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Vehicle

A vehicle (from Latin: vehiculum) is a machine that transports people or cargo. Vehicles include wagons, bicycles, motor vehicles (motorcycles, cars, trucks, buses, mobility scooters for disabled people), railed vehicles (trains, trams), watercraft (ships, boats, underwater vehicles), amphibious vehicles (screw-propelled vehicles, hovercraft), aircraft (airplanes, helicopters, aerostats) and spacecraft.Land vehicles are classified broadly by what is used to apply steering and drive forces against the ground: wheeled, tracked, railed or skied. ISO 3833-1977 is the standard, also internationally used in legislation, for road vehicles types, terms and definitions. History The oldest boats found by archaeological excavation are logboats, with the oldest logboat found, the Pesse canoe found in a bog in the Netherlands, being carbon dated to 8040 - 7510 BC, making it 9,500–10,000 years old, a 7,000-year-old seagoing boat made from reeds and tar has been found in Kuwait. Boats were used between 4000 -3000 BC in Sumer, ancient Egypt and in the Indian Ocean. There is evidence of camel pulled wheeled vehicles about 4000–3000 BC. The earliest evidence of a wagonway, a predecessor of the railway, found so far was the 6 to 8.5 km (4 to 5 mi) long Diolkos wagonway, which transported boats across the Isthmus of Corinth in Greece since around 600 BC. Wheeled vehicles pulled by men and animals ran in grooves in limestone, which provided the track element, preventing the wagons from leaving the intended route. In 200 CE, Ma Jun built a south-pointing chariot, a vehicle with an early form of guidance system. Railways began reappearing in Europe after the Dark Ages. The earliest known record of a railway in Europe from this period is a stained-glass window in the Minster of Freiburg im Breisgau dating from around 1350. In 1515, Cardinal Matthäus Lang wrote a description of the Reisszug, a funicular railway at the Hohensalzburg Fortress in Austria. The line originally used wooden rails and a hemp haulage rope and was operated by human or animal power, through a treadwheel. 1769 Nicolas-Joseph Cugnot is often credited with building the first self-propelled mechanical vehicle or automobile in 1769. In Russia, in the 1780s, Ivan Kulibin developed a human-pedalled, three-wheeled carriage with modern features such as a flywheel, brake, gear box and bearings; however, it was not developed further. 1783 Montgolfier brothers first balloon vehicle 1801 Richard Trevithick built and demonstrated his Puffing Devil road locomotive, which many believe was the first demonstration of a steam-powered road vehicle, though it could not maintain sufficient steam pressure for long periods and was of little practical use. 1817 Push bikes, draisines or hobby horses were the first human means of transport to make use of the two-wheeler principle, the draisienne (or Laufmaschine, "running machine"), invented by the German Baron Karl von Drais, is regarded as the forerunner of the modern bicycle (and motorcycle). It was introduced by Drais to the public in Mannheim in summer 1817. 1885 Karl Benz built (and subsequently patented) the first automobile, powered by his own four-stroke cycle gasoline engine in Mannheim, Germany 1885 Otto Lilienthal began experimental gliding and achieved the first sustained, controlled, reproducible flights. 1903 Wright brothers flew the first controlled, powered aircraft 1907 First helicopters Gyroplane no.1 (tethered) and Cornu helicopter (free flight) 1928 Opel RAK.1 rocket car 1929 Opel RAK.1 rocket glider 1961 Vostok vehicle carried the first human, Yuri Gagarin, into space 1969 Apollo Program first crewed vehicle landed on the moon 2010 The number of road motor vehicles in operation worldwide surpassed the 1 billion mark – roughly one for every seven people. Types of vehicles There are over 1 billion bicycles in use worldwide. In 2002 there were an estimated 590 million cars and 205 million motorcycles in service in the world. At least 500 million Chinese Flying Pigeon bicycles have been made, more than any other single model of vehicle. The most-produced model of motor vehicle is the Honda Super Cub motorcycle, having passed 60 million units in 2008. The most-produced car model is the Toyota Corolla, with at least 35 million made by 2010. The most common fixed-wing airplane is the Cessna 172, with about 44,000 having been made as of 2017. The Soviet Mil Mi-8, at 17,000, is the most-produced helicopter. The top commercial jet airliner is the Boeing 737, at about 10,000 in 2018. At around 14,000 for both, the most produced trams are the KTM-5 and Tatra T3. The most common trolleybus is ZiU-9. Locomotion Locomotion consists of a means that allows displacement with little opposition, a power source to provide the required kinetic energy and a means to control the motion, such as a brake and steering system. By far, most vehicles use wheels which employ the principle of rolling to enable displacement with very little rolling friction. Energy source It is essential that a vehicle have a source of energy to drive it. Energy can be extracted from external sources, as in the cases of a sailboat, a solar-powered car, or an electric streetcar that uses overhead lines. Energy can also be stored, provided it can be converted on demand and the storing mediums energy density and power density are sufficient to meet the vehicles needs. Human power is a simple source of energy that requires nothing more than humans. Despite the fact that humans cannot exceed 500 W (0.67 hp) for meaningful amounts of time, the land speed record for human-powered vehicles (unpaced) is 133 km/h (83 mph), as of 2009 on a recumbent bicycle.The most common type of energy source is fuel. External combustion engines can use almost anything that burns as fuel, whilst internal combustion engines and rocket engines are designed to burn a specific fuel, typically gasoline, diesel or ethanol. Another common medium for storing energy is batteries, which have the advantages of being responsive, useful in a wide range of power levels, environmentally friendly, efficient, simple to install, and easy to maintain. Batteries also facilitate the use of electric motors, which have their own advantages. On the other hand, batteries have low energy densities, short service life, poor performance at extreme temperatures, long charging times, and difficulties with disposal (although they can usually be recycled). Like fuel, batteries store chemical energy and can cause burns and poisoning in event of an accident. Batteries also lose effectiveness with time. The issue of charge time can be resolved by swapping discharged batteries with charged ones; however, this incurs additional hardware costs and may be impractical for larger batteries. Moreover, there must be standard batteries for battery swapping to work at a gas station. Fuel cells are similar to batteries in that they convert from chemical to electrical energy, but have their own advantages and disadvantages. Electrified rails and overhead cables are a common source of electrical energy on subways, railways, trams, and trolleybuses. Solar energy is a more modern development, and several solar vehicles have been successfully built and tested, including Helios, a solar-powered aircraft. Nuclear power is a more exclusive form of energy storage, currently limited to large ships and submarines, mostly military. Nuclear energy can be released by a nuclear reactor, nuclear battery, or repeatedly detonating nuclear bombs. There have been two experiments with nuclear-powered aircraft, the Tupolev Tu-119 and the Convair X-6. Mechanical strain is another method of storing energy, whereby an elastic band or metal spring is deformed and releases energy as it is allowed to return to its ground state. Systems employing elastic materials suffer from hysteresis, and metal springs are too dense to be useful in many cases.Flywheels store energy in a spinning mass. Because a light and fast rotor is energetically favorable, flywheels can pose a significant safety hazard. Moreover, flywheels leak energy fairly quickly and affect a vehicles steering through the gyroscopic effect. They have been used experimentally in gyrobuses. Wind energy is used by sailboats and land yachts as the primary source of energy. It is very cheap and fairly easy to use, the main issues being dependence on weather and upwind performance. Balloons also rely on the wind to move horizontally. Aircraft flying in the jet stream may get a boost from high altitude winds. Compressed gas is currently an experimental method of storing energy. In this case, compressed gas is simply stored in a tank and released when necessary. Like elastics, they have hysteresis losses when gas heats up during compression. Gravitational potential energy is a form of energy used in gliders, skis, bobsleds and numerous other vehicles that go down hill. Regenerative braking is an example of capturing kinetic energy where the brakes of a vehicle are augmented with a generator or other means of extracting energy. Motors and engines When needed, the energy is taken from the source and consumed by one or more motors or engines. Sometimes there is an intermediate medium, such as the batteries of a diesel submarine.Most motor vehicles have internal combustion engines. They are fairly cheap, easy to maintain, reliable, safe and small. Since these engines burn fuel, they have long ranges but pollute the environment. A related engine is the external combustion engine. An example of this is the steam engine. Aside from fuel, steam engines also need water, making them impractical for some purposes. Steam engines also need time to warm up, whereas IC engines can usually run right after being started, although this may not be recommended in cold conditions. Steam engines burning coal release sulfur into the air, causing harmful acid rain. While intermittent internal combustion engines were once the primary means of aircraft propulsion, they have been largely superseded by continuous internal combustion engines: gas turbines. Turbine engines are light and, particularly when used on aircraft, efficient. On the other hand, they cost more and require careful maintenance. They can also be damaged by ingesting foreign objects, and they produce a hot exhaust. Trains using turbines are called gas turbine-electric locomotives. Examples of surface vehicles using turbines are M1 Abrams, MTT Turbine SUPERBIKE and the Millennium. Pulse jet engines are similar in many ways to turbojets, but have almost no moving parts. For this reason, they were very appealing to vehicle designers in the past; however their noise, heat and inefficiency has led to their abandonment. A historical example of the use of a pulse jet was the V-1 flying bomb. Pulse jets are still occasionally used in amateur experiments. With the advent of modern technology, the pulse detonation engine has become practical and was successfully tested on a Rutan VariEze. While the pulse detonation engine is much more efficient than the pulse jet and even turbine engines, it still suffers from extreme noise and vibration levels. Ramjets also have few moving parts, but they only work at high speed, so that their use is restricted to tip jet helicopters and high speed aircraft such as the Lockheed SR-71 Blackbird.Rocket engines are primarily used on rockets, rocket sleds and experimental aircraft. Rocket engines are extremely powerful. The heaviest vehicle ever to leave the ground, the Saturn V rocket, was powered by five F-1 rocket engines generating a combined 180 million horsepower (134.2 gigawatt). Rocket engines also have no need to "push off" anything, a fact that the New York Times denied in error. Rocket engines can be particularly simple, sometimes consisting of nothing more than a catalyst, as in the case of a hydrogen peroxide rocket. This makes them an attractive option for vehicles such as jet packs. Despite their simplicity, rocket engines are often dangerous and susceptible to explosions. The fuel they run off may be flammable, poisonous, corrosive or cryogenic. They also suffer from poor efficiency. For these reasons, rocket engines are only used when absolutely necessary.Electric motors are used in electric vehicles such as electric bicycles, electric scooters, small boats, subways, trains, trolleybuses, trams and experimental aircraft. Electric motors can be very efficient: over 90% efficiency is common. Electric motors can also be built to be powerful, reliable, low-maintenance and of any size. Electric motors can deliver a range of speeds and torques without necessarily using a gearbox (although it may be more economical to use one). Electric motors are limited in their use chiefly by the difficulty of supplying electricity.Compressed gas motors have been used on some vehicles experimentally. They are simple, efficient, safe, cheap, reliable and operate in a variety of conditions. One of the difficulties met when using gas motors is the cooling effect of expanding gas. These engines are limited by how quickly they absorb heat from their surroundings. The cooling effect can, however, double as air conditioning. Compressed gas motors also lose effectiveness with falling gas pressure.Ion thrusters are used on some satellites and spacecraft. They are only effective in a vacuum, which limits their use to spaceborne vehicles. Ion thrusters run primarily off electricity, but they also need a propellant such as caesium, or more recently xenon. Ion thrusters can achieve extremely high speeds and use little propellant; however they are power-hungry. Converting energy to work The mechanical energy that motors and engines produce must be converted to work by wheels, propellers, nozzles, or similar means. Aside from converting mechanical energy into motion, wheels allow a vehicle to roll along a surface and, with the exception of railed vehicles, to be steered. Wheels are ancient technology, with specimens being discovered from over 5000 years ago. Wheels are used in a plethora of vehicles, including motor vehicles, armoured personnel carriers, amphibious vehicles, airplanes, trains, skateboards and wheelbarrows. Nozzles are used in conjunction with almost all reaction engines. Vehicles using nozzles include jet aircraft, rockets and personal watercraft. While most nozzles take the shape of a cone or bell, some unorthodox designs have been created such as the aerospike. Some nozzles are intangible, such as the electromagnetic field nozzle of a vectored ion thruster.Continuous track is sometimes used instead of wheels to power land vehicles. Continuous track has the advantages of a larger contact area, easy repairs on small damage, and high maneuverability. Examples of vehicles using continuous track are tanks, snowmobiles and excavators. Two continuous tracks used together allow for steering. The largest vehicle in the world, the Bagger 288, is propelled by continuous tracks. Propellers (as well as screws, fans and rotors) are used to move through a fluid. Propellers have been used as toys since ancient times, however it was Leonardo da Vinci who devised what was one of the earliest propeller driven vehicles, the "aerial-screw". In 1661, Toogood & Hays adopted the screw for use as a ship propeller. Since then, the propeller has been tested on many terrestrial vehicles, including the Schienenzeppelin train and numerous cars. In modern times, propellers are most prevalent on watercraft and aircraft, as well as some amphibious vehicles such as hovercraft and ground-effect vehicles. Intuitively, propellers cannot work in space as there is no working fluid, however some sources have suggested that since space is never empty, a propeller could be made to work in space.Similarly to propeller vehicles, some vehicles use wings for propulsion. Sailboats and sailplanes are propelled by the forward component of lift generated by their sails/wings. Ornithopters also produce thrust aerodynamically. Ornithopters with large rounded leading edges produce lift by leading-edge suction forces. Research at the University of Toronto Institute for Aerospace Studies lead to a flight with an actual ornithopter on July 31, 2010. Paddle wheels are used on some older watercraft and their reconstructions. These ships were known as paddle steamers. Because paddle wheels simply push against the water, their design and construction is very simple. The oldest such ship in scheduled service is the Skibladner. Many pedalo boats also use paddle wheels for propulsion. Screw-propelled vehicles are propelled by auger-like cylinders fitted with helical flanges. Because they can produce thrust on both land and water, they are commonly used on all-terrain vehicles. The ZiL-2906 was a Soviet-designed screw-propelled vehicle designed to retrieve cosmonauts from the Siberian wilderness. Friction All or almost all of the useful energy produced by the engine is usually dissipated as friction; so minimising frictional losses is very important in many vehicles. The main sources of friction are rolling friction and fluid drag (air drag or water drag). Wheels have low bearing friction and pneumatic tyres give low rolling friction. Steel wheels on steel tracks are lower still.Aerodynamic drag can be reduced by streamlined design features. Friction is desirable and important in supplying traction to facilitate motion on land. Most land vehicles rely on friction for accelerating, decelerating and changing direction. Sudden reductions in traction can cause loss of control and accidents. Control Steering Most vehicles, with the notable exception of railed vehicles, have at least one steering mechanism. Wheeled vehicles steer by angling their front or rear wheels. The B-52 Stratofortress has a special arrangement in which all four main wheels can be angled. Skids can also be used to steer by angling them, as in the case of a snowmobile. Ships, boats, submarines, dirigibles and aeroplanes usually have a rudder for steering. On an airplane, ailerons are used to bank the airplane for directional control, sometimes assisted by the rudder. Stopping With no power applied, most vehicles come to a stop due to friction. But it is often required to stop a vehicle faster than by friction alone: so almost all vehicles are equipped with a braking system. Wheeled vehicles are typically equipped with friction brakes, which use the friction between brake pads (stators) and brake rotors to slow the vehicle. Many airplanes have high performance versions of the same system in their landing gear for use on the ground. A Boeing 757 brake, for example, has 3 stators and 4 rotors. The Space Shuttle also uses frictional brakes on its wheels. As well as frictional brakes, hybrid/electric cars, trolleybuses and electric bicycles can also use regenerative brakes to recycle some of the vehicles potential energy. High-speed trains sometimes use frictionless Eddy-current brakes; however widespread application of the technology has been limited by overheating and interference issues.Aside from landing gear brakes, most large aircraft have other ways of decelerating. In aircraft, air brakes are aerodynamic surfaces that provide braking force by increasing the frontal cross section thus aerodynamic drag of the aircraft. These are usually implemented as flaps that oppose air flow when extended and are flush with aircraft when retracted. Reverse thrust is also used in many aeroplane engines. Propeller aircraft achieve reverse thrust by reversing the pitch of the propellers, while jet aircraft do so by redirecting their engine exhaust forwards. On aircraft carriers, arresting gears are used to stop an aircraft. Pilots may even apply full forward throttle on touchdown, in case the arresting gear does not catch and a go around is needed.Parachutes are used to slow down vehicles travelling very fast. Parachutes have been used in land, air and space vehicles such as the ThrustSSC, Eurofighter Typhoon and Apollo Command Module. Some older Soviet passenger jets had braking parachutes for emergency landings. Boats use similar devices called sea anchors to maintain stability in rough seas. To further increase the rate of deceleration or where the brakes have failed, several mechanisms can be used to stop a vehicle. Cars and rolling stock usually have hand brakes that, while designed to secure an already parked vehicle, can provide limited braking should the primary brakes fail. A secondary procedure called forward-slip is sometimes used to slow airplanes by flying at an angle, causing more drag. Legislation Motor vehicle and trailer categories are defined according to the following international classification: Category M: passenger vehicles. Category N: motor vehicles for the carriage of goods. Category O: trailers and semi-trailers. European Union In the European Union the classifications for vehicle types are defined by: Commission Directive 2001/116/EC of 20 December 2001, adapting to technical progress Council Directive 70/156/EEC on the approximation of the laws of the Member States relating to the type-approval of motor vehicles and their trailers Directive 2002/24/EC of the European Parliament and of the Council of 18 March 2002 relating to the type-approval of two or three wheeled motor vehicles and repealing Council Directive 92/61/EECEuropean Community, is based on the Communitys WVTA (whole vehicle type-approval) system. Under this system, manufacturers can obtain certification for a vehicle type in one Member State if it meets the EC technical requirements and then market it EU-wide with no need for further tests. Total technical harmonization already has been achieved in three vehicle categories (passenger cars, motorcycles, and tractors) and soon will extend to other vehicle categories (coaches and utility vehicles). It is essential that European car manufacturers be ensured access to as large a market as possible. While the Community type-approval system allows manufacturers to benefit fully from internal market opportunities, worldwide technical harmonization in the context of the United Nations Economic Commission for Europe (UNECE) offers a market beyond European borders. Licensing In many cases, it is unlawful to operate a vehicle without a license or certification. The least strict form of regulation usually limits what passengers the driver may carry or prohibits them completely (e.g., a Canadian ultra-light license without endorsements). The next level of licensing may allow passengers, but without any form of compensation or payment. A private drivers license usually has these conditions. Commercial licenses that allow the transport of passengers and cargo are more tightly regulated. The most strict form of licensing is generally reserved for school buses, hazardous materials transports and emergency vehicles. The driver of a motor vehicle is typically required to hold a valid drivers license while driving on public lands, whereas the pilot of an aircraft must have a license at all times, regardless of where in the jurisdiction the aircraft is flying. Registration Vehicles are often required to be registered. Registration may be for purely legal reasons, for insurance reasons or to help law enforcement recover stolen vehicles. Toronto Police Service, for example, offers free and optional bicycle registration online. On motor vehicles, registration often takes the form of a vehicle registration plate, which makes it easy to identify a vehicle. In Russia, trucks and buses have their licence plate numbers repeated in large black letters on the back. On aircraft, a similar system is used where a tail number is painted on various surfaces. Like motor vehicles and aircraft, watercraft also have registration numbers in most jurisdictions, however the vessel name is still the primary means of identification as has been the case since ancient times. For this reason, duplicate registration names are generally rejected. In Canada, boats with an engine power of 10 hp (7.5 kW) or greater require registration, leading to the ubiquitous "9.9 hp (7.4 kW)" engine. Registration may be conditional on the vehicle being approved for use on public highways, as in the case of the UK and Ontario. Many US states also have requirements for vehicles operating on public highways. Aircraft have more stringent requirements, as they pose a high risk of damage to people and property in event of an accident. In the US, the FAA requires aircraft to have an airworthiness certificate. Because US aircraft must be flown for some time before they are certified, there is a provision for an experimental airworthiness certificate. FAA experimental aircraft are restricted in operation, including no overflights of populated areas, in busy airspace or with unessential passengers. Materials and parts used in FAA certified aircraft must meet the criteria set forth by the technical standard orders. Mandatory safety equipment In many jurisdictions, the operator of a vehicle is legally obligated to carry safety equipment with or on them. Common examples include seat belts in cars, helmets on motorcycles and bicycles, fire extinguishers on boats, buses and airplanes and life jackets on boats and commercial aircraft. Passenger aircraft carry a great deal of safety equipment including inflatable slides are rafts, oxygen masks, oxygen tanks, life jackets, satellite beacons and first aid kits. Some equipment such as life jackets has led to debate regarding their usefulness. In the case of Ethiopian Airlines Flight 961, the life jackets saved many people but also led to many deaths when passengers inflated their vests prematurely. Right-of-way There are specific real-estate arrangements made to allow vehicles to travel from one place to another. The most common arrangements are public highways, where appropriately licensed vehicles can navigate without hindrance. These highways are on public land and are maintained by the government. Similarly, toll routes are open to the public after paying a toll. These routes and the land they rest on may be government or privately owned or a combination of both. Some routes are privately owned but grant access to the public. These routes often have a warning sign stating that the government does not maintain the way. An example of this are byways in England and Wales. In Scotland, land is open to un-motorised vehicles if the land meets certain criteria. Public land is sometimes open to use by off-road vehicles. On US public land, the Bureau of Land Management (BLM) decides where vehicles may be used. Railways often pass over land not owned by the railway company. The right to this land is granted to the railway company through mechanisms such as easement. Watercraft are generally allowed to navigate public waters without restriction as long as they do not cause a disturbance. Passing through a lock, however, may require paying a toll. Despite the common law tradition Cuius est solum, eius est usque ad coelum et ad inferos of owning all the air above ones property, the US Supreme Court ruled that aircraft in the US have the right to use air above someone elses property without their consent. While the same rule generally applies in all jurisdictions, some countries such as Cuba and Russia have taken advantage of air rights on a national level to earn money. There are some areas that aircraft are barred from overflying. This is called prohibited airspace. Prohibited airspace is usually strictly enforced due to potential damage from espionage or attack. In the case of Korean Air Lines Flight 007, the airliner entered prohibited airspace over Soviet territory and was shot down as it was leaving. Safety For a comparison of transportation fatality rates, see: Air safety statistics. Several different metrics used to compare and evaluate the safety of different vehicles. The main three are deaths per billion passenger-journeys, deaths per billion passenger-hours and deaths per billion passenger-kilometers. See also Automotive acronyms and abbreviations ISIRI 6924 Narrow-track vehicle Outline of vehicles Personal transporter Propulsion Single-track vehicle Vehicular dynamics Vehicular metrics == References ==

