levels was published in April 2015. This study showed a significant reduction of LDL cholesterol levels in patients taking both Alirocumab and oral statins compared to placebo patients solely taking oral statins. Studies are ongoing to assess the effects of alirocumab in normocholesterolemic individuals.In July 2014, Regeneron and Sanofi announced that they had purchased a priority review voucher that BioMarin had won for a recent rare disease drug approval for $67.5 million; the voucher cut four months off the regulatory review time for alirocumab and was part of their strategy to beat Amgen to market with the first approval of a PCSK9 inhibitor.In July 2015, the FDA approved alirocumab as a second-line treatment to lower LDL cholesterol for adults who have hereditary high cholesterol and people with atherosclerosis who require additional lowering of LDL cholesterol when diet and statin treatment have not worked. This was the first approval of a PCSK9 inhibitor. The FDA approval was contingent on the completion of further clinical trials to better determine efficacy and safety.Regeneron and Amgen had each filed for patent protection on their monoclonal antibodies and the companies ended up in patent litigation in the U.S. In March 2016, a district court found that alirocumab infringed Amgens patents; Amgen then requested an injunction barring Regeneron and Sanofi from marketing alirocumab, which was granted in January 2017. The judge gave Regeneron and Sanofi 30 days to appeal before the injunction went into effect. In October, 2017 the US Court of Appeals reversed the ban and ordered a new trial after finding the jury was given improper instructions and evidence was withheld. Regeneron and Sanofi were allowed to continue marketing alirocumab during the appeals process.The U.S. Food and Drug Administration (FDA) granted approval of Praluent to Regeneron Pharmaceuticals, Inc. Society and culture In 2014 as PCSK9 inhibitors approached regulatory approval, market analysts estimated that the overall market for these drugs could be $10B per year, with each of alirocumab and Amgens competing drugs having sales of $3B per year, and other competitors dividing the remaining $4B, based on estimates of an annual price for alirocumab of $10,000 per year. At the same time, pharmacy benefit managers such as Express Scripts and CVS Caremark, while recognizing that the new drugs could help patients who were otherwise left with uncontrolled cholesterol levels, and recognizing that injectable biopharmaceuticals will always be more expensive than pills, and especially more expensive than generic pills, expressed concerns about the burden of the new costs on the health care system.When the drug was approved in July 2015, the announced price was higher than analysts had predicted: $14,600 a year. Pharmacy benefit managers continued expressing their concerns, as did insurance companies and some doctors, who were especially concerned over the price, in light of the fact that the FDA approval was based on lowering cholesterol alone, and not on better health outcomes, such as fewer heart attacks or longer life.The treatment for people with very high cholesterol that cannot be controlled with diet or statins is apheresis, which is similar to dialysis in that a person visits a clinic each month and his or her blood is mechanically filtered, in this case to remove LDL cholesterol. That treatment costs $8000 per month, or $96,000 per year. The price of alirocumab was determined based in part on making apheresis no longer necessary. Names Alirocumab is the International nonproprietary name. References External links "Alirocumab". Drug Information Portal. U.S. National Library of Medicine.

You function as a medical explainer. Your task is to convey the meanings of medical terms in a detailed, yet easy-to-understand manner.

The term 'Lymphocytic meningoradiculitis' keeps coming up in medical discussions. What does it stand for?

Lymphocytic meningoradiculitis, also known as Bannwarth syndrome, is a neurological disease characterized as intense nerve pain radiating from the spine. The disease is caused by an infection of Borrelia burgdorferi, a tick-borne spirochete bacterium also responsible for causing Lyme disease. Signs and symptoms Lymphocytic meningoradiculitis is characterized by an intense spinal pain in the lumbar and cervical regions, radiating to the extremities. Symptoms may include facial paralysis, abducens palsy, anorexia, tiredness, headache, double vision, paraesthesia, and erythema migrans. Treatment Lymphocytic meningoradiculitis is treated with antibiotics. Oral doxycycline or IV ceftriaxone are typically recommended for 14-21 days. History The disease was first reported in 1941 by German neurologist, Alfred Bannwarth, who described the main symptoms as intense radicular pain, facial palsy, severe headaches, and vomiting. A common feature he observed in his infected patients was an abnormal increase of lymphocytes in their cerebrospinal fluid (CSF). See also Tick-borne disease References == External links ==

You function as a medical explainer. Your task is to convey the meanings of medical terms in a detailed, yet easy-to-understand manner.

I'm trying to understand 'Cutaneous leishmaniasis' within a medical context. Could you shed some light on it?

Cutaneous leishmaniasis is the most common form of leishmaniasis affecting humans. It is a skin infection caused by a single-celled parasite that is transmitted by the bite of a phlebotomine sand fly. There are about thirty species of Leishmania that may cause cutaneous leishmaniasis. This disease is considered to be a zoonosis (an infectious disease that is naturally transmissible from animals to humans), with the exception of Leishmania tropica — which is often an anthroponotic disease (an infectious disease that is naturally transmissible from humans to vertebrate animals). Signs and symptoms Post kala-azar dermal leishmaniasis Post-kala-azar dermal leishmaniasis (PKDL) is a recurrence of kala-azar that may appear on the skin of affected individuals months and up to 20 years after being partially treated, untreated or even in those considered adequately treated. In Sudan, they can be demonstrated in up to 60% of treated cases. They manifest as hypopigmented skin lesions (such as macules, papules, nodules), or facial redness. Though any organism causing kala-azar can lead to PKDL, it is commonly associated with Leishmania donovani which gives different disease patterns in India and Sudan. In the Indian variant, nodules enlarge with time and form plaques but rarely ulcerate, but nodules from the African variety often ulcerate as they progress. Nerve involvement is common in African variety but rare in Indian subcontinent. Histology demonstrates a mixture of chronic inflammatory cells; there can be macrophage or epitheloid granuloma. Parasite concentration is not consistent among studies, perhaps reflecting low sensitivity of diagnostic methods used in earlier entries.Current approach to diagnosis involves demonstration of parasite by microscopy, in vitro culture or animal inoculation; immunodiagnosis of parasite antigen; detection of parasite DNA in tissue.Newer polymerase chain reaction (PCR) based tools have higher sensitivity and specificity. Emergence of PKDL has been reported in HIV affected individuals and may become a problem in the future. Sodium stibogluconate alone or in combination with rifampicin is used for the treatment of PKDL for a long course of up to 4 months. Compliance can be an issue for such a long course. Mucocutaneous leishmaniasis Mucocutaneous leishmaniasis is an especially disturbing form of cutaneous leishmaniasis, because it produces destructive and disfiguring lesions of the face. It is most often caused by Leishmania braziliensis, but cases caused by L. aethiopica have also been described.Mucocutaneous leishmaniasis is very difficult to treat. Treatment involves the use of pentavalent antimonial compounds, which are highly toxic (common side effects include thrombophlebitis, pancreatitis, cardiotoxicity and hepatotoxicity) and not very effective. For example, in one study, despite treatment with high doses of sodium stibogluconate for 28 days, only 30% of patients remained disease-free at 12 months follow-up. Even in those patients who achieve an apparent cure, as many as 19% will relapse. Several drug combinations with immunomodulators have been tested, for example, a combination of pentoxifylline (inhibitor of TNF-α) and a pentavalent antimonial at a high dose for 30 days in a small-scale (23 patients) randomised placebo-controlled study from Brazil achieved cure rates of 90% and reduced time to cure, a result that should be interpreted cautiously in light of inherent limitations of small-scale studies. In an earlier small-scale (12 patients) study, addition of imiquimod showed promising results which need yet to be confirmed in larger trials. Pathophysiology Promastigotes of Leishmania are transmitted to human skin by the bite of a sandfly. Leishmania then invades human macrophages and replicates intracellularly. A raised, red lesion develops at the site of the bite (often weeks or sometimes years afterwards). The lesion then ulcerates and may become secondarily infected with bacteria. In many species (for example, L. major) the lesion often spontaneously heals with atrophic scarring. In some species (for example, L. braziliensis) the lesion may spontaneously heal with scarring, but then reappear elsewhere (especially as destructive mucocutaneous lesions). Lesions of other Leishmania species may spontaneously heal and then reappear as satellite lesions around the site of the original lesion, or along the route of lymphatic drainage.Some species tend to cause cutaneous leishmaniasis (e.g., L. major and L.tropica), whereas some species tend to cause visceral leishmaniasis (e.g., L. infantum and L. donovani), though emerging research (due to high deployment rates of western countries to indigenous areas) is showing these species specific presentation lines are blurring. Diagnosis Diagnosis is based on the characteristic appearance of non-healing raised, scaling lesions that may ulcerate and become secondarily infected with organisms such as Staphylococcus aureus, in someone who has returned from an endemic area.In resource limited settings, fine-needle aspiration of the lesion is confirmatory with identification of amastigote form of Leishmania. The gold standard for diagnosis is a PCR test. Treatment American cutaneous and mucocutaneous leishmaniasis The best treatment for American cutaneous and mucocutaneous leishmaniasis (ACML) is not known. Pentavalent antimonial drugs (sodium stibogluconate (SSG) and meglumine antimonate (Glucantime, MA)) have been used since the 1940s, but they are expensive, toxic, and painful. Treatments that work for one species of Leishmania may not work for another; therefore, it is recommended that the exact species be identified prior to initiating treatment. Unfortunately, leishmaniasis is an orphan disease in developed nations, and almost all the current treatment options are toxic with significant side effects.The best-studied treatments for ACML caused by two Leishmania species are listed below. However, one should note that most of the studies examining treatments of ACML were poorly designed. Therefore, no definitive treatment guidelines or recommendations are currently available, as large-scale and well-conducted studies are necessary to evaluate the long-term effects of current treatments. Leishmania braziliensis and Leishmania panamensis: There is good evidence that oral allopurinol plus intramuscular MA is superior to either medication alone. In addition, a 20-day course of intravenous MA was better than a 7-day course as well as a 3- or 7-day course of intravenous MA with paromomycin + 12% methylbenzethonium chloride. For L. braziliensis, oral pentoxifylline plus intravenous SSG seems to be more efficacious than intravenous SSG alone, and intravenous MA was superior to intramuscular paromomycin sulfate and IV pentamidine. Likewise, intramuscular MA was shown to be better than the Bacillus Calmette-Guerin vaccine. For L. panamensis, oral ketoconazole, oral miltefosine, and topical paromomycin + 12% methylbenzethonium chloride were shown to be superior to placebo.There is no strong evidence for the efficacy of surgery, oral itraconazole and fluconazole, oral antibiotics (rifampicin, metronidazole, cotrimoxazole), intravenous or topical amphotericin B, oral dapsone, photodynamic therapy, promoting healing therapies, laser, or cryotherapy treatments. Old World cutaneous leishmaniasis Similar to ACML, the treatment recommendations for Old World cutaneous leishmaniasis (OWCL) are uncertain due to the variability of and inconsistencies within the research.Most studies done to assess treatments of OWCL included two species of parasites, Leishmania major and Leishmania tropica. The most well-studied treatments for OWCL are oral itraconazole and topical paromomycin.Patients treated with oral itraconazole for an average of 2.5 months had a higher cure rate compared to placebo, but they also had a higher rate of side effects, including gastrointestinal complaints, abnormal liver function, headaches, and dizziness.Patients treated with topical paromomycin showed no difference in cure rate compared to placebo, but patients treated with paromomycin had a higher rate of adverse skin reactions.The treatments for other Leishmania species responsible for OWCL, such as L. infantum, L. aethiopica, and L. donovani, have not been thoroughly studied. In addition, the effects of leishmaniasis treatment in children, women of childbearing age, patients with comorbidities, and immunocompromised patients have not been well established. Epidemiology Cutaneous leishmaniasis is endemic in all tropical and subtropical areas of the world. The distribution of this disease is very tightly linked to geography, and villages even 15 miles apart can have very different rates of cutaneous leishmaniasis.Most species of Leishmania are capable of infecting humans and causing cutaneous leishmaniasis. In the New World, these organisms include L. amazonensis, L. braziliensis, L. guyanensis, L. lainsoni, L. lindenbergi, L. mexicana, L. naiffi, L. panamensis, L. peruviana, L. shawi, and L. venezuelensis. Old World species that cause cutaneous leishmaniasis include L. aethiopica, L. infantum, L. major, and L. tropica. With the exception of L. tropica — which is commonly associated with human settlements and therefore considered to be an anthroponotic species — all of these organisms are zoonotic. As demographic changes occur in developing nations, some species that have traditionally been considered to be zoonotic (e.g., L. panamensis) are becoming primarily human pathogens.Dogs and rodents serve as the primary animal reservoir hosts in the sylvatic cycle, but people with chronic PKDL can also serve as important reservoir hosts for cutaneous leishmaniasis. The most common vectors for cutaneous leishmaniasis in the Old World are sandflies of the genus Phlebotomus, while Lutzomyia and those within the family Psychodidae (especially the genus Psychodopygus) are the most common vectors in the New World. There are more than 600 species of phlebotomine sandflies, and only 30 of these are known vectors. Cutaneous leishmaniasis has been seen in American and Canadian troops coming back from Afghanistan. Means of Prevention The sand fly stings mainly at night, and it usually occurs about half a meter above the ground (so sleeping on high beds can prevent infection). To avoid stinging, apply mosquito repellent, and cover the body.Studies conducted in recent years show that the plant Bougainvillea glabra may protect against the sand fly. The plant was found to be toxic to sand flies and that the life span of flies that ate from this plant was significantly shortened and sometimes led to their premature death before they could spread the disease.Hebrew University study found that some plants attract sand flies. These plants often attract sand flies up to 14 times more than Bougainvillea glabra, but unlike Bougainvillea glabra, are not toxic to the sand flies. Based on this information, the dispersion of sand flies can be controlled by limiting the growth of these plants near populated areas. Alternatively, these plants may serve to capture and control sand flies by using their odor compounds or the plants themselves alongside simple glue traps, or by spraying them with deadly pesticides for sand flies which are safe for humans and mammals (e.g., boric acid or spinosad) thereby stopping the spread of the disease. Of the dozens of plants examined, the three plants that attracted especially sand flies are the Ochradenus baccatus, Prosopis farcta, and Tamarix nilotica. Outbreak in 2016 The Middle East, in 2016, seems to be experiencing an increase in the cutaneous leishmaniasis disease due to migrants fleeing the Islamic State of Iraq and the Levant. Reports of the increase in the disease have surfaced in Turkey, Lebanon, and elsewhere.The huge increase in the spread of the disease is attributed to the refugee crises in the Middle East and North Africa over the past five years, particularly due to the displacement of millions of Syrian refugees. The outbreak among Syrian refugees was documented by the World Health Organization (WHO) in 2012 and recognized as ongoing. Nepal A recent study with large series of cases from Mid-western region of Nepal have demonstrated that cutaneous leishmaniasis is an under recognized medical condition posing health challenges mandating new guidelines for its elimination/ eradication. Other animals Besides humans, cutaneous leishmaniasis often affects other animals, notably in dogs as canine leishmaniasis. References == External links ==

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

I've come across the term 'Chronic fatigue syndrome' in a medical context, but I'm not sure what it means. Can you clarify?

Chronic fatigue syndrome (CFS), also called myalgic encephalomyelitis (ME) or ME/CFS, is a complex, debilitating, long-term medical condition. The causes and mechanisms of the disease are not fully understood. Distinguishing core symptoms are lengthy exacerbations or flare-ups of the illness following ordinary minor physical or mental activity, known as post-exertional malaise (PEM); greatly diminished capacity to accomplish tasks that were routine before the illness; and sleep disturbances.: 7  Orthostatic intolerance (difficulty sitting and standing upright) and cognitive dysfunction are also diagnostic. Frequently and variably, other common symptoms occur involving numerous body systems, and chronic pain is common. The unexplained and often incapacitating fatigue in CFS is different from that caused by normal strenuous ongoing exertion, is not significantly relieved by rest, and is not due to a previous medical condition. Diagnosis is based on the persons symptoms because no confirmed diagnostic test is available.Proposed mechanisms include biological, genetic, epigenetic, infectious, and physical or psychological stress affecting the biochemistry of the body. Persons with CFS may recover or improve over time, but some will become severely affected and disabled for an extended period. No therapies or medications are approved to treat the cause of the illness; treatment is aimed at alleviation of symptoms. The CDC recommends pacing (personal activity management) to keep mental and physical activity from making symptoms worse. Limited evidence suggests that rintatolimod, counseling, and personalized activity management helps improve some patients functional abilities. About 1% of primary-care patients have CFS; estimates of incidence vary widely because epidemiological studies define the illness dissimilarly. It has been estimated that 836,000 to 2.5 million Americans and 250,000 to 1,250,000 people in the United Kingdom have CFS. CFS occurs 1.5 to 2 times as often in women as in men. It most commonly affects adults between ages 40 and 60 years; it can occur at other ages, including childhood. Other studies suggest that about 0.5% of children have CFS, and that it is more common in adolescents than in younger children.: 182  Chronic fatigue syndrome is a major cause of school absence.: 183  CFS reduces health, happiness, productivity, and can also cause socio-emotional disruptions such as loneliness and alienation. However, there is controversy over many aspects of the disorder. Physicians, researchers, and patient advocates promote different names and diagnostic criteria. Results of studies of proposed causes and treatments are often poor or contradictory. Signs and symptoms The United States Centers for Disease Control and Prevention (CDC) recommends these criteria for diagnosis: Greatly lowered ability to do activities that were usual before the illness. This drop in activity level occurs along with fatigue and must last six months or longer. Worsening of symptoms after physical or mental activity that would not have caused a problem before the illness. The amount of activity that might aggravate the illness is difficult for a person to predict, and the decline often presents 12 to 48 hours after the activity. The relapse, or crash, may last days, weeks or longer. This is known as post-exertional malaise (PEM). Sleep problems; people may still feel weary after full nights of sleep, or may struggle to stay awake, fall asleep or stay asleep.Additionally, one of the following symptoms must be present: Problems with thinking and memory (cognitive dysfunction, sometimes described as "brain fog") While standing or sitting upright; lightheadedness, dizziness, weakness, fainting or vision changes may occur (orthostatic intolerance) Other common symptoms Many, but not all people with ME/CFS report: Muscle pain, joint pain without swelling or redness, and headache Tender lymph nodes in the neck or armpits Sore throat Irritable bowel syndrome Chills and night sweats Allergies and sensitivities to foods, odors, chemicals, lights, or noise Shortness of breath Irregular heartbeatIncreased sensitivity to sensory stimuli and pain have also been observed in CFS.The CDC recommends that people with symptoms of CFS consult a physician to rule out other illnesses, which may be treatable. Onset The onset of CFS may be gradual or sudden. When it begins suddenly, it often follows a period of infectious-like symptoms or a known infection, and between 20 and 80% of patients report an onset resembling an infection.: 158  When gradual, the illness may begin over the course of months or years. Studies disagree as to which pattern is more common.: 158 : 181  CFS may also occur after physical trauma such as a car accident or surgery. Physical functioning The functional capacity of individuals with CFS varies greatly. Some persons with mild CFS lead relatively normal lives with vigilant energy management; persons that are severely ill may be totally bed-ridden and unable to care for themselves. For the majority of persons with CFS, work, school, and family activities are significantly reduced for extended periods of time. The severity of symptoms and disability is the same regardless of gender, and many experience strongly disabling chronic pain. Persons report critical reductions in levels of physical activity. Also, a reduction in the complexity of activity has been observed. Reported impairment is comparable to other fatiguing medical conditions including late-stage AIDS, lupus, rheumatoid arthritis, chronic obstructive pulmonary disease (COPD), and end-stage kidney disease. CFS affects a persons functional status and well-being more than major medical conditions such as multiple sclerosis, congestive heart failure, or type II diabetes mellitus.Often, courses of remission and relapse of symptoms occur, which make the illness difficult to manage. Persons who feel better for a period may overextend their activities, and the result can be a worsening of their symptoms with a relapse of the illness.About 25% of people with CFS are house-bound or bed-ridden for long periods during their illness, often for decades.: 32  An estimated 75% are unable to work because of their illness. More than half were on disability benefits or temporary sick leave, and less than a fifth worked full-time. Children who become ill with CFS are a major cause of school absence.: 183 People with CFS have decreased scores on the SF-36 quality-of-life questionnaire, especially in the sub scales on vitality, physical functioning, general health, physical role, and social functioning; however, the sub scales for "role emotional" and mental health in CFS patients were consistent with or not substantially lower than healthy controls. Cognitive functioning Cognitive dysfunction is one of the more disabling aspects of CFS due to its negative impact on occupational and social functioning. Fifty to eighty percent of persons with CFS are estimated to have serious problems with cognition. Cognitive symptoms are mainly due to deficits in attention, memory, and reaction time. Measured cognitive abilities are found to be below projected normal values and likely to affect day-to-day activities; for example, increases in common mistakes, forgetting scheduled tasks, or having difficulty responding when spoken to are observed.Simple and complex information-processing speed and functions entailing working memory over long time periods are moderately to extensively impaired. These deficits are generally consistent with the patients perceptions. Perceptual abilities, motor speed, language, reasoning, and intelligence do not appear to be significantly altered. When poorer health status was reported, a persons perception of their cognitive problems was frequently greater. Better physical functioning in people with CFS is associated with less visuoperceptual difficulty and fewer language-processing complaints.Inconsistencies of subjective and observed values of cognitive dysfunction reported across multiple studies are likely caused by a number of factors. Differences of research participants cognitive abilities pre- and post-illness onset are naturally variable and are difficult to measure because of a lack of specialized analytical tools that can consistently quantify the specific cognitive difficulties in CFS.The frequency of neuropsychiatric and neuropsychological symptoms is increased in the population of persons with CFS; the understanding of why this occurs is unresolved. Various hypotheses have been advanced to try to explain the relationship between the cognitive symptoms and the illness. Some researchers believe psychiatric causes underlie or contribute to the illness, while other researchers believe the illness causes biochemical and sociological changes in people that produce the symptoms. Cause The cause of CFS is unknown. Genetic and physiological factors are thought to work together to precipitate and perpetuate the condition. A 2016 report by the Institute of Medicine states that CFS is a biologically based illness, but that the biologic abnormalities are not sensitive or specific enough to be useful as a diagnosis.Because it may begin as an influenza-like illness with a sudden onset, various infectious causes have been proposed, but evidence is insufficient to support such causation. Infections proposed include mononucleosis, Chlamydophila pneumoniae, human herpesvirus 6, and Lyme disease. Inflammation may be involved. Often, the illness will follow a viral illness such as mononucleosis or gastroenteritis. Risk factors All ages, ethnic groups, and income levels are susceptible to the illness. The CDC states that Caucasians may be diagnosed more frequently than other races in America, but the illness is at least as prevalent among African Americans and Hispanics. A 2009 meta-analysis showed that African Americans and Native Americans have a higher risk of CFS, though it specifically excluded other more common ethnicities worldwide, and it acknowledged that studies and data were limited.More women than men get CFS. A large 2020 meta-analysis estimated that between 1.5 and 2.0 times more cases are women. The review acknowledged that different case definitions and diagnostic methods within datasets yielded a wide range of prevalence rates. The CDC estimates CFS occurs up to four times more often in women than in men. The illness can occur at any age, but has the highest prevalence in persons between the ages of 40 and 60. CFS is less prevalent among children and adolescents than among adults.Blood relatives of those who have CFS appear to be more predisposed, implying that genetic factors may increase the risk of susceptibility to the illness.According to the CDC, "CFS is a biological illness, not a psychologic disorder", and those affected "are neither malingering nor seeking secondary gain". The World Health Organization (WHO) classifies CFS as a neurological disease in the ICD-11 for Mortality and Morbidity Statistics (ICD-11). Viral and other infections Post-viral fatigue syndrome (PVFS) or post-viral syndrome describes a type of chronic fatigue syndrome that occurs following a viral infection. A recent review found Epstein–Barr virus (EBV) antibody activity to be higher in patients with CFS, and that a subset of patients with CFS were likely to have increased EBV activity compared to controls. Viral infection is a significant risk factor for CFS, with one study finding 22% of people with EBV experience fatigue six months later, and 9% having strictly defined CFS. A systematic review found that fatigue severity was the main predictor of prognosis in CFS, and did not identify psychological factors linked to prognosis.Another review found that risk factors for developing CFS after mononucleosis, dengue fever, or Q-fever included longer bed-rest during the illness, poorer pre-illness physical fitness, attributing symptoms to physical illness, belief that a long recovery time is needed, as well as pre-infection distress and fatigue. The same review found biological factors such as CD4 and CD8 activation and liver inflammation are predictors of sub-acute fatigue but not CFS. However, these findings are not generally accepted due to the use of the Oxford criteria in selecting patients. The CDC does not recognize attribution of symptoms as a risk factor.A study comparing diagnostic labels found that people labelled with ME had the worst prognosis, while those with PVFS had the best. Whether this is due to those with more severe or longer-lasting symptoms results in a label with the description of ME, or if being labelled with ME adversely causes a more severe or prolonged illness is unclear. Pathophysiology Neurological A range of neurological structural and functional abnormalities is found in people with CFS, including lowered metabolism at the brain stem and reduced blood flow to areas of the brain; these differences are consistent with neurological illness, but not depression or psychological illness. The World Health Organization classes chronic fatigue syndrome as a central nervous system disease.Some neuroimaging studies have observed prefrontal and brainstem hypometabolism; however, sample size was limited. Neuroimaging studies in persons with CFS have identified changes in brain structure and correlations with various symptoms. Results were not consistent across the neuroimaging brain structure studies, and more research is needed to resolve the discrepancies found between the disparate studies.Tentative evidence suggests a relationship between autonomic nervous system dysfunction and diseases such as CFS, fibromyalgia, irritable bowel syndrome, and interstitial cystitis. However, it is unknown if this relationship is causative. Reviews of CFS literature have found autonomic abnormalities such as decreased sleep efficiency, increased sleep latency, decreased slow wave sleep, and abnormal heart rate response to tilt table tests, suggesting a role of the autonomic nervous system in CFS. However, these results were limited by inconsistency.Central sensitization, or increased sensitivity to sensory stimuli such as pain have been observed in CFS. Sensitivity to pain increases after exertion, which is opposite to the normal pattern. Immunological Immunological abnormalities are frequently observed in those with CFS. Decreased NK cell activity is found more often in people with CFS and this correlates with severity of symptoms. People with CFS have an abnormal response to exercise, including increased production of complement products, increased oxidative stress combined with decreased antioxidant response, and increased Interleukin 10, and TLR4, some of which correlates with symptom severity. Increased levels of cytokines have been proposed to account for the decreased ATP production and increased lactate during exercise; however, the elevations of cytokine levels are inconsistent in specific cytokine, albeit frequently found. Similarities have been drawn between cancer and CFS with regard to abnormal intracellular immunological signaling. Abnormalities observed include hyperactivity of Ribonuclease L, a protein activated by IFN, and hyperactivity of NF-κB. Endocrine Evidence points to abnormalities in the hypothalamic-pituitary-adrenal axis (HPA axis) in some, but not all, persons with CFS, which may include slightly low cortisol levels, a decrease in the variation of cortisol levels throughout the day, decreased responsiveness of the HPA axis, and a high serotonergic state, which can be considered to be a "HPA axis phenotype" that is also present in some other conditions, including post-traumatic stress disorder and some autoimmune conditions. It is unclear whether or not decreased cortisol levels of the HPA axis plays a primary role as a cause of CFS, or has a secondary role in the continuation or worsening of symptoms later in the illness. In most healthy adults, the cortisol awakening response shows an increase in cortisol levels averaging 50% in the first half-hour after waking. In people with CFS, this increase apparently is significantly less, but methods of measuring cortisol levels vary, so this is not certain. Autoimmunity Autoimmunity has been proposed to be a factor in CFS, but there are only a few relevant findings so far. There are a subset of patients with increased B cell activity and autoantibodies, possibly as a result of decreased NK cell regulation or viral mimicry. In 2015, a large German study found 29% of ME/CFS patients had elevated autoantibodies to M3 and M4 muscarinic acetylcholine receptors as well as to ß2 adrenergic receptors. A 2016 Australian study found that ME/CFS patients had significantly greater numbers of single nucleotide polymorphisms associated with the gene encoding for M3 muscarinic acetylcholine receptors. Energy metabolism Studies have observed mitochondrial abnormalities in cellular energy production, but recent focus has concentrated on secondary effects that may result in aberrant mitochondrial function because inherent problems with the mitochondria structure or genetics have not been replicated. Diagnosis No characteristic laboratory abnormalities are approved to diagnose CFS; while physical abnormalities can be found, no single finding is considered sufficient for diagnosis. Blood, urine, and other tests are used to rule out other conditions that could be responsible for the symptoms. The CDC states that a medical history should be taken and a mental and physical examination should be done to aid diagnosis. Diagnostic tools The CDC recommends considering the questionnaires and tools described in the 2015 Institute of Medicine report, which include: The Chalder Fatigue Scale Multidimensional Fatigue Inventory Fisk Fatigue Impact Scale The Krupp Fatigue Severity Scale DePaul Symptom Questionnaire CDC Symptom Inventory for CFS Work and Social Adjustment Scale (WSAS) SF-36 / RAND-36: 270 A two-day cardiopulmonary exercise test (CPET) is not necessary for diagnosis, although lower readings on the second day may be helpful in supporting a claim for social security disability. A two-day CPET cannot be used to rule out chronic fatigue syndrome.: 216 Definitions Notable definitions include: Centers for Disease Control and Prevention (CDC) definition (1994), the most widely used clinical and research description of CFS, is also called the Fukuda definition and is a revision of the Holmes or CDC 1988 scoring system. The 1994 criteria require the presence of four or more symptoms beyond fatigue, while the 1988 criteria require six to eight. The ME/CFS 2003 Canadian Clinical working definition states: "A patient with ME/CFS will meet the criteria for fatigue, post-exertional malaise and/or fatigue, sleep dysfunction, and pain; have two or more neurological/cognitive manifestations and one or more symptoms from two of the categories of autonomic, neuroendocrine, and immune manifestations; and the illness persists for at least 6 months". The Myalgic Encephalomyelitis International Consensus Criteria (ICC) published in 2011 is based on the Canadian working definition and has an accompanying primer for clinicians The ICC does not have a six months waiting time for diagnosis. The ICC requires post-exertional neuroimmune exhaustion (PENE) which has similarities with post-exertional malaise, plus at least three neurological symptoms, at least one immune or gastrointestinal or genitourinary symptom, and at least one energy metabolism or ion transportation symptom. Unrefreshing sleep or sleep dysfunction, headaches or other pain, and problems with thinking or memory, and sensory or movement symptoms are all required under the neurological symptoms criterion. According to the ICC, patients with post-exertional neuroimmune exhaustion but only partially meet the criteria should be given the diagnosis of atypical myalgic encephalomyelitis. The 2015 definition by the National Academy of Medicine (then referred to as the "Institute of Medicine") is not a definition of exclusion (differential diagnosis is still required). "Diagnosis requires that the patient have the following three symptoms: 1) A substantial reduction or impairment in the ability to engage in pre-illness levels of occupational, educational, social, or personal activities, that persists for more than 6 months and is accompanied by fatigue, which is often profound, is of new or definite onset (not lifelong), is not the result of ongoing excessive exertion, and is not substantially alleviated by rest, and 2) post-exertional malaise* 3) Unrefreshing sleep*; At least one of the two following manifestations is also required: 1) Cognitive impairment* 2) Orthostatic intolerance" and notes that "*Frequency and severity of symptoms should be assessed. The diagnosis of ME/CFS should be questioned if patients do not have these symptoms at least half the time with moderate, substantial, or severe intensity."Clinical practice guidelines are generally based on case descriptions, with the aim of improving diagnosis, management and treatment. An example is the ME/CFS guideline for the National Health Services in England and Wales, updated in 2021. Other guidance can be found at the New York Department of Health. Differential diagnosis Certain medical conditions can cause chronic fatigue and must be ruled out before a diagnosis of CFS can be given. Hypothyroidism, anemia, coeliac disease (that can occur without gastrointestinal symptoms), diabetes and certain psychiatric disorders are a few of the diseases that must be ruled out if the patient presents with appropriate symptoms. Other diseases, listed by the Centers for Disease Control and Prevention, include infectious diseases (such as Epstein–Barr virus, influenza, HIV infection, tuberculosis, Lyme disease), neuroendocrine diseases (such as thyroiditis, Addisons disease, adrenal insufficiency, Cushings disease), hematologic diseases (such as occult malignancy, lymphoma), rheumatologic diseases (such as fibromyalgia, polymyalgia rheumatica, Sjögrens syndrome, lupus, giant-cell arteritis, polymyositis, dermatomyositis), psychiatric diseases (such as bipolar disorder, schizophrenia, delusional disorders, dementia, anorexia/bulimia nervosa), neuropsychologic diseases (such as obstructive sleep apnea, parkinsonism, multiple sclerosis), and others (such as nasal obstruction from allergies, sinusitis, anatomic obstruction, autoimmune diseases, cancer, chronic hepatitis, some chronic illness, alcohol or other substance abuse, pharmacologic side effects, heavy metal exposure and toxicity, marked body weight fluctuation). Ehlers–Danlos syndromes (EDS) may also have similar symptoms. Medications can also cause side effects that mimic symptoms of CFS.Persons with fibromyalgia (FM, or fibromyalgia syndrome, FMS), like those with CFS, have muscle pain, severe fatigue and sleep disturbances. The presence of allodynia (abnormal pain responses to mild stimulation) and of extensive tender points in specific locations differentiates FM from CFS, although the two diseases often co-occur.Depressive symptoms, if seen in CFS, may be differentially diagnosed from primary depression by the absence of anhedonia, decreased motivation, and guilt; and the presence of somatic symptoms such as sore throat, swollen lymph nodes, and exercise intolerance with post exertional exacerbation of symptoms. Management There is no approved pharmacological treatment, therapy or cure for CFS, although various drugs have been or are being investigated. A 2014 report prepared by the Agency for Healthcare Research and Quality stated that there are wide variations in patient management, that many receive a multifaceted approach to treatment, and that no medications have been approved by the US Food and Drug Administration (FDA) for the treatment of ME/CFS, although several have been used off label. The report concluded that although counseling and graded exercise therapy (GET) have shown some benefits, these interventions have not been studied fully enough to recommend them for all persons affected. The report expressed concern that GET appears to be associated with worsening symptoms in some. The CDC no longer recommends these interventions, and there is some evidence of patient harm.The CDC guide for the management of CFS states that while there is no cure, a number of methods might improve symptoms. Treatment strategies for sleep problems; pain; depression, stress, and anxiety; dizziness and lightheadedness (orthostatic intolerance); and memory and concentration problems are enumerated. Other useful topics that patients and doctors might discuss include carefully monitoring and managing activity to avoid worsening of symptoms, counseling to cope with the impact the illness may have on quality of life, proper nutrition and nutritional supplements that may support better health, and complementary therapies that might help increase energy or decrease pain.The United Kingdoms National Institute for Health and Clinical Excellence (NICE) 2021 guideline directed toward healthcare professionals and patients, specifies the need for shared decision-making between patients and medical care teams and acknowledges the reality and impact of the condition and the symptoms. The NICE guideline covers diagnosis, illness management, and aspects of symptom management: diet, medications, coexisting conditions, flare-ups, and energy management. The guideline recognized symptoms of severe ME/CFS may be misunderstood as neglect or abuse and recommends assessment for safeguarding of persons suspected of having ME/CFS be evaluated by professionals with experience and understanding of the illness. The guideline states that GET is not an appropriate treatment for ME/CFS. CBT might be offered to help a person manage the difficulties of dealing with a chronic illness, not to cure the illness.Prior to publication of the NICE 2021 guideline, Andrew Goddard, president of the Royal College of Physicians, stated there was concern NICE did not adequately consider the experts support and evidence of the benefits of GET and CBT, and urged they be included in the guideline. Various ME/CFS patient groups disputed the benefits of the therapies and stated that GET can make the illness more severe.Comorbid conditions can occur in CFS that may interact with and exacerbate the symptoms of CFS. Appropriate medical intervention for these conditions may be beneficial. The most commonly diagnosed include fibromyalgia, irritable bowel syndrome, depression, anxiety, allergies, and chemical sensitivities. Pacing Pacing, or activity management, is an illness management strategy based on the observation that symptoms tend to increase following mental or physical exertion, and was recommended for CFS in the 1980s. It is now commonly used as a management strategy in chronic illnesses and in chronic pain.Its two forms are symptom-contingent pacing, in which the decision to stop (and rest or change an activity) is determined by self-awareness of an exacerbation of symptoms, and time-contingent pacing, which is determined by a set schedule of activities that a patient estimates he or she is able to complete without triggering post-exertional malaise (PEM). Thus, the principle behind pacing for CFS is to avoid overexertion and an exacerbation of symptoms. It is not aimed at treating the illness as a whole. Those whose illness appears stable may gradually increase activity and exercise levels, but according to the principle of pacing, must rest or reduce their activity levels if it becomes clear that they have exceeded their limits. Use of a heart-rate monitor with pacing to monitor and manage activity levels is recommended by a number of patient groups, and the CDC considers it useful for some individuals to help avoid post-exertional malaise. Energy envelope theory Energy envelope theory, considered to be consistent with pacing, is a management strategy suggested in the 2011 international consensus criteria for ME, which refers to using an "energy bank budget". Energy envelope theory was devised by psychologist Leonard Jason, who previously had CFS. Energy envelope theory states that patients should stay within, and avoid pushing through, the envelope of energy available to them, so as to reduce the post-exertional malaise "payback" caused by overexertion. This may help them make "modest gains" in physical functioning. Several studies have found energy envelope theory to be a helpful management strategy, noting that it reduces symptoms and may increase the level of functioning in CFS. Energy envelope theory does not recommend unilaterally increasing or decreasing activity and is not intended as a therapy or cure for CFS. It has been promoted by various patient groups. Some patient groups recommend using a heart rate monitor to increase awareness of exertion and enable patients to stay within their aerobic threshold envelope. Despite a number of studies showing positive results for energy envelope theory, randomized controlled trials are lacking. Exercise Stretching, movement therapies, and toning exercises are recommended for pain in patients with CFS, and pain medication is also suggested. In many chronic illnesses, aerobic exercise is beneficial, but in chronic fatigue syndrome, the CDC does not recommend it. The CDC states:Any activity or exercise plan for people with ME/CFS needs to be carefully designed with input from each patient. While vigorous aerobic exercise can be beneficial for many chronic illnesses, patients with ME/CFS do not tolerate such exercise routines. Standard exercise recommendations for healthy people can be harmful for patients with ME/CFS. However, it is important that patients with ME/CFS undertake activities that they can tolerate... Counseling The CDC states that counseling may help patients cope with pain caused by CFS, and that talking with a professional counselor or therapist may help people to more effectively manage the symptoms that affect their quality of daily life. Nutrition A proper diet is a significant contributor to the health of any individual. Medical consultation about diet and supplements is recommended for persons with CFS. Persons with CFS may benefit from a balanced diet and properly supervised administration of nutritional support if deficiencies are detected by medical testing. Risks of nutritional supplements include interactions with prescribed medications. Treatment Cognitive behavioral therapy NICE indicates CBT might be offered to help cope with the difficulty of dealing with the symptoms of ME/CFS, but should not be intended to be curative. The rationale behind the use of CBT to change beliefs about the illness is disputed. The CDC states that speaking with a therapist may help people cope with the illness.A 2015 National Institutes of Health report concluded that while counseling and behavior therapies could produce benefits for some people, they may not yield improvement in quality of life, and because of this limitation such therapies should not be considered as a primary treatment, but rather should be used only as one component of a broader approach. This same report stated that although counseling approaches have shown benefit in some measures of fatigue, function and overall improvement, these approaches have been inadequately studied in subgroups of the wider CFS patient population. Further concern was expressed that reporting of negative effects experienced by patients receiving counseling and behavior therapies had been poor. A report by the Institute of Medicine published in 2015 states that it is unclear whether CBT helps to improve cognitive impairments experienced by patients.: 265 A 2014 systematic review reported that there was only limited evidence that patients increased levels of physical activity after receiving CBT. The authors concluded that, as this finding is contrary to the cognitive behavioural model of CFS, patients receiving CBT were adapting to the illness rather than recovering from it. In a letter published online in the Lancet in 2016, Dr Charles Shepherd, medical advisor to the MEA, expressed the view that the contention between patients and researchers lay in "a flawed model of causation that takes no account of the heterogeneity of both clinical presentations and disease pathways that come under the umbrella diagnosis of ME/CFS".Patient organisations have rebuffed the use of CBT as a treatment for CFS to alter illness beliefs. The ME Association (MEA) recommended in 2015, based on the results of an opinion survey of 493 patients who had received CBT treatment in the UK, CBT in its current form should not be used as a primary intervention for people with CFS. In 2019, a large UK survey of people with ME/CFS reported that CBT was ineffective for more than half of respondents. Graded exercise therapy Recommendation for treatment using graded exercise therapy (GET) was removed from NICEs updated Guidelines for Diagnosis and Management of ME/CFS in October 2021. It was removed due to low quality evidence regarding benefit, with the guidelines now stating that clinicians should not prescribe "any programme that ... uses fixed incremental increases in physical activity or exercise, for example, graded exercise therapy." Previously, the National Institutes of Health concluded that while GET could produce benefits, it may not yield improvement in quality of life, and because of this limitation GET should not be considered as a primary treatment. It was recommended to be used only as one component of a broader approach. It noted that a focus on exercise programs had discouraged patient participation in other types of physical activity due to concerns of increased symptoms. An addendum stated, if studies based on the Oxford criteria were excluded, there would be insufficient evidence of the effectiveness of GET.A 2019 updated Cochrane review stated that, exercise therapy probably has a positive effect on fatigue in adults, and slightly improves sleep, but the long-term effects are unknown and has limited relevance to current definitions of ME/CFS. Cochrane started re-evaluating the effects of exercise therapies in chronic fatigue syndrome in 2020.Patient organisations have long criticised the use of exercise therapy, most notably GET, as a treatment for CFS. Based on an opinion survey of patients who had received GET, in 2015 the ME Association concluded, GET in its current delivered form should not be recommended as a primary intervention for persons with CFS. Adaptive pacing therapy APT, not to be confused with pacing, is a therapy rather than a management strategy. APT is based on the idea that CFS involves a person only having a limited amount of available energy, and using this energy wisely will mean the "limited energy will increase gradually".: 5  A large clinical trial known as the PACE trial found APT was no more effective than usual care or specialized medical care. The PACE trial generated much criticism due to the broad Oxford criteria patient selection, the standards of outcome effectiveness were lowered during the study and that re-analysis of the data did not support the magnitude of improvements initially reported.Unlike pacing, APT is based on the cognitive behavioral model of chronic fatigue syndrome and involves increasing activity levels, which it states may temporarily increase symptoms. In APT, the patient first establishes a baseline level of activity, which can be carried out consistently without any post-exertional malaise ("crashes"). APT states that persons should plan to increase their activity, as able. However, APT also requires patients to restrict their activity level to only 70% of what they feel able to do, while also warning against too much rest. This has been described as contradictory, and Jason states that in comparison with pacing, this 70% limit restricts the activities that patients are capable of and results in a lower level of functioning. Jason and Goudsmit, who first described pacing and the energy envelope theory for CFS, have both criticized APT for being inconsistent with the principles of pacing and highlighted significant differences. APT was promoted by Action for ME, the patient charity involved in the PACE trial, until 2019. Rintatolimod Rintatolimod is a double-stranded RNA drug developed to modulate an antiviral immune reaction through activation of toll-like receptor 3. In several clinical trials of CFS, the treatment has shown a reduction in symptoms, but improvements were not sustained after discontinuation. Evidence supporting the use of rintatolimod is deemed low to moderate. The US FDA has denied commercial approval, called a new drug application, citing several deficiencies and gaps in safety data in the trials, and concluded that the available evidence is insufficient to demonstrate its safety or efficacy in CFS. Rintatolimod has been approved for marketing and treatment for persons with CFS in Argentina, and in 2019, FDA regulatory requirements were met for exportation of rintatolimod to the country. Rintatolimod is currently in an experimental trial in the USA to treat both ME/CFS and Long Covid. Prognosis Information on the prognosis of CFS is limited, and the course of the illness is variable. According to the NICE guideliene, CFS "varies in long-term outlook from person to person." Complete recovery, partial improvement, and worsening are all possible. Symptoms generally fluctuate over days, weeks, or longer periods, and some people may experience periods of remission. Overall, "many will need to adapt to living with ME/CFS." Some people who improve need to manage their activities in order to stay improved. Children and teenagers are more likely to recover or improve than adults.A 2005 systematic review found that for untreated CFS, "the median full recovery rate was 5% (range 0–31%) and the median proportion of patients who improved during follow-up was 39.5% (range 8–63%)," and that 8 to 30% of patients were able to return to work. Age at onset, a longer duration of follow-up, less fatigue severity at baseline, and other factors were occasionally, but non consistently, related to outcome. Another review found that children have a better prognosis than adults, with 54–94% having recovered by follow-up, compared to less than 10% of adults returning to pre-illness levels of functioning. Epidemiology The prevalence rates for CFS/ME vary widely depending on "case definitions and diagnostic methods". Based on the 1994 CDC diagnostic criteria, the global prevalence rate for CFS is 0.89%. In comparison, the prevalence rate for the stricter criteria, such as the 1988 CDC "Holmes" criteria for CFS and the 2003 Canadian criteria for ME (both of which, for example, exclude patients with psychiatric diagnoses), produce an incidence rate of only 0.17%. For an example of how these rates impact a nation: the CDC website notes that between 836,000 and 2.5 million Americans have ME/CFS, "but most remain undiagnosed".Females are diagnosed about 1.5 to 2.0 times more often with CFS than males. An estimated 0.5% of children have CFS, and more adolescents are affected with the illness than younger children.: 182 The incidence rate according to age has two peaks, one at 10–19 and another at 30–39 years. The effect is seen both in female and in male data, but is more pronounce in females. It was suggested that this occurs because these age groups may be more vulnerable to CFS. The rate of prevalence is highest between ages 40 and 60. History Myalgic encephalomyelitis From 1934 onwards, outbreaks of a previously unknown illness began to be recorded by doctors. Initially considered to be occurrences of poliomyelitis, the illness was subsequently referred to as "epidemic neuromyasthenia". In the 1950s, the term "benign myalgic encephalomyelitis" was used in relation to a comparable outbreak at the Royal Free Hospital in London. The descriptions of each outbreak were varied, but included symptoms of malaise, tender lymph nodes, sore throat, pain, and signs of encephalomyelitis. The cause of the condition was not identified, although it appeared to be infectious, and the term "benign myalgic encephalomyelitis" was chosen to reflect the lack of mortality, the severe muscular pains, symptoms suggesting damage to the nervous system, and to the presumed inflammatory nature of the disorder. Björn Sigurðsson disapproved of the name, stating that the illness is rarely benign, does not always cause muscle pain, and is possibly never encephalomyelitic. The syndrome appeared in sporadic as well as epidemic cases. In 1969, benign myalgic encephalomyelitis appeared as an entry to the International Classification of Diseases under Diseases of the nervous system. In 1986, Ramsay published the first diagnostic criteria for ME, in which the condition was characterized by: 1) muscle fatiguability in which, even after minimal physical effort, three or more days elapse before full muscle power is restored; 2) extraordinary variability or fluctuation of symptoms, even in the course of one day; and 3) chronicity. By 1988, the continued work of Ramsay had demonstrated that, although the disease rarely resulted in mortality, it was often severely disabling.: 28–29  Because of this, Ramsay proposed that the prefix "benign" be dropped. Chronic fatigue syndrome In the mid-1980s, two large outbreaks of an illness that resembled mononucleosis drew national attention in the United States. Located in Nevada and New York, the outbreaks involved an illness characterized by "chronic or recurrent debilitating fatigue, and various combinations of other symptoms, including a sore throat, lymph node pain and tenderness, headache, myalgia, and arthralgias". An initial link to the Epstein-Barr virus had the illness acquire the name "chronic Epstein-Barr virus syndrome".: 29  In 1987, the CDC convened a working group to reach a consensus on the clinical features of the illness. The working group concluded that CFS was not new, and that the many different names given to it previously reflected widely differing concepts of the illnesss cause and epidemiology. The CDC working group chose "chronic fatigue syndrome" as a more neutral and inclusive name for the illness, but noted that "myalgic encephalomyelitis" was widely accepted in other parts of the world. In 1988, the first definition of CFS was published. Although the cause of the illness remained unknown, several attempts were made to update this definition, most notably in 1994. The most widely referenced diagnostic criteria and definition of CFS for research and clinical purposes were published in 1994 by the CDC. In 2006, the CDC commenced a national program to educate the American public and health-care professionals about CFS. Other medical terms A range of both theorised and confirmed medical entities and naming conventions have appeared historically in the medical literature dealing with ME and CFS. These include: Epidemic neuromyasthenia was a term used for outbreaks with symptoms resembling poliomyelitis. Iceland disease and Akureyri disease were synonymous terms used for an outbreak of fatigue symptoms in Iceland. Low natural killer syndrome, a term used mainly in Japan, reflected research showing diminished in vitro activity of natural killer cells isolated from patients. Neurasthenia has been proposed as an historical diagnosis that occupied a similar medical and cultural space to CFS. Royal Free disease was named after the historically significant outbreak in 1955 at the Royal Free Hospital used as an informal synonym for "benign myalgic encephalomyelitis". Tapanui flu was a term commonly used in New Zealand, deriving from the name of a town, Tapanui, where numerous people had the syndrome. Society and culture Naming Many names have been proposed for the illness. Currently, the most commonly used are "chronic fatigue syndrome", "myalgic encephalomyelitis", and the umbrella term "ME/CFS". Reaching consensus on a name is challenging because the cause and pathology remain unknown.: 29–30 The term "chronic fatigue syndrome" has been criticized by some patients as being both stigmatizing and trivializing, and which in turn prevents the illness from being seen as a serious health problem that deserves appropriate research. While many patients prefer "myalgic encephalomyelitis", which they believe better reflects the medical nature of the illness, there is resistance amongst some clinicians toward the use of myalgic encephalomyelitis on the grounds that the inflammation of the central nervous system (myelitis) implied by the term has not been demonstrated.A 2015 report from the Institute of Medicine recommended the illness be renamed "systemic exertion intolerance disease", (SEID), and suggested new diagnostic criteria, proposing post-exertional malaise, (PEM), impaired function, and sleep problems are core symptoms of ME/CFS. Additionally, they described cognitive impairment and orthostatic intolerance as distinguishing symptoms from other fatiguing illnesses. Economic impact Reynolds et al. (2004) estimated that the illness caused about $20,000 per person with CFS in lost productivity, which totals to $9.1 billion per year in the United States.: 29  This is comparable to other chronic illnesses that extract some of the biggest medical and socioeconomic costs. Direct healthcare costs are estimated at between $9 and $14 billion annually in the US alone. A 2008 study calculated that the total annual cost burden of ME/CFS to society in the US was extensive, and could approach $24.0 billion. A 2017 estimate for the annual economic burden in the United Kingdom from ME/CFS was 3.3 billion pounds sterling. Awareness day 12 May is designated as ME/CFS International Awareness Day. The day is observed so that stakeholders have an occasion to improve the knowledge of "the public, policymakers, and health-care professionals about the symptoms, diagnosis, and treatment of ME/CFS, as well as the need for a better understanding of this complex illness." It was chosen because it is the birthday of Florence Nightingale, who had an illness appearing similar to ME/CFS or fibromyalgia. Doctor–patient relations Some in the medical community do not recognize CFS as a real condition, nor does agreement exist on its prevalence. There has been much disagreement over proposed causes, diagnosis, and treatment of the illness. This uncertainty can significantly affect doctor-patient relations. A 2006 survey of GPs in southwest England found that despite more than two-thirds of them accepting CFS/ME as a recognizable clinical entity, nearly half did not feel confident with making the diagnosis and/or treating the disease. Three other key factors that were significantly, positively associated with GPs attitudes were knowing someone socially with CFS/ME, being male, and seeing more patients with the condition in the last year.From the patient perspective, one 1997 study found that 77% of individuals with CFS reported negative experiences with health-care providers. In a more recent metaanalysis of qualitative studies, a major theme identified in patient discourses was that they felt severely ill, yet were blamed and dismissed. A study of themes in patient newsgroup postings noted key themes relating to denial of social recognition of suffering and feelings of being accused of "simply faking it". Another theme that emerged strongly was that achieving diagnosis and acknowledgement requires tremendous amounts of "hard work" by patients. Blood donation In 2010, several national blood banks adopted measures to discourage or prohibit individuals diagnosed with CFS from donating blood, based on concern following the 2009 claim of a link, between CFS and a retrovirus which was subsequently shown to be unfounded. Organizations adopting these or similar measures included the Canadian Blood Services, the New Zealand Blood Service, the Australian Red Cross Blood Service and the American Association of Blood Banks, In November 2010, the UK National Blood Service introduced a permanent deferral of donation from ME/CFS patients based on the potential harm to those patients that may result from their giving blood. Donation policy in the UK now states, "The condition is relapsing by nature and donation may make symptoms worse, or provoke a relapse in an affected individual." Controversy Much contention has arisen over the cause, pathophysiology, nomenclature, and diagnostic criteria of CFS. Historically, many professionals within the medical community were unfamiliar with CFS, or did not recognize it as a real condition; nor did agreement exist on its prevalence or seriousness. Some people with CFS reject any psychological component.In 1970, two British psychiatrists, McEvedy and Beard, reviewed the case notes of 15 outbreaks of benign myalgic encephalomyelitis and concluded that it was caused by mass hysteria on the part of patients, or altered medical perception of the attending physicians. Their conclusions were based on previous studies that found many normal physical test results, a lack of a discernible cause, and a higher prevalence of the illness in females. Consequently, the authors recommended that the disease should be renamed "myalgia nervosa". This perspective was rejected in a series of case studies by Dr. Melvin Ramsay and other staff of the Royal Free Hospital, the center of a significant outbreak. The psychological hypothesis posed by McEvedy and Beard created great controversy, and convinced a generation of health professionals in the UK that this could be a plausible explanation for the condition, resulting in neglect by many medical specialties. The specialty that did take a major interest in the illness was psychiatry.Because of the controversy, sociologists hypothesized that stresses of modern living might be a cause of the illness, while some in the media used the term "Yuppie flu" and called it a disease of the middle class. People with disabilities from CFS were often not believed and were accused of being malingerers. The November 1990 issue of Newsweek ran a cover story on CFS, which although supportive of an organic cause of the illness, also featured the term yuppie flu, reflecting the stereotype that CFS mainly affected yuppies. The implication was that CFS is a form of burnout. The term yuppie flu is considered offensive by both patients and clinicians.In 2009, the journal Science published a study that identified the XMRV retrovirus in a population of people with CFS. Other studies failed to reproduce this finding, and in 2011, the editor of Science formally retracted its XMRV paper while the Proceedings of the National Academy of Sciences similarly retracted a 2010 paper which had appeared to support the finding of a connection between XMRV and CFS. Research funding United Kingdom The lack of research funding and the funding bias towards biopsychosocial studies and against biomedical studies has been highlighted a number of times by patient groups and a number of UK politicians. A parliamentary inquiry by an ad hoc group of parliamentarians in the United Kingdom, set up and chaired by former MP, Dr Ian Gibson, called the Group on Scientific Research into CFS/ME,: 169–86  was addressed by a government minister claiming that few good biomedical research proposals have been submitted to the Medical Research Council (MRC) in contrast to those for psychosocial research. They were also told by other scientists of proposals that have been rejected, with claims of bias against biomedical research. The MRC confirmed to the group that from April 2003 to November 2006, it has turned down 10 biomedical applications relating to CFS/ME and funded five applications relating to CFS/ME, mostly in the psychiatric/psychosocial domain.In 2008, the MRC set up an expert group to consider how the MRC might encourage new high-quality research into CFS/ME and partnerships between researchers already working on CFS/ME and those in associated areas. It currently lists CFS/ME with a highlight notice, inviting researchers to develop high-quality research proposals for funding. In February 2010, the All-Party Parliamentary Group on ME (APPG on ME) produced a legacy paper, which welcomed the recent MRC initiative, but felt that far too much emphasis in the past had been on psychological research, with insufficient attention to biomedical research, and that further biomedical research must be undertaken to help discover a cause and more effective forms of management for this disease.Controversy surrounds psychologically oriented models of the disease and behavioral treatments conducted in the UK. United States In 1998, $13 million for CFS research was found to have been redirected or improperly accounted for by the United States CDC, and officials at the agency misled Congress about the irregularities. The agency stated that they needed the funds to respond to other public-health emergencies. The director of a US national patient advocacy group charged the CDC had a bias against studying the disease. The CDC pledged to improve their practices and to restore the $13 million to CFS research over three years.On 29 October 2015, the National Institutes of Health declared its intent to increase research on ME/CFS. The NIH Clinical Center was to study individuals with ME/CFS, and the National Institute of Neurological Disorders and Stroke would lead the Trans-NIH ME/CFS Research Working Group as part of a multi-institute research effort. Notable cases In 1989, The Golden Girls (1985–1992) featured chronic fatigue syndrome in a two-episode arc, "Sick and Tired: Part 1" and "Part 2", in which protagonist Dorothy Zbornak, portrayed by Bea Arthur, after a lengthy battle with her doctors in an effort to find a diagnosis for her symptoms, is finally diagnosed with CFS. American author Ann Bannon had CFS. Laura Hillenbrand, author of the popular book Seabiscuit, has struggled with CFS since age 19. Research The different case definitions used to research the illness influence the types of patients selected for studies, and research also suggests subtypes of patients may exist within a heterogeneous population. In one of the definitions, symptoms are accepted that may suggest a psychiatric disorder, while others specifically exclude primary psychiatric disorders. The lack of a single, unifying case definition was criticized in the Institute of Medicines 2015 report for "creating an unclear picture of the symptoms and signs of the disorder" and "complicating comparisons of the results" (study results).: 72 More robust diagnostic methods are being investigated with the aim of identifying unique biomarkers that may be used in clinical testing. In 2019, two different papers were published proposing blood-based biomarkers for CFS. One found that blood cells of CFS patients could be distinguished from healthy controls by their response to hyperosmotic stress. Another found that the red blood cells of CFS patients were stiffer, and thus less able to deform in order to pass through capilliaries. See also Long COVID Unrest (2017 film) References External links "CDC – Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)". Centers for Disease Control. Retrieved 20 May 2020.

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I need a basic explanation for the medical term 'Corneal dystrophy.'

Corneal dystrophy is a group of rare hereditary disorders characterised by bilateral abnormal deposition of substances in the transparent front part of the eye called the cornea. Signs and symptoms Corneal dystrophy may not significantly affect vision in the early stages. However, it does require proper evaluation and treatment for restoration of optimal vision. Corneal dystrophies usually manifest themselves during the first or second decade but sometimes later. It appears as grayish white lines, circles, or clouding of the cornea. Corneal dystrophy can also have a crystalline appearance.There are over 20 corneal dystrophies that affect all parts of the cornea. These diseases share many traits: They are usually inherited. They affect the right and left eyes equally. They are not caused by outside factors, such as injury or diet. Most progress gradually. Most usually begin in one of the five corneal layers and may later spread to nearby layers. Most do not affect other parts of the body, nor are they related to diseases affecting other parts of the eye or body. Most can occur in otherwise totally healthy people, male or female.Corneal dystrophies affect vision in widely differing ways. Some cause severe visual impairment, while a few cause no vision problems and are diagnosed during a specialized eye examination by an ophthalmologist. Other dystrophies may cause repeated episodes of pain without leading to permanent loss of vision. Genetics Different corneal dystrophies are caused by mutations in the CHST6, KRT3, KRT12, PIP5K3, SLC4A11, TACSTD2, TGFBI, and UBIAD1 genes. Mutations in TGFBI which encodes transforming growth factor beta induced cause several forms of corneal dystrophies including granular corneal dystrophy, lattice corneal dystrophy, epithelial basement membrane dystrophy, Reis-Bucklers corneal dystrophy, and Thiel–Behnke dystrophy.Corneal dystrophies may have a simple autosomal dominant, autosomal recessive or rarely X-linked recessive Mendelian mode of inheritance: Pathophysiology A corneal dystrophy can be caused by an accumulation of extraneous material in the cornea, including lipids and cholesterol crystals. Diagnosis Diagnosis can be established on clinical grounds and this may be enhanced with studies on surgically excised corneal tissue and in some cases with molecular genetic analyses. As clinical manifestations widely vary with the different entities, corneal dystrophies should be suspected when corneal transparency is lost or corneal opacities occur spontaneously, particularly in both corneas, and especially in the presence of a positive family history or in the offspring of consanguineous parents.Superficial corneal dystrophies – Meesmann dystrophy is characterized by distinct tiny bubble-like, punctate opacities that form in the central corneal epithelium and to a lesser extent in the peripheral cornea of both eyes during infancy that persists throughout life. Symmetrical reticular opacities form in the superficial central cornea of both eyes at about 4–5 years of age in Reis-Bücklers corneal dystrophy. Patient remains asymptomatic until epithelial erosions precipitate acute episodes of ocular hyperemia, pain, and photophobia. Visual acuity eventually becomes reduced during the second and third decades of life following a progressive superficial haze and an irregular corneal surface. In Thiel–Behnke dystrophy, sub-epithelial corneal opacities form a honeycomb-shaped pattern in the superficial cornea. Multiple prominent gelatinous mulberry-shaped nodules form beneath the corneal epithelium during the first decade of life in gelatinous drop-like corneal dystrophy which cause photophobia, tearing, corneal foreign body sensation and severe progressive loss of vision. Lisch epithelial corneal dystrophy is characterized by feather shaped opacities and microcysts in the corneal epithelium that are arranged in a band-shaped and sometimes whorled pattern. Painless blurred vision sometimes begins after sixty years of life.Corneal stromal dystrophies – Macular corneal dystrophy is manifested by a progressive dense cloudiness of the entire corneal stroma that usually first appears during adolescence and eventually causing severe visual impairment. In granular corneal dystrophy multiple small white discrete irregular spots that resemble bread crumbs or snowflakes become apparent beneath Bowman zone in the superficial central corneal stroma. They initially appear within the first decade of life. Visual acuity is more or less normal. Lattice dystrophy starts as fine branching linear opacities in Bowmans layer in the central area and spreads to the periphery. Recurrent corneal erosions may occur. The hallmark of Schnyder corneal dystrophy is the accumulation of crystals within the corneal stroma which cause corneal clouding typically in a ring-shaped fashion.Posterior corneal dystrophies – Fuchs corneal dystrophy presents during the fifth or sixth decade of life. The characteristic clinical findings are excrescences on a thickened Descemet membrane (cornea guttae), generalized corneal edema and decreased visual acuity. In advanced cases, abnormalities are found in all the layers of the cornea. In posterior polymorphous corneal dystrophy small vesicles appear at the level of Descemet membrane. Most patients remain asymptomatic and corneal edema is usually absent. Congenital hereditary endothelial corneal dystrophy is characterized by a diffuse ground-glass appearance of both corneas and markedly thickened (2–3 times thicker than normal) corneas from birth or infancy. Differential diagnosis Main differential diagnosis include various causes of monoclonal gammopathy, lecithin-cholesterol-acyltransferase deficiency, Fabry disease, cystinosis, tyrosine transaminase deficiency, systemic lysosomal storage diseases, and several skin diseases (X-linked ichthyosis, keratosis follicularis spinolosa decalvans). Historically, an accumulation of small gray variable shaped punctate opacities of variable shape in the central deep corneal stroma immediately anterior to Descemet membrane were designated deep filiform dystrophy and cornea farinata because of their resemblance to commas, circles, lines, threads (filiform), flour (farina) or dots. These abnormalities are now known to accompany X-linked ichthyosis, steroid sulfatase deficiency, caused by steroid sulfatase gene mutations and are currently usually not included under the rubric of the corneal dystrophies.In the past, the designation vortex corneal dystrophy (corneal verticillata) was applied to a corneal disorder characterized by the presence of innumerable tiny brown spots arranged in curved whirlpool-like lines in the superficial cornea. An autosomal dominant mode of transmission was initially suspected, but later it was realized that these individuals were affected hemizygous males and asymptomatic female carriers of an X-linked systemic metabolic disease caused by a deficiency of α-galactosidase, known as Fabry disease. Classification Corneal dystrophies were commonly subdivided depending on its specific location within the cornea into anterior, stromal, or posterior according to the layer of the cornea affected by the dystrophy.In 2015 the ICD3 classification was published. and has classified disease into four groups as follows: Epithelial and subepithelial dystrophies Epithelial basement membrane dystrophy Epithelial recurrent erosion dystrophies (Franceschetti corneal dystrophy, Dystrophia Smolandiensis, and Dystrophia Helsinglandica) Subepithelial mucinous corneal dystrophy Meesmann corneal dystrophy Lisch epithelial corneal dystrophy Gelatinous drop-like corneal dystrophy Bowman Layer dystrophies Reis–Bücklers corneal dystrophy Thiel–Behnke corneal dystrophy Stromal dystrophies- TGFB1 corneal dystrophies Lattice corneal dystrophy, type 1 variants (III, IIIA, I/IIIA, IV) of lattice corneal dystrophy Granular corneal dystrophy, type 1 Granular corneal dystrophy, type 2 Stromal dystrophies Macular corneal dystrophy Schnyder crystalline corneal dystrophy Congenital stromal corneal dystrophy Fleck corneal dystrophy Posterior amorphous corneal dystrophy Central cloudy dystrophy of François Pre-Descemet corneal dystrophy Endothelial dystrophies Fuchs dystrophy Posterior polymorphous corneal dystrophy Congenital hereditary endothelial dystrophy X-linked endothelial corneal dystrophyThe following (now historic) classification was by Klintworth:Superficial dystrophies: Epithelial basement membrane dystrophy Meesmann juvenile epithelial corneal dystrophy Gelatinous drop-like corneal dystrophy Lisch epithelial corneal dystrophy Subepithelial mucinous corneal dystrophy Reis-Bucklers corneal dystrophy Thiel–Behnke dystrophyStromal dystrophies: Lattice corneal dystrophy Granular corneal dystrophy Macular corneal dystrophy Schnyder crystalline corneal dystrophy Congenital stromal corneal dystrophy Fleck corneal dystrophyPosterior dystrophies: Fuchs dystrophy Posterior polymorphous corneal dystrophy Congenital hereditary endothelial dystrophy Treatment Early stages may be asymptomatic and may not require any intervention. Initial treatment may include hypertonic eyedrops and ointment to reduce the corneal edema and may offer symptomatic improvement prior to surgical intervention.Suboptimal vision caused by corneal dystrophy may be helped with scleral contact lenses but eventually usually requires surgical intervention in the form of corneal transplantation. Penetrating keratoplasty, a common type of corneal transplantation, is commonly performed for extensive corneal dystrophy.With penetrating keratoplasty (corneal transplant), the long-term results are good to excellent. Recent surgical improvements have been made which have increased the success rate for this procedure. However, recurrence of the disease in the donor graft may happen. Superficial corneal dystrophies do not need a penetrating keratoplasty as the deeper corneal tissue is unaffected, therefore a lamellar keratoplasty may be used instead.Phototherapeutic keratectomy (PTK) can be used to excise or ablate the abnormal corneal tissue. Patients with superficial corneal opacities are suitable candidates for this procedure. See also Recurrent corneal erosion Keratoconus Keratoglobus Corneal dystrophies in dogs Dyskeratosis corneal and photophobia in XLPDR == References ==

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I'm not familiar with the medical term 'Syringobulbia.' Could you provide some insights?

Syringobulbia is a medical condition in which syrinxes, or fluid-filled cavities, affect the brainstem (usually the lower brainstem). The exact cause is often unknown, but may be linked to a widening of the central canal of the spinal cord. This may affect one or more cranial nerves, resulting in various kinds of facial palsies. Sensory and motor nerve pathways may be affected by interruption or compression of nerves. This disorder is associated with syringomyelia, a syrinx limited to the spinal cord. It can be diagnosed using magnetic resonance imaging. Symptoms may be treated with tricyclic antidepressants. Signs and symptoms Syringobulbia usually causes pain. It may also cause a loss of sense of temperature. Alveolar hypoventilation (insufficient breathing, a type of central hypoventilation syndrome) may occur, with hypercapnia (excess blood CO2), stridor (an unusual breathing sound), and irregular breathing. Cause Syringobulbia may be caused by a birth defect, trauma or tumor growth. The exact trigger is unknown, but may be linked to a widening of the central canal of the spinal cord. Mechanism Syringobulbia affects the lower part of the brainstem. The central canal of the spinal cord may be widened. A fluid-filled lesion forms, known as a syrinx. This can vary in size significantly between patients. Nerve fibres may be compressed where they cross the midline, or in other parts of the spinal cord. Cranial nerves may be affected.Syringobulbia may be associated with syringomyelia, a syrinx limited to the spinal cord. Diagnosis Syringobulbia may be diagnosed using magnetic resonance imaging. Treatment The pain caused by syringobulbia may be treated with tricyclic antidepressants. See also Syrinx Syringomyelia References External links 14-182d. at Merck Manual of Diagnosis and Therapy Professional Edition

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I'm looking for a concise explanation of the medical term 'Marburg virus disease.'

Marburg virus disease (MVD; formerly Marburg hemorrhagic fever) is a viral hemorrhagic fever in humans and primates caused by either of the two Marburgviruses: Marburg virus (MARV) and Ravn virus (RAVV). Its clinical symptoms are very similar to those of Ebola virus disease (EVD).Egyptian fruit bats are believed to be the normal carrier in nature and Marburg virus RNA has been isolated from them. Signs and symptoms The most detailed study on the frequency, onset, and duration of MVD clinical signs and symptoms was performed during the 1998–2000 mixed MARV/RAVV disease outbreak. A maculopapular rash, petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites) are typical hemorrhagic manifestations. However, contrary to popular belief, hemorrhage does not lead to hypovolemia and is not the cause of death (total blood loss is minimal except during labor). Instead, death occurs due to multiple organ dysfunction syndrome (MODS) due to fluid redistribution, hypotension, disseminated intravascular coagulation, and focal tissue necroses.Clinical phases of Marburg Hemorrhagic Fevers presentation are described below. Note that phases overlap due to variability between cases. Incubation: 2–21 days, averaging 5–9 days. Generalization Phase: Day 1 up to Day 5 from the onset of clinical symptoms. MHF presents with a high fever 104 °F (~40˚C) and a sudden, severe headache, with accompanying chills, fatigue, nausea, vomiting, diarrhea, pharyngitis, maculopapular rash, abdominal pain, conjunctivitis, and malaise. Early Organ Phase: Day 5 up to Day 13. Symptoms include prostration, dyspnea, edema, conjunctival injection, viral exanthema, and CNS symptoms, including encephalitis, confusion, delirium, apathy, and aggression. Hemorrhagic symptoms typically occur late and herald the end of the early organ phase, leading either to eventual recovery or worsening and death. Symptoms include bloody stools, ecchymoses, blood leakage from venipuncture sites, mucosal and visceral hemorrhaging, and possibly hematemesis. Late Organ Phase: Day 13 up to Day 21+. Symptoms bifurcate into two constellations for survivors and fatal cases. Survivors will enter a convalescence phase, experiencing myalgia, fibromyalgia, hepatitis, asthenia, ocular symptoms, and psychosis. Fatal cases continue to deteriorate, experiencing continued fever, obtundation, coma, convulsions, diffuse coagulopathy, metabolic disturbances, shock and death, with death typically occurring between days 8 and 16. Causes MVD is caused by two viruses; Marburg virus (MARV) and Ravn virus (RAVV), family Filoviridae.Marburgviruses are endemic in arid woodlands of equatorial Africa. Most marburgvirus infections were repeatedly associated with people visiting natural caves or working in mines. In 2009, the successful isolation of infectious MARV and RAVV was reported from healthy Egyptian fruit bat caught in caves. This isolation strongly suggests that Old World fruit bats are involved in the natural maintenance of marburgviruses and that visiting bat-infested caves is a risk factor for acquiring marburgvirus infections. Further studies are necessary to establish whether Egyptian rousettes are the actual hosts of MARV and RAVV or whether they get infected via contact with another animal and therefore serve only as intermediate hosts. Another risk factor is contact with nonhuman primates, although only one outbreak of MVD (in 1967) was due to contact with infected monkeys.Contrary to Ebola virus disease (EVD), which has been associated with heavy rains after long periods of dry weather, triggering factors for spillover of marburgviruses into the human population have not yet been described. Diagnosis MVD is clinically indistinguishable from Ebola virus disease (EVD), and it can also easily be confused with many other diseases prevalent in Equatorial Africa, such as other viral hemorrhagic fevers, falciparum malaria, typhoid fever, shigellosis, rickettsial diseases such as typhus, cholera, gram-negative sepsis, borreliosis such as relapsing fever or EHEC enteritis. Other infectious diseases that ought to be included in the differential diagnosis include leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis, trypanosomiasis, visceral leishmaniasis, hemorrhagic smallpox, measles, and fulminant viral hepatitis. Non-infectious diseases that can be confused with MVD are acute promyelocytic leukemia, hemolytic uremic syndrome, snake envenomation, clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura, hereditary hemorrhagic telangiectasia, Kawasaki disease, and even warfarin intoxication. The most important indicator that may lead to the suspicion of MVD at clinical examination is the medical history of the patient, in particular the travel and occupational history (which countries and caves were visited?) and the patients exposure to wildlife (exposure to bats or bat excrements?). MVD can be confirmed by isolation of marburgviruses from or by detection of marburgvirus antigen or genomic or subgenomic RNAs in patient blood or serum samples during the acute phase of MVD. Marburgvirus isolation is usually performed by inoculation of grivet kidney epithelial Vero E6 or MA-104 cell cultures or by inoculation of human adrenal carcinoma SW-13 cells, all of which react to infection with characteristic cytopathic effects. Filovirions can easily be visualized and identified in cell culture by electron microscopy due to their unique filamentous shapes, but electron microscopy cannot differentiate the various filoviruses alone despite some overall length differences. Immunofluorescence assays are used to confirm marburgvirus presence in cell cultures. During an outbreak, virus isolation and electron microscopy are most often not feasible options. The most common diagnostic methods are therefore RT-PCR in conjunction with antigen-capture ELISA, which can be performed in field or mobile hospitals and laboratories. Indirect immunofluorescence assays (IFAs) are not used for diagnosis of MVD in the field anymore. Classification Marburg virus disease (MVD) is the official name listed in the World Health Organizations International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10) for the human disease caused by any of the two marburgviruses Marburg virus (MARV) and Ravn virus (RAVV). In the scientific literature, Marburg hemorrhagic fever (MHF) is often used as an unofficial alternative name for the same disease. Both disease names are derived from the German city Marburg, where MARV was first discovered. Transmission The details of the initial transmission of MVD to humans remain incompletely understood. Transmission most likely occurs from Egyptian fruit bats or another natural host, such as non-human primates or through the consumption of bush meat, but the specific routes and body fluids involved are unknown. Human-to-human transmission of MVD occurs through direct contact with infected bodily fluids such as blood. Prevention There are currently no Food and Drug Administration-approved vaccines for the prevention of MVD. Many candidate vaccines have been developed and tested in various animal models. Of those, the most promising ones are DNA vaccines or based on Venezuelan equine encephalitis virus replicons, vesicular stomatitis Indiana virus (VSIV) or filovirus-like particles (VLPs) as all of these candidates could protect nonhuman primates from marburgvirus-induced disease. DNA vaccines have entered clinical trials. Marburgviruses are highly infectious, but not very contagious. They do not get transmitted by aerosol during natural MVD outbreaks. Due to the absence of an approved vaccine, prevention of MVD therefore relies predominantly on quarantine of confirmed or high probability cases, proper personal protective equipment, and sterilization and disinfection. Endemic zones The natural maintenance hosts of marburg viruses remain to be identified unequivocally. However, the isolation of both MARV and RAVV from bats and the association of several MVD outbreaks with bat-infested mines or caves strongly suggests that bats are involved in marburg virus transmission to humans. Avoidance of contact with bats and abstaining from visits to caves is highly recommended, but may not be possible for those working in mines or people dependent on bats as a food source. During outbreaks Since marburgviruses are not spread via aerosol, the most straightforward prevention method during MVD outbreaks is to avoid direct (skin-to-skin) contact with patients, their excretions and body fluids, and any possibly contaminated materials and utensils. Patients should be isolated, but still are safe to be visited by family members. Medical staff should be trained in and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, should be discouraged or modified, ideally with the help of local traditional healers. In the laboratory Marburgviruses are World Health Organization Risk Group 4 Pathogens, requiring Biosafety Level 4-equivalent containment, laboratory researchers have to be properly trained in BSL-4 practices and wear proper personal protective equipment. Treatment There is currently no effective marburgvirus-specific therapy for MVD. Treatment is primarily supportive in nature and includes minimizing invasive procedures, balancing fluids and electrolytes to counter dehydration, administration of anticoagulants early in infection to prevent or control disseminated intravascular coagulation, administration of procoagulants late in infection to control hemorrhaging, maintaining oxygen levels, pain management, and administration of antibiotics or antifungals to treat secondary infections. Prognosis Prognosis is generally poor. If a patient survives, recovery may be prompt and complete, or protracted with sequelae, such as orchitis, hepatitis, uveitis, parotitis, desquamation, or alopecia. Importantly, MARV is known to be able to persist in some survivors and to either reactivate and cause a secondary bout of MVD or to be transmitted via sperm, causing secondary cases of infection and disease.Of the 252 people who contracted Marburg during the 2004–2005 outbreak of a particularly virulent serotype in Angola, 227 died, for a case fatality rate of 90%. Although all age groups are susceptible to infection, children are rarely infected. In the 1998–2000 Congo epidemic, only 8% of the cases were children less than 5 years old. Epidemiology Below is a table of outbreaks concerning MVD from 1967 to 2021: 1967 outbreak MVD was first documented in 1967, when 31 people became ill in the German towns of Marburg and Frankfurt am Main, and in Belgrade, Yugoslavia. The outbreak involved 25 primary MARV infections and seven deaths, and six nonlethal secondary cases. The outbreak was traced to infected grivets (species Chlorocebus aethiops) imported from an undisclosed location in Uganda and used in developing poliomyelitis vaccines. The monkeys were received by Behringwerke, a Marburg company founded by the first winner of the Nobel Prize in Medicine, Emil von Behring. The company, which at the time was owned by Hoechst, was originally set up to develop sera against tetanus and diphtheria. Primary infections occurred in Behringwerke laboratory staff while working with grivet tissues or tissue cultures without adequate personal protective equipment. Secondary cases involved two physicians, a nurse, a post-mortem attendant, and the wife of a veterinarian. All secondary cases had direct contact, usually involving blood, with a primary case. Both physicians became infected through accidental skin pricks when drawing blood from patients. A popular science account of this outbreak can be found in Laurie Garrett’s book The Coming Plague. 1975 cases In 1975, an Australian tourist became infected with MARV in Rhodesia (today Zimbabwe). He died in a hospital in Johannesburg, South Africa. His girlfriend and an attending nurse were subsequently infected with MVD, but survived. 1980 cases A case of MARV infection occurred in 1980 in Kenya. A French man, who worked as an electrical engineer in a sugar factory in Nzoia (close to Bungoma) at the base of Mount Elgon (which contains Kitum Cave), became infected by unknown means and died on 15 January shortly after admission to Nairobi Hospital. The attending physician contracted MVD, but survived. A popular science account of these cases can be found in Richard Preston’s book The Hot Zone (the French man is referred to under the pseudonym “Charles Monet”, whereas the physician is identified under his real name, Shem Musoke). 1987 case In 1987, a single lethal case of RAVV infection occurred in a 15-year-old Danish boy, who spent his vacation in Kisumu, Kenya. He had visited Kitum Cave on Mount Elgon prior to travelling to Mombasa, where he developed clinical signs of infection. The boy died after transfer to Nairobi Hospital. A popular science account of this case can be found in Richard Preston’s book The Hot Zone (the boy is referred to under the pseudonym “Peter Cardinal”). 1988 laboratory infection In 1988, researcher Nikolai Ustinov infected himself lethally with MARV after accidentally pricking himself with a syringe used for inoculation of guinea pigs. The accident occurred at the Scientific-Production Association "Vektor" (today the State Research Center of Virology and Biotechnology "Vektor") in Koltsovo, USSR (today Russia). Very little information is publicly available about this MVD case because Ustinovs experiments were classified. A popular science account of this case can be found in Ken Alibek’s book Biohazard. 1990 laboratory infection Another laboratory accident occurred at the Scientific-Production Association "Vektor" (today the State Research Center of Virology and Biotechnology "Vektor") in Koltsovo, USSR, when a scientist contracted MARV by unknown means. 1998–2000 outbreak A major MVD outbreak occurred among illegal gold miners around Goroumbwa mine in Durba and Watsa, Democratic Republic of Congo from 1998 to 2000, when co-circulating MARV and RAVV caused 154 cases of MVD and 128 deaths. The outbreak ended with the flooding of the mine. 2004–2005 outbreak In early 2005, the World Health Organization (WHO) began investigating an outbreak of viral hemorrhagic fever in Angola, which was centered in the northeastern Uíge Province but also affected many other provinces. The Angolan government had to ask for international assistance, pointing out that there were only approximately 1,200 doctors in the entire country, with some provinces having as few as two. Health care workers also complained about a shortage of personal protective equipment such as gloves, gowns, and masks. Médecins Sans Frontières (MSF) reported that when their team arrived at the provincial hospital at the center of the outbreak, they found it operating without water and electricity. Contact tracing was complicated by the fact that the countrys roads and other infrastructure were devastated after nearly three decades of civil war and the countryside remained littered with land mines. Americo Boa Vida Hospital in the Angolan capital Luanda set up a special isolation ward to treat infected people from the countryside. Unfortunately, because MVD often results in death, some people came to view hospitals and medical workers with suspicion and treated helpers with hostility. For instance, a specially-equipped isolation ward at the provincial hospital in Uíge was reported to be empty during much of the epidemic, even though the facility was at the center of the outbreak. WHO was forced to implement what it described as a "harm reduction strategy", which entailed distributing disinfectants to affected families who refused hospital care. Of the 252 people who contracted MVD during outbreak, 227 died. 2007 cases In 2007, four miners became infected with marburgviruses in Kamwenge District, Uganda. The first case, a 29-year-old man, became symptomatic on July 4, 2007, was admitted to a hospital on July 7, and died on July 13. Contact tracing revealed that the man had had prolonged close contact with two colleagues (a 22-year-old man and a 23-year-old man), who experienced clinical signs of infection before his disease onset. Both men had been admitted to hospitals in June and survived their infections, which were proven to be due to MARV. A fourth, 25-year-old man, developed MVD clinical signs in September and was shown to be infected with RAVV. He also survived the infection. 2008 cases On July 10, 2008, the Netherlands National Institute for Public Health and the Environment reported that a 41-year-old Dutch woman, who had visited Python Cave in Maramagambo Forest during her holiday in Uganda had MVD due to MARV infection, and had been admitted to a hospital in the Netherlands. The woman died under treatment in the Leiden University Medical Centre in Leiden on July 11. The Ugandan Ministry of Health closed the cave after this case. On January 9 of that year an infectious diseases physician notified the Colorado Department of Public Health and the Environment that a 44-year-old American woman who had returned from Uganda had been hospitalized with a fever of unknown origin. At the time, serologic testing was negative for viral hemorrhagic fever. She was discharged on January 19, 2008. After the death of the Dutch patient and the discovery that the American woman had visited Python Cave, further testing confirmed the patient demonstrated MARV antibodies and RNA. 2017 Uganda outbreak In October 2017 an outbreak of Marburg virus disease was detected in Kween District, Eastern Uganda. All three initial cases (belonging to one family – two brothers and one sister) had died by 3 November. The fourth case – a health care worker – developed symptoms on 4 November and was admitted to a hospital. The first confirmed case traveled to Kenya before the death. A close contact of the second confirmed case traveled to Kampala. It is reported that several hundred people may have been exposed to infection. 2021 Guinean cases In August 2021, two months after the re-emergent Ebola epidemic in the Guéckédou prefecture was declared over, a case of the Marburg disease was confirmed by health authorities through laboratory analysis. Other potential case of the disease in a contact awaits official results. These are the first cases of the Marburg hemorrhagic fever confirmed to happen in West Africa. The cases of Marburg also have been identified in Guéckédou. On August 10, the WHO said health authorities in Guinea have confirmed one death from Marburg virus. 2022 Ghanaian cases In July 2022, preliminary analysis of samples taken from two patients – both deceased – in Ghana indicated the cases were positive for Marburg. However, per standard procedure, the samples were sent to the Pasteur Institute of Dakar for confirmation. On 17 July 2022 the two cases were confirmed by Ghana, which caused the country to declare a Marburg virus disease outbreak. An additional case was identified, bringing the total to three. Research Experimentally, recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of MARV has been used successfully in nonhuman primate models as post-exposure prophylaxis. A vaccine candidate has been effective in nonhuman primates. Experimental therapeutic regimens relying on antisense technology have shown promise, with phosphorodiamidate morpholino oligomers (PMOs) targeting the MARV genome New therapies from Sarepta and Tekmira have also been successfully used in humans as well as primates. See also List of other Filoviridae outbreaks References Further reading External links ViralZone: Marburg virus Centers for Disease Control, Infection Control for Viral Haemorrhagic Fevers In the African Health Care Setting. Center for Disease Control, Marburg Haemorrhagic Fever. Center for Disease Control, Known Cases and Outbreaks of Marburg Haemorrhagic Fever Ebola and Marburg haemorrhagic fever (10 July 2008) factsheet from European Centre for Disease Prevention and Control World Health Organization, Marburg Haemorrhagic Fever. Red Cross PDF Virus Pathogen Database and Analysis Resource (ViPR): Filoviridae

You are a medical lexicon. Explain medical terminology with depth and clarity, making sure the information is both accurate and easy to grasp.