Hodgkin lymphoma

Hodgkin lymphoma (HL) is a type of lymphoma, in which cancer originates from a specific type of white blood cell called lymphocytes, where multinucleated Reed–Sternberg cells (RS cells) are present in the patients lymph nodes. The condition was named after the English physician Thomas Hodgkin, who first described it in 1832. Symptoms may include fever, night sweats, and weight loss. Often, nonpainful enlarged lymph nodes occur in the neck, under the arm, or in the groin. Those affected may feel tired or be itchy.The two major types of Hodgkin lymphoma are classic Hodgkin lymphoma and nodular lymphocyte-predominant Hodgkin lymphoma. About half of cases of Hodgkin lymphoma are due to Epstein–Barr virus (EBV) and these are generally the classic form. Other risk factors include a family history of the condition and having HIV/AIDS. Diagnosis is conducted by confirming the presence of cancer and identifying RS cells in lymph node biopsies. The virus-positive cases are classified as a form of the Epstein–Barr virus-associated lymphoproliferative diseases.Hodgkin lymphoma may be treated with chemotherapy, radiation therapy, and stem cell transplantation. The choice of treatment often depends on how advanced the cancer has become and whether or not it has favorable features. If the disease is detected early, a cure is often possible. In the United States, 88% of people diagnosed with Hodgkin Lymphoma survive for five years or longer. For those under the age of 20, rates of survival are 97%. Radiation and some chemotherapy drugs, however, increase the risk of other cancers, heart disease, or lung disease over the subsequent decades.In 2015, about 574,000 people globally had Hodgkin lymphoma, and 23,900 (4.2%) died. In the United States, 0.2% of people are affected at some point in their life. Most people are diagnosed with the disease between the ages of 20 and 40. Signs and symptoms People with Hodgkin lymphoma may present with the following symptoms: Lymphadenopathy: the most common symptom of Hodgkin is the painless enlargement of one or more lymph nodes. The nodes may also feel rubbery and swollen when examined. The nodes of the neck, armpits and groin (cervical and supraclavicular) are most frequently involved (80–90% of the time, on average). The lymph nodes of the chest are often affected, and these may be noticed on a chest radiograph. Systemic symptoms: about one-third of people with Hodgkin disease may also present with systemic symptoms, including:Itchy skin Night sweats. Unexplained weight loss of at least 10% of the persons total body mass in six months or less. Low-grade fever. Fatigue (lassitude). Systemic symptoms such as fever, night sweats, and weight loss are known as B symptoms; thus, presence of these indicate that the persons stage is, for example, 2B instead of 2A. Splenomegaly: enlargement of the spleen is often present in people with Hodgkin lymphoma. The enlargement is seldom massive, and the size of the spleen may fluctuate during the course of treatment. Hepatomegaly: enlargement of the liver, due to liver involvement, is infrequent in people with Hodgkin Lymphoma. Hepatosplenomegaly: the enlargement of both the liver and spleen caused by the same disease. Pain following alcohol consumption: classically, involved nodes are painful after alcohol consumption, though this phenomenon is very uncommon, occurring in only two to three percent of people with Hodgkin lymphoma, thus having a low sensitivity. On the other hand, its positive predictive value is high enough for it to be regarded as a pathognomonic sign of Hodgkin lymphoma. The pain typically has an onset within minutes after ingesting alcohol, and is usually felt as coming from the vicinity where there is an involved lymph node. The pain has been described as either sharp and stabbing or dull and aching. Back pain: nonspecific back pain (pain that cannot be localised or its cause determined by examination or scanning techniques) has been reported in some cases of Hodgkin lymphoma. The lower back is most often affected. Cyclical fever: people may also present with a cyclical high-grade fever known as the Pel–Ebstein fever, or more simply "P-E fever". However, there is debate as to whether the P-E fever truly exists. Nephrotic syndrome can occur in individuals with Hodgkin lymphoma and is most commonly caused by minimal change disease. May present with airway obstruction, pleural/pericardial effusion, hepatocellular dysfunction, bone marrow infiltration. Diagnosis Hodgkin lymphoma must be distinguished from non-cancerous causes of lymph node swelling (such as various infections) and from other types of cancer. Definitive diagnosis is by lymph node biopsy (usually excisional biopsy with microscopic examination). Blood tests are also performed to assess function of major organs and to assess safety for chemotherapy. Positron emission tomography (PET) is used to detect small deposits that do not show on CT scanning. PET scans are also useful in functional imaging (by using a radiolabeled glucose to image tissues of high metabolism). In some cases, a gallium scan may be used instead of a PET scan. Types There are two main types of Hodgkin lymphoma: classic Hodgkin lymphoma and nodular lymphocyte predominant Hodgkin lymphoma. The prevalence of classic Hodgkin lymphoma and nodular lymphocyte Hodgkin lymphoma are approximately 90% and 10%, respectively. The morphology, phenotype, molecular features, and, therefore, the clinical behaviour and presentation of the two types differ. Classic Classic Hodgkin lymphoma (excluding nodular lymphocyte predominant Hodgkin lymphoma) can be subclassified into four pathologic subtypes based upon Reed–Sternberg cell morphology and the composition of the reactive cell infiltrate seen in the lymph node biopsy specimen (the cell composition around the Reed–Sternberg cell(s)). Presence of EBV in Reed-Sternberg cells is most commonly found in the subtypes lymphocyte depleted HL (>70%) and mixed cellularity HL (70%), whilst being less prevalent in lymphocyte-rich HL (40%) and relatively uncommon by comparison in nodular sclerosing HL. For the other forms, although the traditional B-cell markers (such as CD20) are not expressed on all cells, Reed–Sternberg cells are usually of B cell origin. Although Hodgkins is now frequently grouped with other B-cell malignancies, some T-cell markers (such as CD2 and CD4) are occasionally expressed. However, this may be an artifact of the ambiguity inherent in the diagnosis. Hodgkin cells produce interleukin-21 (IL-21), which was once thought to be exclusive to T-cells. This feature may explain the behavior of classic Hodgkin lymphoma, including clusters of other immune cells gathered around HL cells (infiltrate) in cultures. Nodular lymphocyte predominant Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is another subtype of Hodgkin lymphoma distinct from classic Hodgkin lymphoma and is characterized by the presence of popcorn cells which express CD20. Due to these differences, among others, NLPHL is often treated differently from classic Hodgkin lymphoma, including using rituximab in combination with AVBD chemotherapy, though individual cases vary and clinical trials are ongoing. Staging The staging is the same for both Hodgkin and non-Hodgkin lymphomas. After Hodgkin lymphoma is diagnosed, a person will be staged: that is, they will undergo a series of tests and procedures that will determine what areas of the body are affected. These procedures may include documentation of their histology, a physical examination, blood tests, chest X-ray radiographs, computed tomography (CT)/positron emission tomography (PET)/magnetic resonance imaging (MRI) scans of the chest, abdomen and pelvis, and usually a bone marrow biopsy. PET scan is now used instead of the gallium scan for staging. On the PET scan, sites involved with lymphoma light up very brightly enabling accurate and reproducible imaging. In the past, a lymphangiogram or surgical laparotomy (which involves opening the abdominal cavity and visually inspecting for tumors) were performed. Lymphangiograms or laparotomies are very rarely performed, having been supplanted by improvements in imaging with the CT scan and PET scan.On the basis of this staging, the person will be classified according to a staging classification (the Ann Arbor staging classification scheme is a common one): Stage I is involvement of a single lymph node region (I) (mostly the cervical region) or single extralymphatic site (Ie); Stage II is involvement of two or more lymph node regions on the same side of the diaphragm (II) or of one lymph node region and a contiguous extralymphatic site (IIe); Stage III is involvement of lymph node regions on both sides of the diaphragm, which may include the spleen (IIIs) or limited contiguous extralymphatic organ or site (IIIe, IIIes); Stage IV is disseminated involvement of one or more extralymphatic organs.The absence of systemic symptoms is signified by adding "A" to the stage; the presence of systemic symptoms is signified by adding "B" to the stage. For localised extranodal extension from mass of nodes that does not advance the stage, subscript "E" is added. Splenic involvement is signified by adding "S" to the stage. The inclusion of "bulky disease" is signified by "X". Pathology MacroscopyAffected lymph nodes (most often, laterocervical lymph nodes) are enlarged, but their shape is preserved because the capsule is not invaded. Usually, the cut surface is white-grey and uniform; in some histological subtypes (e.g. nodular sclerosis) a nodular aspect may appear.A fibrin ring granuloma may be seen. Microscopy Microscopic examination of the lymph node biopsy reveals complete or partial effacement of the lymph node architecture by scattered large malignant cells known as Reed-Sternberg cells (RSC) (typical and variants) admixed within a reactive cell infiltrate composed of variable proportions of lymphocytes, histiocytes, eosinophils, and plasma cells. The Reed–Sternberg cells are identified as large often bi-nucleated cells with prominent nucleoli and an unusual CD45-, CD30+, CD15+/- immunophenotype. In approximately 50% of cases, the Reed–Sternberg cells are infected by the Epstein–Barr virus.Characteristics of classic Reed–Sternberg cells include large size (20–50 micrometres), abundant, amphophilic, finely granular/homogeneous cytoplasm; two mirror-image nuclei (owl eyes) each with an eosinophilic nucleolus and a thick nuclear membrane (chromatin is distributed close to the nuclear membrane). Almost all of these cells have an increased copy number of chromosome 9p/9p24.1.Variants: Hodgkin cell (atypical mononuclear RSC) is a variant of RS cell, which has the same characteristics but is mononucleated. Lacunar RSC is large, with a single hyperlobulated nucleus, multiple, small nucleoli and eosinophilic cytoplasm which is retracted around the nucleus, creating an empty space ("lacunae"). Pleomorphic RSC has multiple irregular nuclei. "Popcorn" RSC (lympho-histiocytic variant) is a small cell, with a very lobulated nucleus, small nucleoli. "Mummy" RSC has a compact nucleus with no nucleolus and basophilic cytoplasm.Hodgkin lymphoma can be sub-classified by histological type. The cell histology in Hodgkin lymphoma is not as important as it is in non-Hodgkin lymphoma: the treatment and prognosis in classic Hodgkin lymphoma usually depends on the stage of disease rather than the histotype. Management The current approach for treatment aims to reduce the acute and long-term toxicities associated with Hodgkin lymphoma (e.g. cardiac damage and secondary cancers) and increase overall survival.People with early stage disease (IA or IIA) are effectively treated with radiation therapy or chemotherapy. The choice of treatment depends on the age, sex, bulk and the histological subtype of the disease. Adding localised radiation therapy after the chemotherapy regimen may provide a longer progression-free survival compared with chemotherapy treatment alone. People with later disease (III, IVA, or IVB) are treated with combination chemotherapy alone. People of any stage with a large mass in the chest are usually treated with combined chemotherapy and radiation therapy. The common non-Hodgkin treatment, rituximab (which is a monoclonal antibody against CD20) is not routinely used to treat Hodgkin lymphoma due to the lack of CD20 surface antigens in most cases. The use of rituximab in Hodgkin lymphoma, including the lymphocyte predominant subtype has been recently reviewed. The evidence is very uncertain about the effect of Nivolumab for patients with a Hodgkins lymphoma e.g. on the overall survival.Increased age is an adverse risk factor for Hodgkin lymphoma, but in general elderly people (≥ 60 years of age) without major comorbidities are sufficiently fit to tolerate therapy with curative intent. Despite this, treatment outcome in the elderly patient is not comparable to that of younger people and the disease is a different entity in older people where different considerations enter into treatment decisions.Recently, two novel targeted drugs have been developed for relapsing and refractory HL patients; Brentuximab vedotin, a CD30 antibody conjugated with a cytotoxic component MMAE, and the checkpoint inhibitors, Nivolumab and Pembrolizumab. This has been an important step in the treatment for the few, but still existing refractory patients. For Hodgkin lymphomas, radiation oncologists typically use external beam radiation therapy (sometimes shortened to EBRT or XRT). Radiation oncologists deliver external beam radiation therapy to the lymphoma from a machine called a linear accelerator which produces high energy X-rays and electrons. People usually describe treatments as painless and similar to getting an X-ray. Treatments last less than 30 minutes each. For lymphomas, there are a few different ways radiation oncologists target the cancer cells. Involved site radiation is when the radiation oncologists give radiation only to those parts of the persons body known to have the cancer. Very often, this is combined with chemotherapy. Radiation therapy directed above the diaphragm to the neck, chest or underarms is called mantle field radiation. Radiation to below the diaphragm to the abdomen, spleen or pelvis is called inverted-Y field radiation. Total nodal irradiation is when the therapist gives radiation to all the lymph nodes in the body to destroy cells that may have spread. Adverse effects The high cure rates and long survival of many people with Hodgkin lymphoma has led to a high concern with late adverse effects of treatment, including cardiovascular disease and second malignancies such as acute leukemias, lymphomas, and solid tumors within the radiation therapy field. Most people with early-stage disease are now treated with abbreviated chemotherapy and involved site radiation therapy rather than with radiation therapy alone. Clinical research strategies are exploring reduction of the duration of chemotherapy and dose and volume of radiation therapy in an attempt to reduce late morbidity and mortality of treatment while maintaining high cure rates. Hospitals are also treating those who respond quickly to chemotherapy with no radiation.In childhood cases of Hodgkin lymphoma, long-term endocrine adverse effects are a major concern, mainly gonadal dysfunction and growth retardation. Gonadal dysfunction seems to be the most severe endocrine long-term effect, especially after treatment with alkylating agents or pelvic radiotherapy.It is possible that patients undergoing a chemotherapy need a platelet transfusion. If a stem cell transplantation is necessary for the treatment of a relapse, graft-versus-host diseases might occur. Supportive treatment Adding physical exercises to the standard treatment for adult patients with haematological malignancies like Hodgkin lymphoma may result in little to no difference in the mortality, the quality of life and the physical functioning. These exercises may result in a slight reduction in depression. Furthermore, aerobic physical exercises probably reduce fatigue. The evidence is very uncertain about the effect on anxiety and serious adverse events. Prognosis Treatment of Hodgkins disease has been improving over the past few decades. Recent trials that have made use of new types of chemotherapy have indicated higher survival rates than have previously been seen. In one recent European trial, the five-year survival rate for those people with a favorable prognosis (FFP) was 98%, while that for people with worse outlooks was at least 85%.In 1998, an international effort identified seven prognostic factors that accurately predict the success rate of conventional treatment in people with locally extensive or advanced-stage Hodgkin lymphoma. Freedom from progression (FFP) at five years was directly related to the number of factors present in a person. The five-year FFP for people with zero factors is 84%. Each additional factor lowers the five-year FFP rate by 7%, such that the five-year FFP for a person with five or more factors is 42%.The adverse prognostic factors identified in the international study are: Age ≥ 45 years Stage IV disease Hemoglobin < 10.5 g/dl Lymphocyte count < 600/µl or < 8% Male Albumin < 4.0 g/dl White blood count ≥ 15,000/µlOther studies have reported the following to be the most important adverse prognostic factors: mixed-cellularity or lymphocyte-depleted histologies, male sex, large number of involved nodal sites, advanced stage, age of 40 years or more, the presence of B symptoms, high erythrocyte sedimentation rate, and bulky disease (widening of the mediastinum by more than one third, or the presence of a nodal mass measuring more than 10 cm in any dimension.)More recently, the use of positron emission tomography (PET) early after commencing chemotherapy has demonstrated to have powerful prognostic ability. This enables assessment of an individuals response to chemotherapy as the PET activity switches off rapidly in people who are responding. In this study, after two cycles of ABVD chemotherapy, 83% of people were free of disease at 3 years if they had a negative PET versus only 28% in those with positive PET scans. This prognostic method improves on FFP estimates based on the seven conventional factors. Several trials are underway to see if PET-based risk adapted response can be used to improve a persons outcomes by changing chemotherapy early in people who are not responding. The evidence is very uncertain about the effect of negative (= good prognosis) or positive (= bad prognosis) interim PET scan results for patients with a Hodgkins lymphoma on the progression-free survival. Negative interim PET scan results may result in an increase in progression-free survival compared if the adjusted result was measured. Negative interim PET scan results probably result in a large increase in the overall survival compared to those with a positive interim PET scan result, Epidemiology Unlike some other lymphomas, whose number of new cases per year increases with age, Hodgkin lymphoma has a bimodal curve for the number of cases; that is, it occurs most frequently in two separate age groups, the first being young adulthood (age 15–35) and the second being in those over 55 years old although these peaks may vary slightly with nationality. Overall, it is more common in males, except for the nodular sclerosis variant, which is slightly more common in females. The annual number of cases of Hodgkin lymphoma is 2.7 per 100,000 per persons per year, and the disease accounts for slightly less than 1% of all cancers worldwide.In 2010, globally it resulted in about 18,000 deaths down from 19,000 in 1990. In 2012, there were an estimated 65,950 cases and 25,469 deaths from Hodgkin lymphoma worldwide, with 28,852 and 37,098 cases occurring in developed and developing countries, respectively. However, the age-standardized rates were higher in developed regions, with the greatest rates in the Americas (1.5 per 100,000), East Mediterranean Region (1.5 per 100,000), and Europe (2.0 per 100,000). The East Mediterranean Region also has the highest age-standardized mortality rate of 1.0 per 100,000, which is mainly attributed to lifestyle and environmental risk factors associated with transitional economies such as smoking, obesity, physical inactivity, and reproductive behaviors, as well as availability of diagnostic practices and awareness of the disease.The number of cases of Hodgkin lymphoma is increased in people with HIV infection. In contrast to many other lymphomas associated with HIV infection it occurs most commonly in people with higher CD4 T cell counts. Canada Hodgkin lymphoma accounts for 0.6% of all male cancer cases, and 0.4% of all female cancer cases in Canada. In 2017, approximately 990 Canadians will be diagnosed with Hodgkin lymphoma, and 140 will die of the disease. UK Hodgkin lymphoma accounts for less than 1% of all cancer cases and deaths in the UK. Around 1,800 people were diagnosed with the disease in 2011, and around 330 people died in 2012. United States In 2016, there were 8,389 new cases and 1,000 mortalities attributed to Hodgkin Lymphoma, a decrease from the 8,625 new cases and 1,120 mortalities in 2015. As of January 1, 2016, the 5-year limited duration prevalence of Hodgkin Lymphoma was 37,513 representing 0.71% of all diagnosed cancers in the U.S. History Hodgkin lymphoma was first described in an 1832 report by Thomas Hodgkin, although Hodgkin noted that perhaps an earlier reference to the condition was provided by Marcello Malpighi in 1666. While occupied as museum curator at Guys Hospital, London, Hodgkin studied seven people with painless lymph node enlargement. Of the seven cases, two were under the care of Richard Bright, one was of Thomas Addison, and one was of Robert Carswell. Carswells report of the seventh case was accompanied by numerous illustrations that aided early descriptions of the disease.Hodgkins report on the seven cases, entitled "On some morbid appearances of the absorbent glands and spleen", was presented to the Medical and Chirurgical Society of London in January 1832 and was subsequently published in the societys journal, Medical-Chirurgical Society Transactions. Hodgkins paper went largely unnoticed, however, even though Bright highlighted it in an 1838 publication. Indeed, Hodgkin himself did not view his contribution as particularly significant.In 1856, Samuel Wilks independently reported on a series of patients with the same disease that Hodgkin had previously described. Wilks, a successor to Hodgkin at Guys Hospital, was unaware of Hodgkins prior work on the subject. Bright informed Wilks of Hodgkins contribution and in 1865, Wilks published a second paper, entitled "Cases of enlargement of the lymphatic glands and spleen", in which he named the illness "Hodgkins disease" in honor of his predecessor.Theodor Langhans and WS Greenfield first described the microscopic characteristics of Hodgkin lymphoma in 1872 and 1878, respectively. In 1898 and 1902, respectively, Carl Sternberg and Dorothy Reed independently described the cytogenetic features of the malignant cells of Hodgkin lymphoma, now called Reed–Sternberg cells.Tissue specimens from Hodgkins seven cases were preserved at Guys Hospital. Nearly 100 years after Hodgkins initial publication, histopathologic reexamination confirmed Hodgkin lymphoma in only three of seven of these people. The remaining cases included non-Hodgkin lymphoma, tuberculosis, and syphilis.Hodgkin lymphoma was one of the first cancers to be treated successfully with radiation therapy and, later, it was one of the first to be treated by combination chemotherapy. Notable cases Paul Allen, co-founder of Microsoft was diagnosed with Hodgkin lymphoma in 1982. He later died from non-Hodgkin lymphoma, on October 15, 2018. Eric Berry, All-Pro strong safety for the Kansas City Chiefs of the National Football League, diagnosed in 2014. Howard Carter, Egyptologist and discoverer of the Tomb of Tutankhamun, died in 1939 from Hodgkins disease. Starchild Abraham Cherrix, a teenager whose refusal to undergo further conventional treatment after relapsing in 2006 resulted in a court battle and a change to Virginia laws about medical neglect. James Conner, running back and 2014 ACC Player of the Year for the Pittsburgh Steelers. Michael Cuccione, Canadian child actor, was diagnosed in 1994 at age 9. Treatments that rendered him cancer-free, including chemotherapy, a bone marrow transplant, and radiation, left him with permanent lung and respiratory problems and he died in 2001 just after turning 16. Victoria Duval, American tennis player, was diagnosed in 2014. Gerald Finzi, British composer, was diagnosed in 1951 and died in 1956. Mist Edvardsdóttir, Icelandic football player and member of the Icelandic womens national team. Diagnosed in June 2014 at the age of 23. Continued to play until becoming too ill due to chemotherapy. Made recovery in early 2015. Delta Goodrem, Australian singer, songwriter, and actress. She was diagnosed in July 2003 at the age of 18. Jiří Grossmann, Czechoslovak theatre actor, poet, and composer Michael C. Hall (born February 1, 1971), American actor, best known for his lead role as Dexter Morgan, in Showtimes crime series Dexter. In 2010, aged 38, Hall announced he was undergoing treatment for Hodgkin lymphoma; within two years, the disease was in full remission. Richard Harris, Irish actor who portrayed Albus Dumbledore in the first two Harry Potter movies, died on October 25, 2002, after being diagnosed earlier that year. Daniel Hauser, whose mother fled with him in 2009 in order to prevent him from undergoing chemotherapy. Tessa James, Australian actress, was diagnosed in 2014. Sean Kent, American stand up comedian and actor. Was diagnosed in 2002 while writing on a TV show. After three months in remission the cancer returned and he was given an autologous stem cell transplant at City of Hope Cancer Hospital in Los Angeles. Currently lives in Texas with his wife and family and still performs many weeks a year. Mario Lemieux, Hall of Fame NHL player, co-owner of the Pittsburgh Penguins and founder of the Mario Lemieux Foundation, diagnosed in 1993. Dinu Lipatti (1917–1950), Romanian classical pianist and composer. Diagnosed in 1947, received cortisone treatment in 1949; died from a burst abscess on his one lung. Jack Lisowski, English snooker player, diagnosed in 2008 at the age of 16. Mamta Mohandas, Indian film actress and producer, diagnosed in 2010. Nanni Moretti, Italian actor and director. Laura Packard, health care activist diagnosed in 2017, spoke at the 2020 Democratic National Convention. Nikola Pokrivač, Croatian soccer midfielder, diagnosed in 2015. Anthony Rizzo, MLB All-Star first baseman for the New York Yankees, diagnosed in May 2008 while signed as a minor league player for the Boston Red Sox. Dave Roberts, MLB outfielder and manager of the Los Angeles Dodgers. Diagnosed in March 2010 while he was a coach for the San Diego Padres. Chip Roy, Texas congressman. Flip Saunders, head coach of the NBA team Minnesota Timberwolves, announced in August 2015 that he was diagnosed with Hodgkins disease. He died of the disease in October 2015. Brandon Tartikoff, American television executive, diagnosed around 1974, died in 1997. Ethan Zohn,

Hodgkin lymphoma

American professional soccer player and a winner of the Survivor reality television series. Zohn was diagnosed twice (in 2009 and 2011). Arlen Specter, United States Senator from Pennsylvania (1981 - 2011), diagnosed in 2005. He later died from non-Hodgkin lymphoma in 2012. David Brooks, Welsh professional footballer, diagnosed in 2021 while playing for AFC Bournemouth. Bernardo Tengarrinha, Portuguese professional footballer, diagnosed in 2017 Tengarrinha died on October 30, 2021, at the age of 32. [21] Hours later, his former teams FC Porto and Boavista FC paid tribute to him before the local derby. playing for FC Porto. References Further reading Charlotte DeCroes Jacobs. Henry Kaplan and the Story of Hodgkins Disease (Stanford University Press; 2010) 456 pages; combines a biography of the American radiation oncologist (1918–84) with a history of the lymphatic cancer whose treatment he helped to transform. External links Hodgkin lymphoma at Curlie Hodgkin Lymphoma at American Cancer Society Hodgkin Lymphoma at the American National Cancer Institute

Outline of counseling

Counseling is the professional guidance of the individual by utilizing psychological methods especially in collecting case history data, using various techniques of the personal interview, and testing interests and aptitudes.This is a list of counseling topics. Therapeutic modalities Common areas See also List of psychotherapies Outline of communication Outline of psychology Outline of sociology Subfields of sociology Outline of self Psychopharmacology == References ==

Dipylidium caninum

Dipylidium caninum, also called the flea tapeworm, double-pored tapeworm, or cucumber tapeworm (in reference to the shape of its cucumber-seed-like proglottids, though these also resemble grains of rice or sesame seeds), is a cyclophyllid cestode that infects organisms afflicted with fleas and canine chewing lice, including dogs, cats, and sometimes human pet-owners, especially children. Adult morphology The adult worm is about 18 inches (46 cm) long. Gravid proglottids containing the worms microscopic eggs are either passed in the definitive hosts feces or may leave their host spontaneously and are then ingested by microscopic flea larvae (the intermediate hosts) in the surrounding environment. As in all members of family Dipylidiidae, proglottids of the adult worm have genital pores on both sides (hence the name double-pore tapeworm). Each side has a set of male and female reproductive organs. The uterus is paired with 16 to 20 radial branches each. The scolex has a retractable rostellum with four rows of hooks, along with the four suckers that all cyclophyllid cestodes have. Life cycle The definitive host within this life cycle is primarily canines, and occasionally felines, and in rare cases young children. The intermediate hosts include fleas (Ctenocephalides spp.) and chewing lice. The first stage in the life cycle is when the gravid proglottids are either passed out through faecal matter, or actively crawl out of the anus of the host. The gravid proglottids once out of the definitive host release eggs. Then, an intermediate host (the larval stage of a flea or chewing louse) will ingest an egg, which develops into a cysticercoid larva. The cysticercoid larva remains viable, but is not infective to carnivores until the flea hatches to an adult and begins feeding on a host (e.g. a dog). Approximately 36 hours after the flea has consumed a blood meal, the infective metacestode develops inside the flea. The metacestode larva must be ingested in a flea by the dog or cat during grooming in order to develop. Humans can also become infected by D. caninum by accidentally ingesting an infected flea. In the small intestine of the definitive host, the metacestode develops into an adult tapeworm, which reaches maturity 4-6 weeks after ingestion. This adult tapeworm produces proglottids, and over time, the proglottids mature and become gravid and eventually detach from the tapeworm and the life cycle starts all over again. Geographic Distribution This parasite occurs worldwide in animals, such as dogs and cats, as well as in humans, though to a significantly lesser degree. It is the most common tapeworm of dogs and is relatively common in cats. Despite human diplydiasis being rare, instances have been reported from every inhabited continent.Human instances of diplydiasis are reported globally, and unsurprisingly roughly one third of the cases occur in children less than 6 months of age. The most at-risk age group is those that range from 2 months to 4 years old. Pet infections Tapeworm infection usually does not cause pathology in the dog or cat, and most pets show no adverse reaction to infection other than increased appetite. The bulk of infections are asymptomatic and the infections that do result in symptoms are generally mildly so. Pets behavior may reflect the presence of anal discomfort and itching, or pruritus. This could result in the ‘butt-scooching” across the floor, grass or carpeting. It may be accompanied by slight gastrointestinal disturbances, as this is the region where the worms inhabit. Though not a pathology of the diplydiasis, the most unnerving sign of the infection is the presence of proglottids in the animals, or child’s, feces. These proglottids can also be found near the perianal region, in the feces, and in diapers (children). The motile proglottids can actively crawl out of the anus of the infected animal/person and migrate small distances, thus potentially covering this array of neighboring surfaces. It is from these locations that the larval stage of the flea will come along and ingest them. Then the metacestode stage, a cysticercoid, develops in the coelomic cavity (abdominal cavity; main body cavity) of the flea larvae and remains there as the flea matures into an adult. These freshly passed proglottids are motile, allowing them to also be found on the floor and furniture, from a migration out of a pets anus and could be compared to resembling fly larvae, or maggots.The other tapeworm infecting cats is Taenia taeniaeformis, though this form is much less commonly encountered than D. caninum. A recent (2018) study using genetical analysis and experimental infections and life-cycles showed that two different distinct genotypes of D. caninum occur respectively in dogs and in cats, and suggested that two different species might be involved. Human infections A human infection with D. caninum is rare, but if an infection does occur, it is more likely to occur in young children. As of the early 1960s, the number of cases of D. caninum in the U.S. was a mere 21. Therefore, human infection of Dipylidium caninum, or diplydiasis, is a rare occasion. It is largely agreed across the parasitology community that despite the reports of this disease occurring, there are very likely numerous cases that have gone unnoticed and unreported because of its subtle and minor pathology in humans, in addition to its scarceness in clinical records. The adult tapeworm grows within the host for 3–4 weeks after initial infection. The number of parasites the host is initially infected with is directly related to the number of cysticercoid juveniles present in the fleas coelom. The load of parasites present in the humans is lower, luckily, as the life cycle is not occurring in the ideal conditions or species as humans are not the definitive host.Many cases have an unexciting course of infection, as can be depicted in two cases occurring in the 1960s. The first case occurred in a 9-month-old female. Mother found motile proglottids the child’s diaper, later identified as D. caninum. The child had no apparent signs or symptoms. The presumed source of infections was one of the family’s four Labrador retrievers, two of which were found to already have been infected with D. caninum. The second additional case occurred in an 18-month-old male. Mother found motile proglottids in the child’s diaper and again, the child was symptom-free. A puppy in the household was found to be infected and thus was the source of the child infection. Young children and toddlers are at a greater risk of infection because of how they interact with their pets. A human may attain an infection by accidentally ingesting an infected flea through food contamination or through the saliva of pets. Most infections are asymptomatic, but sometimes these symptoms may be identified in an infected individual: mild diarrhea, abdominal colic, anorexia, restlessness, constipation, rectal itching, and pain due to emerging proglottids through the anal cavity. Treatment and prevention As with most tapeworm infections, the drugs of choice to kill adult tapeworms are praziquantel or niclosamide. Pets can be prevented from becoming infested with tapeworm if they are treated prophylactically with a product which kills the intermediate host (the flea) before the infective metacestode can develop. Some isoxazoline products are registered to prevent flea tapeworm infestations using this method. Gallery References External links tapeworms from The Pet Health Library

Periodontosis

Periodontosis is an obsolete term that was used to describe what was once thought to be certain type of unique and distinguishable chronic periodontal disease that manifested as degenerative bony changes without concomitant inflammation. Although utilized for more than 50 years, the term has since been dropped in favor of a more contemporary disease classification for periodontal disease. Described by Gottlieb as a "diffuse atrophy of the alveolar bone," the term periodontosis was later applied and it gained acceptance as a disease entity, being defined as: "a degenerative, noninflammatory destruction of the periodontium, originating in one or more of the periodontal structures and characterized by migrating and loosening of the teeth in the presence or absence of secondary epithelial proliferation and pocket formation or secondary gingival disease."Noted as a rare disease, periodontosis was said to have been seen primarily in young patients. And despite being defined as being a "noninflammatory destruction of the periodontium," almost all cases did exhibit varying degrees of gingival inflammation. References == External links ==

Human leg

The human leg, in the general word sense, is the entire lower limb of the human body, including the foot, thigh or sometimes even the hip or gluteal region. However, the definition in human anatomy refers only to the section of the lower limb extending from the knee to the ankle, also known as the crus or, especially in non-technical use, the shank. Legs are used for standing, and all forms of locomotion including recreational such as dancing, and constitute a significant portion of a persons mass. Female legs generally have greater hip anteversion and tibiofemoral angles, but shorter femur and tibial lengths than those in males. Structure In human anatomy, the lower leg is the part of the lower limb that lies between the knee and the ankle. Anatomists restrict the term leg to this use, rather than to the entire lower limb. The thigh is between the hip and knee and makes up the rest of the lower limb. The term lower limb or lower extremity is commonly used to describe all of the leg. The leg from the knee to the ankle is called the crus. The calf is the back portion, and the tibia or shinbone together with the smaller fibula make up the front of the lower leg. Evolution has provided the human body with two distinct features: the specialization of the upper limb for visually guided manipulation and the lower limbs development into a mechanism specifically adapted for efficient bipedal gait. While the capacity to walk upright is not unique to humans, other primates can only achieve this for short periods and at a great expenditure of energy.The human adaption to bipedalism has also affected the location of the bodys center of gravity, the reorganization of internal organs, and the form and biomechanism of the trunk. In humans, the double S-shaped vertebral column acts as a great shock-absorber which shifts the weight from the trunk over the load-bearing surface of the feet. The human legs are exceptionally long and powerful as a result of their exclusive specialization for support and locomotion—in orangutans the leg length is 111% of the trunk; in chimpanzees 128%, and in humans 171%. Many of the legs muscles are also adapted to bipedalism, most substantially the gluteal muscles, the extensors of the knee joint, and the calf muscles. Skeleton The major bones of the leg are the femur (thigh bone), tibia (shin bone), and adjacent fibula, and these are all long bones. The patella (kneecap) is the sesamoid bone in front of the knee. Most of the leg skeleton has bony prominences and margins that can be palpated and some serve as anatomical landmarks that define the extent of the leg. These landmarks are the anterior superior iliac spine, the greater trochanter, the superior margin of the medial condyle of tibia, and the medial malleolus. Notable exceptions to palpation are the hip joint, and the neck and body, or shaft of the femur. Usually, the large joints of the lower limb are aligned in a straight line, which represents the mechanical longitudinal axis of the leg, the Mikulicz line. This line stretches from the hip joint (or more precisely the head of the femur), through the knee joint (the intercondylar eminence of the tibia), and down to the center of the ankle (the ankle mortise, the fork-like grip between the medial and lateral malleoli). In the tibial shaft, the mechanical and anatomical axes coincide, but in the femoral shaft they diverge 6°, resulting in the femorotibial angle of 174° in a leg with normal axial alignment. A leg is considered straight when, with the feet brought together, both the medial malleoli of the ankle and the medial condyles of the knee are touching. Divergence from the normal femorotibial angle is called genu varum if the center of the knee joint is lateral to the mechanical axis (intermalleolar distance exceeds 3 cm), and genu valgum if it is medial to the mechanical axis (intercondylar distance exceeds 5 cm). These conditions impose unbalanced loads on the joints and stretching of either the thighs adductors and abductors.The angle of inclination formed between the neck and shaft of the femur (collodiaphysial angle) varies with age—about 150° in the newborn, it gradually decreases to 126–128° in adults, to reach 120° in old age. Pathological changes in this angle result in abnormal posture of the leg: a small angle produces coxa vara and a large angle coxa valga; the latter is usually combined with genu varum, and coxa vara leads genu valgum. Additionally, a line drawn through the femoral neck superimposed on a line drawn through the femoral condyles forms an angle, the torsion angle, which makes it possible for flexion movements of the hip joint to be transposed into rotary movements of the femoral head. Abnormally increased torsion angles result in a limb turned inward and a decreased angle in a limb turned outward; both cases resulting in a reduced range of a persons mobility. Muscles Hip There are several ways of classifying the muscles of the hip: By location or innervation (ventral and dorsal divisions of the plexus layer); By development on the basis of their points of insertion (a posterior group in two layers and an anterior group); and By function (i.e. extensors, flexors, adductors, and abductors).Some hip muscles also act either on the knee joint or on vertebral joints. Additionally, because the areas of origin and insertion of many of these muscles are very extensive, these muscles are often involved in several very different movements. In the hip joint, lateral and medial rotation occur along the axis of the limb; extension (also called dorsiflexion or retroversion) and flexion (anteflexion or anteversion) occur along a transverse axis; and abduction and adduction occur about a sagittal axis.The anterior dorsal hip muscles are the iliopsoas, a group of two or three muscles with a shared insertion on the lesser trochanter of the femur. The psoas major originates from the last vertebra and along the lumbar spine to stretch down into the pelvis. The iliacus originates on the iliac fossa on the interior side of the pelvis. The two muscles unite to form the iliopsoas muscle, which is inserted on the lesser trochanter of the femur. The psoas minor, only present in about 50 per cent of subjects, originates above the psoas major to stretch obliquely down to its insertion on the interior side of the major muscle.The posterior dorsal hip muscles are inserted on or directly below the greater trochanter of the femur. The tensor fasciae latae, stretching from the anterior superior iliac spine down into the iliotibial tract, presses the head of the femur into the acetabulum but also flexes, rotates medially, and abducts to hip joint. The piriformis originates on the anterior pelvic surface of the sacrum, passes through the greater sciatic foramen, and inserts on the posterior aspect of the tip of the greater trochanter. In a standing posture it is a lateral rotator, but it also assists extending the thigh. The gluteus maximus has its origin between (and around) the iliac crest and the coccyx, from where one part radiates into the iliotibial tract and the other stretches down to the gluteal tuberosity under the greater trochanter. The gluteus maximus is primarily an extensor and lateral rotator of the hip joint, and it comes into action when climbing stairs or rising from a sitting to a standing posture. Furthermore, the part inserted into the fascia latae abducts and the part inserted into the gluteal tuberosity adducts the hip. The two deep glutei muscles, the gluteus medius and minimus, originate on the lateral side of the pelvis. The medius muscle is shaped like a cap. Its anterior fibers act as a medial rotator and flexor; the posterior fibers as a lateral rotator and extensor; and the entire muscle abducts the hip. The minimus has similar functions and both muscles are inserted onto the greater trochanter. The ventral hip muscles function as lateral rotators and play an important role in the control of the bodys balance. Because they are stronger than the medial rotators, in the normal position of the leg, the apex of the foot is pointing outward to achieve better support. The obturator internus originates on the pelvis on the obturator foramen and its membrane, passes through the lesser sciatic foramen, and is inserted on the trochanteric fossa of the femur. "Bent" over the lesser sciatic notch, which acts as a fulcrum, the muscle forms the strongest lateral rotators of the hip together with the gluteus maximus and quadratus femoris. When sitting with the knees flexed it acts as an abductor. The obturator externus has a parallel course with its origin located on the posterior border of the obturator foramen. It is covered by several muscles and acts as a lateral rotator and a weak adductor. The inferior and superior gemelli muscles represent marginal heads of the obturator internus and assist this muscle. These three muscles form a three-headed muscle (tricipital) known as the triceps coxae. The quadratus femoris originates at the ischial tuberosity and is inserted onto the intertrochanteric crest between the trochanters. This flattened muscle act as a strong lateral rotator and adductor of the thigh. The adductor muscles of the thigh are innervated by the obturator nerve, with the exception of pectineus which receives fibers from the femoral nerve, and the adductor magnus which receives fibers from the tibial nerve. The gracilis arises from near the pubic symphysis and is unique among the adductors in that it reaches past the knee to attach on the medial side of the shaft of the tibia, thus acting on two joints. It share its distal insertion with the sartorius and semitendinosus, all three muscles forming the pes anserinus. It is the most medial muscle of the adductors, and with the thigh abducted its origin can be clearly seen arching under the skin. With the knee extended, it adducts the thigh and flexes the hip. The pectineus has its origin on the iliopubic eminence laterally to the gracilis and, rectangular in shape, extends obliquely to attach immediately behind the lesser trochanter and down the pectineal line and the proximal part of the linea aspera on the femur. It is a flexor of the hip joint, and an adductor and a weak medial rotator of the thigh. The adductor brevis originates on the inferior ramus of the pubis below the gracilis and stretches obliquely below the pectineus down to the upper third of the linea aspera. Except for being an adductor, it is a lateral rotator and weak flexor of the hip joint.The adductor longus has its origin at superior ramus of the pubis and inserts medially on the middle third of the linea aspera. Primarily an adductor, it is also responsible for some flexion. The adductor magnus has its origin just behind the longus and lies deep to it. Its wide belly divides into two parts: One is inserted into the linea aspera and the tendon of the other reaches down to adductor tubercle on the medial side of the femurs distal end where it forms an intermuscular septum that separates the flexors from the extensors. Magnus is a powerful adductor, especially active when crossing legs. Its superior part is a lateral rotator but the inferior part acts as a medial rotator on the flexed leg when rotated outward and also extends the hip joint. The adductor minimus is an incompletely separated subdivision of the adductor magnus. Its origin forms an anterior part of the magnus and distally it is inserted on the linea aspera above the magnus. It acts to adduct and lateral rotate the femur. Thigh The muscles of the thigh can be classified into three groups according to their location: anterior and posterior muscles and the adductors (on the medial side). All the adductors except gracilis insert on the femur and act on the hip joint, and so functionally qualify as hip muscles. The majority of the thigh muscles, the "true" thigh muscles, insert on the leg (either the tibia or the fibula) and act primarily on the knee joint. Generally, the extensors lie on anterior of the thigh and flexors lie on the posterior. Even though the sartorius flexes the knee, it is ontogenetically considered an extensor since its displacement is secondary. Of the anterior thigh muscles the largest are the four muscles of the quadriceps femoris: the central rectus femoris, which is surrounded by the three vasti, the vastus intermedius, medialis, and lateralis. Rectus femoris is attached to the pelvis with two tendons, while the vasti are inserted to the femur. All four muscles unite in a common tendon inserted into the patella from where the patellar ligament extends it down to the tibial tuberosity. Fibers from the medial and lateral vasti form two retinacula that stretch past the patella on either sides down to the condyles of the tibia. The quadriceps is the knee extensor, but the rectus femoris additionally flexes the hip joint, and articular muscle of the knee protects the articular capsule of the knee joint from being nipped during extension. The sartorius runs superficially and obliquely down on the anterior side of the thigh, from the anterior superior iliac spine to the pes anserinus on the medial side of the knee, from where it is further extended into the crural fascia. The sartorius acts as a flexor on both the hip and knee, but, due to its oblique course, also contributes to medial rotation of the leg as one of the pes anserinus muscles (with the knee flexed), and to lateral rotation of the hip joint.There are four posterior thigh muscles. The biceps femoris has two heads: The long head has its origin on the ischial tuberosity together with the semitendinosus and acts on two joints. The short head originates from the middle third of the linea aspera on the shaft of the femur and the lateral intermuscular septum of thigh, and acts on only one joint. These two heads unite to form the biceps which inserts on the head of the fibula. The biceps flexes the knee joint and rotates the flexed leg laterally—it is the only lateral rotator of the knee and thus has to oppose all medial rotator. Additionally, the long head extends the hip joint. The semitendinosus and the semimembranosus share their origin with the long head of the biceps, and both attaches on the medial side of the proximal head of the tibia together with the gracilis and sartorius to form the pes anserinus. The semitendinosus acts on two joints; extension of the hip, flexion of the knee, and medial rotation of the leg. Distally, the semimembranosus tendon is divided into three parts referred to as the pes anserinus profondus. Functionally, the semimembranosus is similar to the semitendinosus, and thus produces extension at the hip joint and flexion and medial rotation at the knee. Posteriorly below the knee joint, the popliteus stretches obliquely from the lateral femoral epicondyle down to the posterior surface of the tibia. The subpopliteal bursa is located deep to the muscle. Popliteus flexes the knee joint and medially rotates the leg. Lower leg and foot With the popliteus (see above) as the single exception, all muscles in the leg are attached to the foot and, based on location, can be classified into an anterior and a posterior group separated from each other by the tibia, the fibula, and the interosseous membrane. In turn, these two groups can be subdivided into subgroups or layers—the anterior group consists of the extensors and the peroneals, and the posterior group of a superficial and a deep layer. Functionally, the muscles of the leg are either extensors, responsible for the dorsiflexion of the foot, or flexors, responsible for the plantar flexion. These muscles can also classified by innervation, muscles supplied by the anterior subdivision of the plexus and those supplied by the posterior subdivision. The leg muscles acting on the foot are called the extrinsic foot muscles whilst the foot muscles located in the foot are called intrinsic.Dorsiflexion (extension) and plantar flexion occur around the transverse axis running through the ankle joint from the tip of the medial malleolus to the tip of the lateral malleolus. Pronation (eversion) and supination (inversion) occur along the oblique axis of the ankle joint. Extrinsic Three of the anterior muscles are extensors. From its origin on the lateral surface of the tibia and the interosseus membrane, the three-sided belly of the tibialis anterior extends down below the superior and inferior extensor retinacula to its insertion on the plantar side of the medial cuneiform bone and the first metatarsal bone. In the non-weight-bearing leg, the anterior tibialis dorsal flexes the foot and lifts the medial edge of the foot. In the weight-bearing leg, it pulls the leg towards the foot. The extensor digitorum longus has a wide origin stretching from the lateral condyle of the tibia down along the anterior side of the fibula, and the interosseus membrane. At the ankle, the tendon divides into four that stretch across the foot to the dorsal aponeuroses of the last phalanges of the four lateral toes. In the non-weight-bearing leg, the muscle extends the digits and dorsiflexes the foot, and in the weight-bearing leg acts similar to the tibialis anterior. The extensor hallucis longus has its origin on the fibula and the interosseus membrane between the two other extensors and is, similarly to the extensor digitorum, is inserted on the last phalanx of big toe ("hallux"). The muscle dorsiflexes the hallux, and acts similar to the tibialis anterior in the weight-bearing leg. Two muscles on the lateral side of the leg form the fibular (peroneal) group. The fibularis (peroneus) longus and fibularis (peroneus) brevis both have their origins on the fibula, and they both pass behind the lateral malleolus where their tendons pass under the fibular retinacula. Under the foot, the fibularis longus stretches from the lateral to the medial side in a groove, thus bracing the transverse arch of the foot. The fibularis brevis is attached on the lateral side to the tuberosity of the fifth metatarsal. Together, these two fibularis muscles form the strongest pronators of the foot. The fibularis muscles are highly variable, and several variants can occasionally be present. Of the posterior muscles three are in the superficial layer. The major plantar flexors, commonly referred to as the triceps surae, are the soleus, which arises on the proximal side of both leg bones, and the gastrocnemius, the two heads of which arises on the distal end of the femur. These muscles unite in a large terminal tendon, the Achilles tendon, which is attached to the posterior tubercle of the calcaneus. The plantaris closely follows the lateral head of the gastrocnemius. Its tendon runs between those of the soleus and gastrocnemius and is embedded in the medial end of the calcaneus tendon.In the deep layer, the tibialis posterior has its origin on the interosseus membrane and the neighbouring bone areas and runs down behind the medial malleolus. Under the foot it splits into a thick medial part attached to the navicular bone and a slightly weaker lateral part inserted to the three cuneiform bones. The muscle produces simultaneous plantar flexion and supination in the non-weight-bearing leg, and approximates the heel to the calf of the leg. The flexor hallucis longus arises distally on the fibula and on the interosseus membrane from where its relatively thick muscle belly extends far distally. Its tendon extends beneath the flexor retinaculum to the sole of the foot and finally attaches on the base of the last phalanx of the hallux. It plantarflexes the hallux and assists in supination. The flexor digitorum longus, finally, has its origin on the upper part of the tibia. Its tendon runs to the sole of the foot where it forks into four terminal tendon attached to the last phalanges of the four lateral toes. It crosses the tendon of the tibialis posterior distally on the tibia, and the tendon of the flexor hallucis longus in the sole. Distally to its division, the quadratus plantae radiates into it and near the middle phalanges its tendons penetrate the tendons of the flexor digitorum brevis. In the non-weight-bearing leg, it plantar flexes the toes and foot and supinates. In the weight-bearing leg it supports the plantar arch. (For the popliteus, see above.) Intrinsic The intrinsic muscles of the foot, muscles whose bellies are located in the foot proper, are either dorsal (top) or plantar (sole). On the dorsal side, two long extrinsic extensor muscles are superficial to the intrinsic muscles, and their tendons form the dorsal aponeurosis of the toes. The short intrinsic extensors and the plantar and dorsal interossei radiates into these aponeuroses. The extensor digitorum brevis and extensor hallucis brevis have a common origin on the anterior side of the calcaneus, from where their tendons extend into the dorsal aponeuroses of digits 1–4. They act to dorsiflex these digits.The plantar muscles can be subdivided into three groups associated with three regions: those of the big digit, the little digit, and the region between these two. All these muscles are covered by the thick and dense plantar aponeurosis, which, together with two tough septa, form the spaces of the three groups. These muscles and their fatty tissue function as cushions that transmit the weight of the body downward. As a whole, the foot is a functional entity. The abductor hallucis stretches along the medial edge of the foot, from the calcaneus to the base of the first phalanx of the first digit and the medial sesamoid bone. It is an abductor and a weak flexor, and also helps maintain the arch of the foot. Lateral to the abductor hallucis is the flexor hallucis brevis, which originates from the medial cuneiform bone and from the tendon of the tibialis posterior. The flexor hallucis has a medial and a lateral head inserted laterally to the abductor hallucis. It is an important plantar flexor which comes into prominent use in classical ballet (i.e. for pointe work). The adductor hallucis has two heads; a stronger oblique head which arises from the cuboid and lateral cuneiform bones and the bases of the second and third metatarsals; and a transverse head which arises from the distal ends of the third-fifth metatarsals. Both heads are inserted on the lateral sesamoid bone of the first digit. The muscle acts as a tensor to the arches of the foot, but can also adduct the first digit and plantar flex its first phalanx.The opponens digiti minimi originates from the long plantar ligament and the plantar tendinous sheath of the fibularis (peroneus) longus and is inserted on the fifth metatarsal. When present, it acts to plantar flex the fifth digit and supports the plantar arch. The flexor digiti minimi arises from the region of base of the fifth metatarsal and is inserted onto the base of the first phalanx of the fifth digit where it is usually merged with the abductor of the first digit. It acts to plantar flex the last digit. The largest and longest muscles of the little toe is the abductor digiti minimi. Stretching from the lateral process of the calcaneus, with a second attachment on the base of the fifth metatarsal, to the base of the fifth digits first phalanx, the muscle forms the lateral edge of the sole. Except for supporting the arch, it plantar flexes the little toe and also acts as an abductor.The four lumbricales have their origin on the tendons of the flexor digitorum longus, from where they extend to the medial side of the bases of the first phalanx of digits two-five. Except for reinforcing the plantar arch, they contribute to plantar flexion and move the four digits toward the big toe. They are, in contrast to the lumbricales of the hand, rather variable, sometimes absent and sometimes more than four are present. The quadratus plantae arises with two slips from margins of the plantar surface of the calcaneus and is inserted into the tendon(s) of the flexor digitorum longus, and is known as the "plantar head" of this latter muscle. The three plantar interossei arise with their single heads on the medial side of the third-fifth metatarsals and are inserted on the bases of the first phalanges of these digits. The two heads of the four dorsal interossei arise on two adjacent metatarsals and merge in the intermediary spaces. Their distal attachment is on the bases of the proximal phalanges of the second-fourth digits. The interossei are organized with the second digit as a longitudinal axis; the plantars act as adductors and pull digits 3–5 towards the second digit; while the dorsals act as abductors. Additionally, the interossei act as plantar flexors at the metatarsophalangeal joints. Lastly, the flexor digitorum brevis arises from underneath the calcaneus to insert its tendons on the middle phalanges of digit 2–4. Because the tendons of the flexor digitorum longus run between these tendons, the brevis is sometimes called perforatus. The tendons of these two muscles are surrounded by a tendinous sheath. The brevis acts to plantar flex the middle phalanges. Flexibility Flexibility can be simply defined as the available range of motion (ROM) provided by a specific joint or group of joints. For the most part, exercises that increase flexibility are performed with intentions to boost overall muscle length, reduce the risks of injury and to potentially improve muscular performance in physical activity. Stretching muscles after engagement in any physical activity can improve muscular strength, increase flexibility, and reduce muscle soreness. If limited movement is present within a joint, the "insufficient extensibility" of the muscle, or muscle group, could be restricting the activity of the affected joint. Stretching Stretching prior to strenuous physical activity has been thought to increase muscular performance by extending the soft tissue past its attainable length in order to increase range of motion. Many physically active individuals practice these techniques as a “warm-up” in order to achieve a certain level of muscular preparation for specific exercise movements. When stretching, muscles should feel somewhat uncomfortable but not physically agonizing. Plantar flexion: One of the most popular lower leg muscle stretches is the step standing heel raises, which mainly involves the gastrocnemius, soleus, and the Achilles tendon. Standing heel raises allow the individual to activate their calf muscles by standing on a step

Human leg

with toes and forefoot, leaving the heel hanging off the step, and plantar flexing the ankle joint by raising the heel. This exercise is easily modified by holding on to a nearby rail for balance and is generally repeated 5–10 times. Dorsiflexion: In order to stretch the anterior muscles of the lower leg, crossover shin stretches work well. This motion will stretch the dorsiflexion muscles, mainly the anterior tibialis, extensor hallucis longus and extensor digitorum longus, by slowly causing the muscles to lengthen as body weight is leaned on the ankle joint by using the floor as resistance against the top of the foot. Crossover shin stretches can vary in intensity depending on the amount of body weight applied on the ankle joint as the individual bends at the knee. This stretch is typically held for 15–30 seconds. Eversion and inversion: Stretching the eversion and inversion muscles allows for better range of motion to the ankle joint. Seated ankle elevations and depressions will stretch the fibularis (peroneus) and tibilalis muscles that are associated with these movements as they lengthen. Eversion muscles are stretched when the ankle becomes depressed from the starting position. In like manner, the inversion muscles are stretched when the ankle joint becomes elevated. Throughout this seated stretch, the ankle joint is to remain supported while depressed and elevated with the ipsilateral (same side) hand in order to sustain the stretch for 10–15 seconds. This stretch will increase overall eversion and inversion muscle group length and provide more flexibility to the ankle joint for larger range of motion during activity. Blood supply The arteries of the leg are divided into a series of segments. In the pelvis area, at the level of the last lumbar vertebra, the abdominal aorta, a continuation the descending aorta, splits into a pair of common iliac arteries. These immediately split into the internal and external iliac arteries, the latter of which descends along the medial border of the psoas major to exits the pelvis area through the vascular lacuna under the inguinal ligament.The artery enters the thigh as the femoral artery which descends the medial side of the thigh to the adductor canal. The canal passes from the anterior to the posterior side of the limb where the artery leaves through the adductor hiatus and becomes the popliteal artery. On the back of the knee the popliteal artery runs through the popliteal fossa to the popliteal muscle where it divides into anterior and posterior tibial arteries.In the lower leg, the anterior tibial enters the extensor compartment near the upper border of the interosseus membrane to descend between the tibialis anterior and the extensor hallucis longus. Distal to the superior and extensor retinacula of the foot it becomes the dorsal artery of the foot. The posterior tibial forms a direct continuation of the popliteal artery which enters the flexor compartment of the lower leg to descend behind the medial malleolus where it divides into the medial and lateral plantar arteries, of which the posterior branch gives rise to the fibular artery.For practical reasons the lower limb is subdivided into somewhat arbitrary regions: The regions of the hip are all located in the thigh: anteriorly, the subinguinal region is bounded by the inguinal ligament, the sartorius, and the pectineus and forms part of the femoral triangle which extends distally to the adductor longus. Posteriorly, the gluteal region corresponds to the gluteus maximus. The anterior region of the thigh extends distally from the femoral triangle to the region of the knee and laterally to the tensor fasciae latae. The posterior region ends distally before the popliteal fossa. The anterior and posterior regions of the knee extend from the proximal regions down to the level of the tuberosity of the tibia. In the lower leg the anterior and posterior regions extend down to the malleoli. Behind the malleoli are the lateral and medial retromalleolar regions and behind these is the region of the heel. Finally, the foot is subdivided into a dorsal region superiorly and a plantar region inferiorly. Veins The veins are subdivided into three systems. The deep veins return approximately 85 percent of the blood and the superficial veins approximately 15 percent. A series of perforator veins interconnect the superficial and deep systems. In the standing posture, the veins of the leg have to handle an exceptional load as they act against gravity when they return the blood to the heart. The venous valves assist in maintaining the superficial to deep direction of the blood flow.Superficial veins: Great saphenous vein Small saphenousDeep veins: Femoral vein, whose segments are the common femoral vein and the subsartorial vein. Popliteal vein Anterior tibial vein Posterior tibial vein Fibular vein Nerve supply The sensory and motor innervation to the lower limb is supplied by the lumbosacral plexus, which is formed by the ventral rami of the lumbar and sacral spinal nerves with additional contributions from the subcostal nerve (T12) and coccygeal nerve (Co1). Based on distribution and topography, the lumbosacral plexus is subdivided into the lumbar plexus (T12-L4) and the Sacral plexus (L5-S4); the latter is often further subdivided into the sciatic and pudendal plexuses:The lumbar plexus is formed lateral to the intervertebral foramina by the ventral rami of the first four lumbar spinal nerves (L1-L4), which all pass through psoas major. The larger branches of the plexus exit the muscle to pass sharply downward to reach the abdominal wall and the thigh (under the inguinal ligament); with the exception of the obturator nerve which pass through the lesser pelvis to reach the medial part of the thigh through the obturator foramen. The nerves of the lumbar plexus pass in front of the hip joint and mainly support the anterior part of the thigh.The iliohypogastric (T12-L1) and ilioinguinal nerves (L1) emerge from the psoas major near the muscles origin, from where they run laterally downward to pass anteriorly above the iliac crest between the transversus abdominis and abdominal internal oblique, and then run above the inguinal ligament. Both nerves give off muscular branches to both these muscles. Iliohypogastric supplies sensory branches to the skin of the lateral hip region, and its terminal branch finally pierces the aponeurosis of the abdominal external oblique above the inguinal ring to supply sensory branches to the skin there. Ilioinguinalis exits through the inguinal ring and supplies sensory branches to the skin above the pubic symphysis and the lateral portion of the scrotum.The genitofemoral nerve (L1, L2) leaves psoas major below the two former nerves, immediately divides into two branches that descends along the muscles anterior side. The sensory femoral branch supplies the skin below the inguinal ligament, while the mixed genital branch supplies the skin and muscles around the sex organ. The lateral femoral cutaneous nerve (L2, L3) leaves psoas major laterally below the previous nerve, runs obliquely and laterally downward above the iliacus, exits the pelvic area near the iliac spine, and supplies the skin of the anterior thigh.The obturator nerve (L2-L4) passes medially behind psoas major to exit the pelvis through the obturator canal, after which it gives off branches to obturator externus and divides into two branches passing behind and in front of adductor brevis to supply motor innervation to all the other adductor muscles. The anterior branch also supplies sensory nerves to the skin on a small area on the distal medial aspect of the thigh. The femoral nerve (L2-L4) is the largest and longest of the nerves of the lumbar plexus. It supplies motor innervation to iliopsoas, pectineus, sartorius, and quadriceps; and sensory branches to the anterior thigh, medial lower leg, and posterior foot.The nerves of the sacral plexus pass behind the hip joint to innervate the posterior part of the thigh, most of the lower leg, and the foot. The superior (L4-S1) and inferior gluteal nerves (L5-S2) innervate the gluteus muscles and the tensor fasciae latae. The posterior femoral cutaneous nerve (S1-S3) contributes sensory branches to the skin on the posterior thigh. The sciatic nerve (L4-S3), the largest and longest nerve in the human body, leaves the pelvis through the greater sciatic foramen. In the posterior thigh it first gives off branches to the short head of the biceps femoris and then divides into the tibial (L4-S3) and common fibular nerves (L4-S2). The fibular nerve continues down on the medial side of biceps femoris, winds around the fibular neck and enters the front of the lower leg. There it divides into a deep and a superficial terminal branch. The superficial branch supplies the fibularis muscles and the deep branch enters the extensor compartment; both branches reaches into the dorsal foot. In the thigh, the tibial nerve gives off branches to semitendinosus, semimembranosus, adductor magnus, and the long head of the biceps femoris. The nerve then runs straight down the back of the leg, through the popliteal fossa to supply the ankle flexors on the back of the lower leg and then continues down to supply all the muscles in the sole of the foot. The pudendal (S2-S4) and coccygeal nerves (S5-Co2) supply the muscles of the pelvic floor and the surrounding skin.The lumbosacral trunk is a communicating branch passing between the sacral and lumbar plexuses containing ventral fibers from L4. The coccygeal nerve, the last spinal nerve, emerges from the sacral hiatus, unites with the ventral rami of the two last sacral nerves, and forms the coccygeal plexus. Lower leg and foot The lower leg and ankle need to keep exercised and moving well as they are the base of the whole body. The lower extremities must be strong in order to balance the weight of the rest of the body, and the gastrocnemius muscles take part in much of the blood circulation. Exercises Isometric and standard There are a number of exercises that can be done to strengthen the lower leg. For example, in order to activate plantar flexors in the deep plantar flexors one can sit on the floor with the hips flexed, the ankle neutral with knees fully extended as they alternate pushing their foot against a wall or platform. This kind of exercise is beneficial as it hardly causes any fatigue. Another form of isometric exercise for the gastrocnemius would be seated calf raises which can be done with or without equipment. One can be seated at a table with their feet flat on the ground, and then plantar flex both ankles so that the heels are raised off the floor and the gastrocnemius flexed. An alternate movement could be heel drop exercises with the toes being propped on an elevated surface—as an opposing movement this would improve the range of motion. One-legged toe raises for the gastrocnemius muscle can be performed by holding one dumbbell in one hand while using the other for balance, and then standing with one foot on a plate. The next step would be to plantar flex and keep the knee joint straight or flexed slightly. The triceps surae is contracted during this exercise. Stabilization exercises like the BOSU ball squat are also important especially as they assist in the ankles having to adjust to the balls form in order to balance. Clinical significance Lower leg injury Lower leg injuries are common while running or playing sports. About 10% of all injuries in athletes involve the lower extremities. The majority of athletes sprain their ankles; this is mainly caused by the increased loads onto the feet when they move into the foot down or in an outer ankle position. All areas of the foot, which are the forefoot, midfoot, and rearfoot, absorb various forces while running and this can also lead to injuries. Running and various activities can cause stress fractures, tendinitis, musculotendinous injuries, or any chronic pain to our lower extremities such as the tibia. Types of activities Injuries to quadriceps or hamstrings are caused by the constant impact loads to the legs during activities, such as kicking a ball. While doing this type of motion, 85% of that shock is absorbed to the hamstrings; this can cause strain to those muscles. Jumping – is another risk because if the legs do not land properly after an initial jump, there may be damage to the meniscus in the knees, sprain to the ankle by everting or inverting the foot, or damage to the Achilles tendon and gastrocnemius if there is too much force while plantar flexing. Weight lifting – such as the improperly performed deep squat, is also dangerous to the lower limbs, because the exercise can lead to an overextension, or an outstretch, of our ligaments in the knee and can cause pain over time. Running – the most common activity associated with lower leg injury. There is constant pressure and stress being put on the feet, knees, and legs while running by gravitational force. Muscle tears in our legs or pain in various areas of the feet can be a result of poor biomechanics of running. Running The most common injuries in running involve the knees and the feet. Various studies have focused on the initial cause of these running related injuries and found that there are many factors that correlate to these injuries. Female distance runners who had a history of stress fracture injuries had higher vertical impact forces than non-injured subjects. The large forces onto the lower legs were associated with gravitational forces, and this correlated with patellofemoral pain or potential knee injuries. Researchers have also found that these running-related injuries affect the feet as well, because runners with previous injuries showed more foot eversion and over-pronation while running than non-injured runners. This causes more loads and forces on the medial side of the foot, causing more stress on the tendons of the foot and ankle. Most of these running injuries are caused by overuse: running longer distances weekly for a long duration is a risk for injuring the lower legs. Prevention tools Voluntary stretches to the legs, such as the wall stretch, condition the hamstrings and the calf muscle to various movements before vigorously working them. The environment and surroundings, such as uneven terrain, can cause the feet to position in an unnatural way, so wearing shoes that can absorb forces from the grounds impact and allow for stabilizing the feet can prevent some injuries while running as well. Shoes should be structured to allow friction-traction at the shoe surface, space for different foot-strike stresses, and for comfortable, regular arches for the feet. Summary The chance of damaging our lower extremities will be reduced by having knowledge about some activities associated with lower leg injury and developing a correct form of running, such as not over-pronating the foot or overusing the legs. Preventative measures, such as various stretches, and wearing appropriate footwear, will also reduce injuries. Fracture A fracture of the leg can be classified according to the involved bone into: Femoral fracture (in the upper leg) Crus fracture (in the lower leg) Pain management Lower leg and foot pain management is critical in reducing the progression of further injuries, uncomfortable sensations and limiting alterations while walking and running. Most individuals suffer from various pains in their lower leg and foot due to different factors. Muscle inflammation, strain, tenderness, swelling and muscle tear from muscle overuse or incorrect movement are several conditions often experienced by athletes and the common public during and after high impact physical activities. Therefore, suggested pain management mechanisms are provided to reduce pain and prevent the progression of injury. Plantar fasciitis A plantar fasciitis foot stretch is one of the recommended methods to reduce pain caused by plantar fasciitis (Figure 1). To do the plantar fascia stretch, while sitting in a chair place the ankle on the opposite knee and hold the toes of the impaired foot, slowly pulling back. The stretch should be held for approximately ten seconds, three times per day. Medial tibial stress syndrome (shin splint) Several methods can be utilized to help control pain caused by shin splints. Placing ice on the affected area prior to and after running will aid in reducing pain. In addition, wearing orthotic devices including a neoprene sleeve (Figure 2) and wearing appropriate footwear such as a foot arch can help to eliminate the condition. Stretching and strengthening of the anterior tibia or medial tibia by performing exercises of plantar and dorsi flexors such as calf stretch can also help in easing the pain. Achilles tendinopathy There are numerous appropriate approaches to handling pain resulting from Achilles tendinitis. The primary action is to rest. Activities that do not provide additional stress to the affected tendon are also recommended. Wearing orthothics or prostheses will provide cushion and will prevent the affected Achilles tendon from experiencing further stress when walking and performing therapeutic stretches. A few stretch modalities or eccentric exercises such as toe extension and flexion and calf and heel stretch are beneficial in lowering pain with Achilles tendinopathy patients (Figure 4) Society and culture Adolescent and adult women in many Western cultures often remove the hair from their legs. Toned, tanned, shaved legs are sometimes perceived as a sign of youthfulness and are often considered attractive in these cultures. Men generally do not shave their legs in any culture. However, leg-shaving is a generally accepted practice in modeling. It is also fairly common in sports where the hair removal makes the athlete appreciably faster by reducing drag; the most common case of this is competitive swimming. Image gallery See also Distraction osteogenesis (leg lengthening) References Literature specified by multiple pages above: Chaitow, Leon; Walker DeLany, Judith (2000). Clinical Application of Neuromuscular Techniques: The Lower Body. Elsevier Health Sciences. ISBN 0-443-06284-6. Archived from the original on 22 September 2014. consulting editors, Lawrence M. Ross, Edward D. Lamperti; authors, Michael Schuenke, Erik Schulte, Udo Schumacher. (2006). Thieme Atlas of Anatomy: General Anatomy and Musculoskeletal System. Thieme. ISBN 1-58890-419-9. {{cite book}}: |author= has generic name (help)CS1 maint: multiple names: authors list (link) Platzer, Werner (2004). Color Atlas of Human Anatomy, Vol. 1: Locomotor System (5th ed.). Thieme. ISBN 3-13-533305-1. External links Interactive images at InnerBody