I'd like to learn more about the medical term 'Lymphocytopenia.' Can you provide some details?

Lymphocytopenia is the condition of having an abnormally low level of lymphocytes in the blood. Lymphocytes are a white blood cell with important functions in the immune system. It is also called lymphopenia. The opposite is lymphocytosis, which refers to an excessive level of lymphocytes. Lymphocytopenia may be present as part of a pancytopenia, when the total numbers of all types of blood cells are reduced. Classification In some cases, lymphocytopenia can be further classified according to which kind of lymphocytes are reduced. If all three kinds of lymphocytes are suppressed, then the term is used without further qualification. In T lymphocytopenia, there are too few T lymphocytes, but normal numbers of other lymphocytes. It causes, and manifests as, a T cell deficiency. This is usually caused by HIV infection (resulting in AIDS), but may be Idiopathic CD4+ lymphocytopenia (ICL), which is a very rare heterogeneous disorder defined by CD4+ T-cell counts below 300 cells/μL in the absence of any known immune deficiency condition, such as human immunodeficiency virus (HIV) infection or chemotherapy. In B lymphocytopenia, there are too few B lymphocytes, but possibly normal numbers of other lymphocytes. It causes, and manifests as, a humoral immune deficiency. This is usually caused by medications that suppress the immune system. In NK lymphocytopenia, there are too few natural killer cells, but normal numbers of other lymphocytes. This is very rare. Causes The most common cause of temporary lymphocytopenia is a recent infection, such as the common cold.Lymphocytopenia, but not idiopathic CD4+ lymphocytopenia, is associated with corticosteroid use, infections with HIV and other viral, bacterial, and fungal agents, malnutrition, systemic lupus erythematosus, severe stress, intense or prolonged physical exercise (due to cortisol release), rheumatoid arthritis, sarcoidosis, multiple sclerosis, and iatrogenic (caused by other medical treatments) conditions. Lymphocytopenia is a frequent, temporary result from many types of chemotherapy, such as with cytotoxic agents or immunosuppressive drugs. Some malignancies that have spread to involve the bone marrow, such as leukemia or advanced Hodgkins disease, also cause lymphocytopenia. Another cause is infection with Influenza A virus subtype H1N1 (and other subtypes of the Influenza A virus) and is then often associated with Monocytosis; H1N1 was responsible for the Spanish flu, the 2009 flu pandemic and in 2016 for the Influenza-epidemic in Brazil. The SARS disease caused lymphocytopenia. Among patients with laboratory-confirmed COVID-19 in Wuhan China through January 29th, 2020, 83.2 percent had Lymphocytopenia at admission.Large doses of radiation, such as those involved with nuclear accidents or medical whole body radiation, may cause lymphocytopenia. Diagnosis Lymphocytopenia is diagnosed when the complete blood count shows a lymphocyte count lower than the age-appropriate reference interval (for example, below 1.0 x 10(9)/L in an adult). Prognosis Lymphocytopenia that is caused by infections tends to resolve once the infection has cleared. Patients with idiopathic CD4+ lymphocytopenia may have either abnormally low but stable CD4+ cell counts, or abnormally low and progressively falling CD4+ cell counts; the latter condition is terminal. Other animals Lymphocytopenia caused by Feline Leukemia Virus and Feline immunodeficiency virus retroviral infections is treated with Lymphocyte T-Cell Immune Modulator. References == External links ==

You are an assistant in medical learning. Your role is to clarify medical terminology, ensuring the information is both accurate and accessible.

Could you offer a clear explanation of the term 'Korsakoff syndrome' as used in the medical field?

Korsakoff syndrome (KS) is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation. This neurological disorder is caused by a deficiency of thiamine (vitamin B1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. Korsakoff syndrome is often accompanied by Wernicke encephalopathy; this combination is called Wernicke–Korsakoff syndrome.Korsakoff syndrome is named after Sergei Korsakoff, the Russian neuropsychiatrist who described it during the late 19th century. Signs and symptoms There are seven major symptoms of Korsakoff syndrome, an amnestic-confabulatory syndrome: anterograde amnesia, memory loss for events after the onset of the syndrome retrograde amnesia, memory loss extends back for some time before the onset of the syndrome amnesia of fixation, also known as fixation amnesia (loss of immediate memory, a person being unable to remember events of the past few minutes) confabulation, that is, invented memories which are then taken as true, due to gaps in memory, with such gaps sometimes associated with blackouts minimal content in conversation lack of insight apathy – interest in things is quickly lost, and there is an indifference to changeBenon R. and LeHuché R. (1920) described the characteristic signs of Korsakoff syndrome with some additional features including: confabulation (false memories), fixation amnesia, paragnosia or false recognition of places, mental excitation, and euphoria.Thiamine is essential for the decarboxylation of pyruvate, and deficiency during this metabolic process is thought to cause damage to the medial thalamus and mammillary bodies of the posterior hypothalamus, as well as generalized cerebral atrophy. These brain regions are all parts of the limbic system, which is heavily involved in emotion and memory. KS involves neuronal loss, that is, damage to neurons; gliosis, which is a result of damage to supporting cells of the central nervous system, and bleeding also occurs in mammillary bodies. Damage to the medial dorsal nucleus or anterior nuclei of the thalamus (limbic-specific nuclei) is also associated with this disorder. Cortical dysfunction may have arisen from thiamine deficiency, alcohol neurotoxicity, and/or structural damage in the diencephalon.Originally, it was thought that a lack of initiative and a flat affect were important characteristics of emotional presentation in those affected. Studies have questioned this, proposing that neither is necessarily a symptom of KS. Research suggesting that people with Korsakoff syndrome are emotionally unimpaired has made this a controversial topic. It can be argued that apathy, which is a usual characteristic, reflects a deficit of emotional expressions, without affecting the experience or perception of emotion.KS causes deficits in declarative memory in most people, but leaves implicit spatial, verbal, and procedural memory functioning intact. People with KS have deficits in the processing of contextual information. Context memories refers to the where and when of experiences, and is an essential part of recollection. The ability to store and retrieve this information, such as spatial location or temporal order information, is impaired. Research has also suggested that people with Korsakoff syndrome have impaired executive functions, which can lead to behavioral problems and interfere with daily activities. It is unclear, however, which executive functions are affected most. Nonetheless, IQ is usually not affected by the brain damage associated with Korsakoffs syndrome.At first it was thought that those with KS used confabulation to fill in memory gaps. However, it has been found that confabulation and amnesia do not necessarily co-occur. Studies have shown that there is dissociation between provoked confabulation, spontaneous confabulation (which is unprovoked), and false memories. That is, people affected could be led to believe certain things had happened which actually had not, but so could people without Korsakoff syndrome. Causes Conditions resulting in thiamine deficiency and its effects include chronic alcoholism and severe malnutrition. Alcoholism may co-occur with poor nutrition, which in addition to inflammation of the stomach lining, causes thiamine deficiency. Other causes include dietary deficiencies, prolonged vomiting, eating disorders, and the effects of chemotherapy. It can also occur in pregnant women who have a form of extreme morning sickness known as hyperemesis gravidarum. Mercury poisoning can also lead to Korsakoff syndrome. Though it does not always co-occur, this disorder can emerge frequently as a consequential result of Wernickes encephalopathy.PET scans show that there is a decrease of glucose metabolism in the frontal, parietal and cingulated regions of the brain in those with Korsakoff syndrome. This may contribute to memory loss and amnesia. Structural neuroimaging has also shown the presence of midline diencephalic lesions and cortical atrophy.Structural lesions of the central nervous system, though rare, can also contribute to symptoms of KS. Severe damage to the medial dorsal nucleus inevitably results in memory deficit. Additionally, autopsies of people who had KS have showed lesions in both the midline and anterior thalamus, and thalamic infarctions. Bilateral infarctions to the thalamus can result in Korsakoff-induced amnesia as well. These findings imply damage to anterior thalamic nuclei can result in disruptive memory. Risk factors A number of factors may increase a persons risk to develop Korsakoff syndrome. These factors are often related to general health and diet. Age Alcoholism Chemotherapy Dialysis Extreme dieting Genetic factors Diagnosis KS is primarily a clinical diagnosis; imaging and lab tests are not necessary. Prevention The most effective method of preventing AKS is to avoid thiamine deficiency. In Western nations, the most common causes of such a deficiency are alcoholism and eating disorders. Because these are behavioral-induced causes, Korsakoff syndrome is essentially considered a preventable disease. Thus, fortifying foods with thiamine, or requiring companies that sell alcoholic beverages to supplement them with B vitamins in general or thiamine in particular, could avert many cases. Treatment It was once assumed that anyone with KS would eventually need full-time care. This is still often the case, but rehabilitation can help regain some, albeit often limited, level of independence. Treatment involves the replacement or supplementation of thiamine by intravenous or intramuscular injection, together with proper nutrition and hydration. However, the amnesia and brain damage caused by the disease does not always respond to thiamine replacement therapy. In some cases, drug therapy is recommended. Treatment typically requires taking thiamine orally for 3 to 12 months, though only about 20 percent of cases are reversible. If treatment is successful, improvement will become apparent within two years, although recovery is slow and often incomplete.As an immediate form of treatment, a pairing of intravenous or intramuscular thiamine with a high concentration of B-complex vitamins can be administered three times daily for 2–3 days. In most cases, an effective response will be observed. A single dose of 1 gram of thiamine can also be administered to achieve a clinical response. In those who are seriously malnourished, the sudden availability of glucose without proper bodily levels of thiamine to metabolize is thought to cause damage to cells. Thus, the administration of thiamine along with an intravenous form of glucose is often good practice.Treatment for the memory aspect of KS can also include domain-specific learning, which when used for rehabilitation is called the method of vanishing cues. Such treatments aim to use intact memory processes as the basis for rehabilitation. Those who used the method of vanishing cues in therapy were found to learn and retain information more easily.People diagnosed with KS are reported to have a normal life expectancy, presuming that they abstain from alcohol and follow a balanced diet. Empirical research has suggested that good health practices have beneficial effects in Korsakoff syndrome. Epidemiology Rates varies between countries, but it is estimated to affect around 12.5% of heavy drinkers. References == External links ==

You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

What is the significance of the term 'Vascular access steal syndrome' in the medical field?

In nephrology, vascular access steal syndrome is a syndrome caused by ischemia (not enough blood flow) resulting from a vascular access device (such as an arteriovenous fistula or synthetic vascular graft–AV fistula) that was installed to provide access for the inflow and outflow of blood during hemodialysis. Signs Pallor Diminished pulses (distal to the fistula) Necrosis Decreased wrist-brachial index (ratio of blood pressure measured in the wrist and the blood pressure measured in the upper arm), especially if below 0.6 Symptoms Pain distal to the fistula.Symptoms are graded by their severity: Grade 0: No symptoms of steal Grade 1: Mild - cool extremity, improvement in hand pulse with access occlusion Grade 2: Moderate - Ischemic symptoms during dialysis Grade 3: Severe - Ischemic hand pain outside of dialysis; Ulcers or gangrene of the fingers Diagnosis History and physical exam - relief of symptoms with compression of the fistula on exam is highly suggestive of steal Arteriography Duplex ultrasound Treatment The fistula flow can be restricted through banding, or modulated through surgical revision. Revascularization techniques Distal Revascularization and Interval Ligation (DRIL) procedure PAI (Proximalization of the Arterial Inflow) RUDI (Revision Using Distal Inflow) Banding techniques Narrowing suture Plication Minimally invasive MILLER banding Tapering Surgical bandingIf the above methods fail, the fistula is ligated, and a new fistula is created in a more proximal location in the same limb, or in the contralateral limb. Incidence DASS occurs in about 1% of AV fistulas and 2.7-8% of PTFE grafts. Terminology Within the contexts of nephrology and dialysis, vascular access steal syndrome is also less precisely just called steal syndrome (for short), but in wider contexts that term is ambiguous because it can refer to other steal syndromes, such as subclavian steal syndrome or coronary steal syndrome. See also Terms for anatomical location == References ==

You serve as a medical tutor. Your objective is to demystify medical terms, providing thorough explanations that cater to various levels of medical knowledge.

Can you demystify the medical term 'Lupus vasculitis' for me?

Lupus vasculitis is a complication of systemic lupus erythematosus in which the autoimmune response causes the deposition of immune complexes, such as rheumatoid factor, within the blood vessels. It may manifest in as high as 56% of lupus patients throughout their life, in contrast to antiphospholipid syndrome which has a prevalence of 15%. Vasculitis more often affects younger men. == References ==

You serve as an encyclopedia of medical terms. Deliver clear, detailed explanations, making medical language understandable to a diverse audience.

I've come across the term 'Paleness' in a medical context, but I'm not sure what it means. Can you clarify?

Paleness may refer to: Pallor, a medical condition Paleness (color) See also Pale (disambiguation)

You serve as a medical tutor. Your objective is to demystify medical terms, providing thorough explanations that cater to various levels of medical knowledge.

I need a basic explanation for the medical term 'Corneal ectatic disorders.'

Corneal ectatic disorders or corneal ectasia are a group of uncommon, noninflammatory, eye disorders characterised by bilateral thinning of the central, paracentral, or peripheral cornea. Types Keratoconus, a progressive, noninflammatory, bilateral, asymmetric disease, characterized by paraxial stromal thinning and weakening that leads to corneal surface distortion. Keratoglobus, a rare noninflammatory corneal thinning disorder, characterised by generalised thinning and globular protrusion of the cornea. Pellucid marginal degeneration, a bilateral, noninflammatory disorder, characterized by a peripheral band of thinning of the inferior cornea. Posterior keratoconus, a rare condition, usually congenital, which causes a nonprogressive thinning of the inner surface of the cornea, while the curvature of the anterior surface remains normal. Usually only a single eye is affected. Post-LASIK ectasia, a complication of LASIK eye surgery. Terriens marginal degeneration, a painless, noninflammatory, unilateral or asymmetrically bilateral, slowly progressive thinning of the peripheral corneal stroma. Diagnosis Usually diagnosed clinically by several clinical tests. Although some investigations might needed for confirming the diagnosis and to differentiate different types of corneal ectatic diseases. Corneal topography Corneal tomography Treatment Treatment options include contact lenses and intrastromal corneal ring segments for correcting refractive errors caused by irregular corneal surface, corneal collagen cross-linking to strengthen a weak and ectatic cornea, or corneal transplant for advanced cases. References External links International Journal of Keratoconus and Ectatic Corneal Diseases

You serve as a guide in the medical field. Explain medical terms thoroughly, ensuring the information is both insightful and comprehensible.

I'm looking for a concise explanation of the medical term 'Anhedonia.'

Anhedonia is a diverse array of deficits in hedonic function, including reduced motivation or ability to experience pleasure. While earlier definitions emphasized the inability to experience pleasure, anhedonia is currently used by researchers to refer to reduced motivation, reduced anticipatory pleasure (wanting), reduced consummatory pleasure (liking), and deficits in reinforcement learning. In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), anhedonia is a component of depressive disorders, substance-related disorders, psychotic disorders, and personality disorders, where it is defined by either a reduced ability to experience pleasure, or a diminished interest in engaging in pleasurable activities. While the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) does not explicitly mention anhedonia, the depressive symptom analogous to anhedonia as described in the DSM-5 is a loss of interest or pleasure. Definition While anhedonia was originally defined in 1896 by Théodule-Armand Ribot as the reduced ability to experience pleasure, it has been used to refer to deficits in multiple facets of reward. Re-conceptualizations of anhedonia highlight the independence of "wanting" and "liking". "Wanting" is a component of anticipatory positive affect, mediating both the motivation (i.e. incentive salience) to engage with reward, as well as the positive emotions associated with anticipating a reward. "Liking", on the other hand, is associated with the pleasure derived from consuming a reward. The consciousness of reward-related processes has also been used to categorize reward in the context of anhedonia, as studies comparing implicit behavior versus explicit self-reports demonstrate a dissociation of the two. Learning has also been proposed as an independent facet of reward that may be impaired in conditions associated with anhedonia, but empirical evidence dissociating learning from either "liking" or "wanting" is lacking.Anhedonia has also been used to refer to "affective blunting", "restricted range of affect", "emotional numbing", and "flat affect", particularly in the context of post-traumatic stress disorders. In PTSD patients, scales measuring these symptoms correlate strongly with scales that measure more traditional aspects of anhedonia, supporting this association. Causes Studies in clinical populations, healthy populations, and animal models have implicated a number of neurobiological substrates in anhedonia. Regions implicated in anhedonia include the prefrontal cortex as a whole, particularly the orbitofrontal cortex (OFC), the striatum, amygdala, anterior cingulate cortex (ACC), hypothalamus, and ventral tegmental area (VTA). Neuroimaging studies in humans have reported that deficits in consummatory aspects of reward are associated with abnormalities in the ventral striatum and medial prefrontal cortex, while deficits in anticipatory aspects of reward are related to abnormalities in hippocampal, dorsal ACC and prefrontal regions. These abnormalities are generally consistent with animal models, except for inconsistent findings with regard to the OFC. This inconsistency may be related to the difficulty in imaging the OFC due to its anatomical location, or the small number of studies performed on anhedonia; a number of studies have reported reduced activity in the OFC in schizophrenia and major depression, as well as a direct relationship between reduced activity and anhedonia. Researchers theorize that anhedonia may result from the breakdown in the brains reward system, involving the neurotransmitter dopamine. Anhedonia can be characterised as "impaired ability to pursue, experience and/or learn about pleasure, which is often, but not always accessible to conscious awareness".The conditions of akinetic mutism and negative symptoms are closely related. In akinetic mutism, a stroke or other lesion to the anterior cingulate cortex causes reduction in movement (akinetic) and speech (mutism). Occurrence Major depressive disorder Anhedonia occurs in roughly 70% of people with a major depressive disorder. Anhedonia is a core symptom of major depressive disorder; therefore, individuals experiencing this symptom can be diagnosed with depression, even in the absence of low/depressed mood. The Diagnostic and Statistical Manual of Mental Disorders (DSM) describes a "lack of interest or pleasure", but these can be difficult to discern given that people tend to become less interested in things which do not give them pleasure. The DSM criterion of weight loss is probably related, and many individuals with this symptom describe a lack of enjoyment of food. They can portray any of the non-psychotic symptoms and signs of depression. Schizophrenia Anhedonia is one of the negative symptoms of schizophrenia. Although five domains are usually used to classify negative symptoms, factor analysis of questionnaires yield two factors, with one including deficits in pleasure and motivation. People with schizophrenia retrospectively report experiencing fewer positive emotions than healthy individuals. However, "liking" or consummatory pleasure, is intact in people with schizophrenia, as they report experiencing the same degree of positive affect when presented with rewarding stimuli. Neuroimaging studies support this behavioral observation, as most studies report intact responses in the reward system (i.e. ventral striatum, VTA) to simple rewards. However, studies on monetary rewards sometimes report reduced responsiveness. More consistent reductions are observed with regard to emotional response during reward anticipation, which is reflected in a reduced responsiveness of both cortical and subcortical components of the reward system. Schizophrenia is associated with reduced positive prediction errors (a normal pattern of response to an unexpected reward), which a few studies have demonstrated to be correlated with negative symptoms. People with schizophrenia demonstrate impairment in reinforcement learnings tasks only when the task requires explicit learning, or is sufficiently complex. Implicit reinforcement learning, on the other hand, is relatively intact. These deficits may be related to dysfunction in the ACC, OFC and dlPFC leading to abnormal representation of reward and goals. Substance-related disorders Anhedonia is common in people who are dependent upon any one or more of a wide variety of drugs, including alcohol, opioids, and nicotine. Although anhedonia becomes less severe over time, it is a significant predictor of relapse. Post-traumatic stress disorder While PTSD is associated with reduced motivation, part of the anticipatory "wanting", it is also associated with elevated sensation seeking, and no deficits in physiological arousal, or self reported pleasure to positive stimuli. PTSD is also associated with blunted affect, which may be due to the high comorbidity with depression. Parkinsons disease Anhedonia occurs frequently in Parkinsons disease, with rates between 7%–45% being reported. Whether or not anhedonia is related to the high rates of depression in Parkinsons disease is unknown. Bipolar depression Anhedonia is also reported to appear in people with bipolar depression. Attention deficit hyperactivity disorder Anhedonia may be associated with ADHD. Impairments of dopaminergic and serotonergic function in the brain of those with ADHD result in dysregulation of reward processing which can lead to anhedonia. Sexual anhedonia Sexual anhedonia in males is also known as ejaculatory anhedonia. This condition means that the man will ejaculate with no accompanying sense of pleasure.The condition is most frequently found in males, but women can experience lack of pleasure when the body goes through the orgasm process as well. Sexual anhedonia may be caused by: Hyperprolactinaemia Hypoactive sexual desire disorder (HSDD), also called inhibited sexual desire Low levels of the hormone testosterone Spinal cord injury Multiple sclerosis Use of SSRI antidepressants or having used SSRI antidepressants in the past. Use (or previous use) of antidopaminergic neuroleptics (anti-psychotics) Fatigue Physical illnessIt is very uncommon that a neurological examination and blood tests can determine the cause of a specific case of sexual anhedonia. Patients may be prescribed sustained-release bupropion to aid in treatment, which has been shown to relieve sexual dysfunction even in patients without depression. Social anhedonia Definition Social anhedonia is defined as a disinterest in social contact and a lack of pleasure in social situations, and is characterized by social withdrawal. This characteristic typically manifests as an indifference to other people. In contrast to introversion, a nonpathological dimension of human personality, social anhedonia represents a deficit in the ability to experience pleasure. Additionally, social anhedonia differs from social anxiety in that social anhedonia is predominantly typified by diminished positive affect, while social anxiety is distinguished by both decreased positive affect and exaggerated negative affect.This trait is currently seen as a central characteristic, as well as a predictor, of schizophrenia spectrum disorders. Signs and symptoms Decreased ability to experience interpersonal pleasure Social withdrawal/isolation Decreased capacity for social contact and interaction Lack of close friends and intimate relationships, and decreased quality of those relationships Poor social adjustment Decreased positive affect Flat affect Depressed mood State-related anxiety Background and early clinical observation The term anhedonia is derived from the Greek an-, "without" and hēdonē, "pleasure". Interest in the nature of pleasure and its absence dates back to ancient Greek philosophers such as Epicurus. The symptoms of anhedonia were introduced to the realm of psychopathology in 1809 by John Haslam, who characterized a patient with schizophrenia as indifferent to "those objects and pursuits which formerly proved sources of delight and instruction". The concept was formally coined by Théodule-Armand Ribot and later used by psychiatrists Paul Eugen Bleuler and Emil Kraepelin to describe a core symptom of schizophrenia. In particular, Rado postulated that schizotypes, or individuals with the schizophrenic phenotype, have two key genetic deficits, one related to the ability to feel pleasure (anhedonia) and one related to proprioception. In 1962 Meehl furthered Rados theory through the introduction of the concept of schizotaxia, a genetically driven neural integrative defect thought to give rise to the personality type of schizotypy. Loren and Jean Chapman further distinguished between two types of anhedonia: physical anhedonia, or a deficit in the ability to experience physical pleasure, and social, or a deficit in the ability to experience interpersonal pleasure.Recent research suggests that social anhedonia may represent a prodrome of psychotic disorders. First-degree relatives of individuals with schizophrenia show elevated levels of social anhedonia, higher baseline scores of social anhedonia are associated with later development of schizophrenia. These findings provide support for the conjecture that it represents a genetic risk marker for schizophrenia-spectrum disorders. Additionally, elevated levels of social anhedonia in patients with schizophrenia have been linked to poorer social functioning. Socially anhedonic individuals perform worse on a number of neuropsychological tests than non-anhedonic participants, and show similar physiological abnormalities seen in patients with schizophrenia. Comorbidity Anhedonia is present in several forms of psychopathology. Depression Social anhedonia is observed in both depression and schizophrenia. However, social anhedonia is a state related to the depressive episode and the other is trait related to the personality construct associated with schizophrenia. These individuals both tend to score highly on self-report measures of social anhedonia. Blanchard, Horan, and Brown demonstrated that, although both the depression and the schizophrenia patient groups can look very similar in terms of social anhedonia cross-sectionally, over time as individuals with depression experience symptom remission, they show fewer signs of social anhedonia, while individuals with schizophrenia do not. Blanchard and colleagues (2011) found individuals with social anhedonia also had elevated rates of lifetime mood disorders including depression and dysthymia compared to controls. Social anxiety As mentioned above, social anxiety and social anhedonia differ in important ways. However, social anhedonia and social anxiety are also often comorbid. People with social anhedonia may display increased social anxiety and be at increased risk for social phobias and generalized anxiety disorder. It has yet to be determined what the exact relationship between social anhedonia and social anxiety is, and if one potentiates the other. Individuals with social anhedonia may display increased stress reactivity, meaning that they feel more overwhelmed or helpless in response to a stressful event compared to control subjects who experience the same type of stressor. This dysfunctional stress reactivity may correlate with hedonic capacity, providing a potential explanation for the increased anxiety symptoms experienced in people with social anhedonia. In an attempt to separate out social anhedonia from social anxiety, the Revised Social Anhedonia Scale didnt include items that potentially targeted social anxiety. However, more research must be conducted on the underlying mechanisms through which social anhedonia overlaps and interacts with social anxiety. The efforts of the "social processes" RDoC initiative will be crucial in differentiating between these components of social behavior that may underlie mental illnesses such as schizophrenia. Primary relevance in schizophrenia and schizophrenia spectrum disorders Social anhedonia is a core characteristic of schizotypy, which is defined as a continuum of personality traits that can range from normal to disordered and contributes to risk for psychosis and schizophrenia. Social anhedonia is a dimension of both negative and positive schizotypy. It involves social and interpersonal deficits, but is also associated with cognitive slippage and disorganized speech, both of which fall into the category of positive schizotypy. Not all people with schizophrenia display social anhedonia and likewise, people who have social anhedonia may never be diagnosed with a schizophrenia-spectrum disorder if they do not have the positive and cognitive symptoms that are most frequently associated with most schizophrenia-spectrum disorders.Social anhedonia may be a valid predictor of future schizophrenia-spectrum disorders; young adults with social anhedonia perform in a similar direction to schizophrenia patients in tests of cognition and social behavior, showing potential predictive validity. Social anhedonia usually manifests in adolescence, possibly because of a combination of the occurrence of critical neuronal development and synaptic pruning of brain regions important for social behavior and environmental changes, when adolescents are in the process of becoming individuals and gaining more independence. Treatment There is no validated treatment for social anhedonia. Future research should focus on genetic and environmental risk factors to home in on specific brain regions and neurotransmitters that may be implicated in social anhedonias cause and could be targeted with medication or behavioral treatments. Social support may also play a valuable role in the treatment of social anhedonia. Blanchard et al. found that a greater number of social supports, as well as a greater perceived social support network, were related to fewer schizophrenia-spectrum symptoms and to better general functioning within the social anhedonia group. So far, no medicine has been developed to specifically target anhedonia. Gender differences In the general population, males score higher than females on measures of social anhedonia. This sex difference is stable throughout time (from adolescence into adulthood) and is also seen in people with schizophrenia-spectrum disorders. These results may reflect a more broad pattern of interpersonal and social deficits seen in schizophrenia-spectrum disorders. On average, males with schizophrenia are diagnosed at a younger age, have more severe symptoms, worse treatment prognosis, and a decrease in overall quality of life compared to females with the disorder. These results, coupled with the sex difference seen in social anhedonia, outline the necessity for research on genetic and hormonal characteristics that differ between males and females, and that may increase risk or resilience for mental illnesses such as schizophrenia. Assessing social anhedonia There are several self-report psychometric measures of schizotypy which each contain subscales related to social anhedonia: Revised Social Anhedonia Scale—Chapman Psychosis Proneness Scales No Close Friends Subscale – Schizotypal Personality Questionnaire Introverted Anhedonia Subscale—Oxford–Liverpool Inventory of Feelings and Experiences Genetic components L.J. and J.P. Chapman were the first to discuss the possibility that social anhedonia may stem from a genetic vulnerability. The disrupted in schizophrenia 1 (DISC1) gene has been consistently associated with risk for, and cause of, schizophrenia-spectrum disorders and other mental illnesses. More recently, DISC1 has been associated with social anhedonia within the general population. Tomppo identified a specific DISC1 allele that is associated with an increase in characteristics of social anhedonia. They also identified a DISC1 allele associated with decreased characteristics of social anhedonia, that was found to be preferentially expressed in women. More research needs to be conducted, but social anhedonia may be an important intermediate phenotype (endophenotype) between genes associated with risk for schizophrenia and phenotype of the disorder. Neurobiological correlates Researchers studying the neurobiology of social anhedonia posit that this trait may be linked to dysfunction of reward-related systems in the brain. This circuitry is critical for the sensation of pleasure, the computation of reward benefits and costs, determination of the effort required to obtain a pleasant stimulus, deciding to obtain that stimulus, and increasing motivation to obtain the stimulus. In particular, the ventral striatum and areas of the prefrontal cortex (PFC), including the orbitofrontal cortex (OFC) and dorsolateral (dl) PFC, are critically involved in the experience of pleasure and the hedonic perception of rewards. With regards to neurotransmitter systems, opioid, gamma-Aminobutyric acid and endocannabinoid systems in the nucleus accumbens, ventral pallidum, and OFC mediate the hedonic perception of rewards. Activity in the PFC and ventral striatum have been found to be decreased in anhedonic individuals with major depressive disorder (MDD) and schizophrenia. However, schizophrenia may be less associated with decreased hedonic capacity and more with deficient reward appraisal. Specific musical anhedonia Recent studies have found people who do not have any issue processing musical tones or beat, yet receive no pleasure from listening to music. Specific musical anhedonia is distinct from melophobia, the fear of music. See also Avolition Dysthymia References External links Anhedonia – Bipolar Disorder Symptoms No Pleasure, No Reward

You are a medical advisor. Your role is to break down medical terminology into clear, detailed explanations for a general audience.

I'm trying to understand 'Lymphocytosis' within a medical context. Could you shed some light on it?

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 ==

You are a facilitator of medical knowledge. Provide thorough and accessible explanations of medical terms, catering to both specialists and non-specialists.

I'm looking for a concise explanation of the medical term 'Mitochondrial trifunctional protein deficiency.'

Mitochondrial trifunctional protein deficiency (MTP deficiency or MTPD) is an autosomal recessive fatty acid oxidation disorder that prevents the body from converting certain fats to energy, particularly during periods without food. People with this disorder have inadequate levels of an enzyme that breaks down a certain group of fats called long-chain fatty acids. Signs and symptoms The presentation of mitochondrial trifunctional protein deficiency may begin during infancy, features that occur are: low blood sugar, weak muscle tone, and liver problems. Infants with this disorder are at risk for heart problems, breathing difficulties, and pigmentary retinopathy. Signs and symptoms of mitochondrial trifunctional protein deficiency that may begin after infancy include hypotonia, muscle pain, a breakdown of muscle tissue, and a loss of sensation in the extremities called peripheral neuropathy. Some who have MTP deficiency show a progressive course associated with myopathy, and recurrent rhabdomyolysis. Genetics The genetics of mitochondrial trifunctional protein deficiency is based on mutations in the HADHA and HADHB genes which cause this disorder. These genes each provide instructions for making part of an enzyme complex called mitochondrial trifunctional protein. This enzyme complex functions in mitochondria, the energy-producing centers within cells: mitochondrial trifunctional protein contains three enzymes that each perform a different function. This enzyme complex is required to metabolize a group of fats called long-chain fatty acids. These fatty acids are stored in the bodys fat tissues and are a major source of energy for the heart and muscles. During periods of fasting, fatty acids are also an important energy source for the liver and other tissues.Mutations in the HADHA or HADHB genes that cause mitochondrial trifunctional protein deficiency disrupt all functions of this enzyme complex. Without enough of this enzyme complex, long-chain fatty acids cannot be metabolized. As a result, these fatty acids are not converted to energy, which can lead to some features of this disorder. Long-chain fatty acids may also build up and damage the liver, heart, and muscles. This abnormal buildup causes other symptoms of mitochondrial trifunctional protein deficiency.The mechanism of this condition indicates that the mitochondrial trifunction protein catalyzes 3 steps in mitochondrial beta-oxidation of fatty acids: long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD), long-chain enoyl-CoA hydratase, and long-chain thiolase activities. Trifunctional protein deficiency is characterized by decreased activity of all 3 enzymes. Clinically, trifunctional protein deficiency usually results in sudden unexplained infant death, cardiomyopathy, or skeletal myopathy. Diagnosis Diagnosis of mitochondrial trifunctional protein deficiency is often confirmed using tandem mass spectrometry. Genetic counseling is available for this condition. Additionally the following exams are available: CBC Urine test Treatment Management for mitochondrial trifunctional protein deficiency entails the following: Avoiding factors that might precipitate condition Glucose Low fat/high carbohydrate nutrition See also Long-chain acyl-CoA dehydrogenase References Further reading Nyhan, William L.; Hoffman, Georg F.; Barshop, Bruce A.; Al-Aqeel, Aida I. (2012). Atlas of Inherited Metabolic Diseases 3E. CRC Press. ISBN 9781444149487. Thöny, Beat; Duran, Marinus; Gibson, K. Michael; Dionisi-Vici, Carlo (2013). Physicians Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases. Springer. ISBN 9783642403378. External links Media related to Mitochondrial trifunctional protein deficiency at Wikimedia Commons

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Could you offer a clear explanation of the term 'Timolol' as used in the medical field?

Timolol is a beta blocker medication used either by mouth or as eye drops. As eye drops it is used to treat increased pressure inside the eye such as in ocular hypertension and glaucoma. By mouth it is used for high blood pressure, chest pain due to insufficient blood flow to the heart, to prevent further complications after a heart attack, and to prevent migraines.Common side effects with the drops is irritation of the eye. Common side effects by mouth include tiredness, slow heart beat, itchiness, and shortness of breath. Other side effects include masking the symptoms of low blood sugar in those with diabetes. Use is not recommended in those with asthma, uncompensated heart failure, or COPD. It is unclear if use during pregnancy is safe for the baby. Timolol is a non-selective beta blocker.Timolol was patented in 1968, and came into medical use in 1978. It is on the World Health Organizations List of Essential Medicines. Timolol is available as a generic medication. In 2019, it was the 160th most commonly prescribed medication in the United States, with more than 3 million prescriptions. Medical uses By mouth In its by mouth or oral form, it is used: to treat high blood pressure to prevent heart attacks to prevent migraine headachesThe combination of timolol and the alpha-1 blocker prazosin has sedative effects. Eye drops In its eye drop form it is used to treat open-angle and, occasionally, secondary glaucoma. The mechanism of action of timolol is probably the reduction of the formation of aqueous humor in the ciliary body in the eye. It was the first beta blocker approved for topical use in treatment of glaucoma in the United States (1978). When used by itself, it depresses intraocular pressure (IOP) 18–34% below baseline within first few treatments. However, there are short-term escape and long-term drift effects in some people. That is, tolerance develops. It may reduce the extent of the diurnal IOP curve up to 50%. The IOP is higher during sleep. Efficacy of timolol in lowering IOP during the sleep period may be limited. It is a 5–10× more potent β-blocker than propranolol. Timolol is light-sensitive; it is usually preserved with 0.01% benzalkonium chloride (BAC), but also comes BAC-free. It can also be used in combination with pilocarpine, carbonic anhydrase inhibitors or prostaglandin analogs.A Cochrane review compared the effect of timolol versus brimonidine in slowing the progression of open angle glaucoma in adults but found insufficient evidence to come to conclusions. On the skin In its gel form it is used on the skin to treat infantile hemangiomas. Contraindications The medication should not be taken by individuals with: An allergy to timolol or any other beta-blockers Asthma or severe chronic obstructive bronchitis A slow heart rate (bradycardia), or a heart block Heart failure Side effects The most serious possible side effects include cardiac arrhythmias and severe bronchospasms. Timolol can also lead to fainting, congestive heart failure, depression, confusion, worsening of Raynauds syndrome and impotence.Side effects when given in the eye include: burning sensation, eye redness, superficial punctate keratopathy, corneal numbness. Formulations It is available in tablet and liquid formulations.For ophthalmic use, timolol is also available combined: with carbonic anhydrase inhibitors: timolol and brinzolamide timolol and dorzolamide with α2 agonists: timolol and brimonidine with prostaglandin analogs: timolol and latanoprost timolol and travoprost Brand names Timolol is marketed under many trade names worldwide. Timolol eye drops are marketed under the brand name Istalol among others. References External links "Timolol". Drug Information Portal. U.S. National Library of Medicine. "Timolol Ophthalmic". Drug Information Portal. U.S. National Library of Medicine. "Timolol maleate". Drug Information Portal. U.S. National Library of Medicine. "Timolol Ophthalmic". MedlinePlus.

You are a conduit for medical education. Your task is to offer detailed explanations of medical terms, ensuring they are understandable and precise.

I'm trying to expand my medical knowledge. Can you elucidate the term 'Heparin-induced thrombocytopenia'?

Heparin-induced thrombocytopenia (HIT) is the development of thrombocytopenia (a low platelet count), due to the administration of various forms of heparin, an anticoagulant. HIT predisposes to thrombosis (the abnormal formation of blood clots inside a blood vessel) because platelets release microparticles that activate thrombin, thereby leading to thrombosis. When thrombosis is identified the condition is called heparin-induced thrombocytopenia and thrombosis (HITT). HIT is caused by the formation of abnormal antibodies that activate platelets. If someone receiving heparin develops new or worsening thrombosis, or if the platelet count falls, HIT can be confirmed with specific blood tests.The treatment of HIT requires stopping heparin treatment, and both protection from thrombosis and choice of an agent that will not reduce the platelet count any further. Several alternatives are available for this purpose; mainly used are danaparoid, fondaparinux, argatroban, and bivalirudin.While heparin was discovered in the 1930s, HIT was not reported until the 1960s. Signs and symptoms Heparin may be used for both prevention and the treatment of thrombosis. It exists in two main forms: an "unfractionated" form that can be injected under the skin (subcutaneously) or through an intravenous infusion, and a "low molecular weight" form that is generally given subcutaneously. Commonly used low molecular weight heparins are enoxaparin, dalteparin, nadroparin and tinzaparin.In HIT, the platelet count in the blood falls below the normal range, a condition called thrombocytopenia. However, it is generally not low enough to lead to an increased risk of bleeding. Most people with HIT, therefore, do not experience any symptoms. Typically, the platelet count falls 5–14 days after heparin is first given; if someone has received heparin in the previous three months, the fall in platelet count may occur sooner, sometimes within a day.The most common symptom of HIT is enlargement or extension of a previously diagnosed blood clot, or the development of a new blood clot elsewhere in the body. This may take the form of clots either in arteries or veins, causing arterial or venous thrombosis, respectively. Examples of arterial thrombosis are stroke, myocardial infarction ("heart attack"), and acute leg ischemia. Venous thrombosis may occur in the leg or arm in the form of deep vein thrombosis (DVT) and in the lung in the form of a pulmonary embolism (PE); the latter usually originates in the leg, but migrates to the lung.In those receiving heparin through an intravenous infusion, a complex of symptoms ("systemic reaction") may occur when the infusion is started. These include fever, chills, high blood pressure, a fast heart rate, shortness of breath, and chest pain. This happens in about a quarter of people with HIT. Others may develop a skin rash consisting of red spots. Mechanism The administration of heparin can cause the development of HIT antibodies, suggesting heparin may act as a hapten, thus may be targeted by the immune system. In HIT, the immune system forms antibodies against heparin when it is bound to a protein called platelet factor 4 (PF4). These antibodies are usually of the IgG class and their development usually takes about 5 days. However, those who have been exposed to heparin in the last few months may still have circulating IgG, as IgG-type antibodies generally continue to be produced even when their precipitant has been removed. This is similar to immunity against certain microorganisms, with the difference that the HIT antibody does not persist more than three months. HIT antibodies have been found in individuals with thrombocytopenia and thrombosis who had no prior exposure to heparin, but the majority are found in people who are receiving heparin.The IgG antibodies form a complex with heparin and PF4 in the bloodstream. The tail of the antibody then binds to the FcγIIa receptor, a protein on the surface of the platelet. This results in platelet activation and the formation of platelet microparticles, which initiate the formation of blood clots; the platelet count falls as a result, leading to thrombocytopenia. In addition, the reticuloendothelial system (mostly the spleen) removes the antibody-coated platelets, further contributing to the thrombocytopenia. Formation of PF4-heparin antibodies is common in people receiving heparin, but only a proportion of these develop thrombocytopenia or thrombosis. This has been referred to as an "iceberg phenomenon". Diagnosis HIT may be suspected if blood tests show a falling platelet count in someone receiving heparin, even if the heparin has already been discontinued. Professional guidelines recommend that people receiving heparin have a complete blood count (which includes a platelet count) on a regular basis while receiving heparin.However, not all people with a falling platelet count while receiving heparin turn out to have HIT. The timing, severity of the thrombocytopenia, the occurrence of new thrombosis, and the presence of alternative explanations, all determine the likelihood that HIT is present. A commonly used score to predict the likelihood of HIT is the "4 Ts" score introduced in 2003. A score of 0–8 points is generated; if the score is 0–3, HIT is unlikely. A score of 4–5 indicates intermediate probability, while a score of 6–8 makes it highly likely. Those with a high score may need to be treated with an alternative drug, while more sensitive and specific tests for HIT are performed, while those with a low score can safely continue receiving heparin, as the likelihood that they have HIT is extremely low. In an analysis of the reliability of the 4T score, a low score had a negative predictive value of 0.998, while an intermediate score had a positive predictive value of 0.14 and a high score a positive predictive value of 0.64; intermediate and high scores, therefore, warrant further investigation. The first screening test in someone suspected of having HIT is aimed at detecting antibodies against heparin-PF4 complexes. This may be with a laboratory test of the enzyme-linked immunosorbent assay type. This ELISA test, however, detects all circulating antibodies that bind heparin-PF4 complexes, and may also falsely identify antibodies that do not cause HIT. Therefore, those with a positive ELISA are tested further with a functional assay. This test uses platelets and serum from the patient; the platelets are washed and mixed with serum and heparin. The sample is then tested for the release of serotonin, a marker of platelet activation. If this serotonin release assay (SRA) shows high serotonin release, the diagnosis of HIT is confirmed. The SRA test is difficult to perform and is usually only done in regional laboratories.If someone has been diagnosed with HIT, some recommend routine Doppler sonography of the leg veins to identify deep vein thromboses, as this is very common in HIT. Treatment Given the fact that HIT predisposes strongly to new episodes of thrombosis, simply discontinuing the heparin administration is insufficient. Generally, an alternative anticoagulant is needed to suppress the thrombotic tendency while the generation of antibodies stops and the platelet count recovers. To make matters more complicated, the other most commonly used anticoagulant, warfarin, should not be used in HIT until the platelet count is at least 150 x 109/L because a very high risk of warfarin necrosis exists in people with HIT who have low platelet counts. Warfarin necrosis is the development of skin gangrene in those receiving warfarin or a similar vitamin K inhibitor. If the patient was receiving warfarin at the time when HIT is diagnosed, the activity of warfarin is reversed with vitamin K. Transfusing platelets is discouraged, as a theoretical risk indicates that this may worsen the risk of thrombosis; the platelet count is rarely low enough to be the principal cause of significant hemorrhage.Various nonheparin agents are used as alternatives to heparin therapy to provide anticoagulation in those with strongly suspected or proven HIT: danaparoid, fondaparinux, bivalirudin, and argatroban. Not all agents are available in all countries, and not all are approved for this specific use. For instance, argatroban is only recently licensed in the United Kingdom, and danaparoid is not available in the United States. Fondaparinux, a factor Xa inhibitor, is commonly used off label for HIT treatment in the United States.According to a systematic review, people with HIT treated with lepirudin showed a relative risk reduction of clinical outcome (death, amputation, etc.) to be 0.52 and 0.42 when compared to patient controls. In addition, people treated with argatroban for HIT showed a relative risk reduction of the above clinical outcomes to be 0.20 and 0.18. Lepirudin production stopped on May 31, 2012. Epidemiology Up to 8% of patients receiving heparin are at risk to develop HIT antibodies, but only 1–5% on heparin will progress to develop HIT with thrombocytopenia and subsequently one-third of them may develop arterial or venous thrombosis. After vascular surgery, 34% of patients receiving heparin developed HIT antibodies without clinical symptoms. The exact number of cases of HIT in the general population is unknown. What is known is that women receiving heparin after a recent surgical procedure, particularly cardiothoracic surgery, have a higher risk, while the risk is very low in women just before and after giving birth. Some studies have shown that HIT is less common in those receiving low molecular weight heparin. History While heparin was introduced for clinical use in the late 1930s, new thrombosis in people treated with heparin was not described until 1957, when vascular surgeons reported the association. The fact that this phenomenon occurred together with thrombocytopenia was reported in 1969; prior to this time, platelet counts were not routinely performed. A 1973 report established HIT as a diagnosis, as well as suggesting that its features were the result of an immune process.Initially, various theories existed about the exact cause of the low platelets in HIT. Gradually, evidence accumulated on the exact underlying mechanism. In 1984–1986, John G. Kelton and colleagues at McMaster University Medical School developed the laboratory tests that could be used to confirm or exclude heparin-induced thrombocytopenia.Treatment was initially limited to aspirin and warfarin, but the 1990s saw the introduction of a number of agents that could provide anticoagulation without a risk of recurrent HIT. Older terminology distinguishes between two forms of heparin-induced thrombocytopenia: type 1 (mild, nonimmune mediated and self-limiting fall in platelet count) and type 2, the form described above. Currently, the term HIT is used without a modifier to describe the immune-mediated severe form.In 2021 a condition resembling HIT but without heparin exposure was described to explain unusual post-vaccination embolic and thrombotic events after the Oxford–AstraZeneca COVID-19 vaccine. It is a rare adverse event (1:1 million to 1:100,000) resulting from COVID-19 vaccines (particularly adenoviral vector vaccines). This is also known as Thrombosis with Thrombocytopenia Syndrome or TTS. References == External links ==

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

I'm curious about the meaning of the medical term 'Esterified estrogens.' Can you give me some insights?

Esterified estrogens (EEs), sold under the brand names Estratab and Menest among others, is an estrogen medication which is used hormone therapy for menopausal symptoms and low sex hormone levels in women, to treat breast cancer in both women and men, and to treat prostate cancer in men. It is formulated alone or in combination with methyltestosterone. It is taken by mouth.Side effects of EEs include nausea, breast tension, edema, and breakthrough bleeding among others. It is an estrogen, or an agonist of the estrogen receptors, the biological target of estrogens like estradiol. EEs are a prodrug mainly of estradiol and to a lesser extent of equilin.EEs were introduced for medical use by 1970. They are available in only a few countries, such as Chile and the United States. They have also been marketed in Argentina and Switzerland in the past. Medical uses EEs are used in hormone therapy for menopausal symptoms, female hypogonadism, ovariectomy, and primary ovarian failure and in the treatment of breast cancer and prostate cancer. Available forms EEs are available in the form of 0.3 mg, 0.625 mg, 1.25 mg, and 2.5 mg oral tablets. Estratest is a combination formulation of 1.25 mg EEs with 2.5 mg methyltestosterone. Side effects Pharmacology EEs consist primarily of sodium estrone sulfate and sodium equilin sulfate, and are very similar to conjugated estrogens (CEEs, conjugated equine estrogens; brand name Premarin). However, EEs and CEEs differ in the sources of their contents and in the percentages of their constituents; CEEs consist of approximately 53% sodium estrone sulfate and 25% sodium equilin sulfate, while EEs contain about 75 to 85% sodium estrone sulfate and 6 to 11% sodium equilin sulfate. EEs have been found to produce similar serum levels of estrone and estradiol relative to CEEs, although with higher levels of estrone and lower levels of equilin. One study found that the risk of venous thrombosis may be less with EEs relative to CEEs. Chemistry EEs contain synthetic, plant-derived estrogens and are manufactured from soybeans and yams. History EEs were introduced for medical use by 1970. Society and culture Generic names Estrogens, esterified is the generic name of the drug and its USP. It is also known as esterified estrogens. Brand names EEs are marketed under a variety of brand names including Amnestrogen, Estragyn, Estratab, Evex, Femibel, Femogen, Menest, Neo Estrone Tab, and Oestro-Feminal alone, and, in combination with methyltestosterone, under the brand names Covaryx, Delitan, Eemt, Essian, Estratest, Feminova-T, Menogen, and Syntest. Availability EEs are or have been marketed in Argentina, Chile, Switzerland, and the United States. Both EEs and the combination of EEs and methyltestosterone are listed as being marketed only in Chile and the United States as of present. See also Esterified estrogens/methyltestosterone Estrogenic substances Conjugated estriol List of combined sex-hormonal preparations == References ==

You serve as a medical tutor. Your objective is to demystify medical terms, providing thorough explanations that cater to various levels of medical knowledge.

Please help me grasp the concept behind the medical term 'Beta thalassemia.'

Beta thalassemias (β thalassemias) are a group of inherited blood disorders. They are forms of thalassemia caused by reduced or absent synthesis of the beta chains of hemoglobin that result in variable outcomes ranging from severe anemia to clinically asymptomatic individuals. Global annual incidence is estimated at one in 100,000. Beta thalassemias occur due to malfunctions in the hemoglobin subunit beta or HBB. The severity of the disease depends on the nature of the mutation.HBB blockage over time leads to decreased beta-chain synthesis. The bodys inability to construct new beta-chains leads to the underproduction of HbA (adult hemoglobin). Reductions in HbA available overall to fill the red blood cells in turn leads to microcytic anemia. Microcytic anemia ultimately develops in respect to inadequate HBB protein for sufficient red blood cell functioning. Due to this factor, the patient may require blood transfusions to make up for the blockage in the beta-chains. Repeated blood transfusions cause severe problems associated with iron overload. Signs and symptoms Three main forms have been described: thalassemia minor, thalassemia intermedia, and thalassemia major which vary from asymptomatic or mild symptoms to severe anemia requiring lifelong transfusions. Individuals with beta thalassemia major (those who are homozygous for thalassemia mutations, or inheriting 2 mutations) usually present within the first two years of life with symptomatic severe anemia, poor growth, and skeletal abnormalities. Untreated thalassemia major eventually leads to death, usually by heart failure; therefore, prenatal screening is very important. Those with beta thalassemia intermedia (those who are compound heterozygoutes for the beta thalassemia mutation) usually present later in life with mild to moderate symptoms of anemia. Beta thalassemia trait (also known as beta thalassemia minor) involves heterozygous inheritance of a beta-thalassemia mutation and patients usually have borderline microcytic, hypochromic anemia and they are usually asymptomatic or have mild symptoms. Beta thalassemia minor can also present as beta thalassemia silent carriers; those who inherit a beta thalassemic mutation but have no hematologic abnormalities nor symptoms. Some people with thalassemia are susceptible to health complications that involve the spleen (hypersplenism) and gallstones (due to hyperbilirubinemia from peripheral hemolysis). These complications are mostly found in thalassemia major and intermedia patients.Excess iron (from hemolysis or transfusions) causes serious complications within the liver, heart, and endocrine glands. Severe symptoms include liver cirrhosis, liver fibrosis, and in extreme cases, liver cancer. Heart failure, growth impairment, diabetes and osteoporosis are life-threatening conditions which can be caused by beta thalassemia major. The main cardiac abnormalities seen as a result of beta thalassemia and iron overload include left ventricular systolic and diastolic dysfunction, pulmonary hypertension, valvulopathy, arrhythmias, and pericarditis. Increased gastrointestinal iron absorption is seen in all grades of beta thalassemia, and increased red blood cell destruction by the spleen due to ineffective erythropoiesis further releases additional iron into the bloodstream.Additional symptoms of beta thalassemia major or intermedia include the classic symptoms of moderate to severe anemia including fatigue, growth and developmental delay in childhood, leg ulcers and organ failure. Ineffective erythropoiesis (red blood cell production) can also lead to compensatory bone marrow expansion which can then lead to bony changes/deformities, bone pain and craniofacial abnormalities. Extramedullary organs such as the liver and spleen that can also undergo erythropoiesis become activated leading to hepatosplenomegaly (enlargement of the liver and spleen). Other tissues in the body can also become sites of erythropoiesis, leading to extramedullary hematopoietic pseudotumors which may cause compressive symptoms if they occur in the thoracic cavity or spinal canal. Cause Mutations Two major groups of mutations can be distinguished: Nondeletion forms: These defects, in general, involve a single base substitution or small insertions near or upstream of the β globin gene. Most often, mutations occur in the promoter regions preceding the beta-globin genes. Less often, abnormal splice variants are believed to contribute to the disease. Deletion forms: Deletions of different sizes involving the β globin gene produce different syndromes such as (βo) or hereditary persistence of fetal hemoglobin syndromes.Mutations are characterized as (βo) if they prevent any formation of β globin chains, mutations are characterized as (β+) if they allow some β globin chain formation to occur. mRNA assembly Beta thalassemia is a hereditary disease affecting hemoglobin. As with about half of all hereditary diseases, an inherited mutation damages the assembly of the messenger-type RNA (mRNA) that is transcribed from a chromosome. DNA contains both the instructions (genes) for stringing amino acids together into proteins, as well as stretches of DNA that play important roles in regulating produced protein levels.In thalassemia, an additional, contiguous length or a discontinuous fragment of non-coding instructions is included in the mRNA. This happens because the mutation obliterates the boundary between the intronic and exonic portions of the DNA template. Because all the coding sections may still be present, normal hemoglobin may be produced and the added genetic material, if it produces pathology, instead disrupts regulatory functions enough to produce anemia. Hemoblogins normal alpha and beta subunits each have an iron-containing central portion (heme) that allows the protein chain of a subunit to fold around it. Normal adult hemoglobin contains 2 alpha and 2 beta subunits. Thalassemias typically affect only the mRNAs for production of the beta chains (hence the name). Since the mutation may be a change in only a single base (single-nucleotide polymorphism), on-going efforts seek gene therapies to make that single correction. Risk factors Family history and ancestry are factors that increase the risk of beta thalassemia. Depending on family history, if a persons parents or grandparents had beta thalassemia major or intermedia, there is a 75% (3 out of 4) probability (see inheritance chart at top of page) of the mutated gene being inherited by an offspring. Even if a child does not have beta thalassemia major or intermedia, they can still be a carrier, possibly resulting in future generations of their offspring having beta thalassemia.Another risk factor is ancestry. Beta thalassemia occurs most often in people of Italian, Greek, Middle Eastern, Southern Asian, and African ancestry. Diagnosis Abdominal pain due to hypersplenism, splenic infarction and right-upper quadrant pain caused by gallstones are major clinical manifestations. However, diagnosing thalassemia from symptoms alone is inadequate. Physicians note these signs as associative due to this diseases complexity. The following associative signs can attest to the severity of the phenotype: pallor, poor growth, inadequate food intake, splenomegaly, jaundice, maxillary hyperplasia, dental malocclusion, cholelithiasis, systolic ejection murmur in the presence of severe anemia and pathologic fractures. Based on symptoms, tests are ordered for a differential diagnosis. These tests include complete blood count; hemoglobin electrophoresis; serum transferrin, ferritin, total iron-binding capacity; urine urobilin and urobilogen; peripheral blood smear, which may show codocytes, or target cells; hematocrit; and serum bilirubin. The expected pattern on hemoglobin electrophoresis in people with beta-thalassemia is an increased level of hemoglobin A2 and slightly increased hemoglobin F. The diagnosis is confirmed with hemoglobin electrophoresis or high performance liquid chromatography.Skeletal changes associated with expansion of the bone marrow: Chipmunk facies: bossing of the skull, prominent malar eminence, depression of the bridge of the nose, tendency to a mongoloid slant of the eye, and exposure of the upper teeth due to hypertrophy of the maxillae. Hair-on-end (or "crew cut") on skull X-ray: new bone formation due to the inner table. DNA analysis All beta thalassemias may exhibit abnormal red blood cells; a family history is followed by DNA analysis. This test is used to investigate deletions and mutations in the alpha- and beta-globin-producing genes. Family studies can be done to evaluate carrier status and the types of mutations present in other family members. DNA testing is not routine, but can help diagnose thalassemia and determine carrier status. In most cases the treating physician uses a clinical prediagnosis assessing anemia symptoms: fatigue, breathlessness and poor exercise tolerance. Further genetic analysis may include HPLC should routine electrophoresis prove difficult. Prevention Beta thalassemia is a hereditary disease allowing for a preventative treatment by carrier screening and prenatal diagnosis. It can be prevented if one parent has normal genes, giving rise to screenings that empower carriers to select partners with normal hemoglobin. A study aimed at detecting the genes that could give rise to offspring with sickle cell disease. Patients diagnosed with beta thalassemia have MCH ≤ 26 pg and an RDW < 19. Of 10,148 patients, 1,739 patients had a hemoglobin phenotype and RDW consistent with beta thalassemia. After the narrowing of patients, the HbA2 levels were tested presenting 77 patients with beta thalassemia. This screening procedure proved insensitive in populations of West African ancestry because of the indicators has high prevalence of alpha thalassemia. Countries have programs distributing information about the reproductive risks associated with carriers of haemoglobinopathies. Thalassemia carrier screening programs have educational programs in schools, armed forces, and through mass media as well as providing counseling to carriers and carrier couples. Screening has shown reduced incidence; by 1995 the prevalence in Italy reduced from 1:250 to 1:4000, and a 95% decrease in that region. The decrease in incidence has benefitted those affected with thalassemia, as the demand for blood has decreased, therefore improving the supply of treatment. Treatment Beta thalassemia major Affected children require regular lifelong blood transfusions. Bone marrow transplants can be curative for some children. Patients receive frequent blood transfusions that lead to or potentiate iron overload. Iron chelation treatment is necessary to prevent damage to internal organs in cases of iron overload. Advances in iron chelation treatments allow patients with thalassemia major to live long lives with access to proper treatment. Popular chelators include deferoxamine and deferiprone.The oral chelator deferasirox was approved for use in 2005 in some countries. Bone marrow transplantation is the only cure and is indicated for patients with severe thalassemia major. Transplantation can eliminate a patients dependence on transfusions. Absent a matching donor, a savior sibling can be conceived by preimplantation genetic diagnosis (PGD) to be free of the disease as well as to match the recipients human leukocyte antigen (HLA) type.Serum ferritin (the storage form of iron) is routinely measured in those with beta thalassemia to determine the degree of iron overload; with increased ferritin levels directing the use of iron chelation therapy. The three iron chelators; subcutaneous deferoxamine, oral deferiprone and oral deferasirox can be used as monotherapy or in combination, they have all been shown to decrease serum/systemic iron levels, hepatic and cardiac iron levels as well as decreasing the risk of cardiac arrhythmia, heart failure and death. Hepatic and myocardial MRI is also used to quantify the iron deposition in target organs, especially the heart and liver, to guide therapy.Scientists at Weill Cornell Medical College have developed a gene therapy strategy that could feasibly treat both beta-thalassemia and sickle cell disease. The technology is based on delivery of a lentiviral vector carrying both the human β-globin gene and an ankyrin insulator to improve gene transcription and translation, and boost levels of β-globin production.On June 10, 2022, a U.S. federal advisory panel recommended that the FDA approve a gene therapy treatment for use with beta thalassemia. Surgical Patients with thalassemia major are more inclined to have a splenectomy. The use of splenectomies have been declining in recent years due to decreased prevalence of hypersplenism in adequately transfused patients. Splenectomy is also associated with increased risk of infections and increased morbidity due to vascular disease, as the spleen is involved in scavenging to rid the body of pathologic or abnormal red blood cells. Patients with hypersplenism are more likely to have a lower amount of healthy blood cells in their body than normal and reveal symptoms of anemia. The different surgical techniques are the open and laparoscopic method. The laparoscopic method requires longer operating time but a shorter recovery period with a smaller and less prominent surgical scar. If it is unnecessary to remove the entire spleen a partial splenectomy may occur; this method preserves some of the immune function while reducing the probability of hypersplenism. Those undergoing splenectomy should receive an appropriate pneumococcal vaccine at least one week (preferably three weeks) before the surgery. Therapeutic Long-term transfusion therapy (in those with transfusion dependent beta thalassemia) is a treatment used to maintain hemoglobin levels at a target pre-transfusion hemoglobin level of 9–10.5 g/dL (11-12 g/dL in those with concomitant heart disease). To ensure quality blood transfusions, the packed red blood cells should be leucoreduced. By having leucoreduced blood packets, the patient is at a lower risk to develop adverse reactions by contaminated white cells and preventing platelet alloimmunisation. Patients with allergic transfusion reactions or unusual red cell antibodies must receive washed red cells or cryopreserved red cells. Washed red cells have been removed of plasma proteins that would have become a target of the patients antibodies allowing the transfusion to be carried out safely. Cryopreserved red cells are used to maintain a supply of rare donor units for patients with unusual red cell antibodies or missing common red cell antigens. These regular transfusions promote normal growth, physical activities and suppress bone marrow hyperactivity. Pharmaceutical During normal iron homeostasis the circulating iron is bound to transferrin. But with iron overload (such as with frequent blood transfusions), the ability for transferrin to bind iron is exceeded and non-transferrin bound iron accumulated. This unbound iron is toxic due to its high propensity to induce oxygen species and is responsible for cellular damage. The prevention of iron overload protects patients from morbidity and mortality. The primary aim is to bind to and remove iron from the body and a rate equal to the rate of transfusional iron input or greater than iron input. Iron chelation is a medical therapy that may prevent the complications of iron overload. Every unit of transfused blood contains 200–250 mg of iron and the body has no natural mechanism to remove excess iron. The excess iron can be removed by iron chelators (deferoxamine, deferiprone and deferasirox).Luspatercept (ACE-536) is a recombinant fusion protein that is used as a treatment in adults with transfusion dependent beta thalassemia. It consists of a modified extra-cellular domain of human activin receptor type IIB bound to the Fc portion of the human IgG1 antibody. The molecule binds to select transforming growth factor beta superfamily ligands to block SMAD2 and 3 signaling, thus enhancing erythroid maturation. The medication has been shown to reduce the transfusion burden by 33% in adults with transfusion dependent beta thalassemia as compared to placebo and was also associated with decreased ferritin levels (with no significant decreases in liver or cardiac iron levels). Beta thalassemia intermedia Patients with beta thalassemia intermedia require no transfusions or may require episodic blood transfusions during certain circumstances (infection, pregnancy, surgery). Patients with frequent transfusions may develop iron overload and require chelation therapy. Transmission is autosomal recessive; however, dominant mutations and compound heterozygotes have been reported. Genetic counseling is recommended and prenatal diagnosis may be offered. Beta thalassemia minor Patients with beta thalassemia minor are usually asymptomatic and are often monitored without treatment. Beta thalassemia minor may coexist with other conditions such as chronic hepatitis B, chronic hepatitis C, non-alcoholic fatty liver disease and alcoholic liver disease that, when combined or co-existing, may cause a person to have iron overload of the liver and more severe liver disease. Epidemiology The beta form of thalassemia is particularly prevalent among the Mediterranean peoples and this geographical association is responsible for its naming: thalassa (θάλασσα) is the Greek word for sea and haima (αἷμα) is the Greek word for blood. In Europe, the highest concentrations of the disease are found in Greece and the Turkish coastal regions. The major Mediterranean islands (except the Balearics) such as Sicily, Sardinia, Corsica, Cyprus, Malta and Crete are heavily affected in particular. Other Mediterranean peoples, as well as those in the vicinity of the Mediterranean, also have high incidence rates, including people from West Asia and North Africa. The data indicate that 15% of the Greek and Turkish Cypriots are carriers of beta-thalassaemia genes, while 10% of the population carry alpha-thalassaemia genes. Evolutionary adaptation The thalassemia trait may confer a degree of protection against malaria, which is or was prevalent in the regions where the trait is common, thus conferring a selective survival advantage on carriers (known as heterozygous advantage), thus perpetuating the mutation. In that respect, the various thalassemias resemble another genetic disorder affecting hemoglobin, sickle-cell disease. Incidence The disorder is more prevalent in certain ethnicities and age groups. Beta thalassemia is most prevalent in the "thalassemia belt" which includes areas in Sub-Saharan Africa, the Mediterranean extending into the Middle East and Southeast Asia. This geographical distribution is thought to be due to beta-thalassemia carrier state (beta thalassemia minor) conferring a resistance to malaria. In the United States, thalassemias prevalence is approximately 1 in 272,000 or 1,000 people. There have been 4,000 hospitalized cases in England in 2002 and 9,233 consultant episodes for thalassemia. Men accounted for 53% of hospital consultant episodes and women accounted for 47%. The mean patient age is 23, with only 1% of consultants being older than 75, and 69% being 15–59. It is estimated that 1.5% of the worlds population are carriers and 40,000 affected infants are born with the disease annually. Beta thalassemia major is usually fatal in infancy if blood transfusions are not initiated immediately. See also Alpha-thalassemia Anisopoikilocytosis (variance in red blood cell size, usually as a result of beta thalassemia) Delta-thalassemia Hemoglobinopathy References Further reading Cao, Antonio; Galanello, Renzo (2010). "Beta-Thalassemia". In Pagon, Roberta A; Bird, Thomas D; Dolan, Cynthia R; Stephens, Karen; Adam, Margaret P (eds.). GeneReviews. University of Washington, Seattle. PMID 20301599. Bahal, Raman; McNeer, Nicole Ali; Quijano, Elias; Liu, Yanfeng; Sulkowski, Parker; Turchick, Audrey; Lu, Yi-Chien; Bhunia, Dinesh C.; Manna, Arunava; Greiner, Dale L.; Brehm, Michael A.; Cheng, Christopher J.; López-Giráldez, Francesc; Ricciardi, Adele; Beloor, Jagadish; Krause, Diane S.; Kumar, Priti; Gallagher, Patrick G.; Braddock, Demetrios T.; Saltzman, W. Mark; Ly, Danith H.; Glazer, Peter M. (26 October 2016). "In vivo correction of anaemia in β-thalassemic mice by γPNA-mediated gene editing with nanoparticle delivery". Nature Communications. 7: 13304. Bibcode:2016NatCo...713304B. doi:10.1038/ncomms13304. ISSN 2041-1723. PMC 5095181. PMID 27782131. == External links ==

You are a medical advisor. Your role is to break down medical terminology into clear, detailed explanations for a general audience.

I'm not familiar with the medical term 'Monochromacy.' Could you provide some insights?

Monochromacy (from Greek mono, meaning "one" and chromo, meaning "color") is the ability of organisms or machines to perceive only light intensity, without respect to spectral composition (color). Organisms with monochromacy are called monochromats. Many mammals, such as cetaceans, the owl monkey and the Australian sea lion (pictured at right) are monochromats. In humans, absence of color vision is one among several other symptoms of severe inherited or acquired diseases, including achromatopsia or blue cone monochromacy, together affecting about 1 in 30,000 people. The affected can distinguish light, dark, and shades of gray but not color. Humans Human vision relies on a duplex retina, comprising two types of photoreceptor cells. Rods are primarily responsible for dim-light scotopic vision and cones are primarily responsible for day-light photopic vision. For all known vertebrates, scotopic vision is monochromatic, since there is typically only one class of rod cell. However, the presence of multiple cone classes contributing to photopic vision enables color vision during daytime conditions. Most humans have three classes of cones, each with a different class of opsin. These three opsins have different spectral sensitivities, which is a prerequisite for trichromacy. An alteration of any of these three cone opsins can lead to colorblindness. Anomalous Trichromacy, when all three cones are functional, but one or more is altered in its spectral sensitivity. Dichromacy, when one of the cones is non-functional and one of the red-green or blue-yellow opponent channels are fully disabled. Cone Monochromacy, when two of the cones are non-functional and both chromatic opponent channels are disabled. Vision is reduced to blacks, whites, and greys. Rod Monochromacy (Achromatopsia), when all three of the cones are non-functional and therefore photopic vision (and therefore color vision) is disabled.Monochromacy of photopic vision is a symptom of both Cone Monochromacy and Rod Monochromacy, so these two conditions are typically referred to collectively as monochromacy. Rod Monochromacy Rod monochromacy (RM), also called congenital complete achromatopsia or total color blindness, is a rare and extremely severe form of an autosomal recessively inherited retinal disorder resulting in severe visual handicap. People with RM have a reduced visual acuity, (usually about 0.1 or 20/200), have total color blindness, photo-aversion and nystagmus. The nystagmus and photo-aversion usually are present during the first months of life, and the prevalence of the disease is estimated to be 1 in 30,000 worldwide. Since patients with RM have no cone function, they lack photopic vision, relying entirely on their rods and scotopic vision, which is necessarily monochromatic. They therefore cannot see any color but only shades of grey. Cone Monochromacy Cone monochromacy (CM) is a condition defined by the exhibition of only one class of cones. A cone monochromat can have good pattern vision at normal daylight levels, but will not be able to distinguish hues. As humans typically exhibit three classes of cones, cone monochromats can hypothetically derive their photopic vision from any one of them, leading to three categories of cone monochromats: Blue cone monochromacy (BCM), also known as S-cone monochromacy, is an X-linked cone disease. It is a rare congenital stationary cone dysfunction syndrome, affecting less than 1 in 100,000 individuals, and is characterized by the absence of L- and M-cone function. BCM results from mutations in a single red or red–green hybrid opsin gene, mutations in both the red and the green opsin genes or deletions within the adjacent LCR (locus control region) on the X chromosome. Green cone monochromacy (GCM), also known as M-cone monochromacy, is a condition where the blue and red cones are absent in the fovea. The prevalence of this type of monochromacy is estimated to be less than 1 in 1 million. Red cone monochromacy (RCM), also known as L-cone monochromacy, is a condition where the blue and green cones are absent in the fovea. Like GCM, the prevalence of RCM is also estimated at less than 1 in 1 million.Cone Monochromats with normal rod function can sometimes exhibit mild color vision due to conditional dichromacy. In mesopic conditions, both rods and cones are active and opponent interactions between the cones and rods can afford slight color vision.According to Jay Neitz, a color vision researcher at the University of Washington, each of the three standard color-detecting cones in the retina of trichromats can detect approximately 100 gradations of color. The brain can process the combinations of these three values so that the average human can distinguish about one million colors. Therefore, a monochromat would be able to distinguish about 100 colors. Mammals Until the 1960s popular belief held that most mammals outside of primates were monochromats. In the last half-century, however, a focus on behavioral and genetic testing of mammals has accumulated extensive evidence of at least dichromatic color vision in a number of mammalian orders. Mammals are now usually assumed to be dichromats (possessing S- and L-cones), with monochromats viewed as the exceptions. Two mammalian orders containing marine mammals exhibit monochromatic vision: Pinnipeds (including seals, sea lions and walruses) Cetaceans (including dolphins and whales)Unlike the trichromacy exhibited in most primates, Owl monkeys (genus Aotus) are also monochromats. Several members of the family Procyonidae (raccoon, crab-eating raccoon and kinkajou) and a few rodents have been demonstrated as cone monochromats, having lost functionality of the S-cone (retaining the L-cone).The light available in an animals habitat is a significant determiner of a mammals color vision. Marine, Nocturnal or Burrowing mammals, which experience less light, have less evolutionary pressure to preserve dichromacy, so often evolve monochromacy.A recent study using through PCR analysis of genes OPN1SW, OPN1LW, and PDE6C determined that all mammals in the cohort Xenarthra (representing sloths, anteaters and armadillos) developed rod monochromacy through a stem ancestor. See also Achromatopsia Blue cone monochromacy Cone dystrophy Dichromacy Trichromacy Tetrachromacy References External links Rossi, Ethan (February 2013). "Visual Function and Cortical Organization in Carriers of Blue Cone Monochromacy". PLOS ONE. 8 (2): e57956. Bibcode:2013PLoSO...857956R. doi:10.1371/journal.pone.0057956. PMC 3585243. PMID 23469117. Weleber, Richard (June 2002). "Infantile and childhood retinal blindness: A molecular perspective (TheFranceschetti Lecture)". Ophthalmic Genetics. 23 (2): 71–98. doi:10.1076/opge.23.2.71.2214. PMID 12187427. S2CID 30741530.

You are a medical advisor. Your role is to break down medical terminology into clear, detailed explanations for a general audience.

Could you offer a clear explanation of the term 'Sebelipase alfa' as used in the medical field?

Sebelipase alfa, sold under the brand name Kanuma, is a recombinant form of the enzyme lysosomal acid lipase (LAL) that is used as a medication for the treatment of lysosomal acid lipase deficiency (LAL-D). It is administered via intraveneous infusion. It was approved for medical use in the European Union and in the United States in 2015. Medical uses Sebelipase alfa is indicated for long-term enzyme replacement therapy (ERT) in people of all ages with lysosomal acid lipase (LAL) deficiency. History Sebelipase was developed by Synageva that became part of Alexion Pharmaceuticals in 2015. For its production, chickens are genetically modified to produce the recombinant form of LAL (rhLAL) in their egg white. After extraction and purification it becomes available as the medication. On 8 December 2015 the FDA announced that its approval came from two centers: The Center for Drug Evaluation and Research (CDER) approved the human therapeutic application of the medication, while the Center for Veterinary Medicine (CVM) approved the application for a recombinant DNA construct in genetically engineered chicken to produce rhLAL in their egg whites. At the time it gained FDA approval Kanuma was the first only drug manufactured in chicken eggs and intended for use in humans.Sebelipase alfa is an orphan drug; its effectiveness was published after a phase 3 trial in 2015. The disease of LAL affects < 0.2 in 10,000 people in the EU. References External links "Sebelipase alfa". Drug Information Portal. U.S. National Library of Medicine.

You act as a bridge between medical jargon and everyday language. Explain medical terms in a manner that is comprehensive yet approachable for non-experts.

I'm encountering the term 'Tropical sprue' in medical literature. What's its definition?