Fibrothorax

Fibrothorax is a medical condition characterised by severe scarring (fibrosis) and fusion of the layers of the pleural space surrounding the lungs resulting in decreased movement of the lung and ribcage. The main symptom of fibrothorax is shortness of breath. There also may be recurrent fluid collections surrounding the lungs. Fibrothorax may occur as a complication of many diseases, including infection of the pleural space known as an empyema or bleeding into the pleural space known as a haemothorax.Fibrosis in the pleura may be produced intentionally using a technique called pleurodesis to prevent recurrent punctured lung (pneumothorax), and the usually limited fibrosis that this produces can rarely be extensive enough to lead to fibrothorax. The condition is most often diagnosed using an X-ray or CT scan, the latter more readily detecting mild cases. Fibrothorax is often treated conservatively with watchful waiting but may require surgery. The outlook is usually good as long as there is no underlying pulmonary fibrosis or complications following surgery. The disease is highly uncommon. Signs and symptoms Signs Reduced movement of the ribcage during breathing, reduced breath sounds on the affected side(s), and a dull feeling when the chest is pressed are common signs observed during examination for fibrothorax. Sharp chest pain with deep breaths or coughing may be seen in some cases. Severe cases of fibrothorax can lead to respiratory failure due to inadequate ventilation and cause abnormally high levels of carbon dioxide in the bloodstream. Symptoms The condition only causes symptoms if the visceral pleura is affected. Although fibrothorax may not cause any symptoms, people affected by the disorder may report shortness of breath. Persistent, recurrent pleural effusions are a possible symptom, caused by the persistent cavity formed by the hardening pleura around the original fluid collection. Shortness of breath tends to develop gradually and may worsen over time. Less commonly, fibrothorax may cause chest discomfort or a dry cough. Fibrothorax may occur as a complication of other diseases. Symptoms of the underlying problem are sometimes seen, for example, fever in cases of empyema. Causes Fibrothorax is often a complication of other diseases that cause inflammation of the pleura. These include infections such as an empyema or tuberculosis, or bleeding within the pleural space known as a haemothorax. Exposure to certain substances, such as asbestos, can cause generalised fibrosis of the lungs, which may involve the pleura and lead to fibrothorax. Less common causes of fibrothorax include collagen vascular diseases such as systemic lupus erythematosus, sarcoidosis, and rheumatoid arthritis; kidney failure leading to uraemia; and side effects of certain medications. The medications most commonly associated with pleural fibrosis are the ergot alkaloids bromocriptine, pergolide, and methysergide. Fibrothorax may also occur without a clear underlying cause, in which case it is known as idiopathic fibrothorax. A technique called pleurodesis can be used to intentionally create scar tissue within the pleural space, usually as a treatment for repeated episodes of a punctured lung, known as a pneumothorax, or for pleural effusions caused by cancer. While this procedure usually generates only limited scar tissue, in rare cases a fibrothorax can develop. Mechanism Fibrosis can affect one or both of the two layers of tissue forming the pleura—the visceral pleura adjacent to the lung and the parietal pleura adjacent to the ribcage. The term fibrothorax implies severe fibrosis affecting both the visceral and the outer (parietal) pleura, fusing the lung to the chest wall. The condition starts as an undrained pleural effusion. Over time, the undrained pleural effusion causes sustained inflammation of the pleura, which can then lead to deposition of fibrin in the pleura and the development of a fibrotic scar. Eventually, a "peel" that is rich in collagen forms around the fluid collection. From this point, the illness can no longer be treated with thoracentesis, since the fluid will return to the cavity maintained by the peel.Over time, generally over the years, the fibrotic scar tissue slowly tightens and thickens, contracting the contents of one or both halves of the chest and reducing the mobility of the ribs. The peel can become deeper than 2 cm. Within the chest, the lung is compressed and unable to expand (trapped lung), making it vulnerable to collapse and causing breathlessness. Restrictive lung disease from fibrothorax may occur when pleural fibrosis is so severe that it involves the diaphragm and ribcage and results primarily from decreased rib movement. Microscopic At the microscopic level, collagen fibres deposit in a basket weave pattern and form scar tissue. Usually, the underlying condition has to cause intense inflammation of the pleura, though it is unclear exactly how this results in fibrosis. The precise mechanisms producing the fibrosis are not entirely clear. However, research indicates a protein called Transforming Growth Factor beta (TGF-β) plays a central role in producing fibrothorax. Anti-TGF-β antibodies prevent fibrothorax in empyema in animal models. Diagnosis A fibrothorax can typically be diagnosed by taking an appropriate medical history in combination with the use of appropriate imaging techniques such as a plain chest X-ray or CT scan. These imaging techniques can detect fibrothorax and pleural thickening that surround the lungs. The presence of a thickened peel with or without calcification are common features of fibrothorax when imaged. CT scans can more readily differentiate whether pleural thickening is due to extra fat deposition or true pleural thickening than X-rays.If a fibrothorax is severe, the thickening may restrict the lung on the affected side causing a loss of lung volume. Additionally, the mediastinum may be physically shifted toward the affected side. A reduction in the size of one side of the chest (hemithorax) on an X-ray or CT scan of the chest suggests chronic scarring. Signs of the underlying disease causing the fibrothorax are also occasionally seen on the X-ray. A CT scan may show features similar to those seen on a plain X-ray. Lung function testing typically demonstrates findings consistent with restrictive lung disease. Treatment Non-surgical Conservative non-surgical treatment of fibrothorax is generally done by treating its underlying cause and is reserved for milder cases. Tobacco smoking cessation is strongly recommended since tobacco smoke exposure can worsen fibrosis. Severe cases of fibrothorax may require supportive mechanical ventilation if the affected person is unable to breathe adequately on their own.In cases of fibrothorax caused by medication, it is recommended that the offending medications be stopped. Ergot alkaloid medications, which can worsen pleural fibrosis, are typically avoided. Cases of fibrothorax attributable to medication typically stop worsening if the provoking medication is stopped. In some situations, medication-induced fibrothorax improves after stopping the causative medication but fibrothorax usually does not completely resolve.Watchful waiting is appropriate for milder cases of fibrothorax in certain situations. Fibrothorax caused by tuberculosis, empyema, or haemothorax often improves spontaneously 3–6 months after the precipitating illness. Corticosteroids are commonly used to treat fibrothorax but are not well-supported by available evidence. Surgical In severe cases of fibrothorax that are compromising a persons ability to breathe, the scar tissue (fibrous peel) causing fibrothorax can be surgically removed using a technique called decortication. However, surgical decortication is an invasive procedure which carries the risk of complications including a small risk of death, and is therefore generally only considered if severe symptoms are present and have been for many months. Surgical decortication is generally considered for people with fibrothoraces that are severe, causing significant shortness of breath, and have otherwise relatively healthy lungs since this enhances the likelihood of a better outcome. Surgical removal of the pleura (pleurectomy) may be performed in refractory cases, as often happens when asbestosis is the cause. Prognosis Fibrothorax complicating another condition, such as tuberculous pleuritis, empyema, or acute haemothorax often spontaneously resolves in 3-6 months.The prognosis after surgical decortication is variable and depends on the health of the underlying lung before the procedure takes place. If the lung was otherwise healthy, then certain aspects of lung function, such as vital capacity, may improve after decortication. If, however, the lung had significant disease, then lung function often does not improve and may even deteriorate after such intervention. The duration of fibrothorax does not affect prognosis.The mortality of surgery is less than 1% overall, but rises to 4-6% in the elderly. Other factors predicting poorer surgical outcomes include intraoperative complications, incomplete surgery, lung disease beyond the fibrothorax being treated, and specific causes of fibrothorax such as asbestosis. Epidemiology Sporadic cases are rarely reported in the medical literature, for example, due to iatrogenic or postoperative complications. Fibrothorax is rare in developed countries, mainly due to a lower incidence of tuberculosis. The condition is far more common in workers exposed to asbestos, with 5–13.5% of those exposed subsequently developing some degree of pleural fibrosis, sometimes not diagnosed until decades after the initial exposure. == References ==

Hypergammaglobulinemia

Hypergammaglobulinemia is a medical condition with elevated levels of gamma globulin. It is a type of immunoproliferative disorder. Types Hypergammaglobulinemia is a condition that is characterized by the increased levels of a certain immunoglobulin in the blood serum. The name of the disorder refers to an excess of proteins after serum protein electrophoresis (found in the gammaglobulin region).Most hypergammaglobulinemias are caused by an excess of immunoglobulin M (IgM), because this is the default immunoglobulin type prior to class switching. Some types of hypergammaglobulinemia are actually caused by a deficiency in the other major types of immunoglobulins, which are IgA, IgE and IgG. There are 5 types of hypergammaglobulinemias associated with hyper IgM.MeSH considers hyper IgM syndrome to be a form of dysgammaglobulinemia, not a form of hypergammaglobulinemia. Type 1 X-linked immunodeficiency with hyper–immunoglobulin M, which is also called type 1 hyper IgM, is a rare form of primary immunodeficiency disease caused by a mutation in the Tumor Necrosis Factor Super Family member 5 (TNFSF5) gene, which codes for CD40 ligand. This gene is located on the long arm of the X chromosome at position 26, denoted Xq26. Normally, CD40 ligand is expressed on activated T cells, and is necessary to induce immunoglobulin class switching from IgM to the other immunoglobulin types. It does this by binding to its ligand, CD40, which is found expressed on the surface of B cells. The mutation in the TNFSF5 gene causes there to be no recognition of CD40 by CD40 ligand, and thus the T cells do not induce Ig class switching in B cells, so there are markedly reduced levels of IgG, IgA, and IgE, but have normal or elevated levels of IgM. CD40 ligand is also required in the functional maturation of T lymphocytes and macrophages, so patients with this disorder have a variable defect in T-lymphocyte and macrophage effector function, as well as hyper IgM. Type 2 Immunodeficiency with hyper IgM type 2 is caused by a mutation in the Activation-Induced Cytidine Deaminase (AICDA) gene, which is located on the short arm of chromosome 12. The protein that is encoded by this gene is called Activation-Induced Cytidine Deaminase (AICDA) and functions as a DNA-editing deaminase that induces somatic hypermutation, class switch recombination, and immunoglobulin gene conversion in B cells. When a person is homozygous for the mutation in the AICDA gene, the protein fails to function, and thus somatic hypermutation, class switch recombination, and immunoglobulin gene conversion cannot occur, which creates an excess of IgM. Type 3 Immunodeficiency with hyper IgM type 3 is caused by a mutation in the gene that codes for CD40. As mentioned above, CD40 is expressed on the surface of B cells, and its binding to CD40 ligand on activated T cells induces Ig class switching. When the mutation is present, there is no signal for B cells to undergo class switching, so there is an excess of IgM and little to no other immunoglobulin types produced. Type 4 Immunodeficiency with hyper IgM type 4 is poorly characterized. All that is known is that there is an excess of IgM in the blood, with normal levels of the other immunoglobulins. The exact cause is yet to be determined. Type 5 Immunodeficiency with hyper IgM type 5 is caused by a mutation in the Uracil-DNA glycosylase (UNG) gene, which, like AICDA, is located on chromosome 12. This codes for Uracil DNA Glycosylase, which is responsible for excising previous uracil bases that are due to cytosine deamination, or previous uracil misincorporation from double-stranded previous DNA substrates. This enzyme is also responsible for helping with gene conversion during somatic recombination in B cells. The mutation in the gene causes an enzyme that does not function properly, thus gene conversion does not proceed and class switching cannot occur. See also Monoclonal gammopathy of undetermined significance References == External links ==

Femur

The femur (; pl. femurs or femora ), or thigh bone, is the proximal bone of the hindlimb in tetrapod vertebrates. The head of the femur articulates with the acetabulum in the pelvic bone forming the hip joint, while the distal part of the femur articulates with the tibia (shinbone) and patella (kneecap), forming the knee joint. By most measures the two (left and right) femurs are the strongest bones of the body, and in humans, the largest and thickest. Structure The femur is the only bone in the upper leg. The two femurs converge medially toward the knees, where they articulate with the proximal ends of the tibiae. The angle of convergence of the femora is a major factor in determining the femoral-tibial angle. Human females have thicker pelvic bones, causing their femora to converge more than in males. In the condition genu valgum (knock knee) the femurs converge so much that the knees touch one another. The opposite extreme is genu varum (bow-leggedness). In the general population of people without either genu valgum or genu varum, the femoral-tibial angle is about 175 degrees.The femur is the largest and thickest bone in the human body. By some measures, it is also the strongest bone in the human body. This depends on the type of measurement taken to calculate strength. Some strength tests show the temporal bone in the skull to be the strongest bone. The femur length on average is 26.74% of a persons height, a ratio found in both men and women and most ethnic groups with only restricted variation, and is useful in anthropology because it offers a basis for a reasonable estimate of a subjects height from an incomplete skeleton. The femur is categorised as a long bone and comprises a diaphysis (shaft or body) and two epiphyses (extremities) that articulate with adjacent bones in the hip and knee. Upper part The upper or proximal extremity (close to the torso) contains the head, neck, the two trochanters and adjacent structures. The upper extremity is the shortest femoral extremity, the lower extremity is the thickest femoral extremity. The head of the femur, which articulates with the acetabulum of the pelvic bone, comprises two-thirds of a sphere. It has a small groove, or fovea, connected through the round ligament to the sides of the acetabular notch. The head of the femur is connected to the shaft through the neck or collum. The neck is 4–5 cm. long and the diameter is smallest front to back and compressed at its middle. The collum forms an angle with the shaft in about 130 degrees. This angle is highly variant. In the infant it is about 150 degrees and in old age reduced to 120 degrees on average. An abnormal increase in the angle is known as coxa valga and an abnormal reduction is called coxa vara. Both the head and neck of the femur is vastly embedded in the hip musculature and can not be directly palpated. In skinny people with the thigh laterally rotated, the head of the femur can be felt deep as a resistance profound (deep) for the femoral artery.The transition area between the head and neck is quite rough due to attachment of muscles and the hip joint capsule. Here the two trochanters, greater and lesser trochanter, are found. The greater trochanter is almost box-shaped and is the most lateral prominent of the femur. The highest point of the greater trochanter is located higher than the collum and reaches the midpoint of the hip joint. The greater trochanter can easily be felt. The trochanteric fossa is a deep depression bounded posteriorly by the intertrochanteric crest on the medial surface of the greater trochanter. The lesser trochanter is a cone-shaped extension of the lowest part of the femur neck. The two trochanters are joined by the intertrochanteric crest on the back side and by the intertrochanteric line on the front.A slight ridge is sometimes seen commencing about the middle of the intertrochanteric crest, and reaching vertically downward for about 5 cm. along the back part of the body: it is called the linea quadrata (or quadrate line). About the junction of the upper one-third and lower two-thirds on the intertrochanteric crest is the quadrate tubercle located. The size of the tubercle varies and it is not always located on the intertrochanteric crest and that also adjacent areas can be part of the quadrate tubercle, such as the posterior surface of the greater trochanter or the neck of the femur. In a small anatomical study it was shown that the epiphyseal line passes directly through the quadrate tubercle. Body The body of the femur (or shaft) is large, thick and almost cylindrical in form. It is a little broader above than in the center, broadest and somewhat flattened from before backward below. It is slightly arched, so as to be convex in front, and concave behind, where it is strengthened by a prominent longitudinal ridge, the linea aspera which diverges proximally and distal as the medial and lateral ridge. Proximally the lateral ridge of the linea aspera becomes the gluteal tuberosity while the medial ridge continues as the pectineal line. Besides the linea aspera the shaft has two other bordes; a lateral and medial border. These three bordes separates the shaft into three surfaces: One anterior, one medial and one lateral. Due to the vast musculature of the thigh the shaft can not be palpated.The third trochanter is a bony projection occasionally present on the proximal femur near the superior border of the gluteal tuberosity. When present, it is oblong, rounded, or conical in shape and sometimes continuous with the gluteal ridge. A structure of minor importance in humans, the incidence of the third trochanter varies from 17–72% between ethnic groups and it is frequently reported as more common in females than in males. Lower part The lower extremity of the femur (or distal extremity) is the thickest femoral extremity, the upper extremity is the shortest femoral extremity. It is somewhat cuboid in form, but its transverse diameter is greater than its antero-posterior (front to back). It consists of two oblong eminences known as the condyles.Anteriorly, the condyles are slightly prominent and are separated by a smooth shallow articular depression called the patellar surface. Posteriorly, they project considerably and a deep notch, the Intercondylar fossa of femur, is present between them. The lateral condyle is the more prominent and is the broader both in its antero-posterior and transverse diameters. The medial condyle is the longer and, when the femur is held with its body perpendicular, projects to a lower level. When, however, the femur is in its natural oblique position the lower surfaces of the two condyles lie practically in the same horizontal plane. The condyles are not quite parallel with one another; the long axis of the lateral is almost directly antero-posterior, but that of the medial runs backward and medialward. Their opposed surfaces are small, rough, and concave, and form the walls of the intercondyloid fossa. This fossa is limited above by a ridge, the intercondyloid line, and below by the central part of the posterior margin of the patellar surface. The posterior cruciate ligament of the knee joint is attached to the lower and front part of the medial wall of the fossa and the anterior cruciate ligament to an impression on the upper and back part of its lateral wall.The articular surface of the lower end of the femur occupies the anterior, inferior, and posterior surfaces of the condyles. Its front part is named the patellar surface and articulates with the patella; it presents a median groove which extends downward to the intercondyloid fossa and two convexities, the lateral of which is broader, more prominent, and extends farther upward than the medial.Each condyle is surmounted by an elevation, the epicondyle. The medial epicondyle is a large convex eminence to which the tibial collateral ligament of the knee-joint is attached. At its upper part is the adductor tubercle and behind it is a rough impression which gives origin to the medial head of the gastrocnemius. The lateral epicondyle which is smaller and less prominent than the medial, gives attachment to the fibular collateral ligament of the knee-joint. Development The femur develops from the limb buds as a result of interactions between the ectoderm and the underlying mesoderm, formation occurs roughly around the fourth week of development.By the sixth week of development, the first hyaline cartilage model of the femur is formed by chondrocytes. Endochondral ossification begins by the end of the embryonic period and primary ossification centers are present in all long bones of the limbs, including the femur, by the 12th week of development. The hindlimb development lags behind forelimb development by 1–2 days. Function As the femur is the only bone in the thigh, it serves as an attachment point for all the muscles that exert their force over the hip and knee joints. Some biarticular muscles – which cross two joints, like the gastrocnemius and plantaris muscles – also originate from the femur. In all, 23 individual muscles either originate from or insert onto the femur. In cross-section, the thigh is divided up into three separate fascial compartments divided by fascia, each containing muscles. These compartments use the femur as an axis, and are separated by tough connective tissue membranes (or septa). Each of these compartments has its own blood and nerve supply, and contains a different group of muscles. These compartments are named the anterior, medial and posterior fascial compartments. Muscle attachments Clinical significance Fractures A femoral fracture that involves the femoral head, femoral neck or the shaft of the femur immediately below the lesser trochanter may be classified as a hip fracture, especially when associated with osteoporosis. Femur fractures can be managed in a pre-hospital setting with the use of a traction splint. Diversity among animals In primitive tetrapods, the main points of muscle attachment along the femur are the internal trochanter and third trochanter, and a ridge along the ventral surface of the femoral shaft referred to as the adductor crest. The neck of the femur is generally minimal or absent in the most primitive forms, reflecting a simple attachment to the acetabulum. The greater trochanter was present in the extinct archosaurs, as well as in modern birds and mammals, being associated with the loss of the primitive sprawling gait. The lesser trochanter is a unique development of mammals, which lack both the internal and fourth trochanters. The adductor crest is also often absent in mammals or alternatively reduced to a series of creases along the surface of the bone. Structures analogous to the third trochanter are present in mammals, including some primates.Some species of whales, snakes, and other non-walking vertebrates have vestigial femurs. In some snakes the protruding end of a pelvic spur, a vestigial pelvis and femur remnant which is not connected to the rest of the skeleton, plays a role in mating. This role in mating is hypothesized to have possibly occurred in Basilosauridae, an extinct family of whales with well-defined femurs, lower legs and feet. Occasionally, the genes that code for longer extremities cause a modern whale to develop miniature legs (atavism).One of the earliest known vertebrates to have a femur is the eusthenopteron, a prehistoric lobe-finned fish from the Late Devonian period. Viral metagenomics A recent study revealed that bone is a much richer source of persistent DNA viruses than earlier perceived. Besides Parvovirus 19 and hepatitis B virus, ten additional ones were discovered, namely several members of the herpes- and polyomavirus families, as well as human papillomavirus 31 and torque teno virus. Invertebrates In invertebrate zoology the name femur appears in arthropodology. The usage is not homologous with that of vertebrate anatomy; the term "femur" simply has been adopted by analogy and refers, where applicable, to the most proximal of (usually) the two longest jointed segments of the legs of the arthropoda. The two basal segments preceding the femur are the coxa and trochanter. This convention is not followed in carcinology but it applies in arachnology and entomology. In myriapodology another segment, the prefemur, connects the trochanter and femur. Additional media References External links Media related to Femur at Wikimedia Commons The dictionary definition of Femur at Wiktionary The dictionary definition of thighbone at Wiktionary

Histiocytic sarcoma

Histiocytic sarcoma is a tumor derived from histiocytes. The tumor is often positive for CD163 and can appear in the thyroid. However, in some cases it can also appear in the brain. References == External links ==

MELAS syndrome

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is one of the family of mitochondrial diseases, which also include MIDD (maternally inherited diabetes and deafness, MERRF syndrome, and Lebers hereditary optic neuropathy. It was first characterized under this name in 1984. A feature of these diseases is that they are caused by defects in the mitochondrial genome which is inherited purely from the female parent. The most common MELAS mutation is mitochondrial mutation, mtDNA, referred to as m.3243A>G. Signs and symptoms MELAS is a condition that affects many of the bodys systems, particularly the brain and nervous system (encephalo-) and muscles (myopathy). In most cases, the signs and symptoms of this disorder appear in childhood following a period of normal development. Children with MELAS often have normal early psychomotor development until the onset of symptoms between 2 and 10 years old. Though less common, infantile onset may occur and may present as failure to thrive, growth retardation and progressive deafness. Onset in older children typically presents as recurrent attacks of a migraine-like headache, anorexia, vomiting, and seizures. Children with MELAS are also frequently found to have short stature.Most people with MELAS have a buildup of lactic acid in their bodies, a condition called lactic acidosis. Increased acidity in the blood can lead to vomiting, abdominal pain, extreme tiredness (fatigue), muscle weakness, loss of bowel control, and difficulty breathing. Less commonly, people with MELAS may experience involuntary muscle spasms (myoclonus), impaired muscle coordination (ataxia), hearing loss, heart and kidney problems, diabetes, epilepsy, and hormonal imbalances. Differential diagnosis The presentation of some cases is similar to that of Kearns–Sayre syndrome.Myoclonus epilepsy associated with ragged red fibers (MERRF) may be confused with MELAS as they both involve seizures, mental deterioration, and myopathy with ragged red fibers on biopsy. MERRF patients may also have hearing loss, visual disturbance secondary to optic atrophy, and short stature. The characteristic myoclonic seizure in MERRF may help to narrow diagnosis, but genetic testing should be considered to distinguish the two conditions.Leigh syndrome may also present with progressive neurological deterioration, seizures, and vomiting mainly in young children. Genetics MELAS is mostly caused by mutations in the genes in mitochondrial DNA, but it can also be caused by mutations in the nuclear DNA. NADH dehydrogenase Some of the genes (MT-ND1, MT-ND5) affected in MELAS encode proteins that are part of NADH dehydrogenase (also called complex I) in mitochondria, that helps convert oxygen and simple sugars to energy. Transfer RNAs Other genes (MT-TH, MT-TL1, and MT-TV) encode mitochondrial specific transfer RNAs (tRNAs).Mutations in MT-TL1 cause more than 80 percent of all cases of MELAS. They impair the ability of mitochondria to make proteins, use oxygen, and produce energy. Researchers have not determined how changes in mitochondrial DNA lead to the specific signs and symptoms of MELAS. They continue to investigate the effects of mitochondrial gene mutations in different tissues, particularly in the brain. Inheritance This condition is inherited in a mitochondrial pattern, which is also known as maternal inheritance and heteroplasmy. This pattern of inheritance applies to genes contained in mitochondrial DNA. Because egg cells, but not sperm cells, contribute mitochondria to the developing embryo, only females pass mitochondrial conditions to their children. Mitochondrial disorders can appear in every generation of a family and can affect both males and females, but fathers do not pass mitochondrial traits to their children. In most cases, people with MELAS inherit an altered mitochondrial gene from their mother. Less commonly, the disorder results from a new mutation in a mitochondrial gene and occurs in people with no family history of MELAS. Diagnosis MRI: Multifocal infarct-like cortical areas in different stages of ischemic evolution, areas that do not conform to any known vascular territory. Initial lesions often occur in the occipital or parietal lobes with eventual involvement of the cerebellum, cerebral cortex, basal ganglia, and thalamus.Lactate levels are often elevated in serum and cerebrospinal fluid. MR spectroscopy may show an elevated lactate peak in affected and even unaffected brain areas. Muscle biopsy shows ragged red fibers. However, genetic evaluation should be done first, which eliminates the need for muscle biopsy in most cases. Diagnosis may be molecular or clinical: Stroke-like episodes before or after 40 years old Encephalopathy with seizures or dementia Blood lactic acidosis* or ragged red fibers on muscle biopsyDue to mitochondrial heteroplasmy, urine and blood testing is preferable to blood alone. PCR and ARMS-PCR are commonly used, reliable, rapid, and cost-effective techniques for the diagnosis of MELAS.Hearing loss and mitochondrial diabetes are common features. Eyes may have a distinctive speckled pigment in the retina, referred to as a maculopathy. Family members may present differently. Treatment There is no curative treatment. The disease remains progressive and fatal.Patients are managed according to what areas of the body are affected at a particular time. Enzymes, amino acids, antioxidants and vitamins have been used. Treatment for MELAS currently is 1. support the good mitochondria that is left with a mito cocktail and 2. avoid known mito toxins. Also the following supplements may help: CoQ10 has been helpful for some MELAS patients. B complex 100 is recommended as the B vitamins are the energy vitamins. Nicotinamide has been used because complex l accepts electrons from NADH and ultimately transfers electrons to CoQ10. Riboflavin has been reported to improve the function of a patient with complex l deficiency and the 3250T-C mutation. The administration of L-arginine during the acute and interictal periods may represent a potential new therapy for this syndrome to reduce brain damage due to impairment of vasodilation in intracerebral arteries due to nitric oxide depletion. Citrulline is also used as citrulline makes the plasma arginine higher, these doses are being studied at Baylor. Treatment with IV arginine is thought to relax the blood vessels to the brain, via nitric oxide. https://jamanetwork.com/journals/jamaneurology/article-abstract/2499460 Epidemiology The exact incidence of MELAS is unknown. It is one of the more common conditions in a group known as mitochondrial diseases. Together, mitochondrial diseases occur in about 1 in 4,000 people. See also Mitochondrial myopathy References External links melas at NIH/UW GeneTests

Procedure

Procedure may refer to: Medical procedure Instructions or recipes, a set of commands that show how to achieve some result, such as to prepare or make something Procedure (business), specifying parts of a business process Standard operating procedure, a step-by-step instruction to achieve some result, used in industry and military Legal procedure, the body of law and rules used in the administration of justice in the court system, including: Civil procedure Criminal procedure Administrative procedure Parliamentary procedure, a set of rules governing meetings Procedure (computer science), also termed a subroutine, function, or subprogram Stored procedure, a subroutine in the data dictionary of a relational database The Procedure, an American hardcore band See also Procedural (disambiguation)

Browns syndrome

Browns syndrome is a rare form of strabismus characterized by limited elevation of the affected eye. The disorder may be congenital (existing at or before birth), or acquired. Brown syndrome is caused by a malfunction of the superior oblique muscle, causing the eye to have difficulty moving up, particularly during adduction (when eye turns towards the nose). Harold W. Brown first described the disorder in 1950 and initially named it the "superior oblique tendon sheath syndrome". Presentation A simple definition of the syndrome is "limited elevation in adduction from mechanical causes around the superior oblique". This definition indicates that when the head is upright, the eye is restricted in movement due to problems with muscles and tendons that surround the eye.Harold W. Brown characterized the syndrome in many ways such as: Limited elevation in the eye when head is straight up Eyes point out in a straight up gaze (divergence in up gaze) Widening of the eyelids in the affected eye on adduction Head tilts backwards (compensatory chin elevation to avoid double vision) Near normal elevation in abductionHe concluded that all of these features of Brown syndrome were due to the shortening or tightening of the anterior superior oblique tendon. Because this syndrome can be acquired or occur at random and has spontaneous resolution, Brown hypothesized one major truth for this disorder — that the short tendon sheath was due to a complete separation, congenital paresis, of the ipsilateral (on the same side) inferior oblique muscle and secondary to a permanent shortening.After further research, he redefined the sheath syndrome into the following divisions: true sheath syndrome, which categorized only the cases that had a congenital short anterior sheath of the superior oblique tendon, and simulated sheath syndrome, which characterized all cases in which the clinical features of a sheath syndrome caused by something different other than a congenital short anterior sheath of the tendon. The clinical features of the two categories are correct but true sheath syndrome is always congenital. However, in 1970 it was discovered that a tight sheath tendon was not the cause of Browns Syndrome. The real cause was a tight or short superior oblique tendon; studies have confirmed this and have labeled the tendon inelastic. Causes Browns syndrome can be divided in two categories based on the restriction of movement on the eye itself and how it affects the eye excluding the movement: Congenital (present at birth) Browns syndrome results from structural anomalies other than a short tendon sheath but other fibrous adhesions may be present around the trochlear area. Acquired cases arise from trauma, surgery, sinusitis and inflammation of the superior oblique tendon sheath in rheumatoid arthritis. Orbital floor fractures may trap the orbital tissue in such a way as to simulate Browns syndrome. Intermittent forms of vertical retraction syndrome have been associated with click, which occurs as the restriction is released (superior oblique click syndrome). Diagnosis Diagnosis of Browns syndrome usually happens during a routine ophthalmologic appointment. Treatments If binocular vision is present and head position is correct, treatment is not obligatory. Treatment is required for: visual symptoms, strabismus, or incorrect head position.Acquired cases that have active inflammation of the superior oblique tendon may benefit from local corticosteroid injections in the region of the trochlea. The goal of surgery is to restore free ocular rotations. Various surgical techniques have been used: Harold Brown advocated that the superior oblique tendon be stripped. A procedure named sheathotomy. The results of such a procedure are frequently unsatisfactory because of reformation of scar tissue. Tenotomy of the superior oblique tendon (with or without a tendon spacer) has also been advocated. This has the disadvantage that it frequently produces a superior oblique paresis. Weakening of the inferior oblique muscle of the affected eye may be needed to compensate for iatrogenic fourth nerve palsy.During surgery, a traction test is repeated until the eye rotations are free and the eye is anchored in an elevated adducted position for about two weeks after the surgery. This maneuver is intended to prevent the reformation of scar tissue in the same places. Normalization of head position may occur but restoration of full motility is seldom achieved. A second procedure may be required. Epidemiology In Browns original series there was a 3:2 predominance of women to men and nearly twice as many cases involved the right eye as the left. 10% of cases showed bilaterality. Familial occurrence of Browns syndrome has been reported. See also Strabismus Strabismus surgery Pediatric ophthalmology Duane syndrome References == External links ==

Headache

Headache is the symptom of pain in the face, head, or neck. It can occur as a migraine, tension-type headache, or cluster headache. There is an increased risk of depression in those with severe headaches.Headaches can occur as a result of many conditions. There are a number of different classification systems for headaches. The most well-recognized is that of the International Headache Society, which classifies it into more than 150 types of primary and secondary headaches. Causes of headaches may include dehydration; fatigue; sleep deprivation; stress; the effects of medications (overuse) and recreational drugs, including withdrawal; viral infections; loud noises; head injury; rapid ingestion of a very cold food or beverage; and dental or sinus issues (such as sinusitis).Treatment of a headache depends on the underlying cause, but commonly involves pain medication (especially in case of migraine or cluster headache). A headache is one of the most commonly experienced of all physical discomforts.About half of adults have a headache in a given year. Tension headaches are the most common, affecting about 1.6 billion people (21.8% of the population) followed by migraine headaches which affect about 848 million (11.7%). Causes There are more than 200 types of headaches. Some are harmless and some are life-threatening. The description of the headache and findings on neurological examination, determine whether additional tests are needed and what treatment is best.Headaches are broadly classified as "primary" or "secondary". Primary headaches are benign, recurrent headaches not caused by underlying disease or structural problems. For example, migraine is a type of primary headache. While primary headaches may cause significant daily pain and disability, they are not dangerous from a physiological point of view. Secondary headaches are caused by an underlying disease, like an infection, head injury, vascular disorders, brain bleed, stomach irritation, or tumors. Secondary headaches can be dangerous. Certain "red flags" or warning signs indicate a secondary headache may be dangerous. Primary Ninety percent of all headaches are primary headaches. Primary headaches usually first start when people are between 20 and 40 years old. The most common types of primary headaches are migraines and tension-type headaches. They have different characteristics. Migraines typically present with pulsing head pain, nausea, photophobia (sensitivity to light) and phonophobia (sensitivity to sound). Tension-type headaches usually present with non-pulsing "bandlike" pressure on both sides of the head, not accompanied by other symptoms. Such kind of headaches maybe further classified into-episodic and chronic tension type headaches Other very rare types of primary headaches include: cluster headaches: short episodes (15–180 minutes) of severe pain, usually around one eye, with autonomic symptoms (tearing, red eye, nasal congestion) which occur at the same time every day. Cluster headaches can be treated with triptans and prevented with prednisone, ergotamine or lithium. trigeminal neuralgia or occipital neuralgia: shooting face pain hemicrania continua: continuous unilateral pain with episodes of severe pain. Hemicrania continua can be relieved by the medication indomethacin. primary stabbing headache: recurrent episodes of stabbing "ice pick pain" or "jabs and jolts" for 1 second to several minutes without autonomic symptoms (tearing, red eye, nasal congestion). These headaches can be treated with indomethacin. primary cough headache: starts suddenly and lasts for several minutes after coughing, sneezing or straining (anything that may increase pressure in the head). Serious causes (see secondary headaches red flag section) must be ruled out before a diagnosis of "benign" primary cough headache can be made. primary exertional headache: throbbing, pulsatile pain which starts during or after exercising, lasting for 5 minutes to 24 hours. The mechanism behind these headaches is unclear, possibly due to straining causing veins in the head to dilate, causing pain. These headaches can be prevented by not exercising too strenuously and can be treated with medications such as indomethacin. primary sex headache: dull, bilateral headache that starts during sexual activity and becomes much worse during orgasm. These headaches are thought to be due to lower pressure in the head during sex. It is important to realize that headaches that begin during orgasm may be due to a subarachnoid hemorrhage, so serious causes must be ruled out first. These headaches are treated by advising the person to stop sex if they develop a headache. Medications such as propranolol and diltiazem can also be helpful. hypnic headache: a moderate-severe headache that starts a few hours after falling asleep and lasts 15–30 minutes. The headache may recur several times during the night. Hypnic headaches are usually in older women. They may be treated with lithium. Secondary Headaches may be caused by problems elsewhere in the head or neck. Some of these are not harmful, such as cervicogenic headache (pain arising from the neck muscles). The excessive use of painkillers can paradoxically cause worsening painkiller headaches.More serious causes of secondary headaches include the following: meningitis: inflammation of the meninges which presents with fever and meningismus, or stiff neck bleeding inside the brain (intracranial hemorrhage) subarachnoid hemorrhage (acute, severe headache, stiff neck without fever) ruptured aneurysm, arteriovenous malformation, intraparenchymal hemorrhage (headache only) brain tumor: dull headache, worse with exertion and change in position, accompanied by nausea and vomiting. Often, the person will have nausea and vomiting for weeks before the headache starts. temporal arteritis: inflammatory disease of arteries common in the elderly (average age 70) with fever, headache, weight loss, jaw claudication, tender vessels by the temples, polymyalgia rheumatica acute closed-angle glaucoma (increased pressure in the eyeball): a headache that starts with eye pain, blurry vision, associated with nausea and vomiting. On physical exam, the person will have red eyes and a fixed, mid-dilated pupil. Post-ictal headaches: Headaches that happen after a convulsion or other type of seizure, as part of the period after the seizure (the post-ictal state)Gastrointestinal disorders may cause headaches, including Helicobacter pylori infection, celiac disease, non-celiac gluten sensitivity, irritable bowel syndrome, inflammatory bowel disease, gastroparesis, and hepatobiliary disorders. The treatment of the gastrointestinal disorders may lead to a remission or improvement of headaches.Migraine headaches are also associated with Cyclic Vomiting Syndrome (CVS). CVS is characterized by episodes of severe vomiting, and often occur alongside symptoms similar to those of migraine headaches (photophobia, abdominal pain, etc.). Pathophysiology The brain itself is not sensitive to pain, because it lacks pain receptors. However, several areas of the head and neck do have pain receptors and can thus sense pain. These include the extracranial arteries, middle meningeal artery, large veins, venous sinuses, cranial and spinal nerves, head and neck muscles, the meninges, falx cerebri, parts of the brainstem, eyes, ears, teeth, and lining of the mouth. Pial arteries, rather than pial veins are responsible for pain production.Headaches often result from traction to or irritation of the meninges and blood vessels. The pain receptors may be stimulated by head trauma or tumors and cause headaches. Blood vessel spasms, dilated blood vessels, inflammation or infection of meninges and muscular tension can also stimulate pain receptors. Once stimulated, a nociceptor sends a message up the length of the nerve fiber to the nerve cells in the brain, signalling that a part of the body hurts.Primary headaches are more difficult to understand than secondary headaches. The exact mechanisms which cause migraines, tension headaches and cluster headaches are not known. There have been different hypotheses over time that attempt to explain what happens in the brain to cause these headaches.Migraines are currently thought to be caused by dysfunction of the nerves in the brain. Previously, migraines were thought to be caused by a primary problem with the blood vessels in the brain. This vascular theory, which was developed in the 20th century by Wolff, suggested that the aura in migraines is caused by constriction of intracranial vessels (vessels inside the brain), and the headache itself is caused by rebound dilation of extracranial vessels (vessels just outside the brain). Dilation of these extracranial blood vessels activates the pain receptors in the surrounding nerves, causing a headache. The vascular theory is no longer accepted. Studies have shown migraine head pain is not accompanied by extracranial vasodilation, but rather only has some mild intracranial vasodilation.Currently, most specialists think migraines are due to a primary problem with the nerves in the brain. Auras are thought to be caused by a wave of increased activity of neurons in the cerebral cortex (a part of the brain) known as cortical spreading depression followed by a period of depressed activity. Some people think headaches are caused by the activation of sensory nerves which release peptides or serotonin, causing inflammation in arteries, dura and meninges and also cause some vasodilation. Triptans, medications that treat migraines, block serotonin receptors and constrict blood vessels.People who are more susceptible to experiencing migraines without headache are those who have a family history of migraines, women, and women who are experiencing hormonal changes or are taking birth control pills or are prescribed hormone replacement therapy.Tension headaches are thought to be caused by activation of peripheral nerves in the head and neck muscles.Cluster headaches involve overactivation of the trigeminal nerve and hypothalamus in the brain, but the exact cause is unknown. Diagnosis Most headaches can be diagnosed by the clinical history alone. If the symptoms described by the person sound dangerous, further testing with neuroimaging or lumbar puncture may be necessary. Electroencephalography (EEG) is not useful for headache diagnosis.The first step to diagnosing a headache is to determine if the headache is old or new. A "new headache" can be a headache that has started recently, or a chronic headache that has changed character. For example, if a person has chronic weekly headaches with pressure on both sides of his head, and then develops a sudden severe throbbing headache on one side of his head, they have a new headache. Red flags It can be challenging to differentiate between low-risk, benign headaches and high-risk, dangerous headaches since symptoms are often similar. Headaches that are possibly dangerous require further lab tests and imaging to diagnose.The American College for Emergency Physicians published criteria for low-risk headaches. They are as follows: age younger than 30 years features typical of primary headache history of similar headache no abnormal findings on neurologic exam no concerning change in normal headache pattern no high-risk comorbid conditions (for example, HIV) no new concerning history or physical examination findingsA number of characteristics make it more likely that the headache is due to potentially dangerous secondary causes which may be life-threatening or cause long-term damage. These "red flag" symptoms mean that a headache warrants further investigation with neuroimaging and lab tests.In general, people complaining of their "first" or "worst" headache warrant imaging and further workup. People with progressively worsening headache also warrant imaging, as they may have a mass or a bleed that is gradually growing, pressing on surrounding structures and causing worsening pain. People with neurological findings on exam, such as weakness, also need further workup.The American Headache Society recommends using "SSNOOP", a mnemonic to remember the red flags for identifying a secondary headache: Systemic symptoms (fever or weight loss) Systemic disease (HIV infection, malignancy) Neurologic symptoms or signs Onset sudden (thunderclap headache) Onset after age 40 years Previous headache history (first, worst, or different headache)Other red flag symptoms include: Old headaches Old headaches are usually primary headaches and are not dangerous. They are most often caused by migraines or tension headaches. Migraines are often unilateral, pulsing headaches accompanied by nausea or vomiting. There may be an aura (visual symptoms, numbness or tingling) 30–60 minutes before the headache, warning the person of a headache. Migraines may also not have auras. Tension-type headaches usually have bilateral "bandlike" pressure on both sides of the head usually without nausea or vomiting. However, some symptoms from both headache groups may overlap. It is important to distinguish between the two because the treatments are different. The mnemonic POUND helps distinguish between migraines and tension-type headaches. POUND stands for: One review article found that if 4–5 of the POUND characteristics are present, a migraine is 24 times as likely a diagnosis than a tension-type headache (likelihood ratio 24). If 3 characteristics of POUND are present, migraine is 3 times more likely a diagnosis than tension type headache (likelihood ratio 3). If only 2 POUND characteristics are present, tension-type headaches are 60% more likely (likelihood ratio 0.41). Another study found the following factors independently each increase the chance of migraine over tension-type headache: nausea, photophobia, phonophobia, exacerbation by physical activity, unilateral, throbbing quality, chocolate as a headache trigger, and cheese as a headache trigger.Cluster headaches are relatively rare (1 in 1000 people) and are more common in men than women. They present with sudden onset explosive pain around one eye and are accompanied by autonomic symptoms (tearing, runny nose and red eye).Temporomandibular jaw pain (chronic pain in the jaw joint), and cervicogenic headache (headache caused by pain in muscles of the neck) are also possible diagnoses.For chronic, unexplained headaches, keeping a headache diary can be useful for tracking symptoms and identifying triggers, such as association with menstrual cycle, exercise and food. While mobile electronic diaries for smartphones are becoming increasingly common, a recent review found most are developed with a lack of evidence base and scientific expertise. New headaches New headaches are more likely to be dangerous secondary headaches. They can, however, simply be the first presentation of a chronic headache syndrome, like migraine or tension-type headaches.One recommended diagnostic approach is as follows. If any urgent red flags are present such as visual loss, new seizures, new weakness, new confusion, further workup with imaging and possibly a lumbar puncture should be done (see red flags section for more details). If the headache is sudden onset (thunderclap headache), a computed tomography test to look for a brain bleed (subarachnoid hemorrhage) should be done. If the CT scan does not show a bleed, a lumbar puncture should be done to look for blood in the CSF, as the CT scan can be falsely negative and subarachnoid hemorrhages can be fatal. If there are signs of infection such as fever, rash, or stiff neck, a lumbar puncture to look for meningitis should be considered. If there is jaw claudication and scalp tenderness in an older person, a temporal artery biopsy to look for temporal arteritis should be performed and immediate treatment should be started. Neuroimaging Old headaches The US Headache Consortium has guidelines for neuroimaging of non-acute headaches. Most old, chronic headaches do not require neuroimaging. If a person has the characteristic symptoms of a migraine, neuroimaging is not needed as it is very unlikely the person has an intracranial abnormality. If the person has neurological findings, such as weakness, on exam, neuroimaging may be considered. New headaches All people who present with red flags indicating a dangerous secondary headache should receive neuroimaging. The best form of neuroimaging for these headaches is controversial. Non-contrast computerized tomography (CT) scan is usually the first step in head imaging as it is readily available in Emergency Departments and hospitals and is cheaper than MRI. Non-contrast CT is best for identifying an acute head bleed. Magnetic Resonance Imaging (MRI) is best for brain tumors and problems in the posterior fossa, or back of the brain. MRI is more sensitive for identifying intracranial problems, however it can pick up brain abnormalities that are not relevant to the persons headaches.The American College of Radiology recommends the following imaging tests for different specific situations: Lumbar puncture A lumbar puncture is a procedure in which cerebral spinal fluid is removed from the spine with a needle. A lumbar puncture is necessary to look for infection or blood in the spinal fluid. A lumbar puncture can also evaluate the pressure in the spinal column, which can be useful for people with idiopathic intracranial hypertension (usually young, obese women who have increased intracranial pressure), or other causes of increased intracranial pressure. In most cases, a CT scan should be done first. Classification Headaches are most thoroughly classified by the International Headache Societys International Classification of Headache Disorders (ICHD), which published the second edition in 2004. The third edition of the International Headache Classification was published in 2013 in a beta version ahead of the final version. This classification is accepted by the WHO.Other classification systems exist. One of the first published attempts was in 1951. The US National Institutes of Health developed a classification system in 1962. ICHD-2 The International Classification of Headache Disorders (ICHD) is an in-depth hierarchical classification of headaches published by the International Headache Society. It contains explicit (operational) diagnostic criteria for headache disorders. The first version of the classification, ICHD-1, was published in 1988. The current revision, ICHD-2, was published in 2004. The classification uses numeric codes. The top, one-digit diagnostic level includes 14 headache groups. The first four of these are classified as primary headaches, groups 5-12 as secondary headaches, cranial neuralgia, central and primary facial pain and other headaches for the last two groups.The ICHD-2 classification defines migraines, tension-types headaches, cluster headache and other trigeminal autonomic headache as the main types of primary headaches. Also, according to the same classification, stabbing headaches and headaches due to cough, exertion and sexual activity (sexual headache) are classified as primary headaches. The daily-persistent headaches along with the hypnic headache and thunderclap headaches are considered primary headaches as well.Secondary headaches are classified based on their cause and not on their symptoms. According to the ICHD-2 classification, the main types of secondary headaches include those that are due to head or neck trauma such as whiplash injury, intracranial hematoma, post craniotomy or other head or neck injury. Headaches caused by cranial or cervical vascular disorders such as ischemic stroke and transient ischemic attack, non-traumatic intracranial hemorrhage, vascular malformations or arteritis are also defined as secondary headaches. This type of headache may also be caused by cerebral venous thrombosis or different intracranial vascular disorders. Other secondary headaches are those due to intracranial disorders that are not vascular such as low or high pressure of the cerebrospinal fluid pressure, non-infectious inflammatory disease, intracranial neoplasm, epileptic seizure or other types of disorders or diseases that are intracranial but that are not associated with the vasculature of the central nervous system.ICHD-2 classifies headaches that are caused by the ingestion of a certain substance or by its withdrawal as secondary headaches as well. This type of headache may result from the overuse of some medications or exposure to some substances. HIV/AIDS, intracranial infections and systemic infections may also cause secondary headaches. The ICHD-2 system of classification includes the headaches associated with homeostasis disorders in the category of secondary headaches. This means that headaches caused by dialysis, high blood pressure, hypothyroidism, cephalalgia and even fasting are considered secondary headaches. Secondary headaches, according to the same classification system, can also be due to the injury of any of the facial structures including teeth, jaws, or temporomandibular joint. Headaches caused by psychiatric disorders such as somatization or psychotic disorders are also classified as secondary headaches.The ICHD-2 classification puts cranial neuralgias and other types of neuralgia in a different category. According to this system, there are 19 types of neuralgias and headaches due to different central causes of facial pain. Moreover, the ICHD-2 includes a category that contains all the headaches that cannot be classified.Although the ICHD-2 is the most complete headache classification there is and it includes frequency in the diagnostic criteria of some types of headaches (primarily primary headaches), it does not specifically code frequency or severity which are left at the discretion of the examiner. NIH The NIH classification consists of brief definitions of a limited number of headaches.The NIH system of classification is more succinct and only describes five categories of headaches. In this case, primary headaches are those that do not show organic or structural causes. According to this classification, primary headaches can only be vascular, myogenic, cervicogenic, traction, and inflammatory. Management Primary headache syndromes have many different possible treatments. In those with chronic headaches the long term use of opioids appears to result in greater harm than benefit. Migraines Migraine can be somewhat improved by lifestyle changes, but most people require medicines to control their symptoms. Medications are either to prevent getting migraines, or to reduce symptoms once a migraine starts.Preventive medications are generally recommended when people have more than four attacks of migraine per month, headaches last longer than 12 hours or the headaches are very disabling. Possible therapies include beta blockers, antidepressants, anticonvulsants and NSAIDs. The type of preventive medicine is usually chosen based on the other symptoms the person has. For example, if the person also has depression, an antidepressant is a good choice.Abortive therapies for migraines may be oral, if the migraine is mild to moderate, or may require stronger medicine given intravenously or intramuscularly. Mild to moderate headaches should first be treated with acetaminophen (paracetamol) or NSAIDs, like ibuprofen. If accompanied by nausea or vomiting, an antiemetic such as metoclopramide (Reglan) can be given orally or rectally. Moderate to severe attacks should be treated first with an oral triptan, a medication that mimics serotonin (an agonist) and causes mild vasoconstriction. If accompanied by nausea and vomiting, parenteral (through a needle in the skin) triptans and antiemetics can be given.Sphenopalatine ganglion block (SPG block, also known nasal ganglion block or pterygopalatine ganglion blocks) can abort and prevent migraines, tension headaches and cluster headaches. It was originally described by American ENT surgeon Greenfield Sluder in 1908. Both blocks and neurostimulation have been studied as treatment for headaches.Several complementary and alternative strategies can help with migraines. The American Academy of Neurology guidelines for migraine treatment in 2000 stated relaxation training, electromyographic feedback and cognitive behavioral therapy may be considered for migraine treatment, along with medications. Tension-type headaches Tension-type headaches can usually be managed with NSAIDs (ibuprofen, naproxen, aspirin), or acetaminophen. Triptans are not helpful in tension-type headaches unless the person also has migraines. For chronic tension type headaches, amitriptyline is the only medication proven to help. Amitriptyline is a medication which treats depression and also independently treats pain. It works by blocking the reuptake of serotonin and norepinephrine, and also reduces muscle tenderness by a separate mechanism. Studies evaluating acupuncture for tension-type headaches have been mixed. Overall, they show that acupuncture is probably not helpful for tension-type headaches. Cluster headaches Abortive therapy for cluster headaches includes subcutaneous sumatriptan (injected under the skin) and triptan nasal sprays. High flow oxygen therapy also helps with relief.For people with extended periods of cluster headaches, preventive therapy can be necessary. Verapamil is recommended as first line treatment. Lithium can also be useful. For people with shorter bouts, a short course of prednisone (10 days) can be helpful. Ergotamine is useful if given 1–2 hours before an attack. Secondary headaches Treatment of secondary headaches involves treating the underlying cause. For example, a person with meningitis will require antibiotics. A person with a brain tumor may require surgery, chemotherapy or brain radiation. Neuromodulation Peripheral neuromodulation has tentative benefits in primary headaches including cluster headaches and chronic migraine. How it may work is still being looked into. Epidemiology Literature reviews find that approximately 64–77% of adults have had a headache at some point in their lives. During each year, on average, 46–53% of people have headaches. However, the prevalence of headache varies widely depending on how the survey was conducted, with studies finding lifetime prevalence of as low as 8% to as high as 96%. Most of these headaches are not dangerous. Only approximately 1–5% of people who seek emergency treatment for headaches have a serious underlying cause.More than 90% of headaches are primary headaches. Most of these primary headaches are tension headaches. Most people with tension headaches have "episodic" tension headaches that come and go. Only 3.3% of adults have chronic tension headaches, with headaches for more than 15 days in a month.Approximately 12–18% of people in the world have migraines. More women than men experience migraines. In Europe and North America, 5–9% of men experience migraines, while 12–25% of women experience migraines.Cluster headaches are relatively uncommon. They affect only 1–3 per thousand people in the world. Cluster headaches affect approximately three times as many men as women. History The first recorded classification system was published by Aretaeus of Cappadocia, a medical scholar of Greco-Roman antiquity. He made a distinction between three different types of headache: i) cephalalgia, by which he indicates a shortlisting, mild headache; ii) cephalea, referring to a chronic type of headache; and iii) heterochromia, a paroxysmal headache on one side of the head. Another classification system that resembles the modern ones was published by Thomas Willis, in De Cephalalgia in 1672. In 1787 Christian Baur generally divided headaches into idiopathic (primary headaches) and symptomatic (secondary ones), and defined 84 categories. Children In general, children experience the same types of headaches as adults do, but their symptoms may be slightly different. The diagnostic approach to headaches in children is similar to that of adults. However, young children may not be able to verbalize pain well. If a young child is fussy, they may have a headache.Approximately 1% of emergency department visits for children are for headache. Most of these headaches are not dangerous. The most common type of headache seen in pediatric emergency rooms is headache caused by a cold (28.5%). Other headaches diagnosed in the emergency department include post-traumatic headache (20%), headache related to a problem with a ventriculoperitoneal shunt (a device put into the brain to remove excess CSF and reduce pressure in the brain) (11.5%) and migraine (8.5%). The most common serious headaches found in children include brain bleeds (subdural hematoma, epidural hematoma), brain abscesses, meningitis and ventriculoperitoneal shunt malfunction. Only 4–6.9% of kids with a headache have a serious cause.Just as in adults, most headaches are benign, but when head pain is accompanied with other symptoms such as speech problems, muscle weakness, and loss of vision, a more serious underlying cause may exist: hydrocephalus, meningitis, encephalitis, abscess, hemorrhage, tumor, blood clots, or head trauma. In these cases, the headache evaluation may include CT scan or MRI in order to look for possible structural disorders of the central nervous system. If a child with a recurrent headache has a normal physical exam, neuroimaging is not recommended. Guidelines state children with abnormal neurologic exams, confusion, seizures and recent onset of worst headache of life, change in headache type or anything suggesting neurologic problems