Tropical sprue is a malabsorption disease commonly found in tropical regions, marked with abnormal flattening of the villi and inflammation of the lining of the small intestine. It differs significantly from coeliac sprue. It appears to be a more severe form of environmental enteropathy. Signs and symptoms The illness usually starts with an attack of acute diarrhoea, fever and malaise following which, after a variable period, the patient settles into the chronic phase of diarrhoea, steatorrhoea, weight loss, anorexia, malaise, and nutritional deficiencies. The symptoms of tropical sprue are: Diarrhoea Steatorrhoea or fatty stool (often foul-smelling and whitish in colour) Indigestion Cramps Weight loss and malnutrition FatigueLeft untreated, nutrient and vitamin deficiencies may develop in patients with tropical sprue. These deficiencies may have these symptoms: Vitamin A deficiency: hyperkeratosis or skin scales Vitamin B12 and folic acid deficiencies: anaemia, numbness, and tingling sensation Vitamin D and calcium deficiencies: spasm, bone pain, muscle weakness Vitamin K deficiency: bruises Cause The cause of tropical sprue is not known. It may be caused by persistent bacterial, viral, amoebal, or parasitic infections. Folic acid deficiency, effects of malabsorbed fat on intestinal motility, and persistent small intestinal bacterial overgrowth may combine to cause the disorder. A link between small intestinal bacterial overgrowth and tropical sprue has been proposed to be involved in the aetiology of post-infectious irritable bowel syndrome (IBS). Intestinal immunologic dysfunction, including deficiencies in secretory immunoglobulin A (IgA), may predispose people to malabsorption and bacterial colonization, so tropical sprue may be triggered in susceptible individuals following an acute enteric infection. Diagnosis Diagnosis of tropical sprue can be complicated because many diseases have similar symptoms. The following investigation results are suggestive: Abnormal flattening of villi and inflammation of the lining of the small intestine, observed during an endoscopic procedure. Presence of inflammatory cells (most often lymphocytes) in the biopsy of small intestine tissue. Low levels of vitamins A, B12, E, D, and K, as well as serum albumin, calcium, and folate, revealed by a blood test. Excess fat in the feces (steatorrhoea). Thickened small bowel folds seen on imaging.Tropical sprue is largely limited to within about 30 degrees north and south of the equator. Recent travel to this region is a key factor in diagnosing this disease in residents of countries outside of that geographical region.Other conditions which can resemble tropical sprue need to be differentiated. Coeliac disease (also known as coeliac sprue or gluten sensitive enteropathy), has similar symptoms to tropical sprue, with the flattening of the villi and small intestine inflammation and is caused by an autoimmune disorder in genetically susceptible individuals triggered by ingested gluten. Malabsorption can also be caused by protozoan infections, tuberculosis, HIV/AIDS, immunodeficiency, chronic pancreatitis and inflammatory bowel disease. Environmental enteropathy is a less severe, subclinical condition similar to tropical sprue. Prevention Preventive measures for visitors to tropical areas where the condition exists include steps to reduce the likelihood of gastroenteritis. These may comprise using only bottled water for drinking, brushing teeth, and washing food, and avoiding fruits washed with tap water (or consuming only peeled fruits, such as bananas and oranges). Basic sanitation is necessary to reduce fecal-oral contamination and the impact of environmental enteropathy in the developing world. Treatment Once diagnosed, tropical sprue can be treated by a course of the antibiotic tetracycline or sulphamethoxazole/trimethoprim (co-trimoxazole) for 3 to 6 months. Supplementation of vitamins B12 and folic acid improves appetite and leads to a gain in weight. Prognosis The prognosis for tropical sprue may be excellent after treatment. It usually does not recur in people who get it during travel to affected regions. The recurrence rate for natives is about 20%, but another study showed changes can persist for several years. Epidemiology Tropical sprue is common in the Caribbean, Central and South America, and India and southeast Asia. In the Caribbean, it appeared to be more common in Puerto Rico and Haiti. Epidemics in southern India have occurred. History The disease was first described by William Hillary in 1759 in Barbados. Tropical sprue was responsible for one-sixth of all casualties sustained by the Allied forces in India and Southeast Asia during World War II. The use of folic acid and vitamin B12 in the treatment of tropical sprue was promoted in the late 1940s by Dr. Tom Spies of the University of Alabama, while conducting his research in Cuba and Puerto Rico. == References ==

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

Please help me grasp the concept behind the medical term 'Anabolic steroid.'

Anabolic steroids, also known more properly as anabolic–androgenic steroids (AAS), are steroidal androgens that include natural androgens like testosterone as well as synthetic androgens that are structurally related and have similar effects to testosterone. They increase protein within cells, especially in skeletal muscles, and also have varying degrees of virilizing effects, including induction of the development and maintenance of masculine secondary sexual characteristics such as the growth of facial and body hair. The word anabolic, referring to anabolism, comes from the Greek ἀναβολή anabole, "that which is thrown up, mound". Androgens or AAS are one of three types of sex hormone agonists, the others being estrogens like estradiol and progestogens like progesterone. AAS were synthesized in the 1930s, and are now used therapeutically in medicine to stimulate muscle growth and appetite, induce male puberty and treat chronic wasting conditions, such as cancer and AIDS. The American College of Sports Medicine acknowledges that AAS, in the presence of adequate diet, can contribute to increases in body weight, often as lean mass increases and that the gains in muscular strength achieved through high-intensity exercise and proper diet can be additionally increased by the use of AAS in some individuals.Health risks can be produced by long-term use or excessive doses of AAS. These effects include harmful changes in cholesterol levels (increased low-density lipoprotein and decreased high-density lipoprotein), acne, high blood pressure, liver damage (mainly with most oral AAS), and dangerous changes in the structure of the left ventricle of the heart. These risks are further increased when, as they often do, athletes take steroids alongside other drugs, causing significantly more damage to their bodies. The effect of anabolic steroids on the heart can cause myocardial infarction and strokes. Conditions pertaining to hormonal imbalances such as gynecomastia and testicular size reduction may also be caused by AAS. In women and children, AAS can cause irreversible masculinization.Ergogenic uses for AAS in sports, racing, and bodybuilding as performance-enhancing drugs are controversial because of their adverse effects and the potential to gain unfair advantage in physical competitions. Their use is referred to as doping and banned by most major sporting bodies. Athletes have been looking for drugs to enhance their athletic abilities since the Olympics started in Ancient Greece. For many years, AAS have been by far the most detected doping substances in IOC-accredited laboratories. In countries where AAS are controlled substances, there is often a black market in which smuggled, clandestinely manufactured or even counterfeit drugs are sold to users. Uses Medical Since the discovery and synthesis of testosterone in the 1930s, AAS have been used by physicians for many purposes, with varying degrees of success. These can broadly be grouped into anabolic, androgenic, and other uses. Anabolic Bone marrow stimulation: For decades, AAS were the mainstay of therapy for hypoplastic anemias due to leukemia, kidney failure or aplastic anemia. Growth stimulation: AAS can be used by pediatric endocrinologists to treat children with growth failure. However, the availability of synthetic growth hormone, which has fewer side effects, makes this a secondary treatment. Stimulation of appetite and preservation and increase of muscle mass: AAS have been given to people with chronic wasting conditions such as cancer and AIDS. Stimulation of lean body mass and prevention of bone loss in elderly men, as some studies indicate. However, a 2006 placebo-controlled trial of low-dose testosterone supplementation in elderly men with low levels of testosterone found no benefit on body composition, physical performance, insulin sensitivity, or quality of life. Prevention or treatment of osteoporosis in postmenopausal women. Nandrolone decanoate is approved for this use. Although they have been indicated for this indication, AAS saw very little use for this purpose due to their virilizing side effects. Aiding weight gain following surgery or physical trauma, during chronic infection, or in the context of unexplained weight loss. Counteracting the catabolic effect of long-term corticosteroid therapy. Oxandrolone improves both short-term and long-term outcomes in people recovering from severe burns and is well-established as a safe treatment for this indication. Treatment of idiopathic short stature, hereditary angioedema, alcoholic hepatitis, and hypogonadism. Methyltestosterone is used in the treatment of delayed puberty, hypogonadism, cryptorchidism, and erectile dysfunction in males, and in low doses to treat menopausal symptoms (specifically for osteoporosis, hot flashes, and to increase libido and energy), postpartum breast pain and engorgement, and breast cancer in women. Androgenic Androgen replacement therapy for men with low levels of testosterone; also effective in improving libido for elderly males. Induction of male puberty: Androgens are given to many boys distressed about extreme delay of puberty. Testosterone is now nearly the only androgen used for this purpose and has been shown to increase height, weight, and fat-free mass in boys with delayed puberty. Masculinizing hormone therapy for transgender men, other transmasculine people, and intersex people, by producing masculine secondary sexual characteristics such as a voice deepening, increased bone and muscle mass, masculine fat distribution, facial and body hair, and clitoral enlargement, as well as mental changes such as alleviation of gender dysphoria and increased sex drive. Other Treatment of breast cancer in women, although they are now very rarely used for this purpose due to their marked virilizing side effects. In low doses as a component of hormone therapy for postmenopausal and transgender women, for instance to increase energy, well-being, libido, and quality of life, as well as to reduce hot flashes. Testosterone is usually used for this purpose, although methyltestosterone is also used. Male hormonal contraception; currently experimental, but potential for use as effective, safe, reliable, and reversible male contraceptives. Enhancing performance Most steroid users are not athletes. In the United States, between 1 million and 3 million people (1% of the population) are thought to have used AAS. Studies in the United States have shown that AAS users tend to be mostly middle-class men with a median age of about 25 who are noncompetitive bodybuilders and non-athletes and use the drugs for cosmetic purposes. "Among 12- to 17-year-old boys, use of steroids and similar drugs jumped 25 percent from 1999 to 2000, with 20 percent saying they use them for looks rather than sports, a study by insurer Blue Cross Blue Shield found."(Eisenhauer) Another study found that non-medical use of AAS among college students was at or less than 1%. According to a recent survey, 78.4% of steroid users were noncompetitive bodybuilders and non-athletes, while about 13% reported unsafe injection practices such as reusing needles, sharing needles, and sharing multidose vials, though a 2007 study found that sharing of needles was extremely uncommon among individuals using AAS for non-medical purposes, less than 1%. Another 2007 study found that 74% of non-medical AAS users had post-secondary degrees and more had completed college and fewer had failed to complete high school than is expected from the general populace. The same study found that individuals using AAS for non-medical purposes had a higher employment rate and a higher household income than the general population. AAS users tend to research the drugs they are taking more than other controlled-substance users; however, the major sources consulted by steroid users include friends, non-medical handbooks, internet-based forums, blogs, and fitness magazines, which can provide questionable or inaccurate information.AAS users tend to be unhappy with the portrayal of AAS as deadly in the media and in politics. According to one study, AAS users also distrust their physicians and in the sample 56% had not disclosed their AAS use to their physicians. Another 2007 study had similar findings, showing that, while 66% of individuals using AAS for non-medical purposes were willing to seek medical supervision for their steroid use, 58% lacked trust in their physicians, 92% felt that the medical communitys knowledge of non-medical AAS use was lacking, and 99% felt that the public has an exaggerated view of the side-effects of AAS use. A recent study has also shown that long term AAS users were more likely to have symptoms of muscle dysmorphia and also showed stronger endorsement of more conventional male roles. A recent study in the Journal of Health Psychology showed that many users believed that steroids used in moderation were safe.AAS have been used by men and women in many different kinds of professional sports to attain a competitive edge or to assist in recovery from injury. These sports include bodybuilding, weightlifting, shot put and other track and field, cycling, baseball, wrestling, mixed martial arts, boxing, football, and cricket. Such use is prohibited by the rules of the governing bodies of most sports. AAS use occurs among adolescents, especially by those participating in competitive sports. It has been suggested that the prevalence of use among high-school students in the U.S. may be as high as 2.7%. Dosages Available forms The AAS that have been used most commonly in medicine are testosterone and its many esters (but most typically testosterone undecanoate, testosterone enanthate, testosterone cypionate, and testosterone propionate), nandrolone esters (typically nandrolone decanoate and nandrolone phenylpropionate), stanozolol, and metandienone (methandrostenolone). Others that have also been available and used commonly but to a lesser extent include methyltestosterone, oxandrolone, mesterolone, and oxymetholone, as well as drostanolone propionate (dromostanolone propionate), metenolone (methylandrostenolone) esters (specifically metenolone acetate and metenolone enanthate), and fluoxymesterone. Dihydrotestosterone (DHT), known as androstanolone or stanolone when used medically, and its esters are also notable, although they are not widely used in medicine. Boldenone undecylenate and trenbolone acetate are used in veterinary medicine.Designer steroids are AAS that have not been approved and marketed for medical use but have been distributed through the black market. Examples of notable designer steroids include 1-testosterone (dihydroboldenone), methasterone, trenbolone enanthate, desoxymethyltestosterone, tetrahydrogestrinone, and methylstenbolone. Routes of administration There are four common forms in which AAS are administered: oral pills; injectable steroids; creams/gels for topical application; and skin patches. Oral administration is the most convenient. Testosterone administered by mouth is rapidly absorbed, but it is largely converted to inactive metabolites, and only about one-sixth is available in active form. In order to be sufficiently active when given by mouth, testosterone derivatives are alkylated at the 17α position, e.g. methyltestosterone and fluoxymesterone. This modification reduces the livers ability to break down these compounds before they reach the systemic circulation. Testosterone can be administered parenterally, but it has more irregular prolonged absorption time and greater activity in muscle in enanthate, undecanoate, or cypionate ester form. These derivatives are hydrolyzed to release free testosterone at the site of injection; absorption rate (and thus injection schedule) varies among different esters, but medical injections are normally done anywhere between semi-weekly to once every 12 weeks. A more frequent schedule may be desirable in order to maintain a more constant level of hormone in the system. Injectable steroids are typically administered into the muscle, not into the vein, to avoid sudden changes in the amount of the drug in the bloodstream. In addition, because estered testosterone is dissolved in oil, intravenous injection has the potential to cause a dangerous embolism (clot) in the bloodstream. Transdermal patches (adhesive patches placed on the skin) may also be used to deliver a steady dose through the skin and into the bloodstream. Testosterone-containing creams and gels that are applied daily to the skin are also available, but absorption is inefficient (roughly 10%, varying between individuals) and these treatments tend to be more expensive. Individuals who are especially physically active and/or bathe often may not be good candidates, since the medication can be washed off and may take up to six hours to be fully absorbed. There is also the risk that an intimate partner or child may come in contact with the application site and inadvertently dose themselves; children and women are highly sensitive to testosterone and can develop unintended masculinization and health effects, even from small doses. Injection is the most common method used by individuals administering AAS for non-medical purposes.The traditional routes of administration do not have differential effects on the efficacy of the drug. Studies indicate that the anabolic properties of AAS are relatively similar despite the differences in pharmacokinetic principles such as first-pass metabolism. However, the orally available forms of AAS may cause liver damage in high doses. Adverse effects Known possible side effects of AAS include: Dermatological/integumental: oily skin, acne vulgaris, acne conglobata, seborrhea, stretch marks (due to rapid muscle enlargement), hypertrichosis (excessive body hair growth), androgenic alopecia (pattern hair loss; scalp baldness), fluid retention/edema. Reproductive/endocrine: libido changes, reversible infertility, hypogonadotropic hypogonadism. Male-specific: spontaneous erections, nocturnal emissions, priapism, erectile dysfunction, gynecomastia (mostly only with aromatizable and hence estrogenic AAS), oligospermia/azoospermia, testicular atrophy, intratesticular leiomyosarcoma, prostate hypertrophy, prostate cancer. Female-specific: masculinization, irreversible voice deepening, hirsutism (excessive facial/body hair growth), menstrual disturbances (e.g., anovulation, oligomenorrhea, amenorrhea, dysmenorrhea), clitoral enlargement, breast atrophy, uterine atrophy, teratogenicity (in female fetuses). Child-specific: premature epiphyseal closure and associated short stature, precocious puberty in boys, delayed puberty and contrasexual precocity in girls. Psychiatric/neurological: mood swings, irritability, aggression, violent behavior, impulsivity/recklessness, hypomania/mania, euphoria, depression, anxiety, dysphoria, suicidality, delusions, psychosis, withdrawal, dependence, neurotoxicity, cognitive impairment. Musculoskeletal: muscle hypertrophy, muscle strains, tendon ruptures, rhabdomyolysis. Cardiovascular: dyslipidemia (e.g., increased LDL levels, decreased HDL levels, reduced apo-A1 levels), atherosclerosis, hypertension, left ventricular hypertrophy, cardiomyopathy, myocardial hypertrophy, polycythemia/erythrocytosis, arrhythmias, thrombosis (e.g., embolism, stroke), myocardial infarction, sudden death. Hepatic: elevated liver function tests (AST, ALT, bilirubin, LDH, ALP), hepatotoxicity, jaundice, hepatic steatosis, hepatocellular adenoma, hepatocellular carcinoma, cholestasis, peliosis hepatis; all mostly or exclusively with 17α-alkylated AAS. Renal: renal hypertrophy, nephropathy, acute renal failure (secondary to rhabdomyolysis), focal segmental glomerulosclerosis, renal cell carcinoma. Others: glucose intolerance, insulin resistance, immune dysfunction. Physiological Depending on the length of drug use, there is a chance that the immune system can be damaged. Most of these side-effects are dose-dependent, the most common being elevated blood pressure, especially in those with pre-existing hypertension. In addition to morphological changes of the heart which may have a permanent adverse effect on cardiovascular efficiency. AAS have been shown to alter fasting blood sugar and glucose tolerance tests. AAS such as testosterone also increase the risk of cardiovascular disease or coronary artery disease. Acne is fairly common among AAS users, mostly due to stimulation of the sebaceous glands by increased testosterone levels. Conversion of testosterone to DHT can accelerate the rate of premature baldness for males genetically predisposed, but testosterone itself can produce baldness in females.A number of severe side effects can occur if adolescents use AAS. For example, AAS may prematurely stop the lengthening of bones (premature epiphyseal fusion through increased levels of estrogen metabolites), resulting in stunted growth. Other effects include, but are not limited to, accelerated bone maturation, increased frequency and duration of erections, and premature sexual development. AAS use in adolescence is also correlated with poorer attitudes related to health. Cancer WHO organization International Agency for Research on Cancer (IARC) list AAS under Group 2A: Probably carcinogenic to humans. Cardiovascular Other side-effects can include alterations in the structure of the heart, such as enlargement and thickening of the left ventricle, which impairs its contraction and relaxation, and therefore reducing ejected blood volume. Possible effects of these alterations in the heart are hypertension, cardiac arrhythmias, congestive heart failure, heart attacks, and sudden cardiac death. These changes are also seen in non-drug-using athletes, but steroid use may accelerate this process. However, both the connection between changes in the structure of the left ventricle and decreased cardiac function, as well as the connection to steroid use have been disputed.AAS use can cause harmful changes in cholesterol levels: Some steroids cause an increase in LDL cholesterol and a decrease in HDL cholesterol. Growth defects AAS use in adolescents quickens bone maturation and may reduce adult height in high doses. Low doses of AAS such as oxandrolone are used in the treatment of idiopathic short stature, but this may only quicken maturation rather than increasing adult height. Feminization There are also sex-specific side effects of AAS. Development of breast tissue in males, a condition called gynecomastia (which is usually caused by high levels of circulating estradiol), may arise because of increased conversion of testosterone to estradiol by the enzyme aromatase. Reduced sexual function and temporary infertility can also occur in males. Another male-specific side-effect that can occur is testicular atrophy, caused by the suppression of natural testosterone levels, which inhibits production of sperm (most of the mass of the testes is developing sperm). This side-effect is temporary; the size of the testicles usually returns to normal within a few weeks of discontinuing AAS use as normal production of sperm resumes. Masculinization Female-specific side effects include increases in body hair, permanent deepening of the voice, enlarged clitoris, and temporary decreases in menstrual cycles. Alteration of fertility and ovarian cysts can also occur in females. When taken during pregnancy, AAS can affect fetal development by causing the development of male features in the female fetus and female features in the male fetus. Kidney problems Kidney tests revealed that nine of the ten steroid users developed a condition called focal segmental glomerulosclerosis, a type of scarring within the kidneys. The kidney damage in the bodybuilders has similarities to that seen in morbidly obese patients, but appears to be even more severe. Liver problems High doses of oral AAS compounds can cause liver damage. Peliosis hepatis has been increasingly recognised with the use of AAS. Neuropsychiatric A 2005 review in CNS Drugs determined that "significant psychiatric symptoms including aggression and violence, mania, and less frequently psychosis and suicide have been associated with steroid abuse. Long-term steroid abusers may develop symptoms of dependence and withdrawal on discontinuation of AAS". High concentrations of AAS, comparable to those likely sustained by many recreational AAS users, produce apoptotic effects on neurons, raising the specter of possibly irreversible neurotoxicity. Recreational AAS use appears to be associated with a range of potentially prolonged psychiatric effects, including dependence syndromes, mood disorders, and progression to other forms of substance abuse, but the prevalence and severity of these various effects remains poorly understood. There is no evidence that steroid dependence develops from therapeutic use of AAS to treat medical disorders, but instances of AAS dependence have been reported among weightlifters and bodybuilders who chronically administered supraphysiologic doses. Mood disturbances (e.g. depression, [hypo-]mania, psychotic features) are likely to be dose- and drug-dependent, but AAS dependence or withdrawal effects seem to occur only in a small number of AAS users.Large-scale long-term studies of psychiatric effects on AAS users are not currently available. In 2003, the first naturalistic long-term study on ten users, seven of which having completed the study, found a high incidence of mood disorders and substance abuse, but few clinically relevant changes in physiological parameters or laboratory measures were noted throughout the study, and these changes were not clearly related to periods of reported AAS use. A 13-month study, which was published in 2006 and which involved 320 body builders and athletes suggests that the wide range of psychiatric side-effects induced by the use of AAS is correlated to the severity of abuse. Diagnostic Statistical Manual assertion DSM-IV lists General diagnostic criteria for a personality disorder guideline that "The pattern must not be better accounted for as a manifestation of another mental disorder, or to the direct physiological effects of a substance (e.g. drug or medication) or a general medical condition (e.g. head trauma).". As a result, AAS users may get misdiagnosed by a psychiatrist not told about their habit. Personality profiles Cooper, Noakes, Dunne, Lambert, and Rochford identified that AAS-using individuals are more likely to score higher on borderline (4.7 times), antisocial (3.8 times), paranoid (3.4 times), schizotypal (3.1 times), histrionic (2.9 times), passive-aggressive (2.4 times), and narcissistic (1.6 times) personality profiles than non-users. Other studies have suggested that antisocial personality disorder is slightly more likely among AAS users than among non-users (Pope & Katz, 1994). Bipolar dysfunction, substance dependency, and conduct disorder have also been associated with AAS use. Mood and anxiety Affective disorders have long been recognised as a complication of AAS use. Case reports describe both hypomania and mania, along with irritability, elation, recklessness, racing thoughts and feelings of power and invincibility that did not meet the criteria for mania/hypomania. Of 53 bodybuilders who used AAS, 27 (51%) reported unspecified mood disturbance. Aggression and hypomania From the mid-1980s onward, the media reported "roid rage" as a side effect of AAS.: 23 A 2005 review determined that some, but not all, randomized controlled studies have found that AAS use correlates with hypomania and increased aggressiveness, but pointed out that attempts to determine whether AAS use triggers violent behavior have failed, primarily because of high rates of non-participation. A 2008 study on a nationally representative sample of young adult males in the United States found an association between lifetime and past-year self-reported AAS use and involvement in violent acts. Compared with individuals that did not use steroids, young adult males that used AAS reported greater involvement in violent behaviors even after controlling for the effects of key demographic variables, previous violent behavior, and polydrug use. A 1996 review examining the blind studies available at that time also found that these had demonstrated a link between aggression and steroid use, but pointed out that with estimates of over one million past or current steroid users in the United States at that time, an extremely small percentage of those using steroids appear to have experienced mental disturbance severe enough to result in clinical treatments or medical case reports.A 1996 randomized controlled trial, which involved 43 men, did not find an increase in the occurrence of angry behavior during 10 weeks of administration of testosterone enanthate at 600 mg/week, but this study screened out subjects that had previously abused steroids or had any psychiatric antecedents. A trial conducted in 2000 using testosterone cypionate at 600 mg/week found that treatment significantly increased manic scores on the YMRS, and aggressive responses on several scales. The drug response was highly variable. However: 84% of subjects exhibited minimal psychiatric effects, 12% became mildly hypomanic, and 4% (2 subjects) became markedly hypomanic. The mechanism of these variable reactions could not be explained by demographic, psychological, laboratory, or physiological measures.A 2006 study of two pairs of identical twins, in which one twin used AAS and the other did not, found that in both cases the steroid-using twin exhibited high levels of aggressiveness, hostility, anxiety, and paranoid ideation not found in the "control" twin. A small-scale study of 10 AAS users found that cluster B personality disorders were confounding factors for aggression.The relationship between AAS use and depression is inconclusive. There have been anecdotal reports of depression and suicide in teenage steroid users, but little systematic evidence. A 1992 review found that AAS may both relieve and cause depression, and that cessation or diminished use of AAS may also result in depression, but called for additional studies due to disparate data. In the case of suicide, 3.9% of a sample of 77 those classified as AAS users reported attempting suicide during withdrawal (Malone, Dimeff, Lombardo, & Sample, 1995). Reproductive Androgens such as testosterone, androstenedione and dihydrotestosterone are required for the development of organs in the male reproductive system, including the seminal vesicles, epididymis, vas deferens, penis and prostate. AAS are testosterone derivatives designed to maximize the anabolic effects of testosterone. AAS are consumed by elite athletes competing in sports like weightlifting, bodybuilding, and track and field. Male recreational athletes take AAS to achieve an "enhanced" physical appearance.AAS consumption disrupts the hypothalamic–pituitary–gonadal axis (HPG axis) in males. In the HPG axis, gonadotropin-releasing hormone (GnRH) is secreted from the arcuate nucleus of the hypothalamus and stimulates the anterior pituitary to secrete the two gonadotropins, follicle stimulating hormone (FSH) and luteinizing hormone (LH). In adult males, LH stimulates the Leydig cells in the testes to produce testosterone which is required to form new sperm through spermatogenesis. AAS consumption leads to dose-dependent suppression of gonadotropin release through suppression of GnRH from the hypothalamus (long-loop mechanism) or from direct negative feedback on the anterior pituitary to inhibit gonadotropin release (short-loop mechanism), leading to AAS-induced hypogonadism. Pharmacology Mechanism of action The pharmacodynamics of AAS are unlike peptide hormones. Water-soluble peptide hormones cannot penetrate the fatty cell membrane and only indirectly affect the nucleus of target cells through their interaction with the cells surface receptors. However, as fat-soluble hormones, AAS are membrane-permeable and influence the nucleus of cells by direct action. The pharmacodynamic action of AAS begin when the exogenous hormone penetrates the membrane of the target cell and binds to an androgen receptor (AR) located in the cytoplasm of that cell. From there, the compound hormone-receptor diffuses into the nucleus, where it either alters the expression of genes or activates processes that send signals to other parts of the cell. Different types of AAS bind to the AAR with different affinities, depending on their chemical structure.The effect of AAS on muscle mass is caused in at least two ways: first, they increase the production of proteins; second, they reduce recovery time by blocking the effects of stress hormone cortisol on muscle tissue, so that catabolism of muscle is greatly reduced. It has been hypothesized that this reduction in muscle breakdown may occur through AAS inhibiting the action of other steroid hormones called glucocorticoids that promote the breakdown of muscles. AAS also affect the number of cells that develop into fat-storage cells, by favouring cellular differentiation into muscle cells instead. Anabolic and androgenic effects As their name suggests, AAS have two different, but overlapping, types of effects: anabolic, meaning that they promote anabolism (cell growth), and androgenic (or virilizing), meaning that they affect the development and maintenance of masculine characteristics. Some examples of the anabolic effects of these hormones are increased protein synthesis from amino acids, increased appetite, increased bone remodeling and growth, and stimulation of bone marrow, which increases the production of red blood cells. Through a number of mechanisms AAS stimulate the formation of muscle cells and hence cause an increase in the size of skeletal muscles, leading to increased strength.The androgenic effects of AAS are numerous. Depending on the length of use, the side effects of the steroid can be irreversible. Processes affected include pubertal growth, sebaceous gland oil production, and sexuality (especially in fetal development). Some examples of virilizing effects are growth of the clitoris in females and the penis in male children (the adult penis size does not change due to steroids ), increased vocal cord size, increased libido, suppression of natural sex hormones, and impaired production of sperm. Effects on women include deepening of the voice, facial hair growth, and possibly a decrease in breast size. Men may develop an enlargement of breast tissue, known as gynecomastia, testicular atrophy, and a reduced sperm count. The androgenic:anabolic ratio of an AAS is an important factor when determining the clinical application of these compounds. Compounds with a high ratio of androgenic to an anabolic effects are the drug of choice in androgen-replacement therapy (e.g., treating hypogonadism in males), whereas compounds with a reduced androgenic:anabolic ratio are preferred for anemia and osteoporosis, and to reverse protein loss following trauma, surgery, or prolonged immobilization. Determination of androgenic:anabolic ratio is typically performed in animal studies, which has led to the marketing of some compounds claimed to have anabolic activity with weak androgenic effects. This disassociation is less marked in humans, where all AAS have significant androgenic effects.A commonly used protocol for determining the androgenic:anabolic ratio, dating back to the 1950s, uses the relative weights of ventral prostate (VP) and levator ani muscle (LA) of male rats. The VP weight is an indicator of the androgenic effect, while the LA weight is an indicator of the anabolic effect. Two or more batches of rats are castrated and given no treatment and respectively some AAS of interest. The LA/VP ratio for an AAS is calculated as the ratio of LA/VP weight gains produced by the treatment with that compound using castrated but untreated rats as baseline: (LAc,t–LAc)/(VPc,t–VPc). The LA/VP weight gain ratio from rat experiments is not unitary for testosterone (typically 0.3–0.4), but it is normalized for presentation purposes, and used as basis of comparison for other AAS, which have their androgenic:anabolic ratios scaled accordingly (as shown in the table above). In the early 2000s, this procedure was standardized and generalized throughout OECD in what is now known as the Hershberger assay. Body composition and strength improvements Body weight in men may increase by 2 to 5 kg as a result of short-term (<10 weeks) AAS use, which may be attributed mainly to an increase of lean mass. Animal studies also found that fat mass was reduced, but most studies in humans failed to elucidate significant fat mass decrements. The effects on lean body mass have been shown to be dose-dependent. Both muscle hypertrophy and the formation of new muscle fibers have been observed. The hydration of lean mass remains unaffected by AAS use, although small increments of blood volume cannot be ruled out.The upper region of the body (thorax, neck, shoulders, and upper arm) seems to be more susceptible for AAS than other body regions because of predominance of ARs in the upper body. The largest difference in muscle fiber size between AAS users and non-users was observed in type I muscle fibers of the vastus lateralis and the trapezius muscle as a result of long-term AAS self-administration. After drug withdrawal, the effects fade away slowly, but may persist for more than 6–12 weeks after cessation of AAS use.Strength improvements in the range of 5 to 20% of baseline strength, depending largely on the drugs and dose used as well as the administration period. Overall, the exercise where the most significant improvements were observed is the bench press. For almost two decades, it was assumed that AAS exerted significant effects only in experienced strength athletes. A randomized controlled trial demonstrated, however, that even in novice athletes a 10-week strength training program accompanied by testosterone enanthate at 600 mg/week may improve strength more than training alone does. This dose is sufficient to significantly improve lean muscle mass relative to placebo even in subjects that did not exercise at all. The anabolic effects of testosterone enanthate were highly dose dependent. Dissociation of effects Endogenous/natural AAS like testosterone and DHT and synthetic AAS mediate their effects by binding to and activating the AR. On the basis of animal bioassays, the effects of these agents have been divided into two partially dissociable types: anabolic (myotrophic) and androgenic. Dissociation between the ratios of these two types of effects relative to the ratio observed with testosterone is observed in rat bioassays with various AAS. Theories for the dissociation include differences between AAS in terms of their intracellular metabolism, functional selectivity (differential recruitment of coactivators), and non-genomic mechanisms (i.e., signaling through non-AR membrane androgen receptors, or mARs). Support for the latter two theories is limited and more hypothetical, but there is a good deal of support for the intracellular metabolism theory.The measurement of the dissociation between anabolic and androgenic effects among AAS is based largely on a simple but outdated and unsophisticated model using rat tissue bioassays. It has been referred to as the "myotrophic–androgenic index". In this model, myotrophic or anabolic activity is measured by change in the weight of the rat bulbocavernosus/levator ani muscle, and androgenic activity is measured by change in the weight of the rat ventral prostate (or, alternatively, the rat seminal vesicles), in response to exposure to the AAS. The measurements are then compared to form a ratio. Intracellular metabolism Testosterone is metabolized in various tissues by 5α-reductase into DHT, which is 3- to 10-fold more potent as an AR agonist, and by aromatase into estradiol, which is an estrogen and lacks significant AR affinity. In addition, DHT is metabolized by 3α-hydroxysteroid dehydrogenase (3α-HSD) and 3β-hydroxysteroid dehydrogenase (3β-HSD) into 3α-androstanediol and 3β-androstanediol, respectively, which are metabolites with little or no AR affinity. 5α-reductase is widely distributed throughout the body, and is concentrated to various extents in skin (particularly the scalp, face, and genital areas), prostate, seminal vesicles, liver, and the brain. In contrast, expression of 5α-reductase in skeletal muscle is undetectable. Aromatase is highly expressed in adipose tissue and the brain, and is also expressed significantly in skeletal muscle. 3α-HSD is highly expressed in skeletal muscle as well.Natural AAS like testosterone and DHT and synthetic AAS are analogues and are very similar structurally. For this reason, they have the capacity to bind to and be metabolized by the same steroid-metabolizing enzymes. According to the intracellular metabolism explanation, the androgenic-to-anabolic ratio of a given AR agonist is related to its capacity to be transformed by the aforementioned enzymes in conjunction with the AR activity of any resulting products. For instance, whereas the AR activity of testosterone is greatly potentiated by local conversion via 5α-reductase into DHT in tissues where 5α-reductase is expressed, an AAS that is not metabolized by 5α-reductase or is already 5α-reduced, such as DHT itself or a derivative (like mesterolone or drostanolone), would not undergo such potentiation in said tissues. Moreover, nandrolone is metabolized by 5α-reductase, but unlike the case of testosterone and DHT, the 5α-reduced metabolite of nandrolone has much lower affinity for the AR than does nandrolone itself, and this results in reduced AR activation in 5α-reductase-expressing tissues. As so-called "androgenic" tissues such as skin/hair follicles and male reproductive tissues are very high in 5α-reductase expression, while skeletal muscle is virtually devoid of 5α-reductase, this may primarily explain the high myotrophic–androgenic ratio and dissociation seen with nandrolone, as well as with various other AAS.Aside from 5α-reductase, aromatase may inactivate testosterone signaling in skeletal muscle and adipose tissue, so AAS that lack aromatase affinity, in addition to being free of the potential side effect of gynecomastia, might be expected to have a higher myotrophic–androgenic ratio in comparison. In addition, DHT is inactivated by high activity of 3α-HSD in skeletal muscle (and cardiac tissue), and AAS that lack affinity for 3α-HSD could similarly be expected to have a higher myotrophic–androgenic ratio (although perhaps also increased long-term cardiovascular risks). In accordance, DHT, mestanolone (17α-methyl-DHT), and mesterolone (1α-methyl-DHT) are all described as very poorly anabolic due to inactivation by 3α-HSD in skeletal muscle, whereas other DHT derivatives with other structural features like metenolone, oxandrolone, oxymetholone, drostanolone, and stanozolol are all poor substrates for 3α-HSD and are described as potent anabolics.The intracellular metabolism theory explains how and why remarkable dissociation between anabolic and androgenic effects might occur despite the fact that these effects are mediated through the same signaling receptor, and why this dissociation is invariably incomplete. In support of the model is the rare condition congenital 5α-reductase type 2 deficiency, in which the 5α-reductase type 2 enzyme is defective, production of DHT is impaired, and DHT levels are low while testosterone levels are normal. Males with this condition are born with ambiguous genitalia and a severely underdeveloped or even absent prostate gland. In addition, at the time of puberty, such males develop normal musculature, voice deepening, and libido, but have reduced facial hair, a female pattern of body hair (i.e., largely restricted to the pubic triangle and underarms), no incidence of male pattern hair loss, and no prostate enlargement or incidence of prostate cancer. They also notably do not develop gynecomastia as a consequence of their condition. Functional selectivity An animal study found that two different kinds of androgen response elements could differentially respond to testosterone and DHT upon activation of the AR. Whether this is involved in the differences in the ratios of anabolic-to-myotrophic effect of different AAS is unknown however. Non-genomic mechanisms Testosterone signals not only through the nuclear AR, but also through mARs, including ZIP9 and GPRC6A. It has been proposed that differential signaling through mARs may be involved in the dissociation of the anabolic and androgenic effects of AAS. Indeed, DHT has less than 1% of the affinity of testosterone for ZIP9, and the synthetic AAS metribolone and mibolerone are ineffective competitors for the receptor similarly. This indicates that AAS do show differential interactions with the AR and mARs. However, women with complete androgen insensitivity syndrome (CAIS), who have a 46,XY ("male") genotype and testes but a defect in the AR such that it is non-functional, are a challenge to this notion. They are completely insensitive to the AR-mediated effects of androgens like testosterone, and show a perfectly female phenotype despite having testosterone levels in the high end of the normal male range. These women have little or no sebum production, incidence of acne, or body hair growth (including in the pubic and axillary areas). Moreover, CAIS women have lean body mass that is normal for females but is of course greatly reduced relative to males. These observations suggest that the AR is mainly or exclusively responsible for masculinization and myotrophy caused by androgens. The mARs have however been found to be involved in some of the health-related effects of testosterone, like modulation of prostate cancer risk and progression. Antigonadotropic effects Changes in endogenous testosterone levels may also contribute to differences in myotrophic–androgenic ratio between testosterone and synthetic AAS. AR agonists are antigonadotropic – that is, they dose-dependently suppress gonadal testosterone production and hence reduce systemic testosterone concentrations. By suppressing endogenous testosterone levels and effectively replacing AR signaling in the body with that of the exogenous AAS, the myotrophic–androgenic ratio of a given AAS may be further, dose-dependently increased, and this hence may be an additional factor contributing to the differences in myotrophic–androgenic ratio among different AAS. In addition, some AAS, such as 19-nortestosterone derivatives like nandrolone, are also potent progestogens, and activation of the progesterone receptor (PR) is antigonadotropic similarly to activation of the AR. The combination of sufficient AR and PR activation can suppress circulating testosterone levels into the castrate range in men (i.e., complete suppression of gonadal testosterone production and circulating testosterone levels decreased by about 95%). As such, combined progestogenic activity may serve to further increase the myotrophic–androgenic ratio for a given AAS. GABAA receptor modulation Some AAS, such as testosterone, DHT, stanozolol, and methyltestosterone, have been found to modulate the GABAA receptor similarly to endogenous neurosteroids like allopregnanolone, 3α-androstanediol, dehydroepiandrosterone sulfate, and pregnenolone sulfate. It has been suggested that this may contribute as an alternative or additional mechanism to the neurological and behavioral effects of AAS. Comparison of AAS AAS differ in a variety of ways including in their capacities to be metabolized by steroidogenic enzymes such as 5α-reductase, 3-hydroxysteroid dehydrogenases, and aromatase, in whether their potency as AR agonists is potentiated or diminished by 5α-reduction, in their ratios of anabolic/myotrophic to androgenic effect, in their estrogenic, progestogenic, and neurosteroid activities, in their oral activity, and in their capacity to produce hepatotoxicity. 5α-Reductase and androgenicity Testosterone can be robustly converted by 5α-reductase into DHT in so-called androgenic tissues such as skin, scalp, prostate, and seminal vesicles, but not in muscle or bone, where 5α-reductase either is not expressed or is only minimally expressed. As DHT is 3- to 10-fold more potent as an agonist of the AR than is testosterone, the AR agonist activity of testosterone is thus markedly and selectively potentiated in such tissues. In contrast to testosterone, DHT and other 4,5α-dihydrogenated AAS are already 5α-reduced, and for this reason, cannot be potentiated in androgenic tissues. 19-Nortestosterone derivatives like nandrolone can be metabolized by 5α-reductase similarly to testosterone, but 5α-reduced metabolites of 19-nortestosterone derivatives (e.g., 5α-dihydronandrolone) tend to have reduced activity as AR agonists, resulting in reduced androgenic activity in tissues that express 5α-reductase. In addition, some 19-nortestosterone derivatives, including trestolone (7α-methyl-19-nortestosterone (MENT)), 11β-methyl-19-nortestosterone (11β-MNT), and dimethandrolone (7α,11β-dimethyl-19-nortestosterone), cannot be 5α-reduced. Conversely, certain 17α-alkylated AAS like methyltestosterone are 5α-reduced and potentiated in androgenic tissues similarly to testosterone. 17α-Alkylated DHT derivatives cannot be potentiated via 5α-reductase however, as they are already 4,5α-reduced.The capacity to be metabolized by 5α-reductase and the AR activity of the resultant metabolites appears to be one of the major, if not the most important determinant of the androgenic–myotrophic ratio for a given AAS. AAS that are not potentiated by 5α-reductase or that are weakened by 5α-reductase in androgenic tissues have a reduced risk of androgenic side effects such as acne, androgenic alopecia (male-pattern baldness), hirsutism (excessive male-pattern hair growth), benign prostatic hyperplasia (prostate enlargement), and prostate cancer, while incidence and magnitude of other effects such as muscle hypertrophy, bone changes, voice deepening, and changes in sex drive show no difference. Aromatase and estrogenicity Testosterone can be metabolized by aromatase into estradiol, and many other AAS can be metabolized into their corresponding estrogenic metabolites as well. As an example, the 17α-alkylated AAS methyltestosterone and metandienone are converted by aromatase into methylestradiol. 4,5α-Dihydrogenated derivatives of testosterone such as DHT cannot be aromatized, whereas 19-nortestosterone derivatives like nandrolone can be but to a greatly reduced extent. Some 19-nortestosterone derivatives, such as dimethandrolone and 11β-MNT, cannot be aromatized due to steric hindrance provided by their 11β-methyl group, whereas the closely related AAS trestolone (7α-methyl-19-nortestosterone), in relation to its lack of an 11β-methyl group, can be aromatized. AAS that are 17α-alkylated (and not also 4,5α-reduced or 19-demethylated) are also aromatized but to a lesser extent than is testosterone. However, it is notable that estrogens that are 17α-substituted (e.g., ethinylestradiol and methylestradiol) are of markedly increased estrogenic potency due to improved metabolic stability, and for this reason, 17α-alkylated AAS can actually have high estrogenicity and comparatively greater estrogenic effects than testosterone.The major effect of estrogenicity is gynecomastia (woman-like breasts). AAS that have a high potential for aromatization like testosterone and particularly methyltestosterone show a high risk of gynecomastia at sufficiently high dosages, while AAS that have a reduced potential for aromatization like nandrolone show a much lower risk (though still potentially significant at high dosages). In contrast, AAS that are 4,5α-reduced, and some other AAS (e.g., 11β-methylated 19-nortestosterone derivatives), have no risk of gynecomastia. In addition to gynecomastia, AAS with high estrogenicity have increased antigonadotropic activity, which results in increased potency in suppression of the hypothalamic-pituitary-gonadal axis and gonadal testosterone production. Progestogenic activity Many 19-nortestosterone derivatives, including nandrolone, trenbolone, ethylestrenol (ethylnandrol), metribolone (R-1881), trestolone, 11β-MNT, dimethandrolone, and others, are potent agonists of the progesterone receptor (AR) and hence are progestogens in addition to AAS. Similarly to the case of estrogenic activity, the progestogenic activity of these drugs serves to augment their antigonadotropic activity. This results in increased potency and effectiveness of these AAS as antispermatogenic agents and male contraceptives (or, put in another way, increased potency and effectiveness in producing azoospermia and reversible male infertility). Oral activity and hepatotoxicity Non-17α-alkylated testosterone derivatives such as testosterone itself, DHT, and nandrolone all have poor oral bioavailability due to extensive first-pass hepatic metabolism and hence are not orally active. A notable exception to this are AAS that are androgen precursors or prohormones, including dehydroepiandrosterone (DHEA), androstenediol, androstenedione, boldione (androstadienedione), bolandiol (norandrostenediol), bolandione (norandrostenedione), dienedione, mentabolan (MENT dione, trestione), and methoxydienone (methoxygonadiene) (although these are relatively weak AAS). AAS that are not orally active are used almost exclusively in the form of esters administered by intramuscular injection, which act as depots and function as long-acting prodrugs. Examples include testosterone, as testosterone cypionate, testosterone enanthate, and testosterone propionate, and nandrolone, as nandrolone phenylpropionate and nandrolone decanoate, among many others (see here for a full list of testosterone and nandrolone esters). An exception is the very long-chain ester testosterone undecanoate, which is orally active, albeit with only very low oral bioavailability (approximately 3%). In contrast to most other AAS, 17α-alkylated testosterone derivatives show resistance to metabolism due to steric hindrance and are orally active, though they may be esterified and administered via intramuscular injection as well.In addition to oral activity, 17α-alkylation also confers a high potential for hepatotoxicity, and all 17α-alkylated AAS have been associated, albeit uncommonly and only after prolonged use (different estimates between 1 and 17%), with hepatotoxicity. In contrast, testosterone esters have only extremely rarely or never been associated with hepatotoxicity, and other non-17α-alkylated AAS only rarely, although long-term use may reportedly still increase the risk of hepatic changes (but at a much lower rate than 17α-alkylated AAS and reportedly not at replacement dosages). In accordance, D-ring glucuronides of testosterone and DHT have been found to be cholestatic.Aside from prohormones and testosterone undecanoate, almost all orally active AAS are 17α-alkylated. A few AAS that are not 17α-alkylated are orally active. Some examples include the testosterone 17-ethers cloxotestosterone, quinbolone, and silandrone, which are prodrugs (to testosterone, boldenone (Δ1-testosterone), and testosterone, respectively), the DHT 17-ethers mepitiostane, mesabolone, and prostanozol (which are also prodrugs), the 1-methylated DHT derivatives mesterolone and metenolone (although these are relatively weak AAS), and the 19-nortestosterone derivatives dimethandrolone and 11β-MNT, which have improved resistance to first-pass hepatic metabolism due to their 11β-methyl groups (in contrast to them, the related AAS trestolone (7α-methyl-19-nortestosterone) is not orally active). As these AAS are not 17α-alkylated, they show minimal potential for hepatotoxicity. Neurosteroid activity DHT, via its metabolite 3α-androstanediol (produced by 3α-hydroxysteroid dehydrogenase (3α-HSD)), is a neurosteroid that acts via positive allosteric modulation of the GABAA receptor. Testosterone, via conversion into DHT, also produces 3α-androstanediol as a metabolite and hence has similar activity. Some AAS that are or can be 5α-reduced, including testosterone, DHT, stanozolol, and methyltestosterone, among many others, can or may modulate the GABAA receptor, and this may contribute as an alternative or additional mechanism to their central nervous system effects in terms of mood, anxiety, aggression, and sex drive. Chemistry AAS are androstane or estrane steroids. They include testosterone (androst-4-en-17β-ol-3-one) and derivatives with various structural modifications such as: 17α-Alkylation: methyltestosterone, metandienone, fluoxymesterone, oxandrolone, oxymetholone, stanozolol, norethandrolone, ethylestrenol 19-Demethylation: nandrolone, trenbolone, norethandrolone, ethylestrenol, trestolone, dimethandrolone 5α-Reduction: androstanolone, drostanolone, mestanolone, mesterolone, metenolone, oxandrolone, oxymetholone, stanozolol 3β- and/or 17β-esterification: testosterone enanthate, nandrolone decanoate, drostanolone propionate, boldenone undecylenate, trenbolone acetateAs well as others such as 1-dehydrogenation (e.g., metandienone, boldenone), 1-substitution (e.g., mesterolone, metenolone), 2-substitution (e.g., drostanolone, oxymetholone, stanozolol), 4-substitution (e.g., clostebol, oxabolone), and various other modifications. Detection in body fluids The most commonly employed human physiological specimen for detecting AAS usage is urine, although both blood and hair have been investigated for this purpose. The AAS, whether of endogenous or exogenous origin, are subject to extensive hepatic biotransformation by a variety of enzymatic pathways. The primary urinary metabolites may be detectable for up to 30 days after the last use, depending on the specific agent, dose and route of administration. A number of the drugs have common metabolic pathways, and their excretion profiles may overlap those of the endogenous steroids, making interpretation of testing results a very significant challenge to the analytical chemist. Methods for detection of the substances or their excretion products in urine specimens usually involve gas chromatography–mass spectrometry or liquid chromatography-mass spectrometry. History Discovery of androgens The use of gonadal steroids pre-dates their identification and isolation. Extraction of hormones from urines began in China c. 100 BCE. Medical use of testicle extract began in the late 19th century while its effects on strength were still being studied. The isolation of gonadal steroids can be traced back to 1931, when Adolf Butenandt, a chemist in Marburg, purified 15 milligrams of the male hormone androstenone from tens of thousands of litres of urine. This steroid was subsequently synthesized in 1934 by Leopold Ružička, a chemist in Zurich.In the 1930s, it was already known that the testes contain a more powerful androgen than androstenone, and three groups of scientists, funded by competing pharmaceutical companies in the Netherlands, Germany, and Switzerland, raced to isolate it. This hormone was first identified by Karoly Gyula David, E. Dingemanse, J. Freud and Ernst Laqueur in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)." They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The chemical synthesis of testosterone was achieved in August that year, when Butenandt and G. Hanisch published a paper describing "A Method for Preparing Testosterone from Cholesterol." Only a week later, the third group, Ruzicka and A. Wettstein, announced a patent application in a paper "On the Artificial Preparation of the Testicular Hormone Testosterone (Androsten-3-one-17-ol)." Ruzicka and Butenandt were offered the 1939 Nobel Prize in Chemistry for their work, but the Nazi government forced Butenandt to decline the honor, although he accepted the prize after the end of World War II.Clinical trials on humans, involving either PO doses of methyltestosterone or injections of testosterone propionate, began as early as 1937. There are often reported rumors that German soldiers were administered AAS during the Second World War, the aim being to increase their aggression and stamina, but these are, as yet, unproven.: 6  Adolf Hitler himself, according to his physician, was injected with testosterone derivatives to treat various ailments. AAS were used in experiments conducted by the Nazis on concentration camp inmates, and later by the allies attempting to treat the malnourished victims that survived Nazi camps.: 6  President John F. Kennedy was administered steroids both before and during his presidency. Development of synthetic AAS The development of muscle-building properties of testosterone was pursued in the 1940s, in the Soviet Union and in Eastern Bloc countries such as East Germany, where steroid programs were used to enhance the performance of Olympic and other amateur weight lifters. In response to the success of Russian weightlifters, the U.S. Olympic Team physician John Ziegler worked with synthetic chemists to develop an AAS with reduced androgenic effects. Zieglers work resulted in the production of methandrostenolone, which Ciba Pharmaceuticals marketed as Dianabol. The new steroid was approved for use in the U.S. by the Food and Drug Administration (FDA) in 1958. It was most commonly administered to burn victims and the elderly. The drugs off-label users were mostly bodybuilders and weight lifters. Although Ziegler prescribed only small doses to athletes, he soon discovered that those having abused Dianabol developed enlarged prostates and atrophied testes. AAS were placed on the list of banned substances of the International Olympic Committee (IOC) in 1976, and a decade later the committee introduced out-of-competition doping tests because many athletes used AAS in their training period rather than during competition.Three major ideas governed modifications of testosterone into a multitude of AAS: Alkylation at C17α position with methyl or ethyl group created POly active compounds because it slows the degradation of the drug by the liver; esterification of testosterone and nortestosterone at the C17β position allows the substance to be administered parenterally and increases the duration of effectiveness because agents soluble in oily liquids may be present in the body for several months; and alterations of the ring structure were applied for both PO and parenteral agents to seeking to obtain different anabolic-to-androgenic effect ratios. Society and culture Etymology Androgens were discovered in the 1930s and were characterized as having effects described as androgenic (i.e., virilizing) and anabolic (e.g., myotrophic, renotrophic). The term anabolic steroid can be dated as far back as at least the mid-1940s, when it was used to describe the at-the-time hypothetical concept of a testosterone-derived steroid with anabolic effects but with minimal or no androgenic effects. This concept was formulated based on the observation that steroids had ratios of renotrophic to androgenic potency that differed significantly, which suggested that anabolic and androgenic effects might be dissociable.In 1953, a testosterone-derived steroid known as norethandrolone (17α-ethyl-19-nortestosterone) was synthesized at G. D. Searle & Company and was studied as a progestin, but was not marketed. Subsequently, in 1955, it was re-examined for testosterone-like activity in animals and was found to have similar anabolic activity to testosterone, but only one-sixteenth of its androgenic potency. It was the first steroid with a marked and favorable separation of anabolic and androgenic effect to be discovered, and has accordingly been described as the "first anabolic steroid". Norethandrolone was introduced for medical use in 1956, and was quickly followed by numerous similar steroids, for instance nandrolone phenylpropionate in 1959 and stanozolol in 1962. With these developments, anabolic steroid became the preferred term to refer to such steroids (over "androgen"), and entered widespread use. Although anabolic steroid was originally intended to specifically describe testosterone-derived steroids with a marked dissociation of anabolic and androgenic effect, it is applied today indiscriminately to all steroids with AR agonism-based anabolic effects regardless of their androgenic potency, including even non-synthetic steroids like testosterone. While many anabolic steroids have diminished androgenic potency in comparison to anabolic potency, there is no anabolic steroid that is exclusively anabolic, and hence all anabolic steroids retain at least some degree of androgenicity. (Likewise, all "androgens" are inherently anabolic.) Indeed, it is probably not possible to fully dissociate anabolic effects from androgenic effects, as both types of effects are mediated by the same signaling receptor, the AR. As such, the distinction between the terms anabolic steroid and androgen is questionable, and this is the basis for the revised and more recent term anabolic–androgenic steroid (AAS). Legal status The legal status of AAS varies from country to country: some have stricter controls on their use or prescription than others though in many countries they are not illegal. In the U.S., AAS are currently listed as Schedule III controlled substances under the Controlled Substances Act, which makes simple possession of such substances without a prescription a federal crime punishable by up to one year in prison for the first offense. Unlawful distribution or possession with intent to distribute AAS as a first offense is punished by up to ten years in prison. In Canada, AAS and their derivatives are part of the Controlled Drugs and Substances Act and are Schedule IV substances, meaning that it is illegal to obtain or sell them without a prescription; however, possession is not punishable, a consequence reserved for schedule I, II, or III substances. Those guilty of buying or selling AAS in Canada can be imprisoned for up to 18 months. Import and export also carry similar penalties. In Canada, researchers have concluded that steroid use among student athletes is extremely widespread. A study conducted in 1993 by the Canadian Centre for Drug-Free Sport found that nearly 83,000 Canadians between the ages of 11 and 18 use steroids. AAS are also illegal without prescription in Australia, Argentina, Brazil, and Portugal, and are listed as Class C Controlled Drugs in the United Kingdom. AAS are readily available without a prescription in some countries such as Mexico and Thailand. United States The history of the U.S. legislation on AAS goes back to the late 1980s, when the U.S. Congress considered placing AAS under the Controlled Substances Act following the controversy over Ben Johnsons victory at the 1988 Summer Olympics in Seoul. AAS were added to Schedule III of the Controlled Substances Act in the Anabolic Steroids Control Act of 1990.The same act also introduced more stringent controls with higher criminal penalties for offenses involving the illegal distribution of AAS and human growth hormone. By the early 1990s, after AAS were scheduled in the U.S., several pharmaceutical companies stopped manufacturing or marketing the products in the U.S., including Ciba, Searle, Syntex, and others. In the Controlled Substances Act, AAS are defined to be any drug or hormonal substance chemically and pharmacologically related to testosterone (other than estrogens, progestins, and corticosteroids) that promote muscle growth. The act was amended by the Anabolic Steroid Control Act of 2004, which added prohormones to the list of controlled substances, with effect from January 20, 2005.Even though they can still be prescribed by a medical doctor in the U.S, the use of anabolic steroids for injury recovery purposes has been a taboo subject, even amongst the majority of sports medicine doctors and endocrinologists. United Kingdom In the United Kingdom, AAS are classified as class C drugs for their illegal abuse potential, which puts them in the same class as benzodiazepines. AAS are in Schedule 4, which is divided in 2 parts; Part 1 contains most of the benzodiazepines and Part 2 contains the AAS. Part 1 drugs are subject to full import and export controls with possession being an offence without an appropriate prescription. There is no restriction on the possession when it is part of a medicinal product. Part 2 drugs require a Home Office licence for importation and export unless the substance is in the form of a medicinal product and is for self-administration by a person. Status in sports AAS are banned by all major sports bodies including Association of Tennis Professionals, Major League Baseball, Fédération Internationale de Football Association the Olympics, the National Basketball Association, the National Hockey League, World Wrestling Entertainment and the National Football League. The World Anti-Doping Agency (WADA) maintains the list of performance-enhancing substances used by many major sports bodies and includes all anabolic agents, which includes all AAS and precursors as well as all hormones and related substances. Spain has passed an anti-doping law creating a national anti-doping agency. Italy passed a law in 2000 where penalties range up to three years in prison if an athlete has tested positive for banned substances. In 2006, Russian President Vladimir Putin signed into law ratification of the International Convention Against Doping in Sport which would encourage cooperation with WADA. Many other countries have similar legislation prohibiting AAS in sports including Denmark, France, the Netherlands and Sweden. Usage Law enforcement United States federal law enforcement officials have expressed concern about AAS use by police officers. "Its a big problem, and from the number of cases, its something we shouldnt ignore. Its not that we set out to target cops, but when were in the middle of an active investigation into steroids, there have been quite a few cases that have led back to police officers," says Lawrence Payne, a spokesman for the United States Drug Enforcement Administration. The FBI Law Enforcement Bulletin stated that "Anabolic steroid abuse by police officers is a serious problem that merits greater awareness by departments across the country". It is also believed that police officers across the United Kingdom "are using criminals to buy steroids" which he claims to be a top risk factor for police corruption. Professional wrestling Following the murder-suicide of Chris Benoit in 2007, the Oversight and Government Reform Committee investigated steroid usage in the wrestling industry. The Committee investigated WWE and Total Nonstop Action Wrestling (now known as Impact Wrestling), asking for documentation of their companies drug policies. WWE CEO and chairman, Linda and Vince McMahon respectively, both testified. The documents stated that 75 wrestlers—roughly 40 percent—had tested positive for drug use since 2006, most commonly for steroids. Economics AAS are frequently produced in pharmaceutical laboratories, but, in nations where stricter laws are present, they are also produced in small home-made underground laboratories, usually from raw substances imported from abroad. In these countries, the majority of steroids are obtained illegally through black market trade. These steroids are usually manufactured in other countries, and therefore must be smuggled across international borders. As with most significant smuggling operations, organized crime is involved.In the late 2000s, the worldwide trade in illicit AAS increased significantly, and authorities announced record captures on three continents. In 2006, Finnish authorities announced a record seizure of 11.8 million AAS tablets. A year later, the DEA seized 11.4 million units of AAS in the largest U.S seizure ever. In the first three months of 2008, Australian customs reported a record 300 seizures of AAS shipments.In the U.S., Canada, and Europe, illegal steroids are sometimes purchased just as any other illegal drug, through dealers who are able to obtain the drugs from a number of sources. Illegal AAS are sometimes sold at gyms and competitions, and through the mail, but may also be obtained through pharmacists, veterinarians, and physicians. In addition, a significant number of counterfeit products are sold as AAS, in particular via mail order from websites posing as overseas pharmacies. In the U.S., black-market importation continues from Mexico, Thailand, and other countries where steroids are more easily available, as they are legal. Research AAS, alone and in combination with progestogens, have been studied as potential male hormonal contraceptives. Dual AAS and progestins such as trestolone and dimethandrolone undecanoate have also been studied as male contraceptives, with the latter under active investigation as of 2018.Topical androgens have been used and studied in the treatment of cellulite in women. Topical androstanolone on the abdomen has been found to significantly decrease subcutaneous abdominal fat in women, and hence may be useful for improving body silhouette. However, men and hyperandrogenic women have higher amounts of abdominal fat than healthy women, and androgens have been found to increase abdominal fat in postmenopausal women and transgender men as well. See also References Further reading External links Media related to Anabolic-androgenic steroids at Wikimedia Commons

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I've encountered the term 'Taeniasis' while reading about medical topics. What does it refer to exactly?

Taeniasis is an infection within the intestines by adult tapeworms belonging to the genus Taenia. There are generally no or only mild symptoms. Symptoms may occasionally include weight loss or abdominal pain. Segments of tapeworm may be seen in the stool. Complications of pork tapeworm may include cysticercosis.Types of Taenia that cause infections in humans include Taenia solium (pork tapeworm), Taenia saginata (beef tapeworm), and Taenia asiatica (Asian tapeworm). Taenia saginata is due to eating contaminated undercooked beef while Taenia solium and Taenia asiatica is from contaminated undercooked pork. Diagnosis is by examination of stool samples.Prevention is by properly cooking meat. Treatment is generally with praziquantel, though niclosamide may also be used. Together with cysticercosis, infections affect about 50 million people globally. The disease is most common in the developing world. In the United States less than 1,000 cases occur a year. Signs and symptoms Taeniasis generally has few or no symptoms. It takes about 8 weeks from infection for adult worms to form and can last for years without treatment.Infection may be suspected when a portion of the worm is passed in the stool. It is not generally fatal. Pork tapeworm Infection in the intestines by the adult T. solium worms is normally asymptomatic. Heavy infection can result in anaemia and indigestion.A complication, known as cysticercosis, may occur if the eggs of the pork tapeworm are eaten. This typically occurs from vegetables or water contaminated by feces from someone with pork tapeworm taeniasis. The eggs enter the intestine where they develop into larvae which then enter the bloodstream and invade host tissues. This is the most frequent and severe disease caused by any tapeworm. It can lead to headaches, dizziness, seizures, dementia, hypertension, lesions in the brain, blindness, tumor-like growths, and low eosinophil levels. It is a cause of major neurological problems, such as hydrocephalus, paraplegy, meningitis, and death. Beef tapeworm Taenia saginata infection is usually asymptomatic, but heavy infection causes weight loss, dizziness, abdominal pain, diarrhea, headaches, nausea, constipation, chronic indigestion, and loss of appetite. It can cause antigen reaction that induce allergic reaction. It is also a rare cause of ileus, pancreatitis, cholecystitis, and cholangitis. Asian tapeworm Taenia asiatica is also usually asymptomatic. It is unclear if T. asiatica can cause cysticercosis.In pigs, the cysticercus can produce cysticercosis. Cysts develop in liver and lungs. (T. saginata does not cause cysticercosis.) Transmission Taeniasis is contracted after eating undercooked pork or beef that contain the larvae. The adult worms develop and live in the lumen of the intestine. They acquire nutrients from the intestine. The gravid proglottids, body segments containing fertilised eggs, are released in the faeces.If consumed by an intermediate host such as a cow or pig, they hatch within the duodenum to become larvae, penetrate through the intestinal wall into nearby blood vessels, and enter the bloodstream. Once they reach organs such as the skeletal muscles, liver or lungs, the larvae then develop into a cyst, a fluid-filled cysticercus. These contaminated tissues are then consumed through raw or undercooked meat.Cysticercosis occurs when contaminated food, water, or soil that contain T. solium eggs is eaten. Diagnosis Diagnosis of taeniasis is mainly using stool sample, particularly by identifying the eggs. However, this has limitation at the species level because tapeworms basically have similar eggs. Examination of the scolex or the gravid proglottids can resolve the exact species. But body segments are not often available, therefore, laborious histological observation of the uterine branches and PCR detection of ribosomal 5.8S gene are sometimes necessary. Ziehl–Neelsen stain is also used for T. saginata and T. solium, in most cases only the former will stain, but the method is not entirely reliable. Loop-mediated isothermal amplification (LAMP) is highly sensitive (~2.5 times that of multiplex PCR), without false positives, for differentiating the taenid species from faecal samples.To date the most relevant test for T. asiatica is by enzyme-linked immunoelectrotransfer blot (EITB). EITB can effectively identify asiatica from other taenid infections since the serological test indicates an immunoblot band of 21.5 kDa exhibited specifically by T. asiatica. Even though it gives 100% sensitivity, it has not been tested with human sera for cross-reactivity, and it may show a high false positive result. Prevention Prevention efforts include properly cooking meat, treating active cases in humans, vaccinating and treating pigs against the disease, stricter meat-inspection standards, health education, improved sanitation, and improved pig raising practices.Preventing human faeces from contaminating pig feeds also plays a role. Infection can be prevented with proper disposal of human faeces around pigs, cooking meat thoroughly and/or freezing the meat at −10 °C for 5 days. For human cysticercosis, contaminated hands are the primary cause, and especially concerning among food handlers.Proper cooking of meat is an effective prevention. For example, cooking (56 °C for 5 minutes) of beef viscera destroys cysticerci. Refrigeration, freezing (−10 °C for 9 days) or long periods of salting is also lethal to cysticerci. Treatment Praziquantel is the treatment of choice. Usual treatments are with praziquantel (5–10 mg/kg, single-administration) or niclosamide (adults and children over 6 years: 2 g, single-administration after a light breakfast, followed after 2 hours by a laxative; children aged 2–6 years: 1 g; children under 2 years: 500 mg). One study showed albendazole is effective against animal beef tapeworm cysticercosis. Mepacrine is quite effective but has adverse effects in humans. Epidemiology The total global infection is estimated to be between 40 and 60 million people. In the US, the incidence of infection is low, but 25% of cattle sold are still infected. Regions Taeniasis is predominantly found in Asia, Africa, Latin America, particularly on farms in which pigs are exposed to human excrement. At a low level though, it occurs everywhere where beef and pork are eaten, even in countries with strict sanitation policies such as the United States. Taenia saginata is relatively common in Africa, some parts of Eastern Europe, the Philippines, and Latin America. It is most prevalent in Sub-Saharan Africa and the Middle East. Taenia asiatica is restricted to East Asia, including Taiwan, Korea, Indonesia, Nepal, Thailand and China. See also Tapeworm infection References == External links ==

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I need a basic explanation for the medical term 'Macimorelin.'

Macimorelin (INN) – or Macrilen (trade name) – is a drug that was developed by Æterna Zentaris for use in the diagnosis of adult growth hormone deficiency. Macimorelin acetate, the salt formulation, is a synthetic growth hormone secretagogue receptor agonist. It is a growth hormone secretagogue receptor (ghrelin receptor) agonist causing release of growth hormone from the pituitary gland.Macimorelin acetate is described chemically as D-Tryptophanamide, 2-methylalanyl-N-[(1R)-1-(formylamino)-2-(1H-indol-3-yl)ethyl]-acetate. Macimorelin (Macrilen™) was invented and first synthesized by the research group of Professor Martinez at University of Montpellier, Centre National de la Recherche Scientitifique (CNRS), France. This transpired from a long-lasting research collaboration with Aeterna Zentaris. Aeterna Zentaris later in-licensed macimorelin as a development candidate from the CNRS and proceeded with the pre-clinical and clinical development of the compound. As of January 2014, it was in Phase III clinical trials. The phase III trial for growth hormone deficiency is expected to be complete in December 2016.As of December 2017, it became FDA-approved as a method to diagnose growth hormone deficiency. Traditionally, growth hormone deficiency was diagnosed via means of insulin tolerance test (IST) or glucagon stimulation test (GST). These two means are done parenterally, whereas Macrilen boasts an oral formulation for ease of administration for patients and providers. The U.S. Food and Drug Administration (FDA) considers it to be a first-in-class medication. See also List of growth hormone secretagogues References External links "Macimorelin". Drug Information Portal. U.S. National Library of Medicine. "Macimorelin acetate". Drug Information Portal. U.S. National Library of Medicine.

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Could you please explain the term 'Scarring hair loss' in simple language?

Scarring hair loss, also known as cicatricial alopecia, is the loss of hair which is accompanied with scarring. This is in contrast to non scarring hair loss. It can be caused by a diverse group of rare disorders that destroy the hair follicle, replace it with scar tissue, and cause permanent hair loss. A variety of distributions are possible. In some cases, hair loss is gradual, without symptoms, and is unnoticed for long periods. In other cases, hair loss is associated with severe itching, burning and pain and is rapidly progressive. The inflammation that destroys the follicle is below the skin surface and there is usually no "scar" seen on the scalp. Affected areas of the scalp may show little signs of inflammation, or have redness, scaling, increased or decreased pigmentation, pustules, or draining sinuses. Scarring hair loss occurs in otherwise healthy men and women of all ages and is seen worldwide. Signs and symptoms It is important to continue to watch for symptoms and signs of active disease during and after treatment to ensure that the disease is responding adequately and has not re-activated after therapy has been discontinued. Response to therapy may be indicated by the resolution of scalp symptoms such as itching, pain, tenderness, or burning, by improvement in the signs of scalp inflammation such as decreased redness, scaling or pustules, and by halting or slowing the progression of hair loss. A dermatologist can document and monitor a patients cicatricial alopecia using these guidelines, and with the pull test. Photographs of the scalp may be useful in monitoring the course of the disease and response to treatment. Causes The cause of the various cicatricial alopecias is poorly understood. However, all cicatricial alopecias involve inflammation directed at the upper part of the hair follicle where the stem cells and sebaceous gland (oil gland) are located. If the stem cells and sebaceous gland are destroyed, there is then no possibility for regeneration of the hair follicle, and permanent hair loss results. Cicatricial alopecias are not contagious. In general, cicatricial alopecias are not associated with other illnesses, and usually occur in otherwise healthy men and women. Cicatricial alopecias affect both men and women, most commonly adults, although all ages may be affected. Epidemiologic studies have not been performed to determine the incidence of cicatricial alopecias. In general, they are not common. The majority of patients with cicatricial alopecia have no family history of a similar condition. The one exception is Central centrifugal cicatricial alopecia, which primarily affects women of African ancestry and may occur in several women in the same family. While it is possible to have more than one type of hair loss condition, non-scarring forms of hair loss do not turn into scarring forms of hair loss. Diagnosis A scalp biopsy is essential for the diagnosis of cicatricial alopecia and is the necessary first step, as it can be hard to know the diagnosis for sure without a biopsy. Findings of the scalp biopsy, including the type of inflammation present, location and amount of inflammation, and other changes in the scalp, are necessary to diagnose the type of cicatricial alopecia, to determine the degree of activity, and to select appropriate therapy. Clinical evaluation of the scalp is also important. Symptoms of itching, burning, pain, or tenderness usually signal ongoing activity. Signs of scalp inflammation include redness, scaling, and pustules. However, in some cases there are few symptoms or signs and only the scalp biopsy demonstrates the active inflammation. The overall extent and pattern of hair loss is noted and sometimes photographed for future comparison. A hair "pull test" is performed to see if growing, or anagen, where hairs are pulled out easily. The pulled hairs are mounted on a slide and the hair bulbs are viewed with a light microscope to determine how many are growing hairs and how many are resting hairs. In addition, if pustules are present, cultures are taken to identify which microbes, if any, may be contributing to the inflammation. A thorough evaluation that includes all of these parameters is important in diagnosing a cicatricial alopecia and in identifying features in individual patients that will help the selection of therapy. New diagnostic techniques, such as trichoscopy may be used for non-invasive differential diagnosis of cicatricial alopecia. Diagnosis and treatment of cicatricial alopecias is often challenging. For this reason, it is helpful to be evaluated by a dermatologist with a special interest or expertise in scalp and hair disorders, and who is familiar with current diagnostic methods and therapies. Classification Cicatricial alopecias are classified as primary or secondary. This discussion is confined to the primary cicatricial alopecias in which the hair follicle is the target of the destructive inflammatory process. In secondary cicatricial alopecias, destruction of the hair follicle is incidental to a non-follicle-directed process or external injury, such as severe infections, burns, radiation, tumors, or traction. Primary cicatricial alopecias are further classified by the type of inflammatory cells that destroy the hair follicle during the active stage of the disease. The inflammation may predominantly involve lymphocytes or neutrophils. Cicatricial alopecias that predominantly involve lymphocytic inflammation include lichen planopilaris, frontal fibrosing alopecia, central centrifugal alopecia, and pseudopelade (Brocq). Cicatricial alopecias that are due to predominantly neutrophilic inflammation include folliculitis decalvans, tufted folliculitis, and dissecting cellulitis of the scalp. Sometimes the inflammation shifts from a predominantly neutrophilic process to a lymphocytic process. A cicatricial alopecia with a mixed inflammatory infiltrate is folliculitis keloidalis. Treatment As mentioned above, primary cicatricial alopecias are classified by the predominant type of inflammatory cells that attack the hair follicles, such as lymphocytes, neutrophils, or mixed inflammatory cells. Treatment strategies are different for each subtype and detailed treatment options are beyond the scope of this discussion. However, certain general principals are reviewed below. Treatment of the lymphocytic group of cicatricial alopecias (including lichen planopilaris, frontal fibrosing alopecia, central centrifugal alopecia, and pseudopelade (Brocq) involves use of anti-inflammatory medications. The goal of treatment is to decrease or eliminate the lymphocytic inflammatory cells that are attacking and destroying the hair follicle. Oral medications may include hydroxychloroquine, doxycycline, mycophenolate mofetil, cyclosporine, or corticosteroids. Topical medications may include corticosteroids, tacrolimus, pimecrolimus, or Derma-Smoothe/FS scalp oil. Triamcinolone acetonide, a corticosteroid, may be injected into inflamed, symptomatic areas of the scalp. Treatment of the neutrophilic group of cicatricial alopecias (folliculitis decalvans, tufted folliculitis) is directed at eliminating the predominant pathogenic microbes that are invariably involved in the inflammatory process. Oral antibiotics are the mainstay of therapy, and topical antibiotics may be used to supplement the oral antibiotics. In dissecting cellulitis, pathogenic microbes are not usually present. Isotretinoin in small doses may be helpful in treating dissecting cellulitis.Treatment of the mixed group of cicatricial alopecias (folliculitis keloidalis) may include antimicrobials, isotretinoin, and anti-inflammatory medications. Patients are recommended to discuss any treatment with a dermatologist, who also explains potential side effects, as well as laboratory tests that are needed before starting treatment and sometimes are monitored during treatment. The course of cicatricial alopecia is usually prolonged. Treatment is continued until the symptoms and signs of scalp inflammation are controlled, and progression of the condition has been slowed. In other words, itching, pain, tenderness, and burning have cleared, scalp redness, scaling, and/or pustules are no longer present, and the progression of the hair loss has been stopped or slowed. Treatment may then be stopped. Unfortunately, the cicatricial alopecias may reactivate after a quiet period and treatment may have to be repeated. Surgical treatment for cosmetic benefit is an option in some cases after the disease has been inactive for one to two or more years. Hair restoration surgery or scalp reduction may be considered in these instances. Hair regrowth Hair will not regrow once the follicle is destroyed. However, it may be possible to treat the inflammation in and around surrounding follicles before they are destroyed, and for this reason it is important to begin treatment as early as possible to halt the inflammatory process. Minoxidil solution (2% or 5%) applied twice daily to the scalp may be helpful to stimulate any small, remaining, unscarred follicles. The progression of hair loss is unpredictable. In some cases, progression is slow and there is always sufficient hair remaining to cover the affected scalp areas; in other cases, progression can be rapid and extensive. Hair care Hair care products and shampoos can generally be used with any frequency desired, as long as the products are gentle and non-irritating to the scalp. Hair pieces, wigs, hats, and scarves may be used freely. See also Noncicatricial alopecia List of cutaneous conditions References External links Cicatricial Alopecia Overview - US National Institute of Arthritis and Musculoskeletal and Skin Diseases

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What does the medical term 'Polymyxin B' encompass?

Polymyxin B, sold under the brand name Poly-Rx among others, is an antibiotic used to treat meningitis, pneumonia, sepsis, and urinary tract infections. While it is useful for many Gram negative infections, it is not useful for Gram positive infections. It can be given by injection into a vein, muscle, or cerebrospinal fluid or inhaled. The injectable form is generally only used if other options are not available. It is also available as the combinations bacitracin/polymyxin B and neomycin/polymyxin B/bacitracin for use on the skin.Common side effects when given by injection include kidney problems, neurological problems, fever, itchiness, and rash. Injections into muscle may result in significant pain. Other serious side effects may include fungal infections, anaphylaxis, and muscle weakness. It is unclear if use during pregnancy is safe for the baby. Polymyxin B works by breaking down the cytoplasmic membrane which generally results in bacterial cell death.Polymyxin B was approved for medical use in the United States in 1964. It is on the World Health Organizations List of Essential Medicines. It is available as a generic medication. In Europe it is only approved to be applied to the skin as of 2015. It is derived from the bacterium Paenibacillus polymyxa (formerly known as Bacillus polymyxa). Medical uses Spectrum of susceptibility Polymyxin B has been used to treat urinary tract infections and meningitis caused by Pseudomonas aeruginosa and Haemophilus influenzae, respectively. The following represents MIC susceptibility data for a few medically significant microorganisms. Haemophilus influenzae: ≥0.8 μg/ml Pseudomonas aeruginosa: 0.25 μg/ml – 1 μg/ml Endotoxin adsorption An effective use of polymyxin B is found in patients with refractory septic shock, that is, without positive outcome to the administration of standard treatments (increase in volemia and other antibiotics). The obstacle of the toxicity of polymyxin B is bypassed by extracorporeal circulation with perfusion of venous blood through a cartridge on whose fibers polymyxin B is covalently fixed; in this way the antibiotic exerts its bactericidal function but is not released into the blood since it remains fully attached to the fiber. Through this perfusion the cartridge retains the endotoxin, recognized as the trigger of septic shock. The treatment of the cartridge to polymyxin B (Toraymyxin, medical device designed and produced by the Japanese Toray), takes place in two sessions of two hours each, carried out at a distance of 24 hours. Mechanism of action Alters bacterial outer membrane permeability by binding to a negatively charged site in the lipopolysaccharide layer, which has an electrostatic attraction for the positively charged amino groups in the cyclic peptide portion (this site normally is a binding site for calcium and magnesium counter ions); the result is a destabilized outer membrane Fatty acid portion dissolves in hydrophobic region of cytoplasmic membrane and disrupts membrane integrity Leakage of cellular molecules, inhibition of cellular respiration Binds and inactivates endotoxin Relative absence of selective toxicity: nonspecific for cell membranes of any type, highly toxic.Removal of the hydrophobic tail of polymyxin B yields polymyxin nonapeptide (PMBN), which still binds to LPS, but no longer kills the bacterial cell. However, it still detectably increases the permeability of the bacterial cell wall to other antibiotics, indicating that it still causes some degree of membrane disorganization. Mixture composition Polymyxin B is composed of polymyxins B1, B1-I, B2, B3, and B6. Polymyxins B1 and B2 are considered major components. These related components are structurally identical with the exception of a variable fatty acid group on each fraction. Results from in vitro studies have shown marginal differences in MIC data when comparing the fractions. Research application Polymyxin B is also used to induce envelope stress in order to study the organisms response to such stress. Polymyxin envelope stress assays such as this have been used for the study of small RNA (sRNA) responses in Salmonella enterica. See also Polymyxin References External links "Polymyxin B". Drug Information Portal. U.S. National Library of Medicine.

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Can you demystify the medical term 'Chemotherapy-induced acral erythema' for me?

Chemotherapy-induced acral erythema, also known as palmar-plantar erythrodysesthesia or hand-foot syndrome is reddening, swelling, numbness and desquamation (skin sloughing or peeling) on palms of the hands and soles of the feet (and, occasionally, on the knees, elbows, and elsewhere) that can occur after chemotherapy in patients with cancer. Hand-foot syndrome is also rarely seen in sickle-cell disease. These skin changes usually are well demarcated. Acral erythema typically disappears within a few weeks after discontinuation of the offending drug. Signs and symptoms The symptoms can occur anywhere between days to months after administration of the offending medication, depending on the dose and speed of administration. The patient first experiences tingling and/or numbness of the palms and soles. This is followed 2-4 days later by bright redness, which is symmetrical and sharply defined.In severe cases this may be followed by burning pain and swelling, blistering and ulceration, peeling of the skin. Healing occurs without scarring unless there has been skin ulceration or necrosis (skin loss/death). With each subsequent cycle of chemotherapy, the reaction will appear more quickly, be more severe and will take longer to heal. Causes Acral erythema is a common adverse reaction to cytotoxic chemotherapy drugs, particularly cabozantinib, cytarabine, doxorubicin, and fluorouracil and its prodrug capecitabine.Targeted cancer therapies, especially the tyrosine kinase inhibitors sorafenib and sunitinib, have also been associated with a high incidence of acral erythema. However, acral erythema due to tyrosine kinase inhibitors seems to differ somewhat from acral erythema due to classic chemotherapy drugs. Pathogenesis The cause of Palmar-plantar erythrodysesthesia (PPE) is unknown. Existing hypotheses are based on the fact that only the hands and feet are involved and posit the role of temperature differences, vascular anatomy, differences in the types of cells (rapidly dividing epidermal cells and eccrine glands).In the case of PPE caused by PLD, the following mechanism has been demonstrated: sweat deposits and spreads the drug on the skin surface; then the drug penetrates into the stratum corneum like an external agent; palms and soles have high density of sweat glands, and their stratum corneum is approximately 10 times thicker than the rest of the body, and becomes an efficient long-term reservoir for the penetrating PLD, which was deposited on the skin before. Diagnosis Painful red swelling of the hands and feet in a patient receiving chemotherapy is usually enough to make the diagnosis. The problem can also arise in patients after bone marrow transplants, as the clinical and histologic features of PPE can be similar to cutaneous manifestations of acute (first three weeks) graft-versus-host disease. It is important to differentiate PPE, which is benign, from the more dangerous graft-versus-host disease. As time progresses, patients with graft-versus-host disease progress to have other body parts affected, while PPE is limited to hands and feet. Serial biopsies every 3 to 5 days can also be helpful in differentiating the two disorders. Prevention The cooling of hands and feet during chemotherapy may help prevent PPE. Support for this and a variety of other approaches to treat or prevent acral erythema comes from small clinical studies, although none has been proven in a randomised controlled clinical trial of sufficient size.Modifying some daily activities to reduce friction and heat exposure to your hands and feet for a period of time following treatment (approximately one week after IV medication, much as possible during the time you are taking oral (by mouth) medication such as capecitabine). Avoid long exposure of hands and feet to hot water such as washing dishes, long showers, or tub baths. Short showers in tepid water will reduce exposure of the soles of your feet to the drug. Dishwashing gloves should not be worn, as the rubber will hold heat against your palms. Avoid increased pressure on the soles of the feet or palms of hands. No jogging, aerobics, power walking, jumping - avoid long days of walking. You should also avoid using garden tools, household tools such as screwdrivers, and other tasks where you are squeezing your hand on a hard surface. Using knives to chop food may also cause excessive pressure and friction on your palms. Treatment The main treatment for acral erythema is discontinuation of the offending drug, and symptomatic treatment to provide analgesia, lessen edema, and prevent superinfection. However, the treatment for the underlying cancer of the patient must not be neglected. Often, the discontinued drug can be substituted with another cancer drug or cancer treatment.Symptomatic treatment can include wound care, elevation, and pain medication. Various emollients (creams) are recommended to keep skin moist. Corticosteroids and pyridoxine have also been used to relieve symptoms. Other studies do not support the conclusion. A number of additional remedies are listed in recent medical literature. Among them henna and 10% uridine ointment which went through clinical trial. Prognosis Hand-foot invariably recurs with the resumption of chemotherapy. Long-term chemotherapy may also result in reversible palmoplantar keratoderma. Symptoms resolve 1–2 weeks after cessation of chemotherapy (Apisarnthanarax and Duvic 2003). The range is 1-5 wks, so it has recovered by the time the next cycle is due. Healing occurs without scarring unless there has been skin ulceration or necrosis (skin loss/death). With each subsequent cycle of chemotherapy, the reaction will appear more quickly, be more severe and will take longer to heal. History Hand-foot syndrome was first reported in association with chemotherapy by Zuehlke in 1974. Synonyms for acral erythema (AE) include: hand-foot syndrome, palmar-plantar erythrodysesthesia, peculiar AE, chemotherapy-induced AE, toxic erythema of the palms and soles, palmar-plantar erythema, and Burgdorfs reaction. Common abbreviations are HFS and PPE. References Further reading Farr, Katherina Podlekareva; Safwat, Akmal (2011). "Palmar-Plantar Erythrodysesthesia Associated with Chemotherapy and Its Treatment". Case Reports in Oncology. 4 (1): 229–235. doi:10.1159/000327767. PMC 3085037. PMID 21537373. Hand-Foot Syndrome or Palmar-Plantar Erythrodysesthesia (1 & 2)

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I'm encountering the term 'Trisomy 22' in medical literature. What's its definition?

Trisomy 22 is a chromosomal disorder in which three copies of chromosome 22 are present rather than two. It is a frequent cause of spontaneous abortion during the first trimester of pregnancy. Progression to the second trimester and live birth are rare. This disorder is found in individuals with an extra copy or a variation of chromosome 22 in some or all cells of their bodies. Associated disorders Many kinds of disorders are associated with trisomy 22: Emanuel syndrome is named after the genetic contributions made by researcher Dr. Beverly Emanuel. This condition is assigned to individuals born with an unbalanced 11/22 translocation. That is, a fragment of chromosome 11 is moved, or translocated, to chromosome 22. 22q11 deletion syndrome is a rare condition which occurs in about one in 4000 births. This condition is identified when a band in the q11.2 section of the arm of chromosome 22 is missing or deleted. This condition has several different names: 22q11.2 deletion syndrome, velocardiofacial syndrome, DiGeorge syndrome, conotruncal anomaly face syndrome, Opitz G/BBB syndrome, and Cayler cardiofacial syndrome. The effects of this disorder are different in each individual, but similarities exist, such as heart defects, immune system problems, a distinctive facial appearance, learning challenges, cleft palate, hearing loss, kidney problems, hypocalcemia, and sometimes psychiatric issues. 22q11 microduplication syndrome is the opposite of the 22q11 deletion syndrome; in this condition, a band of q.11.2 section of chromosome 22 is duplicated. Individuals carrying this deficiency are relatively "normal", as in they do not possess any major birth defects or major medical illnesses. This microduplication is more common than the deletion; this might relate to the milder phenotype of the individuals. 22q13 deletion syndrome (Phelan–McDermid syndrome) is a condition caused by the deletion of the tip of the q arm on chromosome 22. Most individuals with this disorder experience cognitive delays, low muscle tone, and sleeping, eating, and behavioural issues. Chromosome ring 22 is a rare disorder caused by the break and rejoining of both ends of chromosome 22, forming a ring. The effects on the individual with this disorder are dependent on the amount of genetic information lost during the process. Major characteristics for this disorder are intellectual disability, muscle weakness, and lack of coordination. Cat eye syndrome (Schmid Fraccaro syndrome) is a condition caused by a partial trisomy or tetrasomy in chromosome 22. A small extra chromosome is found, made up of the top half of chromosome 22 and a portion of the q arm at the q11.2 break. This chromosome can be found three or four times. This syndrome is referred as "cat eye" due to the eye appearance of reported affected individuals who have coloboma of the iris, but this feature is only seen in about half of the cases. Mosaic trisomy 22 is a disorder in which an extra chromosome 22 is found only in some cells of the body. The severity of each case is determined by the number of cells with this extra copy. Some characteristics of individuals with this condition are cardiac abnormalities, growth retardation, mental delay, etc. Complete trisomy 22, in contrast with mosaic trisomy 22, is characterized by an extra copy of chromosome 22 found in each cell of the body of the affected individual. As of 2014, 29 live-born human cases have been reported, with all of them dying before the age of 12 months. References Further reading Mokate T, Leask K, Mehta S, et al. (2006). "Non-mosaic trisomy 22: a report of 2 cases". Prenat. Diagn. 26 (10): 962–5. doi:10.1002/pd.1537. PMID 16906599. S2CID 43499352. External links Humpath 6236

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I'm seeking clarification on the medical term 'Ivermectin.' Could you explain it?

Ivermectin (, EYE-vər-MEK-tin) is an antiparasitic drug. After its discovery in 1975, its first uses were in veterinary medicine to prevent and treat heartworm and acariasis. Approved for human use in 1987, today it is used to treat infestations including head lice, scabies, river blindness (onchocerciasis), strongyloidiasis, trichuriasis, ascariasis and lymphatic filariasis. It works through many mechanisms to kill the targeted parasites, and can be taken orally, or applied to the skin for external infestations. It belongs to the avermectin family of medications.William Campbell and Satoshi Ōmura won the 2015 Nobel Prize in Physiology or Medicine for its discovery and applications. It is on the World Health Organizations List of Essential Medicines, and is approved by the U.S. Food and Drug Administration as an antiparasitic agent. In 2018, it was the 420th most commonly prescribed medication in the United States, with more than 100,000 prescriptions. It is available as a generic medicine.During the COVID-19 pandemic, misinformation has been widely spread claiming that ivermectin is beneficial for treating and preventing COVID-19. Such claims are not backed by credible scientific evidence. Multiple major health organizations, including the Food and Drug Administration, U.S. Centers for Disease Control, the European Medicines Agency, and the World Health Organization have stated that ivermectin is not authorized or approved to treat COVID-19. Medical uses Ivermectin is used to treat human diseases caused by roundworms and ectoparasites. Worm infections For river blindness (onchocerciasis) and lymphatic filariasis, ivermectin is typically given as part of mass drug administration campaigns that distribute the drug to all members of a community affected by the disease. For river blindness, a single oral dose of ivermectin (150 micrograms per kilogram of body weight) clears the body of larval Onchocerca volvulus worms for several months, preventing transmission and disease progression. Adult worms survive in the skin and eventually recover to produce larval worms again; to keep the worms at bay, ivermectin is given at least once per year for the 10–15-year lifespan of the adult worms. For lymphatic filariasis, oral ivermectin (200 micrograms per kilogram body weight) is part of a combination treatment given annually: ivermectin, diethylcarbamazine citrate and albendazole in places without onchocerciasis; and ivermectin and albendazole in places with onchocerciasis.The World Health Organization (WHO) considers ivermectin the drug of choice for strongyloidiasis. Most cases are treated with two daily doses of oral ivermectin (200 μg per kg body weight), while severe infections are treated with five to seven days of ivermectin. Ivermectin is also the primary treatment for Mansonella ozzardi and cutaneous larva migrans. The U.S. Centers for Disease Control and Prevention (CDC) recommends ivermectin, albendazole, or mebendazole as treatments for ascariasis. Ivermectin is sometimes added to albendazole or mebendazole for whipworm treatment, and is considered a second-line treatment for gnathostomiasis. Mites and insects Ivermectin is also used to treat infection with parasitic arthropods. Scabies – infestation with the mite Sarcoptes scabiei – is most commonly treated with topical permethrin or oral ivermectin. For most scabies cases, ivermectin is used in a two dose regimen: a first dose kills the active mites, but not their eggs. Over the next week, the eggs hatch, and a second dose kills the newly hatched mites. For severe "crusted scabies", the U.S. Centers for Disease Control and Prevention (CDC) recommends up to seven doses of ivermectin over the course of a month, along with a topical antiparasitic. Both head lice and pubic lice can be treated with oral ivermectin, an ivermectin lotion applied directly to the affected area, or various other insecticides. Ivermectin is also used to treat rosacea and blepharitis, both of which can be caused or exacerbated by Demodex folliculorum mites. Contraindications The only absolute contraindication to the use of ivermectin is hypersensitivity to the active ingredient or any component of the formulation. In children under the age of five or those who weigh less than 15 kilograms (33 pounds), there is limited data regarding the efficacy or safety of ivermectin, though the available data demonstrate few adverse effects. However, the American Academy of Pediatrics cautions against use of ivermectin in such patients, as the blood-brain barrier is less developed, and thus there may be an increased risk of particular CNS side effects such as encephalopathy, ataxia, coma, or death. Such patients should be monitored very closely when given ivermectin. The American Academy of Family Physicians also recommends against use in these patients, given a lack of sufficient data to prove drug safety. Ivermectin is secreted in very low concentration in breast milk. It remains unclear if ivermectin is safe during pregnancy. Adverse effects Side effects, although uncommon, include fever, itching, and skin rash when taken by mouth; and red eyes, dry skin, and burning skin when used topically for head lice. It is unclear if the drug is safe for use during pregnancy, but it is probably acceptable for use during breastfeeding.Ivermectin is considered relatively free of toxicity in standard doses (around 300 µg/kg). Based on the data drug safety sheet for ivermectin, side effects are uncommon. However, serious adverse events following ivermectin treatment are more common in people with very high burdens of larval Loa loa worms in their blood. Those who have over 30,000 microfilaria per milliliter of blood risk inflammation and capillary blockage due to the rapid death of the microfilaria following ivermectin treatment.One concern is neurotoxicity after large overdoses, which in most mammalian species may manifest as central nervous system depression, ataxia, coma, and even death, as might be expected from potentiation of inhibitory chloride channels.Since drugs that inhibit the enzyme CYP3A4 often also inhibit P-glycoprotein transport, the risk of increased absorption past the blood-brain barrier exists when ivermectin is administered along with other CYP3A4 inhibitors. These drugs include statins, HIV protease inhibitors, many calcium channel blockers, lidocaine, the benzodiazepines, and glucocorticoids such as dexamethasone.During the course of a typical treatment, ivermectin can cause minor aminotransferase elevations. In rare cases it can cause mild clinically apparent liver disease.To provide context for the dosing and toxicity ranges, the LD50 of ivermectin in mice is 25 mg/kg (oral), and 80 mg/kg in dogs, corresponding to an approximated human-equivalent dose LD50 range of 2.02-43.24 mg/kg, which is far in excess of its FDA-approved usage (a single dose of 0.150-0.200 mg/kg to be used for specific parasitic infections). While ivermectin has also been studied for use in COVID-19, and while it has some ability to inhibit SARS-CoV-2 in vitro, achieving 50% inhibition in vitro was found to require an estimated oral dose of 7.0 mg/kg (or 35x the maximum FDA-approved dosage), high enough to be considered ivermectin poisoning. Despite insufficient data to show any safe and effective dosing regimen for ivermectin in COVID-19, doses have been taken far in excess of FDA-approved dosing, leading the CDC to issue a warning of overdose symptoms including nausea, vomiting, diarrhea, hypotension, decreased level of consciousness, confusion, blurred vision, visual hallucinations, loss of coordination and balance, seizures, coma, and death. The CDC advises against consuming doses intended for livestock or doses intended for external use and warns that increasing misuse of ivermectin-containing products is resulting in an increasing rate of harmful overdoses. Veterinary use Ivermectin is routinely used to control parasitic worms in the gastrointestinal tract of ruminant animals. These parasites normally enter the animal when it is grazing, pass the bowel, and set and mature in the intestines, after which they produce eggs that leave the animal via its droppings and can infest new pastures. Ivermectin is only effective in killing some of these parasites, this is because of an increase in anthelmintic resistance. This resistance has arisen from the persistent use of the same anthelmintic drugs for the past 40 years.In dogs, ivermectin is routinely used as prophylaxis against heartworm. Dogs with defects in the P-glycoprotein gene (MDR1), often collie-like herding dogs, can be severely poisoned by ivermectin. The mnemonic "white feet, dont treat" refers to Scotch collies that are vulnerable to ivermectin. Some other dog breeds (especially the Rough Collie, the Smooth Collie, the Shetland Sheepdog, and the Australian Shepherd), also have a high incidence of mutation within the MDR1 gene (coding for P-glycoprotein) and are sensitive to the toxic effects of ivermectin. Clinical evidence suggests kittens are susceptible to ivermectin toxicity. A 0.01% ivermectin topical preparation for treating ear mites in cats is available.Ivermectin is sometimes used as an acaricide in reptiles, both by injection and as a diluted spray. While this works well in some cases, care must be taken, as several species of reptiles are very sensitive to ivermectin. Use in turtles is particularly contraindicated.A characteristic of the antinematodal action of ivermectin is its potency: for instance, to combat Dirofilaria immitis in dogs, ivermectin is effective at 0.001 milligram per kilogram of body weight when administered orally.For dogs, the insecticide spinosad may have the effect of increasing the toxicity of ivermectin. Pharmacology Mechanism of action Ivermectin and its related drugs act by interfering with the nerve and muscle functions of helminths and insects. The drug binds to glutamate-gated chloride channels common to invertebrate nerve and muscle cells. The binding pushes the channels open, which increases the flow of chloride ions and hyper-polarizes the cell membranes, paralyzing and killing the invertebrate. Ivermectin is safe for mammals (at the normal therapeutic doses used to cure parasite infections) because mammalian glutamate-gated chloride channels only occur in the brain and spinal cord: the causative avermectins usually do not cross the blood–brain barrier, and are unlikely to bind to other mammalian ligand-gated channels. Pharmacokinetics Ivermectin can be given by mouth, topically, or via injection. It does not readily cross the blood–brain barrier of mammals due to the presence of P-glycoprotein (the MDR1 gene mutation affects the function of this protein). Crossing may still become significant if ivermectin is given at high doses, in which case brain levels peak 2–5 hours after administration. In contrast to mammals, ivermectin can cross the blood–brain barrier in tortoises, often with fatal consequences. Chemistry Fermentation of Streptomyces avermitilis yields eight closely related avermectin homologues, of which B1a and B1b form the bulk of the products isolated. In a separate chemical step, the mixture is hydrogenated to give ivermectin, which is an approximately 80:20 mixture of the two 22,23-dihydroavermectin compounds.Ivermectin is a macrocyclical lactone. History The avermectin family of compounds was discovered by Satoshi Ōmura of Kitasato University and William Campbell of Merck. In 1970, Ōmura isolated a strain of Streptomyces avermitilis from woodland soil near a golf course along the south east coast of Honshu, Japan. Ōmura sent the bacteria to William Campbell, who showed that the bacterial culture could cure mice infected with the roundworm Heligmosomoides polygyrus. Campbell isolated the active compounds from the bacterial culture, naming them "avermectins" and the bacterium Streptomyces avermitilis for the compounds ability to clear mice of worms (in Latin: a without, vermis worms). Of the various avermectins, Campbells group found the compound "avermectin B1" to be the most potent when taken orally. They synthesized modified forms of avermectin B1 to improve its pharmaceutical properties, eventually choosing a mixture of at least 80% 22,23-dihydroavermectin B1a and up to 20% 22,23-dihydroavermectin B1b, a combination they called "ivermectin".The discovery of ivermectin has been described as a combination of "chance and choice." Merck was looking for a broad-spectrum anthelmintic, which ivermectin is indeed; however, Campbell noted that they "...also found a broad-spectrum agent for the control of ectoparasitic insects and mites."Merck began marketing ivermectin as a veterinary antiparasitic in 1981. By 1986, ivermectin was registered for use in 46 countries and was administered massively to cattle, sheep and other animals. By the late 1980s, ivermectin was the bestselling veterinary medicine in the world. Following its blockbuster success as a veterinary antiparasitic, another Merck scientist, Mohamed Aziz, collaborated with the World Health Organization to test the safety and efficacy of ivermectin against onchocerciasis in humans. They found it to be highly safe and effective, triggering Merck to register ivermectin for human use as "Mectizan" in France in 1987. A year later, Merck CEO Roy Vagelos agreed that Merck would donate all ivermectin needed to eradicate river blindness. In 1998, that donation would be expanded to include ivermectin used to treat lymphatic filariasis.Ivermectin earned the title of "wonder drug" for the treatment of nematodes and arthropod parasites. Ivermectin has been used safely by hundreds of millions of people to treat river blindness and lymphatic filariasis.Half of the 2015 Nobel Prize in Physiology or Medicine was awarded jointly to Campbell and Ōmura for discovering avermectin, "the derivatives of which have radically lowered the incidence of river blindness and lymphatic filariasis, as well as showing efficacy against an expanding number of other parasitic diseases". Society and culture COVID-19 misinformation Economics The initial price proposed by Merck in 1987 was US$6 per treatment, which was unaffordable for patients who most needed ivermectin. The company donated hundreds of millions of courses of treatments since 1988 in more than 30 countries. Between 1995 and 2010, using donated ivermectin to prevent river blindness, the program is estimated to have prevented seven million years of disability at a cost of US$257 million.Ivermectin is considered an inexpensive drug. As of 2019, ivermectin tablets (Stromectol) in the United States were the least expensive treatment option for lice in children at approximately US$9.30, while Sklice, an ivermectin lotion, cost around US$300 for 120 mL (4 US fl oz).As of 2019, the cost effectiveness of treating scabies and lice with ivermectin has not been studied. Brand names It is sold under the brand names Heartgard, Sklice and Stromectol in the United States, Ivomec worldwide by Merial Animal Health, Mectizan in Canada by Merck, Iver-DT in Nepal by Alive Pharmaceutical and Ivexterm in Mexico by Valeant Pharmaceuticals International. In Southeast Asian countries, it is marketed by Delta Pharma Ltd. under the trade name Scabo 6. The formulation for rosacea treatment is sold under the brand name Soolantra. While in development, it was assigned the code MK-933 by Merck. Research Parasitic disease Ivermectin has been researched in laboratory animals, as a potential treatment for trichinosis. Tropical diseases As of 2016 ivermectin was studied as a potential antiviral agent against chikungunya and yellow fever. In chikungunya, ivermectin showed a wide in vitro safety margin as an antiviral.Ivermectin is also of interest in the prevention of malaria, as it is toxic to both the malaria plasmodium itself and the mosquitos that carry it. A direct effect on malaria parasites could not be shown in an experimental infection of volunteers with Plasmodium falciparum. Use of ivermectin at higher doses necessary to control malaria is probably safe, though large clinical trials have not yet been done to definitively establish the efficacy or safety of ivermectin for prophylaxis or treatment of malaria. Mass drug administration of a population with ivermectin to treat and prevent nematode infestation is effective for eliminating malaria-bearing mosquitos and thereby reducing infection with residual malaria parasites.One alternative to ivermectin is moxidectin, which has been approved by the Food and Drug Administration for use in people with river blindness. Moxidectin has a longer half-life than ivermectin and may eventually supplant ivermectin as it is a more potent microfilaricide, but there is a need for additional clinical trials, with long-term follow-up, to assess whether moxidectin is safe and effective for treatment of nematode infection in children and women of childbearing potential.There is tentative evidence that ivermectin kills bedbugs, as part of integrated pest management for bedbug infestations. However, such use may require a prolonged course of treatment which is of unclear safety. NAFLD In 2013, ivermectin was demonstrated as a novel ligand of the farnesoid X receptor, a therapeutic target for nonalcoholic fatty liver disease. COVID-19 During the COVID-19 pandemic, ivermectin was researched for possible utility in preventing and treating COVID-19, but no good evidence of benefit was found. See also Notes References External links "Ivermectin". Drug Information Portal. U.S. National Library of Medicine. Archived from the original on October 19, 2021. The Carter Center River Blindness (Onchocerciasis) Control Program "ivermectin (Rx) Stromectol". Medscape. Archived from the original on October 19, 2021. "Ivermectin Topical". MedlinePlus. Archived from the original on October 19, 2021.

You function as a medical explainer. Your task is to convey the meanings of medical terms in a detailed, yet easy-to-understand manner.

I'm seeking clarification on the medical term 'Anosmia.' Could you explain it?

Anosmia, also known as smell blindness, is the loss of the ability to detect one or more smells. Anosmia may be temporary or permanent. It differs from hyposmia, which is a decreased sensitivity to some or all smells.Anosmia can be due to a number of factors, including an inflammation of the nasal mucosa, blockage of nasal passages or a destruction of one temporal lobe. Inflammation is due to chronic mucosa changes in the lining of the paranasal sinus and in the middle and superior turbinates.When anosmia is caused by inflammatory changes in the nasal passageways, it is treated simply by reducing inflammation. It can be caused by chronic meningitis and neurosyphilis that would increase intracranial pressure over a long period of time, and in some cases by ciliopathy, including ciliopathy due to primary ciliary dyskinesia.The term derives from the New Latin anosmia, based on Ancient Greek ἀν- (an-) + ὀσμή (osmḗ smell; another related term, hyperosmia, refers to an increased ability to smell). Some people may be anosmic for one particular odor, a condition known as "specific anosmia". The absence of the sense of smell from birth is known as congenital anosmia.In the United States, 3% of people aged over 40 are affected by anosmia.Anosmia is a common symptom of COVID-19 and can persist as long COVID. Definition Anosmia is the inability to smell. It may be partial or total, and can be specific to certain smells. Reduced sensitivity to some or all smells is hyposmia. Signs and symptoms Anosmia can have a number of harmful effects. People with sudden onset anosmia may find food less appetizing, though congenital anosmics rarely complain about this, and none report a loss in weight. Loss of smell can also be dangerous because it hinders the detection of gas leaks, fire, and spoiled food. The common view of anosmia as trivial can make it more difficult for a patient to receive the same types of medical aid as someone who has lost other senses, such as hearing or sight.Many experience one sided loss of smell, often as a result of minor head trauma. This type of anosmia is normally only detected if both of the nostrils are tested separately. Using this method of testing each nostril separately will often show a reduced or even completely absent sense of smell in either one nostril or both, something which is often not revealed if both nostrils are simultaneously tested.Losing an established and sentimental smell memory (e.g. the smell of grass, of the grandparents attic, of a particular book, of loved ones, or of oneself) has been known to cause feelings of depression.Loss of the ability to smell may lead to the loss of libido, though this usually does not apply to loss of smell present at birth.Often people who have loss of smell at birth report that they pretended to be able to smell as children because they thought that smelling was something that older/mature people could do, or did not understand the concept of smelling but did not want to appear different from others. When children get older, they often realize and report to their parents that they do not actually possess a sense of smell, often to the surprise of their parents. Causes A temporary loss of smell can be caused by a blocked nose or infection. In contrast, a permanent loss of smell may be caused by death of olfactory receptor neurons in the nose or by brain injury in which there is damage to the olfactory nerve or damage to brain areas that process smell (see olfactory system). The lack of the sense of smell at birth, usually due to genetic factors, is referred to as congenital anosmia. Family members of the patient with congenital anosmia are often found with similar histories; this suggests that the anosmia may follow an autosomal dominant pattern. Anosmia may very occasionally be an early sign of a degenerative brain disease such as Parkinsons disease and Alzheimers disease.Another specific cause of permanent loss could be from damage to olfactory receptor neurons because of use of certain types of nasal spray; i.e., those that cause vasoconstriction of the nasal microcirculation. To avoid such damage and the subsequent risk of loss of smell, vasoconstricting nasal sprays should be used only when absolutely necessary and then for only a short amount of time. Non-vasoconstricting sprays, such as those used to treat allergy-related congestion, are safe to use for prescribed periods of time. Anosmia can also be caused by nasal polyps. These polyps are found in people with allergies, histories of sinusitis, and family history. Individuals with cystic fibrosis often develop nasal polyps.Amiodarone is a drug used in the treatment of arrhythmias of the heart. A clinical study demonstrated that the use of this drug induced anosmia in some patients. Although rare, there was a case in which a 66-year-old male was treated with amiodarone for ventricular tachycardia. After the use of the drug he began experiencing olfactory disturbance, however after decreasing the dosage of amiodarone, the severity of the anosmia decreased accordingly, suggesting a relationship between use of amiodarone to the development of anosmia. COVID-19-related anosmia Chemosensory disturbances, including loss of smell or taste, are the predominant neurological symptom of COVID-19. As many as 80% of COVID-19 patients exhibit some change in chemesthesis, including smell. Loss of smell has also been found to be more predictive of COVID-19 than all other symptoms, including fever, cough or fatigue, based on a survey of 2 million participants in the UK and US. Google searches for "smell", "loss of smell", "anosmia", and other similar terms increased since the early months of the pandemic, and strongly correlated with increases in daily cases and deaths. Research into the mechanisms underlying these symptoms is currently ongoing.Many countries list anosmia as an official COVID-19 symptom, and some have developed "smell tests" as potential screening tools.In 2020, the Global Consortium for Chemosensory Research, a collaborative research organization of international smell and taste researchers, formed to investigate loss of smell and related chemosensory symptoms. List of causes Diagnosis Doctors will begin with a detailed elicitation of history. Then the doctor will ask for any related injuries in relation to anosmia which could include upper respiratory infections or head injury. Psychophysical Assessment of order and taste identification can be used to identify anosmia. A nervous system examination is performed to see if the cranial nerves are damaged. The diagnosis, as well as the degree of impairment, can now be tested much more efficiently and effectively than ever before thanks to "smell testing kits" that have been made available as well as screening tests which use materials that most clinics would readily have. Occasionally, after accidents, there is a change in a patients sense of smell. Particular smells that were present before are no longer present. On occasion, after head traumas, there are patients who have unilateral anosmia. The sense of smell should be tested individually in each nostril.Many cases of congenital anosmia remain unreported and undiagnosed. Since the disorder is present from birth the individual may have little or no understanding of the sense of smell, hence is unaware of the deficit. It may also lead to reduction of appetite. Treatment Though anosmia caused by brain damage cannot be treated, anosmia caused by inflammatory changes in the mucosa may be treated with glucocorticoids. Reduction of inflammation through the use of oral glucocorticoids such as prednisone, followed by long term topical glucocorticoid nasal spray, would easily and safely treat the anosmia. A prednisone regimen is adjusted based on the degree of the thickness of mucosa, the discharge of oedema and the presence or absence of nasal polyps. However, the treatment is not permanent and may have to be repeated after a short while. Together with medication, pressure of the upper area of the nose must be mitigated through aeration and drainage.Anosmia caused by a nasal polyp may be treated by steroidal treatment or removal of the polyp.One experiment, where two people were given a single dose of 1,000 mg of turmeric, reported to find improvements in COVID-19-induced anosmia (and ageusia), however actual studies have yet to be done regarding this.Although very early in development, gene therapy has restored a sense of smell in mice with congenital anosmia when caused by ciliopathy. In this case, a genetic condition had affected cilia in their bodies which normally enabled them to detect air-borne chemicals, and an adenovirus was used to implant a working version of the IFT88 gene into defective cells in the nose, which restored the cilia and allowed a sense of smell. Epidemiology In the United States 3% of people aged over 40 are affected by anosmia.In 2012, smell was assessed in persons aged 40 years and older with rates of anosmia/severe hyposmia of 0.3% at age 40–49 rising to 14.1% at age 80+. Rates of hyposmia were much higher: 3.7% at age 40–49 and 25.9% at 80+. See also Phantosmia Parosmia Anosmia Awareness Day Zicam, a medicine that caused some users to permanently lose their sense of smell Ageusia, the loss of the sense of taste References Further reading == External links ==

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

The term 'Orchitis' keeps coming up in medical discussions. What does it stand for?

Orchitis is inflammation of the testes. It can also involve swelling, pains and frequent infection, particularly of the epididymis, as in epididymitis. The term is from the Ancient Greek ὄρχις meaning "testicle"; same root as orchid. Signs and symptoms Symptoms of orchitis are similar to those of testicular torsion. These can include: hematospermia (blood in the semen) hematuria (blood in the urine) severe pain visible swelling of a testicle or testicles and often the inguinal lymph nodes on the affected side. Causes Orchitis can be related to epididymitis infection that has spread to the testicles (then called "epididymo-orchitis"), sometimes caused by the sexually transmitted diseases chlamydia and gonorrhea. It has also been reported in cases of males infected with brucellosis. Orchitis can also be seen during active mumps, particularly in adolescent boys.Ischemic orchitis may result from damage to the blood vessels of the spermatic cord during inguinal herniorrhaphy, and may in the worst event lead to testicular atrophy. Diagnosis Blood – ESR high Urine – Cultural & Sensitivity test Ultrasound scanning Treatment In most cases where orchitis is caused by epididymitis, treatment is an oral antibiotic such as cefalexin or ciprofloxacin until infection clears up. In both causes non-steroidal anti-inflammatory drugs such as naproxen or ibuprofen are recommended to relieve pain. Sometimes stronger pain medications in the opiate category are called for and are frequently prescribed by experienced emergency department physicians. Other animals Orchitis is not rare in bulls and rams. It has also been described in roosters. References Further reading Lefort C, Thoumas D, Badachi Y, et al. (July 2001). "Orchites ischémiques: À propos de 5 cas diagnostiqués en écho-Doppler couleur" [Ischemic orchiditis: review of 5 cases diagnosed by color Doppler ultrasonography]. Journal de Radiologie (in French). 82 (7): 839–42. PMID 11507447. INIST:1080037. Chung JJ, Kim MJ, Lee T, Yoo HS, Lee JT (September 1997). "Sonographic findings in tuberculous epididymitis and epididymo-orchitis". Journal of Clinical Ultrasound. 25 (7): 390–4. doi:10.1002/(SICI)1097-0096(199709)25:7<390::AID-JCU7>3.0.CO;2-5. PMID 9282805. S2CID 23653479. Fong Y, Wantz GE (May 1992). "Prevention of ischemic orchitis during inguinal hernioplasty". Surgery, Gynecology & Obstetrics. 174 (5): 399–402. PMID 1570618. Beard CM, Benson RC, Kelalis PP, Elveback LR, Kurland LT (January 1977). "The incidence and outcome of mumps orchitis in Rochester, Minnesota, 1935 to 1974". Mayo Clinic Proceedings. 52 (1): 3–7. PMID 609284. Bigazzi PE, Kosuda LL, Hsu KC, Andres GA (February 1976). "Immune complex orchitis in vasectomized rabbits". The Journal of Experimental Medicine. 143 (2): 382–404. doi:10.1084/jem.143.2.382. PMC 2190126. PMID 129498. Lynch VP, Eakins D, Morrison E (August 1968). "Granulomatous orchitis". British Journal of Urology. 40 (4): 451–8. doi:10.1111/j.1464-410X.1968.tb11832.x. PMID 5678169. Dreyfuss W (April 1954). "Acute granulomatous orchiditis". The Journal of Urology. 71 (4): 483–7. doi:10.1016/S0022-5347(17)67813-3. PMID 13152871. Lambert B (1951). "The frequency of mumps and of mumps orchitis and the consequences for sexuality and fertility". Acta Genetica et Statistica Medica. 2 (Suppl. 1): 1–166. PMID 15444009. Grünberg H (1926). "Three unusual cases of chronic orchitis clinically resembling tumors of the testis". Frankfurt Z Pathol. 33: 217–27. == External links ==

You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

Can you break down the meaning of the medical term 'Tooth decay' for me?

Tooth decay, also known as cavities or caries, is the breakdown of teeth due to acids produced by bacteria. The cavities may be a number of different colors from yellow to black. Symptoms may include pain and difficulty with eating. Complications may include inflammation of the tissue around the tooth, tooth loss and infection or abscess formation.The cause of cavities is acid from bacteria dissolving the hard tissues of the teeth (enamel, dentin and cementum). The acid is produced by the bacteria when they break down food debris or sugar on the tooth surface. Simple sugars in food are these bacterias primary energy source and thus a diet high in simple sugar is a risk factor. If mineral breakdown is greater than build up from sources such as saliva, caries results. Risk factors include conditions that result in less saliva such as: diabetes mellitus, Sjögren syndrome and some medications. Medications that decrease saliva production include antihistamines and antidepressants. Dental caries are also associated with poverty, poor cleaning of the mouth, and receding gums resulting in exposure of the roots of the teeth.Prevention of dental caries includes regular cleaning of the teeth, a diet low in sugar, and small amounts of fluoride. Brushing ones teeth twice per day and flossing between the teeth once a day is recommended. Fluoride may be acquired from water, salt or toothpaste among other sources. Treating a mothers dental caries may decrease the risk in her children by decreasing the number of certain bacteria she may spread to them. Screening can result in earlier detection. Depending on the extent of destruction, various treatments can be used to restore the tooth to proper function or the tooth may be removed. There is no known method to grow back large amounts of tooth. The availability of treatment is often poor in the developing world. Paracetamol (acetaminophen) or ibuprofen may be taken for pain.Worldwide, approximately 3.6 billion people (48% of the population) have dental caries in their permanent teeth as of 2016. The World Health Organization estimates that nearly all adults have dental caries at some point in time. In baby teeth it affects about 620 million people or 9% of the population. They have become more common in both children and adults in recent years. The disease is most common in the developed world due to greater simple sugar consumption and less common in the developing world. Caries is Latin for "rottenness". Signs and symptoms A person experiencing caries may not be aware of the disease. The earliest sign of a new carious lesion is the appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of enamel. This is referred to as a white spot lesion, an incipient carious lesion or a "micro-cavity". As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation ("cavity"). Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated. A lesion that appears dark brown and shiny suggests dental caries were once present but the demineralization process has stopped, leaving a stain. Active decay is lighter in color and dull in appearance.As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through the enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed, resulting in pain that can be transient, temporarily worsening with exposure to heat, cold, or sweet foods and drinks. A tooth weakened by extensive internal decay can sometimes suddenly fracture under normal chewing forces. When the decay has progressed enough to allow the bacteria to overwhelm the pulp tissue in the center of the tooth, a toothache can result and the pain will become more constant. Death of the pulp tissue and infection are common consequences. The tooth will no longer be sensitive to hot or cold but can be very tender to pressure. Dental caries can also cause bad breath and foul tastes. In highly progressed cases, an infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig angina can be life-threatening. Cause Four things are required for caries to form: a tooth surface (enamel or dentin), caries-causing bacteria, fermentable carbohydrates (such as sucrose), and time. This involves adherence of food to the teeth and acid creation by the bacteria that makes up the dental plaque. However, these four criteria are not always enough to cause the disease and a sheltered environment promoting development of a cariogenic biofilm is required. The caries disease process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures that are retained within the bone.Tooth decay is caused by biofilm (dental plaque) lying on the teeth and maturing to become cariogenic (causing decay). Certain bacteria in the biofilm produce acid in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose.Caries occur more often in people from the lower end of the socio-economic scale than people from the upper end of the socio-economic scale, due to lack of education about dental care, and lack of access to professional dental care which may be expensive. Bacteria The most common bacteria associated with dental cavities are the mutans streptococci, most prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. However, cariogenic bacteria (the ones that can cause the disease) are present in dental plaque, but they are usually in too low concentrations to cause problems unless there is a shift in the balance. This is driven by local environmental change, such as frequent sugar intake or inadequate biofilm removal (toothbrushing). If left untreated, the disease can lead to pain, tooth loss and infection.The mouth contains a wide variety of oral bacteria, but only a few specific species of bacteria are believed to cause dental caries: Streptococcus mutans and Lactobacillus species among them. Streptococcus mutans are gram-positive bacteria which constitute biofilms on the surface of teeth. These organisms can produce high levels of lactic acid following fermentation of dietary sugars and are resistant to the adverse effects of low pH, properties essential for cariogenic bacteria. As the cementum of root surfaces is more easily demineralized than enamel surfaces, a wider variety of bacteria can cause root caries, including Lactobacillus acidophilus, Actinomyces spp., Nocardia spp., and Streptococcus mutans. Bacteria collect around the teeth and gums in a sticky, creamy-coloured mass called plaque, which serves as a biofilm. Some sites collect plaque more commonly than others, for example, sites with a low rate of salivary flow (molar fissures). Grooves on the occlusal surfaces of molar and premolar teeth provide microscopic retention sites for plaque bacteria, as do the interproximal sites. Plaque may also collect above or below the gingiva, where it is referred to as supra- or sub-gingival plaque, respectively. These bacterial strains, most notably S. mutans, can be inherited by a child from a caretakers kiss or through feeding pre-masticated food. Dietary sugars Bacteria in a persons mouth convert glucose, fructose, and most commonly sucrose (table sugar) into acids such as lactic acid through a glycolytic process called fermentation. If left in contact with the tooth, these acids may cause demineralization, which is the dissolution of its mineral content. The process is dynamic, however, as remineralization can also occur if the acid is neutralized by saliva or mouthwash. Fluoride toothpaste or dental varnish may aid remineralization. If demineralization continues over time, enough mineral content may be lost so that the soft organic material left behind disintegrates, forming a cavity or hole. The impact such sugars have on the progress of dental caries is called cariogenicity. Sucrose, although a bound glucose and fructose unit, is in fact more cariogenic than a mixture of equal parts of glucose and fructose. This is due to the bacteria utilising the energy in the saccharide bond between the glucose and fructose subunits. S.mutans adheres to the biofilm on the tooth by converting sucrose into an extremely adhesive substance called dextran polysaccharide by the enzyme dextran sucranase. Exposure The frequency with which teeth are exposed to cariogenic (acidic) environments affects the likelihood of caries development. After meals or snacks, the bacteria in the mouth metabolize sugar, resulting in an acidic by-product that decreases pH. As time progresses, the pH returns to normal due to the buffering capacity of saliva and the dissolved mineral content of tooth surfaces. During every exposure to the acidic environment, portions of the inorganic mineral content at the surface of teeth dissolve and can remain dissolved for two hours. Since teeth are vulnerable during these acidic periods, the development of dental caries relies heavily on the frequency of acid exposure. The carious process can begin within days of a tooths erupting into the mouth if the diet is sufficiently rich in suitable carbohydrates. Evidence suggests that the introduction of fluoride treatments has slowed the process. Proximal caries take an average of four years to pass through enamel in permanent teeth. Because the cementum enveloping the root surface is not nearly as durable as the enamel encasing the crown, root caries tend to progress much more rapidly than decay on other surfaces. The progression and loss of mineralization on the root surface is 2.5 times faster than caries in enamel. In very severe cases where oral hygiene is very poor and where the diet is very rich in fermentable carbohydrates, caries may cause cavities within months of tooth eruption. This can occur, for example, when children continuously drink sugary drinks from baby bottles (see later discussion). Teeth There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for cavities. Molar incisor hypo-mineralization, which seems to be increasingly common. While the cause is unknown it is thought to be a combination of genetic and environmental factors. Possible contributing factors that have been investigated include systemic factors such as high levels of dioxins or polychlorinated biphenyl (PCB) in the mothers milk, premature birth and oxygen deprivation at birth, and certain disorders during the childs first 3 years such as mumps, diphtheria, scarlet fever, measles, hypoparathyroidism, malnutrition, malabsorption, hypo-vitaminosis D, chronic respiratory diseases, or undiagnosed and untreated coeliac disease, which usually presents with mild or absent gastrointestinal symptoms.Amelogenesis imperfecta, which occurs in between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth. In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Approximately 96% of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries. The evidence for linking malocclusion and/or crowding to dental caries is weak; however, the anatomy of teeth may affect the likelihood of caries formation. Where the deep developmental grooves of teeth are more numerous and exaggerated, pit and fissure caries is more likely to develop (see next section). Also, caries is more likely to develop when food is trapped between teeth. Other factors Reduced salivary flow rate is associated with increased caries since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions that reduce the amount of saliva produced by salivary glands, in particular the submandibular gland and parotid gland, are likely to lead to dry mouth and thus to widespread tooth decay. Examples include Sjögren syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also occlude the flow of saliva to an extreme degree. This is known as meth mouth. Tetrahydrocannabinol (THC), the active chemical substance in cannabis, also causes a nearly complete occlusion of salivation, known in colloquial terms as "cotton mouth". Moreover, 63% of the most commonly prescribed medications in the United States list dry mouth as a known side-effect. Radiation therapy of the head and neck may also damage the cells in salivary glands, somewhat increasing the likelihood of caries formation.Susceptibility to caries can be related to altered metabolism in the tooth, in particular to fluid flow in the dentin. Experiments on rats have shown that a high-sucrose, cariogenic diet "significantly suppresses the rate of fluid motion" in dentin.The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries. Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede. As the gingiva loses attachment to the teeth due to gingival recession, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel. Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root-surface caries. Exposure of children to secondhand tobacco smoke is associated with tooth decay.Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium, such as cadmium, mimic the calcium ion and therefore exposure to them may promote tooth decay.Poverty is also a significant social determinant for oral health. Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.Forms are available for risk assessment for caries when treating dental cases; this system using the evidence-based Caries Management by Risk Assessment (CAMBRA). It is still unknown if the identification of high-risk individuals can lead to more effective long-term patient management that prevents caries initiation and arrests or reverses the progression of lesions.Saliva also contains iodine and EGF. EGF results effective in cellular proliferation, differentiation and survival. Salivary EGF, which seems also regulated by dietary inorganic iodine, plays an important physiological role in the maintenance of oral (and gastro-oesophageal) tissue integrity, and, on the other hand, iodine is effective in prevention of dental caries and oral health. Pathophysiology Teeth are bathed in saliva and have a coating of bacteria on them (biofilm) that continually forms. The development of biofilm begins with pellicle formation. Pellicle is an acellular proteinaceous film which covers the teeth. Bacteria colonize on the teeth by adhering to the pellicle-coated surface. Over time, a mature biofilm is formed and this create a cariogenic environment on the tooth surface. The minerals in the hard tissues of the teeth (enamel, dentin and cementum) are constantly undergoing processes of demineralization and remineralization. Dental caries results when the demineralization rate is faster than the remineralization and there is net mineral loss. This happens when there is an ecologic shift within the dental biofilm, from a balanced population of micro-organisms to a population that produce acids and can survive in an acid environment. Enamel Tooth enamel is a highly mineralized acellular tissue, and caries act upon it through a chemical process brought on by the acidic environment produced by bacteria. As the bacteria consume the sugar and use it for their own energy, they produce lactic acid. The effects of this process include the demineralization of crystals in the enamel, caused by acids, over time until the bacteria physically penetrate the dentin. Enamel rods, which are the basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the dentin. Since demineralization of enamel by caries, in general, follows the direction of the enamel rods, the different triangular patterns between pit and fissure and smooth-surface caries develop in the enamel because the orientation of enamel rods are different in the two areas of the tooth.As the enamel loses minerals, and dental caries progresses, the enamel develops several distinct zones, visible under a light microscope. From the deepest layer of the enamel to the enamel surface, the identified areas are the: translucent zone, dark zones, body of the lesion, and surface zone. The translucent zone is the first visible sign of caries and coincides with a one to two percent loss of minerals. A slight remineralization of enamel occurs in the dark zone, which serves as an example of how the development of dental caries is an active process with alternating changes. The area of greatest demineralization and destruction is in the body of the lesion itself. The surface zone remains relatively mineralized and is present until the loss of tooth structure results in a cavitation. Dentin Unlike enamel, the dentin reacts to the progression of dental caries. After tooth formation, the ameloblasts, which produce enamel, are destroyed once enamel formation is complete and thus cannot later regenerate enamel after its destruction. On the other hand, dentin is produced continuously throughout life by odontoblasts, which reside at the border between the pulp and dentin. Since odontoblasts are present, a stimulus, such as caries, can trigger a biologic response. These defense mechanisms include the formation of sclerotic and tertiary dentin.In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the advancing front, the zone of bacterial penetration, and the zone of destruction. The advancing front represents a zone of demineralized dentin due to acid and has no bacteria present. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. The zone of destruction has a more mixed bacterial population where proteolytic enzymes have destroyed the organic matrix. The innermost dentin caries has been reversibly attacked because the collagen matrix is not severely damaged, giving it potential for repair. Sclerotic dentin The structure of dentin is an arrangement of microscopic channels, called dentinal tubules, which radiate outward from the pulp chamber to the exterior cementum or enamel border. The diameter of the dentinal tubules is largest near the pulp (about 2.5 μm) and smallest (about 900 nm) at the junction of dentin and enamel. The carious process continues through the dentinal tubules, which are responsible for the triangular patterns resulting from the progression of caries deep into the tooth. The tubules also allow caries to progress faster. In response, the fluid inside the tubules brings immunoglobulins from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules. This results in a constriction of the tubules, which is an attempt to slow the bacterial progression. In addition, as the acid from the bacteria demineralizes the hydroxyapatite crystals, calcium and phosphorus are released, allowing for the precipitation of more crystals which fall deeper into the dentinal tubule. These crystals form a barrier and slow the advancement of caries. After these protective responses, the dentin is considered sclerotic. According to hydrodynamic theory, fluids within dentinal tubules are believed to be the mechanism by which pain receptors are triggered within the pulp of the tooth. Since sclerotic dentin prevents the passage of such fluids, pain that would otherwise serve as a warning of the invading bacteria may not develop at first. Tertiary dentin In response to dental caries, there may be production of more dentin toward the direction of the pulp. This new dentin is referred to as tertiary dentin. Tertiary dentin is produced to protect the pulp for as long as possible from the advancing bacteria. As more tertiary dentin is produced, the size of the pulp decreases. This type of dentin has been subdivided according to the presence or absence of the original odontoblasts. If the odontoblasts survive long enough to react to the dental caries, then the dentin produced is called "reactionary" dentin. If the odontoblasts are killed, the dentin produced is called "reparative" dentin. In the case of reparative dentin, other cells are needed to assume the role of the destroyed odontoblasts. Growth factors, especially TGF-β, are thought to initiate the production of reparative dentin by fibroblasts and mesenchymal cells of the pulp. Reparative dentin is produced at an average of 1.5 μm/day, but can be increased to 3.5 μm/day. The resulting dentin contains irregularly shaped dentinal tubules that may not line up with existing dentinal tubules. This diminishes the ability for dental caries to progress within the dentinal tubules. Cementum The incidence of cemental caries increases in older adults as gingival recession occurs from either trauma or periodontal disease. It is a chronic condition that forms a large, shallow lesion and slowly invades first the roots cementum and then dentin to cause a chronic infection of the pulp (see further discussion under classification by affected hard tissue). Because dental pain is a late finding, many lesions are not detected early, resulting in restorative challenges and increased tooth loss. Diagnosis The presentation of caries is highly variable. However, the risk factors and stages of development are similar. Initially, it may appear as a small chalky area (smooth surface caries), which may eventually develop into a large cavitation. Sometimes caries may be directly visible. However other methods of detection such as X-rays are used for less visible areas of teeth and to judge the extent of destruction. Lasers for detecting caries allow detection without ionizing radiation and are now used for detection of interproximal decay (between the teeth). Primary diagnosis involves inspection of all visible tooth surfaces using a good light source, dental mirror and explorer. Dental radiographs (X-rays) may show dental caries before it is otherwise visible, in particular caries between the teeth. Large areas of dental caries are often apparent to the naked eye, but smaller lesions can be difficult to identify. Visual and tactile inspection along with radiographs are employed frequently among dentists, in particular to diagnose pit and fissure caries. Early, uncavitated caries is often diagnosed by blowing air across the suspect surface, which removes moisture and changes the optical properties of the unmineralized enamel. Some dental researchers have cautioned against the use of dental explorers to find caries, in particular sharp ended explorers. In cases where a small area of tooth has begun demineralizing but has not yet cavitated, the pressure from the dental explorer could cause a cavity. Since the carious process is reversible before a cavity is present, it may be possible to arrest caries with fluoride and remineralize the tooth surface. When a cavity is present, a restoration will be needed to replace the lost tooth structure. At times, pit and fissure caries may be difficult to detect. Bacteria can penetrate the enamel to reach dentin, but then the outer surface may remineralize, especially if fluoride is present. These caries, sometimes referred to as "hidden caries", will still be visible on X-ray radiographs, but visual examination of the tooth would show the enamel intact or minimally perforated. The differential diagnosis for dental caries includes dental fluorosis and developmental defects of the tooth including hypomineralization of the tooth and hypoplasia of the tooth.The early carious lesion is characterized by demineralization of the tooth surface, altering the tooths optical properties. Technology utilizing laser speckle image (LSI) techniques may provide a diagnostic aid to detect early carious lesions. Classification Caries can be classified by location, etiology, rate of progression, and affected hard tissues. These forms of classification can be used to characterize a particular case of tooth decay in order to more accurately represent the condition to others and also indicate the severity of tooth destruction. In some instances, caries is described in other ways that might indicate the cause. The G. V. Black classification is as follows: Class I – occlusal surfaces of posterior teeth, buccal or lingual pits on molars, lingual pit near cingulum of maxillary incisors Class II – proximal surfaces of posterior teeth Class III – interproximal surfaces of anterior teeth without incisal edge involvement Class IV – interproximal surfaces of anterior teeth with incisal edge involvement Class V – cervical third of facial or lingual surface of tooth Class VI – incisal or occlusal edge is worn away due to attrition Early childhood caries Early childhood caries (ECC), also known as "baby bottle caries," "baby bottle tooth decay" or "bottle rot," is a pattern of decay found in young children with their deciduous (baby) teeth. This must include the presence of at least one carious lesion on a primary tooth in a child under the age of 6 years. The teeth most likely affected are the maxillary anterior teeth, but all teeth can be affected. The name for this type of caries comes from the fact that the decay usually is a result of allowing children to fall asleep with sweetened liquids in their bottles or feeding children sweetened liquids multiple times during the day.Another pattern of decay is "rampant caries", which signifies advanced or severe decay on multiple surfaces of many teeth. Rampant caries may be seen in individuals with xerostomia, poor oral hygiene, stimulant use (due to drug-induced dry mouth), and/or large sugar intake. If rampant caries is a result of previous radiation to the head and neck, it may be described as radiation-induced caries. Problems can also be caused by the self-destruction of roots and whole tooth resorption when new teeth erupt or later from unknown causes. Children at 6–12 months are at increased risk of developing dental caries. For other children aged 12–18 months, dental caries develop on primary teeth and approximately twice yearly for permanent teeth.A range of studies have reported that there is a correlation between caries in primary teeth and caries in permanent teeth. Rate of progression Temporal descriptions can be applied to caries to indicate the progression rate and previous history. "Acute" signifies a quickly developing condition, whereas "chronic" describes a condition that has taken an extended time to develop, in which thousands of meals and snacks, many causing some acid demineralization that is not remineralized, eventually result in cavities. Recurrent caries, also described as secondary, are caries that appear at a location with a previous history of caries. This is frequently found on the margins of fillings and other dental restorations. On the other hand, incipient caries describes decay at a location that has not experienced previous decay. Arrested caries describes a lesion on a tooth that was previously demineralized but was remineralized before causing a cavitation. Fluoride treatment can help recalcification of tooth enamel as well as the use of amorphous calcium phosphate. Micro-invasive interventions (such as dental sealant or resin infiltration) have been shown to slow down the progression of proximal decay. Affected hard tissue Depending on which hard tissues are affected, it is possible to describe caries as involving enamel, dentin, or cementum. Early in its development, caries may affect only enamel. Once the extent of decay reaches the deeper layer of dentin, the term "dentinal caries" is used. Since cementum is the hard tissue that covers the roots of teeth, it is not often affected by decay unless the roots of teeth are exposed to the mouth. Although the term "cementum caries" may be used to describe the decay on roots of teeth, very rarely does caries affect the cementum alone. Prevention Oral hygiene The primary approach to dental hygiene care consists of tooth-brushing and flossing. The purpose of oral hygiene is to remove and prevent the formation of plaque or dental biofilm, although studies have shown this effect on caries is limited. While there is no evidence that flossing prevents tooth decay, the practice is still generally recommended.A toothbrush can be used to remove plaque on accessible surfaces, but not between teeth or inside pits and fissures on chewing surfaces. When used correctly, dental floss removes plaque from areas that could otherwise develop proximal caries but only if the depth of sulcus has not been compromised. Additional aids include interdental brushes, water picks, and mouthwashes. The use of rotational electric toothbrushes might reduce the risk of plaque and gingivitis, though it is unclear whether they are of clinical importance.However, oral hygiene is effective at preventing gum disease (gingivitis / periodontal disease). Food is forced inside pits and fissures under chewing pressure, leading to carbohydrate-fuelled acid demineralisation where the brush, fluoride toothpaste, and saliva have no access to remove trapped food, neutralise acid, or remineralise tooth enamel. (Occlusal caries accounts for between 80 and 90% of caries in children (Weintraub, 2001).) Unlike brushing, fluoride leads to proven reduction in caries incidence by approximately 25%; higher concentrations of fluoride (>1,000 ppm) in toothpaste also helps prevents tooth decay, with the effect increasing with concentration up to a plateau. A randomized clinical trial demonstrated that toothpastes that contain arginine have greater protection against tooth cavitation than the regular fluoride toothpastes containing 1450 ppm alone. A Cochrane review has confirmed that the use of fluoride gels, normally applied by a dental professional from once to several times a year, assists in the prevention of tooth decay in children and adolescents, reiterating the importance of fluoride as the principal means of caries prevention. Another review concluded that the supervised regular use of a fluoride mouthwash greatly reduced the onset of decay in the permanent teeth of children.Professional hygiene care consists of regular dental examinations and professional prophylaxis (cleaning). Sometimes, complete plaque removal is difficult, and a dentist or dental hygienist may be needed. Along with oral hygiene, radiographs may be taken at dental visits to detect possible dental caries development in high-risk areas of the mouth (e.g. "bitewing" X-rays which visualize the crowns of the back teeth). Alternative methods of oral hygiene also exist around the world, such as the use of teeth cleaning twigs such as miswaks in some Middle Eastern and African cultures. There is some limited evidence demonstrating the efficacy of these alternative methods of oral hygiene. Dietary modification People who eat more free sugars get more cavities, with cavities increasing exponentially with increasing sugar intake. Populations with less sugar intake have fewer cavities. In one population, in Nigeria, where sugar consumption was about 2g/day, only two percent of the population, of any age, had had a cavity.Chewy and sticky foods (such as candy, cookies, potato chips, and crackers) tend to adhere to teeth longer. However, dried fruits such as raisins and fresh fruit such as apples and bananas disappear from the mouth quickly, and do not appear to be a risk factor. Consumers are not good at guessing which foods stick around in the mouth.For children, the American Dental Association and the European Academy of Paediatric Dentistry recommend limiting the frequency of consumption of drinks with sugar, and not giving baby bottles to infants during sleep (see earlier discussion). Parents are also recommended to avoid sharing utensils and cups with their infants to prevent transferring bacteria from the parents mouth.Xylitol is a naturally occurring sugar alcohol that is used in different products as an alternative to sucrose (table sugar). As of 2015 the evidence concerning the use of xylitol in chewing gum was insufficient to determine if it is effective at preventing caries. Other measures The use of dental sealants is a means of prevention. A sealant is a thin plastic-like coating applied to the chewing surfaces of the molars to prevent food from being trapped inside pits and fissures. This deprives resident plaque bacteria of carbohydrate, preventing the formation of pit and fissure caries. Sealants are usually applied on the teeth of children, as soon as the teeth erupt but adults are receiving them if not previously performed. Sealants can wear out and fail to prevent access of food and plaque bacteria inside pits and fissures and need to be replaced so they must be checked regularly by dental professionals. Dental sealants have been shown to be more effective at preventing occlusal decay when compared to fluoride varnish applications.Calcium, as found in food such as milk and green vegetables, is often recommended to protect against dental caries. Fluoride helps prevent decay of a tooth by binding to the hydroxyapatite crystals in enamel. Streptococcus mutans is the leading cause of tooth decay. Low concentration fluoride ions act as bacteriostatic therapeutic agent and high concentration fluoride ions are bactericidal. The incorporated fluorine makes enamel more resistant to demineralization and, thus, resistant to decay. Fluoride can be found in either topical or systemic form. Topical fluoride is more highly recommended than systemic intake to protect the surface of the teeth. Topical fluoride is used in toothpaste, mouthwash and fluoride varnish. Standard fluoride toothpaste (1,000–1,500 ppm) is more effective than low fluoride toothpaste (< 600ppm) to prevent dental caries. It is recommended that all adult patients to use fluoridated toothpaste with at least 1350ppm fluoride content, brushing at least 2 times per day and brush right before bed. For children and young adults, use fluoridated toothpaste with 1350ppm to 1500ppm fluoride content, brushing 2 times per day and also brush right before bed. American Dental Association Council suggest that for children <3 years old, caregivers should begin brushing their teeth by using fluoridated toothpaste with an amount no more than a smear. Supervised toothbrushing must also be done to children below 8 years of age to prevent swallowing of toothpaste. After brushing with fluoride toothpaste, rinsing should be avoided and the excess spat out. Many dental professionals include application of topical fluoride solutions as part of routine visits and recommend the use of xylitol and amorphous calcium phosphate products. Silver diamine fluoride may work better than fluoride varnish to prevent cavities. Systemic fluoride is found as lozenges, tablets, drops and water fluoridation. These are ingested orally to provide fluoride systemically. Water fluoridation has been shown to be beneficial to prevent tooth decay, especially in low social economical areas, where other forms of fluoride is not available. However, a Cochrane systematic review found no evidence to suggest that taking fluoride systemically daily in pregnant women was effective in preventing dental decay in their offspring. While some products containing chlorhexidine have been shown to limit the progression of existing tooth decay; there is currently no evidence suggesting that chlorhexidine gels and varnishes can prevent dental caries or reduce the population of Streptococcus mutans in the mouth.An oral health assessment carried out before a child reaches the age of one may help with management of caries. The oral health assessment should include checking the childs history, a clinical examination, checking the risk of caries in the child including the state of their occlusion and assessing how well equipped the childs parent or carer is to help the child prevent caries. In order to further increase a childs cooperation in caries management, good communication by the dentist and the rest of the staff of a dental practice should be used. This communication can be improved by calling the child by their name, using eye contact and including them in any conversation about their treatment.Vaccines are also under development. Treatment Most importantly, whether the carious lesion is cavitated or non-cavitated dictates the management. Clinical assessment of whether the lesion is active or arrested is also important. Noncavitated lesions can be arrested and remineralization can occur under the right conditions. However, this may require extensive changes to the diet (reduction in frequency of refined sugars), improved oral hygiene (toothbrushing twice per day with fluoride toothpaste and daily flossing), and regular application of topical fluoride. More recently, Immunoglobulin Y specific to Streptococcus mutans has been used to suppress growth of S mutans. Such management of a carious lesion is termed "non-operative" since no drilling is carried out on the tooth. Non-operative treatment requires excellent understanding and motivation from the individual, otherwise the decay will continue. Once a lesion has cavitated, especially if dentin is involved, remineralization is much more difficult and a dental restoration is usually indicated ("operative treatment"). Before a restoration can be placed, all of the decay must be removed otherwise it will continue to progress underneath the filling. Sometimes a small amount of decay can be left if it is entombed and there is a seal which isolates the bacteria from their substrate. This can be likened to placing a glass container over a candle, which burns itself out once the oxygen is used up. Techniques such as stepwise caries removal are designed to avoid exposure of the dental pulp and overall reduction of the amount of tooth substance which requires removal before the final filling is placed. Often enamel which overlies decayed dentin must also be removed as it is unsupported and susceptible to fracture. The modern decision-making process with regards the activity of the lesion, and whether it is cavitated, is summarized in the table.Destroyed tooth structure does not fully regenerate, although remineralization of very small carious lesions may occur if dental hygiene is kept at optimal level. For the small lesions, topical fluoride is sometimes used to encourage remineralization. For larger lesions, the progression of dental caries can be stopped by treatment. The goal of treatment is to preserve tooth structures and prevent further destruction of the tooth. Aggressive treatment, by filling, of incipient carious lesions, places where there is superficial damage to the enamel, is controversial as they may heal themselves, while once a filling is performed it will eventually have to be redone and the site serves as a vulnerable site for further decay.In general, early treatment is quicker and less expensive than treatment of extensive decay. Local anesthetics, nitrous oxide ("laughing gas"), or other prescription medications may be required in some cases to relieve pain during or following treatment or to relieve anxiety during treatment. A dental handpiece ("drill") is used to remove large portions of decayed material from a tooth. A spoon, a dental instrument used to carefully remove decay, is sometimes employed when the decay in dentin reaches near the pulp. Some dentists remove dental caries using a laser rather than the traditional dental drill. A Cochrane review of this technique looked at Er:YAG (erbium-doped yttrium aluminium garnet), Er,Cr:YSGG (erbium, chromium: yttrium-scandium-gallium-garnet) and Nd:YAG (neodymium-doped yttrium aluminium garnet) lasers and found that although people treated with lasers (compared to a conventional dental "drill") experienced less pain and had a lesser need for dental anaesthesia, that overall there was little difference in caries removal. Another alternative to drilling or lasers for small caries is the use of air abrasion, in which small abrasive particles are blasted at decay using pressurized air (similar to sand blasting). Once the cary is removed, the missing tooth structure requires a dental restoration of some sort to return the tooth to function and aesthetic condition. Restorative materials include dental amalgam, composite resin, glass ionomer cement, porcelain, and gold. Composite resin and porcelain can be made to match the color of a patients natural teeth and are thus used more frequently when aesthetics are a concern. Composite restorations are not as strong as dental amalgam and gold; some dentists consider the latter as the only advisable restoration for posterior areas where chewing forces are great. When the decay is too extensive, there may not be enough tooth structure remaining to allow a restorative material to be placed within the tooth. Thus, a crown may be needed. This restoration appears similar to a cap and is fitted over the remainder of the natural crown of the tooth. Crowns are often made of gold, porcelain, or porcelain fused to metal. For children, preformed crowns are available to place over the tooth. These are usually made of metal (usually stainless steel but increasingly there are aesthetic materials). Traditionally teeth are shaved down to make room for the crown but, more recently, stainless steel crowns have been used to seal decay into the tooth and stop it progressing. This is known as the Hall Technique and works by depriving the bacteria in the decay of nutrients and making their environment less favorable for them. It is a minimally invasive method of managing decay in children and does not require local anesthetic injections in the mouth. In certain cases, endodontic therapy may be necessary for the restoration of a tooth. Endodontic therapy, also known as a "root canal", is recommended if the pulp in a tooth dies from infection by decay-causing bacteria or from trauma. In root canal therapy, the pulp of the tooth, including the nerve and vascular tissues, is removed along with decayed portions of the tooth. The canals are instrumented with endodontic files to clean and shape them, and they are then usually filled with a rubber-like material called gutta percha. The tooth is filled and a crown can be placed. Upon completion of root canal therapy, the tooth is non-vital, as it is devoid of any living tissue. An extraction can also serve as treatment for dental caries. The removal of the decayed tooth is performed if the tooth is too far destroyed from the decay process to effectively restore the tooth. Extractions are sometimes considered if the tooth lacks an opposing tooth or will probably cause further problems in the future, as may be the case for wisdom teeth. Extractions may also be preferred by people unable or unwilling to undergo the expense or difficulties in restoring the tooth. Epidemiology Worldwide, approximately 3.6 billion people have dental caries in their permanent teeth. In baby teeth it affects about 620 million people or 9% of the population. The disease is most common in Latin American countries, countries in the Middle East, and South Asia, and least prevalent in China. In the United States, dental caries is the most common chronic childhood disease, being at least five times more common than asthma. It is the primary pathological cause of tooth loss in children. Between 29% and 59% of adults over the age of 50 experience caries.Treating dental cavities costs 5–10% of health-care budgets in industrialized countries, and can easily exceed budgets in lower-income countries.The number of cases has decreased in some developed countries, and this decline is usually attributed to increasingly better oral hygiene practices and preventive measures such as fluoride treatment. Nonetheless, countries that have experienced an overall decrease in cases of tooth decay continue to have a disparity in the distribution of the disease. Among children in the United States and Europe, twenty percent of the population endures sixty to eighty percent of cases of dental caries. A similarly skewed distribution of the disease is found throughout the world with some children having none or very few caries and others having a high number. Australia, Nepal, and Sweden (where children receive dental care paid for by the government) have a low incidence of cases of dental caries among children, whereas cases are more numerous in Costa Rica and Slovakia.The classic DMF (decay/missing/filled) index is one of the most common methods for assessing caries prevalence as well as dental treatment needs among populations. This index is based on in-field clinical examination of individuals by using a probe, mirror and cotton rolls. Because the DMF index is done without X-ray imaging, it underestimates real caries prevalence and treatment needs.Bacteria typically associated with dental caries have been isolated from vaginal samples from females who have bacterial vaginosis. History There is a long history of dental caries. Over a million years ago, hominins such as Paranthropus had cavities. The largest increases in the prevalence of caries have been associated with dietary changes.Archaeological evidence shows that tooth decay is an ancient disease dating far into prehistory. Skulls dating from a million years ago through the Neolithic period show signs of caries, including those from the Paleolithic and Mesolithic ages. The increase of caries during the neolithic period may be attributed to the increased consumption of plant foods containing carbohydrates. The beginning of rice cultivation in South Asia is also believed to have caused an increase in caries especially for women, although there is also some evidence from sites in Thailand, such as Khok Phanom Di, that shows a decrease in overall percentage of dental caries with the increase in dependence on rice agriculture.A Sumerian text from 5000 BC describes a "tooth worm" as the cause of caries. Evidence of this belief has also been found in India, Egypt, Japan, and China. Unearthed ancient skulls show evidence of primitive dental work. In Pakistan, teeth dating from around 5500 BC to 7000 BC show nearly perfect holes from primitive dental drills. The Ebers Papyrus, an Egyptian text from 1550 BC, mentions diseases of teeth. During the Sargonid dynasty of Assyria during 668 to 626 BC, writings from the kings physician specify the need to extract a tooth due to spreading inflammation. In the Roman Empire, wider consumption of cooked foods led to a small increase in caries prevalence. The Greco-Roman civilization, in addition to the Egyptian civilization, had treatments for pain resulting from caries.The rate of caries remained low through the Bronze Age and Iron Age, but sharply increased during the Middle Ages. Periodic increases in caries prevalence had been small in comparison to the 1000 AD increase, when sugar cane became more accessible to the Western world. Treatment consisted mainly of herbal remedies and charms, but sometimes also included bloodletting. The barber surgeons of the time provided services that included tooth extractions. Learning their training from apprenticeships, these health providers were quite successful in ending tooth pain and likely prevented systemic spread of infections in many cases. Among Roman Catholics, prayers to Saint Apollonia, the patroness of dentistry, were meant to heal pain derived from tooth infection.There is also evidence of caries increase when Indigenous people in North America changed from a strictly hunter-gatherer diet to a diet with maize. Rates also increased after contact with colonizing Europeans, implying an even greater dependence on maize.During the European Age of Enlightenment, the belief that a "tooth worm" caused caries was also no longer accepted in the European medical community. Pierre Fauchard, known as the father of modern dentistry, was one of the first to reject the idea that worms caused tooth decay and noted that sugar was detrimental to the teeth and gingiva. In 1850, another sharp increase in the prevalence of caries occurred and is believed to be a result of widespread diet changes. Prior to this time, cervical caries was the most frequent type of caries, but increased availability of sugar cane, refined flour, bread, and sweetened tea corresponded with a greater number of pit and fissure caries. In the 1890s, W. D. Miller conducted a series of studies that led him to propose an explanation for dental caries that was influential for current theories. He found that bacteria inhabited the mouth and that they produced acids that dissolved tooth structures when in the presence of fermentable carbohydrates. This explanation is known as the chemoparasitic caries theory. Millers contribution, along with the research on plaque by G. V. Black and J. L. Williams, served as the foundation for the current explanation of the etiology of caries. Several of the specific strains of lactobacilli were identified in 1921 by Fernando E. Rodríguez Vargas. In 1924 in London, Killian Clarke described a spherical bacterium in chains isolated from carious lesions which he called Streptococcus mutans. Although Clarke proposed that this organism was the cause of caries, the discovery was not followed up. Later, in 1954 in the US, Frank Orland working with hamsters showed that caries was transmissible and caused by acid-producing Streptococcus thus ending the debate whether dental caries were resultant from bacteria. It was not until the late 1960s that it became generally accepted that the Streptococcus isolated from hamster caries was the same as S. mutans.Tooth decay has been present throughout human history, from early hominids millions of years ago, to modern humans. The prevalence of caries increased dramatically in the 19th century, as the Industrial Revolution made certain items, such as refined sugar and flour, readily available. The diet of the "newly industrialized English working class" then became centered on bread, jam, and sweetened tea, greatly increasing both sugar consumption and caries. Etymology and usage Naturalized from Latin into English (a loanword), caries in its English form originated as a mass noun that means "rottenness", that is, "decay". The word is an uncountable noun. Cariesology or cariology is the study of dental caries. Society and culture It is estimated that untreated dental caries results in worldwide productivity losses in the size of about US$27 billion yearly. Other animals Dental caries are uncommon among companion animals. See also Cariogram References Cited sources Nanci, A. (2013). Ten Cates Oral Histology. Elsevier. ISBN 978-0323078467. External links Tooth decay at Curlie Centers for Disease Control: Dental Caries

You are an assistant in medical learning. Your role is to clarify medical terminology, ensuring the information is both accurate and accessible.

I'm encountering the term 'Anorectal abscess' in medical literature. What's its definition?

Anorectal abscess (also known as an anal/rectal abscess, or perianal/perirectal abscess) is an abscess adjacent to the anus. Most cases of perianal abscesses are sporadic, though there are certain situations which elevate the risk for developing the disease, such as diabetes mellitus, Crohns disease, chronic corticosteroid treatment and others. It arises as a complication of paraproctitis. Ischiorectal, inter- and intrasphincteric abscesses have been described. Signs and symptoms Pain in the perianal area is the most common symptom of an anorectal abscess. The pain may be dull, aching, or throbbing. It is worst when the person sits down and right before a bowel movement. After the individual has a bowel movement, the pain usually lessens. Other signs and symptoms of anorectal abscess include constipation, drainage from the rectum, fever and chills, or a palpable mass near the anus. The condition can become extremely painful, and usually worsens over the course of just a few days. The pain may be limited and sporadic at first, but may worsen to a constant pain which can become very severe when body position is changed (e.g., when standing up, rolling over, and so forth). Depending upon the exact location of the abscess, there can also be excruciating pain during bowel movements, though this is not always the case. This condition may occur in isolation, but is frequently indicative of another underlying disorder, such as Crohns disease. Complications If left untreated, an anal fistula will almost certainly form, connecting the rectum to the skin. This requires more intensive surgery. Furthermore, any untreated abscess may (and most likely will) continue to expand, eventually becoming a serious systemic infection. Cause Abscesses are caused by a high-density infection of (usually) common bacteria which collect in one place or another for any variety of reasons. Anal abscesses, without treatment, are likely to spread and affect other parts of the body, particularly the groin and rectal lumen. All abscesses can progress to serious generalized infections requiring lengthy hospitalizations if not treated. Historically, many rectal abscesses are caused by bacteria common in the digestive system, such as E. coli. While this still continues often to be the case, there has recently been an increase in the causative organism being staphylococcus, as well as the difficult to treat community-acquired methicillin-resistant S. aureus. Because of the increasing appearance of more exotic bacteria in anal abscesses, microbiological examination will always be performed on the surgical exudate to determine the proper course of any antibiotic treatment. Diagnosis Diagnosis of anorectal abscess begins with a medical history and physical exam. Imaging studies which can help determine the diagnosis in cases of a deep non-palpable perirectal abscess include pelvic CT scan, MRI or trans-rectal ultrasound. These studies are not necessary, though, in cases which the diagnosis can be made upon physical exam. Classification Anorectal abscesses are classified according to their anatomic location and the following are the most common types: perianal abscess, ischiorectal abscess, intersphincteric abscess and supralevator abscess. Perianal abscess, which represents the most common type of anorectal abscesses accounting for about 60% of reported cases, are superficial collections of purulent material just beneath the skin of the anal canal.Ischiorectal abscess is formed when suppuration transverses the external anal sphincter into the ischiorectal space.Intersphincteric abscess results from suppuration contained between the internal and external anal sphincters.Supralevator abscess forms from cephalad extension of the intersphincteric abscess above the levator ani or from caudal extension of a suppurative abdominal process like appendicitis, diverticular or gynaecologic sepsis. Differential diagnosis This condition is often initially misdiagnosed as hemorrhoids, since this is almost always the cause of any sudden anal discomfort. The presence of the abscess, however, is suspected when the pain quickly worsens over one or two days and usual hemorrhoid treatments are ineffective in bringing relief. Furthermore, any serious abscess will eventually begin to cause signs and symptoms of general infection, including fever and nighttime chills. A physician can rule out a hemorrhoid with a simple visual inspection, and usually appreciate an abscess by touch. Treatment Anal abscesses are rarely treated with a simple course of antibiotics. In almost all cases surgery will need to take place to remove the abscess. Treatment is possible in an emergency department under local anesthesia, but it is highly preferred to be formally admitted to a hospital and to have the surgery performed in an operating room under general anesthesia. Generally speaking, a fairly small but deep incision is performed close to the root of the abscess. The surgeon will allow the abscess to drain its exudate and attempt to discover any other related lesions in the area. This is one of the most basic types of surgery, and is usually performed in less than thirty minutes by the anal surgical team. Generally, a portion of the exudate is sent for microbiological analysis to determine the type of infecting bacteria. The incision is not closed (stitched), as the damaged tissues must heal from the inside toward the skin over a period of time. The affected individual is often sent home within twenty-four hours of the surgery, and may be instructed to perform several sitz baths per day. These involve a small basin which is filled with warm water, and possibly with salts; usually fits over a toilet; and soaks the affected area for a period of time. Another method of recovery involves the use of surgical packing. The initial packing is inserted by the surgical team, with redressing generally performed by hospital staff or a district nurse. During the week following the surgery, many patients will have some form of antibiotic therapy, along with some form of pain management therapy, consistent with the nature of the abscess. It is unclear whether internal packing of the perianal abscess influences time taken for healing, wound pain, development of fistulae, or abscess recurrence.The patient usually experiences an almost complete relief of the severe pain associated to his/her abscess upon waking from anesthesia; the pain associated with the opening and draining incision during the post-operative period is often mild in comparison. Gallery References == External links ==

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Could you please explain the term 'Exanthem' in simple language?

An exanthem is a widespread rash occurring on the outside of the body and usually occurring in children. An exanthem can be caused by toxins, drugs, or microorganisms, or can result from autoimmune disease. The term exanthem is from the Greek ἐξάνθημα, exánthēma, a breaking out. It can be contrasted with enanthems which occur inside the body, such as on mucous membranes. Infectious exanthem In 1905, the Russian-French physician Léon Cheinisse (1871–1924), proposed a numbered classification of the six most common childhood exanthems.Of these six "classical" infectious childhood exanthems, four are viral. Numbers were provided in 1905.The four viral exanthema have much in common, and are often studied together as a class. They are: Scarlet fever, or "second disease", is associated with the bacterium Streptococcus pyogenes. Fourth disease, also known as "Dukes disease" is a condition whose existence is not widely accepted today. It was described in 1900 and is postulated to be related to the bacterium Staphylococcus aureus.In 1979 and 2001 a possible "seventh diease" was postulated following reports of a condition in Japan also referred to as acute febrile infantile mucocutaneous lymph node syndrome (MCLS).Many other common viruses apart from the ones mentioned above can also produce an exanthem as part of their presentation, though they are not considered part of the classic numbered list: Varicella zoster virus (chickenpox or shingles) Mumps rhinovirus (the common cold) unilateral laterothoracic exanthem of childhood Some types of viral haemorrhagic fever are also known to produce a systemic rash of this kind during the progression of the disease. Tick-borne diseases like Rocky Mountain spotted fever produce a rash that may become extensive enough so as to be classified as exanthemous in as many as 90% of children with the disease. See also List of cutaneous conditions References External links Overview at About.com Definition at MedTerms Differential diagnosis Dermatology Quiz Includes photo, diagnosis, and treatment of unilateral laterothoracic exanthem (ULE).

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The term 'Uterine inversion' keeps coming up in medical discussions. What does it stand for?