Headache

should receive neuroimaging.When children complain of headaches, many parents are concerned about a brain tumor. Generally, headaches caused by brain masses are incapacitating and accompanied by vomiting. One study found characteristics associated with brain tumor in children are: headache for greater than 6 months, headache related to sleep, vomiting, confusion, no visual symptoms, no family history of migraine and abnormal neurologic exam.Some measures can help prevent headaches in children. Drinking plenty of water throughout the day, avoiding caffeine, getting enough and regular sleep, eating balanced meals at the proper times, and reducing stress and excess of activities may prevent headaches. Treatments for children are similar to those for adults, however certain medications such as narcotics should not be given to children.Children who have headaches will not necessarily have headaches as adults. In one study of 100 children with headache, eight years later 44% of those with tension headache and 28% of those with migraines were headache free. In another study of people with chronic daily headache, 75% did not have chronic daily headaches two years later, and 88% did not have chronic daily headaches eight years later. See also Eye strain References External links Headache at Curlie

Viral cardiomyopathy

Viral cardiomyopathy occurs when viral infections cause myocarditis with a resulting thickening of the myocardium and dilation of the ventricles. These viruses include Coxsackie B and adenovirus, echoviruses, influenza H1N1, Epstein–Barr virus, rubella (German measles virus), varicella (chickenpox virus), mumps, measles, parvoviruses, yellow fever, dengue fever, polio, rabies and the viruses that cause hepatitis A and C, as well as COVID-19, which has been seen to cause this in persons otherwise thought to have a "low risk" of the viruss effects. COVID-19 Cardiomyopathy Patients with Covid-19 frequently experience heart issues. According to studies, people who have had previous cardiovascular conditions like cardiomyopathy, hypertension, coronary heart disease, or arrhythmia are more likely to become critically ill from SARS-CoV-2 infection. Myocarditis may result from a direct viral infection of the myocardium. Cardiovascular biomarkers like troponin, lactate dehydrogenase, high sensitivity amino-terminal B-type natriuretic peptide, creatinine kinase, and creatinine kinase myocardial band, which indicate myocardial damage, increase in concentration in response to covid-19. Hundreds of studies have reported myocarditis/myopericarditis caused by Covid-19 infection in living patients, with a male predominance (58%), and a median age of 50 years. See also Coxsackievirus-induced cardiomyopathy Myocarditis Pericarditis Vaccine adverse event References External links Myocarditis on emedicine

Argyll Robertson pupil

Argyll Robertson pupils (AR pupils) are bilateral small pupils that reduce in size on a near object (i.e., they accommodate), but do not constrict when exposed to bright light (i.e., they do not react). They are a highly specific sign of neurosyphilis; however, Argyll Robertson pupils may also be a sign of diabetic neuropathy. In general, pupils that accommodate but do not react are said to show light-near dissociation (i.e., it is the absence of a miotic reaction to light, both direct and consensual, with the preservation of a miotic reaction to near stimulus (accommodation/convergence).AR pupils are extremely uncommon in the developed world. There is continued interest in the underlying pathophysiology, but the scarcity of cases makes ongoing research difficult. Pathophysiology The two different types of near response are caused by different underlying disease processes. Adies pupil is caused by damage to peripheral pathways to the pupil (parasympathetic neurons in the ciliary ganglion that cause pupillary constriction to bright light and with near vision). The pathophysiologic mechanism which produces an Argyll Robertson pupil is unclear, but is believed to be the result of bilateral damage to the pretectal nuclei in the midbrain. Studies have failed to demonstrate a focal localising lesion. Research has implicated the rostral midbrain in the vicinity of the cerebral aqueduct of the third ventricle as the most likely region of damage. A lesion in this area would involve efferent pupillary fibres on the dorsal aspect of the Edinger-Westphal nucleus (associated with the response to light) while sparing the fibres associated with the response to near, which lie slightly more ventrally. The exact relationship between syphilis and the two types of pupils (AR pupils and tonic pupils) is not known at the present time. The older literature on AR pupils did not report the details of pupillary constriction (brisk vs. tonic) that are necessary to distinguish AR pupils from tonic pupils. Tonic pupils can occur in neurosyphilis. It is not known whether neurosyphilis itself (infection by Treponema pallidum) can cause tonic pupils, or whether tonic pupils in syphilis simply reflect a coexisting peripheral neuropathy. Thompson and Kardon summarize the present view: The evidence supports a midbrain cause of the AR pupil, provided one follows Loewenfeld’s definition of the AR pupil as small pupils that react very poorly to light and yet seem to retain a normal pupillary near response that is definitely not tonic.To settle the question of whether the AR pupil is of central or peripheral origin, it will be necessary to perform iris transillumination (or a magnified slit-lamp examination) in a substantial number of patients who have a pupillary light-near dissociation (with and without tonicity of the near reaction), perhaps in many parts of the world. Parinaud syndrome A third cause of light-near dissociation is Parinaud syndrome, also called dorsal midbrain syndrome. This uncommon syndrome involves vertical gaze palsy associated with pupils that “accommodate but do not react." The causes of Parinaud syndrome include brain tumors (pinealomas), multiple sclerosis and brainstem infarction. Due to the lack of detail in the older literature and the scarcity of AR pupils at the present time, it is not known whether syphilis can cause Parinaud syndrome. It is not known whether AR pupils are any different from the pupils seen in other dorsal midbrain lesions. The condition is diagnosed clinically by a physician. Treatment There is no definite treatment, but, because syphilis may be an underlying cause, it should be treated. However, because this sign is associated with neurosyphilis, it should be treated with crystalline penicillin 24 mU intravenous per day for 10 to 14 days. If the patient is allergic to penicillin, they should undergo desensitization and then be treated. History Argyll Robertson pupils were named after Douglas Argyll Robertson (1837–1909), a Scottish ophthalmologist and surgeon who described the condition in the mid-1860s in the context of neurosyphilis. In the early 20th century, William John Adie described a second type of pupil that could "accommodate but not react". Adies tonic pupil is usually associated with a benign peripheral neuropathy (Adie syndrome), not with syphilis.When penicillin became widely available in the 1940s, the prevalence of AR pupils (which develop only after decades of untreated infection) decreased dramatically. AR pupils are now quite rare. A patient whose pupil “accommodates but does not react” almost always has a tonic pupil, not an AR pupil. In the 1950s, Loewenfeld distinguished between the two types of pupils by carefully observing the exact way in which the pupils constrict with near vision. The near response in AR pupils is brisk and immediate. The near response in tonic pupils is slow and prolonged. See also References Further reading Pearce JM (2004). "The Argyll Robertson pupil". J. Neurol. Neurosurg. Psychiatry. 75 (9): 1345. doi:10.1136/jnnp.2003.014225. PMC 1739227. PMID 15314131. == External links ==

Hypernasal speech

Hypernasal speech is a disorder that causes abnormal resonance in a humans voice due to increased airflow through the nose during speech. It is caused by an open nasal cavity resulting from an incomplete closure of the soft palate and/or velopharyngeal sphincter. In normal speech, nasality is referred to as nasalization and is a linguistic category that can apply to vowels or consonants in a specific language. The primary underlying physical variable determining the degree of nasality in normal speech is the opening and closing of a velopharyngeal passage way between the oral vocal tract and the nasal vocal tract. In the normal vocal tract anatomy, this opening is controlled by lowering and raising the velum or soft palate, to open or close, respectively, the velopharyngeal passageway. Anatomy The palate comprises two parts, the hard palate (palatum durum) and the soft palate (palatum molle), which is connected to the uvula. The movements of the soft palate and the uvula are made possible by the velopharyngeal sphincter. During speech or swallowing, the soft palate lifts against the back throat wall to close the nasal cavity. When producing nasal consonants (such as "m", "n", and "ng"), the soft palate remains relaxed, thereby enabling the air to go through the nose. The Eustachian tube, which opens near the velopharyngeal sphincter, connects the middle ear and nasal pharynx. Normally, the tube ensures aeration and drainage (of secretions) of the middle ear. Narrow and closed at rest, it opens during swallowing and yawning, controlled by the tensor veli palatini and the levator veli palatini (muscles of the soft palate). Children with a cleft palate have difficulties controlling these muscles and thus are unable to open the Eustachian tube. Secretions accumulate in the middle ear when the tube remains dysfunctional over a long period of time, which cause hearing loss and middle ear infections. Ultimately, hearing loss can lead to impaired speech and language development. Causes The general term for disorders of the velopharyngeal valve is velopharyngeal dysfunction (VPD). It includes three subterms: velopharyngeal insufficiency, velopharyngeal inadequacy, and velopharyngeal mislearning. Velopharyngeal insufficiency can be caused by an anatomical abnormality of the throat. It occurs in children with a history of cleft palate or submucous cleft, who have short or otherwise abnormal vela. Velopharyngeal insufficiency can also occur after adenoidectomy. Velopharyngeal incompetence is a defective closure of the velopharyngeal valve due to its lack of speed and precision. It is caused by a neurologic disorder or injury (e.g. cerebral palsy or traumatic brain injury). Sometimes children present no abnormalities yet still have hypernasal speech: this can be due to velopharyngeal mislearning, indicating that the child has been imitating or has never learned how to use the valve correctly. Diagnosis There are several methods for diagnosing hypernasality. A speech therapist listens to and records the child while analysing perceptual speech. In hypernasality, the child cannot produce oral sounds (vowels and consonants) correctly. Only the nasal sounds can be correctly produced. A hearing test is also desirable. A mirror is held beneath the nose while the child pronounces the vowels. Nasal air escape, and thus hypernasality, is indicated if the mirror fogs up. A pressure-flow technique is used to measure velopharyngeal orifice area during the speech. The patient must be at least three to four years old. A video nasopharyngeal endoscopy observes velopharyngeal function, movements of the soft palate, and pharyngeal walls. It utilises a very small scope placed in the back of the nasal cavity. The doctor will then ask the child to say a few words. The patient must be at least three to four years old to ensure cooperation. A cinefluoroscopy gives dynamic visualisation and can easier be applied to younger children, though it has the disadvantage of exposing the patient to radiation. A nasometer calculates the ratio of nasality. The patient wears a headset, where the oral and nasal cavities are separated by a plate. On both sides of the plate are microphones. The ratio calculated by the nasometer indicates the amount of nasality, with a higher ratio indicating more nasality. Effects on Speech Hypernasality is generally segmented into so-called resonance effects in vowels and some voiced or sonorant consonants and the effects of excess nasal airflow during those consonants requiring a buildup of oral air pressure, such as stop consonants (as /p/) or sibilants (as /s/). The latter nasal airflow problem is termed nasal emission, and acts to prevent the buildup of air pressure and thus prevent the normal production of the consonant. In testing for resonance effects without the aid of technology, speech pathologists are asked to rate the speech by listening to a recorded sentence or paragraph, though there is much variability in such subjective ratings, for at least two reasons. First, the acoustic effect of a given velopharyngeal opening varies greatly depending on the degree of occlusion of the nasal passageways. (This is the reason why a stuffy nose from an allergy or cold will sound more nasal than when the nose is clear.) Secondly, for many persons with hypernasal speech, especially hearing impaired, there are also mispronunciations of the articulation of the vowels. It is extremely difficult to separate the acoustic effects of hypernasality from the acoustic effects of mispronounced vowels (examples). Of course, in speech training of the hearing impaired, there is little possibility of making nasality judgments aurally, and holding a finger to the side of the nose, to feel voice frequency vibration, is sometimes recommended. Treatment Speech therapy In cases of muscle weakness or cleft palate, special exercises can help to strengthen the soft palate muscles with the ultimate aim of decreasing airflow through the nose and thereby increasing intelligibility. Intelligibility requires the ability to close the nasal cavity, as all English sounds, except the nasal sounds "m" [m], "n" [n], and "ng" [ŋ], have airflow only through the mouth. Normally, by age three, a child can raise the muscles of the soft palate to close to nasal cavity. Without the use of a technological aid, nasal emission is sometimes judged by listening for any turbulence that may be produced by the nasal airflow, as when there is a small velopharyngeal opening and there is some degree of mucous in the opening. More directly, methods recommended include looking for the fogging of a mirror held near the nares or listening through a tube, the other end of which is held in or near a nares opening.There have been many attempts to use technological augmentation more than a mirror or tube to aid the speech pathologist or provide meaningful feedback to the person attempting to correct their hypernasality. Among the more successful of these attempts, the incompleteness of velopharyngeal closure during vowels and sonorants that causes nasal resonance can be estimated and displayed for evaluation or biofeedback in speech training through the nasalance of the voice, with nasalance defined as a ratio of acoustic energy at the nostrils to that at the mouth, with some form of acoustic separation present between the mouth and nose. In the nasalance measurement system sold by WEVOSYS, the acoustic separation is provided by a mask-tube system, nasalance measurement system sold by Kay-Pentax, the acoustic separation is provided by a solid flat partition held against the upper lip, while in the system sold by Glottal Enterprises the acoustic separation can be by either a solid flat partition or a two-chamber mask.However, devices for measuring nasalance do not measure nasal emission during pressure consonants. Because of this, a means for measuring the degree of velopharyngeal closure in consonants is also needed. A commercially available device for making such measurements is the Perci-Sar system from Microtronics. The Nasality Visualization System from Glottal Enterprises allows both the measurement of Nasal Emission and Nasalance. In the presence of a cleft palate, either of these systems can be helpful in evaluating the need for an appliance or surgical intervention to close the cleft or the success of an appliance or a surgical attempt to close the cleft. Exercises If a child finds it difficult to blow, pinching the nose can help regulate airflow. The child should then practice speech sounds without pinching the nose. These exercises only work as treatments if hypernasality is small. Severe deviations should be treated surgically. CPAP There is insufficient evidence to support the use of traditional non-speech oral motor exercises can reduce hypernasality. Velopharyngeal closure patterns and their underlying neuromotor control may differ for speech and nonspeech activities. Therefore, the increase in velar movement through blowing, sucking, and swallowing may not transfer to speech tasks. Thus, hypernasality remains while individual speak. Kuehn proposed a new way of treatment by using a CPAP machine during speech tasks. The positive pressure provided by a CPAP machine provides resistance to strengthen velopharyngeal muscles. With nasal mask in place, an individual is asked to produce VNCV syllables and short sentences. It is believed that CPAP therapy can increase both muscle endurance as well as strength because it overloads the levator veli palatini muscle and involves a regimen with a large number of repetitions of velar elevation. Research findings proved that patients with hypernasality due to flaccid dysarthria, TBI or cleft palate do eliminate hypernasality after receiving this training program. Surgery The two main surgical techniques for correcting the aberrations the soft palate present in hypernasality are the posterior pharyngeal flap and the sphincter pharyngoplasty. After surgical interventions, speech therapy is necessary to learn how to control the newly constructed flaps. Posterior pharyngeal flap Posterior pharyngeal flap surgery is mostly used for vertical clefts of the soft palate. The surgeon cuts through the upper layers of the back of the throat, creating a small square of tissue. This flap remains attached on one side (usually at the top). The other side is attached to (parts of) the soft palate. This ensures that the nasal cavity is partially separated from the oral cavity. When the child speaks, the remaining openings close from the side due to the narrowing of the throat caused by the muscle movements necessary for speech. In a relaxed state, the openings allow breathing through the nose. Sphincter pharyngoplasty Sphincter pharyngoplasty is mostly used for horizontal clefts of the soft palate. Two small flaps are made on the left and right side of the entrance to the nasal cavity, attached to the back of the throat. For good results, the patient must have good palatal motion, as the occlusion of the nasal cavity is mainly carried out by muscles already existing and functioning. Complications The most common complications of the posterior pharyngeal wall flap are hyponasality, nasal obstruction, snoring, and sleep apnea. Rarer complications include flap separation, sinusitis, postoperative bleeding, and aspiration pneumonia. Possible complications of the sphincter pharyngoplasty are snoring, nasal obstruction, difficulty blowing the nose. Some researches suggest that sphincter pharyngoplasty introduces less hyponasality and obstructive sleep symptoms than the posterior pharyngeal wall flap. Both surgeries have a favourable effect on the function of the Eustachian tube. See also Rhinolalia clausa Nasalization Nasalance References == External links ==

Sister

A sister is a woman or a girl who shares one or more parents with another individual; a female sibling. The male counterpart is a brother. Although the term typically refers to a familial relationship, it is sometimes used endearingly to refer to non-familial relationships. A full sister is a first degree relative. Overview The English word sister comes from Old Norse systir which itself derives from Proto-Germanic *swestēr, both of which have the same meaning, i.e. sister. Some studies have found that sisters display more traits indicating jealousy around their siblings than their male counterparts, brothers. In some cultures, sisters are afforded a role of being under the protection by male siblings, especially older brothers from issues ranging from bullies or sexual advances by womanizers. In some quarters the term sister has gradually broadened its colloquial meaning to include individuals stipulating kinship. In response, in order to avoid equivocation, some publishers prefer the usage of female sibling over sister. Males with a twin sister sometimes view her as their female alter ego, or what they would have been like, if they had two X chromosomes. A study in Perth Australia found that girls having only youngers brothers resulted in a chastity effect, losing their virginity on average more than a year later than average. This has been hypothesized as being attributed to the pheromones in their brothers sweat and household-related errands. Sororal relationships Various studies have shown that older sisters are likely to give a varied gender role to their younger siblings as well as being more likely to develop a close bond with their younger siblings. Older sisters are more likely to play with their younger siblings. Younger siblings display a more needy behavior when in close proximity to their older sister and are more likely to be tolerant of an older sisters bad behavior. Boys with only an older sister are more likely to display stereotypically male behavior, and such masculine boys increased their masculine behavior with the more sisters they have. The reverse is true for young boys with several sisters, as they tend to be feminine, however, they outgrow this by the time they approach pubescence. Boys with older sisters were less likely to be delinquent or have emotional and behavioral disorders. A younger sister is less likely to be scolded by older siblings than a younger brother. The most common recreational activity between older brother/younger sister pairs is art drawing. Some studies also found a correlation between having an older sister and constructive discussions about safe sexual practices. Some studies have shown that men without sisters are more likely to be ineffectual at courtship and romantic relationships. Fictional works about sisters Films What Ever Happened to Baby Jane? (1962) Hannah and Her Sisters (1986) Hanging Up (2000) Frozen (2013) Little Women (2019) Literature Little Women Laura Lee Hopes Bobbsey Twins novels, which included two sets of fraternal twins: 12-year-old Nan and Bert, and six-year-old Flossie and Freddie In Her Shoes (2002), novel #Toots (2019), novel Television Hope & Faith, American sitcom Sisters (TV series) What I Like About You, TV series Sister, Sister, TV series Games Jessica & Zofia Blazkowicz , Wolfenstein: Youngblood Mileena & Kitana, Mortal Kombat Kat and Ana, WarioWare See also Brother Sisterhood (disambiguation) Religious sister References External links The dictionary definition of sister at Wiktionary

Monocytosis

Monocytosis is an increase in the number of monocytes circulating in the blood. Monocytes are white blood cells that give rise to macrophages and dendritic cells in the immune system. In humans, monocytosis occurs when there is a sustained rise in monocyte counts greater than 800/mm3 to 1000/mm3.Monocytosis has sometimes been called mononucleosis, but that name is usually reserved specifically for infectious mononucleosis. Causes Monocytosis often occurs during chronic inflammation. Diseases that produce such a chronic inflammatory state: Infections: tuberculosis, brucellosis, listeriosis, subacute bacterial endocarditis, syphilis, and other viral infections and many protozoal and rickettsial infections (e.g. kala azar, malaria, Rocky Mountain spotted fever). Blood and immune causes: chronic neutropenia and myeloproliferative disorders. Autoimmune diseases and vasculitis: systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel disease. Malignancies: Hodgkins disease and certain leukaemias, such as chronic myelomonocytic leukaemia (CMML) and monocytic leukemia. Recovery phase of neutropenia or an acute infection. Obesity (cf. Nagareddy et al. (2014), Cell Metabolism, Vol. 19, pp 821–835) Miscellaneous causes: sarcoidosis, lipid storage disease and ZNFX1 deficiency.During these stages of extreme inflammation, monocytosis can damage tissues because it increases the activation of the immune response and prevents the inflammation from subsiding which is seen in cases where sepsis occurs. Diagnosis Blood Test (CBC) (Normal range of Monocytes: 1-10%) (Normal range in males: 0.2-0.8 x 103/microliter) Blood test checking for monocytosis (Abnormal ranges: >10%) (Abnormal range in males: >0.8 x 103/microliter) Treatment Ceftriaxone if there is typhoid fever and levofloxacin or moxifloxacin. Gentamicin and doxycyclin if brucellosis. References == External links ==

Plica syndrome

Plica syndrome is a condition that occurs when a plica (a vestigial extension of the protective synovial capsule of usually the knee) becomes irritated, enlarged, or inflamed. Cause This inflammation is typically caused by the plica being caught on the femur, or pinched between the femur and the patella. The most common location of plica tissue is along the medial (inside) side of the knee. The plica can tether the patella to the femur, be located between the femur and patella, or be located along the femoral condyle. If the plica tethers the patella to the femoral condyle, the symptoms may cause it to be mistaken for chondromalacia. The plica themselves are remnants of the fetal stage of development where the knee is divided into three compartments. The plica normally diminish in size during the second trimester of fetal development, as the three compartments develop into the synovial capsule. In adults, they normally exist as sleeves of tissue called synovial folds. The plica are usually harmless and unobtrusive; plica syndrome only occurs when the synovial capsule becomes irritated, which thickens the plica themselves (making them prone to irritation/inflammation, or being caught on the femur). Diagnosis If the plica tethers the patella to the femoral condyle, the symptoms may cause it to be mistaken for chondromalacia patellae. Diagnosis is often complicated by the thin structures of plicae, fenestrated septum or unfenestrated septum all being too fine to resolve well even in MRI. Treatment Plica syndrome treatment focuses on decreasing inflammation of the synovial capsule. A nonsteroidal anti-inflammatory drug (NSAID) is often used in conjunction with therapeutic exercise and modalities. Iontophoresis and phonophoresis have been utilized successfully against inflammation of the plica and synovial capsule. Failing these, surgical removal of the plica of the affected knee may be necessary. See also Knee pain Patellofemoral pain syndrome Iliotibial band syndrome References == External links ==

Disorder

Disorder may refer to randomness, non-order, or no intelligible pattern. Disorder may also refer to: Healthcare Disorder (medicine), a functional abnormality or disturbance Mental disorder or psychological disorder, a psychological pattern associated with distress or disability that occurs in an individual and is not a part of normal development or culture:Anxiety disorder, different forms of abnormal and pathological fear and anxiety Conversion disorder, neurological symptoms such as numbness, blindness, paralysis, or fits, where no neurological explanation is possible Obsessive–compulsive disorder, an anxiety disorder characterized by repetitive behaviors aimed at reducing anxiety Obsessive–compulsive personality disorder, obsession with perfection, rules, and organization Personality disorder, an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the culture of the individual who exhibits it Law enforcement Civil disorder, one or more forms of disturbance caused by a group of people Lawlessness, a lack of laws or law enforcement Science Crystallographic disorder, disordered atom locations in crystals Order and disorder Arts, entertainment, and media Films Disorder (1962 film), a film by Franco Brusati Disorder (2009 film), a Chinese documentary Disorder (2015 film), a French film Music Disorder (band), a Bristol-based hardcore punk band Disorder (album), an album by The Gazette Disorder (EP), an EP by Front Line Assembly "Disorder", a song by Joy Division from the 1979 album Unknown Pleasures Other uses Dis-order, the mail order service of Displeased Records See also Chaos Order

Tinea manuum

Tinea manuum is a fungal infection of the hand, mostly a type of dermatophytosis, often part of two feet-one hand syndrome. There is diffuse scaling on the palms or back of usually one hand and the palmer creases appear more prominent. When both hands are affected, the rash looks different on each hand, with palmer creases appearing whitish if the infection has been present for a long time. It can be itchy and look slightly raised. Nails may also be affected.The most common cause is Trichophyton rubrum. The infection can result from touching another area of the body with a fungal infection such as athletes foot or fungal infection of groin, contact with an infected person or animal, or from contact with soil or contaminated towels. Risk factors include diabetes, high blood pressure, weak immune system, humid surroundings, excessive sweating, recurrent hand trauma and cracks in feet. Pet owners and farmworkers are also at higher risk. Machine operators, mechanics, gas/electricity workers and people who work with chemicals have also been reported to be at greater risk.Diagnosis is by visualization, direct microscopy and culture. Psoriasis of the palms, pompholyx and contact dermatitis may appear similar. Treatment is usually with long-term topical antifungal medications. If not resolving, terbinafine or itraconazole taken by mouth might be options.It occurs worldwide. One large study revealed around 84% of tinea manuum was associated with athletes foot, of which 80% admitted scratching their feet, and 60% were male, Signs and symptoms There is usually an itch, with generalised dry flaky thick skin of the palm of a hand. Frequently, one hand is affected, but it can be in both. If the back of the hand is affected, it may appear as reddish circles like in ringworm. Sometimes there are no symptoms. The feet may be affected as in two feet-one hand syndrome. Cause and mechanism The most common cause is Trichophyton rubrum. Other causes include Trichophyton verrucosum (from cattle), Microsporum canis (from a cat or dog), Trichophyton erinacei (from a hedgehog), Trichophyton mentagrophytes, Epidermophyton floccosum, Trichophyton interdigitale, and more rarely Microsporum gypseum, Trichophyton eriotrephon, and Arhroderma benhamiae.Tinea manuum can result from touching another area of the body with a fungal infection such as athletes foot or tinea cruris, contact with an infected person or animal, or from contact with soil or contaminated towels. Risk factors Diabetes, high blood pressure, weak immune system, humid surroundings, excessive sweating, recurrent hand trauma and cracks in feet are risk factors for tinea manuum. Pet owners and farmworkers are also at higher risk. Diagnosis Diagnosis is by visualization, direct microscopy and culture. Differential diagnosis Psoriasis of the palms, pompholyx and contact dermatitis may appear similar. Treatment Treatment is usually with long-term topical antifungal medications. If not resolving, terbinafine or itraconazole by mouth might be options. Other options include clotrimazole, fluconazole and ketoconazole. Prevention Prevention is focussed on hygiene such as washing hands, avoiding scratching the feet or touching fungal toe infections. Epidemiology Tinea manuum is most common in young adult males. Dermatophyte infections occur in up to a quarter of the worlds population, of which the hands and feet are most commonly involved. It occurs worldwide. One large study revealed around 84% of tinea manuum was associated with athletes foot, of which 80% admitted scratching their feet, and 60% were male, See also List of cutaneous conditions References == External links ==