Uterine inversion is when the uterus turns inside out, usually following childbirth. Symptoms include postpartum bleeding, abdominal pain, a mass in the vagina, and low blood pressure. Rarely inversion may occur not in association with pregnancy.Risk factors include pulling on the umbilical cord or pushing on the top of the uterus before the placenta has detached. Other risk factors include uterine atony, placenta previa, and connective tissue disorders. Diagnosis is by seeing the inside of the uterus either in or coming out of the vagina.Treatment involves standard resuscitation together with replacing the uterus as rapidly as possible. If efforts at manual replacement are not successful surgery is required. After the uterus is replaced oxytocin and antibiotics are typically recommended. The placenta can then be removed if it is still attached.Uterine inversion occurs in about 1 in 2,000 to 1 in 10,000 deliveries. Rates are higher in the developing world. The risk of death of the mother is about 15% while historically it has been as high as 80%. The condition has been described since at least 300 BC by Hippocrates. Signs and symptoms Uterine inversion is often associated with significant postpartum bleeding. Traditionally it was thought that it presented with haemodynamic shock "out of proportion" with blood loss, however blood loss has often been underestimated. The parasympathetic effect of traction on the uterine ligaments may cause bradycardia. Causes The most common cause is the mismanagement of 3rd stage of labor, such as: Fundal pressure Excess cord traction during the 3rd stage of laborOther natural causes can be: Uterine weakness, congenital or not Precipitate delivery Short umbilical cordIt is more common in multiple gestation than in singleton pregnancies. Associations Placenta praevia Fundal Placental Implantation Use of Magnesium Sulfate Vigorous fundal pressure Repeated cord traction short umbilical cord Types One: Complete. Visible outside the cervix. Two: Incomplete. Visible only at the cervix. Treatment Treatment involves standard resuscitation together with replacing the uterus as rapidly as possible. If efforts at manual replacement are not successful surgery is required. After the uterus is replaced oxytocin and antibiotics are typically recommended. The placenta can then be removed if it is still attached. Epidemiology Uterine inversion occurs in about 1 in 2,000 to 1 in 10,000 deliveries. Rates are higher in the developing world. == References ==

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I'd like to learn more about the medical term 'Gastric erosion.' Can you provide some details?

Gastric erosion occurs when the mucous membrane lining the stomach becomes inflamed. Specifically, the term "erosion," in this context means damage that is limited to the mucosa (which consists of three distinct layers: The epithelium (in the case of a healthy stomach, this is non-ciliated simple columnar epithelium), basement membrane, and lamina propria). An erosion is different from an ulcer. An "ulcer" is an area of damage to the gastrointestinal wall (in this case the gastric wall) that extends deeper through the wall than an erosion (an ulcer can extend anywhere from beyond the lamina propria to right through the wall, potentially causing a perforation). See gastrointestinal wall. Some drugs, as tablets, can irritate this mucous membrane, especially drugs taken for arthritis and muscular disorders, steroids, and aspirin. A gastric erosion may also occur because of emotional stress, or as a side effect of burns or stomach injuries. See acute gastritis. Symptoms There is basically one symptom of gastric erosion: bleeding from the area where the stomach lesion is. Bowel movements may contain blood. Vomit may be bloody as well, but a gastric erosion may not cause vomiting. Blood may be black because it will be partially digested. Loss of blood may cause one to develop anemia. Risks Anemia and other problems related to blood loss may occur. Sometimes a person with a gastric erosion will experience severe bleeding all at once; red (bloody) vomiting and/or black bowel movements may occur. Sources "Gastric Erosion." Encyclopædia Britannica, Micropaedia. Encyclopædia Britannica Inc., 1998 ed.

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I'm seeking clarification on the medical term 'Chilblain lupus erythematosus.' Could you explain it?

Chilblain lupus erythematosus is a chronic, unremitting form of lupus erythematosus with the fingertips, rims of ears, calves, and heels affected, especially in women. See also Lupus erythematosus List of cutaneous conditions References == External links ==

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Can you demystify the medical term 'African tick bite fever' for me?

African tick bite fever (ATBF) is a bacterial infection spread by the bite of a tick. Symptoms may include fever, headache, muscle pain, and a rash. At the site of the bite there is typically a red skin sore with a dark center. The onset of symptoms usually occurs 4–10 days after the bite. Complications are rare but may include joint inflammation. Some people do not develop symptoms.Tick bite fever is caused by the bacterium Rickettsia africae. The bacterium is spread by ticks of the Amblyomma type. These generally live in tall grass or bush rather than in cities. The diagnosis is typically based on symptoms. It can be confirmed by culture, PCR, or immunofluorescence.There is no vaccine. Prevention is by avoiding tick bites by covering the skin, using DEET, or using permethrin treated clothing. Evidence regarding treatment, however, is limited. The antibiotic doxycycline appears useful. Chloramphenicol or azithromycin may also be used. The disease will also tend to resolve without treatment.The disease occurs in sub-Saharan Africa, the West Indies, and Oceania. It is relatively common among travelers to sub-Saharan Africa. Most infections occur between November and April. Outbreaks of the disease may occur. The earliest descriptions of the condition are believed to be from 1911. African tick bite fever is a type of spotted fever. It has previously been confused with Mediterranean spotted fever. Signs and symptoms African tick bite fever is often asymptomatic or mild in clinical presentation and complications are rare. The onset of illness is typically 5–7 days after the tick bite, although in some cases it may take up to 10 days for symptoms to occur. Symptoms can persist for several days to up to three weeks. Common presenting symptoms include: Fever Headache Muscle aches Inoculation eschar, which is dead, often black, tissue around a bite site (see photo above) Eschars may or may not be present. Amblyomma ticks actively attack cattle or humans and can bite more than once. In African tick bite fever, unlike what is typically seen with other Rickettsial spotted fevers when only one eschar is identified, multiple eschars may be seen and are considered pathognomonic. Swollen lymph nodes near the site of the bite Maculopapular and/or vesicular rash Complications Complications are rare and are not life-threatening. No deaths due to African tick bite fever have been reported. Reported complications include: Prolonged fever > 3 weeks in duration Reactive arthritis Moderate to severe headache Cause Bacteriology Rickettsia africae is a gram-negative, obligate intracellular, pleomorphic bacterium. It belongs to the genus Rickettsia, which includes many bacterial species that are transmitted to humans by arthropods. Vectors Two species of hard ticks, Amblyoma variegatum and Amblyomma hebraeum are the most common vectors of R. africae. Typically, Amblyomma hebraeum transmits the bacteria in South Africa while Amblyoma variegatum carries R. africae throughout West, Central and East Africa and through the French West Indies. Other species of Amblyomma in sub-Saharan Africa can also transmit R. africae and it may be that up to 100% of Amblyomma ticks in sub-Saharan Africa carry R. africae. Amblyomma ticks are most active from November to April. These tick species frequently feed on cattle and other livestock, but can also be found feeding on wild animals in areas where farm animals are not found. Unlike other hard tick species, which passively seek hosts by clinging to plants and waiting for a potential host to brush by in passing, the Amblyomma hard ticks actively seek out hosts.Groups of tourists visiting Africa have returned to their own countries and were diagnosed there as having been infected.Up until 1998, it was thought that only ticks in sub-Saharan Africa carried R. africae. However, a case of locally transmitted African tick bite fever in the French West Indies led to the discovery of R. africae carried by Amblyomma varigatum ticks introduced through cattle shipped from Senegal to Gaudeluope more than a century ago. R. africae has been isolated from ticks on several Caribbean islands, though the only cases in humans in the Caribbean have occurred in the French West Indies. R. africae has also been found in Amblyomma loculosum ticks in Oceania. Pathogenesis After the rickettsia bacteria infects humans through a tick bite, it invades endothelial cells in the circulatory system (veins, arteries, capillaries). The body then releases chemicals that cause inflammation, resulting in the characteristic symptoms like headache and fever. The hallmark of all rickettsial diseases is a histology (cellular) finding called lymphohistiocytic vasculitis that involves immune cell deposition into the endothelial cells that make up vessels. This occurs secondary to the chemicals mentioned above, as well as damage from the infection, and involves signals to immune cells (T cells and macrophages) to come to the site of the infection.Rickettsia bacteria species like R. africae replicate around the area of the initial tick bite, causing necrosis (cell death) and lymph node inflammation. This is the cause of the characteristic eschar. Diagnosis Many patients with ATBF who live in areas with a high number of infections (Africa and the West Indies) do not visit a doctor, as most patients only have mild symptoms. This disease can, however, cause more serious symptoms in travelers who have never been exposed to the Rickettsia africae bacterium before and are not immune. Travelers who present to a doctor after a trip to affected areas can be hard to diagnose, as many tropical diseases cause a fever similar to that of ATBF. Other diseases that may look similar are malaria, dengue fever, tuberculosis, acute HIV and respiratory infections. In addition to questions about symptoms, doctors will ask patients for an accurate travel history and whether he/she was near animals or ticks. Microbiological tests are available for doctors, but are expensive and often must be done by special laboratories.The antibiotic treatment available for rickettsiae infections has very few side effects, so if a doctor has a high suspicion of the disease, he or she may simply treat without doing more laboratory tests. Blood tests Diagnosis of ATBF is mostly based on symptoms, as many laboratory tests are not specific for ATBF. Common laboratory test signs of ATBF are a low white blood cell count (lymphopenia) and low platelet count (thrombocytopenia), a high C-reactive protein, and mildly high liver function tests. Microbiological tests Biopsies or cultures of a persons tick wound (eschar) are used to diagnose ATBF. However, this requires special culture media and can only be done by a laboratory with biohazard protection. There are more specialized laboratory tests available that use quantitative polymerase chain reactions (qPCR), but can only be done by laboratories with special equipment. Immunofluorescence assays can also be used, but are hard to interpret because of cross-reactions with other rickettsiae bacteria. Prevention Prevention of ATBF centers around protecting oneself from tick bites by wearing long pants and shirt, and using insecticides like DEET on the skin. Travelers to rural areas in Africa and the West Indies should be aware that they may come in contact with ATBF tick vectors. Infection is more likely to occur in people who are traveling to rural areas or plan to spend time participating in outdoor activities. Extra caution should be taken in November - April, when Amblyomma ticks are more active. Inspection of the body, clothing, gear, and any pets after time outdoors can help to identify and remove ticks early. Treatment African tick bite fever is usually mild, and most patients do not need more than at-home treatment with antibiotics for their illness. However, because so few patients with this infection visit a doctor, the best antibiotic choice, dose and length of treatment are not well known. Typically doctors treat this disease with antibiotics that have been used effectively for the treatment of other diseases caused by bacteria of similar species, such as Rocky Mountain Spotted Fever. For mild cases, people are usually treated with one of the following: doxycycline chloramphenicol ciprofloxacinIf a person has more severe symptoms, like a high fever or serious headache, the infection can be treated with doxycycline for a longer amount of time. Pregnant women should not use doxycycline or ciprofloxacin as both antibiotics can cause problems in fetuses. Josamycin has been used effectively for treatment of pregnant women with other rickettsial diseases, but it is unclear if it has a role in the treatment of ATBF. Epidemiology Cases of African tick bite fever have been more frequently reported in the literature among international travelers. Data examining rates in local populations are limited. Among locals who live in endemic areas, exposure at a young age and mild symptoms or lack of symptoms, as well as decreased access to diagnostic tools, may lead to decreased diagnosis. In Zimbabwe, where R. africae is endemic, one study reported an estimated yearly incidence of 60-80 cases per 10,000 patients.Looking at published data over the past 35 years, close to 200 confirmed cases of African tick bite fever in international travelers have been reported. The majority (~80%) of these cases occurred in travelers returning from South Africa. See also Boutonneuse fever Rocky Mountain spotted fever Flea-borne spotted fever References == External links ==

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Could you please explain the term 'Primary familial brain calcification' in simple language?

Primary Indiana familial brain calcification (PFBC), also known as familial idiopathic basal ganglia calcification (FIBGC) and Fahrs disease, is a rare, genetically dominant, inherited neurological disorder characterized by abnormal deposits of calcium in areas of the brain that control movement. Through the use of CT scans, calcifications are seen primarily in the basal ganglia and in other areas such as the cerebral cortex. Signs and symptoms Symptoms of this disease include deterioration of motor functions and speech, seizures, and other involuntary movement. Other symptoms are headaches, dementia, and vision impairment. Characteristics of Parkinsons Disease are also similar to PFBC.The disease usually manifests itself in the third to fifth decade of life but may appear in childhood or later in life. It usually presents with clumsiness, fatigability, unsteady gait, slow or slurred speech, difficulty swallowing, involuntary movements or muscle cramping. Seizures of various types are common. Neuropsychiatric symptoms, which may be the first or the most prominent manifestations, range from mild difficulty with concentration and memory to changes in personality and/or behavior, to psychosis and dementia. Causes This condition can be inherited in an autosomal dominant or recessive fashion. Several genes has been associated with this condition Mutation A locus at 14q has been suggested, but no gene has been identified. A second locus has been identified on chromosome 8 and a third has been reported on chromosome 2. This suggests there may be some genetic heterogeneity in this disease.A mutation in the gene encoding the type III sodium dependent phosphate transporter 2 (SLC20A2) located on chromosome 8 has been reported. Biochemical evidence suggests that phosphate transport may be involved in this disease.Two other genes have been associated with this condition: PDGFB on chromosome 22 and PDGFRB on chromosome 5. These genes are biochemically linked: PDGFRB encodes the platelet-derived growth factor receptor β and PDGFB encodes the ligand of PDGF-Rβ. These genes are active during angiogenesis to recruit pericytes which suggests that alterations in the blood brain barrier may be involved in the pathogenesis of this condition.A fourth gene associated with this condition is XPR1. This gene is the long arm of located on chromosome 1 (1q25.3).Another gene that has been associated with this condition is MYORG. This gene is located on the long arm of chromosome 9 (9p13.3). This gene is associated with an autosomal recessive inheritance pattern in this condition.Another gene junctional adhesion molecule 2 (JAM2) has been associated with an autosomal recessive form of this condition. Other genes that have been associated with this condition are Junctional adhesion molecule C (JAM3) and Occludin (OCLN). Pathology The most commonly affected region of the brain is the lenticular nucleus and in particular the internal globus pallidus. Calcifications in the caudate, dentate nuclei, putamen and thalami are also common. Occasionally calcifications begin or predominate in regions outside the basal ganglia.Calcification seems to be progressive, since calcifications are generally more extensive in older individuals and an increase in calcification can sometimes be documented on follow up of affected subjects.As well as the usual sites the cerebellar gyri, brain stem, centrum semiovale and subcortical white matter may also be affected. Diffuse atrophic changes with dilatation of the subarachnoid space and/or ventricular system may coexist with the calcifications. Histologically concentric calcium deposits within the walls of small and medium-sized arteries are present. Less frequently the veins may also be affected. Droplet calcifications can be observed along capillaries. These deposits may eventually lead to closure of the lumina of vessels.The pallidal deposits stain positively for iron. Diffuse gliosis may surround the large deposits but significant loss of nerve cells is rare. On electron microscopy the mineral deposits appear as amorphous or crystalline material surrounded by a basal membrane. Calcium granules are seen within the cytoplasm of neuronal and glial cells. The calcifications seen in this condition are indistinguishable from those secondary to hypoparathyroidism or other causes. Diagnosis In addition to the usual routine haematologic and biochemical investigations, the serum calcium, phosphorus, magnesium, alkaline phosphatase, calcitonin and parathyroid hormone should also be measured. The cerebrospinal fluid (CSF) should be examined to exclude bacteria, viruses and parasites. The Ellsworth Howard test (a 10-20 fold increase of urinary cyclic AMP excretion following stimulation with 200 micromoles of parathyroid hormone) may be worth doing also. Serology for toxoplasmosis is also indicated. Brain CT scan is the preferred method of localizing and assessing the extent of cerebral calcifications.Elevated levels of copper, iron, magnesium and zinc but not calcium have been reported in the CSF but the significance of this finding — if any — is not known.The diagnosis requires the following criteria be met: the presence of bilateral calcification of the basal ganglia the presence of progressive neurologic dysfunction the absence of an alternative metabolic, infectious, toxic or traumatic cause a family history consistent with autosomal dominant inheritanceThe calcification is usually identified on CT scan but may be visible on plain films of the skull. Differential diagnosis Basal ganglia calcification may occur as a consequence of several other known genetic conditions and these have to be excluded before a diagnosis can be made. Management There is currently no cure for PFBC nor a standard course of treatment. The available treatment is directed symptomatic control. If parkinsonian features develop, there is generally poor response to levodopa therapy. Case reports have suggested that haloperidol or lithium carbonate may help with psychotic symptoms. One case report described an improvement with the use of a bisphosphonate. Prognosis The prognosis for any individual with PFBC is variable and hard to predict. There is no reliable correlation between age, extent of calcium deposits in the brain, and neurological deficit. Since the appearance of calcification is age-dependent, a CT scan could be negative in a gene carrier who is younger than the age of 55.Progressive neurological deterioration generally results in disability and death. History The disease was first noted by German pathologist Karl Theodor Fahr in 1930. A less common name for the condition is Chavany-Brunhes syndrome and Fritsches syndrome, the former named after Jacques Brunhes, Jean Alfred Émile Chavany, while the later named after R. Fritsche.Fewer than 20 families had been reported in the literature up to 1997. In literature Fahrs syndrome features in Norwegian Jo Nesbøs crime fiction novel "The Snowman" (the seventh novel in the Harry Hole detective series). See also Primrose syndrome References External links Fahr Syndrome Images (MedPix) National Organization for Rare Disorders (NORD) National Institute on Aging (NIA) National Institute of Mental Health (NIMH)

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I'm seeking clarification on the medical term 'Bartholins cyst.' Could you explain it?

A Bartholins cyst occurs when a Bartholins gland within the labia becomes blocked. Small cysts may result in minimal or no symptoms. Larger cysts may result in swelling on one side of the vagina, as well as pain during sex or walking. If the cyst becomes infected, an abscess can occur, which is typically red and very painful. If there are no symptoms, no treatment is needed. Bartholins cysts affect about 2% of women at some point in their life. They most commonly occur during childbearing years.When the cyst becomes uncomfortable or painful, drainage is recommended. The preferred method is the insertion of a Word catheter for four weeks, as recurrence following simple incision and drainage is common. A surgical procedure known as marsupialization may be used or, if the problems persist, the entire gland may be removed. Removal is sometimes recommended in those older than 40 to ensure cancer is not present. Antibiotics are not generally needed to treat a Bartholins cyst.The cause of a Bartholins cyst is unknown. An abscess results from a bacterial infection, but it is not usually a sexually transmitted infection (STI). Rarely, gonorrhea may be involved. Diagnosis is typically based on symptoms and examination. In women over the age of 40, a tissue biopsy is often recommended to rule out cancer.The cyst is named after Caspar Bartholin who accurately described the glands in 1677. The underlying mechanism of the cyst was determined in 1967 by 20th Century obstetrician Samuel Buford Word. Signs and symptoms Most Bartholins cysts do not cause any symptoms, although some may cause pain during walking, sitting, or sexual intercourse (dyspareunia). They are usually between 1 and 4 cm, and are located just medial to the labia minora. Most Bartholins cysts only affect the left or the right side (unilateral). While small cysts are usually not painful, larger cysts can cause significant pain. Pathophysiology A Bartholins gland cyst develops when the duct that drains the gland becomes blocked. Blockage may be caused by an infection or a mucus plug. The secretions from the Bartholins gland are retained, forming a cyst. Diagnosis Other conditions that may present similarly include hidradenoma papilliferum, lipomas, epidermoid cysts and Skenes duct cysts, among others conditions. In women who are more than 40 years, a biopsy may be recommended to rule out cancer. Treatment If the Bartholins cysts is not painful or uncomfortable, treatment may not be necessary. Small, asymptomatic cysts can be observed over time to assess their development. In cases that require intervention, a catheter may be placed to drain the cyst, or the cyst may be surgically opened to create a permanent pouch (marsupialization). Intervention has a success rate of 85%, regardless of the method used, to alleviate swelling and discomfort.Catheterization is a minor procedure that can be performed locally as an outpatient procedure. A small tube with a balloon on the end (known as a Word catheter) may be inserted into the cyst. The balloon is then inflated to keep it in place. The catheter stays in place for 2 to 4 weeks, draining the fluid and causing a normal gland opening to form, after which the catheter is removed. The catheters do not generally impede normal activity, but sexual intercourse is generally abstained from while the catheter is in place.Cysts may also be opened permanently, a procedure called marsupialization, which involves opening the gland through an incision to ensure that the secretion channel remains open. If a cyst is infected, it may break open and start to heal on its own after 3 to 4 days. Nonprescription pain medication such as ibuprofen relieves pain, and a sitz bath may increase comfort and reduce pain. Warm compresses can also speed up healing. If a Bartholin gland abscess comes back several times, the gland and duct can be surgically removed. Prognosis While Bartholin cysts can be quite painful, they are not life-threatening. New cysts cannot absolutely be prevented from forming, but surgical or laser removal of a cyst makes it less likely that a new one will form at the same site. Those with a cyst are more likely than those without a cyst to get one in the future. They can recur every few years or more frequently. Many women who have marsupialization done find that the recurrences may slow, but do not actually stop. Epidemiology Two percent of women will have a Bartholins gland cyst at some point in their lives. They occur at a rate of 0.55 per 1000 person-years and in women aged 35–50 years at a rate of 1.21 per 1000 person-years. The incidence of Bartholin duct cysts increases with age until menopause, and decreases thereafter. Hispanic women may be more often affected than white women and black women. The risk of developing a Bartholins gland cyst increases with the number of childbirths. References == External links ==

You are a medical advisor. Your role is to break down medical terminology into clear, detailed explanations for a general audience.

Please help me grasp the concept behind the medical term 'Foix–Alajouanine syndrome.'

Foix–Alajouanine syndrome, also called subacute ascending necrotizing myelitis, is a disease caused by an arteriovenous malformation of the spinal cord. In particular, most cases involve dural arteriovenous malformations that present in the lower thoracic or lumbar spinal cord. The condition is named after Charles Foix and Théophile Alajouanine who first described the condition in 1926. Signs and symptoms The patients can present with symptoms indicating spinal cord involvement such as (paralysis of arms and legs, numbness and loss of sensation and sphincter dysfunction), and pathological examination reveals disseminated nerve cell death in the spinal cord. Diagnosis Clinically, the patient may present with neurological symptoms such as numbness, weakness, loss of reflexes, or even sudden or progressive paralysis. The affected portion of the body will correlate to where the lesion lies within the spinal cord. The disease typically has an insidious onset, but symptoms may manifest suddenly. A thorough physical exam may lead a physician toward targeted imaging, with MRI being the most appropriate imaging modality for initial diagnosis. A spinal MRA will serve as a superior imaging technique to visualize the extent of the arteriovenous malformation within the cord and may be especially useful if surgical treatment is attempted. Treatment Surgical treatment may be attempted with endovascular embolization or ligation of the arteriovenous malformation within the spinal cord.Corticosteroids may be used acutely to help slow the progression of symptoms or they may be used chronically in a poor surgical candidate. In either case, physical therapy will be an important part of the recovery process in helping the patient regain strength and coordination. See also Vascular myelopathy References External links synd/1526 at Who Named It? synd/1755 at Who Named It?

You function as a medical explainer. Your task is to convey the meanings of medical terms in a detailed, yet easy-to-understand manner.

I'm trying to expand my medical knowledge. Can you elucidate the term 'Familial hypercholesterolemia'?

Familial hypercholesterolemia (FH) is a genetic disorder characterized by high cholesterol levels, specifically very high levels of low-density lipoprotein (LDL cholesterol), in the blood and early cardiovascular disease. The most common mutations diminish the number of functional LDL receptors in the liver. Since the underlying body biochemistry is slightly different in individuals with FH, their high cholesterol levels are less responsive to the kinds of cholesterol control methods which are usually more effective in people without FH (such as dietary modification and statin tablets). Nevertheless, treatment (including higher statin doses) is usually effective. FH is classified as a type 2 familial dyslipidemia. There are five types of familial dyslipidemia (not including subtypes), and each are classified from both the altered lipid profile and by the genetic abnormality. For example, high LDL (often due to LDL receptor defect) is type 2. Others include defects in chylomicron metabolism, triglyceride metabolism, and metabolism of other cholesterol-containing particles, such as VLDL and IDL. About 1 in 100 to 200 people have mutations in the LDLR gene that encodes the LDL receptor protein, which normally removes LDL from the circulation, or apolipoprotein B (ApoB), which is the part of LDL that binds with the receptor; mutations in other genes are rare. People who have one abnormal copy (are heterozygous) of the LDLR gene may develop cardiovascular disease prematurely at the age of 30 to 40. Having two abnormal copies (being homozygous) may cause severe cardiovascular disease in childhood. Heterozygous FH is a common genetic disorder, inherited in an autosomal dominant pattern, occurring in 1:250 people in most countries; homozygous FH is much rarer, occurring in 1 in 300,000 people.Heterozygous FH is normally treated with statins, bile acid sequestrants, or other lipid-lowering agents that lower cholesterol levels. New cases are generally offered genetic counseling. Homozygous FH often does not respond to medical therapy and may require other treatments, including LDL apheresis (removal of LDL in a method similar to dialysis) and occasionally liver transplantation. Signs and symptoms Physical signs High cholesterol levels normally do not cause any symptoms. Yellow deposits of cholesterol-rich fat may be seen in various places on the body such as around the eyelids (known as xanthelasma palpebrarum), the outer margin of the iris (known as arcus senilis corneae), and in the tendons of the hands, elbows, knees and feet, particularly the Achilles tendon (known as a tendon xanthoma). Cardiovascular disease Accelerated deposition of cholesterol in the walls of arteries leads to atherosclerosis, the underlying cause of cardiovascular disease. The most common problem in FH is the development of coronary artery disease (atherosclerosis of the coronary arteries that supply the heart) at a much younger age than would be expected in the general population. This may lead to angina pectoris (chest pain or tightness on exertion) or heart attacks. Less commonly, arteries of the brain are affected; this may lead to transient ischemic attacks (brief episodes of weakness on one side of the body or inability to talk) or occasionally stroke. Peripheral artery occlusive disease (obstruction of the arteries of the legs) occurs mainly in people with FH who smoke; this can cause pain in the calf muscles during walking that resolves with rest (intermittent claudication) and problems due to a decreased blood supply to the feet (such as gangrene). Atherosclerosis risk is increased further with age and in those who smoke, have diabetes, high blood pressure and a family history of cardiovascular disease. Diagnosis Approximately 85% of individuals with this disorder have not been diagnosed and consequently are not receiving lipid-lowering treatments. Physical examination findings can help a physician make the diagnosis of FH. Tendon xanthomas are seen in 20-40% of individuals with FH and are pathognomonic for the condition. A xanthelasma or corneal arcus may also be seen. These common signs are supportive of the diagnosis, but are non-specific findings. Lipid measurements Cholesterol levels may be determined as part of health screening for health insurance or occupational health, when the external physical signs such as xanthelasma, xanthoma, arcus are noticed, symptoms of cardiovascular disease develop, or a family member has been found to have FH. A pattern compatible with hyperlipoproteinemia type IIa on the Fredrickson classification is typically found: raised level of total cholesterol, markedly raised level of low-density lipoprotein (LDL), normal level of high-density lipoprotein (HDL), and normal level of triglycerides. Total cholesterol levels of 350–550 mg/dL are typical of heterozygous FH while total cholesterol levels of 650–1000 mg/dL are typical of homozygous FH. The LDL is typically above the 75th percentile, that is, 75% of the healthy population would have a lower LDL level. Cholesterol levels can be drastically higher in people with FH who are also obese. Mutation analysis On the basis of the isolated high LDL and clinical criteria (which differ by country), genetic testing for LDL receptor mutations and ApoB mutations can be performed. Mutations are detected in between 50 and 80% of cases; those without a mutation often have higher triglyceride levels and may in fact have other causes for their high cholesterol, such as combined hyperlipidemia due to metabolic syndrome. Differential diagnosis FH needs to be distinguished from familial combined hyperlipidemia and polygenic hypercholesterolemia. Lipid levels and the presence of xanthomata can confirm the diagnosis. Sitosterolemia and cerebrotendineous xanthomatosis are two rare conditions that can also present with premature atherosclerosis and xanthomas. The latter condition can also involve neurological or psychiatric manifestations, cataracts, diarrhea and skeletal abnormalities. Genetics The most common genetic defects in FH are LDLR mutations (prevalence 1 in 250, depending on the population), ApoB mutations (prevalence 1 in 1000), PCSK9 mutations (less than 1 in 2500) and LDLRAP1. The related disease sitosterolemia, which has many similarities with FH and also features cholesterol accumulation in tissues, is due to ABCG5 and ABCG8 mutations. LDL receptor The LDL receptor gene is located on the short arm of chromosome 19 (19p13.1-13.3). It comprises 18 exons and spans 45 kb, and the protein gene product contains 839 amino acids in mature form. A single abnormal copy (heterozygote) of FH causes cardiovascular disease by the age of 50 in about 40% of cases. Having two abnormal copies (homozygote) causes accelerated atherosclerosis in childhood, including its complications. The plasma LDL levels are inversely related to the activity of LDL receptor (LDLR). Homozygotes have LDLR activity of less than 2%, while heterozygotes have defective LDL processing with receptor activity being 2–25%, depending on the nature of the mutation. Over 1000 different mutations are known.There are five major classes of FH due to LDLR mutations: Class I: LDLR is not synthesized at all. Class II: LDLR is not properly transported from the endoplasmic reticulum to the Golgi apparatus for expression on the cell surface. Class III: LDLR does not properly bind LDL on the cell surface because of a defect in either apolipoprotein B100 (R3500Q) or in LDL-R. Class IV: LDLR bound to LDL does not properly cluster in clathrin-coated pits for receptor-mediated endocytosis (pathway step 2). Class V: LDLR is not recycled back to the cell surface (pathway step 5). Apolipoprotein B Apolipoprotein B, in its ApoB100 form, is the main apolipoprotein, or protein part of the lipoprotein particle. Its gene is located on the second chromosome (2p24-p23) and is 46.2 kb long. FH is often associated with the mutation of R3500Q, which causes replacement of arginine by glutamine at position 3500. The mutation is located on a part of the protein that normally binds with the LDL receptor, and binding is reduced as a result of the mutation. Like LDLR, the number of abnormal copies determines the severity of the hypercholesterolemia. PCSK9 Mutations in the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene were linked to autosomal dominant (i.e. requiring only one abnormal copy) FH in a 2003 report. The gene is located on the first chromosome (1p34.1-p32) and encodes a 666 amino acid protein that is expressed in the liver. It has been suggested that PCSK9 causes FH mainly by reducing the number of LDL receptors on liver cells. LDLRAP1 Abnormalities in the ARH gene, also known as LDLRAP1, were first reported in a family in 1973. In contrast to the other causes, two abnormal copies of the gene are required for FH to develop (autosomal recessive). The mutations in the protein tend to cause the production of a shortened protein. Its real function is unclear, but it seems to play a role in the relation between the LDL receptor and clathrin-coated pits. People with autosomal recessive hypercholesterolemia tend to have more severe disease than LDLR-heterozygotes but less severe than LDLR-homozygotes. Pathophysiology LDL cholesterol normally circulates in the body for 2.5 days, and subsequently the apolipoprotein B portion of LDL cholesterol binds to the LDL receptor on the liver cells, triggering its uptake and digestion. This process results in the removal of LDL from the circulatory system. Synthesis of cholesterol by the liver is suppressed in the HMG-CoA reductase pathway. In FH, LDL receptor function is reduced or absent, and LDL circulates for an average duration of 4.5 days, resulting in significantly increased level of LDL cholesterol in the blood with normal levels of other lipoproteins. In mutations of ApoB, reduced binding of LDL particles to the receptor causes the increased level of LDL cholesterol. It is not known how the mutation causes LDL receptor dysfunction in mutations of PCSK9 and ARH.Although atherosclerosis occurs to a certain degree in all people, people with FH may develop accelerated atherosclerosis due to the excess level of LDL. The degree of atherosclerosis approximately depends on the number of LDL receptors still expressed and the functionality of these receptors. In many heterozygous forms of FH, the receptor function is only mildly impaired, and LDL levels will remain relatively low. In the more serious homozygous forms, the receptor is not expressed at all.Some studies of FH cohorts suggest that additional risk factors are generally at play when a person develops atherosclerosis. In addition to the classic risk factors such as smoking, high blood pressure, and diabetes, genetic studies have shown that a common abnormality in the prothrombin gene (G20210A) increases the risk of cardiovascular events in people with FH. Several studies found that a high level of lipoprotein(a) was an additional risk factor for ischemic heart disease. The risk was also found to be higher in people with a specific genotype of the angiotensin-converting enzyme (ACE). Screening Cholesterol screening and genetic testing among family members of people with known FH is cost-effective. Other strategies such as universal screening at the age of 16 were suggested in 2001. The latter approach may however be less cost-effective in the short term. Screening at an age lower than 16 was thought likely to lead to an unacceptably high rate of false positives.A 2007 meta-analysis found that "the proposed strategy of screening children and parents for familial hypercholesterolaemia could have considerable impact in preventing the medical consequences of this disorder in two generations simultaneously." "The use of total cholesterol alone may best discriminate between people with and without FH between the ages of 1 to 9 years."Screening of toddlers has been suggested, and results of a trial on 10,000 one-year-olds were published in 2016. Work was needed to find whether screening was cost-effective, and acceptable to families. Genetic counseling can help assist in genetic testing following a positive cholesterol screen for FH. Treatment Heterozygous FH FH is usually treated with statins. Statins act by inhibiting the enzyme hydroxymethylglutaryl CoA reductase (HMG-CoA-reductase) in the liver. In response, the liver produces more LDL receptors, which remove circulating LDL from the blood. Statins effectively lower cholesterol and LDL levels, although sometimes add-on therapy with other drugs is required, such as bile acid sequestrants (cholestyramine or colestipol), nicotinic acid preparations or fibrates. Control of other risk factors for cardiovascular disease is required, as risk remains somewhat elevated even when cholesterol levels are controlled. Professional guidelines recommend that the decision to treat a person with FH with statins should not be based on the usual risk prediction tools (such as those derived from the Framingham Heart Study), as they are likely to underestimate the risk of cardiovascular disease; unlike the rest of the population, FH have had high levels of cholesterol since birth, probably increasing their relative risk. Prior to the introduction of the statins, clofibrate (an older fibrate that often caused gallstones), probucol (especially in large xanthomas) and thyroxine were used to reduce LDL cholesterol levels. More controversial is the addition of ezetimibe, which inhibits cholesterol absorption in the gut. While it reduces LDL cholesterol, it does not appear to improve a marker of atherosclerosis called the intima-media thickness. Whether this means that ezetimibe is of no overall benefit in FH is unknown.There are no interventional studies that directly show mortality benefit of cholesterol lowering in FH. Rather, evidence of benefit is derived from a number of trials conducted in people who have polygenic hypercholesterolemia (in which heredity plays a smaller role). Still, a 1999 observational study of a large British registry showed that mortality in people with FH had started to improve in the early 1990s when statins were introduced.A cohort study suggested that treatment of FH with statins leads to a 48% reduction in death from coronary heart disease to a point where people are no more likely to die of coronary heart disease than the general population. However, if the person already had coronary heart disease the reduction was 25%. The results emphasize the importance of early identification of FH and treatment with statins.Alirocumab and evolocumab, both monoclonal antibodies against PCSK9, are specifically indicated as adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia, who require additional lowering of LDL cholesterol.More recently Inclisiran has been approved for the treatment of HeFH Homozygous FH Homozygous FH is harder to treat. The LDL (Low Density Lipoprotein) receptors are minimally functional, if at all. Only high doses of statins, often in combination with other medications, are modestly effective in improving lipid levels. If medical therapy is not successful at reducing cholesterol levels, LDL apheresis may be used; this filters LDL from the bloodstream in a process reminiscent of dialysis. Very severe cases may be considered for a liver transplant; this provides a liver with normally functional LDL receptors, and leads to rapid improvement of the cholesterol levels, but at the risk of complications from any solid organ transplant (such as rejection, infections, or side-effects of the medication required to suppress rejection). Other surgical techniques include partial ileal bypass surgery, in which part of the small bowel is bypassed to decrease the absorption of nutrients and hence cholesterol, and portacaval shunt surgery, in which the portal vein is connected to the vena cava to allow blood with nutrients from the intestine to bypass the liver.Lomitapide, an inhibitor of the microsomal triglyceride transfer protein, was approved by the US FDA in December 2012 as an orphan drug for the treatment of homozygous familial hypercholesterolemia. In January 2013, The US FDA also approved mipomersen, which inhibits the action of the gene apolipoprotein B, for the treatment of homozygous familial hypercholesterolemia. Gene therapy is a possible future alternative.Evinacumab, a monoclonal antibody inhibiting angiopoietin-like protein 3, was approved in 2021 for adjunct therapy. Children Given that FH is present from birth and atherosclerotic changes may begin early in life, it is sometimes necessary to treat adolescents or even teenagers with agents that were originally developed for adults. Due to safety concerns, many physicians prefer to use bile acid sequestrants and fenofibrate as these are licensed in children. Nevertheless, statins seem safe and effective, and in older children may be used as in adults.An expert panel in 2006 advised on early combination therapy with LDL apheresis, statins, and cholesterol absorption inhibitors in children with homozygous FH at the highest risk. Epidemiology The global prevalence of FH is approximately 10 million people. In most populations studied, heterozygous FH occurs in about 1:250 people, but not all develop symptoms. Homozygous FH occurs in about 1:1,000,000.LDLR mutations are more common in certain populations, presumably because of a genetic phenomenon known as the founder effect—they were founded by a small group of individuals, one or several of whom was a carrier of the mutation. The Afrikaner, French Canadians, Lebanese Christians, and Finns have high rates of specific mutations that make FH particularly common in these groups. APOB mutations are more common in Central Europe. History The Norwegian physician Dr Carl Müller first associated the physical signs, high cholesterol levels and autosomal dominant inheritance in 1938. In the early 1970s and 1980s, the genetic cause for FH was described by Dr Joseph L. Goldstein and Dr Michael S. Brown of Dallas, Texas. Initially, they found increased activity of HMG-CoA reductase, but studies showed that this did not explain the very abnormal cholesterol levels in people with FH. The focus shifted to the binding of LDL to its receptor, and effects of impaired binding on metabolism; this proved to be the underlying mechanism for FH. Subsequently, numerous mutations in the protein were directly identified by sequencing. They later won the 1985 Nobel Prize in Medicine for their discovery of the LDL receptor and its impact on lipoprotein metabolism. See also Primary hyperlipoproteinemia Familial hypertriglyceridemia Lipoprotein lipase deficiency Familial apoprotein CII deficiency Akira Endo, discoverer of the first statin References External links MedicinePlus: Familial Hypercholesterolemia

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I'd like to learn more about the medical term 'Trichilemmal cyst.' Can you provide some details?

A trichilemmal cyst is a common cyst that forms from a hair follicle, most often on the scalp, and is smooth, mobile, and filled with keratin, a protein component found in hair, nails, skin, and horns. Trichilemmal cysts are clinically and histologically distinct from trichilemmal horns, hard tissue that is much rarer and not limited to the scalp. Rarely, these cysts may grow more extensively and form rapidly multiplying trichilemmal tumors, also called proliferating trichilemmal cysts, which are benign, but may grow aggressively at the cyst site. Very rarely, trichilemmal cysts can become cancerous. Classification Trichilemmal cysts may be classified as sebaceous cysts, although technically speaking are not sebaceous. "True" sebaceous cysts, which originate from sebaceous glands and which contain sebum, are relatively rare and are known as steatocystoma simplex or, if multiple, as steatocystoma multiplex. Medical professionals have suggested that the term "sebaceous cyst" be avoided since it can be misleading.: 31  In practice, however, the term is still often used for epidermoid and pilar cysts. Pathogenesis Trichilemmal cysts are derived from the outer root sheath of the hair follicle. Their origin is currently unknown, but they may be produced by budding from the external root sheath as a genetically determined structural aberration. They arise preferentially in areas of high hair follicle concentrations, so 90% of cases occur on the scalp. They are solitary in 30% and multiple in 70% of cases.Histologically, they are lined by stratified squamous epithelium that lacks a granular cell layer and are filled with compact "wet" keratin. Areas consistent with proliferation can be found in some cysts. In rare cases, this leads to formation of a tumor, known as a proliferating trichilemmal cyst. The tumor is clinically benign, although it may display nuclear atypia, dyskeratotic cells, and mitotic figures. These features can be misleading, and a diagnosis of squamous cell carcinoma may be mistakenly rendered. Treatment Surgical excision is required to treat a trichilemmal cyst. The method of treatment varies depending on the physicians training. Most physicians perform the procedure under local anesthetic. Others prefer a more conservative approach. This involves the use of a small punch biopsy about one-fourth the diameter of the cyst. The punch biopsy is used to enter the cyst cavity. The contents of the cyst are emptied, leaving an empty sac. As the pilar cyst wall is the thickest and most durable of the many varieties of cysts, it can be grabbed with forceps and pulled out of the small incision. This method is best performed on cysts larger than a pea that have formed a thick enough wall to be easily identified after the sac is emptied. Small cysts have thin walls, so are easily fragmented on traction. This increases the likelihood of cyst recurrence. This method often results in only a small scar, and very little if any bleeding. See also Proliferating epidermoid cyst List of cutaneous conditions References == External links ==

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

I'm curious about the meaning of the medical term 'Cadmium poisoning.' Can you give me some insights?

Cadmium is a naturally occurring toxic metal with common exposure in industrial workplaces, plant soils, and from smoking. Due to its low permissible exposure in humans, overexposure may occur even in situations where trace quantities of cadmium are found. Cadmium is used extensively in electroplating, although the nature of the operation does not generally lead to overexposure. Cadmium is also found in some industrial paints and may represent a hazard when sprayed. Operations involving removal of cadmium paints by scraping or blasting may pose a significant hazard. The primary use of cadmium is in the manufacturing of NiCd rechargeable batteries. The primary source for cadmium is as a byproduct of refining zinc metal. Exposures to cadmium are addressed in specific standards for the general industry, shipyard employment, the construction industry, and the agricultural industry. Signs and symptoms Acute Acute exposure to cadmium fumes may cause flu-like symptoms including chills, fever, and muscle ache sometimes referred to as "the cadmium blues." Symptoms may resolve after a week if there is no respiratory damage. More severe exposures can cause tracheobronchitis, pneumonitis, and pulmonary edema. Symptoms of inflammation may start hours after the exposure and include cough, dryness and irritation of the nose and throat, headache, dizziness, weakness, fever, chills, and chest pain. Chronic Complications of cadmium poisoning include cough, anemia, and kidney failure (possibly leading to death). Cadmium exposure increases ones chances of developing cancer. Similar to zinc, long-term exposure to cadmium fumes can cause life long anosmia. Bone and joints One of the main effects of cadmium poisoning is weak and brittle bones. The bones become soft (osteomalacia), lose bone mineral density (osteoporosis), and become weaker. This results in joint and back pain, and increases the risk of fractures. Spinal and leg pain is common, and a waddling gait often develops due to bone deformities caused by the long-term cadmium exposure. The pain eventually becomes debilitating, with fractures becoming more common as the bone weakens. Permanent deformation in bones can occur. In extreme cases of cadmium poisoning, more body weight causes a fracture. Renal The kidney damage inflicted by cadmium poisoning is irreversible. The kidneys can shrink up to 30 percent. The kidneys lose their function to remove acids from the blood in proximal renal tubular dysfunction. The proximal renal tubular dysfunction causes hypophosphatemia, leading to muscle weakness and sometimes coma. Hyperchloremia also occurs. Kidney dysfunction also causes gout, a form of arthritis due to the accumulation of uric acid crystals in the joints because of high acidity of the blood (hyperuricemia). Cadmium exposure is also associated with the development of kidney stones. Sources of exposure Smoking is a significant source of cadmium exposure. Even small amounts of cadmium from smoking are highly toxic to humans, as the lungs absorb cadmium more efficiently than the stomach. Cadmium is emitted to the electronic cigarette (EC) aerosol but, on currently available data, the lifetime cancer risk (LCR) calculated doesn’t exceed the acceptable risk limit. Environmental Buildup of cadmium levels in the water, air, and soil has been occurring particularly in industrial areas. Environmental exposure to cadmium has been particularly problematic in Japan where many people have consumed rice that was grown in cadmium-contaminated irrigation water. This phenomenon is known as itai-itai disease.People who live near hazardous waste sites or factories that release cadmium into the air have the potential for exposure to cadmium in air. However, numerous state and federal regulations in the United States control the amount of cadmium that can be released to the air from waste sites and incinerators so that properly regulated sites are not hazardous. The general population and people living near hazardous waste sites may be exposed to cadmium in contaminated food, dust, or water from unregulated or accidental releases. Numerous regulations and use of pollution controls are enforced to prevent such releases.Some sources of phosphate in fertilizers contain cadmium in amounts of up to 100 mg/kg, which can lead to an increase in the concentration of cadmium in soil (for example in New Zealand). Cadmium can be removed from soil using nanopolymers. Food Food is another source of cadmium. Plants may contain small or moderate amounts in non-industrial areas, but high levels may be found in the liver and kidneys of adult animals. The daily intake of cadmium through food varies by geographic region. Intake is reported to be approximately 8 to 30μg in Europe and the United States versus 59 to 113 μg in various areas of Japan. Occupational exposure In the 1950s and 1960s industrial exposure to cadmium was high, but as the toxic effects of cadmium became apparent, industrial limits on cadmium exposure have been reduced in most industrialized nations and many policy makers agree on the need to reduce exposure further. While working with cadmium it is important to do so under a fume hood to protect against dangerous fumes. Brazing fillers which contain cadmium should be handled with care. Serious toxicity problems have resulted from long-term exposure to cadmium plating baths. Workers can be exposed to cadmium in air from the smelting and refining of metals, or from the air in plants that make cadmium products such as batteries, coatings, or plastics. Workers can also be exposed when soldering or welding metal that contains cadmium. Approximately 512,000 workers in the United States are in environments each year where cadmium exposure may occur. Regulations that set permissible levels of exposure, however, are enforced to protect workers and to make sure that levels of cadmium in the air are considerably below levels thought to result in harmful effects.Artists who work with cadmium pigments, which are commonly used in strong oranges, reds, and yellows, can easily accidentally ingest dangerous amounts, particularly if they use the pigments in dry form, as with chalk pastels, or in mixing their own paints. Consumer products Cadmium is used in nickel-cadmium batteries; these are some of the most popular and most common cadmium-based products. In February 2010, cadmium was found in an entire line of Wal-Mart exclusive Miley Cyrus jewelry. The charms were tested at the behest of the Associated Press and were found to contain high levels of cadmium. Wal-Mart did not stop selling the jewelry until May 12 because "it would be too difficult to test products already on its shelves". On June 4 cadmium was detected in the paint used on promotional drinking glasses for the movie Shrek Forever After, sold by McDonalds Restaurants, triggering a recall of 12 million glasses. Toxicology Cadmium is an extremely toxic industrial and environmental pollutant classified as a human carcinogen: Group 1, according to the International Agency for Research on Cancer; Group 2a, according to Environmental Protection Agency (EPA); and a 1B carcinogen as classified by European Chemical Agency. Toxicodynamics Cellular toxicology Inside cells, cadmium ions act as a catalytic hydrogen peroxide generator. This sudden surge of cytosolic hydrogen peroxide causes increased lipid peroxidation and additionally depletes ascorbate and glutathione stores. Hydrogen peroxide can also convert thiol groups on proteins into nonfunctional sulfonic acids and is also capable of directly attacking nuclear DNA. This oxidative stress causes the afflicted cell to manufacture large amounts of inflammatory cytokines. Toxicokinetics Inhaling cadmium-laden dust quickly leads to respiratory tract and kidney problems which can be fatal (often from kidney failure). Ingestion of any significant amount of cadmium causes immediate poisoning and damage to the liver and the kidneys. Compounds containing cadmium are also carcinogenic. Diagnosis Biomarkers of excessive exposure Increased concentrations of urinary beta-2 microglobulin can be an early indicator of kidney dysfunction in persons chronically exposed to low but excessive levels of environmental cadmium. The urinary beta-2 microglobulin test is an indirect method of measuring cadmium exposure. Under some circumstances, the Occupational Health and Safety Administration requires screening for kidney damage in workers with long-term exposure to high levels of cadmium. Blood or urine cadmium concentrations provide a better index of excessive exposure in industrial situations or following acute poisoning, whereas organ tissue (lung, liver, kidney) cadmium concentrations may be useful in fatalities resulting from either acute or chronic poisoning. Cadmium concentrations in healthy persons without excessive cadmium exposure are generally less than 1 μg/L in either blood or urine. The ACGIH biological exposure indices for blood and urine cadmium levels are 5 μg/L and 5 μg/g creatinine, respectively, in random specimens. Persons who have sustained kidney damage due to chronic cadmium exposure often have blood or urine cadmium levels in a range of 25-50 μg/L or 25-75 μg/g creatinine, respectively. These ranges are usually 1000-3000 μg/L and 100-400 μg/g, respectively, in survivors of acute poisoning and may be substantially higher in fatal cases. Treatment Any person with cadmium poisoning must seek immediate medical attention. For a single exposure by ingestion, gastric decontamination by emesis or gastric lavage may be beneficial soon after exposure. Administration of activated charcoal has not been proven effective.Chelation therapies to remove cadmium are not effective, so the most important action is to prevent additional exposure. Detoxification of Cadmium (Cd) with EDTA and other chelators is possible. Clinically available chelators include EDTA, DMPS, DMSA, and British Anti-Lewisite (BAL). BAL is more toxic than its derivatives, DMPS and DMSA, and is seldom used clinically. EDTA, DMPS, and DMSA increase urinary excretion of Cd. Studies in vitro and in vivo suggest that EDTA is superior to DMSA in mobilizing intracellular Cd. As EDTA is approved by the FDA for lead and other heavy metals, and has a long history of safe use, it is most widely accepted for clinical use. Use of such chelators as has been seen as therapeutically beneficial to humans and animals when done using established protocols. Epidemiology In a mass cadmium poisoning in Japan, a marked prevalence for skeletal complications has been noted for older, postmenopausal women, however, the cause of the phenomenon is not fully understood, and is under investigation. Cadmium poisoning in postmenopausal women may result in an increased risk for osteoporosis. Current research has pointed to general malnourishment, as well as poor calcium metabolism relating to the womens age. Studies are pointing to damage of the mitochondria of kidney cells by cadmium as a key factor of the disease. History An experiment during the early 1960s involving the spraying of cadmium over Norwich was declassified in 2005 by the UK government, as documented in a BBC News article. See also Cobalt poisoning Itai-itai disease References Footnotes Shannon M. Heavy Metal Poisoning, in Haddad LM, Shannon M, Winchester JF(editors): Clinical Management of Poisoning and Drug Overdose, Third Edition, 1998. "Cadmium and you" (PDF). Redgrave Court, Merton Road, Bootle, Merseyside, L20 7HS, United Kingdom: Health and Safety Executive. March 2010. Retrieved January 29, 2011.{{cite web}}: CS1 maint: location (link) Hartwig, Andrea (2013). "Cadmium and Cancer". Cadmium: From Toxicity to Essentiality. Metal Ions in Life Sciences. Vol. 11. pp. 491–507. doi:10.1007/978-94-007-5179-8_15. ISBN 978-94-007-5178-1. PMID 23430782. External links ATSDR Case Studies in Environmental Medicine: Cadmium Toxicity U.S. Department of Health and Human Services CDC - Cadmium - NIOSH Workplace Safety and Health Topic U.S. Department of Health and Human Services National Pollutant Inventory - Cadmium and compounds http://www.canoshweb.org/odp/html/cadmium.htm Archived 2021-03-09 at the Wayback Machine

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

Could you provide a brief overview of 'Abdominal pregnancy' in a medical context?

An abdominal pregnancy is a rare type of ectopic pregnancy where the embryo or fetus is growing and developing outside the womb in the abdomen, but not in the Fallopian tube (usual location), ovary or broad ligament.Because tubal, ovarian and broad ligament pregnancies are as difficult to diagnose and treat as abdominal pregnancies, their exclusion from the most common definition of abdominal pregnancy has been debated.Others—in the minority—are of the view that abdominal pregnancy should be defined by a placenta implanted into the peritoneum. Signs and symptoms Symptoms may include abdominal pain or vaginal bleeding during pregnancy. As this is nonspecific in areas where ultrasound is not available the diagnosis was often only discovered during surgery to investigate the abnormal symptoms. They are typically diagnosed later in the developing world than the developed. In about half of cases from a center in the developing world the diagnosis was initially missed.It is a dangerous condition as there can be bleeding into the abdomen that results in low blood pressure and can be fatal. Other causes of death in women with an abdominal pregnancy include anemia, pulmonary embolus, coagulopathy, and infection. Risk factors Risk factors are similar to tubal pregnancy with sexually transmitted disease playing a major role; however about half of those with ectopic pregnancy have no known risk factors (which include damage to the Fallopian tubes from previous surgery or from previous ectopic pregnancy, and tobacco smoking). Mechanism Implantation sites can be anywhere in the abdomen but can include the peritoneum outside of the uterus, the rectouterine pouch (culdesac of Douglas), omentum, bowel and its mesentery, mesosalpinx, and the peritoneum of the pelvic wall and the abdominal wall. The growing placenta may be attached to several organs including tube and ovary. Rare other sites have been the liver and spleen, giving rise to a hepatic pregnancy or splenic pregnancy, respectively. Even an early diaphragmatic pregnancy has been described in a patient where an embryo began growing on the underside of the diaphragm. Primary versus secondary implantation A primary abdominal pregnancy refers to a pregnancy that first implanted directly in the peritoneum, save for the tubes and ovaries; such pregnancies are very rare, only 24 cases having been reported by 2007. Typically an abdominal pregnancy is a secondary implantation which means that it originated from a tubal (less common an ovarian) pregnancy and re-implanted. Other mechanisms for secondary abdominal pregnancy include uterine rupture, rupture of a uterine rudimentary horn and fimbrial abortion. Diagnosis Suspicion of an abdominal pregnancy is raised when the fetal anatomy can be easily felt, or the lie is abnormal, the cervix is displaced, or there is failed induction of labor. X-rays can be used to aid diagnosis. Sonography can demonstrate that the pregnancy is outside an empty uterus, there is reduced to no amniotic fluid between the placenta and the fetus, no uterine wall surrounding the fetus, fetal parts are close to the abdominal wall, the fetus has an abnormal lie, the placenta looks abnormal and there is free fluid in the abdomen. MRI has also been used with success to diagnose abdominal pregnancy and plan for surgery. Elevated alpha-fetoprotein levels are another clue of the presence of an abdominal pregnancy. Ultrasound Most cases can be diagnosed by ultrasound. The diagnosis however may be missed with ultrasound depending on the operators skill. Criteria To diagnose the rare primary abdominal pregnancy, Studdifords criteria need to be fulfilled: tubes and ovaries should be normal, there is no abnormal connection (fistula) between the uterus and the abdominal cavity, and the pregnancy is related solely to the peritoneal surface without signs that there was a tubal pregnancy first. Studdifords criteria were refined in 1968 by Friedrich and Rankin to include microscopic findings. Differential diagnosis Depending on gestational age the differential diagnoses for abdominal pregnancy include miscarriage, intrauterine fetal death, placental abruption, an acute abdomen with an intrauterine pregnancy and a fibroid uterus with an intrauterine pregnancy . Treatment Ideally the management of abdominal pregnancy should be done by a team that has medical personnel from multiple specialties. Potential treatments consist of surgery with termination of the pregnancy (removal of the fetus) via laparoscopy or laparotomy, use of methotrexate, embolization, and combinations of these. Sapuri and Klufio indicate that conservative treatment is also possible if the following criteria are met: 1. there are no major congenital malformations; 2. the fetus is alive; 3. there is continuous hospitalization in a well-equipped and well-staffed maternity unit which has immediate blood transfusion facilities; 4. there is careful monitoring of maternal and fetal well-being; and 5. placental implantation is in the lower abdomen away from the liver and spleen. The choice is largely dictated by the clinical situation. Generally, treatment is indicated when the diagnosis is made; however, the situation of the advanced abdominal pregnancy is more complicated. Advanced abdominal pregnancy Advanced abdominal pregnancy refers to situations where the pregnancy continues past 20 weeks of gestation (versus early abdominal pregnancy < 20 weeks). In those situations, live births have been reported in the lay press where the babies are not uncommonly referred to as Miracle babies. A patient may carry a dead fetus but will not go into labor. Over time, the fetus calcifies and becomes a lithopedion.It is generally recommended to perform a laparotomy when the diagnosis of an abdominal pregnancy is made. However, if the baby is alive and medical support systems are in place, careful watching could be considered to bring the baby to viability. Women with an abdominal pregnancy will not go into labor. Delivery in a case of an advanced abdominal pregnancy will have to be via laparotomy. The survival of the baby is reduced and high perinatal mortality rates between 40% and 95% have been reported.Babies of abdominal pregnancies are prone to birth defects due to compression in the absence of the uterine wall and the often reduced amount of amniotic fluid surrounding the unborn baby. The rate of malformations and deformations is estimated to be about 21%; typical deformations are facial and cranial asymmetries and joint abnormalities and the most common malformations are limb defects and central nervous malformations.Once the baby has been delivered placental management becomes an issue. In normal deliveries the contraction of uterus provides a powerful mechanism to control blood loss, however, in an abdominal pregnancy the placenta is located over tissue that cannot contract and attempts of its removal may lead to life-threatening blood loss. Thus blood transfusion is frequent in the management of patients with this kind of pregnancy, with others even using tranexamic acid and recombinant factor VIIa, which both minimize blood loss.Generally, unless the placenta can be easily tied off or removed, it may be preferable to leave it in place and allow for a natural regression. This process may take several months and can be monitored by clinical examination, checking human chorionic gonadotropin levels and by ultrasound scanning (in particular using doppler ultrasonography. Use of methotrexate to accelerate placental regression is controversial as the large amount of necrotic tissue is a potential site for infection, mifepristone has also be used to promote placental regression. Placental vessels have also been blocked by angiographic embolization. Complications of leaving the placenta can include residual bleeding, infection, bowel obstruction, pre-eclampsia (which may all necessitate further surgery) and failure to breast feed due to placental hormones.Outcome with abdominal pregnancy can be good for the baby and mother, Lampe described an abdominal pregnancy baby and her mother who were well more than 22 years after surgery. Epidemiology About 1.4% of ectopic pregnancies are abdominal, or about 1 out of every 8,000 pregnancies. A report from Nigeria places the frequency in that country at 34 per 100,000 deliveries and a report from Zimbabwe, 11 per 100,000 deliveries. The maternal mortality rate is estimated to be about 5 per 1,000 cases, about seven times the rate for ectopics in general, and about 90 times the rate for a "normal" delivery (1987 US data). History Al-Zahrawi (936–1013) is credited with first recognizing abdominal pregnancy which was apparently unknown to Greek and Roman physicians and was not mentioned in the writings of Hippocrates; Jacopo Berengario da Carpi (1460–1530) the Italian physician is credited with the first detailed anatomical description of abdominal pregnancy. Natural experiment Because pregnancy is outside the uterus, abdominal pregnancy serves as a model of human male pregnancy or for females who lack a uterus, although such pregnancy would be dangerous. Abdominal pregnancy has served to further clarify the disease pre-eclampsia which was previously thought (1980s) to require a uterus for it to occur, however pre-eclampsias occurrence in abdominal pregnancy (with the conceptus outside the uterus) helped throw light on pre-eclampsias etiology. Cases of combined simultaneous abdominal and intrauterine pregnancy have been reported. References == External links ==

You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

Could you please explain the term 'Meningioma' in simple language?

Meningioma, also known as meningeal tumor, is typically a slow-growing tumor that forms from the meninges, the membranous layers surrounding the brain and spinal cord. Symptoms depend on the location and occur as a result of the tumor pressing on nearby tissue. Many cases never produce symptoms. Occasionally seizures, dementia, trouble talking, vision problems, one sided weakness, or loss of bladder control may occur.Risk factors include exposure to ionizing radiation such as during radiation therapy, a family history of the condition, and neurofibromatosis type 2. As of 2014 they do not appear to be related to cell phone use. They appear to be able to form from a number of different types of cells including arachnoid cells. Diagnosis is typically by medical imaging.If there are no symptoms, periodic observation may be all that is required. Most cases that result in symptoms can be cured by surgery. Following complete removal fewer than 20% recur. If surgery is not possible or all the tumor cannot be removed radiosurgery may be helpful. Chemotherapy has not been found to be useful. A small percentage grow rapidly and are associated with worse outcomes.About one per thousand people in the United States are currently affected. Onset is usually in adults. In this group they represent about 30% of brain tumors. Women are affected about twice as often as men. Meningiomata were reported as early as 1614 by Felix Plater. Signs and symptoms Small tumors (e.g., < 2.0 cm) usually are incidental findings at autopsy without having caused symptoms. Larger tumors may cause symptoms, depending on the size and location. Focal seizures may be caused by meningiomata that overlie the cerebrum. Progressive spastic weakness in legs and incontinence may be caused by tumors that overlie the parasagittal frontoparietal region. Tumors of the Sylvian aqueduct may cause myriad motor, sensory, aphasic, and seizure symptoms, depending on the location. Increased intracranial pressure eventually occurs, but is less frequent than in gliomas. Diplopia (Double vision) or uneven pupil size may be symptoms if related pressure causes a third and/or sixth nerve palsy. Causes The causes of meningiomata are not well understood. Most cases are sporadic, appearing randomly, while some are familial. Persons who have undergone radiation, especially to the scalp, are more at risk for developing meningiomata, as are those who have had a brain injury. Atomic bomb survivors from Hiroshima had a higher than typical frequency of developing meningiomata, with the incidence increasing the closer that they were to the site of the explosion. Dental X-rays are correlated with an increased risk of meningioma, in particular for people who had frequent dental X-rays in the past, when the X-ray dose of a dental X-ray was higher than in the present.Having excess body fat increases the risk.A 2012 review found that mobile telephone use was unrelated to meningioma.People with neurofibromatosis type 2 (NF-2) have a 50% chance of developing one or more meningiomata.Ninety-two percent of meningiomata are benign. Eight percent are either atypical or malignant. Genetics The most frequent genetic mutations (~50%) involved in meningiomata are inactivation mutations in the neurofibromatosis 2 gene (merlin) on chromosome 22q.TRAF7 mutations are present in about one-fourth of meningiomata. Mutations in the TRAF7, KLF4, AKT1, and SMO genes are commonly expressed in benign skull-base meningiomata. Mutations in NF2 are commonly expressed in meningiomata located in the cerebral and cerebellar hemispheres. Pathophysiology Meningiomata arise from arachnoidal cap cells, most of which are near the vicinity of the venous sinuses, and this is the site of greatest prevalence for meningioma formation. Some subtypes may arise from the pial cap cells that migrate during the development together with blood vessels into the brain parenchyma. They most frequently are attached to the dura over the superior parasagittal surface of frontal and parietal lobes, along the sphenoid ridge, in the olfactory grooves, the sylvian region, superior cerebellum along the falx cerebri, cerebellopontine angle, and the spinal cord. The tumor is usually gray, well-circumscribed, and takes on the form of the space it occupies. They usually are dome-shaped, with the base lying on the dura. Locations Parasagittal/falcine (25%) Convexity (surface of the brain) (19%) Sphenoid ridge (17%) Suprasellar (9%) Posterior fossa (8%) Olfactory groove (8%) Middle fossa/Meckels cave (4%) Tentorial (3%) Peri-torcular (3%) Intraparenchymal (rare)Other uncommon locations are the lateral ventricle, foramen magnum, and the orbit/optic nerve sheath. Meningiomata also may occur as a spinal tumor, more often in women than in men. This occurs more often in Western countries than Asian.Histologically, meningioma cells are relatively uniform, with a tendency to encircle one another, forming whorls and psammoma bodies (laminated calcific concretions). As such, they also have a tendency to calcify and are highly vascularized.Meningiomata often are considered benign tumors that can be removed by surgery, but most recurrent meningiomata correspond to histologic benign tumors. The metabolic phenotype of these benign recurrent meningiomata indicated an aggressive metabolism resembling that observed for atypical meningioma. Diagnosis Meningiomata are visualized readily with contrast CT, MRI with gadolinium, and arteriography, all attributed to the fact that meningiomata are extra-axial and vascularized. CSF protein levels are usually found to be elevated when lumbar puncture is used to obtain spinal fluid. On T1-weighted contrast-enhanced MRI, they may show a typical dural tail sign absent in some rare forms of meningiomas.Although the majority of meningiomata are benign, they may have malignant presentations. Classification of meningiomata are based upon the WHO classification system. Benign (Grade I) – (90%) – meningothelial, fibrous, transitional, psammomatous, angioblastic Atypical (Grade II) – (7%) – chordoid, clear cell, atypical (includes brain invasion) Anaplastic/malignant (Grade III) – (2%) – papillary, rhabdoid, anaplastic (most aggressive)In a 2008 review of the latter two categories, atypical and anaplastic-meningioma cases, the mean overall survival for atypical meningiomata was found to be 11.9 years vs. 3.3 years for anaplastic meningiomata. Mean relapse-free survival for atypical meningiomata was 11.5 years vs. 2.7 years for anaplastic meningiomata.Malignant anaplastic meningioma is aggressive. Although anaplastic meningioma has higher chances of distant metastasis than the other two types, the overall incidence of meningioma metastasis is only 0.18%; which is considered rare. Even if, by general rule, neoplasms of the nervous system (brain tumors) cannot metastasize into the body because of the blood–brain barrier, anaplastic meningioma can. Although they are inside the cerebral cavity, they are located on the bloodside of the BBB, because meningiomata tend to be connected to blood vessels. Thus, cancerized cells can escape into the bloodstream, which is why meningiomata, when they metastasize, often turn up around the lungs.Anaplastic meningioma and hemangiopericytoma are difficult to distinguish, even by pathological means, as they look similar, especially, if the first occurrence is a meningeal tumor, and both tumors occur in the same types of tissue.Although usually benign a "petro-clival" menigioma is typically fatal without treatment due to its location. Until the 1970s no treatment was available for this type of meningioma; however, since that time a range of surgical and radiological treatments have evolved. Nevertheless, the treatment of this type of meningioma remains a challenge with relatively frequent poor outcomes. Prevention The risk of meningioma can be reduced by maintaining a normal body weight, and by avoiding unnecessary dental x-rays. Treatment Observation Observation with close imaging follow-up may be used in select cases if a meningioma is small and asymptomatic. In a retrospective study on 43 patients, 63% of patients were found to have no growth on follow-up, and the 37% found to have growth at an average of 4 mm / year. In this study, younger patients were found to have tumors that were more likely to have grown on repeat imaging; thus are poorer candidates for observation. In another study, clinical outcomes were compared for 213 patients undergoing surgery vs. 351 patients under watchful observation. Only 6% of the conservatively treated patients developed symptoms later, while among the surgically treated patients, 5.6% developed persistent morbid condition, and 9.4% developed surgery-related morbid condition.Observation is not recommended in tumors already causing symptoms. Furthermore, close follow-up with imaging is required with an observation strategy to rule out an enlarging tumor. Surgery Meningiomata usually can be surgically resected (removed) and result in a permanent cure if the tumor is superficial on the dural surface and easily accessible. Transarterial embolization has become a standard preoperative procedure in the preoperative management. If invasion of the adjacent bone occurs, total removal is nearly impossible. It is rare for benign meningiomata to become malignant.The probability of a tumor recurring or growing after surgery may be estimated by comparing the tumors WHO (World Health Organization) grade and by the extent of surgery by the Simpson Criteria. Radiation therapy Radiation therapy may include photon-beam or proton-beam treatment, or fractionated external beam radiation. Radiosurgery may be used in lieu of surgery in small tumors located away from critical structures. Fractionated external-beam radiation also can be used as primary treatment for tumors that are surgically unresectable or, for patients who are inoperable for medical reasons.Radiation therapy often is considered for WHO grade I meningiomata after subtotal (incomplete) tumor resections. The clinical decision to irradiate after a subtotal resection is somewhat controversial, as no class I randomized, controlled trials exist on the subject. Numerous retrospective studies, however, have suggested strongly that the addition of postoperative radiation to incomplete resections improves both progression-free survival (i.e. prevents tumor recurrence) and improves overall survival.In the case of a grade III meningioma, the current standard of care involves postoperative radiation treatment regardless of the degree of surgical resection. This is due to the proportionally higher rate of local recurrence for these higher-grade tumors. Grade II tumors may behave variably and there is no standard of whether to give radiotherapy following a gross total resection. Subtotally resected grade II tumors should be radiated. Chemotherapy Likely, current chemotherapies are not effective. Antiprogestin agents have been used, but with variable results. A 2007 study of whether hydroxyurea has the capacity to shrink unresectable or recurrent meningiomata is being further evaluated. Epidemiology Many individuals have meningiomata, but remain asymptomatic, so the meningiomata are discovered during an autopsy. One to two percent of all autopsies reveal meningiomata that were unknown to the individuals during their lifetime, since there were never any symptoms. In the 1970s, tumors causing symptoms were discovered in 2 out of 100,000 people, while tumors discovered without causing symptoms occurred in 5.7 out of 100,000, for a total incidence of 7.7/100,000. With the advent of modern sophisticated imaging systems such as CT scans, the discovery of asymptomatic meningiomata has tripled.Meningiomata are more likely to appear in women than men, though when they appear in men, they are more likely to be malignant. Meningiomata may appear at any age, but most commonly are noticed in men and women age 50 or older, with meningiomata becoming more likely with age. They have been observed in all cultures, Western and Eastern, in roughly the same statistical frequency as other possible brain tumors. History The neoplasms currently referred to as meningiomata were referred to with a wide range of names in older medical literature, depending on the source. Various descriptors included "fungoid tumors", "fungus of the dura mater", "epithelioma", "psammoma", "dural sarcoma", "dural endothelioma", "fibrosarcoma", "angioendothelioma", "arachnoidal fibroboastoma", "endotheliosis of the meninges", "meningeal fibroblastoma", "meningoblastoma", "mestothelioma of the meninges", "sarcoma of the dura", and others.The modern term of "meningioma" was used first by Harvey Cushing (1869–1939) in 1922, to describe a set of tumors that occur throughout the neuraxis (brain and spinal cord), but have various commonalities. Charles Oberling then separated these into subtypes based on cell structure and, over the years, several other researchers have defined dozens of different subtypes as well. In 1979, the World Health Organization (WHO) classified seven subtypes, upgraded in 2000 to a classification system with nine low-grade variants (grade I tumors) and three variants each of grade II and grade III meningiomata. The most common subtypes are Meningotheliomatous (63%), transitional or mixed-type (19%), fibrous (13%), and psammomatous (2%).The earliest evidence of a probable meningioma is from a skull approximately 365,000 years old, which was found in Germany. Other probable examples have been discovered in other continents around the world, including North and South America, and Africa.The earliest written record of what was probably a meningioma is from the 1600s, when Felix Plater (1536–1614) of the University of Basel performed an autopsy on Sir Caspar Bonecurtius. Surgery for removal of meningiomata was first attempted in the sixteenth century, but the first known successful surgery for removal of a meningioma of the convexity (parasagittal) was performed in 1770 by Anoine Luis. The first documented successful removal of a skull base meningioma was performed in 1835 by Zanobi Pecchioli, Professor of Surgery at the University of Siena. Other notable meningioma researchers have been William Macewen (1848–1924), and William W. Keen (1837–1932).Improvements in meningioma research and treatment over the last century have occurred in terms of the surgical techniques for removal of the tumor, and related improvements in anesthesia, antiseptic methods, techniques to control blood loss, better ability to determine which tumors are and are not operable, and to effectively differentiate between the different meningioma subtypes. Notable cases Leonard Wood (1860–1927), underwent successful surgery by Dr. Harvey Cushing for a meningioma circa 1910, a major advance in neurosurgery at the time. Crystal Lee Sutton (1940–2009), American union organizer and inspiration for the film Norma Rae, died of a malignant meningioma. Elizabeth Taylor (1932–2011), American actress, underwent surgery in February 1997 to remove a benign meningioma. Kathi Goertzen (1958–2012), television news anchor in Seattle who underwent a very public battle with recurring tumors. She died on August 13, 2012, of complications related to her treatment. Eileen Ford (1922–2014), American model agency executive and co-founder of Ford Models. Died on July 9, 2014, from complications of meningioma and osteoporosis. Mary Tyler Moore (1936–2017), American actress, underwent surgery in May 2011 to remove a benign meningioma. Jack Daulton (1956–), American trial lawyer and art collector, underwent three surgeries in 2011–2012 in connection with the removal of a golf-ball-size benign meningioma over his left motor cortex; he fully recovered without disability or recurrence. Simone Giertz (1990–), Swedish inventor and professional YouTuber, underwent surgery to remove a grade I meningioma in 2018 and radiation therapy after tumor regrowth in 2019. References External links MR/CT scans of meningioma from MedPix MR/CT scans of pneumosinus dilatans from MedPix Cancer.Net: Meningioma

You function as a medical informant. Please provide in-depth yet accessible descriptions of medical terms, suitable for a broad audience.

Could you offer a clear explanation of the term 'Pressure ulcer' as used in the medical field?