Pantothenate kinase-associated neurodegeneration

Pantothenate kinase-associated neurodegeneration (PKAN), formerly called Hallervorden–Spatz syndrome, is a genetic degenerative disease of the brain that can lead to parkinsonism, dystonia, dementia, and ultimately death. Neurodegeneration in PKAN is accompanied by an excess of iron that progressively builds up in the brain. PKAN is caused by loss of function of the enzyme PANK2, due to bi-allelic genetic mutations. It follows autosomal recessive inheritance. This enzyme is the first step in the pathway converting vitamin B5 into coenzyme A. There are currently no treatments that modify disease progress, though there are a number of medications and therapies that can help improve symptoms and there is active research into treatments. Signs and symptoms Symptoms typically begin in childhood and are progressive, often resulting in death by early adulthood. Symptoms of PKAN begin before middle childhood, and most often are noticed before ten years of age. Symptoms include: dystonia (repetitive uncontrollable muscle contractions that may cause jerking or twisting of certain muscle groups) dysphagia & dysarthria due to muscle groups involved in speech being involved rigidity/stiffness of limbs tremor writhing movements dementia spasticity weakness seizures (rare) toe walking retinitis pigmentosa, another degenerative disease that affects the individuals retina, often causing alteration of retinal color and progressive deterioration of the retina at first causing night blindness and later resulting in a complete loss of vision.25% of individuals experience an uncharacteristic form of PKAN that develops post-10 years of age and follows a slower, more gradual pace of deterioration than those pre-10 years of age. These individuals face significant speech deficits as well as psychiatric and behavioral disturbances.Being a progressive, degenerative nerve illness, PKAN leads to early immobility and often death by early adulthood. Death occurs prematurely due to infections such as pneumonia, and the disease in itself is technically not life limiting. Genetics PKAN is an autosomal recessive disorder. Both the parents of an affected child must be heterozygous carriers for the disease and therefore must carry one mutant allele. As it is an autosomal disorder, those heterozygous for the disorder may not display any atypical characteristics that are considered suggestive of the disorder, however there have been reported cases of compound heterozygosity in which heterozygous individuals do develop the classic form of the disease.The disorder is caused by a mutant PANK2 gene located at the chromosomal locus: 20p13-p12.3. PANK2 is responsible for coding the protein Pantothenate kinase 2. PANK2 encodes the enzyme pantothenate kinase, and mutations in the gene lead to an inborn error of vitamin B5 (pantothenate) metabolism. Vitamin B5 is required for the production of coenzyme A in cells. Disruption of this enzyme affects energy and lipid metabolism and may lead to accumulation of potentially harmful compounds in the brain, including iron.PANK2 encodes a 1.85Kb transcript which is derived from seven exons covering a total distance of approximately 3.5Mb of genomic DNA. The PANK2 gene also encodes a 50.5-kDaprotein that is a functional pantothenate kinase, an essential regulatory enzyme in coenzyme A (CoA) biosynthesis, and catalyzing the phosphorylation of pantothenate (vitamin B5), N-pantothenoyl-cysteine, and pantetheine (OMIM). Mutant PANK2 gene coded proteins are often caused by null or missense mutations most notably a 7bp deletion in the PANK2 gene coding sequence.This disorder has been reported in specific communities based on intra-community marriages where both parents of the child are carrying the same mutation. One of the communities reported is Agrawal (Agarwal) Community mainly based in Northern Part of India. The known mutation in Agarwal community is pathogenic mutation 1c.215_216insA in PANK2 gene. This is also coded as chr20:3870292-3870293insA by some labs. It results in a frameshift and premature truncation of the protein 47 amino acids downstream to codon 183 (p.Arg183GlufsTer47; ENST00000316562). Diagnosis A neurological examination would show evidence of muscle rigidity; weakness; and abnormal postures, movements, and tremors. If other family members are also affected, this may help determine the diagnosis. Genetic tests can confirm an abnormal gene causing the disease. However, this test is not yet widely available. Other movement disorders and diseases must be ruled out. Individuals exhibiting any of the above listed symptoms are often tested using MRI (Magnetic Resonance Imaging) for a number of neuro-related disorders. An MRI usually shows iron deposits in the basal ganglia. Development of diagnostic criteria continues in the hope of further separating PKAN from other forms of neurodegenerative diseases featuring NBIA. Neuropathology Microscopic features of PKAN include high levels of iron in the globus pallidus and the pars reticulata of substantia nigra, evident as a characteristic rust-brown discoloration in a pattern called the eye-of-the-tiger sign; lipofuscin and neuromelanin concentrated in the iron-accumulating areas; oval, nonnucleated structures representing swollen axons whose cytoplasm swells with vacuoles, referred to as spheroids, axon schollen, or neuroaxonal dystrophy; and Lewy bodies. Treatment Phosphopantothenate has been shown to treat PKAN in a human, and also in a mouse model of the disease. Pantethine (a precursor of pantetheine) has been studied and shown to be effective in a mouse and in a fruit fly model of the disease. Prognosis Survival rates for those diagnosed with typical PKAN, and left untreated is 11.18 years with a standard deviation of 7.8 years. A study reporting good outcomes in a single patient with late onset PKAN has been performed. Epidemiology Prevalence data regarding this disorder remains incomplete, however it is estimated that anywhere between 1 in 1,000,000 to 3 in 1,000,000 individuals will be affected by this disorder (based upon observed cases in a population), but once again this is only an estimate as the disease is so rare it is difficult to statistically and accurately ascertain. History PKAN was first described by Hallervorden and Spatz (1922). Their discovery was brought about by a diagnosis of a family of 12 in which five sisters exhibited progressively increasing dementia and dysarthria. Autopsies revealed brown discolorations in different areas of the brain (particularly of interest were the globus pallidus and substantia nigra regions). Further investigation and description was brought about by Meyer (1958) who diagnosed 30 separate cases of PKAN. Meyer(1958) was followed by Elejalde et al. (1978) who described 5 affected family members and hypothesized that the disorder originated in central Europe, backing up his hypothesis with clinical and genetic analysis. Further investigation and insights were provided by Malmstrom-Groth and Kristensson (1982) and Jankovic et al. (1985).Diagnosis of PKAN hit a milestone with the availability of MRIs, as well as the in-depth descriptions of those MRIs provided by Littrup and Gebarski (1985), Tanfani et al. (1987), Sethi et al. (1988), Angelini et al. (1992), Casteels et al. (1994), and Malandrini et al. (1995). The gene was localized to chromosome 20p by Taylor et al. (1996) who suggested that this disorder should be referred to as neurodegeneration with brain iron accumulation (NBIA1) to avoid the objectionable eponym of Hallervorden-Spatz. The disease was renamed pantothenate kinase-associated neurodegeneration or PKAN by Zhou et al. (2001) who suggested the name to avoid misinterpretation and to better reflect the true nature of the disorder. Most recently Pellecchia et al. (2005) published a report of 16 patients affected by PKAN, confirmed by genetic analysis. References External links 02041 at CHORUSsynd/1082 at Who Named It? nbia at NINDS

Activity

Activity may refer to: Action (philosophy), in general Human activity: human behavior, in sociology behavior may refer to all basic human actions, economics may study human economic activities and along with cybernetics and psychology may study their modulation Recreation, or activities of leisure The Aristotelian concept of energeia, Latinized as actus Activity (UML), a major task in Unified Modeling Language Activity, the rate of catalytic activity, such as enzyme activity (enzyme assay), in physical chemistry and enzymology Thermodynamic activity, the effective concentration of a solute for the purposes of mass action Activity (project management) Activity, the number of radioactive decays per second Activity (software engineering) Activity (soil mechanics) HMS Activity (D94), an aircraft carrier of the Royal Navy "Activity", a song by Way Out West from Intensify Cultural activities, activities referred to culture. See also Activity theory, a learning theory in education Social activity (disambiguation), several concepts in the social sciences Activiti (software), an open source Business Process Management platform Active (disambiguation)

Thoracic cavity

The thoracic cavity (or chest cavity) is the chamber of the body of vertebrates that is protected by the thoracic wall (rib cage and associated skin, muscle, and fascia). The central compartment of the thoracic cavity is the mediastinum. There are two openings of the thoracic cavity, a superior thoracic aperture known as the thoracic inlet and a lower inferior thoracic aperture known as the thoracic outlet. The thoracic cavity includes the tendons as well as the cardiovascular system which could be damaged from injury to the back, spine or the neck. Structure Structures within the thoracic cavity include: structures of the cardiovascular system, including the heart and great vessels, which include the thoracic aorta, the pulmonary artery and all its branches, the superior and inferior vena cava, the pulmonary veins, and the azygos vein structures of the respiratory system, including the diaphragm, trachea, bronchi and lungs structures of the digestive system, including the esophagus, endocrine glands, including the thymus gland, structures of the nervous system including the paired vagus nerves, and the paired sympathetic chains, lymphatics including the thoracic duct.It contains three potential spaces lined with mesothelium: the paired pleural cavities and the pericardial cavity. The mediastinum comprises those organs which lie in the centre of the chest between the lungs. The cavity also contains two openings one at the top, the superior thoracic aperture also called the thoracic inlet, and a lower inferior thoracic aperture which is much larger than the inlet. Clinical significance If the pleural cavity is breached from the outside, as by a bullet wound or knife wound, a pneumothorax, or air in the cavity, may result. If the volume of air is significant, one or both lungs may collapse, which requires immediate medical attention. Additional images See also References External links thoraxlesson3 at The Anatomy Lesson by Wesley Norman (Georgetown University)

Trichorrhexis nodosa

Trichorrhexis nodosa is a defect in the hair shaft characterized by thickening or weak points (nodes) that cause the hair to break off easily.: 766 : 636  This group of conditions contributes to the appearance of hair loss, lack of growth, and damaged-looking hair. Symptoms Among the symptoms (and signs) for this condition are the following: lack of apparent hair growth hair appears patchy hair breaks easily close to scalp hair may have thickenings or nodes in the shaft ends of hair thinned or split whitish discoloration of hair tips hair breaks easily at tips Complications This condition is not dangerous but may affect self-esteem. Causes Trichorrhexis may have a genetic basis but appears to be precipitated by environmental factors. Among Caucasians the defect often appears at the ends of the hair shaft with splitting of the ends, thinning and whitish discoloration. These conditions are directly related to environmental causes such as "perming", blow drying, aggressive hair brushing, and excessive chemical exposure. In some cases, trichorrhexis nodosa may be caused by an underlying disorder such as argininosuccinic aciduria, Menkes kinky hair syndrome, Nethertons syndrome, hypothyroidism, or trichothiodystrophy. Diagnosis Examination of the hair shafts with a microscope may reveal changes of trichorrhexis nodosa. Prevention Avoid aggressive brushing and grooming, strong chemicals, permanents, straightening, and similar hair-damaging habits. Treatment Improving environmental factors will reduce damage to the hair. Gentle brushing with a soft brush should replace more aggressive brushing, ratting, or other procedures. Harsh chemicals such as hair straightening compounds and permanents should be avoided. The hair should not be ironed. Excessively harsh shampoo should be avoided. Hair conditioners should be used. Prognosis This condition is self-limiting. Improvements in grooming techniques and in environmental conditions will correct the abnormality. See also Trichomegaly Infrared Heat & Negative Ion Straighteners List of cutaneous conditions Notes References MedlinePlus Encyclopedia: Trichorrhexis nodosa == External links ==

Alcohol dependence

Alcohol dependence is a previous (DSM-IV and ICD-10) psychiatric diagnosis in which an individual is physically or psychologically dependent upon alcohol (also chemically known as ethanol). In 2013, it was reclassified as alcohol use disorder in DSM-5, which combined alcohol dependence and alcohol abuse into this diagnosis. Definition Diagnosis DSM: Alcohol dependence According to the DSM-IV criteria for alcohol dependence, at least three out of seven of the following criteria must be manifest during a 12-month period: Tolerance Withdrawal symptoms or clinically defined alcohol withdrawal syndrome Use in larger amounts or for longer periods than intended Persistent desire or unsuccessful efforts to cut down on alcohol use Time is spent obtaining alcohol or recovering from effects Social, occupational and recreational pursuits are given up or reduced because of alcohol use Use is continued despite knowledge of alcohol-related harm (physical or psychological) Other alcohol-related disorders Because only 3 of the 7 DSM-IV criteria for alcohol dependence are required, not all patients meet the same criteria and therefore not all have the same symptoms and problems related to drinking. Not everyone with alcohol dependence, therefore, experiences physiological dependence. Alcohol dependence is differentiated from alcohol abuse by the presence of symptoms such as tolerance and withdrawal. Both alcohol dependence and alcohol abuse are sometimes referred to by the less specific term alcoholism. However, many definitions of alcoholism exist, and only some are compatible with alcohol abuse. There are two major differences between alcohol dependence and alcoholism as generally accepted by the medical community. Alcohol dependence refers to an entity in which only alcohol is the involved addictive agent. Alcoholism refers to an entity in which alcohol or any cross-tolerant addictive agent is involved. In alcohol dependence, reduction of alcohol, as defined within DSM-IV, can be attained by learning to control the use of alcohol. That is, a client can be offered a social learning approach that helps them to cope with external pressures by re-learning their pattern of drinking alcohol. In alcoholism, patients are generally not presumed to be in remission unless they are abstinent from alcohol.The following elements are the template for which the degree of dependence is judged: Narrowing of the drinking repertoire. Increased salience of the need for alcohol over competing needs and responsibilities. An acquired tolerance to alcohol. Withdrawal symptoms. Relief or avoidance of withdrawal symptoms by further drinking. Subjective awareness of compulsion to drink. Reinstatement after abstinence. Screening AUDIT has replaced older screening tools such as CAGE but there are many shorter alcohol screening tools, mostly derived from the AUDIT. The Severity of Alcohol Dependence Questionnaire (SAD-Q) is a more specific twenty-item inventory for assessing the presence and severity of alcohol dependence. AUDIT The Alcohol Use Disorders Identification Test (AUDIT) is considered the most accurate alcohol screening tool for identifying potential alcohol misuse, including dependence. It was developed by the World Health Organisation, designed initially for use in primary healthcare settings with supporting guidance. CAGE The CAGE questionnaire, the name of which is an acronym of its four questions, is a widely used method of screening for alcoholism. Online version of the CAGE questionnaire SADQ The Severity of Alcohol Dependence Questionnaire (SADQ or SAD-Q) is a 20 item clinical screening tool designed to measure the presence and level of alcohol dependence. Withdrawal Withdrawals from alcohol dependence is a common side effect that occurs when a person with the dependency stops drinking abruptly or even cuts back on their drinking after a prolonged period of indulgence. Withdrawal from alcohol dependence can vary from mild, moderate to severe, depending on several factors such as: how long the person has been drinking, are they a binge drinker, do they relapse chronically, how much do they drink daily. All these factors can vary from one person to the next depending on psychological, environmental, and biological factors. Some common withdrawal side effects are as listed: Mild Nausea Vomiting Rapid heartbeat Elevated blood pressure Fatigue Body aches / tremors Anxiety / Irritability / Depression Fuzzy brain Issues with sleeping Severe Vomiting Hypertensive crisis Seizures / Tremors Delusions / Hallucinations Dehydration Fever Chills / Shakes Extreme mood lability Mental pandemonium Little to no appetiteThe spectrum of alcohol withdrawal symptoms range from such minor symptoms as insomnia and tremulousness to severe complications such as withdrawal seizures and delirium tremens. Alcohol withdrawal syndrome can be very tricky to diagnose, due to other preliminary conditions that may exist from individual to individual. Treatment Treatments for alcohol dependence can be separated into two groups, those directed towards severely alcohol-dependent people, and those focused for those at risk of becoming dependent on alcohol. Treatment for alcohol dependence often involves utilizing relapse prevention, support groups, psychotherapy, and setting short-term goals. The Twelve-Step Program is also a popular faith-based process used by those wishing to recover from alcohol dependence.The ultimate goal when it comes to treating alcohol dependence or as the DSM-5 now calls it alcohol use disorder, is to help with establishing abstinence from drinking. There are several other benefits that come along with treatment. For some, it is reconnecting with themselves and obtaining self-esteem and confidence, a healthier lifestyle (physically and mentally), creating new relationships with other like-minded people as well as rekindling or mending old relationships if possible. The treatment process consists typically of two parts short-term and long-term. First, there is the path to abstinence and/or recovery. There are several reasons why someone with alcohol use disorder or alcohol dependency would seek treatment. This can either be a personal reason or because of law enforcement. There is a series of different levels of treatment processes depending on the severity subtype. Some would or could benefit from medication treatment with psychosocial treatment, while others could just benefit from psychosocial treatment. Listed below are different some different types of treatments that are used with treating alcohol dependency/alcohol use disorder depending on several factors that vary from person to person. Types of treatments: Withdrawals (no medication aid needed) Withdrawals (depending on severity of symptoms, could be accompanied with supervision by medical personal and medication) Psychosocial treatment (counseling, CBT, psychoeducation, assertive community treatment) Alcoholics Anonymous Inpatient or outpatient programs Social services (case management) Al-Anon/Alateen Epidemiology About 12% of American adults have had an alcohol dependence problem at some time in their life. In the UK the NHS estimates that around 9% of men and 4% of UK women show signs of alcohol dependence. History The term alcohol dependence has replaced alcoholism as a term in order that individuals do not internalize the idea of cure and disease, but can approach alcohol as a chemical they may depend upon to cope with outside pressures. The contemporary definition of alcohol dependence is still based upon early research. There has been considerable scientific effort over the past several decades to identify and understand the core features of alcohol dependence. This work began in 1976, when the British psychiatrist Griffith Edwards and his American colleague Milton M. Gross collaborated to produce a formulation of what had previously been understood as alcoholism – the alcohol dependence syndrome. The alcohol dependence syndrome was seen as a cluster of seven elements that concur. It was argued that not all elements may be present in every case, but the picture is sufficiently regular and coherent to permit clinical recognition. The syndrome was also considered to exist in degrees of severity rather than as a categorical absolute. Thus, the proper question is not whether a person is dependent on alcohol, but how far along the path of dependence has a person progressed. See also Alcohol intoxication Alcoholic drink Alcohol-related dementia CRAFFT Screening Test Disulfiram-like drug High-functioning alcoholic Long-term effects of alcohol consumption Paddington alcohol test Notes External links Arnold Little, MD Alcohol Dependence – extensive article SADD – Short Alcohol Dependence Data Questionnaire. A brief, self-administered questionnaire sometimes utilised in individual or group treatments. R.R.Garifullin Using coding therapy to treat alcohol and drug addiction. Manipulations in psychotherapy. Rostov-on-Don, Feniks, 251 p. 2004. 251 p. ISBN 5-222-04382-7

Sputum

Sputum is mucus that is coughed up from the lower airways (the trachea and bronchi). In medicine, sputum samples are usually used for a naked eye examination, microbiological investigation of respiratory infections and cytological investigations of respiratory systems. It is crucial that the specimen does not include any mucoid material from the nose or oral cavity. A naked eye exam of the sputum can be done at home by a patient in order to note the various colors (see below). Any hint of yellow or green color (pus) suggests an airway infection (but does not indicate the type of organism causing it). Such color hints are best detected when the sputum is viewed on a very white background such as white paper, a white pot or a white sink surface. The more intense the yellow color, the more likely it is a caused by an infection (bronchitis, bronchopneumonia or pneumonia). Having green, yellow, or thickened phlegm (sputum) does not always indicate the presence of an infection. Also, if an infection is present, the color of the phlegm (sputum) does not determine whether a virus, a bacterium or another pathogen has caused it. Simple allergies can also cause changes in the color of the mucus. Description The best sputum samples contain very little saliva, as saliva contaminates the sample with oral bacteria. This is especially true for samples for laboratory testing in cytology or microbiology. Specimen adequacy is assessed by the laboratory technologists by examining a Gram stain or cytology stain of the sputum. More than 25 squamous epithelial cells at low power magnification exam under the microscope strongly suggest salivary contamination. Sputum samples have been used to quantify the degree of airway inflammation in human diseases such as asthma. Specifically, this work has demonstrated that a subgroup of severe asthma patients has airway inflammation that is resistant to treatment with corticosteroids.When a sputum specimen is plated out in microbiology, it is best to get the portion of the sample that almost looks like yellow pus onto the swab. If there is any blood in the sputum, this should also be on the swab. Microbiological sputum samples are used to look for infections, such as Moraxella catarrhalis, Mycobacterium tuberculosis, Streptococcus pneumoniae, and Haemophilus influenzae. Other pathogens can also be found. Purulent sputum contains pus, composed of white blood cells, cellular debris, dead tissue, serous fluid, and viscous liquid (mucus). Purulent sputum is typically yellow or green. It is seen in cases of pneumonia, bronchiectasis, lung abscess, or an advanced stage of bronchitis. Interpretation Sputum can be (when examined by the naked eye): Bloody (hemoptysis) Blood-streaked sputum –an indicator of possible inflammation of the throat (larynx and/or trachea) or bronchi; lung cancer; other bleeding erosions, ulcers, or tumors of the lower airway. Pink sputum – it indicates sputum evenly mixed with blood from alveoli and/or small peripheral bronchi as is seen in potential pulmonary edema. Massive blood – an indicator of possible cavitary tuberculosis or tumor such as lung cancer, or lung abscess; bronchiectasis; lung infarction; pulmonary embolism. Red, jelly-like sputum - an indicator of possible pneumonia caused by Klebsiella. Green or greenish colored - indicative of potential longstanding respiratory infection (green from degenerative changes in cell debris) as in pneumonia, ruptured lung abscess, chronic infectious bronchitis, and infected bronchiectasis or cystic fibrosis. Rust colored – usually caused by pneumococcal bacteria (in pneumonia), pulmonary embolism, lung cancer or pulmonary tuberculosis. Brownish –potential indicator of chronic bronchitis (greenish/yellowish/brown); chronic pneumonia (whitish-brown); tuberculosis; lung cancer. Yellow, yellowish purulent – an indicator of the sample containing pus. "The sputum color of patients with acute cough and no underlying chronic lung disease does not imply therapeutic consequences such as prescription of antibiotics." The color can provide hints as to effective treatment in chronic bronchitis patients:A yellow-greenish (mucopurulent) color suggests that treatment with antibiotics can reduce symptoms. The green color is caused by degenerating neutrophil verdoperoxidase. Whitish gray sputum color against a white color background (such as a white sink surface) tends to indicate either a specimen from someone who is dehydrated, and/or from an older person, and/or a specimen with a mixed, modest number of eosinophils and maybe some acute inflammatory neutrophil cells (this last choice tends to suggest chronic allergic bronchitis). A white, milky, or opaque (mucoid) appearance means that antibiotics are less likely to be effective in treatment because the likelihood is greater of a viral infection or allergy (even asthma...thick sputum) than of antibiotic-responsive micro-organisms. Foamy white – may come from earlier-phase pulmonary edema. Frothy pink – may indicate more severe pulmonary edema. Antibiotics may not be necessary at this time. Clear – pulmonary embolism (clear to frothy); COPD chronic obstructive pulmonary disease (clear to gray); viral respiratory infection (clear to whitish and sometimes a hint of yellow); asthma (thick and white to yellowish). See also Phlegm References == External links ==

Congenital heart defect

A congenital heart defect (CHD), also known as a congenital heart anomaly and congenital heart disease, is a defect in the structure of the heart or great vessels that is present at birth. A congenital heart defect is classed as a cardiovascular disease. Signs and symptoms depend on the specific type of defect. Symptoms can vary from none to life-threatening. When present, symptoms may include rapid breathing, bluish skin (cyanosis), poor weight gain, and feeling tired. CHD does not cause chest pain. Most congenital heart defects are not associated with other diseases. A complication of CHD is heart failure.The cause of a congenital heart defect is often unknown. Risk factors include certain infections during pregnancy such as rubella, use of certain medications or drugs such as alcohol or tobacco, parents being closely related, or poor nutritional status or obesity in the mother. Having a parent with a congenital heart defect is also a risk factor. A number of genetic conditions are associated with heart defects, including Down syndrome, Turner syndrome, and Marfan syndrome. Congenital heart defects are divided into two main groups: cyanotic heart defects and non-cyanotic heart defects, depending on whether the child has the potential to turn bluish in color. The defects may involve the interior walls of the heart, the heart valves, or the large blood vessels that lead to and from the heart.Congenital heart defects are partly preventable through rubella vaccination, the adding of iodine to salt, and the adding of folic acid to certain food products. Some defects do not need treatment. Others may be effectively treated with catheter based procedures or heart surgery. Occasionally a number of operations may be needed, or a heart transplant may be required. With appropriate treatment, outcomes are generally good, even with complex problems.Congenital heart defects are the most common birth defect. In 2015, they were present in 48.9 million people globally. They affect between 4 and 75 per 1,000 live births, depending upon how they are diagnosed. In about 6 to 19 per 1,000 they cause a moderate to severe degree of problems. Congenital heart defects are the leading cause of birth defect-related deaths: in 2015, they resulted in 303,300 deaths, down from 366,000 deaths in 1990. Signs and symptoms Signs and symptoms are related to type and severity of the heart defect. Symptoms frequently present early in life, but it is possible for some CHDs to go undetected throughout life. Some children have no signs while others may exhibit shortness of breath, cyanosis, fainting, heart murmur, under-development of limbs and muscles, poor feeding or growth, or respiratory infections. Congenital heart defects cause abnormal heart structure resulting in production of certain sounds called heart murmur. These can sometimes be detected by auscultation; however, not all heart murmurs are caused by congenital heart defects. Associated conditions Congenital heart defects are associated with an increased incidence of seven other specific medical conditions, together being called the VACTERL association: V — Vertebral anomalies A — Anal atresia C — Cardiovascular anomalies T — Tracheoesophageal fistula E — Esophageal atresia R — Renal (Kidney) and/or radial anomalies L — Limb defectsVentricular septal defect (VSD), atrial septal defects, and tetralogy of Fallot are the most common congenital heart defects seen in the VACTERL association. Less common defects in the association are truncus arteriosus and transposition of the great arteries. Causes The cause of congenital heart disease may be genetic, environmental, or a combination of both. Genetic Genetic mutations, often sporadic, represent the largest known cause of congenital heart defects. They are described in the table below. Molecular pathways The genes regulating the complex developmental sequence have only been partly elucidated. Some genes are associated with specific defects. A number of genes have been associated with cardiac manifestations. Mutations of a heart muscle protein, α-myosin heavy chain (MYH6) are associated with atrial septal defects. Several proteins that interact with MYH6 are also associated with cardiac defects. The transcription factor GATA4 forms a complex with the TBX5 which interacts with MYH6. Another factor, the homeobox (developmental) gene, NKX2-5 also interacts with MYH6. Mutations of all these proteins are associated with both atrial and ventricular septal defects; In addition, NKX2-5 is associated with defects in the electrical conduction of the heart and TBX5 is related to the Holt–Oram syndrome which includes electrical conduction defects and abnormalities of the upper limb. The Wnt signaling co-factors BCL9, BCL9L and PYGO might be part of this molecular pathways, as when their genes are mutated, this causes phenotypes similar to the features present in Holt-Oram syndrome. Another T-box gene, TBX1, is involved in velo-cardio-facial syndrome DiGeorge syndrome, the most common deletion which has extensive symptoms including defects of the cardiac outflow tract including tetralogy of Fallot. The notch signaling pathway, a regulatory mechanism for cell growth and differentiation, plays broad roles in several aspects of cardiac development. Notch elements are involved in determination of the right and left sides of the body plan, so the directional folding of the heart tube can be impacted. Notch signaling is involved early in the formation of the endocardial cushions and continues to be active as the develop into the septa and valves. It is also involved in the development of the ventricular wall and the connection of the outflow tract to the great vessels. Mutations in the gene for one of the notch ligands, Jagged1, are identified in the majority of examined cases of arteriohepatic dysplasia (Alagille syndrome), characterized by defects of the great vessels (pulmonary artery stenosis), heart (tetralogy of Fallot in 13% of cases), liver, eyes, face, and bones. Though less than 1% of all cases, where no defects are found in the Jagged1 gene, defects are found in Notch2 gene. In 10% of cases, no mutation is found in either gene. For another member of the gene family, mutations in the Notch1 gene are associated with bicuspid aortic valve, a valve with two leaflets instead of three. Notch1 is also associated with calcification of the aortic valve, the third most common cause of heart disease in adults.Mutations of a cell regulatory mechanism, the Ras/MAPK pathway are responsible for a variety of syndromes, including Noonan syndrome, LEOPARD syndrome, Costello syndrome and cardiofaciocutaneous syndrome in which there is cardiac involvement. While the conditions listed are known genetic causes, there are likely many other genes which are more subtle. It is known that the risk for congenital heart defects is higher when there is a close relative with one. Environmental Known environmental factors include certain infections during pregnancy such as rubella, drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus). Alcohol exposure in the father also appears to increase the risk of congenital heart defects.Being overweight or obese increases the risk of congenital heart disease. Additionally, as maternal obesity increases, the risk of heart defects also increases. A distinct physiological mechanism has not been identified to explain the link between maternal obesity and CHD, but both pre-pregnancy folate deficiency and diabetes have been implicated in some studies. Mechanism There is a complex sequence of events that result in a well formed heart at birth and disruption of any portion may result in a defect. The orderly timing of cell growth, cell migration, and programmed cell death ("apoptosis") has been studied extensively and the genes that control the process are being elucidated. Around day 15 of development, the cells that will become the heart exist in two horseshoe shaped bands of the middle tissue layer (mesoderm), and some cells migrate from a portion of the outer layer (ectoderm), the neural crest, which is the source of a variety of cells found throughout the body. On day 19 of development, a pair of vascular elements, the "endocardial tubes", form. The tubes fuse when cells between then undergo programmed death and cells from the first heart field migrate to the tube, and form a ring of heart cells (myocytes) around it by day 21. On day 22, the heart begins to beat and by day 24, blood is circulating.At day 22, the circulatory system is bilaterally symmetrical with paired vessels on each side and the heart consisting of a simple tube located in the midline of the body layout. The portions that will become the atria and will be located closest to the head are the most distant from the head. From days 23 through 28, the heart tube folds and twists, with the future ventricles moving left of center (the ultimate location of the heart) and the atria moving towards the head.On day 28, areas of tissue in the heart tube begin to expand inwards; after about two weeks, these expansions, the membranous "septum primum" and the muscular "endocardial cushions", fuse to form the four chambers of the heart. A failure to fuse properly will result in a defect that may allow blood to leak between chambers. After this happens, cells that have migrated from the neural crest begin to divide the bulbus cordis, the main outflow tract is divided in two by the growth a spiraling septum, becoming the great vessels—the ascending segment of the aorta and the pulmonary trunk. If the separation is incomplete, the result is a "persistent truncus arteriosus". The vessels may be reversed ("transposition of the great vessels"). The two halves of the split tract must migrate into the correct positions over the appropriate ventricles. A failure may result in some blood flowing into the wrong vessel (e.g.overriding aorta). The four-chambered heart and the great vessels have features required for fetal growth. The lungs are unexpanded and cannot accommodate the full circulatory volume. Two structures exist to shunt blood flow away from the lungs. Cells in part of the septum primum die creating a hole while muscle cells, the "septum secundum", grow along the right atrial side the septum primum, except for one region, leaving a gap through which blood can pass from the right artium to the left atrium, the foramen ovale. A small vessel, the ductus arteriosus allows blood from the pulmonary artery to pass to the aorta. Changes at birth The ductus arteriosus stays open because of circulating factors including prostaglandins. The foramen ovale stays open because of the flow of blood from the right atrium to the left atrium. As the lungs expand, blood flows easily through the lungs and the membranous portion of the foramen ovale (the septum primum) flops over the muscular portion (the septum secundum). If the closure is incomplete, the result is a patent foramen ovale. The two flaps may fuse, but many adults have a foramen ovale that stays closed only because of the pressure difference between the atria. Theories Rokitansky (1875) explained congenital heart defects as breaks in heart development at various ontogenesis stages. Spitzer (1923) treats them as returns to one of the phylogenesis stages. Krimski (1963), synthesizing two previous points of view, considered congenital heart diseases as a stop of development at the certain stage of ontogenesis, corresponding to this or that stage of the phylogenesis. Hence these theories can explain feminine and neutral types of defects only. Diagnosis Many congenital heart defects can be diagnosed prenatally by fetal echocardiography. This is a test which can be done during the second trimester of pregnancy, when the woman is about 18–24 weeks pregnant. It can be an abdominal ultrasound or transvaginal ultrasound.If a baby is born with cyanotic heart disease, the diagnosis is usually made shortly after birth due to the blue colour of their skin (called cyanosis).If a baby is born with a septal defect or an obstruction defect, often their symptoms are only noticeable after several months or sometimes even after many years. Classification A number of classification systems exist for congenital heart defects. In 2000 the International Congenital Heart Surgery Nomenclature was developed to provide a generic classification system. Hypoplasia Hypoplasia can affect the heart, typically resulting in the underdevelopment of the right ventricle or the left ventricle. This causes only one side of the heart to be capable of pumping blood to the body and lungs effectively. Hypoplasia of the heart is rare but is the most serious form of CHD. It is called hypoplastic left heart syndrome when it affects the left side of the heart and hypoplastic right heart syndrome when it affects the right side of the heart. In both conditions, the presence of a patent ductus arteriosus (and, when hypoplasia affects the right side of the heart, a patent foramen ovale) is vital to the infants ability to survive until emergency heart surgery can be performed, since without these pathways blood cannot circulate to the body (or lungs, depending on which side of the heart is defective). Hypoplasia of the heart is generally a cyanotic heart defect. Obstructive defects Obstructive defects occur when heart valves, arteries, or veins are abnormally narrow or blocked. Common defects include pulmonic stenosis, aortic stenosis, and coarctation of the aorta, with other types such as bicuspid aortic valve stenosis and subaortic stenosis being comparatively rare. Any narrowing or blockage can cause heart enlargement or hypertension. Septal defects The septum is a wall of tissue which separates the left heart from the right heart. Defects in the interatrial septum or the interventricular septum allow blood to flow from the left side of the heart to the right, reducing the hearts efficiency. Ventricular septal defects are collectively the most common type of CHD, although approximately 30% of adults have a type of atrial septal defect called probe patent foramen ovale. Cyanotic defects Cyanotic heart defects are called such because they result in cyanosis, a bluish-grey discoloration of the skin due to a lack of oxygen in the body. Such defects include persistent truncus arteriosus, total anomalous pulmonary venous connection, tetralogy of Fallot, transposition of the great vessels, and tricuspid atresia. Defects Aortic stenosis Arrhythmogenic right ventricular cardiomyopathy Atrial septal defect (ASD) Atrioventricular septal defect (AVSD) Bicuspid aortic valve Cardiomyopathy Complete heart block (CHB) Dextrocardia Double inlet left ventricle (DILV) Double outlet right ventricle (DORV) Ebsteins anomaly Early Repolarization Syndrome Hypoplastic left heart syndrome (HLHS) Hypoplastic right heart syndrome (HRHS) Mitral stenosis Myocardial bridge Persistent truncus arteriosus Pulmonary atresia Pulmonary stenosis Rhabdomyomas (Tumors of the Heart) Transposition of the great vessels dextro-Transposition of the great arteries (d-TGA) levo-Transposition of the great arteries (l-TGA) Tricuspid atresia Ventricular septal defect (VSD) Wolff–Parkinson–White syndrome (WPW)Some conditions affect the great vessels or other vessels in close proximity to the heart, but not the heart itself, but are often classified as congenital heart defects. Coarctation of the aorta (CoA) Double aortic arch, aberrant subclavian artery, and other malformations of the great arteries Interrupted aortic arch (IAA) Patent ductus arteriosus (PDA) Scimitar syndrome (SS) Partial anomalous pulmonary venous connection (PAPVC) Total anomalous pulmonary venous connection (TAPVC)Some constellations of multiple defects are commonly found together. Tetralogy of Fallot (ToF) Pentalogy of Cantrell Shones syndrome/ Shones complex / Shones anomaly Treatment CHD may require surgery and medications. Medications include diuretics, which aid the body in eliminating water, salts, and digoxin for strengthening the contraction of the heart. This slows the heartbeat and removes some fluid from tissues. Some defects require surgical procedures to restore circulation back to normal and in some cases, multiple surgeries are needed.Interventional cardiology now offers minimally invasive alternatives to surgery for some patients. The Melody Transcatheter Pulmonary Valve (TPV), approved in Europe in 2006 and in the U.S. in 2010 under a Humanitarian Device Exemption (HDE), is designed to treat congenital heart disease patients with a dysfunctional conduit in their right ventricular outflow tract (RVOT). The RVOT is the connection between the heart and lungs; once blood reaches the lungs, it is enriched with oxygen before being pumped to the rest of the body. Transcatheter pulmonary valve technology provides a less-invasive means to extend the life of a failed RVOT conduit and is designed to allow physicians to deliver a replacement pulmonary valve via a catheter through the patients blood vessels.Many people require lifelong specialized cardiac care, first with a pediatric cardiologist and later with an adult congenital cardiologist. There are more than 1.8 million adults living with congenital heart defects. Epidemiology Heart defects are among the most common birth defect, occurring in 1% of live births (2–3% including bicuspid aortic valve). In 2013, 34.3 million people had CHD. In 2010, they resulted in 223,000 deaths, down from 278,000 deaths in 1990.For congenital heart defects that arise without a family history (de novo), the recurrence risk in offspring is 3–5%. This risk is higher in left ventricular outflow tract obstructions, heterotaxy, and atrioventricular septal defects. Terminology Congenital heart defects are known by a number of names including congenital heart anomaly, congenital heart disease, heart defects, and congenital cardiovascular malformations. See also Congenital Heart Surgeons Society Congenital heart block References External links Congenital heart defect at Curlie Congenital heart disease information for parents.