Pressure ulcers, also known as pressure sores, bed sores or pressure injuries, are localised damage to the skin and/or underlying tissue that usually occur over a bony prominence as a result of usually long-term pressure, or pressure in combination with shear or friction. The most common sites are the skin overlying the sacrum, coccyx, heels, and hips, though other sites can be affected, such as the elbows, knees, ankles, back of shoulders, or the back of the cranium. Pressure ulcers occur due to pressure applied to soft tissue resulting in completely or partially obstructed blood flow to the soft tissue. Shear is also a cause, as it can pull on blood vessels that feed the skin. Pressure ulcers most commonly develop in individuals who are not moving about, such as those who are on chronic bedrest or consistently use a wheelchair. It is widely believed that other factors can influence the tolerance of skin for pressure and shear, thereby increasing the risk of pressure ulcer development. These factors are protein-calorie malnutrition, microclimate (skin wetness caused by sweating or incontinence), diseases that reduce blood flow to the skin, such as arteriosclerosis, or diseases that reduce the sensation in the skin, such as paralysis or neuropathy. The healing of pressure ulcers may be slowed by the age of the person, medical conditions (such as arteriosclerosis, diabetes or infection), smoking or medications such as anti-inflammatory drugs. Although often prevented and treatable if detected early, pressure ulcers can be very difficult to prevent in critically ill people, frail elders and individuals with impaired mobility such as wheelchair users (especially where spinal injury is involved). Primary prevention is to redistribute pressure by regularly turning the person. The benefit of turning to avoid further sores is well documented since at least the 19th century. In addition to turning and re-positioning the person in the bed or wheelchair, eating a balanced diet with adequate protein and keeping the skin free from exposure to urine and stool is important.The rate of pressure ulcers in hospital settings is high; the prevalence in European hospitals ranges from 8.3% to 23%, and the prevalence was 26% in Canadian healthcare settings from 1990 to 2003. In 2013, there were 29,000 documented deaths from pressure ulcers globally, up from 14,000 deaths in 1990. Presentation Complications Pressure ulcers can trigger other ailments, cause considerable suffering, and can be expensive to treat. Some complications include autonomic dysreflexia, bladder distension, bone infection, pyarthrosis, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation (Marjolins ulcer - secondary carcinomas in chronic wounds). Sores may recur if those with pressure ulcers do not follow recommended treatment or may instead develop seromas, hematomas, infections, or wound dehiscence. Paralyzed individuals are the most likely to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from kidney failure and amyloidosis. Pressure ulcers are also painful, with individuals of all ages and all stages of pressure ulcers reporting pain. Cause There are four mechanisms that contribute to pressure ulcer development: External (interface) pressure applied over an area of the body, especially over the bony prominences can result in obstruction of the blood capillaries, which deprives tissues of oxygen and nutrients, causing ischemia (deficiency of blood in a particular area), hypoxia (inadequate amount of oxygen available to the cells), edema, inflammation, and, finally, necrosis and ulcer formation. Ulcers due to external pressure occur over the sacrum and coccyx, followed by the trochanter and the calcaneus (heel). Friction is damaging to the superficial blood vessels directly under the skin. It occurs when two surfaces rub against each other. The skin over the elbows can be injured due to friction. The back can also be injured when patients are pulled or slid over bed sheets while being moved up in bed or transferred onto a stretcher. Shearing is a separation of the skin from underlying tissues. When a patient is partially sitting up in bed, their skin may stick to the sheet, making them susceptible to shearing in case underlying tissues move downward with the body toward the foot of the bed. This may also be possible on a patient who slides down while sitting in a chair. Moisture is also a common pressure ulcer culprit. Sweat, urine, feces, or excessive wound drainage can further exacerbate the damage done by pressure, friction, and shear. It can contribute to maceration of surrounding skin thus potentially expanding the deleterious effects of pressure ulcers. Risk factors There are over 100 risk factors for pressure ulcers. Factors that may place a patient at risk include immobility, diabetes mellitus, peripheral vascular disease, malnutrition, cerebral vascular accident and hypotension. Other factors are age of 70 years and older, current smoking history, dry skin, low body mass index, urinary and fecal incontinence, physical restraints, malignancy, and history of pressure ulcers. Pathophysiology Pressure ulcers may be caused by inadequate blood supply and resulting reperfusion injury when blood re-enters tissue. A simple example of a mild pressure sore may be experienced by healthy individuals while sitting in the same position for extended periods of time: the dull ache experienced is indicative of impeded blood flow to affected areas. Within 2 hours, this shortage of blood supply, called ischemia, may lead to tissue damage and cell death. The sore will initially start as a red, painful area. The other process of pressure ulcer development is seen when pressure is high enough to damage the cell membrane of muscle cells. The muscle cells die as a result and skin fed through blood vessels coming through the muscle die. This is the deep tissue injury form of pressure ulcers and begins as purple intact skin.According to Centers for Medicare and Medicaid Services, pressure ulcers are one of the eight preventable iatrogenic illnesses. If a pressure ulcer is acquired in the hospital, the hospital will no longer receive reimbursement for the persons care. Hospitals spend about $5 billion annually for treatment of pressure ulcers. Sites Common pressure sore sites include the skin over the ischial tuberosity, the sacrum, the heels of the feet, over the heads of the long bones of the foot, buttocks, over the shoulder, and over the back of the head. Biofilm Biofilm is one of the most common reasons for delayed healing in pressure ulcers. Biofilm occurs rapidly in wounds and stalls healing by keeping the wound inflamed. Frequent debridement and antimicrobial dressings are needed to control the biofilm. Infection prevents healing of pressure ulcers. Signs of pressure ulcer infection include slow or delayed healing and pale granulation tissue. Signs and symptoms of systemic infection include fever, pain, redness, swelling, warmth of the area, and purulent discharge. Additionally, infected wounds may have a gangrenous smell, be discolored, and may eventually produce more pus.In order to eliminate this problem, it is imperative to apply antiseptics at once. Hydrogen peroxide (a near-universal toxin) is not recommended for this task as it increases inflammation and impedes healing. Dressings with cadexomer iodine, silver, or honey have been shown to penetrate bacterial biofilms. Systemic antibiotics are not recommended in treating local infection in a pressure ulcer, as it can lead to bacterial resistance. They are only recommended if there is evidence of advancing cellulitis, bony infection, or bacteria in the blood. Diagnosis Classification The definitions of the pressure ulcer stages are revised periodically by the National Pressure Injury Advisory Panel (NPUAP) in the United States and the European Pressure Ulcer Advisory Panel (EPUAP) in Europe. Different classification systems are used around the world, depending upon the health system, the health discipline and the purpose for the classifying (e.g. health care versus, prevalence studies versus funding. Briefly, they are as follows: Stage I: Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area differs in characteristics such as thickness and temperature as compared to adjacent tissue. Stage 1 may be difficult to detect in individuals with dark skin tones. May indicate "at risk" persons (a heralding sign of risk). Stage II: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising. This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation. Stage III: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a stage 3 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and stage 3 ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage 3 pressure ulcers. Bone/tendon is not visible or directly palpable. Stage IV: Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling. The depth of a stage 4 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and these ulcers can be shallow. Stage 4 ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis likely to occur. Exposed bone/tendon is visible or directly palpable. In 2012, the National Pressure Injury Advisory Panel stated that pressure ulcers with exposed cartilage are also classified as a stage 4. Unstageable: Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels is normally protective and should not be removed. Suspected deep tissue injury: A purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. A deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.The term medical device related pressure ulcer refers to a cause rather than a classification. Pressure ulcers from a medical device are classified according to the same classification system being used for pressure ulcers arising from other causes, but the cause is usually noted. Ischemic fasciitis Ischemic fasciitis (IF) is a benign tumor in the class of fibroblastic and myofibroblastic tumors that, like pressure ulcers, may develop in elderly, bed-ridden individuals. These tumors commonly form in the subcutaneous tissues (i.e. lower most tissue layer of the skin) that overlie bony protuberances such as those in or around the hip, shoulder, greater trochanter of the femur, iliac crest, lumbar region, or scapular region. IF tumors differ from pressure ulcers in that they typically do not have extensive ulcerations of the skin and on histopathological microscopic analysis lack evidence of acute inflammation as determined by the presence of various types of white blood cells. These tumors are commonly treated by surgical removal. Prevention In the United Kingdom, the Royal College of Nursing has published guidelines in Pressure Ulcer Risk Assessment and Prevention that call for identifying people at risk and taking preventive action; the UK National Standards for Care Homes to do so as well. Recent efforts in the United States and South Korea have sought to automate risk assessment and classification by training machine learning models on electronic health records.Internationally, the NPIAP, EPUAP and Pan Pacific Pressure Injury Alliance, together with wound organizations from 15 countries around the world, published updated the international evidence-based clinical practice guideline in 2019. The 2019 guideline was developed by an international team of over 180 clinical specialists and updates the 2009 EPUAP/NPUAP clinical guideline and the 2014 NPUAP/EPUAP/PPPIA clinical guideline. The guideline includes recommendations on strategies to treat pressure ulcers, including the use of bed rest, pressure redistributing support surfaces, nutritional support, repositioning, wound care (e.g. debridement, wound dressings) and biophysical agents (e.g. electrical stimulation). Reliable scientific evidence to support the use of many of these interventions, though, is lacking. More research is needed to assess how to best support the treatment of pressure ulcers, for example by repositioning. Also, the benefit of using systemic or topical antibiotics in the management of pressure ulcer is still unclear. Redistributing pressure The most important care for a person at risk for pressure ulcers and those with bedsores is the redistribution of pressure so that no pressure is applied to the pressure ulcer. In the 1940s Ludwig Guttmann introduced a program of turning paraplegics every two hours thus allowing bedsores to heal. Previously such individuals had a two-year life-expectancy, normally succumbing to blood and skin infections. Guttmann had learned the technique from the work of Boston physician Donald Munro.There is lack of evidence on prevention of pressure ulcer whether the patient is put in 30 degrees position or at the standard 90 degrees position.Nursing homes and hospitals usually set programs in place to avoid the development of pressure ulcers in those who are bedridden, such as using a routine time frame for turning and repositioning to reduce pressure. The frequency of turning and repositioning depends on the persons level of risk. Support surfaces A 2015 Cochrane systematic review found that people who lay on high specification or high density foam mattresses were 60% less likely to develop new pressure ulcers compared to regular foam mattresses. Sheepskin overlays on top of mattresses were also found to prevent new pressure ulcer formation. There is unclear research on the effectiveness of alternating pressure mattresses. Pressure-redistributive mattresses are used to reduce high values of pressure on prominent or bony areas of the body. There are several important terms used to describe how these support surfaces work. These terms were standardized through the Support Surface Standards Initiative of the NPUAP. Many support surfaces redistribute pressure by immersing and/or enveloping the body into the surface. Some support surfaces, including antidecubitus mattresses and cushions, contain multiple air chambers that are alternately pumped. Methods to standardize the products and evaluate the efficacy of these products have only been developed in recent years through the work of the S3I within NPUAP. For individuals with paralysis, pressure shifting on a regular basis and using a wheelchair cushion featuring pressure relief components can help prevent pressure wounds. A 2022 Cochrane systematic review aimed to find out how effective pressure redistributing static chairs (as opposed to wheelchairs) are for preventing pressure ulcers. Static chairs can include: standard hospital chairs; chairs with no cushions or manual/dynamic function; and chairs with integrated pressure redistributing surfaces and recline, rise or tilt functions. The authors did not find any randomised controlled trials that were eligible for inclusion. More research is needed to establish how effective pressure redistributing static chairs are for preventing pressure ulcers. Controlling the heat and moisture levels of the skin surface, known as skin microclimate management, also plays a significant role in the prevention and control of pressure ulcers. Nutrition In addition, adequate intake of protein and calories is important. Vitamin C has been shown to reduce the risk of pressure ulcers. People with higher intakes of vitamin C have a lower frequency of bed sores in those who are bedridden than those with lower intakes. Maintaining proper nutrition in newborns is also important in preventing pressure ulcers. If unable to maintain proper nutrition through protein and calorie intake, it is advised to use supplements to support the proper nutrition levels. Skin care is also important because damaged skin does not tolerate pressure. However, skin that is damaged by exposure to urine or stool is not considered a pressure ulcer. These skin wounds should be classified as Incontinence Associated Dermatitis. Organisational changes There is some suggestion that organisational changes may reduce incidence of pressure ulcers. Cochrane systematic reviews on organisation of health services, risk assessment tools, wound care teams, and education have concluded that evidence is uncertain as to the benefit of these organisational changes. This is largely due to the lack of high-quality research in these areas. Other prevention therapies A Cochrane systematic review found use of creams containing fatty acids may be more effective in reducing incidence of pressure ulcers compared to creams without fatty acids. Silicone dressings may also reduce pressure ulcer incidence. There is no evidence that massage reduces pressure ulcer incidence. Treatment Internationally, the NPIAP, EPUAP and Pan Pacific Pressure Injury Alliance, together with wound organizations from 15 countries around the world published updated their international evidence-based clinical practice guideline in 2019. The 2019 guideline was developed by an international team of over 180 clinical specialists and updates the 2009 EPUAP/NPUAP clinical guideline and the 2014 NPUAP/EPUAP/PPPIA clinical guideline. The guideline includes recommendations on strategies to treat pressure ulcers, including the use of bed rest, pressure redistributing support surfaces, nutritional support, repositioning, wound care (e.g. debridement, wound dressings) and biophysical agents (e.g. electrical stimulation). Reliable scientific evidence to support the use of many of these interventions, though, is lacking. More research is needed to assess how to best support the treatment of pressure ulcers, for example by repositioning. A 2020 Cochrane systematic review of randomized controlled trials concluded that more research is needed to determine whether or not electrical stimulation is an effective treatment for pressure ulcers. In addition, the benefit of using systemic or topical antibiotics in the management of pressure ulcer is still unclear. Debridement Necrotic tissue should be removed in most pressure ulcers. The heel is an exception in many cases when the limb has an inadequate blood supply. Necrotic tissue is an ideal area for bacterial growth, which has the ability to greatly compromise wound healing. There are five ways to remove necrotic tissue. Autolytic debridement is the use of moist dressings to promote autolysis with the bodys own enzymes and white blood cells. It is a slow process, but mostly painless, and is most effective in individuals with a properly functioning immune system. Biological debridement, or maggot debridement therapy, is the use of medical maggots to feed on necrotic tissue and therefore clean the wound of excess bacteria. Although this fell out of favor for many years, in January 2004, the FDA approved maggots as a live medical device. Chemical debridement, or enzymatic debridement, is the use of prescribed enzymes that promote the removal of necrotic tissue. Mechanical debridement, is the use of debriding dressings, whirlpool or ultrasound for slough in a stable wound. Surgical debridement, or sharp debridement, is the fastest method, as it allows a surgeon to quickly remove dead tissue. Dressings A 2017 Cochrane review found that it was unclear whether one topical agent or dressing was better than another for treating pressure ulcers. Protease-modulating dressings, foam dressings or collagenase ointment may be better at healing than gauze. The wound dressing should be selected based on the wound and condition of the surrounding skin. There are some studies that indicate that antimicrobial products that stimulate the epithelization may improve the wound healing. However, there is no international consensus on the selection of the dressings for pressure ulcers. Cochrane reviews summarise evidence on alginate dressings, foam dressings, and hydrogel dressings. Due to a lack of robust evidence, the benefits of these dressings over other treatments is unclear. Some guidelines for dressing are: Other treatments Other treatments include anabolic steroids, negative pressure wound therapy, phototherapy, support surfaces, reconstructive surgery, ultrasound, topical phenytoin and pressure relieving devices. There is little or no evidence to support or refute the benefits of most of these treatments compared to each other and placebo. When selecting treatments, consideration should be given to patients quality of life as well as the interventions ease of use, reliability, and cost. Epidemiology Pressure ulcers resulted in 29,000 deaths worldwide in 2013 up from 14,000 deaths in 1990.Each year, more than 2.5 million people in the United States develop pressure ulcers. In acute care settings in the United States, the incidence of bedsores is 0.4% to 38%; within long-term care it is 2.2% to 23.9%, and in home care, it is 0% to 17%. Similarly, there is wide variation in prevalence: 10% to 18% in acute care, 2.3% to 28% in long-term care, and 0% to 29% in home care. There is a much higher rate of bedsores in intensive care units because of immunocompromised individuals, with 8% to 40% of those in the ICU developing bedsores. However, pressure ulcer prevalence is highly dependent on the methodology used to collect the data. Using the European Pressure Ulcer Advisory Panel (EPUAP) methodology there are similar figures for pressure ulcers in acutely sick people in the hospital. There are differences across countries, but using this methodology, pressure ulcer prevalence in Europe was consistently high, from 8.3% (Italy) to 22.9% (Sweden). A recent study in Jordan also showed a figure in this range. Some research shows differences in pressure-ulcer detection among white and black residents in nursing homes. See also Perfusion—systemic biomechanics of blood delivery References Nathaniel Avilla, John Soto, Toni Tweedy, The Cochrane Database of Systematic Reviews diariodelyaqui Further reading External links Media related to Pressure ulcers at Wikimedia Commons

You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

Could you please explain the term 'Saber shin' in simple language?

Saber shin is a malformation of the tibia. It presents as a sharp anterior bowing, or convexity, of the tibia. Causes Periosteal reaction along the shaft of the tibia. It can result from congenital syphilis, yaws, Pagets disease of bone, vitamin D deficiency or Weismann-Netter–Stuhl syndrome. It can be due to osteomalacia. Prognosis Etymology Saber refers to the tibias resemblance to the curve of a saber sword. See also Saddle nose List of cutaneous conditions Rickets References Bibliography Mosbys Medical, Nursing, & Allied Health Dictionary. Edition 5, 1998 p7B49.

You are a medical lexicon. Explain medical terminology with depth and clarity, making sure the information is both accurate and easy to grasp.

Could you provide a brief overview of 'Cestoda' in a medical context?

Cestoda is a class of parasitic worms in the flatworm phylum (Platyhelminthes). Most of the species—and the best-known—are those in the subclass Eucestoda; they are ribbon-like worms as adults, known as tapeworms. Their bodies consist of many similar units known as proglottids—essentially packages of eggs which are regularly shed into the environment to infect other organisms. Species of the other subclass, Cestodaria, are mainly fish infecting parasites. All cestodes are parasitic; many have complex life histories, including a stage in a definitive (main) host in which the adults grow and reproduce, often for years, and one or two intermediate stages in which the larvae develop in other hosts. Typically the adults live in the digestive tracts of vertebrates, while the larvae often live in the bodies of other animals, either vertebrates or invertebrates. For example, Diphyllobothrium has at least two intermediate hosts, a crustacean and then one or more freshwater fish; its definitive host is a mammal. Some cestodes are host-specific, while others are parasites of a wide variety of hosts. Some six thousand species have been described; probably all vertebrates can host at least one species. The adult tapeworm has a scolex (head), a short neck, and a strobila (segmented body) formed of proglottids. Tapeworms anchor themselves to the inside of the intestine of their host using their scolex, which typically has hooks, suckers, or both. They have no mouth, but absorb nutrients directly from the hosts gut. The neck continually produces proglottids, each one containing a reproductive tract; mature proglottids are full of eggs, and fall off to leave the host, either passively in the feces or actively moving. All tapeworms are hermaphrodites, with each individual having both male and female reproductive organs. Humans are subject to infection by several species of tapeworms if they eat undercooked meat such as pork (Taenia solium), beef (T. saginata), and fish (Diphyllobothrium), or if they live in, or eat food prepared in, conditions of poor hygiene (Hymenolepis or Echinococcus species). The unproven concept of using tapeworms as a slimming aid has been touted since around 1900. Diversity and habitat All 6,000 species of Cestoda are parasites, mainly intestinal; their definitive hosts are vertebrates, both terrestrial and marine, while their intermediate hosts include insects, crustaceans, molluscs, and annelids as well as other vertebrates.T. saginata, the beef tapeworm, can grow up to 20 m (65 ft); the largest species, the whale tapeworm Tetragonoporus calyptocephalus, can grow to over 30 m (100 ft). Species with small hosts tend to be small. For example, vole and lemming tapeworms are only 13–240 mm (0.5–9.4 in) in length, and those parasitizing shrews only 0.8–60 mm (0.03–2.36 in). Anatomy Cestodes have no gut or mouth and absorb nutrients from the hosts alimentary tract through their specialised neodermal cuticle, or tegument, through which gas exchange also takes place. The tegument also protects the parasite from the hosts digestive enzymes and allows it to transfer molecules back to the host.The body form of adult eucestodes is simple, with a scolex, or grasping head, adapted for attachment to the definitive host, a short neck, and a strobila, or segmented trunk formed of proglottids, which makes up the worms body. Members of the subclass Cestodaria, the Amphilinidea and Gyrocotylidea, are wormlike but not divided into proglottids. Amphilinids have a muscular proboscis at the front end; Gyrocotylids have a sucker or proboscis which they can pull inside or push outside at the front end, and a holdfast rosette at the posterior end.The Cestodaria have 10 larval hooks while Eucestoda have 6 larval hooks. Scolex The scolex, which attaches to the intestine of the definitive host, is often minute in comparison with the proglottids. It is typically a four-sided knob, armed with suckers or hooks or both. In some species, the scolex is dominated by bothria, or "sucking grooves" that function like suction cups. Cyclophyllid cestodes can be identified by the presence of four suckers on their scolices. Other species have ruffled or leaflike scolices, and there may be other structures to aid attachment.In the larval stage the scolex is similarly shaped and is known as the protoscoleces. Body systems Circular and longitudinal muscles lie under the neodermis, beneath which further longitudinal, dorso-ventral and transverse muscles surround the central parenchyma. Protonephridial cells drain into the parenchyma. There are four longitudinal collection canals, two dorso-lateral and two ventro-lateral, running along the length of the worm, with a transverse canal linking the ventral ones at the posterior of each segment. When the proglottids begin to detach, these canals open to the exterior through the terminal segment.The main nerve centre of a cestode is a cerebral ganglion in its scolex. Nerves emanate from the ganglion to supply the general body muscular and sensory endings, with two lateral nerve cords running the length of the strobila. The cirrus and vagina are innervated, and sensory endings around the genital pore are more plentiful than in other areas. Sensory function includes both tactoreception (touch) and chemoreception (smell or taste). Proglottids Once anchored to the hosts intestinal wall, tapeworms absorb nutrients through their surface as their food flows past them. Cestodes are unable to synthesise lipids, which they use for reproduction, and are therefore entirely dependent on their hosts.The tapeworm body is composed of a series of segments called proglottids. These are produced from the neck by mitotic growth, which is followed by transverse constriction. The segments become larger and more mature as they are displaced backwards by newer segments. Each proglottid contains an independent reproductive tract, and like some other flatworms, cestodes excrete waste through flame cells (protonephridia) located in the proglottids. The sum of the proglottids is called a strobila, which is thin and resembles a strip of tape; from this is derived the common name "tapeworm". Proglottids are continually being produced by the neck region of the scolex, as long as the scolex is attached and alive.Mature proglottids are essentially bags of eggs, each of which is infective to the proper intermediate host. They are released and leave the host in feces, or migrate outwards as independent motile proglottids. The number of proglottids forming the tapeworm ranges from three to four thousand. Their layout comes in two forms: craspedote, meaning any given proglottid is overlapped by the previous proglottid, or acraspedote, indicating the proglottids do not overlap. Reproduction Cestodes are exclusively hermaphrodites, with both male and female reproductive systems in each body. The reproductive system includes one or more testes, cirri, vas deferens, and seminal vesicles as male organs, and a single lobed or unlobed ovary with the connecting oviduct and uterus as female organs. The common external opening for both male and female reproductive systems is known as the genital pore, which is situated at the surface opening of the cup-shaped atrium. Though they are sexually hermaphroditic and cross-fertilization is the norm, self-fertilization sometimes occurs and makes possible the reproduction of a worm when it is the only individual in its hosts gut. During copulation, the cirri of one individual connect with those of the other through the genital pore, and then spermatozoa are exchanged. Life cycle Cestodes are parasites of vertebrates, with each species infecting a single definitive host or group of closely related host species. All but amphilinids and gyrocotylids (which burrow through the gut or body wall to reach the coelom) are intestinal, though some life-cycle stages rest in muscle or other tissues. The definitive host is always a vertebrate but in nearly all cases, one or more intermediate hosts are involved in the lifecycle, typically arthropods or other vertebrates. Infections can be long-lasting; in humans, tapeworm infection may last as much as 30 years. No asexual phases occur in the lifecycle, as they do in other flatworms, but the lifecycle pattern has been a crucial criterion for assessing evolution among Platyhelminthes.Cestodes produce large numbers of eggs, but each one has a low probability of finding a host. To increase their chances, different species have adopted various strategies of egg release. In the Pseudophyllidea, many eggs are released in the brief period when their aquatic intermediate hosts are abundant (semelparity). In contrast, in the terrestrial Cyclophyllidea, proglottids are released steadily over a period of years, or as long as their host lives (iteroparity). Another strategy is to have very long-lived larvae; for example, in Echinococcus, the hydatid larvae can survive for ten years or more in humans and other vertebrate hosts, giving the tapeworm an exceptionally long time window in which to find another host.Many tapeworms have a two-phase lifecycle with two types of host. The adult Taenia saginata lives in the gut of a primate such as a human, its definitive host. Proglottids leave the body through the anus and fall to the ground, where they may be eaten with grass by a grazing animal such as a cow. This animal then becomes an intermediate host, the oncosphere boring through the gut wall and migrating to another part of the body such as the muscle. Here it encysts, forming a cysticercus. The parasite completes its lifecycle when the intermediate host passes on the parasite to the definitive host, usually when the definitive host eats contaminated parts of the intermediate host, for example a human eating raw or undercooked meat. Another two-phase lifecycle is exhibited by Anoplocephala perfoliata, the definitive host being an equine and the intermediate host an oribatid mite.Diphyllobothrium exhibits a more complex, three-phase lifecycle. If the eggs are laid in water, they develop into free-swimming oncosphere larvae. After ingestion by a suitable freshwater crustacean such as a copepod, the first intermediate host, they develop into procercoid larvae. When the copepod is eaten by a suitable second intermediate host, typically a minnow or other small freshwater fish, the procercoid larvae migrate into the fishs flesh where they develop into plerocercoid larvae. These are the infective stages for the mammalian definitive host. If the small fish is eaten by a predatory fish, its muscles too can become infected.Schistocephalus solidus is another three-phase example. The intermediate hosts are copepods and small fish, and the definitive hosts are waterbirds. This species has been used to demonstrate that cross-fertilisation produces a higher infective success rate than self-fertilisation. Host immunity Hosts can become immune to infection by a cestode if the lining, the mucosa, of the gut is damaged. This exposes the hosts immune system to cestode antigens, enabling the host to mount an antibody defence. Host antibodies can kill or limit cestode infection by damaging their digestive enzymes, which reduces their ability to feed and therefore to grow and to reproduce; by binding to their bodies; and by neutralising toxins that they produce. When cestodes feed passively in the gut, they do not provoke an antibody reaction. Evolution and phylogeny Fossil history Parasite fossils are rare, but recognizable clusters of cestode eggs, some with an operculum (lid) indicating that they had not erupted, one with a developing larva, have been discovered in fossil shark coprolites dating to the Permian, some 270 million years ago.The fossil Rugosusivitta, which was found in China at base of the Cambrian deposits in Yunnan just above the Ediacaran-Cambrian border, has great similarities to present day Cestodians. If correct, this would be the earliest example of a Platyzoan and also one of the earliest bilaterian body-fossils and might thus provide an insight to the living mode of Cestodians before they became specialized parasites. External The position of the Cestoda within the Platyhelminthes and other Spiralian phyla based on genomic analysis is shown in the phylogenetic tree. The non-parasitic flatworms, traditionally grouped as the "Turbellaria", are paraphyletic, as the parasitic Neodermata including the Cestoda arose within that grouping. The approximate times when major groups first appeared is shown in millions of years ago. Internal The evolutionary history of the Cestoda has been studied using ribosomal RNA, mitochondrial and other DNA, and morphological analysis and continues to be revised. "Tetraphyllidea" is seen to be paraphyletic; "Pseudophyllidea" has been broken up into two orders, Bothriocephalidea and Diphyllobothriidea. Hosts, whose phylogeny often mirrors that of the parasites (Fahrenholzs rule), are indicated in italics and parentheses, the life-cycle sequence (where known) shown by arrows as (intermediate host1 [→ intermediate host2 ] → definitive host). Alternatives, generally for different species within an order, are shown in square brackets. The Taeniidae, including species such as the pork tapeworm and the beef tapeworm that often infect humans, may be the most basal of the 12 orders of the Cyclophyllidea. Interactions with humans Infection and treatment Like other species of mammal, humans can become infected with tapeworms. There may be few or no symptoms, and the first indication of the infection may be the presence of one or more proglottids in the stools. The proglottids appear as flat, rectangular, whitish objects about the size of a grain of rice, which may change size or move about. Bodily symptoms which are sometimes present include abdominal pain, nausea, diarrhea, increased appetite and weight loss.There are several classes of anthelminthic drugs, some effective against many kinds of parasite, others more specific; these can be used both preventatively and to treat infections. For example, praziquantel is an effective treatment for tapeworm infection, and is preferred over the older niclosamide. While accidental tapeworm infections in developed countries are quite rare, such infections are more likely to occur in countries with poor sanitation facilities or where food hygiene standards are low. History and culture In ancient Greece, the comic playwright Aristophanes and philosopher Aristotle described the lumps that form during cysticercosis as "hailstones". In Medieval times, in The Canon of Medicine, completed in 1025, the Persian physician Avicenna recorded parasites including tapeworms. In the Early Modern period, Francesco Redi described and illustrated many parasites, and was the first to identify the cysts of Echinococcus granulosus seen in dogs and sheep as parasitic in origin; a century later, in 1760, Peter Simon Pallas correctly suggested that these were the larvae of tapeworms.Tapeworms have occasionally appeared in fiction. Peter Marren and Richard Mabey in Bugs Britannica write that Irvine Welshs sociopathic policeman in his 1998 novel Filth owns a talking tapeworm, which they call "the most attractive character in the novel"; it becomes the policemans alter ego and better self. Mira Grants 2013 novel Parasite envisages a world where peoples immune systems are maintained by genetically engineered tapeworms. Tapeworms are prominently mentioned in the System of a Down song "Needles": their inclusion within the song result in a lyrical dispute among band members.There are unproven claims that, around 1900, tapeworm eggs were marketed to the public as slimming tablets. A full-page coloured image, purportedly from a womens magazine of that period, reads "Fat: the enemy ... that is banished! How? With sanitized tape worms. Jar packed. No ill effects!" When television presenter Michael Mosley deliberately infected himself with tapeworms he gained weight due to increased appetite. Dieters still sometimes risk intentional infection, evidenced by a 2013 warning on American television. Notes References Further reading Merck Manual of Medication Information, Second Home Edition, Online Version, Tapeworm Infection 2005 Mayo Clinic Website on infectious diseases, Mayo Clinic - Tapeworm Infection, 2006 Medline Plus - Taeniasis (tapeworm infection) University of South Carolina - School of Medicine - Cestodes (tapeworms)

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

What is the significance of the term 'Hyperprolactinaemia' in the medical field?

Hyperprolactinaemia is the presence of abnormally high levels of prolactin in the blood. Normal levels average to about 13 ng/mL in women, and 5 ng/mL in men, with an upper normal limit of serum prolactin levels being 15-25 ng/mL for both. When the fasting levels of prolactin in blood exceed this upper limit, hyperprolactinemia is indicated. Prolactin (PRL) is a peptide hormone produced by lactotroph cells in the anterior pituitary gland. PRL is involved in lactation after pregnancy and plays a vital role in breast development. Hyperprolactinemia may cause galactorrhea (production and spontaneous flow of breast milk), infertility, and disruptions in the normal menstrual period in women; as well as hypogonadism, infertility and erectile dysfunction in men. Although hyperprolactinemia can result from normal physiological changes during pregnancy and breastfeeding, it can also be caused by other etiologies. For example, high prolactin levels could result from diseases affecting the hypothalamus and pituitary gland. Other organs, such as the liver and kidneys, could affect prolactin clearance and consequently, prolactin levels in the serum. The disruption of prolactin regulation could also be attributed to external sources such as medications.In the general population, the prevalence of hyperprolactinemia is 0.4%. The prevalence increases to as high as 17% in women with reproductive diseases, such as polycystic ovary syndrome. In cases of tumor-related hyperprolactinemia, prolactinoma is the most common culprit of consistently high levels of prolactin as well as the most common type of pituitary tumor. For non-tumor related hyperprolactinemia, the most common cause is medication-induced prolactin secretion. Particularly, antipsychotics have been linked to a majority of non-tumor related hyperprolactinemia cases due to their prolactin-rising and prolactin-sparing mechanisms. Typical antipsychotics have been shown to induce significant, dose-dependent increases in prolactin levels up to 10-fold the normal limit. Atypical antipsychotics vary in their ability to elevate prolactin levels, however, medications in this class such as risperidone and paliperidone carry the highest potential to induce hyperprolactinemia in a dose-dependent manner similar to typical antipsychotics. Signs and symptoms In women, high blood levels of prolactin are typically associated with hypoestrogenism, anovulatory infertility, and changes in menstruation. Menstruation disturbances experienced in women commonly manifests as amenorrhea or oligomenorrhea. In the latter case, irregular menstrual flow may result in abnormally heavy and prolonged bleeding (menorrhagia). Women who are not pregnant or nursing may also unexpectedly begin producing breast milk (galactorrhea), a condition that is not always associated with high prolactin levels. For instance, many premenopausal women experiencing hyperprolactinemia do not experience galactorrhea and only some women who experience galactorrhea will be diagnosed with hyperprolactinemia. Thus, galactorrhea may be observed in individuals with normal prolactin levels and does not necessarily indicate hyperprolactinemia. This phenomenon is likely due to galactorrhea requiring adequate levels of progesterone or estrogen to prepare the breast tissue. Additionally, some women may also experience loss of libido and breast pain, particularly when prolactin levels rise initially, as the hormone promotes tissue changes in the breast.In men, the most common symptoms of hyperprolactinemia are decreased libido, sexual dysfunction, erectile dysfunction/impotence, infertility, and gynecomastia. Unlike women, men do not experience reliable indicators of elevated prolactin such as menstruation to prompt immediate medical consultation. As a result, the early signs of hyperprolactinemia are generally more difficult to detect and may go unnoticed until more severe symptoms are present. For instance, symptoms such as loss of libido and sexual dysfunction are subtle, arise gradually, and may falsely indicate a differential cause. Many men with pituitary tumor-associated hyperprolactinemia may forego clinical help until they begin to experience serious endocrine and vision complications, such as major headaches or eye problems.Long-term hyperprolactinaemia can lead to detrimental changes in bone metabolism as a result of hypoestrogenism and hypoandrogenism. Studies have shown that chronically elevated prolactin levels lead to increased bone resorption and suppression of bone formation, leading to reduced bone density, increased risk of fractures, and increased risk of osteoporosis. The chronic presence of hyperprolactinemia can lead to hypogonadism and osteolysis in men. Causes Prolactin secretion is regulated by both stimulatory and inhibitory mechanisms. Dopamine acts on pituitary lactotroph D2 receptors to inhibit prolactin secretion while other peptides and hormones, such as thyrotropin releasing hormone (TRH), stimulate prolactin secretion. As a result, hyperprolactinemia may be caused by disinhibition (e.g., compression of the pituitary stalk or reduced dopamine levels) or excess production. The most common cause of hyperprolactinemia is prolactinoma (a type of pituitary adenoma). A blood serum prolactin level of 1000–5000 mIU/L (47-235 ng/mL) may arise from either mechanism, however levels >5000 mIU/L (>235 ng/mL) is likely due to the activity of an adenoma. Prolactin blood levels are typically correlated to the size the tumors. Pituitary tumors smaller than 10 mm in diameter, or microadenomas, tend to have prolactin levels <200 ng/mL. Macroadenomas larger than 10 mm in diameter possess prolactin >1000 ng/mL.Hyperprolactinemia inhibits the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus, which in turn inhibits the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland and results in diminished gonadal sex hormone production (termed hypogonadism). This is the cause of many of the symptoms described below. In many people, elevated prolactin levels remain unexplained and may represent a form of hypothalamic–pituitary–adrenal axis dysregulation. Physiological causes Physiological (i.e., non-pathological) causes include: ovulation, pregnancy, breastfeeding, chest wall injury, stress, stress-associated REM sleep, and exercise. During pregnancy, prolactin levels can range up to 600 ng/mL, depending on estrogen concentration. At 6 weeks post-birth (postpartum), estradiol concentrations decrease, and prolactin concentrations return to normal even during breastfeeding. Stress-related factors include physical, exercise, hypoglycemia, myocardial infarction, and surgery. Coitus and sleep can also contribute to an increased prolactin release. Medications Prolactin secretion in the pituitary is normally suppressed by the brain chemical dopamine, which binds to dopamine receptors. Drugs that block the effects of dopamine at the pituitary or deplete dopamine stores in the brain may cause the pituitary to secrete prolactin without an inhibitory effect. These drugs include the typical antipsychotics: phenothiazines such as chlorpromazine (Thorazine), and butyrophenones such as haloperidol (Haldol); atypical antipsychotics such as risperidone (Risperdal) and paliperidone (Invega); gastroprokinetic drugs used to treat gastro-esophageal reflux and medication-induced nausea (such as that from chemotherapy): metoclopramide (Reglan) and domperidone; less often, alpha-methyldopa and reserpine, used to control hypertension; and TRH. The use of estrogen-containing oral contraceptives are also known to increase prolactin levels when taken in high doses >35 μg. The sleep drug ramelteon (Rozerem) also increases the risk of hyperprolactinaemia. Particularly, the dopamine antagonists metoclopramide and domperidone are both powerful prolactin stimulators and have been used to stimulate breast milk secretion for decades. However, since prolactin is antagonized by dopamine and the body depends on the two being in balance, the risk of prolactin stimulation is generally present with all drugs that deplete dopamine, either directly or as a rebound effect. Specific diseases Prolactinoma or other tumors arising in or near the pituitary — such as those that cause acromegaly may block the flow of dopamine from the brain to the prolactin-secreting cells, likewise, division of the pituitary stalk or hypothalamic disease. Other causes include chronic kidney failure, hypothyroidism, bronchogenic carcinoma and sarcoidosis. Some women with polycystic ovary syndrome may have mildly-elevated prolactin levels. Nonpuerperal mastitis may induce transient hyperprolactinemia (neurogenic hyperprolactinemia) of about three weeks duration; conversely, hyperprolactinemia may contribute to nonpuerperal mastitis.Apart from diagnosing hyperprolactinemia and hypopituitarism, prolactin levels are often checked by physicians in those who have had a seizure, when there is need to differentiate between epileptic seizure or a non-epileptic seizure. Shortly after epileptic seizures, prolactin levels often rise, whereas they are normal in non-epileptic seizures. Diagnosis An appropriate diagnosis of hyperprolactinemia starts with conducting a complete clinical history before performing any treatment. Physiological causes, systemic disorders, and the use of certain drugs must be ruled out before the condition is diagnosed. Screening is indicated for those who are asymptomatic and those with elevated prolactin without an associated cause. The most common causes of hyperprolactinemia are prolactinomas, drug-induced hyperprolactinemia, and macroprolactinemia. Individuals with hyperprolactinemia may present with symptoms including galactorrhea, hypogonadism effects, and/or infertility. The magnitude that prolactin is elevated can be used as an indicator of the etiology of the hyperprolactinemia diagnosis. Prolactin levels over 250 ng/mL may suggest prolactinoma. Prolactin levels less than 100 ng/mL may suggest drug-induced hyperprolactinemia, macroprolactinemia, nonfunctioning pituitary adenomas, or systemic disorders.Elevated prolactin blood levels are typically assessed in women with unexplained breast milk secretion (galactorrhea) or irregular menses or infertility, and in men with impaired sexual function and milk secretion. If high prolactin levels are present, all known conditions and medications which raises prolactin secretion must be assessed and excluded for diagnosis. After ruling out other causes and prolactin levels remain high, TSH levels are assessed. If TSH levels are elevated, hyperprolactinemia is secondary to hypothyroidism and treated accordingly. If TSH levels are normal, an MRI or CT scan is conducted to assess for any pituitary adenomas. Although hyperprolactinemia is often uncommon in postmenopausal women, prolactinomas detected after menopause are typically macroadenomas. While a plain X-ray of the bones surrounding the pituitary may reveal the presence of a large macroadenoma, small microadenomas will not be apparent. Magnetic resonance imaging (MRI) is the most sensitive test for detecting pituitary tumors and determining their size. MRI scans may be repeated periodically to assess tumor progression and the effects of therapy. Computed Tomography (CT scan) is another indicator of abnormalities in pituitary gland size; it also gives an image of the pituitary, but is less sensitive than the MRI. In addition to assessing the size of the pituitary tumor, physicians also look for damage to surrounding tissues, and perform tests to assess whether production of other pituitary hormones are normal. Depending on the size of the tumor, physicians may request an eye exam that includes the measurement of visual fields.However, a high measurement of prolactin may also result from the presence of macroprolactin, otherwise known as big prolactin or big-big prolactin, in the serum. Macroprolactin occurs when prolactin polymerizes together and can bind with IgG to form complexes. Although this can result in high prolactin levels in some assay tests, macroprolactin is biologically inactive and will not cause symptoms typical of hyperprolactinemia. In those who are asymptomatic or without obvious causes of hyperprolactinemia, macroprolactin should be assessed and ruled out. Treatment Treatment for hyperprolactinemia is usually dependent upon its cause, ranging from hypothyroidism, drug-induced hyperprolactinemia, hypothalamic disease, idiopathic hyperprolactinemia, macroprolactin, or prolactinoma. Therefore, in order to provide the proper management of hyperprolactinemia, the pathological form and physiological increase in prolactin levels are differentiated, and the correct cause of hyperprolactinemia must be identified before treatment. For functional asymptomatic hyperprolactinemia, the treatment of choice is removing the associated cause, including antipsychotic therapy. However, prolactin levels should be drawn and monitored both prior to any discontinuation or changes to therapy, and afterwards. With symptomatic hyperprolactinemia, stopping antipsychotic drugs for a short trial period are not recommended due to the risk of exacerbation or relapse of symptoms. Options for treatment include decreasing the dose of antipsychotics, adding aripiprazole as an adjunctive therapy, and switching antipsychotics as a last resort. In pharmacologic hyperprolactinemia, the concerning drug can be switched to another treatment or discontinued entirely. Vitex agnus-castus extract may be tried in cases of mild hyperprolactinemia. No treatment is required in asymptomatic macroprolactin and instead, serial prolactin measurements and pituitary imaging is monitored in a regular follow-up appointments.Medical therapy is the preferred treatment in prolactinomas. In most cases, medications that are dopamine agonists, such as cabergoline and bromocriptine (often preferred when pregnancy is possible), are the treatment of choice used to decrease prolactin levels and tumor size upon the presence of microadenomas or macroadenomas. A systematic review and meta-analyses has shown that cabergoline is more effective in treatment of hyperprolactinemia than bromocriptine. Other dopamine agonists that have been used less commonly to suppress prolactin include dihydroergocryptine, ergoloid, lisuride, metergoline, pergolide, quinagolide, and terguride. If the prolactinoma does not initially respond to dopamine agonist therapy, such that prolactin levels are still high or the tumor is not shrinking as expected, the dose of the dopamine agonist can be increased in a stepwise fashion to the maximum tolerated dose. Another option is to consider switching between dopamine agonists. It is possible for the prolactinoma to be resistant to bromocriptine but respond well to cabergoline and vice versa. Surgical therapy can be considered if pharmacologic options have been exhausted.There is evidence to support improvement in outcomes of hyperprolactinemic individuals who have shown to be resistant to or intolerant of the treatment of choice, dopamine agonists, through radiotherapy and surgery. See also Hypothalamic–pituitary–prolactin axis Hypopituitarism References == External links ==

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

I'm not familiar with the medical term 'Oxazepam.' Could you provide some insights?

Oxazepam is a short-to-intermediate-acting benzodiazepine. Oxazepam is used for the treatment of anxiety and insomnia and in the control of symptoms of alcohol withdrawal syndrome. It is a metabolite of diazepam, prazepam, and temazepam, and has moderate amnesic, anxiolytic, anticonvulsant, hypnotic, sedative, and skeletal muscle relaxant properties compared to other benzodiazepines.It was patented in 1962 and approved for medical use in 1964. Medical uses It is an intermediate-acting benzodiazepine with a slow onset of action, so it is usually prescribed to individuals who have trouble staying asleep, rather than falling asleep. It is commonly prescribed for anxiety disorders with associated tension, irritability, and agitation. It is also prescribed for drug and alcohol withdrawal, and for anxiety associated with depression. Physicians may use oxazepam outside its approved indications to treat social phobia, post-traumatic stress disorder, insomnia, premenstrual syndrome, and other conditions. Side effects The side effects of oxazepam are similar to those of other benzodiazepines, and may include dizziness, drowsiness, headache, memory impairment, paradoxical excitement, and anterograde amnesia, but does not affect transient global amnesia. Side effects due to rapid decrease in dose or abrupt withdrawal from oxazepam may include abdominal and muscle cramps, convulsions, depression, inability to fall asleep or stay asleep, sweating, tremors, or vomiting.In September 2020, the U.S. Food and Drug Administration (FDA) required the boxed warning be updated for all benzodiazepine medicines to describe the risks of abuse, misuse, addiction, physical dependence, and withdrawal reactions consistently across all the medicines in the class. Tolerance, dependence and withdrawal Oxazepam, as with other benzodiazepine drugs, can cause tolerance, physical dependence, addiction, and benzodiazepine withdrawal syndrome. Withdrawal from oxazepam or other benzodiazepines often leads to withdrawal symptoms which are similar to those seen during alcohol and barbiturate withdrawal. The higher the dose and the longer the drug is taken, the greater the risk of experiencing unpleasant withdrawal symptoms. Withdrawal symptoms can occur, though, at standard dosages and also after short-term use. Benzodiazepine treatment should be discontinued as soon as possible by a slow and gradual dose reduction regimen. Contraindications Oxazepam is contraindicated in myasthenia gravis, chronic obstructive pulmonary disease, and limited pulmonary reserve, as well as severe hepatic disease. Special precautions Benzodiazepines require special precautions if used in the elderly, during pregnancy, in children, alcohol- or drug-dependent individuals, and individuals with comorbid psychiatric disorders. Benzodiazepines including oxazepam are lipophilic drugs and rapidly penetrate membranes, so rapidly crosses over into the placenta with significant uptake of the drug. Use of benzodiazepines in late pregnancy, especially high doses, may result in floppy infant syndrome. Pregnancy Oxazepam when taken during the third trimester, causes a definite risk to the neonate including a severe benzodiazepine withdrawal syndrome including hypotonia, and reluctance to suck, to apnoeic spells, cyanosis, and impaired metabolic responses to cold stress. Floppy infant syndrome and sedation in the newborn may also occur. Symptoms of floppy infant syndrome and the neonatal benzodiazepine withdrawal syndrome have been reported to persist from hours to months after birth. Interactions As oxazepam is an active metabolite of diazepam, an overlap in possible interactions is likely with other drugs or food, with exception of the pharmacokinetic CYP450 interactions (e.g. with cimetidine). Precautions and following the prescription are required when taking oxazepam (or other benzodiazepines) in combinations with antidepressant medication (SSRIs such as fluoxetine, sertraline, and paroxetine, or multiple reuptake inhibitors such as bupropion, duloxetine, or venlafaxine), potent painkillers (opioids, e.g. morphine, oxycodone or methadone). Concurrent use of these medicines (as well as other benzodiazepines) can interact in a way that is difficult to predict. Drinking alcohol when taking oxazepam is not recommended. Concomitant use of oxazepam and alcohol can lead to increased sedation, severe problems with coordination (ataxia), decreased muscle tone, and in severe cases or in predisposed patients, even to life-threatening intoxications with respiratory depression, coma, and collapse. There is a risk of blood circulation collapse, possibly the same condition as blood circulation syncope, when oxazepam is used in combination with quetiapine, an antipsychotic. Overdose Oxazepam is generally less toxic in overdose than other benzodiazepines. Important factors which affect the severity of a benzodiazepine overdose include the dose ingested, the age of the patient, and health status prior to overdose. Benzodiazepine overdoses can be much more dangerous if a coingestion of other CNS depressants such as opiates or alcohol has occurred. Symptoms of an oxazepam overdose include: Respiratory depression Excessive somnolence Altered consciousness Central nervous system depression Occasionally cardiovascular and pulmonary toxicity Rarely, deep coma Pharmacology Oxazepam is an intermediate-acting benzodiazepine of the 3-hydroxy family; it acts on benzodiazepine receptors, resulting in increased effect of GABA to the GABAA receptor which results in inhibitory effects on the central nervous system. The half-life of oxazepam is between 6 and 9 hours. It has been shown to suppress cortisol levels. Oxazepam is the most slowly absorbed and has the slowest onset of action of all the common benzodiazepines according to one British study.Oxazepam is an active metabolite formed during the breakdown of diazepam, nordazepam, and certain similar drugs. It may be safer than many other benzodiazepines in patients with impaired liver function because it does not require hepatic oxidation, but rather, it is simply metabolized by glucuronidation, so oxazepam is less likely to accumulate and cause adverse reactions in the elderly or people with liver disease. Oxazepam is similar to lorazepam in this respect. Preferential storage of oxazepam occurs in some organs, including the heart of the neonate. Absorption by any administered route and the risk of accumulation is significantly increased in the neonate, and withdrawal of oxazepam during pregnancy and breast feeding is recommended, as oxazepam is excreted in breast milk.2 mg of oxazepam equates to 1 mg of diazepam according to the benzodiazepine equivalency converter, therefore 20 mg of oxazepam according to BZD equivalency equates to 10 mg of diazepam and 15 mg oxazepam to 7.5 mg diazepam (rounded up to 8 mg of diazepam). Some BZD equivalency converters use 3 to 1 (oxazepam to diazepam), 1 to 3 (diazepam to oxazepam) as the ratio (3:1 and 1:3), so 15 mg of oxazepam would equate to 5 mg of diazepam. Chemistry Oxazepam exists as a racemic mixture. Early attempts to isolate enantiomers were unsuccessful; the corresponding acetate has been isolated as a single enantiomer. Given the different rates of epimerization that occur at different pH levels, it was determined that there would be no therapeutic benefit to the administration of a single enantiomer over the racemic mixture. Frequency of use Oxazepam, along with diazepam, nitrazepam, and temazepam, were the four benzodiazepines listed on the pharmaceutical benefits scheme and represented 82% of the benzodiazepine prescriptions in Australia in 1990–1991. It is in several countries the benzodiazepine of choice for novice users, due to a low chance of accumulation and a relatively slow absorption speed. Society and culture Misuse Oxazepam has the potential for misuse, defined as taking the drug to achieve a high, or continuing to take the drug in the long term against medical advice. Benzodiazepines, including diazepam, oxazepam, nitrazepam, and flunitrazepam, accounted for the largest volume of forged drug prescriptions in Sweden from 1982 to 1986. During this time, a total of 52% of drug forgeries were for benzodiazepines, suggesting they were a major prescription drug class of abuse.However, due to its slow rate of absorption and its slow onset of action, oxazepam has a relatively low potential for abuse compared to some other benzodiazepines, such as temazepam, flunitrazepam, or triazolam, which have a high potential for abuse similar to barbiturates. Legal status Oxazepam is a Schedule IV drug under the Convention on Psychotropic Substances. Brand names It is marketed under many brand names worldwide, including: Alepam, Alepan, Anoxa, Anxiolit, Comedormir, durazepam, Murelax, Nozepam, Oksazepam, Opamox, Ox-Pam, Oxa-CT, Oxabenz, Oxamin, Oxapam, Oxapax, Oxascand, Oxaze, Oxazepam, Oxazépam, Oxazin, Oxepam, Praxiten, Purata, Selars, Serax, Serenal, Serepax, Seresta, Séresta, Serpax, Sobril, Tazepam, Vaben, and Youfei.It is also marketed in combination with hyoscine as Novalona and in combination with alanine as Pausafrent T. Environmental concerns In 2013, a laboratory study which exposed European perch to oxazepam concentrations equivalent to those present in European rivers (1.8 micrograms liter−1) found that they exhibited increased activity, reduced sociality, and higher feeding rate. In 2016, a follow-up study which exposed salmon smolt to oxazepam for seven days before letting them migrate observed increased intensity of migratory behaviour compared to controls. A 2019 study associated this faster, bolder behaviour in exposed smolt to increased mortality due to a higher likelihood of being predated on.On the other hand, a 2018 study from the same authors, which kept 480 European perch and 12 northern pikes in 12 ponds over 70 days, half of them control and half spiked with oxazepam, found no significant difference in either perch growth or mortality. However, it suggested that the latter could be explained by the exposed perch and pike being equally hampered by oxazepam, rather than the lack of an overall effect. Lastly, a 2021 study built on these results by comparing two whole lakes filled with perch and pikes - one control while the other was exposed to oxazepam 11 days into experiment, at concentrations between 11 and 24 μg L−1, which is 200 times greater than the reported concentrations in the European rivers. Even so, there were no measurable effects on pike behaviour after the addition of oxazepam, while the effects on perch behaviour were found to be negligible. The authors concluded that the effects previously attributed to oxazepam were instead likely caused by a combination of fish being stressed by human handling and small aquaria, followed by being exposed to a novel environment. References External links Inchem - Oxazepam

You are an assistant in medical learning. Your role is to clarify medical terminology, ensuring the information is both accurate and accessible.

Could you offer a clear explanation of the term 'Gallstone ileus' as used in the medical field?

Gallstone ileus is a rare form of small bowel obstruction caused by an impaction of a gallstone within the lumen of the small intestine. Such a gallstone enters the bowel via a cholecysto-enteric fistula. The presence of large stones, >2.5 cm in diameter, within the gallbladder are thought to predispose to fistula formation by gradual erosion through the gallbladder fundus. Once a fistula has formed, a stone may travel from the gallbladder into the bowel and become lodged almost anywhere along the gastrointestinal tract. Obstruction occurs most commonly at the near the distal ileum, within 60 cm proximally to the ileocecal valve. Rarely, gallstone ileus may recur if the underlying fistula is not treated.First described by Thomas Bartholin in 1654, the name "gallstone ileus" is a misnomer because an ileus is, by definition, a non-mechanical bowel motility failure (as opposed to a mechanical obstruction by a stone). Diagnosis Diagnosis of gallstone ileus requires radiographic studies. Classic radiographic findings are known as Riglers triad: pneumobilia (air within the biliary tree) evidence of small bowel obstruction radiopaque gallstone on abdominal radiograph Treatment Initial management involves fluid resuscitation and potentially nasogastric suctioning. Since gallstone ileus constitutes a form of mechanical small bowel obstruction, it can be a surgical emergency and requires open or laparoscopic surgery to remove an impacted stone. The different strategies for surgical management are either enterolithotomy alone, allowing a delayed cholecystectomy after an inflammation-free period of 4–6 weeks (and therefore two-stage surgery) or enterolithotomy in combination with a cholecystectomy and fistula division (one-stage surgery). The different strategies for surgical management are controversial, and depend on factors such as patient fitness for surgery and comorbidities. Eponym Bouverets syndrome refers to reverse gallstone ileus where the gallstone propagates proximally and causes gastric outlet obstruction by being impacted in first part of duodenum. References == External links ==

You function as a medical dictionary. Offer comprehensive and accurate descriptions of medical terms, ensuring clarity and depth in your explanations.

Could you offer a clear explanation of the term 'Weakness' as used in the medical field?

Weakness is a symptom of a number of different conditions. The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis. Pathophysiology Muscle cells work by detecting a flow of electrical impulses from the brain, which signals them to contract through the release of calcium by the sarcoplasmic reticulum. Fatigue (reduced ability to generate force) may occur due to the nerve, or within the muscle cells themselves. New research from scientists at Columbia University suggests that muscle fatigue is caused by calcium leaking out of the muscle cell. This makes less calcium available for the muscle cell. In addition, the Columbia researchers propose that an enzyme activated by this released calcium eats away at muscle fibers.Substrates within the muscle generally serve to power muscular contractions. They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate. ATP binds to the myosin head and causes the ratchetting that results in contraction according to the sliding filament model. Creatine phosphate stores energy so ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5–7 seconds. Glycogen is the intramuscular storage form of glucose, used to generate energy quickly once intramuscular creatine stores are exhausted, producing lactic acid as a metabolic byproduct. Contrary to common belief, lactic acid accumulation doesnt actually cause the burning sensation felt when people exhaust their oxygen and oxidative metabolism, but in actuality, lactic acid in presence of oxygen recycles to produce pyruvate in the liver, which is known as the Cori cycle.Substrates produce metabolic fatigue by being depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions. In essence, the muscle stops contracting because it lacks the energy to do so. Differential diagnosis True vs. perceived weakness True weakness (or neuromuscular) describes a condition where the force exerted by the muscles is less than would be expected, for example muscular dystrophy. Perceived weakness (or non-neuromuscular) describes a condition where a person feels more effort than normal is required to exert a given amount of force but actual muscle strength is normal, for example chronic fatigue syndrome.In some conditions, such as myasthenia gravis, muscle strength is normal when resting, but true weakness occurs after the muscle has been subjected to exercise. This is also true for some cases of chronic fatigue syndrome, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions. Asthenia vs. myasthenia Asthenia (Greek: ἀσθένεια, lit lack of strength but also disease) is a medical term referring to a condition in which the body lacks or has lost strength either as a whole or in any of its parts. It denotes symptoms of physical weakness and loss of strength. General asthenia occurs in many chronic wasting diseases (such as tuberculosis and cancer), sleep disorders or chronic disorders of the heart, lungs or kidneys, and is probably most marked in diseases of the adrenal gland. Asthenia may be limited to certain organs or systems of organs, as in asthenopia, characterized by ready fatiguability. Asthenia is also a side effect of some medications and treatments, such as Ritonavir (a protease inhibitor used in HIV treatment). Differentiating psychogenic (perceived) asthenia and true asthenia from myasthenia is often difficult, and in time apparent psychogenic asthenia accompanying many chronic disorders is seen to progress into a primary weakness.Myasthenia (my- from Greek μυο meaning "muscle" + -asthenia ἀσθένεια meaning "weakness"), or simply muscle weakness, is a lack of muscle strength. The causes are many and can be divided into conditions that have either true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular diseases, such as myasthenia gravis. Types Muscle fatigue can be central, neuromuscular, or peripheral muscular. Central muscle fatigue manifests as an overall sense of energy deprivation, and peripheral muscle weakness manifests as a local, muscle-specific inability to do work. Neuromuscular fatigue can be either central or peripheral. Central fatigue The central fatigue is generally described in terms of a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output. It has been suggested that the reduced neural drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity. The exact mechanisms of central fatigue are unknown, though there has been considerable interest in the role of serotonergic pathways. Neuromuscular fatigue Nerves control the contraction of muscles by determining the number, sequence, and force of muscular contraction. When a nerve experiences synaptic fatigue it becomes unable to stimulate the muscle that it innervates. Most movements require a force far below what a muscle could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue.For extremely powerful contractions that are close to the upper limit of a muscles ability to generate force, neuromuscular fatigue can become a limiting factor in untrained individuals. In novice strength trainers, the muscles ability to generate force is most strongly limited by nerves ability to sustain a high-frequency signal. After an extended period of maximum contraction, the nerves signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the muscle appears to simply stop listening and gradually cease to move, often lengthening. As there is insufficient stress on the muscles and tendons, there will often be no delayed onset muscle soreness following the workout. Part of the process of strength training is increasing the nerves ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force. It is this "neural training" that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force. Peripheral muscle fatigue Peripheral muscle fatigue during physical work is considered an inability for the body to supply sufficient energy or other metabolites to the contracting muscles to meet the increased energy demand. This is the most common case of physical fatigue—affecting a national average of 72% of adults in the work force in 2002. This causes contractile dysfunction that manifests in the eventual reduction or lack of ability of a single muscle or local group of muscles to do work. The insufficiency of energy, i.e. sub-optimal aerobic metabolism, generally results in the accumulation of lactic acid and other acidic anaerobic metabolic by-products in the muscle, causing the stereotypical burning sensation of local muscle fatigue, though recent studies have indicated otherwise, actually finding that lactic acid is a source of energy.The fundamental difference between the peripheral and central theories of muscle fatigue is that the peripheral model of muscle fatigue assumes failure at one or more sites in the chain that initiates muscle contraction. Peripheral regulation therefore depends on the localized metabolic chemical conditions of the local muscle affected, whereas the central model of muscle fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating muscle fatigue through muscle derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. Therefore, the feedback that is read by this central regulator could include chemical and mechanical as well as cognitive cues. The significance of each of these factors will depend on the nature of the fatigue-inducing work that is being performed.Though not universally used, "metabolic fatigue" is a common alternative term for peripheral muscle weakness, because of the reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the myocytes. This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca2+ to stimulate actin and myosin to contract. Management References External links McArdles disease

You are a facilitator of medical knowledge. Provide thorough and accessible explanations of medical terms, catering to both specialists and non-specialists.

I'm encountering the term 'Quintuplets' in medical literature. What's its definition?

Quintuplets is an American sitcom that aired 22 episodes on Fox from June 16, 2004 to January 12, 2005. The program starred Andy Richter and Rebecca Creskoff and shared some of their experiences parenting teenage quintuplets. Synopsis The series is set in Nutley, New Jersey, and looks like a typical family sitcom. Much of the storyline focuses on the difficulty of supporting a large family of teens, both financially and emotionally, as they grapple with the reality that theyre no longer as cute as when they were babies. The house is a typical three-bedroom family home. The three male siblings share a room with bunk beds, the two females share another room. The kitchen contains a double-wide beer cooler as a refrigerator, and the basement contains a walk-in freezer, both to store the large amounts of food such a large family requires. The situation may be seen to parallel and parody the old sitcom The Brady Bunch, by highlighting the impracticality of the large family. The theme song, "Suck or Shine," was performed by Chris and Tad. Cast and characters Bob Chase (Andy Richter) – The father sells office cubicles and barely makes enough money to support his large family. Most of his time is spent trying to save money, and he only occasionally provides parenting for his five teens, but hed prefer to get away whenever he has the chance. He also opines that he thinks half his children are freaks, blaming this and the fact that there were so many at once, on the fact that they were artificially inseminated. Carol Chase (Rebecca Creskoff) – The mother maintains the large family and house in "typical sitcom homemaker" mode. In one episode she attempts to go back to work, but nobody wants her because shes been raising kids for 15 years. She goes back to being a homemaker and remains one for the rest of the show. She enforces the house rules. Parker Chase (Jake McDorman) – The popular boy. Tallest of the children, good-looking, successful in academics and sports. He teases his brothers mercilessly, especially Pearce, but is also quick to defend them. The male quints share a deep bond, probably from sharing the womb. At one point the youngest and shortest, Patton, says that Parker took all the good genes and left him with the short ones and Pearce with the weird ones. Pearce Chase (Johnny K. Lewis) – The curly-haired weirdest quint. He boldly shares with anyone his strange perspective on just about any subject, and is so odd that he no longer responds to rejection. Penny Chase (April Matson) – The intellectual, who is vigorously nonconformist. Her taste in clothing and hairstyle frequently gets her mistaken for the typical goth. She enjoys reading and sometimes feels inadequate to Paige. Paige Chase (Sarah Wright) – The beautiful girl. She spends most of her time thinking of and attending to her appearance. Shes not the brightest of the family, but shes bubbly and kind. Patton Chase (Ryan Pinkston) – The youngest of the children, and the shortest at 410". This is a source of amusement to the family and shame to the father, and the mother is often overly-nurturing. He takes growth hormones. He is girl-crazy and his typical line to girls (and, in one episode, a guy when he was pretending to be gay to avoid being pulverized) is, "Yes I am, you likey?." It usually works, but his sisters often find it disgusting. Episodes See also Arrested Development – in which Richter himself played a set of identical quintuplets. References External links Quintuplets at IMDb

You function as a medical informant. Please provide in-depth yet accessible descriptions of medical terms, suitable for a broad audience.

Could you provide a brief overview of 'Chylomicron retention disease' in a medical context?

Chylomicron retention disease is a disorder of fat absorption. It is associated with SAR1B. Mutations in SAR1B prevent the release of chylomicrons in the circulation which leads to nutritional and developmental problems. It is a rare autosomal recessive disorder with around 40 cases reported worldwide. Since the disease allele is recessive, parents usually do not show symptoms.Without functional chylomicrons, certain fat-soluble vitamins such as vitamin D and vitamin E cannot be absorbed. Chylomicrons have a crucial role in fat absorption and transport, thus a deficiency in chylomicron functioning reduces available levels of dietary fats and fat-soluble vitamins. History Chylomicron Retention Disease, also called Andersons disease, is an autosomal recessive lipid malabsorption syndrome characterized by abnormally low amounts of cholesterol in the blood. This disease most frequently is diagnosed in infants. Charlotte Anderson first published a description of the disorder in 1961, where she observed a seven month old girl who developed intestinal mucosa filled with fat droplets. In 2003, Jones and colleagues identified mutations in the SAR1B gene, which transcripts the SAR1B protein involved in COPII transport and proposed this was the molecular defect of the disorder. To present day, 17 mutations of the SAR1B gene have been discovered. This disease is rare, with only 50 cases diagnosed worldwide. Genetics The Sar1B GTPase is an enzyme located in epithelial cells of the gastrointestinal tract. These proteins are critical for release of chylomicrons in the body.Chylomicron retention disease is an autosomal homozygous recessive disorder arising from mutations in the gene encoding the Sar1B GTPase. The Sar1B gene is located at position 5q31.1 in the fifth chromosome and is composed of eight exons. Alternative splicing of the second exon results into two different splice isoforms for the Sar1B transcript RNA. In CMRD, a mutation of this genomic sequence affects the Sar1B enzymes ability to interact with Guanine Exchange Factors (GEFs) and GTP-Activating Proteins (GAPs). The mutation of exon 6 of the sequence can eliminate the critical chain that is responsible for recognizing guanine. This strips the GTPase of its capability to hydrolyze GTP, its hallmark trait. This overall affects the ability of Sar1B GTPase to control chylomicron release. A third mutant allele containing a missense mutation has also been reported to cause CMRD. All three of these alleles display recessive inheritance, suggesting that they loss-of-function mutations cause the symptoms of CMRD. Physiology During digestion, fats, or triglycerides(TGs), are enzymatically catabolized by lipases into two fatty acids and a monoglyceride molecule. Those components are then transported across the enterocyte membrane as micelles and reformed into triglycerides once across the membrane.Once transported to the ER the triglycerides are incorporated into pre-chylomicrons which are made up of TGs, cholesterol, and phospholipids. The pre-chylomicrons are then packaged into PCTV in order to be transported to the Golgi apparatus for additional maturation prior to exocytosis into the lymphatic system. From the lymphatic system, they enter general circulation, where they are produced in various forms that can be absorbed by bodily tissues and metabolized or stored by adipose tissue. Before the PCTV leaves the ER, it is incorporated into a COPII coatomer of five proteins. The PCTV undergoes a similar mechanism for budding as normal COPII transport vesicles. Though PCTV does not require COPII coatomer proteins for budding from the ER, association with the coatomer is necessary for docking and fusion with the cis-golgi network. In chylomicron retention disease, the PCTV vesicles are competent for budding from the ER membrane but are defective for fusion with the cis-golgi body. Sar1B is a GTPase and one of the five proteins of the COPll coatomer. A mutation in the sar1B gene and subsequently the sar1B protein are the common genetic origins of chylomicron retention disorder. Without the fully functional sar1B protein, the COPll coatomer proteins engulf pre-chylomicrons exiting the ER but are unable to disassemble upon arrival at the cis-Golgi, preventing membrane fusion with this organelle. Signs and symptoms Physical symptoms of CMRD involving development and function of the gastrointestinal tract and nervous system typically manifest between infancy and adolescence. The symptoms of CmRD are similar to the physical symptoms of malnutrition, as the disease arises due to the poor absorption of lipids and fat-soluble nutrients such as vitamin E. For this reason, the disease is likely to be under-diagnosed by physicians . Fat-soluble nutrients are essential for growth, development, and normal bodily function. Vitamin E deficiency is especially serious, as the vitamin is necessary for proper neurological function and development. Without Vitamin E, neurons cannot operate correctly and signals from the brain are weakened. This leads to reduced muscle development and reduced muscle contraction. Symptoms that manifest in the GI tract are likely to be a consequence of both reduced absorption of fats and physiological stress imposed on enterocytes that can not shuttle fats into circulation . Additional symptoms that occur throughout the body can be attributed to the lack of sufficient lipid sources. Chronic Malabsorptive Diarrhea- Diarrhea that results from the poor absorption of fats Steatorrhea- Abnormal stools, often foul smelling, due to the increased presence of undigested fats Vomiting Vitamin E Deficiency- Low levels of Vitamin E due to the malabsorption of fats in the diet, causes poor brain, muscle, and eye development. Cardiomyopathy- A class of disease that affects heart muscle, causing shortness of breath, tiredness, and swelling of the legs Slowed Growth Failure to Thrive- Insufficient weight gain, or drastic levels of weight loss in children Hypocholesterolemia- Low blood cholesterol levels Hepatic Steatosis (Fatty Liver)- Excessive fat buildup in the liver, a result of the abnormal lipid panels of CMRD patients Hyporeflexia- Absent or low levels of muscle reflexes Amyotrophy- Muscle tissue “wasting,” the loss of muscle tissue Diagnosis There is no medical consensus on methodology of diagnosis for CMRD itself. There are, however, protocols used to diagnose the family of genetic disorders to which CMRD belongs. Assessment of hypobetalipoproteinemia relies chiefly on blood lipid analysis following a 12-hr fasting period. Lipids analyzed are LDL (low-density lipoproteins), triglyceride, and apolipoprotein B levels. A patient could be diagnosed with CMRD should they lack sufficient apolipoprotein B levels in the blood. Furthermore, a minimally invasive endoscopic procedure can be used to examine the bowel. A pale intestine can also be indicative of CMRD.Because patient outcomes rely on early diagnosis, it is recommended that candidates for the disorder should receive lipid panel testing prior to 6 months of age. In patients with only CMRD, lipid panels are expected to display normal triglyceride levels, but LDL and HDL levels may >50% below normal range. The test should also reveal low levels of Vitamin E and heightened levels of creatine kinase in the blood. Prognosis As of March 2020, only 50 cases of CMRD have been documented in the medical literature. This small number speaks to the rarity of the disease as well as the lack of thorough research and documentation. As a result, the full course of the disease, life expectancy, and mortality are also poorly documented. Clinical manifestation of CMRD symptoms begin during infancy and early childhood but may go undetected due to the non-specific symptoms associated with the disease. Many of these symptoms can be attributed to malnutrition and nonspecific postnatal diarrhea, confounding early diagnosis. Careful regulation of diet and nutrition are required for management of CMRD since the disease results from the poor absorption of nutrients from food. Treatment It is recommended that patients with CMRD follow a strict low-fat diet in addition to fat-soluble vitamin supplementation. The fat soluble vitamins are A,D,E, and K. A combination of vitamin A and vitamin E are effective for combating ophthalmologic complications. When vitamin D is administered early, it aids in preventing osteopenia. People with CMRD are at an increased risk for essential fatty acid deficiency, so dietary counseling is required in order to maintain the low-fat diet, while attaining sufficient caloric intake and essential fatty acid intake. Proposed Treatment Plan Early diagnosis is important for improving patient outcomes. Patients with delayed diagnoses experienced decreased growth compared to those diagnosed earlier in life. Long-term treatment plans center around dietary management, but because long term results have not been documented due to a lack of thorough research, careful monitoring of the disease is required. Yearly check-ups are recommended to track the growth of children affected by the disease. Evaluations tracking liver function that involve the use of ultrasounds to monitor liver growth, are recommended to be administered every three years. At about ten years of age (pre-puberty), neurological and ophthalmological exams may be required every three years to track muscle and eye activity/strength. In adulthood, past eighteen years of age, echocardiograms are recommended to track heart activity. Thorough and vigorous testing warrant themselves to the treatment of a disease of which we know so little. == References ==

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I've come across the term 'Effusion' in a medical context, but I'm not sure what it means. Can you clarify?

In physics and chemistry, effusion is the process in which a gas escapes from a container through a hole of diameter considerably smaller than the mean free path of the molecules. Such a hole is often described as a pinhole and the escape of the gas is due to the pressure difference between the container and the exterior. Under these conditions, essentially all molecules which arrive at the hole continue and pass through the hole, since collisions between molecules in the region of the hole are negligible. Conversely, when the diameter is larger than the mean free path of the gas, flow obeys the Sampson flow law. In medical terminology, an effusion refers to accumulation of fluid in an anatomic space, usually without loculation. Specific examples include subdural, mastoid, pericardial and pleural effusions. Etymology The word effusion derives from the Latin word, effundo, which means "shed, pour forth, pour out, utter, lavish, waste." Effusion into vacuum Effusion from an equilibrated container into outside vacuum can be calculated based on kinetic theory. The number of atomic or molecular collisions with a wall of a container per unit area per unit time (impingement rate) is given by: assuming mean free path is much greater than pinhole diameter and the gas can be treated as an ideal gas.If a small area A {\displaystyle A} on the container is punched to become a small hole, the effusive flow rate will be where M {\displaystyle M} is the molar mass, N A {\displaystyle N_{A}} is the Avogadro constant, and R = N A k B {\displaystyle R=N_{A}k_{B}} is the gas constant. The average velocity of effused particles is Combined with the effusive flow rate, the recoil/thrust force on the system itself is An example is the recoil force on a balloon with a small hole flying in vacuum. Measures of flow rate According to the kinetic theory of gases, the kinetic energy for a gas at a temperature T {\displaystyle T} is 1 2 m v r m s 2 = 3 2 k B T {\displaystyle {\frac {1}{2}}mv_{\rm {rms}}^{2}={\frac {3}{2}}k_{\rm {B}}T} where m {\displaystyle m} is the mass of one molecule, v r m s {\displaystyle v_{\rm {rms}}} is the root-mean-square speed of the molecules, and k B {\displaystyle k_{\rm {B}}} is the Boltzmann constant. The average molecular speed can be calculated from the Maxwell speed distribution as v a v g = 8 / 3 π v r m s ≈ 0.921 v r m s {\textstyle v_{\rm {avg}}={\sqrt {8/3\pi }}\ v_{\rm {rms}}\approx 0.921\ v_{\rm {rms}}} (or, equivalently, v r m s = 3 π / 8 v a v g ≈ 1.085 v a v g {\textstyle v_{\rm {rms}}={\sqrt {3\pi /8}}\ v_{\rm {avg}}\approx 1.085\ v_{\rm {avg}}} ). The rate Φ N {\displaystyle \Phi _{N}} at which a gas of molar mass M {\displaystyle M} effuses (typically expressed as the number of molecules passing through the hole per second) is then Φ N = Δ P A N A 2 π M R T . {\displaystyle \Phi _{N}={\frac {\Delta PAN_{A}}{\sqrt {2\pi MRT}}}.} Here Δ P {\displaystyle \Delta P} is the gas pressure difference across the barrier, A {\displaystyle A} is the area of the hole, N A {\displaystyle N_{A}} is the Avogadro constant, R {\displaystyle R} is the gas constant and T {\displaystyle T} is the absolute temperature. Assuming the pressure difference between the two sides of the barrier is much smaller than P a v g {\displaystyle P_{\rm {avg}}} , the average absolute pressure in the system (i.e. Δ P ≪ P a v g {\displaystyle \Delta P\ll P_{\rm {avg}}} ), it is possible to express effusion flow as a volumetric flow rate as follows: Φ V = Δ P d 2 P a v g π k B T 32 m {\displaystyle \Phi _{V}={\frac {\Delta Pd^{2}}{P_{\rm {avg}}}}{\sqrt {\frac {\pi k_{B}T}{32m}}}} or Φ V = Δ P d 2 P a v g π R T 32 M {\displaystyle \Phi _{V}={\frac {\Delta Pd^{2}}{P_{\rm {avg}}}}{\sqrt {\frac {\pi RT}{32M}}}} where Φ V {\displaystyle \Phi _{V}} is the volumetric flow rate of the gas, P a v g {\displaystyle P_{\rm {avg}}} is the average pressure on either side of the orifice, and d {\displaystyle d} is the hole diameter. Effect of molecular weight At constant pressure and temperature, the root-mean-square speed and therefore the effusion rate are inversely proportional to the square root of the molecular weight. Gases with a lower molecular weight effuse more rapidly than gases with a higher molecular weight, so that the number of lighter molecules passing through the hole per unit time is greater. Grahams law Scottish chemist Thomas Graham (1805–1869) found experimentally that the rate of effusion of a gas is inversely proportional to the square root of the mass of its particles. In other words, the ratio of the rates of effusion of two gases at the same temperature and pressure is given by the inverse ratio of the square roots of the masses of the gas particles. Rate of effusion of gas 1 Rate of effusion of gas 2 = M 2 M 1 {\displaystyle {{\mbox{Rate of effusion of gas}}_{1} \over {\mbox{Rate of effusion of gas}}_{2}}={\sqrt {M_{2} \over M_{1}}}} where M 1 {\displaystyle M_{1}} and M 2 {\displaystyle M_{2}} represent the molar masses of the gases. This equation is known as Grahams law of effusion. The effusion rate for a gas depends directly on the average velocity of its particles. Thus, the faster the gas particles are moving, the more likely they are to pass through the effusion orifice. Knudsen effusion cell The Knudsen effusion cell is used to measure the vapor pressures of a solid with very low vapor pressure. Such a solid forms a vapor at low pressure by sublimation. The vapor slowly effuses through a pinhole, and the loss of mass is proportional to the vapor pressure and can be used to determine this pressure. The heat of sublimation can also be determined by measuring the vapor pressure as a function of temperature, using the Clausius–Clapeyron relation. == References ==

You are a facilitator of medical knowledge. Provide thorough and accessible explanations of medical terms, catering to both specialists and non-specialists.

Could you please explain the term 'Psychogenic alopecia' in simple language?

Psychogenic alopecia, also called over-grooming or psychological baldness, is a compulsive behavior that affects domestic cats. Generally, psychogenic alopecia does not lead to serious health consequences or a decreased lifespan. Causes Grooming is a natural behavior for cats. Cats spend 5–25% of their waking hours grooming. Grooming becomes excessive when it takes precedence over other activities or no longer seems functional. Excessive grooming, which can lead to hair loss, skin wounds, and ulceration, can result from chronic stress or develop in cats who already exhibit nervous temperaments. Even when the source of stress is resolved or removed, excessive grooming may continue. There may be some genetic basis for the behavior, and it predominantly affects purebred cats of oriental breeds, but can develop in any feline. Female cats appear more susceptible. Environmental factors suspected of causing over-grooming include flea allergy, boredom, food allergy, dust or pollen causing an allergic reaction, constipation and urinary tract infection caused by avoidance of a dirty litter tray, dermatitis, and anxiety caused by inconsistent meal times. Deprivation of sunlight could be the part of the problem for indoors only cats. Symptoms Areas affected are those the cat can access most easily, including the abdomen, legs, flank, and chest. Baldness, usually beginning with the abdomen. Obvious over-grooming (although some cats may only engage in the behavior in the absence of owners). Redness, rashes, pus, scabs on the bald area or areas traumatized by over-grooming. A highly irritable cat may even cut its face with the claw of its hind foot if over-zealously scratching the back of its head. Treatment The cat should be taken to a veterinarian. The most suspected cause of skin problems in cats will be fleas. Other causes of over-grooming are not as easily ascertained. As household antiseptics are known to be toxic to cats, veterinary antiseptics for cats can be used to treat open sores, if they do occur. Sores can also be treated with cream, oral or injected anti-inflammatories, however if the problem continues to recur it may be more cost effective to subject the cat to laboratory testing early on. It may be difficult to keep a clean dressing on a cats belly, and an anti-lick collar is adequate to let the wound heal. If an anti-lick collar is used, a soft anti-lick collar is less cumbersome, although they are less durable. If the cat wears a plastic anti-lick collar, it may use the edge of the collar to grind against existing wounds, making them worse. A soft anti-lick collar will become less effective as it is kicked out of the shape by the cats hind leg, and will need prompt replacement. The cat can sanitize the wound if the collar is removed for daily short periods of time, also giving the cat an opportunity for an overall grooming. Scratches and wounds can heal completely using this method. When the cat stops wearing the collar, thinned hair, redness of skin or cracked nipples on the cat are early indicators that the cat has started to over-groom again. Antidepressants for cats may be suggested by a vet. See also Cat flea Cat health Cat skin disorders Feather-plucking Trichotillomania: a compulsive hair-pulling behavior in humans that can cause hair loss == References ==

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What does the medical term 'Small plaque parapsoriasis' encompass?

Small plaque parapsoriasis characteristically occurs with skin lesions that are round, oval, discrete patches or thin plaques, mainly on the trunk.: 452 : 207 Subtypes: Xanthoerythrodermia perstans is a distinct variant with lesions that are yellow in color.: 452  Digitate dermatosis is a distinct variant with lesions in the shape of a finger and distributed symmetrically on the flanks.: 452 See also Parapsoriasis List of cutaneous conditions References == External links ==

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Can you demystify the medical term 'Metatarsophalangeal joint sprain' for me?

A metatarsophalangeal joint sprain is an injury to the connective tissue between the foot and a toe (at a metatarsophalangeal joint, one of the joints in the ball of the foot). When the big toe is involved, it is known as "turf toe". Causes Turf toe is named from the injury being associated with playing sports on rigid surfaces such as artificial turf and is a fairly common injury among professional American football players. Often, the injury occurs when someone or something falls on the back of the calf while that legs knee and tips of the toes are touching the ground. The toe is hyperextended and thus the joint is injured. Additionally, athletic shoes with very flexible soles combined with cleats that "grab" the turf will cause overextension of the big toe. This can occur on the lesser toes as well. It has also been observed in sports beyond American football, including soccer, baseball, basketball, rugby, volleyball, and tae kwon do. This is a primary reason why many athletes prefer natural grass to turf, because it is softer. Treatment The injury can be debilitating for athletes of many sports who need to accelerate, quickly change direction, or jump. Use of the toes is not possible during the healing process. Since the toes are necessary for proper push-off when accelerating, those sorts of athletic activities should be almost completely curtailed. An extended healing period of one or more months is often required.Because of the anatomy of the distal foot and the unique use of the foot, it is often impossible to properly tape or brace the joint. Although difficult, it is not impossible to tape the toe to limit extension (upward bend of toe). Additionally, wearing a shoe with a rigid sole (often a metal plate) and cushioned innersole will help minimize extension of the joint. Anti-inflammatory medication, as well as physical therapy, is recommended.Turf toe is usually healed in about 2–3 weeks. It can become more serious if left untreated, and may cause serious problems for the athlete. Treating the injury includes icing of the area, elevating the foot, or possibly the use of custom orthotics. See also Broken toe Joggers toe References == External links ==

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I'm seeking clarification on the medical term 'Naftifine.' Could you explain it?

Naftifine hydrochloride (brand names include Exoderil and Naftin) is an allylamine antifungal drug for the topical treatment of tinea pedis, tinea cruris, and tinea corporis (topical fungal infections). Naftifine has triple action: antifungal, antibacterial, and anti-inflammatory. Its fungistatic activity is believed to be based on inhibition of the squalene-2,3-epoxidase enzyme, which in turn results in the shortage of ergosterol required for the formation of fungal cell membranes. With some fungal species, there is also fungicidal activity from a resulting accumulation of squalenes, leading to damage of the fungal cell membranes, including at the endoplasmatic reticulum. The half-life is approximately 2–3 days. The metabolites are excreted in the urine and feces.Naftifine was invented at the Sandoz Research Institute in Vienna, Austria. It was the first succesful antifungal medication of the allylamine class. Naftifine shows mostly fungicidal activity toward dematophytes and molds, and mostly fungistatic activity toward yeasts. It is also effective as an antibacterial agent in treating pyoderma. Naftifine is almost completely metabolized in the human body, with a half-life of 2–3 days. Its metabolytes do not have antifungal activity, and they are excreted with urine and bile. == References ==

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Could you offer a clear explanation of the term 'Erythema nodosum' as used in the medical field?

Erythema nodosum (EN) is an inflammatory condition characterized by inflammation of the fat cells under the skin, resulting in tender red nodules or lumps that are usually seen on both shins. It can be caused by a variety of conditions, and typically resolves spontaneously within 30 days. It is common in young people aged 12–20 years. Signs and symptoms Pre-eruptive phase The first signs of erythema nodosum are often flu-like symptoms such as a fever, cough, malaise, and aching joints. Some people also experience stiffness or swelling in the joints and weight loss. Eruptive stage Erythema nodosum is characterised by 1–2-inch (25–51 mm) nodules (rounded lumps) below the skin surface, usually on the shins. These subcutaneous nodules can appear anywhere on the body, but the most common sites are the shins, arms, thighs, and torso. Each nodule typically disappears after around two weeks, though new ones may continue to form for up to six or eight weeks. A new nodule usually appears red and is hot and firm to the touch. The redness starts to fade and it gradually becomes softer and smaller until it disappears. Each nodule usually heals completely without scarring over the course of about two weeks. Joint pain and inflammation sometimes continue for several weeks or months after the nodules appear.Less common variants of erythema nodosum include: Ulcerating forms, seen in Crohns disease Erythema contusiforme, when a subcutaneous hemorrhage (bleeding under the skin) occurs with an erythema nodosum lesion, causing the lesion to look like a contusion (bruise) Erythema nodosum migrans (also known as subacute nodular migratory panniculitis), a rare form of chronic erythema nodosum characterized by asymmetrical nodules that are mildly tender and migrate over time. Causes EN is associated with a wide variety of conditions. Idiopathic About 30–50% of EN cases are idiopathic (of an unknown cause). Infection Infections associated with EN include: Streptococcal infection which, in children, is by far the most common precipitant Primary infection of tuberculosis Mycoplasma pneumoniae Histoplasma capsulatum Yersinia Lymphogranuloma venereum (LGV), caused by the bacteria Chlamydia trachomatis Epstein-Barr virus Coccidioides immitis (Valley fever) Cat scratch disease Autoimmune disorders Autoimmune disorders associated with EN include: Inflammatory bowel disease (IBD): about 15% of patients develop erythema nodosum. Behçets disease Sarcoidosis Pregnancy Pregnancy may be associated with EN. Medications Medications associated with EN include: Omeprazole Sulfonamides Penicillins Bromides Hepatitis B vaccination Cancer Cancers associated with EN include: Non-Hodgkins lymphoma (NHL) Carcinoid tumours Pancreatic cancerEN may also be due to excessive antibody production in lepromatous leprosy leading to deposition of immune complexes.There is an association with the HLA-B27 histocompatibility antigen, which is present in 65% of patients with erythema nodosum.A useful mnemonic for causes is SORE SHINS (Streptococci, OCP, Rickettsia, Eponymous (Behçet), Sulfonamides, Hansens Disease (Leprosy), IBD, NHL, Sarcoidosis. Pathophysiology Erythema nodosum is probably a delayed hypersensitivity reaction to a variety of antigens. Although circulating immune complexes have been demonstrated in patients with inflammatory bowel disease, they have not been found in idiopathic or uncomplicated cases. Diagnosis Erythema nodosum is diagnosed clinically. A biopsy can be taken and examined microscopically to confirm an uncertain diagnosis. Microscopic examination usually reveals a neutrophilic infiltrate surrounding capillaries that results in septal thickening, with fibrotic changes in the fat around blood vessels. A characteristic microscopic finding is radial granulomas, well-defined nodular aggregates of histiocytes surrounding a stellate cleft.Additional evaluation should be performed to determine the underlying cause of erythema nodosum. This may include a full blood count, erythrocyte sedimentation rate (ESR), antistreptolysin-O (ASO) titer and throat culture, urinalysis, intradermal tuberculin test, and a chest x-ray. The ESR is typically high, the C-reactive protein elevated, and the blood showing an increase in white blood cells.The ESR is initially very high and falls as the nodules of erythema nodosum. The ASO titer is high in cases associated with a streptococcal throat infection. A chest X-ray should be performed to rule out pulmonary diseases, in particular sarcoidosis and Löfgren syndrome. Treatment Erythema nodosum is self-limiting and usually resolves itself within 3–6 weeks. A recurring form does exist, and in children, it is attributed to repeated infections with streptococcus. Treatment should focus on the underlying cause. Symptoms can be treated with bed rest, leg elevation, compressive bandages, wet dressings, and nonsteroidal anti-inflammatory agents (NSAIDs). NSAIDs are usually more effective at the onset of EN versus with chronic disease.Potassium iodide can be used for persistent lesions whose cause remains unknown. Corticosteroids and colchicine can be used in severe refractory cases. Thalidomide has been used successfully in the treatment of Erythema nodosum leprosum, and it was approved by the U.S. FDA for this use in July 1998. According to a 2009 meta-analysis, there is some evidence of benefit for both thalidomide and clofazimine in the treatment of erythema nodosum leprosum. Epidemiology Erythema nodosum is the most common form of panniculitis. It is most common in the ages of 20–30, and affects women 3–6 times more than men. Eponym The term, Subacute Migratory Panniculitis of Vilanova and Piñol, was named after the two Catalan dermatologists who provided a brief description and explanation of the disease, Xavier Montiu Vilanova (1902–1965) and Joaquin Aguade Piñol (1918–1977), in 1954, and was named in 1956. References == External links ==

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

Can you demystify the medical term 'Granuloma faciale' for me?

Granuloma faciale is an uncommon benign chronic skin disease of unknown origin characterized by single or multiple cutaneous nodules, usually occurring over the face.: 836  Occasionally, extrafacial involvement is noted, most often on sun-exposed areas. Diagnosis Skin biopsy for histopathology: Focal LCV, diffuse dermal neutrophilia with leukocytoclasia, tissue eosinophilia & perivascular fibrosis. Differential diagnosis The disease mimics many other dermatoses and can be confused with conditions, such as sarcoidosis, discoid lupus erythematosus, mycosis fungoides, and fixed drug eruption. Treatment Topical corticosteroid, Intralesional corticosteroid, Dapsone, Colchicine, Antimalarial, Pulse dye laser, Carbon dioxide laser. History GF was first described in 1945 by John Edwin Mackonochie Wigley (1892–1962). See also Cutaneous small-vessel vasculitis List of cutaneous conditions References == External links ==

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I'm seeking clarification on the medical term 'Dissociated vertical deviation.' Could you explain it?

Dissociated vertical deviation (DVD) is an eye condition which occurs in association with a squint, typically infantile esotropia. The exact cause is unknown, although it is logical to assume it is from faulty innervation of eye muscles. Presentation The eye drifts upward spontaneously or after being covered. The condition usually affects both eyes, but can occur unilaterally or asymmetrically. It is often associated with latent or manifest-latent nystagmus and, as well as occurring with infantile esotropia, can also be found associated with exotropias and vertical deviations. DVDs are usually controlled from occurring with both eyes open, but may become manifest with inattention. Usually some level of dissociative occlusion is required - to trigger the brain to suppress vision in that eye and then not control a DVD from occurring. The level of dissociative occlusion required may involve using a red filter, a darker filter or complete occlusion (e.g. with a hand). Onset DVD typically becomes apparent between 18 months and three years of age, however, the difficulties of achieving the prolonged occlusion required for accurate detection in the very young make it possible that onset is generally earlier than these figures suggest. Mechanism Dissociation refers to the situation where the innervation of one eye causes it to move involuntarily and independently of the other eye. Usually both eyes work together as described by Herings and Sherringtons laws of innervation. A DVD is a slow upward and sometimes temporal movement of one eye, with cortical suppression of the vision in that eye while it is deviated. On returning downward and possibly inward to take up fixation, the DVD slow movement will be reversed. The dissociative movement seen objectively should not be confused with the dissociation that occurs subjectively - as when the brain begins to not visualise both images simultaneously (by ignoring or suppressing vision in that eye). Diagnosis A test called the Bielschowsky Darkening Wedge Test can be used to reveal and diagnose the presence of dissociated vertical deviation, although any (or no) amount of dissociative occlusion may also prompt it to occur. The patient is asked to look at a light. One eye is covered and a filter is placed in front of the other eye. The density or opacity of this filter is gradually increased, and the behaviour of the eye under the cover (not of the eye beneath the filter) is observed. Initially, if DVD is present, the covered eye will have elevated, but as the filter opacity is increased the eye under the cover will gradually move downwards. This Bielschowsky phenomenon is present in over 50% of persons with prominent DVD, all the more if the DVD is asymmetric and amblyopia is present as well.The Bielschowsky phenomenon is also present in the horizontal plane in patients with prominent DHD (dissociated horizontal deviation). Differential diagnosis DVD is often mistaken for over-action of the inferior oblique extra-ocular muscles. DVD can be revealed on ocular movement testing when one eye is occluded by the nose on lateral gaze. This eye will then elevate, simulating an inferior oblique over action. However, in a unilateral case, overaction of the superior rectus muscle in the unaffected dominant eye, can also be a causing factor as well as causing a V pattern exophoria. Treatment Management of this condition is surgical and typically involves reducing the strength of the superior rectus muscle or anterior transposition of the inferior oblique muscle of the affected eyes.Several different surgical procedures exist for the correction of DVD including: inferior oblique anteriorization, inferior oblique anteriorization plus resection, superior rectus recession, superior rectus recession plus posterior fixation suture, and inferior oblique myectomy, though there is insufficient evidence to determine which procedure results in the best outcomes for patients. See also Strabismus Strabismus surgery Pediatric ophthalmology Infantile esotropia == References ==

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I'm trying to expand my medical knowledge. Can you elucidate the term 'Larsen syndrome'?

Larsen syndrome (LS) is a congenital disorder discovered in 1950 by Larsen and associates when they observed dislocation of the large joints and face anomalies in six of their patients. Patients with Larsen syndrome normally present with a variety of symptoms, including congenital anterior dislocation of the knees, dislocation of the hips and elbows, flattened facial appearance, prominent foreheads, and depressed nasal bridges. Larsen syndrome can also cause a variety of cardiovascular and orthopedic abnormalities. This rare disorder is caused by a genetic defect in the gene encoding filamin B, a cytoplasmic protein that is important in regulating the structure and activity of the cytoskeleton. The gene that influences the emergence of Larsen syndrome is found in chromosome region, 3p21.1-14.1, a region containing human type VII collagen gene. Larsen syndrome has recently been described as a mesenchyme disorder that affects the connective tissue of an individual. Autosomal dominant and recessive forms of the disorder have been reported, although most cases are autosomal dominant. Reports have found that in Western societies, Larsen syndrome can be found in one in every 100,000 births, but this is most likely an underestimate because the disorder is frequently unrecognized or misdiagnosed. Signs and symptoms Common symptoms Symptoms are related to defects in connective tissue. Congenital anterior dislocation of the knees Dislocation of hips and shoulders Flattened facial appearance Prominent forehead Depressed nasal bridge Club foot Cervical kyphosis Cardiac anomalies Cardiac defects are similar to those associated with Marfans syndrome, a disorder of the connective tissue. Elongation of aorta Bicuspid aortic valve Subaortic stenosis Mitral valve prolapse with mitral regurgitation Atrial septal defect Patent ductus arteriosus Tricuspid valve prolapse Aortic dissection and aneurysm Aneurysm of ductus arteriosus Other reported symptoms These symptoms were found in rare cases of Larsen syndrome. Cataracts Cleft palate Extra bones of wrist Malocclusion Microdontia and hypodontia Complete agenesis of anus Bifid uterus Bifid tongue Causes Mutations in gene encoding filamin B Filamins are cytoplasmic proteins that regulate the structure and activity of the cytoskeleton. These proteins serve as scaffolds on which intracellular signaling and protein trafficking are organized. Filamin B has been found to be expressed in human growth plate chondrocytes, which are especially important in vertebrae segmentation and skeleton morphogenesis. Genetic analysis of patients with Larsen syndrome has found the syndrome is caused by missense mutations in the gene that codes for filamin B. These mutations cause an accelerated rate of apoptosis in the epiphyseal growth plates of individuals with the mutation. The defects can cause short stature and other symptoms associated with Larsen syndrome. Localization Genetic analysis has found that a gene linked to Larsen syndrome, LAR1, is strongly linked to chromosome 3p markers. The locus of this gene is found in a region defined distally by D3S1581 and proximally by D3S1600. This location can be mapped to chromosome region 3p21.1-14.1. Human type VII collagen gene is found within this region in chromosome region 3p21.1. It is reasonable to believe that the joint abnormalities and cardiac anomalies associated with Larsen syndrome are related to the fact that the human type VII collagen gene is found within the same chromosome region as the LAR1 gene. Genetics Both autosomal dominant and recessive forms of Larsen syndrome have been reported. The former is significantly more common than the latter. Symptoms such as syndactyly, cleft palate, short stature, and cardiac defects are seen more commonly in individuals with the autosomal recessive form of the disorder. A lethal form of the disorder has been reported. It is described as being a combination of the Larsen phenotype and pulmonary hypoplasia. Diagnosis Ultrasound remains as one of the only effective ways of prenatally diagnosing Larsen syndrome. Prenatal diagnosis is extremely important, as it can help families prepare for the arrival of an infant with specifics necessities. Ultrasound can capture prenatal images of multiple joint dislocations, abnormal positioning of legs and knees, depressed nasal bridge, prominent forehead, and club feet. These symptoms are all associated with Larsen syndrome, so they can be used to confirm that a fetus has the disorder. Treatment Treatment for Larsen syndrome varies according to the symptoms of the individual. Orthopedic surgery can be performed to correct the serious joint defects associated with Larsen syndrome. Reconstructive surgery can be used to treat the facial abnormalities. Cervical kyphosis can be very dangerous to an individual because it can cause the vertebrae to disturb the spinal cord. Posterior cervical arthrodesis has been performed on patients with cervical kyphosis, and the results have been successful Propranolol has been used to treat some of the cardiac defects associated with Marfans syndrome, so the drug also has been suggested to treat cardiac defects associated with Larsen syndrome. Prognosis While Larsen syndrome can be lethal if untreated, the prognosis is relatively good if individuals are treated with orthopedic surgery, physical therapy, and other procedures used to treat the symptoms linked with Larsen syndrome. See also Boomerang dysplasia References External links WebMD abstract

You are a medical knowledge base. Your task is to elucidate medical terminology, offering insights into their meanings, origins, and applications.

I'm trying to understand 'Pamabrom' within a medical context. Could you shed some light on it?

Pamabrom manufactured by Chattem Chemicals, and is a product included in retail drugs available in over-the-counter medications. The active diuretic ingredient in pamabrom is 8-bromotheophylline and it also contains aminoisobutanol. Pamabrom is available in combination with acetaminophen (paracetamol) for various conditions such as back pain and menstrual relief. The acetaminophen helps reduce menstrual pains and the pamabrom reduces associated bloating. The combination is available in a number of products from various brands under different names. The dosages are essentially the same for each brand, including generic drug store varieties. A diuretic is also used to reduce fluid buildup in the body. When the body has fluid buildup, it can cause swelling of the extremities, like in your ankles and feet. Excess fluid can make it harder for your heart to work properly. Buildup of these fluids are sometimes related to congestive heart failure. References External links Are For-Women Products for Real? https://www.webmd.com/hypertension-high-blood-pressure/guide/diuretic-treatment-high-blood-pressure#1

You function as a medical informant. Please provide in-depth yet accessible descriptions of medical terms, suitable for a broad audience.

I've encountered the term 'California encephalitis orthobunyavirus' while reading about medical topics. What does it refer to exactly?

California encephalitis orthobunyavirus type strain California encephalitis virus was discovered in Kern County, California, and causes encephalitis in humans. Encephalitis is an acute inflammation of the brain that can cause minor symptoms, such as headaches, to more severe symptoms such as seizures. Mosquitoes serve as its carrier and for this reason this virus is known as an arbovirus (arthropod-borne virus). California encephalitis orthobunyavirus belongs to the Bunyavirales order of viruses. The La Crosse Virus from the same genus is also a common cause of encephalitis in the United States. Other viruses with similar disease symptoms but genetically unrelated include: Saint Louis encephalitis and West Nile virus. Signs and symptoms The incubation period of California encephalitis is usually 3–7 days. An early symptoms phase of 1–4 days commonly precedes the onset of encephalitis, manifesting as fever, chills, nausea, vomiting, headache, lethargy and abdominal pain.The encephalitis is characterized by fever, drowsiness, and lack of mental alertness and orientation. Seizures occur in 50% of children. Focal neurologic findings, like focal motor abnormalities and paralysis, irregular and abnormal reflexes develop in 20% of children. 10% of patients develop coma. The total duration of illness rarely exceeds 10–14 days. Recurrent unprovoked seizures occur even after the illness has passed develops in 20% of patients, especially those who had seizures during the acute illness. In adults, infection is asymptomatic, which means that the patient is a carrier of the infection, but experiences no symptoms or only mild feverish illness.The mortality rate is less than 1% and most patients with encephalitis clinical symptoms recover completely. Up to 20% of patients develop behavioral problems or recurrent seizures. Pathophysiology Initial infection by the virus and primary spread of the virus causes the onset of non-specific symptoms such as headache and fever. Secondary spread and the multiplication of the virus in the CNS (central nervous system) causes symptoms such as stiff neck, lethargy and seizures. It then can result in encephalitis, when inflammation of the brain, produced by infection by the virus, damages nerve cells, which affects signaling of the brain to the body. After the virus enters the body via a mosquito bite, the virus undergoes local replication at the skin site where virus entered the body. A primary spread of virus occurs, with seeding of the reticuloendothelial system, mainly in the liver, spleen, and lymph nodes. With the ongoing replication of the virus a secondary spread occurs, with the seeding of the CNS. Not all the cases reach this stage, depending on the efficiency of viral replication at the different stages and the degree of virus spread. The California encephalitis virus invades the CNS through either the cerebral capillary endothelial cells or the choroid plexus. Treatment Treatments are given to manage the symptoms the patient is having. In patients who are very sick, supportive treatment, such as mechanical ventilation, is equally important. Corticosteroids are used to reduce brain swelling and inflammation. Sedatives may be needed for irritability or restlessness. Acetaminophen is used for fever and headache. Anticonvulsants are used to prevent seizures. If brain function is severely affected, interventions like physical therapy and speech therapy may be needed after the illness is controlled. Epidemiology Factors influencing the transmission and control of arboviral encephalitis, in general, include: the season, geographical location, patient age, and the regional climate. There are approximately 75 cases reported per year. In the US the highest occurrence is in the Midwestern states, with most cases occurring in the late summer to early fall. Outdoor activities, especially in woodland areas, are associated with an increased risk of infection. History It was first discovered and isolated in 1943, from mosquitoes collected in Kern County, California. Two years later the first human cases of encephalitis were attributed to this new virus. Three cases in total were reported, and all three cases were in residents of Kern County in the Central Valley of California. In all three cases there was strong laboratory evidence confirming infection, due to the presence of neutralizing antibodies linked to California encephalitis. Since then, most cases of encephalitis have been associated with the La Crosse virus, and California encephalitis is a rare cause of disease in the Western world.The original California Encephalitis virus was isolated and put alongside fifteen other related viruses that are now categorized as the "California serogroup". From 1996 to 1998, approximately three times as many reported human cases of arboviral encephalitis were caused by California serogroup viruses than were reported for western equine encephalomyelitis viruses, St. Louis encephalitis, and eastern equine encephalomyelitis viruses combined. Subtypes California encephalitis virus (CEV) – type strain Inkoo virus (INKV) South river virus (SORV) References == External links ==

You are a medical interpreter. Your duty is to translate medical terms into easily digestible information, maintaining accuracy and detail.

What does the medical term 'Fungemia' encompass?

Fungemia is the presence of fungi or yeasts in the blood. The most common type, also known as candidemia, candedemia, or systemic candidiasis, is caused by Candida species; candidemia is also among the most common bloodstream infections of any kind. Infections by other fungi, including Saccharomyces, Aspergillus and Cryptococcus, are also called fungemia. It is most commonly seen in immunosuppressed or immunocompromised patients with severe neutropenia, cancer patients, or in patients with intravenous catheters. It has been suggested the otherwise immunocompetent patients taking infliximab may be at a higher risk for fungemia. Diagnosis is difficult, as routine blood cultures have poor sensitivity. Signs and symptoms Symptoms can range from mild to extreme—often described as extreme flu-like symptoms. Many symptoms may be associated with fungemia, including pain, acute confusion, chronic fatigue, and infections. Skin infections can include persistent or non-healing wounds and lesions, sweating, itching, and unusual discharge or drainage. Risk factors Pathogens The most commonly known pathogen is Candida albicans, causing roughly 70% of fungemias, followed by Candida glabrata with 10%, Aspergillus with 1% and Saccharomyces as the fourth most common. However, the frequency of infection by C. glabrata, Saccharomyces boulardii, Candida tropicalis, C. krusei and C. parapsilosis is increasing, perhaps because significant use of fluconazole is common or due to increase in antibiotic use.Candida auris is an emerging multidrug-resistant (MDR) yeast that can cause invasive infections and is associated with high mortality. It was first described in 2009 after being isolated from external ear discharge of a patient in Japan. Since the 2009 report, C. auris infections, specifically fungemia, have been reported from South Korea, India, South Africa, and Kuwait. Although published reports are not available, C. auris has also been identified in Colombia, Venezuela, Pakistan, and the United Kingdom.In a single reported instance, Psilocybe cubensis was reported to have been cultured from a case of fungemia in which an individual self-injected an underprocessed decoction of fungal matter. The patient, who had been suffering from mild depression, attempted to self-medicate with the mushrooms but was frustrated by the lag time between eating the mushrooms and experiencing the psychedelic effects. In an attempt to bypass this, the patient boiled and filtered the mushrooms into a mushroom tea which was then administered by injection. The patient had multiple organ failure, but this was successfully reversed and the infection treated with antifungal drugs. Two other examples of fungemia as a result of injecting fungal matter in this way have been described in medical literature, both dating to 1985. Diagnosis The gold standard for the diagnosis of invasive candidiasis and candidemia is a positive culture. Blood cultures should be obtained in all patients with suspected candidemia. Treatment Neutropenic vs non-neutropenic candidemia is treated differently.An intravenous echinocandin such as anidulafungin, caspofungin or micafungin is recommended as first-line therapy for fungemia, specifically candidemia. Oral or intravenous fluconazole is an acceptable alternative. The lipid formulation amphotericin B is a reasonable alternative if there is limited antifungal availability, antifungal resistance, or antifungal intolerance. See also Bacteremia Candidiasis Fungicide Mycosis References == External links ==

You serve as a guide in the medical field. Explain medical terms thoroughly, ensuring the information is both insightful and comprehensible.

I'd like to learn more about the medical term 'Nervous.' Can you provide some details?

Nervous may refer to: nervousness Nervous system, a network of cells in an animals body that coordinates movement and the senses Nervous tissue, the cells of the nervous system that work in aggregate to transmit signals Music "Nervous" (Gene Summers song), 1958; covered by several performers "Nervous" (Gavin James song), 2016 "Nervous" (Shawn Mendes song), 2018 "Nervous", a song by K.Flay from Solutions, 2019 "Nervous", a song by L Devine, 2018 "Nervous", a song by Nick Jonas from Spaceman, 2021 Nervous Records, a UK record label Nervous Records (US), a US record label See also "Nervousness", a song by the Gigolo Aunts from Tales from the Vinegar Side Nervous Norvus (1912–1968), the performing name of Jimmy Drake Nervous shark, a species of requiem shark All pages with titles beginning with Nervous

You are a medical knowledge base. Your task is to elucidate medical terminology, offering insights into their meanings, origins, and applications.

What is the significance of the term 'Lattice corneal dystrophy' in the medical field?

Lattice corneal dystrophy type is a rare form of corneal dystrophy. It has no systemic manifestations, unlike the other type of the dystrophy, Lattice corneal dystrophy type II. Lattice corneal dystrophy was first described by Swiss ophthalmologist Hugo Biber in 1890.Lattice dystrophy gets its name from an accumulation of amyloid deposits, or abnormal protein fibers, throughout the middle and anterior stroma. Presentation Filamentous opacities appear in the cornea with intertwining delicate branching processes. During an eye examination, the doctor sees these deposits in the stroma as clear, comma-shaped overlapping dots and branching filaments, creating a lattice effect. Over time, the lattice lines will grow opaque and involve more of the stroma. They will also gradually converge, giving the cornea a cloudiness that may also reduce vision. The disease is bilateral, usually noted before the end of the first decade of life. Although lattice dystrophy can occur at any time in life, the condition usually arises in children between the ages of two and seven.In some people, these abnormal protein fibers can accumulate under the corneas outer layer—the epithelium. This can cause erosion of the epithelium. This condition is known as recurrent epithelial erosion. These erosions alter the corneas normal curvature, resulting in temporary vision problems, and expose the nerves that line the cornea, causing severe pain. Even the involuntary act of blinking can be painful. In systemic cases, kidney failure, heart failure and neuropathy such as facial nerve palsy, laxity of the skin may be noted. Genetics Lattice corneal dystrophy has three types: type I: with no systemic association. It is caused by mutations in TGFBI gene encoding keratoepithelin, which maps to chromosome 5q. type II or Finnish type amyloidosis: associated with manifestations of systemic amyloidosis due to accumulation of gelsolin. Associated conditions may include cutis laxa and ataxia. type III is also described which has an onset at age 70 to 90 years and is not associated with systemic amyloidosis. Diagnosis In the examination of biomicroscopy, it appears as branches spread on the corneal stroma in the appearance of ghost vessels. diagnosis can also be confirmed with anterior segment OCT (Visante OCT, spectral domain OCT).The interwoven linear opaque filaments have some resemblance to NERVES, but may not be observed in all affected members of families with the condition. Recurrent corneal erosions may precede the corneal opacities and even appear in individuals lacking recognizable stromal disease. Amyloid deposits are found throughout the corneal stroma. Linear and other shaped opaque areas accumulate particularly within the central corneal stroma, while the peripheral cornea remains relatively transparent. Treatment In case of corneal erosion, a doctor may prescribe eye drops and ointments to reduce the friction on the eroded cornea. In some cases, an eye patch may be used to immobilize the eyelids. With effective care, these erosions usually heal within three to seven days, although occasional sensations of pain may occur for the next six-to-eight weeks. As patients with LCD suffer with dry eyes as a result of erosion, a new technique involving the insertion of punctal plugs (both upper and lower) can reduce the amount of drops used a day, aiding ocular stability.By about age 40, some people with lattice dystrophy will have scarring under the epithelium, resulting in a haze on the cornea that can greatly obscure vision. In this case, a corneal transplantation may be needed. There have been many cases in which teenage patients have had the procedure, which accounts for the change in severity of the condition from person to person.Although people with lattice dystrophy have an excellent chance for a successful corneal transplantation, the disease may also arise in the donor cornea in as little as three years. In one study, about half of the transplant patients with lattice dystrophy had a recurrence of the disease between two and 26 years after the operation. Of these, 15 percent required a second corneal transplant. Early lattice and recurrent lattice arising in the donor cornea responds well to treatment with the excimer laser. Phototherapeutic keratectomy (PTK) using [Excimer laser] can restore and preserve useful visual function for a significant period of time in patients with anterior corneal dystrophies. References == External links ==

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I'm seeking clarification on the medical term 'Isodicentric 15.' Could you explain it?

Isodicentric 15, also called marker chromosome 15 syndrome, idic(15), partial tetrasomy 15q, or inverted duplication 15 (inv dup 15), is a chromosome abnormality in which a child is born with extra genetic material from chromosome 15. People with idic(15) are typically born with 47 chromosomes in their body cells, instead of the normal 46. The extra chromosome, which is classified as a small supernumerary marker chromosome, is made up of a piece of chromosome 15 that has been duplicated end-to-end like a mirror image. It is the presence of this extra genetic material that is thought to account for the symptoms seen in some people with idic(15). Individuals with idic(15) have a total of four copies of this chromosome 15 region instead of the usual two copies (1 copy each on the maternal and paternal chromosomes). The syndrome is also often referred to by the term Chromosome 15q11.2-q13.1 Duplication Syndrome, shortened to Dup15q Syndrome, or marker chromosome 15 syndrome (mainly in the United States). Dup15q Syndrome includes both idic(15) and interstitial 15q11.2-q13.1, another type of duplication that causes similar clinical traits. The extra chromosome is occasionally found in the mosaic state, i.e. some of the cells carry the marker chromosome. However, mostly because of the markers instability and tendency to be lost during cell division (mitosis), some cells are completely normal with 46 chromosomes. Occasionally, cells may have more than one idic(15), resulting in 48 or 49 chromosomes in all or some of their cells. A similar clinical picture albeit to a milder degree could be expected in individuals that have the extra chromosome 15 material as an interstitial duplication (when the extra piece of chromosome 15 is included within the long arm of one of the two copies of chromosome 15, rather than as a small extra marker chromosome) - often abbreviated to int dup(15); the individual thus having 46 chromosomes. Signs and symptoms The severity of symptoms of idic(15) vary greatly between individuals. Individuals with idic(15) usually have delays in language development and motor skills such as walking or sitting up. Other traits may include low muscle tone (hypotonia), seizures (>50%), short stature, and intellectual disability. Distinctive facial features associated with idic(15) - where present at all - are usually very subtle but may include epicanthal folds (skin folds at the inner corners of one or both eyes), downward slanting palpebral fissures, broad forehead, a flattened nasal bridge, button nose, and a high arched palate (roof of the mouth). Some individuals show other signs that can often be associated with chromosomal conditions, such as pectus excavatum, or a unilateral or bilateral single transverse palmar crease. Many individuals with idic(15) display features of autism, such as problems with communication and social interactions, obsessional interests (often with interactive mechanisms like wheels, doors or switches), unpredictable sleep cycles (and a reduced need for sleep), and repetitive and stereotyped behaviors (e.g., lining up toys, playing with a toy in the same manner over and over again, hand flapping, rocking back and forth). Sensory processing is often affected, especially the vestibular system. A high pain threshold is often observed. If speech develops, it is often echolalic but some individuals do grasp some language. With a severely affected person there may be an inability to walk or talk. Genetics Generally, idic(15) is not inherited; it is said to appear de novo, in one member of the family, by chance. In most cases, the abnormal chromosome is generated in the mothers germ cells: the oocytes. This finding is due to ascertainment bias; cases with maternally derived idic(15) usually have clinical findings and attract attention, but those with paternally derived idic(15) usually do not. Thus, diagnosed cases are usually patients where the duplicated material is derived from the mothers egg cell rather than the fathers sperm cell.People with idic(15) have extra genetic material that has developed from chromosome 15. The material usually exists as a little extra chromosome 15; sometimes called a marker chromosome or an extra structurally abnormal chromosome (ESAC). The marker usually exists as an isodicentric chromosome; i.e. 2 copies of a specific part of the long arm of chromosome 15q11.2-q13.1 that is mirrored and doubled, with 2 centromeres and 2 DNA satellites. The smallest markers appear to be harmless and they may go undetected. However, if they are large enough to contain a number of important genes, they may result in "idic(15) syndrome" which is characterized by learning disabilities, autism and other neurological symptoms. One of the regions responsible for the symptoms of idic(15) syndrome is the critical PWS/AS-region named after the Prader-Willi and/or Angelman syndromes. Isodicentric chromosome 15 and autism For more than 12 years, scientists have noticed that some individuals with autism also have idic(15). In fact, idic(15) is the most frequently identified chromosome problem in individuals with autism. (A chromosome anomaly involves extra or missing chromosomal material, not changes within the genes such as Fragile X syndrome). It is suggested that the co-occurrence of autism and idic(15) is not by chance. There may be a gene or genes in the 15q11-q13 region that is/are related to the development of autism in some individuals.Genetic research studies of individuals without chromosome anomalies also support this idea that an autism-related gene may be present in 15q11.2-q13.1 Specifically, research studies found that certain DNA markers from the (15q1.2-q13.1) region were found more often in individuals with autism than in individuals without autism. Although these DNA markers are too small to be genes, they suggest that researchers may be getting close to finding an autism gene in this region.A recent study reported the introduction of two extra copies of just a single gene present in the 15q11.2-q13.1 region, Ube3a, into mice to model the gene copy number expressed in the brain in idic(15). These mice displayed autism-related behavioral deficits including impaired social interaction, reduced ultrasonic vocal communication, and increased repetitive behavior (self-grooming). Diagnosis The extra chromosome in people with idic(15) can be easily detected through chromosome analysis (karyotyping). Additional tests are usually required. FISH (Fluorescent in situ hybridization) is used to confirm the diagnosis by distinguishing idic(15) from other supernumerary marker chromosomes. Array CGH can be used to determine the gene content and magnitude of copy number variation so that the clinical picture can be foreseen. Interstitial duplications of chromosome 15 can be more difficult to detect on a routine chromosome analysis but are clearly identifiable using a 15q FISH study. Families should always discuss the results of chromosome and FISH studies with a genetic counselor or other genetics professionals to ensure accurate interpretation. Screening In general, idic(15) occurs de novo but the parents must be karyotyped to make sure it is not inherited, mostly because this will affect the course of genetic counseling given to the family. If the abnormality is found prenatally and one of the parents harbour the marker, the child has a chance of not carrying the mutation. Further tests should however be done to prove the marker has not been rearranged while being inherited. This information is also necessary for counseling of future pregnancies. Each family is unique and should therefore be handled individually. Management At the present time, there is no specific treatment that can undo any chromosomal abnormality, nor the genetic pattern seen in people with idic(15). The extra chromosomal material in those affected was present at or shortly after conception, and its effects on brain development began taking place long before the child was born. Therapies are available to help address many of the symptoms associated with idic(15). Physical, occupational, and speech therapies along with special education techniques can stimulate children with idic(15) to develop to their full potential.In terms of medical management of the symptoms associated with Chromosome 15q11.2-q13.1 Duplication Syndrome, families should be aware that individuals with chromosome 15 duplications may tolerate medications differently and may be more sensitive to side effects for some classes of medications, such as the serotonin reuptake inhibitor type medications (SSRI). Thus, these should be used with caution and any new medication should be instituted in a controlled setting, with slow titration of levels and with a clear endpoint as to what the expected outcome for treatment is.There is an increased risk of sudden, unexpected death among children and adults with this syndrome. The full cause is not yet understood but it is generally attributed to SUDEP (Sudden Unexplained Death in Epilepsy). Epidemiology About half of all marker chromosomes are idic(15) but idic(15) in itself is one of the rare chromosome abnormalities. Incidence at birth appears to be 1 in 30,000 with a sex ratio of almost 1:1; however, since dysmorphic features are absent or subtle and major malformations are rare, chromosome analysis may not be thought to be indicated, and some individuals, particularly in the older age groups, probably remain undiagnosed. There are organizations for families with idic(15) children that offer extensive information and support. Research Patients with idic(15) and int dup(15) often feature a distinctive electroencephalography (EEG) signature or biomarker in the form of high amplitude spontaneous beta frequency (12–30 Hz) oscillations. This EEG signature was first noted as a qualitative pattern in clinical EEG readings and was later described quantitatively by researchers at the University of California, Los Angeles and their collaborators within the network of national Dup15q clinics. This group of researchers found that beta activity in children with Dup15q syndrome is significantly greater than that observed in (1) healthy, typically developing children of the same age and (2) children of the same age and IQ with autism not caused by a known genetic disorder (i.e., nonsyndromic ASD). The EEG signature appears almost identical to beta oscillations induced by benzodiazepine drugs that modulate GABAA receptors, suggesting that the signature is driven by overexpression of duplicated GABAA receptor genes GABRA5, GABRB3, and GABRG3 found on 15q11.2-q13.1. Treatment monitoring and identification of molecular disease mechanisms may be facilitated by this biomarker. See also marker chromosome 15 syndrome References == External links ==

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

I'm looking for a concise explanation of the medical term 'Proliferating angioendotheliomatosis.'

Proliferating Angioendotheliomatosis has historically been divided into two groups, (1) a reactive, involuting type and (2) a malignant, rapidly fatal type.: 598 The reactive involuting type, reactive Angioendotheliomatosis is an rare cutaneous condition characterized histologically by a dense proliferation of small capillaries, and occurs in people with various diseases including subacute bacterial endocarditis and end-stage atherosclerotic disease. These people present with various skin lesions and rashes - most commonly on the thighs. Treatment aimed at the underlying condition hastens the resolution of the lesions. The malignant type is an intravascular lymphoma, usually of the diffuse B-cell type, known as intravascular large B-cell lymphoma. It progresses rapidly through involvement of multiple body systems and mortality occurs in less than a year from the initial diagnosis. The average age of diagnosis being 55 years. The causative mechanism is unknown. In a few cases treatment with palliative chemotherapy has been effective.: 598 Classification of Proliferating Angioendotheliomatosis Proliferating angioendotheliomatosis may be divided into two types: a reactive type – Reactive angioendotheliomatosis a malignant type – Intravascular large B-cell lymphoma Treatment In few cases palliative chemotherapy is effective. A 30-year-old woman was diagnosed with cutaneous proliferating angioendotheliomatosis. She was treated with a local excision and radiotherapy. See also List of cutaneous conditions References External links == External links ==

You are a medical interpreter. Your duty is to translate medical terms into easily digestible information, maintaining accuracy and detail.

What is the significance of the term '1q21.1 deletion syndrome' in the medical field?

1q21.1 deletion syndrome is a rare aberration of chromosome 1. A human cell has one pair of identical chromosomes on chromosome 1. With the 1q21.1 deletion syndrome, one chromosome of the pair is not complete, because a part of the sequence of the chromosome is missing. One chromosome has the normal length and the other is too short. In 1q21.1, the 1 stands for chromosome 1, the q stands for the long arm of the chromosome and 21.1 stands for the part of the long arm in which the deletion is situated. The syndrome is a form of the 1q21.1 copy number variations, and it is a deletion in the distal area of the 1q21.1 part. The CNV leads to a very variable phenotype, and the manifestations in individuals are quite variable. Some people who have the syndrome can function in a normal way, while others have symptoms of intellectual impairment and various physical anomalies.1q21.1 microdeletion is a very rare chromosomal condition. Only 46 individuals with this deletion have been reported in medical literature as of August 2011. Symptoms and signs Recognised symptoms are: Only one set of genes on the two chromosomes function (haploinsufficiency) Thrombocytopenia-absent radius (TAR syndrome), in case of a class II-deletion Neurological-psychiatric problems: schizophrenia; epilepsy; learning problems; cognitive disabilities — mild to moderate; developmental delay — mild to moderate (milestones like sitting, standing and walking; come at a later period in childhood); children show an ataxic gait and fall down a lot Dysmorphism: slightly unusual facial appearance; disturbed growth; skeletal malformations; small head (microcephaly); prominent forehead; bulbous nose; deep-set eyes; broad thumbs; broad toes; squint; very flexible joints; clavicular pseudoarthrosis (the collarbone doesnt develop normally) (class II-deletion); an extra transverse crease of the fifth finger (class II-deletion)); problems with the development of the vagina (Müllerian aplasia) Eyes: cataracts Heart abnormalities and cardiovascular anomalies (30% of the cases): anomalous origin of the coronary artery (Class II-deletion) Kidneys: missing kidney or floating kidneys Cancer: neuroblastoma Sleep disturbancesIt is not clear whether the list of symptoms is complete. Very little information is known about the syndrome. The syndrome can have completely different effects on members of the same family.A common deletion is between 1.0–1.9Mb. Mefford states that the standard for a deletion is 1.35Mb. The largest deletion seen on a living human is over 5 Mb. Cause Meiosis is the process of dividing cells in humans. In meiosis, the chromosome pairs split and a representative of each pair goes to one daughter cell. In this way the number of chromosomes will be halved in each cell, while all the parts on the chromosome (genes) remain, after being randomized. Which information of the parent cell ends up in the daughter cell is purely decided by chance. Besides this random process, there is a second random process. In this second random process the DNA will be scrambled in a way that pieces are omitted (deletion), added (duplication), moved from one place to another (translocation) and inverted (inversion). This is a common process, which leads to about 0.4% variation in the DNA.A problem of the second random process is that genetic mistakes can occur. Because of the deletion and duplication process, the chromosomes that come together in a new cell may be shorter or longer. The result of this spontaneous change in the structure of DNA is a so-called copy number variation. Due to the copy number variation chromosomes of different sizes can be combined in a new cell. If this occurs around conception, the result will be a first cell of a human with a genetic variation. This can be either positive or negative. In positive cases this new human will be capable of a special skill that is assessed positively, for example, in sports or science. In negative cases, you have to deal with a syndrome or a severe disability, as in this case the 1q21.1 deletion syndrome.Based on the meiotic process, the syndrome may occur in two ways. a spontaneous deviation (a de novo situation): two chromosomes come together of which one has a copy number variation as a result of the meiosis process. a parent is unknowingly the carrier of a chromosome with a copy number variation and passes it at conception to the child, with different consequences for the child.Due to this genetic misprint, the embryo may experience problems in the development during the first months of pregnancy. Approximately 20 to 40 days after fertilization, something goes wrong in the construction of the body parts and brain, which leads to a chain reaction. Genetics The structure of 1q21.1 The structure of 1q21.1 is complex. The area has a size of approximately 6 Megabase (Mb) (from 141.5 Mb to 147.9 Mb). Within 1q21.1 there are two areas where the CNVs can be found: the proximal area or TAR area (144.1 to 144.5) and the distal area (144.7 to 145.9). The 1q21.1 deletion syndrome will commonly be found in the distal area, but an overlap with the TAR-area is possible. 1q21.1 has multiple repetitions of the same structure (areas with the same color in the picture have equal structures) Only 25% of the structure is not duplicated. There are several gaps in the sequence. There is no further information available about the DNA-sequence in those areas up until now. The gaps represent approximately 700 Kilobase. New genes are expected in the gaps. Because the gaps are still a topic of research, it is hard to find the exact start and end markers of a deletion. The area of 1q21.1 is one of the most difficult parts of the human genome to map.Because of the repetitions in 1q21.1, there is a larger chance of an unequal crossing-over during meiosis. CNVs occur due to non-allelic homologous recombination mediated by low copy repeats (sequentially similar regions). Typing A common deletion is restricted to the distal area. This is a Class I-deletion.In some cases the deletion is so large that the proximal area is involved as well, the so-called Class II-deletion. There are some complex cases in which both the proximal area and the distal area are affected, while the area in between is normal. There are also some a-typical variants. Related genes Genes related to 1q21.1 deletion in the distal area are PDE4DIP, HYDIN2, PRKAB2, PDIA3P, FMO5, CHD1L, BCL9, ACP6, GJA5, GJA8, NBPF10, GPR89B, GPR89C, PDZK1P1 and NBPF11. Diagnostics A de novo-situation appears in about 75% of the cases. In 25% of the cases, one of the parents is carrier of the syndrome, without any effect on the parent. Sometimes adults have mild problems with the syndrome. To find out whether either of the parents carries the syndrome, both parents have to be tested. In several cases, the syndrome was identified with the child, because of a developmental disorder or another problem, and later it appeared that the parent was affected as well. In families where both parents have tested negative for the syndrome, chances of a second child with the syndrome are extremely low. If the syndrome was found in the family, chances of a second child with the syndrome are 50%, because the syndrome is autosomal dominant. The effect of the syndrome on the child cannot be predictedThe syndrome can be detected with fluorescence in situ hybridization. For parents with a child with the syndrome, it is advisable to consult a physician before another pregnancy. Management Treatment of cause: Due to the genetic cause, no treatment of the cause is possible.Treatment of manifestations: routine treatment of ophthalmologic, cardiac, and neurologic findings; speech, occupational, and physical therapies as appropriate; specialized learning programs to meet individual needs; antiepileptic drugs or antipsychotic medications as needed.Surveillance: routine pediatric care; routine developmental assessments; monitoring of specific identified medical issues. Prevalence As of October 2012, Unique, an international rare chromosome disorder group and registry, has 64 genetically confirmed cases of this deletion worldwide. Research On several locations in the world people are studying on the subject of 1q21.1 deletion syndrome. The syndrome was identified for the first time with people with heart abnormalities. The syndrome has later been found in patients with schizophrenia. Research is done on patients with a symptom of the syndrome, to find more patients with the syndrome.There may be a relation between autism and schizophrenia. Literature shows that nine locations have been found on the DNA where the syndromes related to autism or schizophrenia can be found, the so-called "hotspots": 1q21.1, 3q29, 15q13.3, 16p11.2, 16p13.1, 16q21, 17p12, 21q11.2 and 21q13.3. With a number of hotspots, either autism and schizophrenia were observed depending on the copy-number variation (CNV) at that location.Statistical research showed that schizophrenia is more common in combination with 1q21.1 deletion syndrome. On the other side, autism is significantly more common with 1q21.1 duplication syndrome. Further research confirmed that the odds on a relation between schizophrenia and deletions at 1q21.1, 3q29, 15q13.3, 22q11.21 en Neurexin 1 (NRXN1) and duplications at 16p11.2 are at 7.5% or higher. Common variations in the BCL9 gene, which is in the distal area, confer risk of schizophrenia and may also be associated with bipolar disorder and major depressive disorder.Research is done on 10–12 genes on 1q21.1 that produce DUF1220-locations. DUF1220 is an unknown protein, which is active in the neurons of the brain near the neocortex. Based on research on apes and other mammals, it is assumed that DUF1220 is related to cognitive development (man: 212 locations; chimpanzee: 37 locations; monkey: 30 locations; mouse: 1 location). It appears that the DUF1220-locations on 1q21.1 are in areas that are related to the size and the development of the brain. The aspect of the size and development of the brain is related to autism (macrocephaly) and schizophrenia (microcephaly). It has been proposed that a deletion or duplication of a gene that produces DUF1220-areas might cause growth and development disorders in the brain Another relation between macrocephaly with duplications and microcephaly with deletions has been seen in research on the HYDIN Paralog or HYDIN2. This part of 1q21.1 is involved in the development of the brain. It is assumed to be a dosage-sensitive gene. When this gene is not available in the 1q21.1 area, it leads to microcephaly. HYDIN2 is a recent duplication (found only in humans) of the HYDIN gene found on 16q22.2. Research on the genes CHD1L and PRKAB2 within lymphoblast cells lead to the conclusion that anomalies appear with the 1q21.1-deletion syndrome: CHD1L is an enzyme which is involved in untangling the chromatides and the DNA repair system. With 1q21.1 deletion syndrome a disturbance occurs, which leads to increased DNA breaks. The role of CHD1L is similar to that of helicase with the Werner syndrome PRKAB2 is involved in maintaining the energy level of cells. With 1q21.1-deletion syndrome this function was attenuated.GJA5 has been identified as the gene that is responsible for the phenotypes observed with congenital heart diseases on the 1q21.1 location. In case of a duplication of GJA5 tetralogy of Fallot is more common. In case of a deletion other congenital heart diseases than tetralogy of Fallot are more common. References Further reading External links DECIPHER database entry for 1q21.1 deletion syndrome 1q21.1 deletion, GeneReviews NCBI Bookshelf Orpha.net

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I'm not familiar with the medical term 'Recurrent miscarriage.' Could you provide some insights?

Recurrent miscarriage is three or more consecutive pregnancy losses. In contrast, infertility is the inability to conceive. In many cases the cause of RPL is unknown. After three or more losses, a thorough evaluation is recommended by American Society of Reproductive Medicine. About 1% of couples trying to have children are affected by recurrent miscarriage. Causes There are various causes for recurrent miscarriage, and some can be treated. Some couples never have a cause identified, often after extensive investigations. About 50–75% of cases of recurrent miscarriage are unexplained. Chromosomal disorders A balanced translocation or Robertsonian translocation in one of the partners leads to unviable fetuses that are miscarried. This explains why a karyogram is often performed in both partners if a woman has experienced repeated miscarriages.Aneuploidy may be a cause of a random spontaneous as well as recurrent pregnancy loss. Aneuploidy is more common with advanced reproductive age reflecting decreased germ cell quality.Larger chromosomal disorders are generally detected on karyotype. In couples where a miscarried embryo has an abnormal karyotype, 76% of subsequent miscarried embryos have shown abnormal karyotypes as well. On the other hand, this group of couples have a better long-term live birth rate than those where miscarried embryos have normal karyotype. Lifestyle factors While lifestyle factors have been associated with increased risk for miscarriage in general, and are usually not listed as specific causes for RPL, every effort should be made to address these issues in patients with RPL. Of specific concern are chronic exposures to toxins including smoking, alcohol, and drugs. Anatomical conditions Fifteen percent of women who have experienced three or more recurring miscarriages have some anatomical reason for the inability to complete the pregnancy. The structure of the uterus has an effect on the ability to carry a child to term. Anatomical differences are common and can be congenital. Cervical conditions In the second trimester a weak cervix can become a recurrent problem. Such cervical incompetence leads to premature pregnancy loss resulting in miscarriages or preterm deliveries. It has been estimated that cervical insufficiency is a cause in about 8% of women with second trimester recurrent miscarriages. Endocrine disorders Women with hypothyroidism are at increased risk for pregnancy losses. Unrecognized or poorly treated diabetes mellitus leads to increased miscarriages. Women with polycystic ovary syndrome also have higher loss rates possibly related to hyperinsulinemia or excess androgens. Inadequate production of progesterone in the luteal phase may set the stage for RPL (see below). Thrombophilia An important example is the possible increased risk of miscarriage in women with thrombophilia (propensity for blood clots). The most common problem is the factor V Leiden and prothrombin G20210A mutation. Some preliminary studies suggest that anticoagulant medication may improve the chances of carrying pregnancy to term but these studies need to be confirmed before they are adopted in clinical practice. Note that many women with thrombophilia go through one or more pregnancies with no difficulties, while others may have pregnancy complications. Thrombophilia may explain up to 49–65% of recurrent miscarriages. Immune factors A common feature of immune factors in causing recurrent pregnancy loss appears to be a decreased maternal immune tolerance towards the fetus. Antiphospholipid syndrome The antiphospholipid syndrome is an autoimmune disease that is a common cause of recurrent pregnancy loss. Around 15% of the women who have recurrent miscarriages have high levels of antiphospholipid antibodies. Women who have had more than one miscarriage in the first trimester, or a miscarriage in the second trimester, may have their blood tested for antibodies, to determine if they have antiphospholipid syndrome. Women diagnosed with antiphospholipid syndrome generally take aspirin or heparin in subsequent pregnancies, but questions remain due to the lack of high quality trials. Thyroid antibodies Anti-thyroid autoantibodies are associated with an increased risk of recurrent miscarriage with an odds ratio of 2.3 with a 95% confidence interval of 1.5–3.5. Increased uterine NK cells Natural killer cells, a type of white blood cell, are present in uterine tissue. High levels of these cells may be linked to RPL but high numbers or the presence of these cells is not a predictor of pregnancy loss in women who have not have had a miscarriage. Parental HLA sharing Earlier studies that perhaps paternal sharing of HLA genes would be associated with increased pregnancy loss have not been confirmed. Male-specific minor histocompatibility Immunization of mothers against male-specific minor histocompatibility (H-Y) antigens has a pathogenic role in many cases of secondary recurrent miscarriage, that is, recurrent miscarriage in pregnancies succeeding a previous live birth. An example of this effect is that the male:female ratio of children born prior and subsequent to secondary recurrent miscarriage is 1.49 and 0.76 respectively. Ovarian factors Luteal phase defect The issue of a luteal phase defect is complex. The theory behind the concept suggests that an inadequate amount of progesterone is produced by the corpus luteum to maintain the early pregnancy. Assessment of this situation was traditionally carried out by an endometrial biopsy, however recent studies have not confirmed that such assessment is valid. Studies about the value of progesterone supplementation remain deficient, however, such supplementation is commonly carried out on an empirical basis. Infection Infections are estimated to be responsible for between 0.5 and 5% of cases with recurrent miscarriage. The main suspected pathogens are mycoplasma, ureaplasma, Chlamydia trachomatis, Listeria monocytogenes, and herpes simplex virus. An infectious evaluation may be warranted in people with immunodeficiency, or with signs of chronic endometritis/cervicitis on examination. Otherwise, there is no evidence that routine infectious evaluation is appropriate or productive.Chronic endometritis (CE) due to common bacteria has been found to be prevalent in some women with a history of recurrent miscarriage. One study found that 71 percent of women who tested positive for this condition were successfully treated by an antibiogram-based antibiotic treatment. 78.4 percent of these women subsequently became pregnant in the year following treatment. The study concludes that "CE is frequent in women with recurrent miscarriages," and that "antibiotic treatment seems to be associated with an improved reproductive outcome." The authors also conclude, "that hysteroscopy should be a part of the diagnostic workup of infertile women complaining of unexplained recurrent miscarriage." Despite challenges in diagnosing chronic endometritis, often done by identifying plasma cells within the lining of the womb, a recent study identified women with chronic endometritis were more likely to have a miscarriage than women without. Assessment Transvaginal ultrasonography has become the primary method of assessment of the health of an early pregnancy. In non-pregnant patients who are evaluated for recurrent pregnancy loss the following tests are usually performed. Parental chromosome testing (karyogram) is generally recommended after 2 or 3 pregnancy losses. Blood tests for thrombophilia, ovarian function, thyroid function and diabetes are performed. Treatment If the likely cause of recurrent pregnancy loss can be determined treatment is to be directed accordingly. In pregnant women with a history of recurrent miscarriage, anticoagulants seem to increase the live birth rate among those with antiphospholipid syndrome and perhaps those with congenital thrombophilia but not in those with unexplained recurrent miscarriage. One study found that in many women with chronic endometritis, "fertility was restored after appropriate antibiotic treatment."There are currently no treatments for women with unexplained recurrent pregnancy loss. The majority of patients are counseled to try to conceive again, and chances are about 60% that the next pregnancy is successful without treatment. However, each additional loss worsens the prognostic for a successful pregnancy and increases the psychological and physical risks to the mother. Aspirin has no effect in preventing recurrent miscarriage in women with unexplained recurrent pregnancy loss. Immunotherapy has not been found to help. There is currently one drug in development, NT100, which is in clinical trials for the treatment of unexplained recurrent miscarriage. The study investigates the role of NT100 in improving maternal-fetal tolerance for women with unexplained recurrent miscarriage.In certain chromosomal situations, while treatment may not be available, in vitro fertilization with preimplantation genetic diagnosis may be able to identify embryos with a reduced risk of another pregnancy loss which then would be transferred. However, in vitro fertilization does not improve maternal-fetal tolerance imbalances.Close surveillance during pregnancy is generally recommended for pregnant patients with a history of recurrent pregnancy loss. Even with appropriate and correct treatment another pregnancy loss may occur as each pregnancy develops its own risks and problems. Psychological effects of miscarriages There is significant, and often unrecognized, psychological and psychiatric trauma for the mother – for many, miscarriage represents the loss of a future child, of motherhood, and engenders doubts regarding her ability to procreate."There is tremendous psychological impact of recurrent miscarriage. Psychological support in the form of frequent discussions and sympathetic counseling are crucial to the successful evaluation and treatment of the anxious couple. When no etiologic factor is identified, no treatment started at 60% to 80% fetal salvage rate still may be expected. Therefore, couples with unexplained recurrent miscarriage should be offered appropriate emotional support and reassurance." Association with later disease Recurrent miscarriage in itself is associated with later development of coronary artery disease with an odds ratio of approximately 2, increased risk of ovarian cancer, increased risk of cardiovascular complications, and an increased risk of all-cause mortality of 44%, 86%, and 150% for women with a history of 1, 2, or 3 miscarriages, respectively.Women with a history of recurrent miscarriage are at risk of developing preeclampsia in later pregnancies. References Bibliography Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 9780071716727. == External links ==

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I'm curious about the meaning of the medical term 'Irritant diaper dermatitis.' Can you give me some insights?

Irritant diaper dermatitis (IDD, also called a diaper/nappy rash) is a generic term applied to skin rash in the diaper nappy area that are caused by various skin disorders and/or irritants. Generic irritant diaper/nappy dermatitis is characterized by joined patches of erythema and scaling mainly seen on the convex surfaces, with the skin folds spared. Diaper/nappy dermatitis with secondary bacterial or fungal involvement tends to spread to concave surfaces (i.e. skin folds), as well as convex surfaces, and often exhibits a central red, beefy erythema with satellite pustules around the border. It is usually considered a form of irritant contact dermatitis. The word "diaper" is in the name not because the diaper/nappy itself causes the rash but rather because the rash is associated with diaper use, being caused by the materials trapped by the diaper (usually feces). Allergic contact dermatitis has also been suggested, but there is little evidence for this cause. In adults with incontinence (fecal, urinary, or both), the rash is sometimes called incontinence-associated dermatitis (IAD).The term diaper candidiasis is used when a fungal origin is identified. The distinction is critical because the treatment (antifungals) is completely different. Causes Irritant diaper dermatitis develops when skin is exposed to prolonged wetness, increased skin pH caused by the combination, and subsequent reactions, of urine and feces, and resulting breakdown of the stratum corneum, or outermost layer of the skin. This may be due to diarrhea, frequent stools, tight diapers, overexposure to ammonia, or allergic reactions. In adults, the stratum corneum is composed of 25 to 30 layers of flattened dead keratinocytes, which are continuously shed and replaced from below. These dead cells are interlaid with lipids secreted by the stratum granulosum just underneath, which help to make this layer of the skin a waterproof barrier. The stratum corneums function is to reduce water loss, repel water, protect deeper layers of the skin from injury, and to repel microbial invasion of the skin. In infants, this layer of the skin is much thinner and more easily disrupted. Urine Although wetness alone has the effect of macerating the skin, softening the stratum corneum, and greatly increasing susceptibility to friction injury, urine has an additional impact on skin integrity because of its effect on skin pH. While studies show that ammonia alone is only a mild skin irritant, when urea breaks down in the presence of fecal urease it increases pH because ammonia is released, which in turn promotes the activity of fecal enzymes such as protease and lipase. These fecal enzymes increase the skins hydration and permeability to bile salts which also act as skin irritants. There is no detectable difference in rates of diaper rash in conventional disposable diaper wearers and reusable cloth diaper wearers. "Babies wearing superabsorbent disposable diapers with a central gelling material have fewer episodes of diaper dermatitis compared with their counterparts wearing cloth diapers. However, keep in mind that superabsorbent diapers contain dyes that were suspected to cause allergic contact dermatitis (ACD)." Whether wearing cloth or disposable diapers they should be changed frequently to prevent diaper rash, even if they dont feel wet. To reduce the incidence of diaper rash, disposable diapers have been engineered to pull moisture away from the babys skin using synthetic non-biodegradable gel. Today, cloth diapers use newly available superabsorbent microfiber cloth placed in a pocket with a layer of light permeable material that contacts the skin. This design serves to pull moisture away from the skin in to the microfiber cloth. This technology is used in most major pocket cloth diapers brands today. Diet The interaction between fecal enzyme activity and IDD explains the observation that infant diet and diaper rash are linked because fecal enzymes are in turn affected by diet. Breast-fed babies, for example, have a lower incidence of diaper rash, possibly because their stools have higher pH and lower enzymatic activity. Diaper rash is also most likely to be diagnosed in infants 8–12 months old, perhaps in response to an increase in eating solid foods and dietary changes around that age that affect fecal composition. Any time an infants diet undergoes a significant change (i.e. from breast milk to formula or from milk to solids) there appears to be an increased likelihood of diaper rash.The link between feces and IDD is also apparent in the observation that infants are more susceptible to developing diaper rash after treating with antibiotics, which affect the intestinal microflora. Also, there is an increased incidence of diaper rash in infants who have had diarrhea in the previous 48 hours, which may be because fecal enzymes such as lipase and protease are more active in feces which have passed rapidly through the gastrointestinal tract. Secondary infections The significance of secondary infection in IDD remains controversial. There seems to be no link between presence or absence of IDD and microbial counts. Although apparently healthy infants sometimes culture positive for Candida and other organisms without exhibiting any symptoms, there does seem to be a positive correlation between the severity of the diaper rash noted and the likelihood of secondary involvement. A wide variety of infections has been reported, including Staphylococcus aureus, Streptococcus pyogenes, Proteus mirabilis, enterococci and Pseudomonas aeruginosa, but it appears that Candida is the most common opportunistic invader in diaper areas. Diagnosis The diagnosis of IDD is made clinically, by observing the limitation of an erythematous eruption to the convex surfaces of the genital area and buttocks. If the diaper dermatitis occurs for greater than 3 days it may be colonized with Candida albicans, giving it the beefy red, sharply marginated, appearance of diaper candidiasis. Differential diagnosis Other rashes that occur in the diaper area include seborrhoeic dermatitis and atopic dermatitis. Both Seborrheic and Atopic dermatitis require individualized treatment; they are not the subject of this article. Seborrheic dermatitis, typified by oily, thick yellowish scales, is most commonly seen on the scalp (cradle cap) but can also appear in the inguinal folds. Atopic dermatitis, or eczema, is associated with allergic reaction, often hereditary. This class of rashes may appear anywhere on the body and is characterized by intense itchiness. Treatments Possible treatments include minimizing diaper use, barrier creams, mild topical cortisones, and antifungal agents. A variety of other inflammatory and infectious processes can occur in the diaper area and an awareness of these secondary types of diaper dermatitis aids in the accurate diagnosis and treatment of patients.Overall, there is sparse evidence of sufficient quality to be certain of the effectiveness of the various treatments. Washcloths with cleansing, moisturising and protective properties may be better than soap and water, and skin cleansers may also be better than soap and water, but the certainty of evidence with regard other treatments is very low. Diaper changing The most effective treatment, although not the most practical one, is to discontinue use of diapers, allowing the affected skin to air out. Another option is simply to increase the frequency of diaper changing. Thorough drying of the skin before diapering is a good preventive measure because it is the excess moisture, either from urine and feces or from sweating, that sets the conditions for a diaper rash to occur. Diaper type Some sources claim that diaper rash is more common with cloth diapers. Others claim the material of the diaper is relevant insofar as it can wick and keep moisture away from the babys skin, and preventing secondary Candida infection. However, there may not be enough data from good-quality, randomized controlled trials to support or refute disposable diaper use thus far. Furthermore, the effect of non-biodegradable diapers on the environment is a concerning matter for public policy. Creams, ointments Another approach is to block moisture from reaching the skin, and commonly recommended remedies using this approach include oil-based protectants or barrier cream, various over-the-counter "diaper creams", petroleum jelly, dimethicone and other oils. Such sealants sometimes accomplish the opposite if the skin is not thoroughly dry, in which case they serve to seal the moisture inside the skin rather than outside. Zinc oxide-based ointments such as Pinxav can be quite effective, especially in prevention, because they have both a drying and an astringent effect on the skin, being mildly antiseptic without causing irritation.A 2005 meta-analysis found no evidence to support the use of topical vitamin A to treat the condition. Dangers of using powders Various moisture-absorbing powders, such as talcum or starch, reduce moisture but may introduce other complications. Airborne powders of any sort can irritate lung tissue, and powders made from starchy plants (corn, arrowroot) provide food for fungi and are not recommended by the American Academy of Dermatology. Antifungals In persistent or especially bad rashes, an antifungal cream often has to be used. In cases that the rash is more of an irritation, a mild topical corticosteroid preparation, e.g. hydrocortisone cream, is used. As it is often difficult to tell a fungal infection apart from a mere skin irritation, many physicians prefer an corticosteroid-and-antifungal combination cream such as hydrocortisone/miconazole. References == External links ==

You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

Please help me grasp the concept behind the medical term 'Pemphigus herpetiformis.'

Pemphigus herpetiformis is a cutaneous condition, a clinical variant of pemphigus that combines the clinical features of dermatitis herpetiformis with the immunopathologic features of pemphigus. Pathophysiology Pemphigus Herpetiformis is an IGg mediated autoantibodies that affect the epidermal layer of the skin. Diagnosis See also Adult linear IgA disease List of cutaneous conditions == References ==

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I've come across the term 'Short bowel syndrome' in a medical context, but I'm not sure what it means. Can you clarify?

Short bowel syndrome (SBS, or simply short gut) is a rare malabsorption disorder caused by a lack of functional small intestine. The primary symptom is diarrhea, which can result in dehydration, malnutrition, and weight loss. Other symptoms may include bloating, heartburn, feeling tired, lactose intolerance, and foul-smelling stool. Complications can include anemia and kidney stones.Most cases are due to the surgical removal of a large portion of the small intestine. This is most often required due to Crohns disease in adults and necrotising enterocolitis in young children. Other causes include damage to the small intestine from other means and being born with an abnormally short intestine. It usually does not develop until less than 2 m (6.6 ft) of the normally 6.1 m (20 ft) small intestine remains.Treatment may include a specific diet, medications, or surgery. The diet may include slightly salty and slightly sweet liquids, vitamin and mineral supplements, small frequent meals, and the avoidance of high fat food. Occasionally nutrients need to be given through an intravenous line, known as parenteral nutrition. Medications used may include antibiotics, antacids, loperamide, teduglutide, and growth hormone. Different types of surgery, including an intestinal transplant, may help some people.Short bowel syndrome newly occurs in about three per million people each year. There are estimated to be about 15,000 people with the condition in the United States. The prevalence in the United States is approximately 30 cases per million and in Europe it is approximately 1.4 cases per million (but the rate varies widely between countries). The prevalence of short bowel syndrome has increased by more than 2 fold in the last 40 years. It is classified as a rare disease by the European Medicines Agency. Outcomes depend on the amount of bowel remaining and whether or not the small bowel remains connected with the large bowel. Signs and symptoms The symptoms of short bowel syndrome can include: Abdominal pain Diarrhea and steatorrhea (oily, bulky stool, which can be malodorous) Fluid depletion Weight loss and malnutrition FatiguePersons with short bowel syndrome may have complications caused by malabsorption of vitamins and minerals, such as deficiencies in vitamins A, D, E, K, B9 (folic acid), and B12, calcium, magnesium, iron, and zinc. These may appear as anemia, hyperkeratosis (scaling of the skin), easy bruising, muscle spasms, poor blood clotting, and bone pain. Causes Short bowel syndrome in adults and children is most commonly caused by surgery (intestinal resection). In those who undergo intestinal resection, approximately 15% eventually develop small bowel syndrome (75% of those due to 1 large resection and 25% due to multiple separate intestinal resections). This surgery may be done for: Crohns disease, an inflammatory disorder of the digestive tract Mesenteric ischemia, embolic or thrombotic events that may occur in the arteries or veins that supply or drain the intestines respectively, leading to disruption of blood supply to the intestines and ischemia. Volvulus, a twisting of the small intestine often caused by intestinal malrotation that quickly cuts off blood supply and leads to tissue death Tumors of the small intestine Radiation enteropathy, radiation injury to the small intestine, due to radiation therapy for cancer Injury or trauma to the small intestine Necrotizing enterocolitis (premature newborn) Bypass surgery to treat obesity Surgery to remove diseases or damaged portion of the small intestineSome children are also born with an abnormally short small intestine, known as congenital short bowel.Surgical complications, requiring re-surgery, are a common cause of small bowel syndrome, contributing up to 50% of cases based on some estimates. These surgical complications include internal hernias, volvuli, ischemia or profound hypotension. Pathophysiology The length of the small intestine can vary greatly, from as short as 2.75 m (9.0 ft) to as long as 10.49 m (34.4 ft). On average it is about 6.1 m (20 ft). Due to this variation it is recommended that following surgery the amount of bowel remaining be specified rather than the amount removed.Short bowel syndrome usually develops when there is less than 2 meters (6.6 feet) of the small intestine left to absorb sufficient nutrients.The resection of specific areas of the small bowel can lead to distinct symptoms in short bowel syndrome. The resection of the ileum leads to a malabsorption of vitamin B12, bile acids and the fat soluble vitamins A, D, E and K. Loss of the distal ileum also leads to loss of inhibitory hormones; leading to gastric hypersecretion, intestinal hypermotility (decreases in the intestinal transit time) leading to secretory diarrhea and macronutrient, micronutrient, vitamin and mineral deficiencies. Loss of the ileocecal valve leads to small intestinal bacterial overgrowth(SIBO) as bacterial flora normally found in the large intestines migrate proximally and colonize the small intestines leading to further malabsorption. SIBO leads to malabsorption as the bacteria colonizing the small intestine metabolize nutrients, directly competing with the intestinal absorption of nutrients. The bacteria colonizing the small intestines in SIBO may also cause bile acid deconjugation leading to malabsorption of lipids.In a process called intestinal adaptation, physiological changes to the remaining portion of the small intestine occur to increase its absorptive capacity. These changes usually take place over 1-2 years. These changes include: Enlargement (increased diameter) and lengthening of the villi found in the lining Increase in the diameter of the small intestine Slow down in peristalsis or movement of food through the small intestine (an increase in the transit time) to increase the time available for nutrient absorptionOsteoporosis is a very common comorbidity in people with short bowel syndrome who are on parenteral nutrition, with an estimated prevalence of 57-67%. The contributing factors to the osteoporosis include malnutrition, vitamin D deficiency due to malabsorption and vitamin D deficiency due to scarce sunlight exposure due to chronic disability. Diagnosis Definition Intestinal failure is decreased intestinal function such that nutrients, water, and electrolytes are not sufficiently absorbed. Short bowel syndrome is when there is less than 2 m (6.6 ft) of working bowel and is the most common cause of intestinal failure. Treatments Symptoms of short bowel syndrome are usually addressed with medication. These include: Anti-diarrheal medicine (e.g. loperamide, codeine) Vitamin, mineral supplements and L-glutamine powder mixed with water H2 blocker and proton pump inhibitors to reduce stomach acid Lactase supplement (to improve the bloating and diarrhea associated with lactose intolerance)In 2004, the USFDA approved a therapy that reduces the frequency and volume of total parenteral nutrition (TPN), comprising: NutreStore (oral solution of glutamine) and Zorbtive (growth hormone, of recombinant DNA origin, for injection) together with a specialized oral diet. After 24 weeks of successful Phase III patient treatment trials, Teduglutide was shown to be relatively safe and effective with varying degrees of benefits and adverse effects per patient. Adequate safety evaluations prove to be difficult due to a limited sample size available for study, however. In 2012, an advisory panel to the USFDA voted unanimously to approve for treatment of SBS the agent teduglutide, a glucagon-like peptide-2 analog developed by NPS Pharmaceuticals, who intend to market the agent in the United States under the brandname Gattex. Teduglutide had been previously approved for use in Europe and is marketed under the brand Revestive by Nycomed.Surgical procedures to lengthen dilated bowel include the Bianchi procedure, where the bowel is cut in half and one end is sewn to the other, and a newer procedure called serial transverse enteroplasty (STEP), where the bowel is cut and stapled in a zigzag pattern. Heung Bae Kim, MD, and Tom Jaksic, MD, both of Childrens Hospital Boston, devised the STEP procedure in the early 2000s. The procedure lengthens the bowel of children with SBS and may allow children to avoid the need for intestinal transplantation. As of June 2009, Kim and Jaksic have performed 18 STEP procedures. The Bianchi and STEP procedures are usually performed by pediatric surgeons at quaternary hospitals who specialize in small bowel surgery. Prognosis After resection; having a remnant small bowel length of less than 75 cm and a remaining large bowel length of less than 57% of the original length are both associated with subsequent dependence on parenteral nutrition.There is no cure for short bowel syndrome except transplant. In newborn infants, the 4-year survival rate on parenteral nutrition is approximately 70%. In newborn infants with less than 10% of expected intestinal length, 5 year survival is approximately 20%. Some studies suggest that much of the mortality is due to a complication of the total parenteral nutrition (TPN), especially chronic liver disease. Much hope is, as of 2006, vested in Omegaven, a type of lipid TPN feed, in which recent case reports suggest the risk of liver disease is much lower.Although promising, small intestine transplant has a mixed success rate, with postoperative mortality rate of up to 30%. One-year and 4-year survival rate are 90% and 60%, respectively. See also Bowel-associated dermatosis–arthritis syndrome, another syndrome that can result from small-bowel bypass (or other causes) References External links Short bowel syndrome at Curlie National Digestive Diseases Information Clearinghouse - Short Bowel Syndrome Archived 2014-03-21 at the Wayback Machine

You are a medical lexicon. Explain medical terminology with depth and clarity, making sure the information is both accurate and easy to grasp.

I'm trying to expand my medical knowledge. Can you elucidate the term 'Dolutegravir/rilpivirine'?

Dolutegravir/rilpivirine, sold under the brand name Juluca, is a fixed-dose combination antiretroviral medication for the treatment of HIV/AIDS. It contains the medicines dolutegravir and rilpivirine. It is taken by mouth.The most common adverse reactions (of all severity grades) are diarrhea and headache.Dolutegravir/rilpivirine was approved for use in the United States in November 2017, and for use in the European Union in May 2018. Medical uses Dolutegravir/rilpivirine is indicated for the treatment of human immunodeficiency virus type 1 (HIV-1) infection in adults who are virologically-suppressed (HIV-1 RNA <50 copies/mL) on a stable antiretroviral regimen for at least six months with no history of virological failure and no known or suspected resistance to any non-nucleoside reverse transcriptase inhibitor or integrase inhibitor. References External links "Dolutegravir mixture with rilpivirine". Drug Information Portal. U.S. National Library of Medicine.

You function as a medical explainer. Your task is to convey the meanings of medical terms in a detailed, yet easy-to-understand manner.

I'd like to learn more about the medical term 'Postterm pregnancy.' Can you provide some details?

Postterm pregnancy is when a woman has not yet delivered her baby after 42 weeks of gestation, two weeks beyond the typical 40-week duration of pregnancy. Postmature births carry risks for both the mother and the baby, including fetal malnutrition, meconium aspiration syndrome, and stillbirths. After the 42nd week of gestation, the placenta, which supplies the baby with nutrients and oxygen from the mother, starts aging and will eventually fail. Postterm pregnancy is a reason to induce labor. Definitions The management of labor and delivery may vary depending on the gestational age. It is common to encounter the following terms when describing different time periods of pregnancy. Postterm – ≥ 42 weeks + 0 days of gestation (> 293 days from the first day of last menstrual period, or > 13 days from the estimated due date) Late term – 41 weeks + 0 days to 41 weeks + 6 days of gestation Full term – 39 weeks + 0 days to 40 weeks + 6 days of gestation Early term – 37 weeks + 0 days to 38 weeks + 6 days of gestation Preterm – ≤ 36 weeks + 6 days of gestationBesides postterm pregnancy, other terminologies have been used to describe the same condition (≥ 42w+0d), such as prolonged pregnancy, postdates, and postdatism. However, these terminologies are less commonly used to avoid confusion.Postterm pregnancy should not be confused with postmaturity, postmaturity syndrome, or dysmaturity. These terms describe the neonatal condition that may be caused by postterm pregnancy instead of the duration of pregnancy. Signs and symptoms Because postterm pregnancy is a condition solely based on gestational age, there are no confirming physical signs or symptoms. While it is difficult to determine gestational age physically, infants that are born postterm may be associated with a physical condition called postmaturity. The most common symptoms for this condition are dry skin, overgrown nails, creases on the babys palms and soles of their feet, minimal fat, abundant hair on their head, and either a brown, green, or yellow discoloration of their skin. Doctors diagnose postmature birth based on the babys physical appearance and the length of the mothers pregnancy. However, some postmature babies may show no or few signs of postmaturity. Baby Reduced placental perfusion – Once a pregnancy has surpassed the 40-week gestation period, doctors closely monitor the mother for signs of placental deterioration. Toward the end of pregnancy, calcium is deposited on the walls of blood vessels, and proteins are deposited on the surface of the placenta, which changes the placenta. This limits the blood flow through the placenta and ultimately leads to placental insufficiency, and the baby is no longer properly nourished. Induced labor is strongly encouraged if this happens. Oligohydramnios – Low volume of amniotic fluid surrounding the fetus. It is associated with complications such as cord compression, abnormal heart rate, fetal acidosis, and meconium amniotic fluid. Meconium aspiration syndrome – Respiratory compromise secondary to meconium present in infants lungs. Macrosomia – Estimated fetal weight of ≥ 4.5 kg. It can further increase the risk of prolonged labor and shoulder dystocia. Shoulder dystocia – Difficulty in delivering the shoulders due to increased body size. Increased forceps-assisted or vacuum-assisted birth – When postterm babies are larger than average, forceps or vacuum delivery may be used to resolve the difficulties at the delivery time, such as shoulder dystocia. Complications include lacerations, skin markings, external eye trauma, intracranial injury, facial nerve injury, skull fracture, and rarely death. Mother Increased labor induction – Induction may be needed if labor progression is abnormal. Oxytocin, a medication used in induction, may have side effects such as low blood pressure. Increased forceps assisted or vacuum assisted birth – operative vaginal deliveries increase maternal risks of genital trauma. Increased Caesarean birth – Postterm babies may be larger than an average baby, thus increasing the length of labor. The labor is increased because the babys head is too big to pass through the mothers pelvis. This is called cephalopelvic disproportion. Caesarean sections are encouraged if this happens. Complications include bleeding, infection, abnormal wound healing, abnormal placenta in future pregnancies, and rarely death.A 2019 randomized control trial of induced labor at 42 or 43 weeks was terminated early due to statistical evidence of "significantly increased risk for women induced at the start of week 43". The study implies clinical guidelines for induction of labor no later than at 41 gestational weeks. Causes The causes of post-term births are unknown, but postmature births are more likely when the mother has experienced a previous postmature birth. Due dates are easily miscalculated when the mother is unsure of her last menstrual period. When there is a miscalculation, the baby could be delivered before or after the expected due date. Postmature births can also be attributed to irregular menstrual cycles. When the menstrual period is irregular it is difficult to judge the moment of ovulation and subsequent fertilization and pregnancy. Some postmature pregnancies may not be postmature in reality due to the uncertainty of mothers last menstrual period. However, in most countries where gestation is measured by ultrasound scan technology, this is less likely. Monitoring Once a pregnancy is diagnosed postterm, usually at or greater than 42 weeks of gestational age, the mother should be offered additional monitoring as this can provide valuable clues that the fetal health is being maintained. Fetal movement recording Regular movements of the fetus is the best sign indicating that it is still in good health. The mother should keep a "kick-chart" to record the movements of her fetus. If there is a reduction in the number of movements it could indicate placental deterioration. Doppler fetal monitor Doppler fetal monitor is a hand-held device that is routinely used in prenatal care. When it is used correctly, it can quickly measure the fetal heart rate. The baseline of fetal heart rate is typically between 110 and 160 beats per minute. Doppler flow study Doppler flow study is a type of ultrasound that measures the amount of blood flowing in and out of the placenta. The ultrasound machine can also detect the direction of blood flow and display it in red or blue. Usually, a red color indicates a flow toward the ultrasound transducer, while blue indicates a flow away from the transducer. Based on the display, doctors can evaluate blood flow to the umbilical arteries, umbilical veins, or other organs such as heart and brain. Nonstress test Nonstress test (NST) is a type of electronic fetal monitoring that uses a cardiotocograph to monitor fetal heartbeat, fetal movement and mothers contraction. NST is typically monitored for at least 20 minutes. Signs of a reactive (normal) NST include a baseline fetal heart rate (FHR) between 110 and 160 beats per minute (bpm) and 2 accelerations of FHR of at least 15 bpm above baseline for over 15 seconds. Vibroacoustic stimulation and longer monitoring may be needed if NST is non-reactive. Biophysical profile A biophysical profile is a noninvasive procedure that uses the ultrasound to evaluate the fetal health based on NST and four ultrasound parameters: fetal movement, fetal breathing, fetal muscle tone, and the amount of amniotic fluid surrounding the fetus. A score of 2 points is given for each category that meets the criteria or 0 points if the criteria are not met (no 1 point). Sometimes, the NST is omitted, making the highest score 8/8 instead of 10/10. Generally, a score of 8/10 or 10/10 is considered a normal test result, unless 0 points is given for amniotic fluid. A score of 6/10 with normal amniotic fluid is considered equivocal, and a repeated test within 24 hours may be needed. A score of 4/10 or less is considered abnormal, and delivery may be indicated. Low amniotic fluid can cause pinching umbilical cord, decreasing blood flow to the fetus. Therefore, a score of 0 points for amniotic fluid may indicate the fetus is at risk. Management Expectant A woman who has reached 42 weeks of pregnancy is likely to be offered induction of labour. Alternatively, she can choose expectant management, that is, she waits for the natural onset of labour. Women opting for expectant management may also choose to carry on with additional monitoring of their baby, with regular CTG, ultrasound, and biophysical profile. Risks of expectant management vary between studies.In many places in the World, according to the World Health Organization and others, such services are rudimentary or not available, and deserve improvement. Inducing labor Inducing labor artificially starts the labor process by using medication and other techniques. Labor is usually only induced if there is potential danger on the mother or child. There are several reasons for labor induction; the mothers water breaks, and contractions have not started, the child is postmature, the mother has diabetes or high blood pressure, or there is not enough amniotic fluid around the baby. Labor induction is not always the best choice because it has its own risks. Sometimes mothers will request to be induced for reasons that are not medical. This is called an elective induction. Doctors try to avoid inducing labor unless it is completely necessary. Procedure There are four common methods of starting contractions. The four most common are stripping the membranes, breaking the mothers water, giving the hormone prostaglandin, and giving the synthetic hormone pitocin. Stripping the membranes does not work for all women, but can for most. A doctor inserts a finger into the mothers cervix and moves it around to separate the membrane connecting the amniotic sac, which houses the baby, from the walls of the uterus. Once this membrane is stripped, the hormone prostaglandin is naturally released into the mothers body and initiates contractions. Most of the time doing this only once will not immediately start labor. It may have to be done several times before the stimulant hormone is released, and contractions start. The next method is breaking the mothers water, which is also referred to as an amniotomy. The doctor uses a plastic hook to break the membrane and rupture the amniotic sac. Within a few hours labor usually begins. Giving the hormone prostaglandin ripens the cervix, meaning the cervix softens, thins out, or dilates. The drug Cervidil is administered by mouth in tablet form or in gel form as an insert. This is most often done in the hospital overnight. The hormone oxytocin is usually given in the synthetic form of Pitocin. It is administered through an IV throughout the labor process. This hormone stimulates contractions. Pitocin is also used to "restart" labor when it is lagging.The use of misoprostol is also allowed, but close monitoring of the mother is required. Feelings Stripping the membranes: Stripping the membranes only takes a few minutes and causes a few intense cramps. Many women report a feeling similar to urination, others report it to be quite painful. Breaking the water: Having ones water broken feels like a slight tug and then a warm flow of liquid. Pitocin: When the synthetic hormone, pitocin, is used, contractions occur more frequently than a natural occurring birth; they are also more intense. Epidemiology Prevalence of postterm pregnancy may vary between countries due to different population characteristics or medical management. Factors include number of first-time pregnancies, genetic predisposition, timing of ultrasound assessment, and Caesarean section rates, etc. The incidence is approximately 7%. Postterm pregnancy occurs in 0.4% of pregnancies approximately in the United States according to birth certificate data. Notes == External links ==

You are a medical knowledge base. Your task is to elucidate medical terminology, offering insights into their meanings, origins, and applications.

What is the significance of the term 'Retroperitoneal fibrosis' in the medical field?

Retroperitoneal fibrosis or Ormonds disease is a disease featuring the proliferation of fibrous tissue in the retroperitoneum, the compartment of the body containing the kidneys, aorta, renal tract, and various other structures. It may present with lower back pain, kidney failure, hypertension, deep vein thrombosis, and other obstructive symptoms. It is named after John Kelso Ormond, who rediscovered the condition in 1948. Causes The association of idiopathic retroperitoneal fibrosis with various immune-related conditions and response to immunosuppression led to a search for an autoimmune cause of idiopathic RPF. Many of these previously idiopathic cases can now be attributed to IgG4-related disease, an autoimmune disorder proposed in 2003. Otherwise, one-third of cases are secondary to malignancy, medication (methysergide, hydralazine, beta blockers), prior radiotherapy, or certain infections.Other associations include: connective tissue disease Riedels thyroiditis sclerosing cholangitis membranous nephropathy ankylosing spondylitis inflammatory bowel disease ANCA-associated vasculitis autoimmune pancreatitis sarcoidosis primary biliary cirrhosis inflammatory abdominal aortic aneurysm Diagnosis The diagnosis of retroperitoneal fibrosis cannot be made on the basis of the results of laboratory studies. CT is the best diagnostic modality: a confluent mass surrounding the aorta and common iliac arteries can be seen. On MRI, it has low T1 signal intensity and variable T2 signal. Malignant retroperitoneal fibrosis usually gives uneven MRI signals, is bulky, extends above the origins of renal arteries, or displaces the aorta anteriorly. Additionally, malignant retroperitoneal fibrosis less frequently displaces the ureters medially when compared to other causes of retroperitoneal fibrosis.On fludeoxyglucose (18F) (FDG) positron emission tomography (PET) scan, FDG accumulation is shown in the affected area.Although biopsy is not usually recommended, it is appropriate when malignancy or infection is suspected. Biopsy should also be done if the location of fibrosis is atypical or if there is an inadequate response to initial treatment. Treatment In the absence of severe urinary tract obstruction (which generally requires surgery with omental wrapping), treatment is generally with glucocorticoids initially, followed by DMARDs either as steroid-sparing agents or if refractory on steroids. The selective estrogen receptor modulator tamoxifen has shown to improve the condition in various small trials, although the exact mechanism of its action remains unclear. References == External links ==

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

I need a basic explanation for the medical term 'Neurotrophic keratitis.'

Neurotrophic keratitis (NK) is a degenerative disease of the cornea caused by damage of the trigeminal nerve, which results in impairment of corneal sensitivity, spontaneous corneal epithelium breakdown, poor corneal healing and development of corneal ulceration, melting and perforation. This is because, in addition to the primary sensory role, the nerve also plays a role maintaining the integrity of the cornea by supplying it with trophic factors and regulating tissue metabolism.Neurotrophic keratitis is classified as a rare disease, with an estimated prevalence of less than 5 in 10,000 people in Europe. It has been recorded that on average, 6% of herpetic keratitis cases may evolve to this disease, with a peak of 12.8% of cases of keratitis due to varicella zoster virus.The diagnosis, and particularly the treatment of neurotrophic keratitis are the most complex and challenging aspects of this disease, as a satisfactory therapeutic approach is not yet available. Causes The cornea lacks blood vessels and is among the most densely innervated structures of the human body. Corneal nerves are responsible for maintaining the anatomical and functional integrity of the cornea, conveying tactile, temperature and pain sensations, playing a role in the blink reflex, in wound healing and in the production and secretion of tears.Most corneal nerve fibres are sensory in origin and are derived from the ophthalmic branch of the trigeminal nerve. Congenital or acquired ocular and systemic diseases can determine a lesion at different levels of the trigeminal nerve, which can lead to a reduction (hypoesthesia) or loss (anesthesia) of sensitivity of the cornea. The most common causes of loss of corneal sensitivity are viral infections (herpes simplex and herpes zoster ophthalmicus), chemical burns, physical injuries, corneal surgery, neurosurgery, chronic use of topical medications, or chronic use of contact lenses.Possible causes also include systemic diseases such as diabetes mellitus, multiple sclerosis or leprosy. Other, albeit less frequent, potential causes of the disease are: intracranial space-occupying lesions such as neuroma, meningioma and aneurysms, which may compress the trigeminal nerve and reduce corneal sensitivity.Conversely, congenital conditions that may lead to this disorder are very rare. Diagnosis NK is diagnosed on the basis of the patients medical history and a careful examination of the eye and surrounding area.With regard to the patients medical history, special attention should be paid to any herpes virus infections and possible surgeries on the cornea, trauma, abuse of anaesthetics or chronic topical treatments, chemical burns or, use of contact lenses. It is also necessary to investigate the possible presence of diabetes or other systemic diseases such as multiple sclerosis. The clinical examination is usually performed through a series of assessments and tools: General examination of cranial nerves, to determine the presence of nerve damage. Eye examinations:Complete eye examination: examination of the eyelids, blink rate, presence of inflammatory reactions and secretions, corneal epithelial alterations. Corneal sensitivity test: performed by placing a cotton wad or cotton thread in contact with the corneal surface: this only allows to determine whether corneal sensitivity is normal, reduced or absent; or using an esthesiometer that allows to assess corneal sensitivity. Tear film function test, such as Schirmers test, and tear film break-up time. Fluorescein eye stain test, which shows any damage to the corneal and conjunctival epithelium Classification According to Mackies classification, neurotrophic keratitis can be divided into three stages based on severity: Stage I: characterized by alterations of the corneal epithelium, which is dry and opaque, with superficial punctate keratopathy and corneal oedema. Long-lasting neurotrophic keratitis may also cause hyperplasia of the epithelium, stromal scarring and neovascularization of the cornea. Stage II: characterized by development of epithelial defects, often in the area near the centre of the cornea. Stage III: characterized by ulcers of the cornea accompanied by stromal oedema and/or melting that may result in corneal perforation. Treatment Early diagnosis, targeted treatment according to the severity of the disease, and regular monitoring of patients with neurotrophic keratitis are critical to prevent damage progression and the occurrence of corneal ulcers, especially considering that the deterioration of the condition is often poorly symptomatic.The purpose of treatment is to prevent the progression of corneal damage and promote healing of the corneal epithelium. The treatment should always be personalized according to the severity of the disease. Conservative treatment is typically the best option.In stage I, the least serious, treatment consists of the administration of preservative-free artificial tears several times a day in order to lubricate and protect the ocular surface, improving the quality of the epithelium and preventing the possible loss of transparency of the cornea.In stage II, treatment should be aimed at preventing the development of corneal ulcers and promoting the healing of epithelial lesions. In addition to artificial tears, topical antibiotics may also be prescribed to prevent possible infections. Patients should be monitored very carefully since, being the disease poorly symptomatic, the corneal damage may progress without the patient noticing any worsening of the symptoms. Corneal contact lenses can also be used in this stage of the disease, for their protective action to improve corneal healing.In the most severe forms (stage III), it is necessary to stop the progression towards corneal perforation: in these cases, a possible surgical treatment option is tarsorrhaphy, i.e. the temporary or permanent closure of the eyelids by means of sutures or botulinum toxin injection. This protects the cornea, although the aesthetic result of these procedures may be difficult to accept for patients. Similarly, a procedure that entails the creation of a conjunctival flap has been shown to be effective in the treatment of chronic corneal ulcers with or without corneal perforation.In addition, another viable therapeutic option is amniotic membrane graft, which has recently been shown to play a role in stimulating corneal epithelium healing and in reducing vascularisation and inflammation of the ocular surface. Other approaches used in severe forms include the administration of autologous serum eye drops.Research studies have focused on developing novel treatments for neurotrophic keratitis, and several polypeptides, growth factors and neuromediators have been proposed. Studies were conducted on topical treatment with Substance P and IGF-1 (insulin-like growth factor-1), demonstrating an effect on epithelial healing. Nerve Growth Factor (NGF) play a role in the epithelial proliferation and differentiation and in the survival of corneal sensory nerves. Topical treatment with murine NGF showed to promote recovery of epithelial integrity and corneal sensitivity in NK patients. Recently, a recombinant human nerve growth factor eye drop formulation has been developed for clinical use.Cenegermin, a recombinant form of human NGF, has recently been approved in Europe in an eye drop formulation for neurotrophic keratitis. Cenegermin as an eye drop formulation for treatment of NK is approved by FDA in August 2018 See also Keratitis Cornea Rare disease References == External links ==

You are a conduit for medical education. Your task is to offer detailed explanations of medical terms, ensuring they are understandable and precise.

I'd like to learn more about the medical term 'Benzonatate.' Can you provide some details?

Benzonatate, sold under the brand name Tessalon among others, is a medication used to try to help with the symptoms of cough and hiccups. It is taken by mouth. Use is not recommended in those under the age of ten. Effects generally begin within 20 minutes and last up to eight hours.Side effects include sleepiness, dizziness, headache, upset stomach, skin rash, hallucinations, and allergic reactions. Excessive doses may cause seizures, irregular heartbeat, and death. Chewing or sucking on the capsule can lead to laryngospasm, bronchospasm, and circulatory collapse. It is unclear if use in pregnancy or breastfeeding is safe. It works by numbing stretch receptors in the lungs and suppressing the cough reflex in the brain.Benzonatate was approved for medical use in the United States in 1958. It is available as a generic medication. It is not available in many countries. In 2019, it was the 105th most commonly prescribed medication in the United States, with more than 6 million prescriptions. Medical uses Cough Benzonatate is a prescription non-opioid alternative for the symptomatic relief of cough. It has been shown to improve cough associated with a variety of respiratory conditions including asthma, bronchitis, pneumonia, tuberculosis, pneumothorax, opiate-resistant cough in lung cancer, and emphysema.Benzonatate also reduces the consistency and volume of sputum production associated with cough in those with chronic obstructive pulmonary disorder (COPD).Compared to codeine, benzonatate has been shown to be more effective in reducing the frequency of induced cough in experiments.Benzonatate does not treat the underlying cause of the cough. Hiccups Benzonatate has been shown to have use in the suppression of hiccups. Intubation Benzonatate acts as a local anesthetic and the liquid inside the capsule can be applied in the mouth to numb the oropharynx for awake intubation. However, there can be life-threatening adverse effects when the medication is absorbed by the oral mucosa, including choking, hypersensitivity reactions, and circulatory collapse. Contraindications Hypersensitivity to benzonatate or any related compounds is a contraindication to its administration. Side effects Benzonatate is generally well-tolerated if the liquid-capsule is swallowed intact. Potential adverse effects to benzonatate include: Constipation, dizziness, fatigue, stuffy nose, nausea, headache are frequently reported. Sedation, a feeling of numbness in the chest, sensation of burning in the eyes, a vague "chilly" sensation, itchiness, and rashes are also possible. Ingestion of a small handful of capsules has caused seizures, cardiac arrhythmia, and death in adults. Hypersensitivity reactions Benzonatate is structurally related to anesthetic medications of the para-aminobenzoic acid (PABA) class which includes procaine and tetracaine. Procaine and tetracaine, previously used heavily in the fields of dentistry and anesthesiology, have fallen out of favor due to allergies associated with their metabolites. Similarly, severe hypersensitivity reactions to benzonatate have been reported and include symptoms of laryngospasm, bronchospasm, and cardiovascular collapse. These reactions are possibly associated with chewing, sucking, or crushing the capsule in the mouth. Improper use Benzonatate should be swallowed whole. Crushing or sucking on the liquid-filled capsule, or "softgel," will cause release of benzonatate from the capsule and can produce a temporary local anesthesia of the oral mucosa. Rapid development of numbness of the tongue and choking can occur. In severe cases, excessive absorption can lead to laryngospasm, bronchospasm, seizures, and circulatory collapse. This may be due to a hypersensitivity reaction to benzonatate or a systemic local anesthetic toxicity, both of which have similar symptoms. There is a potential for these adverse effects to occur at a therapeutic dose, that is, a single capsule, if chewed or sucked on in the mouth. Psychiatric effects Isolated cases of bizarre behavior, mental confusion, and visual hallucinations have been reported during concurrent use with other prescribed medications. Central nervous system effects associated with other para-aminobenozic acid (PABA) derivative local anesthetics, for example procaine or tetracaine, could occur with benzonatate and should be considered. Children Safety and efficacy in children below the age of 10 have not been established. Accidental ingestion resulting in death has been reported in children below the age of 10. Benzonatate may be attractive to children due to its appearance, a round-shaped liquid-filled gelatin capsule, which looks like candy. Chewing or sucking of a single capsule can cause death of a small child. Signs and symptoms can occur rapidly after ingestion (within 15–20 minutes) and include restlessness, tremors, convulsions, coma, and cardiac arrest. Death has been reported within one hour of ingestion. Pregnancy and breast feeding In the U.S., benzonatate is classified by the U.S. Food and Drug Administration (FDA) as pregnancy category C. It is not known if benzonatate can cause fetal harm to a pregnant woman or if it can affect reproduction capacity. Animal reproductive studies have not yet been conducted with benzonatate to evaluate its teratogenicity. Benzonatate should only be given to a pregnant woman if it is clearly needed.It is not known whether benzonatate is excreted in human milk. It is recommended to exercise caution when benzonatate is given to a nursing woman. Overdose Benzonatate is chemically similar to other local anesthetics such as tetracaine and procaine, and shares their pharmacology and toxicology.Benzonatate overdose is characterized by symptoms of restlessness, tremors, seizures, abnormal heart rhythms (cardiac arrhythmia), cerebral edema, absent breathing (apnea), fast heart beat (tachycardia), and in severe cases, coma and death. Symptoms develop rapidly, typically within 1 hour of ingestion. Treatment focuses on removal of gastric contents and on managing symptoms of sedation, convulsions, apnea, and cardiac arrhythmia.Despite a long history of safe and appropriate usage, the safety margin of benzonatate is reportedly narrow. Toxicity above the therapeutic dose is relatively low and ingestion of a small handful of pills can cause symptoms of overdose. Children are at an increased risk for toxicity, which have occurred with administration of only one or two capsules.Due to increasing usage of benzonatate and rapid onset of symptoms, there are accumulating cases of benzonatate overdose deaths, especially in children. Pharmacology Benzonatate is chemically similar to other local anesthetics such as tetracaine and procaine, and shares their pharmacology. Mechanism of action Similar to other local anesthetics, benzonatate is a potent voltage-gated sodium channel inhibitor. After absorption and circulation to the respiratory tract, benzonatate acts as a local anesthetic, decreasing the sensitivity of vagal afferent fibers and stretch receptors in the bronchi, alveoli, and pleura in the lower airway and lung. This dampens their activity and reduces the cough reflex. Benzonatate also has central antitussive activity on the cough center in central nervous system at the level of the medulla. However, there is minimal inhibition of the respiratory center at a therapeutic dosage. Pharmacokinetics The antitussive effect of benzonatate begins within 15 to 20 minutes after oral administration and typically lasts between 3 and 8 hours.Benzonatate is hydrolyzed by plasma butyrylcholinesterase (BChE) to the metabolite 4-(butylamino)benzoic acid (BABA) as well as polyethylene glycol monomethyl esters. Like many other local anesthetic esters, the hydrolysis of the parent compound is rapid. There are concerns that those with pseudocholinesterase deficiencies may have an increased sensitivity to benzonatate as this hydrolysis is impaired, leading to increased levels of circulating medication. Chemical structure Benzonatate is a butylamine, structurally related to other polyglycol ester local anesthetics such as procaine and tetracaine. The molecular weight of benzonatate is 603.7 g/mol. However, the reference standard for benzonatate is a mixture of n-ethoxy compounds, differing in the abundance of 7-9 repeating units, with an average molecular weight of 612.23 g/mol. There is also evidence that the compound is not uniform between manufacturers. Society and culture Benzonatate was first made available in the U.S. in 1958 as a prescription medication for the treatment of cough in individuals over the age of 10. There are a variety of prescription opioid-based cough relievers, such as hydrocodone and codeine, but have unwanted side effects and potential of abuse and diversion. However, benzonatate is currently the only prescription non-opioid antitussive and its usage has been rapidly increasing. The exact reasons of this increase are unclear. Economics In the United States between 2004 and 2009, prescriptions increased 50% from 3.1 million to 4.7 million, the market share of benzonatate among antitussives increased from 6.3% to 13%, and the estimated number of children under the age of 10 years receiving benzonatate increased from 10,000 to 19,000. Throughout this same period, greater than 90% of prescriptions were given to those 18 or older. The majority of prescriptions were given by general, family, internal, and osteopathic physicians with pediatricians account for about 3% of prescribed benzonatate.In 2019, it was the 105th most commonly prescribed medication in the United States, with more than 6 million prescriptions. Brand names Tessalon is a brand name version of benzonatate manufactured by Pfizer, Inc. It is available as perles or capsules. Zonatuss was a brand name manufactured by Atley Pharmaceuticals, Inc. and Vertical Pharmaceuticals, Inc. References External links "Benzonatate". Drug Information Portal. U.S. National Library of Medicine.

You function as a medical informant. Please provide in-depth yet accessible descriptions of medical terms, suitable for a broad audience.

I need a basic explanation for the medical term 'Field.'

Field may refer to: Expanses of open ground Field (agriculture), an area of land used for agricultural purposes Airfield, an aerodrome that lacks the infrastructure of an airport Battlefield Lawn, an area of mowed grass Meadow, a grassland that is either natural or allowed to grow unmowed and ungrazed Playing field, used for sports or games Arts and media In decorative art, the main area of a decorated zone, often contained within a border, often the background for motifs Field (heraldry), the background of a shield In flag terminology, the background of a flag FIELD (magazine), a literary magazine published by Oberlin College in Oberlin, Ohio Field (sculpture), by Anthony Gormley Organizations Field department, the division of a political campaign tasked with organizing local volunteers and directly contacting voters Field Enterprises, a defunct private holding company Field Communications, a division of Field Enterprises Field Museum of Natural History, in Chicago People Field (surname) Field Cate (born 1997), American child actor Places Field, British Columbia, Canada Field, Kentucky, United States Field, Minneapolis, Minnesota, United States Field, Ontario, Canada Field, Staffordshire, England, United Kingdom Field, South Australia Field Hill, British Columbia, Canada Field Island, Nunavut, Canada Mount Field (disambiguation), mountains in Canada, the United States, Australia and Antarctica Science, technology, and mathematics Computing Field (computer science), a smaller piece of data from a larger collection (e.g., database fields) Field-programmability, an electronic devices capability of being reprogrammed with new logic Geology Field (mineral deposit), a mineral deposit containing valuable resources in a cost-competitive concentration Polje or karst field, a characteristic landform in karst topography Mathematics Field (mathematics), type of algebraic structure Number field, specific type of the above algebraic structure Scalar field, assignment of a scalar to each point in a mathematical space Tensor field, assignment of a tensor to each point in a mathematical space Vector field, assignment of a vector to each point in a mathematical space Field of sets, a mathematical structure of sets in an abstract space Field of a binary relation, union of its domain and its range Optics Field of view, the area of a view imaged by a lens Visual field, the part of the field of view which can be perceived by the eyes retina Depth of field, the distance from before to beyond the subject that appears to be in focus (and likewise, field, in the context of depth, is the portion of a scene for which objects within its range are or would be in focus) Physics Field (physics), a mathematical construct for analysis of remote effects Electric field, term in physics to describe the energy that surrounds electrically charged particles Magnetic field, force produced by moving electric charges Electromagnetic field, combination of an electric field and magnetic field Gravitational field, a representation of the combined effects of remote masses on a test particle at each point Sociology Field (Bourdieu), a sociological term coined by Pierre Bourdieu to describe the system of objective relations constituted by various species of capital Sexual field, the systems of objective relations within collective sexual life Other uses in science and technology Field (geography), a spatially dependent variable Field (video), one half of a frame in an interlaced display Field coil, of an electric motor or generator Field experiment Field magnet, a magnet used to produce a magnetic field Field research or fieldwork, the collection of information outside a laboratory, library or workplace setting Field of heliostats, an assembly of heliostats acting together Sports Pitch (sports field) Other uses Field of study, a subdivision of an academic discipline Field of use, permissible operation by the licensee of a patent Track and field, a group of sports See also The Field (disambiguation) Fields (disambiguation) The Fields (disambiguation) Fielding (disambiguation) Feeld, a location-based social discovery service application for iOS and Android Feild, surname All pages with titles beginning with Field All pages with titles containing Field

You act as a medical communicator. Your goal is to translate medical terms into comprehensive, yet straightforward language for all readers.

I'm encountering the term 'Caffeine-induced sleep disorder' in medical literature. What's its definition?

Caffeine-induced sleep disorder is a psychiatric disorder that results from overconsumption of the stimulant caffeine. Caffeine is one of the most widely consumed psychoactive drugs: almost 90% of Americans in a survey consume some type of caffeine each day. "When caffeine is consumed immediately before bedtime or .... throughout the day, sleep onset may be delayed, total sleep time reduced, normal stages of sleep altered, and the quality of sleep decreased." Caffeine reduces slow-wave sleep in the early part of the sleep cycle and can reduce rapid eye movement sleep later in the cycle. Caffeine increases episodes of wakefulness, and high doses in the late evening can increase sleep onset latency. In elderly people, there is an association between use of medication containing caffeine and difficulty in falling asleep.The specific criteria for this disorder in the fourth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) include that there must be a significant inability to sleep which is caused entirely by the physiological effects of caffeine as proven by an examination; if sleeping issues can be accounted for due to a breathing-related sleep disorder, narcolepsy, a circadian rhythm sleep disorder or a mental disorder, then caffeine-induced sleep disorder is not the cause. This condition causes a notable impairment in functioning. The ICD-10 criteria for the principally same disorder is F15:982. Caffeine and age Most studies now, find that there is relatively no association between caffeine and its effects on sleep for infants. There was very little difference between mothers who had high caffeine consumption during pregnancy as opposed to mothers who did not have high consumption of caffeine during their pregnancy.Caffeine in younger children has been found to shorten their sleep duration and increase daytime sleepiness. One study, which looked at children ages six to ten years of age, found that those who consistently consumed caffeine lost about 15 minutes of sleep each night. In most cases where younger children are drinking high amounts of caffeine, parents usually buy their children soft drinks, iced tea, or energy drinks without realizing the amount of caffeine these drinks contain or the implications they have on their children.30% of adolescent adults in a survey were found to consume caffeine daily. Individuals with higher caffeine consumption, tended to feel an increase in wakefulness after sleep onset, shorter sleep durations, and longer daytime sleep. Those who consumed high amounts of caffeine daily, were found to be 1.9 times more likely to have difficulty sleeping and 1.8 times more likely to feel sleepy in the morning compared to those who consume almost no caffeine. Individuals with higher caffeine consumption felt an increase in wakefulness after sleep onset, shorter sleep durations, and longer daytime sleep. The higher consumption time for adolescent adults tends to be on the weekends, while the lowest consumption is midweek. This is assumed to be from greater social opportunities among adolescence. Mechanism of caffeine Caffeine is an adenosine receptor antagonist. This means that caffeine mainly works by occupying adenosine receptors in the brain, specifically, receptors that influence sleep, arousal, and cognition. Once it is in the body, caffeine will persist for several hours, and takes about six hours for one half of the caffeine consumed to be eliminated. When caffeine reaches the brain, it increases the secretion of norepinephrine which is related to the "fight or flight" response. The rise in norepinephrine levels increases activity of neurons in areas of the brain and the symptoms resemble those of a panic attack.The half-life of caffeine is roughly 3–4 hours in healthy adults, however, it is dependent on a variety of variables such as age, liver function, medications, level of enzymes, pregnancy. This short half-life has been found to help out daytime functioning, but increase the side effect of sleep problems. So, while caffeine has the potential to increase performance, it comes at a cost of sleep deprivation which in its own way can counter the main point of caffeine. Sleep deprivation alone can cause a variety of problems associated with cognitive control and functions. This can include reduced alertness, attention, vigilance, speed of motor functions.Though caffeine can be shown to decrease the quality of sleep, there is no evidence that caffeine affects all people the same way. In fact, some people report no sleep problems despite regularly consuming caffeine. Regular intake of caffeine may be normal for a person so it is understandable how they may still get satisfactory sleep. This finding shows that caffeine interferes with a modulatory mechanism in sleep regulation rather than a fundamental sleep regulatory brain circuit. Ultimately, regular sleep habits are important in overall quality and timing of sleep. Caffeine consumption Overconsumption Although the maximum daily consumption of caffeine varies with consideration of couple of aspects such as sex, age, race, physical activity and smoking, excessive ingestion of caffeine can lead to a state of intoxication. This period of intoxication is characterized by restlessness, agitation, excitement, rambling thought or speech, and even insomnia. Even doses of caffeine relating to just one cup of coffee can increase sleep latency and decrease the quality of sleep especially in non-REM deep sleep. A dose of caffeine taken in the morning can have these effects the following night, so one of the main practices of sleep hygiene a person can do is to cease the consumption of caffeine. Moderation Keeping in mind that caffeine content in beverages and food varies and that some individuals are more sensitive to caffeine consumption than others are, moderation of caffeine is key. Between 200 and 300 mg of caffeine is considered "moderate" for most adults. While children can consume caffeine, it is advised to refrain children and adolescents from consuming caffeine due to their growing brains and to allow them to develop healthy sleep patterns. Consequences of sleep disruption Normal healthy sleep is described as having sufficient duration, quality, timing, regulation, and the absence of sleep disturbances or disorders. Even though the suggested amounts of sleep is relatively well known, there are increasing high numbers in the lack of healthy and good quality sleep.Risk factors of sleep can range across many different arrays such as environmental, lifestyle, psychosocial, sleep disorders, or medical conditions. These are all circumstances which put individuals at risk for sleep disruption. Environmental risk factors for sleep disruption can include living in an area where there is excessive noise such as near an interstate, keeping an individual up later than normal. A lifestyle risk factor would include drinking alcohol, drug abuse, or a late shift at work. Psychosocial risk factors include being a caregiver for someone who needs constant attention, parents of young children, anxiety, worry, or stress, etc.Sleep plays an essential part in brain functions and has crucial implications across almost all body systems. Numerous studies have shown caffeine consumption to heavily disrupt sleep patterns. This can lead to other implications such as lengthening the onset of sleep latency and decrease the efficiency and duration of sleep. Disruption of sleep also affects pressure for sleep and lowers electroencephalogram power in the frontal, central, and parietal regions of the brain. Short-term consequences of sleep disruption include: an increase in stress, emotional distress, mood and other mental health problems, cognition, memory, and performance deficits as well as an increase in behavioral problems in normally heathy individuals. Long-term consequences of sleep disruption include: cardiovascular problems such as cardiovascular disease, hypertension, higher concentration of fats in the body, weight issues such as metabolic syndrome, increased likelihood of cancer, and gastrointestinal disorders. References Further reading Broderick P, Benjamin AB (December 2004). "Caffeine and psychiatric symptoms: a review". J Okla State Med Assoc. 97 (12): 538–42. PMID 15732884. == External links ==

You are an expert in medical terminology. Explain medical terms in a way that is both precise and easy to understand for non-medical audiences.

I'm curious about the meaning of the medical term 'Banki syndrome.' Can you give me some insights?

Banki syndrome is a rare disorder in which two or more bones are fused. The symptoms may include: abnormality of the long bone of hand; short fingers or toes; permanent curving of the pinkie finger; fusion of wrist bones. The disorder has been reported in three generations of a single Hungarian family. First described by Z. Banki in a 1965 paper, it has been noted as being similar to Liebenberg syndrome, featuring lunatotriquetral fusion of the lunate bone with the triquetral bone, clinodactyly of the fingers, overall short metacarpals, and thin diaphysis of the longer bones, but unlike Liebenberg, no elbow dysplasia is observed. Sources == References ==

You are a medical educator. Your role is to provide detailed and clear explanations for medical terms, suitable for both professionals and laypersons.

Could you provide a brief overview of 'Cerocorticium molle' in a medical context?

Cerocorticium molle is a species of crust fungus in the family Meruliaceae. Taxonomy The fungus was first described by Miles Berkeley and Moses Ashley Curtis in 1868 as Corticium molle. They described the fruit body of the type specimen as resembling "a thin coating of wax poured over the surface". It was transferred to genus Cerocorticium by Walter Jülich in 1975. Habitat and distribution Cerocorticium molle grows on the dead bark and wood of a variety of angiosperms, and it has occasionally been recorded growing on or under the bark of living trees. It is found in tropical and subtropical regions of Africa, Asia, North America, and South America. == References ==

You serve as an encyclopedia of medical terms. Deliver clear, detailed explanations, making medical language understandable to a diverse audience.

I'm trying to understand 'System' within a medical context. Could you shed some light on it?

A system is a group of interacting or interrelated elements that act according to a set of rules to form a unified whole. A system, surrounded and influenced by its environment, is described by its boundaries, structure and purpose and expressed in its functioning. Systems are the subjects of study of systems theory and other systems sciences. Systems have several common properties and characteristics, including structure, function(s), behavior and interconnectivity. Etymology The term system comes from the Latin word systēma, in turn from Greek σύστημα systēma: "whole concept made of several parts or members, system", literary "composition". History According to Marshall McLuhan, "System" means "something to look at". You must have a very high visual gradient to have systematization. But in philosophy, prior to Descartes, there was no "system". Plato had no "system". Aristotle had no "system". In the 19th century the French physicist Nicolas Léonard Sadi Carnot, who studied thermodynamics, pioneered the development of the concept of a system in the natural sciences. In 1824 he studied the system which he called the working substance (typically a body of water vapor) in steam engines, in regards to the systems ability to do work when heat is applied to it. The working substance could be put in contact with either a boiler, a cold reservoir (a stream of cold water), or a piston (on which the working body could do work by pushing on it). In 1850, the German physicist Rudolf Clausius generalized this picture to include the concept of the surroundings and began to use the term working body when referring to the system. The biologist Ludwig von Bertalanffy became one of the pioneers of the general systems theory. In 1945 he introduced models, principles, and laws that apply to generalized systems or their subclasses, irrespective of their particular kind, the nature of their component elements, and the relation or forces between them.Norbert Wiener and Ross Ashby, who pioneered the use of mathematics to study systems, carried out significant development in the concept of a system.In the 1980s John Henry Holland, Murray Gell-Mann and others coined the term complex adaptive system at the interdisciplinary Santa Fe Institute. Concepts Environment and boundaries Systems theory views the world as a complex system of interconnected parts. One scopes a system by defining its boundary; this means choosing which entities are inside the system and which are outside—part of the environment. One can make simplified representations (models) of the system in order to understand it and to predict or impact its future behavior. These models may define the structure and behavior of the system.Natural and human-made systems There are natural and human-made (designed) systems. Natural systems may not have an apparent objective but their behavior can be interpreted as purposeful by an observer. Human-made systems are made with various purposes that are achieved by some action performed by or with the system. The parts of a system must be related; they must be "designed to work as a coherent entity" — otherwise they would be two or more distinct systems. Theoretical framework Most systems are open systems, exchanging matter and energy with their respective surroundings; like a car, a coffeemaker, or Earth. A closed system exchanges energy, but not matter, with its environment; like a computer or the project Biosphere 2. An isolated system exchanges neither matter nor energy with its environment. A theoretical example of such system is the Universe.Process and transformation process An open system can also be viewed as a bounded transformation process, that is, a black box that is a process or collection of processes that transform inputs into outputs. Inputs are consumed; outputs are produced. The concept of input and output here is very broad. For example, an output of a passenger ship is the movement of people from departure to destination.System model A system comprises multiple views. Man-made systems may have such views as concept, analysis, design, implementation, deployment, structure, behavior, input data, and output data views. A system model is required to describe and represent all these views.Systems architecture A systems architecture, using one single integrated model for the description of multiple views, is a kind of system model. Subsystem A subsystem is a set of elements, which is a system itself, and a component of a larger system. The IBM Mainframe Job Entry Subsystem family (JES1, JES2, JES3, and their HASP/ASP predecessors) are examples. The main elements they have in common are the components that handle input, scheduling, spooling and output; they also have the ability to interact with local and remote operators. A subsystem description is a system object that contains information defining the characteristics of an operating environment controlled by the system. The Data tests are performed to verify the correctness of the individual subsystem configuration data (e.g. MA Length, Static Speed Profile, …) and they are related to a single subsystem in order to test its Specific Application (SA). Analysis There are many kinds of systems that can be analyzed both quantitatively and qualitatively. For example, in an analysis of urban systems dynamics, A .W. Steiss defined five intersecting systems, including the physical subsystem and behavioral system. For sociological models influenced by systems theory, Kenneth D. Bailey defined systems in terms of conceptual, concrete, and abstract systems, either isolated, closed, or open. Walter F. Buckley defined systems in sociology in terms of mechanical, organic, and process models. Bela H. Banathy cautioned that for any inquiry into a system understanding its kind is crucial, and defined "natural" and "designed", i. e. artificial, systems. It is important not to confuse these abstract definitions. For example, natural systems include subatomic systems, living systems, the Solar System, galaxies, and the Universe, while artificial systems include man-made physical structures, hybrids of natural and artificial systems, and conceptual knowledge. The human elements of organization and functions are emphasized with their relevant abstract systems and representations. Artificial systems inherently have a major defect: they must be premised on one or more fundamental assumptions upon which additional knowledge is built. This is in strict alignment to the Gödels incompleteness theorems. The Artificial system can be defined as a "consistent formalized system which contains elementary arithmetic". These fundamental assumptions are not inherently deleterious, but they must by definition be assumed as true, and if they are actually false then the system is not as structurally integral as is assumed (i.e. it is evident that if the initial expession is false, then the Artificial system is not a "consistent formalized system"). For example, in geometry this is very evident in the postulation of theorems and extrapolation of proofs from them. George J. Klir maintained that no "classification is complete and perfect for all purposes", and defined systems as abstract, real, and conceptual physical systems, bounded and unbounded systems, discrete to continuous, pulse to hybrid systems, etc. The interactions between systems and their environments are categorized as relatively closed and open systems. It seems most unlikely that an absolutely closed system can exist or, if it did, that it could be known by man. Important distinctions have also been made between hard systems – technical in nature and amenable to methods such as systems engineering, operations research, and quantitative systems analysis – and soft systems that involve people and organisations, commonly associated with concepts developed by Peter Checkland and Brian Wilson through Soft Systems Methodology (SSM) involving methods such as action research and emphasis of participatory designs. Where hard systems might be identified as more "scientific", the distinction between them is often elusive. Cultural system A cultural system may be defined as the interaction of different elements of culture. While a cultural system is quite different from a social system, sometimes both together are referred to as a "sociocultural system". A major concern of the social sciences is the problem of order. Economic system An economic system is a mechanism (social institution) which deals with the production, distribution and consumption of goods and services in a particular society. The economic system is composed of people, institutions and their relationships to resources, such as the convention of property. It addresses the problems of economics, like the allocation and scarcity of resources. The international sphere of interacting states is described and analysed in systems terms by several international relations scholars, most notably in the neorealist school. This systems mode of international analysis has however been challenged by other schools of international relations thought, most notably the constructivist school, which argues that an over-large focus on systems and structures can obscure the role of individual agency in social interactions. Systems-based models of international relations also underlies the vision of the international sphere held by the liberal institutionalist school of thought, which places more emphasis on systems generated by rules and interaction governance, particularly economic governance. Applications Systems modeling is generally a basic principle in engineering and in social sciences. The system is the representation of the entities under concern. Hence inclusion to or exclusion from system context is dependent on the intention of the modeler. No model of a system will include all features of the real system of concern, and no model of a system must include all entities belonging to a real system of concern. Information and computer science In computer science and information science, system is a hardware system, software system, or combination, which has components as its structure and observable inter-process communications as its behavior. Again, an example will illustrate: There are systems of counting, as with Roman numerals, and various systems for filing papers, or catalogues, and various library systems, of which the Dewey Decimal Classification is an example. This still fits with the definition of components which are connected together (in this case to facilitate the flow of information). System can also refer to a framework, aka platform, be it software or hardware, designed to allow software programs to run. A flaw in a component or system can cause the component itself or an entire system to fail to perform its required function, e.g., an incorrect statement or data definition Engineering and physics In engineering and physics, a physical system is the portion of the universe that is being studied (of which a thermodynamic system is one major example). Engineering also has the concept of a system referring to all of the parts and interactions between parts of a complex project. Systems engineering is the branch of engineering that studies how this type of system should be planned, designed, implemented, built, and maintained. Expected result is the behavior predicted by the specification, or another source, of the component or system under specified conditions. Sociology, cognitive science and management research Social and cognitive sciences recognize systems in human person models and in human societies. They include human brain functions and mental processes as well as normative ethics systems and social/cultural behavioral patterns. In management science, operations research and organizational development (OD), human organizations are viewed as systems (conceptual systems) of interacting components such as subsystems or system aggregates, which are carriers of numerous complex business processes (organizational behaviors) and organizational structures. Organizational development theorist Peter Senge developed the notion of organizations as systems in his book The Fifth Discipline. Organizational theorists such as Margaret Wheatley have also described the workings of organizational systems in new metaphoric contexts, such as quantum physics, chaos theory, and the self-organization of systems. Pure logic There is also such a thing as a logical system. The most obvious example is the calculus developed simultaneously by Leibniz and Isaac Newton. Another example is George Booles Boolean operators. Other examples have related specifically to philosophy, biology, or cognitive science. Maslows hierarchy of needs applies psychology to biology by using pure logic. Numerous psychologists, including Carl Jung and Sigmund Freud have developed systems which logically organize psychological domains, such as personalities, motivations, or intellect and desire. Often these domains consist of general categories following a corollary such as a theorem. Logic has been applied to categories such as taxonomy, ontology, assessment, and hierarchies. Strategic thinking In 1988, military strategist, John A. Warden III introduced the Five Ring System model in his book, The Air Campaign, contending that any complex system could be broken down into five concentric rings. Each ring—Leadership, Processes, Infrastructure, Population and Action Units—could be used to isolate key elements of any system that needed change. The model was used effectively by Air Force planners in the First Gulf War. In the late 1990s, Warden applied his model to business strategy. See also References Bibliography External links Definitions of Systems and Models by Michael Pidwirny, 1999–2007. Publications with the title "System" (1600–2008) by Roland Müller. Definitionen von "System" (1572–2002) by Roland Müller, (most in German).

You are a resource for medical understanding. Offer detailed explanations of medical terms, making complex concepts clear and comprehensible.

Could you offer a clear explanation of the term 'Autoimmune encephalitis' as used in the medical field?

Autoimmune encephalitis is a type of encephalitis that can result from a number of autoimmune diseases including: Rasmussen encephalitis Systemic lupus erythematosus Behçets disease Hashimotos encephalopathy Autoimmune limbic encephalitis Sydenhams chorea == References ==

You act as a medical communicator. Your goal is to translate medical terms into comprehensive, yet straightforward language for all readers.

I need a basic explanation for the medical term 'Vici syndrome.'

Vici syndrome, also called immunodeficiency with cleft lip/palate, cataract, hypopigmentation and absent corpus callosum (or absent corpus callosum cataract immunodeficiency), is a rare autosomal recessive congenital disorder characterized by albinism, agenesis of the corpus callosum, cataracts, cardiomyopathy, severe psychomotor retardation, seizures, immunodeficiency and recurrent severe infections. To date, about 50 cases have been reported. Presentation This syndrome consists of a number of typical features. These include Agenesis of the corpus callosum (80–99% patients) Hypopigmentation of the eyes and hair (80–99% patients) Cardiomyopathy (80–99% patients) Combined immunodeficiency (80–99% patients) Muscular hypotonia (80–99% patients) Abnormality of retinal pigmentation (80–99% patients) Recurrent chest infections (80–99% patients) Abnormal EEG (80–99% patients) Intellectual disability (80–99% patients) Cataracts (75%) Seizures (65%) Renal abnormalities (15%)Infections of the gastrointestinal and urinary tracts are common. Swallowing and feeding difficulties early on may result in a failure to thrive. Optic nerve hypoplasia, nystagmus and photophobia may occur. Facial dysmorphism (cleft lip/palate and micrognathia) and syndactyly may be present. Sensorineural hearing loss may also be present.Death in infancy is not uncommon and is usually due to cardiac complications or severe infections. Genetics Inheritance Vici syndrome is inherited in an autosomal recessive manner. This means the defective gene responsible for the disorder is located on an autosome, and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder. The hypothesis of autosomal recessive inheritance of Vici syndrome was strengthened in 2002 with the clinical description of two new cases, one brother and one sister, by Chiyonobu et al. Gene Vici syndrome is caused by mutations in the gene EPG5 (OMIM # 615068), which encodes an important regulator of the autophagy pathway, the ectopic P-granules autophagy protein 5, involved in the formation of lysosomes. EPG5 is the human homolog of the C.elegans epg5 gene. The gene EPG5 has been cloned for the first time by Nagase et al. by sequencing clones obtained from a size-fractionated fetal brain cDNA library, and was initially named KIAA1632.The EPG5 human gene is located on chromosome 18q12.3, has a length of 119,67Kb (NC_000018.10), consists of 44 exons and is transcriptionally driven from the centromere toward the telomere. The messenger RNA (mRNA) is 12633bp long (NM_020964.2) and contains a CDS of 7740 bp translated into a protein sequence of 2579 amino acids (NP_066015.2) with a molecular weight of 280kDa, presumed. The protein EPG5 is expressed primarily in the central nervous system (CNS), skeletal muscle, heart, thymus, cells of the immune system, lungs and kidneys.Mutations in the EPG5 gene interfere with the autophagy. This appears to be due to a block in the autophagosome-lysosome fusion mechanism. Diagnosis The diagnostic workup usually includes an MRI of the brain, an EEG, ophthalmic examination and a cardiac ECHO. Muscle biopsy – which is not commonly done – may show storage of abnormal material and secondary mitochondrial abnormalities in skeletal muscle. Other features that may be seen on muscle biopsy include variability in fibre size, increase in internal and centralized nuclei, type 1 fibre hypotrophy with normally sized type 2 fibres, increased glycogen storage and variable vacuoles on light microscopy The diagnosis is confirmed by sequencing of the EPG5. Differential diagnosis This includes ataxia–telangiectasia, Chédiak–Higashi syndrome, DiGeorge syndrome, Griscelli syndrome and Marinesco–Sjögren syndrome. Treatment There is no known curative treatment presently. Hearing aids and cataract surgery may be of use. Control of seizures, heart failure, and treatment of infection is essential. Tube feeding may be needed. Eponym Vici syndrome was first described by Carlo Dionisi-Vici et al. (Rome, Italy) in an article from 1988 about two brothers with a previously unreported disorder. Since then, a few articles have reported the same disorder, which subsequently obtained the name Vici syndrome.About 10 years later, del Campo et al. described 4 patients (including 2 sibs, a male and a female) with clinical features very similar to those reported by Dionisi-Vici.In 2007 the renal tubular acidosis was another clinical complication described in only one case report of two brothers with Vici syndrome.In 2010 and 2012 it has also been reported a neuromuscular involvement in patients suffering from this syndrome.In 2013 Vici syndrome has been associated with mutations in the gene EPG5 (OMIM # 615068), which encodes an important regulator of the autophagy pathway, the ectopic P-granules autophagy protein 5, involved in the formation of lysosomes.In 2014 the ophthalmologic features of Vici syndrome were carefully evaluated.In 2015 the doctoral thesis entitled "Deciphering the mechanism of immune dysfunction in Vici Syndrome", University of Rome "La Sapienza" by Dr. Evangelos Axiotis, clarifies the molecular mechanisms and the role of the mutations in EPG5, all responsible for the immunodeficiency present in patients with Vici syndrome. References == External links ==

You function as a medical explainer. Your task is to convey the meanings of medical terms in a detailed, yet easy-to-understand manner.

I'm seeking clarification on the medical term 'Acute posterior multifocal placoid pigment epitheliopathy.' Could you explain it?

Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) is an acquired inflammatory uveitis that belongs to the heterogenous group of white dot syndromes in which light-coloured (yellowish-white) lesions begin to form in the macular area of the retina. Early in the course of the disease, the lesions cause acute and marked vision loss (if it interferes with the optic nerve) that ranges from mild to severe but is usually transient in nature. APMPPE is classified as an inflammatory disorder that is usually bilateral and acute in onset but self-limiting. The lesions leave behind some pigmentation, but visual acuity eventually improves even without any treatment (providing scarring doesnt interfere with the optic nerve). It occurs more commonly in females and is more likely to affect persons between 20 and 30 years of age, but has been seen in people aged 16 to 40. It is known to occur after or concurrently with a systemic infection (but not always), showing that it is related generally to an altered immune system. Recurrent episodes can happen, but are extremely rare. Signs and symptoms The onset of ocular symptoms are usually preceded by episode of viral or flu-like symptoms such as fever, cough or sore throat (however this is not always the case). Patients can typically present erythema nodosum, livido reticularus, bilateral uveitis, and sudden onset of marked visual loss associated with the appearance of multiple lesions in the retina. These lesions may be colored from grey-white to cream-shaded yellow. Other symptoms include scotomata and photopsia. In weeks to a month times the lesions begin to clear and disappear (with prednisone) leaving behind areas of retinal pigment epithelial atrophy and diffuse fine pigmentation (scarring). Rarely choroidal neovascularization occur as a late onset complication. Cause Since The cause of the inflammation remains unknown, with various theories of it occurring as an autoimmune response to a mild infection, or the possibility of it being viral because of the preceding flu-like illness that generally accompanies it. It is usually associated with HLA-B7 and HLA-DR2. The underlying etiology of APMPPE continues to cause debate. The term Pigment Epitheliopathy was chosen by Gass to reflect what he thought was the tissue most significantly affected. Van Buskirk et al., and Deutman et al. proposed choriocapillaris ischemia as the more likely primary etiology. Indocyanine green angiography (ICGA), and OCT angiography (OCTA) studies have provided support for choriocapillaris involvement. However, a novel hypothesis has recently been proposed implicating a direct neurotropic infection as a possible underlying cause given the dynamic changes observed along the neuronal pathway of the retina Diagnosis Diagnosis is usually made on clinical appearance alone on fundoscopy and/or retinal imaging. Supplementary tests such as Optical coherence tomography(OCT) and fundus fluorescein angiography/Indocyanine angiography together with OCT-Angiography are commonly performed to help aid diagnosis and monitoring. Treatment Owing to the self-limiting nature of the disease, treatment is generally not required. In cases where lesions appear to be interfering with the optic nerve, methyl prednisone is prescribed. Prognosis Vision improves in almost all cases. In rare cases, a patient may suffer permanent visual loss associated with lesions on their optic nerve. Rarely, coexisting vasculitis may cause neurological complications. These occurrences can start with mild headaches that steadily worsen in pain and onset, and can include attacks of dysesthesia. This type of deterioration happens usually if the lesions involve the fovea. See also White dot syndromes Uveitis References == External links ==

You are a guide to medical language. Please provide in-depth and understandable explanations of medical terms, highlighting their significance in healthcare.

I'm curious about the meaning of the medical term 'Hemothorax.' Can you give me some insights?

A hemothorax (derived from hemo- [blood] + thorax [chest], plural hemothoraces) is an accumulation of blood within the pleural cavity. The symptoms of a hemothorax may include chest pain and difficulty breathing, while the clinical signs may include reduced breath sounds on the affected side and a rapid heart rate. Hemothoraces are usually caused by an injury, but they may occur spontaneously due to cancer invading the pleural cavity, as a result of a blood clotting disorder, as an unusual manifestation of endometriosis, in response to a collapsed lung, or rarely in association with other conditions. Hemothoraces are usually diagnosed using a chest X-ray, but they can be identified using other forms of imaging including ultrasound, a CT scan, or an MRI. They can be differentiated from other forms of fluid within the pleural cavity by analysing a sample of the fluid, and are defined as having a hematocrit of greater than 50% that of the persons blood. Hemothoraces may be treated by draining the blood using a chest tube. Surgery may be required if the bleeding continues. If treated, the prognosis is usually good. Complications of a hemothorax include infection within the pleural cavity and the formation of scar tissue. Background The lungs are surrounded by two layers of tissue called the pulmonary pleurae. In most healthy people, these two layers are tightly apposed, separated only by a small amount of pleural fluid. In certain disease states, the space between these two layers, called the pleural cavity, swells with fluid. This accumulation of fluid in the pleural cavity is called pleural effusion. Pleural effusions are given specific names depending on the nature of the fluid: hydrothorax for serous fluid, pyothorax for pus, hemothorax for blood, and urinothorax for urine. Signs and symptoms Signs and symptoms include anxiety, rapid breathing, restlessness, shock, and pale, cool, clammy skin. When the affected area is percussed, a dull feeling may be observed. Neck veins may be flat and breathing sounds reduced. It can also cause a collapsed lung (atelectasis). Massive hemothorax, often defined as over 1.5 liters of blood initially when an intercostal drain is placed, or a bleeding rate greater than .2 liters/hr, can result in shock with two causes: massive bleeding resulting from hypovolemic shock, and venous pressure from the retained blood, impairing blood flow. Causes Hemothoraces are classified in three broad categories according to the cause and in order of frequency: traumatic, iatrogenic, or nontraumatic. All three categories have the potential to affect major arteries and result in death by blood loss. Traumatic Hemothorax is most often caused by blunt or penetrating trauma to the chest. In blunt traumatic cases, hemothorax typically occurs when rib fracture damages the intercostal vessels or the intraparenchymal pulmonary vessel, while in penetrating trauma, hemothorax occurs due to injuries directly affecting blood vessels in the thoracic wall, lung parenchyma, or the heart. If large blood vessels such as the aorta are damaged, the blood loss can be massive. Minor chest trauma can cause hemothorax when the bloods ability to clot is diminished as result either of anticoagulant medications or when there are bleeding disorders such as hemophilia. Iatrogenic Iatrogenic hemothorax can occur as a complication of heart and lung surgery, for example the rupture of lung arteries caused by the placement of catheters, thoracotomy, thoracostomy, or thoracentesis. The most common iatrogenic causes include subclavian venous catheterizations and chest tube placements, with an occurrence rate of around 1% Sometimes, a Swan-Ganz catheter causes rupture of the pulmonary artery, causing a massive hemothorax. It can also be caused by other procedures like pleural, lung, or transbronchial biopsies, CPR, Nuss procedure, or endoscopic treatment of esophageal varices. Iatrogenic hemothorax is more common in people who have chronic kidney disease in the intensive care unit. Nontraumatic Less frequently, hemothoraces may occur spontaneously. Nontraumatic hemothoraces most frequently occur as a complication of some forms of cancer if the tumour invades the pleural space. Cancers responsible for hemothoraces include angiosarcomas, schwannomas, mesothelioma, thymomas, germ cell tumours, and lung cancer. Significant hemothoraces can occur with spontaneous rupture of small vessels when the bloods ability to clot is diminished as result of anticoagulant medications. In cases caused by anticoagulant therapy, the hemothorax becomes noticeable 4–7 days after anticoagulant therapy is started. In cases of hemothorax complicating pulmonary embolism treatment, the hemothorax is usually on the side of the original embolism. Those with an abnormal accumulation of air within the pleural space (a pneumothorax) can bleed into the cavity, which occurs in about 5% of cases of spontaneous pneumothorax, especially when lung bullae rupture. The resulting combination of air and blood within the pleural space is known as a hemopneumothorax. Bone growth in exostosis can create sharp edges, which can result in hemothorax by damaging adjacent arteries. It can occur postpartum due to the change in thoracic pressure during labor. Vascular Vascular causes of hemothorax include rupture of the descending aorta, in which case it initially involves the left pleural and mediastinal area due to the close vicinity of the pleural cavity. Rarely, a rupture of the thoracic aorta can result in a hemothorax, but the bleeding usually occurs in the pericardial space. Spontaneous tearing of blood vessels is more likely to occur in those with disorders that weaken blood vessels such as some forms of Ehlers-Danlos syndrome, disorders that lead to malformed blood vessels as seen in Rendu-Osler-Weber syndrome, or in bleeding disorders such as hemophilia and Glanzmann thromboastenia. Other rare causes of hemothorax include neurofibromatosis type 1 and extramedullary hematopoiesis. Catamenial Rarely, hemothoraces can arise due to extrapelvic endometriosis, a condition in which tissue similar to the lining that normally covers the inside of the uterus forms in unusual locations outside the pelvis. Endometriotic tissue that implants on the pleural surface can bleed in response to the hormonal changes of the menstrual cycle, causing what is known as a catamenial hemothorax as part of thoracic endometriosis along with catamenial pneumothorax, catamenial hemoptysis, and lung nodules of endometriosis. Catamenial hemothorax represents 14% of cases of thoracic endometriosis syndrome while catamenial pneumothorax is seen in 73%, catamenial hemoptysis in 7%, and pulmonary nodules in 6%. Mechanism When a hemothorax occurs, blood enters the pleural cavity. The blood loss from the circulation has several effects. Firstly, as blood builds up within the pleural cavity, it begins to interfere with the normal movement of the lungs, preventing one or both lungs from fully expanding and thereby interfering with the normal transfer of oxygen and carbon dioxide to and from the blood. Secondly, blood that has been lost into the pleural cavity can no longer be circulated. Hemothoraces can lead to significant blood loss – each half of the thorax can hold more than 1500 milliliters of blood, representing more than 25% of an average adults total blood volume. The body may struggle to cope with this blood loss, and tries to compensate by maintaining blood pressure by forcing the heart to pump harder and faster, and by squeezing or constricting small blood vessels in the arms and legs. These compensatory mechanisms can be recognised by a rapid resting heart rate and cool fingers and toes.If the blood within the pleural cavity is not removed, it will eventually clot. This clot tends to stick the parietal and visceral pleura together and has the potential to lead to scarring within the pleura, which if extensive leads to the condition known as a fibrothorax. Following the initial loss of blood, a small hemothorax may irritate the pleura, causing additional fluid to seep out, leading to a bloodstained pleural effusion. Furthermore, as enzymes in the pleural fluid begin to break down the clot, the protein concentration of the pleural fluid increases. As a result, the osmotic pressure of the pleural cavity increases, causing fluid to leak into the pleural cavity from the surrounding tissues. Diagnosis Hemothoraces are most commonly detected using a chest X-ray, although ultrasound is sometimes used in an emergency setting. It can be suspected in any person with any form of chest trauma. However, plain X-rays may miss smaller hemothoraces while other imaging modalities such as computed tomography (CT), or magnetic resonance imaging may be more sensitive. In cases where the nature of an effusion is in doubt, a sample of fluid can be aspirated and analysed in a procedure called thoracentesis. Physical examination is used initially. Auscultation has been reported to have an accuracy of nearly 100% in diagnosing hemopneumothorax. Chest X-ray A chest X-ray is the most common technique used to diagnosis a hemothorax. X-rays should ideally be taken in an upright position (an erect chest X-ray), but may be performed with the person lying on their back (supine) if an erect chest X-ray is not feasible. On an erect chest X-ray, a hemothorax is suggested by blunting of the costophrenic angle or partial or complete opacification of the affected half of the thorax. On a supine film the blood tends to layer in the pleural space, but can be appreciated as a haziness of one half of the thorax relative to the other. A small hemothorax may be missed on a chest X-ray as several hundred milliliters of blood can be hidden by the diaphragm and abdominal viscera on an erect film. Supine X-rays are even less sensitive and as much as one liter of blood can be missed on a supine film. Other methods Ultrasonography may be used to detect hemothorax and other pleural effusions. This technique is of particular use in the critical care and trauma settings as it provides rapid, reliable results at the bedside. Ultrasound is more sensitive than chest x-ray in detecting hemothorax. Ultrasound can cause issues in people who are morbidly obese or have subcutaneous emphysema. When CT is unavailable in the current setting or the person cannot be moved to the scan, ultrasound is used.Computed tomography (CT or CAT) scans may be useful for diagnosing retained hemothorax as this form of imaging can detect much smaller amounts of fluid than a plain chest X-ray. However, CT is less used as a primary means of diagnosis within the trauma setting, as these scans require a critically ill person to be transported to a scanner, are slower, and require the subject to remain supine.Magnetic resonance imaging (MRI) can be used to differentiate between a hemothorax and other forms of pleural effusion, and can suggest how long the hemothorax has been present for. Fresh blood can be seen as a fluid with low T1 but high T2 signals, while blood that has been present for more than a few hours displays both low T1 and T2 signals. MRI is used infrequently in the trauma setting due to the prolonged time required to perform an MRI, and the deterioration in image quality that occurs with motion. Thoracentesis Although imaging techniques can demonstrate that fluid is present within the pleural space, it may be unclear what this fluid represents. To establish the nature of the fluid, a sample can be removed by inserting a needle into the pleural cavity in a procedure known as a thoracentesis or pleural tap. In this context, the most important assessment of the pleural fluid is the percentage by volume that is taken up by red blood cells (the hematocrit) A hemothorax is defined as having a hematocrit of at least 50% of that found in the affected persons blood, although the hematocrit of a chronic hemothorax may be between 25 and 50% if additional fluid has been secreted by the pleura. Pleural fluid can dilute hemothoraces in as low as 3–4 days. The red blood cells in the effusion spontaneously break down. Distinguishing the pleural fluid from blood by colour is impossible when the hematocrit value is over 5%. For these reasons, even if there is a hematocrit value under 50%, further investigations can be done in order to figure out if there is a source of bleeding. Hematocrit can be roughly calculated by dividing the red blood cell count of the pleural fluid by 100,000. Thoracentesis is the test most commonly used to diagnose a hemothorax in animals. Hemothorax can itself be a rare complication of thoracentesis if the intercostal artery is punctured. Treatment The treatment of a hemothorax depends largely on the extent of bleeding. While small hemothoraces may require little in the way of treatment, larger hemothoraces may require fluid resuscitation to replace the blood that has been lost, drainage of the blood within the pleural space using a procedure known as a tube thoracostomy, and potentially surgery in the form of a thoracotomy or video-assisted thoracoscopic surgery (VATS) to prevent further bleeding. Occasionally, transcatheter arterial embolization may be used to stop ongoing arterial bleeding. Additional treatment options include antibiotics to reduce the risk of infection and fibrinolytic therapy to break down clotted blood within the pleural space. Thoracostomy Blood in the cavity can be removed by inserting a drain (chest tube) in a procedure called a tube thoracostomy. This procedure is indicated for most causes of hemothorax, but should be avoided in aortic rupture which should be managed with immediate surgery. The thoracostomy tube is usually placed between the ribs in the sixth or seventh intercostal space at the mid-axillary line. It is important to avoid a chest tube becoming obstructed by clotted blood as obstruction prevents adequate drainage of the pleural space. Clotting occurs as the clotting cascade is activated when the blood leaves the blood vessels and comes into contact with the pleural surface, injured lung or chest wall, or the thoracostomy tube. Inadequate drainage may lead to a retained hemothorax, increasing the risk of infection within the pleural space (empyema) or the formation of scar tissue (fibrothorax). Thoracostomy tubes with a diameter of 24–36 F (large-bore tubes) should be used, as these reduce the risk of blood clots obstructing the tube. Manual manipulation of chest tubes (referred to as milking, stripping, or tapping) is commonly performed to maintain an open tube, but no conclusive evidence has demonstrated that this improves drainage. If a chest tube does become obstructed, the tube can be cleared using open or closed techniques. Tubes should be removed as soon as drainage has stopped, as prolonged tube placement increases the risk of empyema. Surgery About 10–20% of traumatic hemothoraces require surgical management. Larger hemothoraces, or those that continue to bleed following drainage, may require surgery. This surgery may take the form of a traditional open-chest procedure (a thoracotomy), but may be performed using video-associated thoracoscopic surgery (VATS). While there is no universally accepted cutoff for the volume of blood loss required before surgery is indicated, generally accepted indications include more than 1500 mL of blood drained from a thoracostomy, bleeding rate of over 500mL/hr in the first hour followed by over 200 mL, hemodynamic instability, or the need for repeat blood transfusions. VATS is less invasive and cheaper than an open thoracotomy, and can reduce the length of hospital stay, but a thoracotomy may be preferred when hypovolemic shock is present, in order to watch bleeding. The procedure should ideally be performed within 72 hours of the injury as delay may increase the risk of complications. In clotted hemothorax, VATS is the generally preferred procedure to remove the clot, and is indicated if the hemothorax fills 1/3 or more of a hemithorax. The ideal time to remove a clot using VATS is at 48–96 hours, but can be attempted up to nine days after the injury. Other Thoracentesis is no longer used in the treatment of hemothorax, although it may still be used to treat small hemothoraces. In catamenial hemothorax, the bleeding is typically self-limiting and mild. Most people with the condition are stable and can be treated with hormonal therapies. They are only partially effective. Surgical removal of the endometrial tissue may be necessary in recurrent cases. However, the disease frequently recurs. Resuscitation with intravenous fluids or with blood products may be required. In fulminant cases, transfusions may be administered before admission to the hospital. Clotting abnormalities, such as those caused by anticoagulant medications, should be reversed. Prophylactic antibiotics are given for 24 hours in the case of trauma. Blood clots may be retained within the pleural cavity despite chest tube drainage. They are a risk factor for complications like fibrothorax and empyema. Such retained clots should be removed, preferably with video-assisted thoracoscopic surgery (VATS). If VATS is unavailable, an alternative is fibrinolytic therapy such as streptokinase or urokinase given directly into the pleural space seven to ten days after the injury. The issues with fibrinolytic therapy include having a high cost and lengthened hospital stay. Residual clot that does not dissipate in response to fibrinolytics may require surgical removal in the form of decortication. Prognosis The prognosis following a hemothorax depends on its size, the treatment given, and the underlying cause. While small hemothoraces may cause little in the way of problems, in severe cases an untreated hemothorax may be rapidly fatal due to uncontrolled blood loss. If left untreated, the accumulation of blood may put pressure on the mediastinum and the trachea, limiting the hearts ability to fill. However, if treated, the prognosis following a traumatic hemothorax is usually favourable and dependent on other non-thoracic injuries that have been sustained at the same time, the age of the person, and the need for mechanical ventilation. Hemothoraces caused by benign conditions such as endometriosis have a good prognosis, while those caused by neurofibromatosis type 1 has a 36% rate of death, and those caused by aortic rupture are often fatal. Penetrating trauma is significantly less common, and has a much higher death rate, with up to 90% dying before arriving at the hospital. Gunshot wounds are associated with a higher death rates compared to stab wounds. In cases of penetrating trauma involving the heart, less than 1% survive. Complications Complications can occur following a hemothorax, and are more likely to occur if the blood has not been adequately drained from the pleural cavity. Blood that remains within the pleural space can become infected, and is known as an empyema. It occurs in 3–4% of traumatic cases, and 27-33% of retained hemothoraces. It is more likely in people who develop shock, had a contaminated pleural space during the injury, persistent bronchopleural fistulae, and lung contusions. The likelihood of it can be reduced by keeping thoracostomy tubes sterile and by keeping the pleural surfaces close together to prevent fluid or blood from accumulating between the surfaces. The retained blood can irritate the pleura, causing scar tissue (adhesions) to form. If extensive, this scar tissue can encase the lung, restricting movement of the chest wall, and is then referred to as a fibrothorax. Less than 1 percent of cases go on to develop a fibrothorax. Cases with hemopneumothorax or infection more often develop fibrothorax. After the chest tube is removed, over 10% of cases develop pleural effusions that are mostly self-limited and leave no lasting complications. In such cases, thoracentesis is performed to eliminate the possibility of an infection being present. Other potential complications include atelectasis, lung infection, pneumothorax, sepsis, respiratory distress, hypotension, tachycardia, pneumonia, adhesions, and impaired lung function. Epidemiology Trauma to the thorax results in approximately 16,000 to 30,000 deaths every year. There are about 300,000 cases of hemothorax in the U.S every year. Polytrauma (injury to multiple body systems) involves chest injuries in 60% of cases and commonly leads to hemothorax. In a case study, 37% of people hospitalized for blunt chest trauma had traumatic hemothorax. Hemothorax commonly occurs with a displaced rib fracture. Other animals Horses In horses, hemothorax is uncommon and usually traumatic. It may occur along with pneumothorax. It is mainly diagnosed by ultrasound. Treatment involves supportive care, correction of the underlying cause, and occasionally drainage. The prognosis is variable. Hemothorax is usually caused by trauma to the thorax. It can result from any injury that involves the pleural, intercostal, intervertebral, cardiac, or thoracic wall muscle. It can rarely be caused by diaphragmatic rupture that results in abdominal herniation. Hemothorax can be caused be cancers involving the thoracic, pulmonary, and mediastinal wall. The most common cancer resulting in hemothorax is a hemangiosarcoma.Clinical signs and symptoms may be variable and cause-dependant. They may include rapid breathing, pain, and shallow breathing in cases with a rib fracture. In the case of extensive bleeding, signs of hypovolemia may occur, and rapid death may result within hours. In less acute cases with slower bleeding, anemia and hypoproteinemia may gradually develop.Ultrasound can detect blood in the pleural cavity. Blood in the thorax is shown by a uniform area without flocculation. Pleural effusions without blood are usually hypoechoic. Echogenicity is indicated by cellular debris and/or fibrin. Bloody pleural effusions are shows by a swirling, hyperechoic pattern. When a stethoscope is used (auscultation), the heartbeat sounds are faint. When percussion is performed, it produces a dull area. However, especially in traumatic cases, percussion may be painful. Although nonspecific, physical examinations may show reduced lung sounds and muffled, widespread heart sounds. Similar signs and symptoms may occur when other fluids are in the pleural cavity.Treatment includes correction of the underlying cause. Drainage is not always required, but can be performed in case of infection or fluid levels resulting in respiratory compromise. However, drainage in contraindicated in cases caused by clotting disorders. Additionally, broad spectrum antibiotics can be given in the case of open trauma or pulmonary rupture. Supportive care may be required. It may include intranasal oxygen, painkillers, blood transfusions, and fluids. In order to avoid fluid overload, fluids are given slowly.The prognosis significantly depends on the underlying cause of the hemothorax. In cases caused by uncomplicated thoracic trauma, the prognosis may be good, but the prognosis is worse in cases that are complicated by pleuritis. Cases caused by cancer or clotting disorders have a poor prognosis, as do cases with massive bleeding due to injury to the heart or very large blood vessels. References == External links ==

You are a medical advisor. Your role is to break down medical terminology into clear, detailed explanations for a general audience.

I'm encountering the term 'Cerebral atherosclerosis' in medical literature. What's its definition?

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 ==

You function as a medical explainer. Your task is to convey the meanings of medical terms in a detailed, yet easy-to-understand manner.

I've encountered the term 'Pethidine' while reading about medical topics. What does it refer to exactly?

Pethidine, also known as meperidine and sold under the brand name Demerol among others, is a synthetic opioid pain medication of the phenylpiperidine class. Synthesized in 1938 as a potential anticholinergic agent by the German chemist Otto Eisleb, its analgesic properties were first recognized by Otto Schaumann while working for IG Farben, Germany. Pethidine is the prototype of a large family of analgesics including the pethidine 4-phenylpiperidines (piminodine, anileridine and others), the prodines (alphaprodine, MPPP, etc.), bemidones (ketobemidone, etc.) and others more distant, including diphenoxylate and analogues.Pethidine is indicated for the treatment of moderate to severe pain, and is delivered as a hydrochloride salt in tablets, as a syrup, or by intramuscular, subcutaneous, or intravenous injection. For much of the 20th century, pethidine was the opioid of choice for many physicians; in 1975, 60% of doctors prescribed it for acute pain and 22% for chronic severe pain.It was patented in 1937 and approved for medical use in 1943. Compared with morphine, pethidine was thought to be safer, carry a lower risk of addiction, and to be superior in treating the pain associated with biliary spasm or renal colic due to its putative anticholinergic effects. These were later discovered to be inaccurate assumptions, as it carries an equal risk of addiction, possesses no advantageous effects on biliary spasm or renal colic compared to other opioids, and due to its toxic metabolite, norpethidine, it is more toxic than other opioids—especially during long-term use. The norpethidine metabolite was found to have serotonergic effects, so pethidine could, unlike most opioids, contribute to serotonin syndrome. Medical uses Pethidine is the most widely used opioid in labour and delivery but has fallen out of favour in some countries such as the United States in favour of other opioids, due to its potential drug interactions (especially with serotonergics) and its neurotoxic metabolite, norpethidine. It is still commonly used in the United Kingdom and New Zealand, and was the preferred opioid in the United Kingdom for use during labour, but has been superseded somewhat by diamorphine and other strong semi-synthetic opioids (e.g. hydromorphone) to avoid serotonin interactions since the mid-2000s. Pethidine is the preferred painkiller for diverticulitis, because it decreases intestinal intraluminal pressure.Before 2003 it was on the World Health Organizations List of Essential Medicines, the most effective and safe medicines needed in a health system. Adverse effects The adverse effects of pethidine administration are primarily those of the opioids as a class: nausea, vomiting, dizziness, diaphoresis, urinary retention, and constipation. Due to moderate stimulant effects mediated by dopamine and norepinephrine, sedation is less likely compared to other opioids. Unlike other opioids, it does not cause miosis because of its anticholinergic properties. Overdose can cause muscle flaccidity, respiratory depression, obtundation, psychosis, cold and clammy skin, hypotension, and coma. A narcotic antagonist such as naloxone is indicated to reverse respiratory depression and other effects of pethidine. Serotonin syndrome has occurred in patients receiving concurrent antidepressant therapy with selective serotonin reuptake inhibitors (SSRIs) or monoamine oxidase inhibitors, or other medication types (see Interactions below). Convulsive seizures sometimes observed in patients receiving parenteral pethidine on a chronic basis have been attributed to accumulation in plasma of the metabolite norpethidine (normeperidine). Fatalities have occurred following either oral or intravenous pethidine overdose. Interactions Pethidine has serious interactions that can be dangerous with monoamine oxidase inhibitors (e.g., furazolidone, isocarboxazid, moclobemide, phenelzine, procarbazine, selegiline, tranylcypromine). Such patients may suffer agitation, delirium, headache, convulsions, and/or hyperthermia. Fatal interactions have been reported including the death of Libby Zion. Seizures may develop when tramadol is given intravenously following, or with, pethidine. It can interact as well with SSRIs and other antidepressants, antiparkinson agents, migraine therapy, stimulants and other agents causing serotonin syndrome. It is thought to be caused by an increase in cerebral serotonin concentrations. It is probable that pethidine can also interact with a number of other medications, including muscle relaxants, benzodiazepines, and ethanol. Mechanism of action Like morphine, pethidine exerts its analgesic effects by acting as an agonist at the μ-opioid receptor.Pethidine is often employed in the treatment of postanesthetic shivering. The pharmacologic mechanism of this antishivering effect is not fully understood, but it may involve the stimulation of κ-opioid receptors.Pethidine has structural similarities to atropine and other tropane alkaloids and may have some of their effects and side effects. In addition to these opioidergic and anticholinergic effects, it has local anesthetic activity related to its interactions with sodium ion channels. Pethidines apparent in vitro efficacy as an antispasmodic agent is due to its local anesthetic effects. It does not have antispasmodic effects in vivo. Pethidine also has stimulant effects mediated by its inhibition of the dopamine transporter (DAT) and norepinephrine transporter (NET). Because of its DAT inhibitory action, pethidine will substitute for cocaine in animals trained to discriminate cocaine from saline.Several analogs of pethidine such as 4-fluoropethidine have been synthesized that are potent inhibitors of the reuptake of the monoamine neurotransmitters dopamine and norepinephrine via DAT and NET. It has also been associated with cases of serotonin syndrome, suggesting some interaction with serotonergic neurons, but the relationship has not been definitively demonstrated.It is more lipid-soluble than morphine, resulting in a faster onset of action. Its duration of clinical effect is 120–150 minutes, although it is typically administered at 4– to 6-hour intervals. Pethidine has been shown to be less effective than morphine, diamorphine, or hydromorphone at easing severe pain, or pain associated with movement or coughing.Like other opioid drugs, pethidine has the potential to cause physical dependence or addiction. It may be more likely to be abused than other prescription opioids, perhaps because of its rapid onset of action. A study which compared 75 mg pethidine administered via intravenous injection (IV) and 100 mg administered orally (PO) to 10 mg oxycodone (IV) and 10 mg (PO), 10 mg morphine (IV) and 20 mg (PO), 2 mg hydromorphone (IV) and 4 mg (PO), and placebo (C) in the subjects self-reported subjective effects such as drug-liking (how many of the subjects enjoyed or not, the experience; if yes, what was the most enjoyable part and why?, etc.) and how eagerly did subject want to re-experience it, and after IV doses were administered, pethidine 75 mg second-highest rates of drug-liking, after morphine 10 mg. Descriptive adjectives for morphine by subjects were: “more sedating”, “more relaxing” and in comparison to the others, many subjects described that the experience was “more intense”. Pethidine followed, then hydromorphone, oxycodone and last was placebo. Upon oral administration, preference went from (greatest>least): oxycodone 10 mg>morphine 20 mg>hydromorphone 4 mg>pethidine 100 mg>placebo. The especially severe side effects unique to pethidine among opioids—serotonin syndrome, seizures, delirium, dysphoria, tremor—are primarily or entirely due to the action of its metabolite, norpethidine. Pharmacokinetics Pethidine is quickly hydrolysed in the liver to pethidinic acid and is also demethylated to norpethidine, which has half the analgesic activity of pethidine but a longer elimination half-life (8–12 hours); accumulating with regular administration, or in kidney failure. Norpethidine is toxic and has convulsant and hallucinogenic effects. The toxic effects mediated by the metabolites cannot be countered with opioid receptor antagonists such as naloxone or naltrexone, and are probably primarily due to norpethidines anticholinergic activity probably due to its structural similarity to atropine, though its pharmacology has not been thoroughly explored. The neurotoxicity of pethidines metabolites is a unique feature of pethidine compared to other opioids. Pethidines metabolites are further conjugated with glucuronic acid and excreted into the urine. Recreational use Trends In data from the U.S. Drug Abuse Warning Network, mentions of hazardous or harmful use of pethidine declined between 1997 and 2002, in contrast to increases for fentanyl, hydromorphone, morphine, and oxycodone. The number of dosage units of pethidine reported lost or stolen in the U.S. increased 16.2% between 2000 and 2003, from 32,447 to 37,687.This article uses the terms "hazardous use", "harmful use", and "dependence" in accordance with Lexicon of alcohol and drug terms, published by the World Health Organization (WHO) in 1994. In WHO usage, the first two terms replace the term "abuse" and the third term replaces the term "addiction". Synthesis Pethidine can be produced in a two-step synthesis. The first step is reaction of benzyl cyanide and chlormethine in the presence of sodium amide to form a piperidine ring. The nitrile is then converted to an ester. Control Pethidine is in Schedule II of the Controlled Substances Act 1970 of the United States as a Narcotic with ACSCN 9230 with a 6250 kilo aggregate manufacturing quota as of 2014. The free base conversion ratio for salts includes 0.87 for the hydrochloride and 0.84 for the hydrobromide. The A, B, and C intermediates in production of pethidine are also controlled, with ACSCN being 9232 for A (with a 6 gram quota) and 9233 being B (quota of 11 grams) and 9234 being C (6 gram quota). It is listed under the Single Convention for the Control of Narcotic Substances 1961 and is controlled in most countries in the same fashion as is morphine. Society and culture In Raymond Chandlers novel The Long Goodbye (1953), in response to "How is Mrs. Wade?", police Lieutenant Bernie Ohls answers, "Too relaxed. She must have grabbed some pills. Theres a dozen kinds up there -- even demerol. Thats bad stuff." Harold Shipman once got addicted to pethidine.Danish writer Tove Ditlevsen suffered a lifelong addiction to pethidine since her husband, a dodgy doctor, had injected her a dose as a painkiller.Pethidine is referenced by its brand name Demerol in the song "Morphine" by singer Michael Jackson on his 1997 album Blood on the Dance Floor: HIStory in the Mix. Pethidine was one of several prescription drugs which Michael Jackson was addicted to at the time and the singer describes this in the lyrics of the song with phrases such as "Relax/This wont hurt you" and "Yesterday you had his trust/Today hes taking twice as much".Pethidine is referenced in the television show Broadchurch, season 2, episode 3, as it was given to the character Beth after she has her baby. In the 1987 Malayalam movie, Amrutham Gamaya, Mohanlals character, Dr. P.K. Haridas injects pethidine in himself and gets addicted to it. A doctor in the TV show Call the Midwife becomes addicted to pethidine.In William Gibsons book Neuromancer, one of the characters say "A mixture of cocaine and meperidine, yes." The Armenian went back to the conversation he was having with the Sanyo. "Demerol, they used to call that," said the Finn.South Carolina-based modern rock group Crossfade mentions Demerol in the lyrics of their 2004 song, "Dead Skin". In the episode "The Fight" of the TV show Parks and Recreation, some characters become intoxicated on a mixed drink called Snake Juice. The character Ann (Rashida Jones), who is a nurse, asks, "What the hell is in Snake Juice? Demerol?" In David Foster Wallaces book Infinite Jest, one of the main characters, Don Gately, is a Demerol addict in recovery. See also Libby Zion Law (a case involving phenelzine and pethidine) == References ==

You are a medical lexicon. Explain medical terminology with depth and clarity, making sure the information is both accurate and easy to grasp.

Can you break down the meaning of the medical term 'Esophageal web' for me?

Esophageal webs are thin membranes occurring anywhere along the esophagus. Presentation Its main symptoms are pain and difficulty in swallowing (dysphagia).Esophageal webs are thin 2–3 mm (0.08–0.12 in) membranes of normal esophageal tissue consisting of mucosa and submucosa that can partially protrude/obstruct the esophagus. They can be congenital or acquired. Congenital webs commonly appear in the middle and inferior third of the esophagus, and they are more likely to be circumferential with a central or eccentric orifice. Acquired webs are much more common than congenital webs and typically appear in the cervical area (postcricoid).Clinical symptoms of this condition are selective (solid more than liquids) dysphagia, thoracic pain, nasopharyngeal reflux, aspiration, perforation and food impaction (the last two are very rare). Causes They are mainly observed in the Plummer–Vinson syndrome, which is associated with chronic iron deficiency anemia. One in 10 patients with Plummer-Vinson syndrome will eventually develop squamous cell carcinoma of the esophagus, but it is unclear if esophageal webs in and of themselves are a risk factor. Esophageal webs are associated with bullous diseases (such as epidermolysis bullosa, pemphigus, and bullous pemphigoid), with graft versus host disease involving the esophagus, and with celiac disease.Esophageal webs are more common in white individuals and in women (with a ratio of 2:1). The literature describes relations between these webs and Plummer-Vinson Syndrome, bullous dermatologic disorders, inlet patch, graft-versus-host disease and celiac disease. The postulated mechanisms are sideropenic anemia (mechanism unknown) or some interference of the immune system. Esophageal webs can be ruptured during upper endoscopy. Diagnosis The diagnostic test of choice is a barium swallow. Treatment Esophageal webs and rings can be treated with endoscopic dilation. References == External links ==