Levocardia

Levocardia is where the heart is on the normal side of the body (the left), as opposed to dextrocardia, in which the heart is in the right side of the thoracic cavity. This can be associated with situs solitus, where the remainder of the organs are on normal side as well; or situs inversus, in which the viscera (stomach, liver, intestines, lungs, etc.) on the opposite side as normal. The latter condition may or may not be associated with clinically relevant abnormalities. See also Isolated levocardia References == External links ==

Thalassemia

Thalassemias are inherited blood disorders characterized by decreased hemoglobin production. Symptoms depend on the type and can vary from none to severe. Often there is mild to severe anemia (low red blood cells or hemoglobin). Anemia can result in feeling tired and pale skin. There may also be bone problems, an enlarged spleen, yellowish skin, and dark urine. Slow growth may occur in children.Thalassemias are genetic disorders inherited from a persons parents. There are two main types, alpha thalassemia and beta thalassemia. The severity of alpha and beta thalassemia depends on how many of the four genes for alpha globin or two genes for beta globin are missing. Diagnosis is typically by blood tests including a complete blood count, special hemoglobin tests, and genetic tests. Diagnosis may occur before birth through prenatal testing.Treatment depends on the type and severity. Treatment for those with more severe disease often includes regular blood transfusions, iron chelation, and folic acid. Iron chelation may be done with deferoxamine, deferasirox or deferiprone. Occasionally, a bone marrow transplant may be an option. Complications may include iron overload from the transfusions with resulting heart or liver disease, infections, and osteoporosis. If the spleen becomes overly enlarged, surgical removal may be required. Thalassemia patients who do not respond well to blood transfusions can take hydroxyurea or thalidomide, and sometimes a combination of both. Hydroxyurea is the only FDA approved drug for thalassemia. Patients who took 10 mg/kg of hydroxyurea every day for a year had significantly higher hemoglobin levels, and it was a well-tolerated treatment for patients who did not respond well to blood transfusions. Another hemoglobin-inducer includes thalidomide, although it has not been tested in a clinical setting. The combination of thalidomide and hydroxyurea resulted in hemoglobin levels increasing significantly in transfusion-dependent and non-transfusion dependent patients As of 2015, thalassemia occurs in about 280 million people, with about 439,000 having severe disease. It is most common among people of Greek, Italian, Middle Eastern, South Asian, and African descent. Males and females have similar rates of disease. It resulted in 16,800 deaths in 2015, down from 36,000 deaths in 1990. Those who have minor degrees of thalassemia, similar to those with sickle-cell trait, have some protection against malaria, explaining why they are more common in regions of the world where malaria exists. Signs and symptoms Iron overload: People with thalassemia can get an overload of iron in their bodies, either from the disease itself or from frequent blood transfusions. Too much iron can result in damage to the heart, liver, and endocrine system, which includes glands that produce hormones that regulate processes throughout the body. The damage is characterized by excessive deposits of iron. Without adequate iron chelation therapy, almost all patients with beta-thalassemia accumulate potentially fatal iron levels. Infection: People with thalassemia have an increased risk of infection. This is especially true if the spleen has been removed. Bone deformities: Thalassemia can make the bone marrow expand, which causes bones to widen. This can result in abnormal bone structure, especially in the face and skull. Bone marrow expansion also makes bones thin and brittle, increasing the risk of broken bones. Enlarged spleen: The spleen aids in fighting infection and filters unwanted material, such as old or damaged blood cells. Thalassemia is often accompanied by the destruction of a large number of red blood cells and the task of removing these cells causes the spleen to enlarge. Splenomegaly can make anemia worse, and it can reduce the life of transfused red blood cells. Severe enlargement of the spleen may necessitate its removal. Slowed growth rates: anemia can cause the growth of a child to slow down. Puberty may also be delayed in children with thalassemia. Heart problems: Diseases, such as congestive heart failure and abnormal heart rhythms, may be associated with severe thalassemia. Hemoglobin structural biology Normal human hemoglobins are tetrameric proteins composed of two pairs of globin chains, each of which contains one alpha-like (α-like) chain and one beta-like (β-like) chain. Each globin chain is associated with an iron-containing heme moiety. Throughout life, the synthesis of the alpha-like and the beta-like (also called non-alpha-like) chains is balanced so that their ratio is relatively constant and there is no excess of either type.The specific alpha and beta-like chains that are incorporated into Hb are highly regulated during development: Embryonic Hbs are expressed as early as four to six weeks of embryogenesis and disappear around the eighth week of gestation as they are replaced by fetal Hb. Embryonic Hbs include: Hb Gower-1, composed of two ζ globins (zeta globins) and two ε globins (epsilon globins) (ζ2ε2) Hb Gower-2, composed of two alpha globins and two epsilon globins (α2ε2) Hb Portland, composed of two zeta globins and two gamma globins (ζ2γ2) Fetal Hb (Hb F) is produced from approximately eight weeks of gestation through birth and constitutes approximately 80 percent of Hb in the full-term neonate. It declines during the first few months of life and, in the normal state, constitutes <1 percent of total Hb by early childhood. Hb F is composed of two alpha globins and two gamma globins (α2γ2). Adult Hb (Hb A) is the predominant Hb in children by six months of age and onward; it constitutes 96-97% of total Hb in individuals without a hemoglobinopathy. It is composed of two alpha globins and two beta globins (α2β2). Hb A2 is a minor adult Hb that normally accounts for approximately 2.5-3.5% of total Hb from six months of age onward. It is composed of two alpha globins and two delta globins (α2δ2). Cause Both α- and β-thalassemias are often inherited in an autosomal recessive manner. Cases of dominantly inherited α- and β-thalassemias have been reported, the first of which was in an Irish family with two deletions of 4 and 11 bp in exon 3 interrupted by an insertion of 5 bp in the β-globin gene. For the autosomal recessive forms of the disease, both parents must be carriers for a child to be affected. If both parents carry a hemoglobinopathy trait, the risk is 25% for each pregnancy for an affected child.The genes involved in thalassemia control the production of healthy hemoglobin. Hemoglobin binds oxygen in the lungs and releases it when the red cells reach peripheral tissues, such as the liver. The binding and release of oxygen by hemoglobin are essential for survival. Evolution Having a single genetic variant for thalassemia may protect against malaria and thus can be an advantage.People diagnosed with heterozygous (carrier) β-thalassemia have some protection against coronary heart disease. Pathophysiology Normally, the majority of adult hemoglobin (HbA) is composed of four protein chains, two α and two β-globin chains arranged into a heterotetramer. In thalassemia, patients have defects in either the α or β-globin chain, causing production of abnormal red blood cells.The thalassemias are classified according to which chain of the hemoglobin molecule is affected. In α-thalassemias, production of the α-globin chain is affected, while in β-thalassemia, production of the β-globin chain is affected.The β-globin chains are encoded by a single gene on chromosome 11; α-globin chains are encoded by two closely linked genes on chromosome 16. Thus, in a normal person with two copies of each chromosome, two loci encode the β chain, and four loci encode the α chain. Deletion of one of the α loci has a high prevalence in people of African or Asian descent, making them more likely to develop α-thalassemia. β-Thalassemias are not only common in Africans, but also in Greeks and Turks. Alpha-thalassemias The α-thalassemias involve the genes HBA1 and HBA2, inherited in a Mendelian recessive fashion. Two gene loci and so four alleles exist. Two genetic loci exist for α-globin, thus four alleles are in diploid cells. Two alleles are maternal and two alleles are paternal in origin. The severity of the α-thalassemias is correlated with the number of affected α-globin; alleles: the greater, the more severe will be the manifestations of the disease. Alpha-thalassemias result in decreased alpha-globin production; therefore, fewer alpha-globin chains are produced, resulting in an excess of β chains in adults and excess γ chains in newborns. The excess β chains form unstable tetramers (called hemoglobin H or HbH of 4 beta chains), which have abnormal oxygen dissociation curves. Alpha thalassemias often are found in people from Southeast Asia, the Middle East, China, and in those of African descent. Beta-thalassemia Beta thalassemias are due to mutations in the HBB gene on chromosome 11, also inherited in an autosomal, recessive fashion. The severity of the disease depends on the nature of the mutation and on the presence of mutations in one or both alleles. Mutated alleles are called β+ when partial function is conserved (either the protein has a reduced function, or it functions normally but is produced in reduced quantity) or βo, when no functioning protein is produced. The situation of both alleles determines the clinical picture: β thalassemia major (Mediterranean anemia or Cooley anemia) is caused by a βo/βo genotype. No functional β chains are produced, and thus no hemoglobin A can be assembled. This is the most severe form of β-thalassemia; β thalassemia intermedia is caused by a β+/βo or β+/β+ genotype. In this form, some hemoglobin A is produced; β thalassemia minor is caused by a β/βo or β/β+ genotype. Only one of the two β globin alleles contains a mutation, so β chain production is not terribly compromised and patients may be relatively asymptomatic.Beta thalassemia most often occurs in people of Mediterranean origin. To a lesser extent, Chinese, other Asians, and African Americans can be affected. Delta-thalassemia As well as alpha and beta chains present in hemoglobin, about 3% of adult hemoglobin is made of alpha and delta chains. Just as with beta thalassemia, mutations that affect the ability of this gene to produce delta chains can occur. Combination hemoglobinopathies Thalassemia can coexist with other hemoglobinopathies. The most common of these are: Hemoglobin E/thalassemia: common in Cambodia, Thailand, and parts of India, it is clinically similar to β thalassemia major or thalassemia intermedia. Hemoglobin S/thalassemia: common in African and Mediterranean populations, it is clinically similar to sickle-cell anemia, with the additional feature of splenomegaly. Hemoglobin C/thalassemia: common in Mediterranean and African populations, hemoglobin C/βo thalassemia causes a moderately severe hemolytic anemia with splenomegaly; hemoglobin C/β+ thalassemia produces a milder disease. Hemoglobin D/thalassemia: common in the northwestern parts of India and Pakistan (Punjab region). Diagnosis Thalassemia can be diagnosed via a complete blood count, hemoglobin electrophoresis or high-performance liquid chromatography, and DNA testing. Hemoglobin electrophoresis is not widely available in developing countries, but the Mentzer index can also be used for diagnosis of thalassemia; it is not a definitive test but it can suggest the possibility of thalassemia. The Mentzer index can be calculated from a complete blood count report. Prevention The American College of Obstetricians and Gynecologists recommends all people thinking of becoming pregnant be tested to see if they have thalassemia. Genetic counseling and genetic testing are recommended for families who carry a thalassemia trait.A screening policy exists in Cyprus to reduce the rate of thalassemia, which, since the programs implementation in the 1970s (also including prenatal screening and abortion), has reduced the number of children born with the disease from one of every 158 births to almost zero. Greece also has a screening program to identify people who are carriers.In Iran as a premarital screening, the mans red cell indices are checked first. If he has microcytosis (mean cell hemoglobin < 27 pg or mean red cell volume < 80 fl), the woman is tested. When both are microcytic, their hemoglobin A2 concentrations are measured. If both have a concentration above 3.5% (diagnostic of thalassemia trait) they are referred to the local designated health post for genetic counseling.Large-scale awareness campaigns are being organized in India both by government and non-government organizations to promote voluntary premarital screening, with marriage between carriers strongly discouraged. Management Mild thalassemia: people with thalassemia traits do not require medical or follow-up care after the initial diagnosis is made. People with β-thalassemia trait should be warned that their condition can be misdiagnosed as the more common iron-deficiency anemia. They should avoid routine use of iron supplements, but iron deficiency may develop during pregnancy or from chronic bleeding. Counseling is indicated for all persons with genetic disorders, especially when the family is at risk of a severe form of disease that may be prevented. Anemia People with severe thalassemia require medical treatment. A blood transfusion regimen is the first effective measure in prolonging life. Growth hormone therapy There is some evidence that growth hormone replacement therapy may help to increase the rate at which children with thalassemia grow taller. Iron overload Multiple blood transfusions may result in iron overload. The iron overload related to thalassemia may be treated by chelation therapy with the medications deferoxamine, deferiprone, or deferasirox. These treatments have resulted in longer life expectancy for those with thalassemia major.Deferoxamine is only effective as a daily injection, complicating its long-term use. However, it is inexpensive and safe. Adverse effects include primary skin reactions around the injection site and hearing loss.Deferasirox and deferiprone are both oral medications, whose common side effects include nausea, vomiting and diarrhea. Deferasirox is not effective for all patients and may not be suitable for those with significant cardiac issues related to iron overload, while deferiprone appears to be the most effective agent when the heart is involved. Furthermore, the cost of deferasirox is also significant.There is no evidence from randomized controlled trial to support zinc supplementation for those with thalassemia. Bone-marrow transplantation Bone-marrow transplantation may offer the possibility of a cure in young people who have an HLA-matched donor. Success rates have reached the 80–90% range. Mortality from the procedure is about 3%. There are no randomized controlled trials that have tested the safety and efficacy of non-identical donor bone-marrow transplantation in persons with β- thalassemia who are dependent on blood transfusion.Graft-versus-host diseases (GvHD) are one relevant side effect of bone-marrow transplantation. Further research is necessary to evaluate whether mesenchymal stromal cells can be used as prophylaxis or treatment for GvHD.If the patient does not have an HLA-matched compatible donor, bone-marrow transplantation from haploidentical mother to child (mismatched donor) may be attempted. In a study of 31 people, the thalassemia-free survival rate was 70%, rejection 23% and mortality 7%. The most positive results tend to occur with very young people. Epidemiology The beta form of thalassemia is particularly prevalent among Mediterranean peoples, and this geographical association is responsible for its original name. Thalassemia resulted in 25,000 deaths in 2013 down from 36,000 deaths in 1990.In Europe, the highest concentrations of the disease are found in Greece, coastal regions in Turkey (particularly the Aegean Region such as İzmir, Balıkesir, Aydın, Muğla, and Mediterranean Region such as Antalya, Adana, Mersin), in southern Spain, in parts of Italy, particularly southern Italy. With the exception of the Balearics, the major Mediterranean Islands, such as Sicily, Sardinia, Malta, Corsica, Cyprus, and Crete are heavily affected. Other Mediterranean peoples, as well as those in the vicinity of the Mediterranean, also have high rates of thalassemia, including people from North Africa and West Asia. Far from the Mediterranean, South Asians are also affected, with the worlds highest concentration of carriers (16–18% of the population) in the Maldives.The disease is also found in populations living in Africa, the Americas, and in Tharu people in the Terai region of Nepal and India. It is believed to account for much lower rates of malaria illnesses and deaths, accounting for the historic ability of Tharus to survive in areas with heavy malaria infestation while others could not. Thalassemias are particularly associated with people of Mediterranean origin, Arabs (especially Palestinians and people of Palestinian descent), and Asians. The estimated prevalence is 16% in people from Cyprus, 1% in Thailand, and 3–8% in populations from Bangladesh, China, India, Malaysia and Pakistan. Estimates suggest that approximately 1.5% of the global population (80 – 90 million people) are β-thalassemia carriers. However, exact data on carrier rates in many populations are lacking, particularly in developing areas of the world known or expected to be heavily affected. Because of the prevalence of the disease in countries with little knowledge of thalassemia, access to proper treatment and diagnosis can be difficult. While there are some diagnostic and treatment facilities in developing countries, in most cases these are not provided by government services and are available only to patients who can afford them. In general, poorer populations only have access to limited diagnostic facilities and blood transfusions. In some developing countries, there are virtually no facilities for diagnosis or management of thalassemia. Etymology and synonym The word thalassemia () derives from the Greek thalassa (θάλασσα), "sea", and New Latin -emia (from the Greek compound stem -aimia (-αιμία), from haima (αἷμα), "blood"). It was coined because the condition called "Mediterranean anemia" was first described in people of Mediterranean ethnicities. "Mediterranean anemia" was renamed thalassemia major once the genetics were better understood. The word thalassemia was first used in 1932.: 877 Society and culture In 2008, in Spain, a baby was selectively implanted to be a cure for his brothers thalassemia. The child was born from an embryo screened to be free of the disease before implantation with in vitro fertilization. The babys supply of immunologically compatible cord blood was saved for transplantation to his brother. The transplantation was considered successful. In 2009, a group of doctors and specialists in Chennai and Coimbatore registered the successful treatment of thalassemia in a child using an unaffected siblings umbilical cord blood. Research Gene therapy Gene therapy is being studied for thalassemia. The procedure involves collecting hematopoietic stem cells (HSCs) from the affected persons blood. The HSCs then have a beta-globin gene added using a lentiviral vector. After destroying the affected persons bone marrow with a dose of chemotherapy (a myeloablative conditioning regimen), the altered HSCs are infused back into the affected person where they become engrafted in the bone marrow where they proliferate. This potentially results in a progressive increase in hemoglobin A2 synthesis in all subsequent developing red blood cells, with resultant resolution of the anemia.While one person with beta thalassemia has no longer required blood transfusions following treatment within a research trial, it is not an approved treatment as of 2018. HbF induction HbF induction is an attempt to reactivate fetal globin gene transcription. Efforts involve trying to disrupt the fetal globin gene promoter. References External links Thalassemia at Curlie Learning About Thalassemia published by the National Human Genome Research Institute.

Orthostatic albuminuria

Orthostatic proteinuria (synonyms: orthostatic albuminuria, postural proteinuria) is a benign condition. A change in renal hemodynamics, which in some otherwise normal individuals, causes protein (mostly albumin) to appear in urine when they are in the standing position. Urine formed when these individuals are lying down is protein-free.There is normal urinary protein excretion during the night but increased excretion during the day, associated with activity and upright posture. Total urinary protein excretion may be increased but levels above 1 g per 24 hours are more likely to be associated with underlying renal disease. The exact cause for orthostatic proteinuria is not known. == References ==

Mast cell leukemia

Mast cell leukemia is an extremely aggressive subtype of acute myeloid leukemia that usually occurs de novo but can, rarely, evolve from transformation of chronic myeloid leukemia into the more aggressive acute myeloid leukemia. In a small proportion of cases, acute mast cell leukemia may evolve from a more progressive form of systemic mastocytosis. The diagnosis of acute mast cell leukemia by the WHO criteria includes the requirement for a prevalence of 20% neoplastic mast cells in marrow and 10% in blood. If the mast cells represent less than 10% of blood cells, the tumor is called "aleukemic" mast cell leukemia. Signs and symptoms Acute mast cell leukemia is a rapidly progressive disorder with leukemic mast cells in blood and in large numbers in marrow. The common signs and symptoms include fever, headache, flushing of face and trunk. The typical cutaneous mast cell infiltrates of urticaria pigmentosa are usually not present before, during, or after diagnosis in patients who have mast cell leukemia. Symptoms include abdominal pain, bone pain, and peptic ulcer which are more prevalent than in other subtypes of acute myeloid leukemia. These former symptoms are due to release of a substance called histamine from neoplastic mast cells. Enlargement of the liver and spleen, or hepatosplenomegaly is characteristic. The mast cells release also many anticoagulants like heparin which can lead to serious bleeding. Liver and splenic dysfunction also contributes to hemorrhage. Involvement of the bone can lead to osteoporosis. Abdominal ultrasound or computerized tomography (CT) scanning is used to look for hepatosplenomegaly and lymphadenopathy. Plain radiography and bone densitometry can be used to assess bone involvement and the presence of osteoporosis. Endoscopy and biopsy can be useful if gut involvement is suspected. Diagnosis Cytochemistry Cytochemical properties of the leukemic cells must be typical of mast cell derivation (presence of metachromatic granules staining with alpha-naphthyl chloroacetate esterase, but not with peroxidase). Mast cell tryptase is an enzyme contained in mast cell granules. Mast cell numbers are best estimated by tryptase immunostaining because very poorly granulated cells may stain very weakly if at all for alpha-naphthol chloroacetate esterase. Tumor markers The leukemic cells usually are strongly positive for CD13, CD33, CD68, and CD117. Characteristically, basophil (e.g. CD11b, CD123) and monocyte markers (CD14, CD15) are absent. The cells usually express CD2 and CD25. Malignant mast cells overexpress the anti-apoptosis gene, bcl-2. A mutation called KIT mutation is detected in most patients. Biochemistry Total serum tryptase is elevated in mast cell leukemia. Normal total (alpha + beta) serum tryptase is approximately 6 micro g/L (range 0 to 11 micro g/L). Values of several hundred micro g/L are characteristic of mast cell leukemia. Plasma and urinary histamine levels are frequently elevated in mast cell leukemia. Histidine decarboxylase (HDC) is the enzyme that catalyzes the reaction which produces histamine from histidine. Measurement of histidine carboxylase in the marrow cells of patients with mast cell leukemia is a very sensitive marker of mast cells. Treatment Immunoglobulin E (IgE) is important in mast cell function. Immunotherapy with anti-IgE immunoglobulin raised in sheep resulted in a transient decrease in the numbers of circulating mast cells in one patient with mast cell leukemia. Although splenectomy has led to brief responses in patients with mast cell leukemia, no firm conclusions as to the efficacy of this treatment are possible. Chemotherapy with combination of cytosine arabinoside and either idarubicin, daunomycin, or mitoxantrone as for acute myeloid leukemia has been used. Stem cell transplantation is an option, although no experience exists concerning responses and outcome. Prognosis Acute mast cell leukemia is extremely aggressive and has a grave prognosis. In most cases, multi-organ failure including bone marrow failure develops over weeks to months. Median survival after diagnosis is only about 6 months. References == External links ==

Anterior compartment syndrome

A compartment syndrome is an increased pressure within a muscular compartment that compromises the circulation to the muscles. Symptoms and signs Diffuse tightness and tenderness over the entire belly of the tibialis anterior muscle that does not respond to elevation or pain medication can be early warning signs and suggestive of Anterior Compartment Syndrome. Other common symptoms include excessive swelling that causes the skin to become hot, stretched and glossy. Pain, paresthesias, and tenderness in both the ischemic muscles and the region supplied by the deep common fibular nerve are exhibited by patients with this condition. Sensitivity to passive stretch and active contraction are common, and tend to increase the symptoms. Pathology A compartment space is anatomically determined by an unyielding fascial (and osseous) enclosure of the muscles. The anterior compartment syndrome of the lower leg (often referred to simply as anterior compartment syndrome), can affect any and all four muscles of that compartment: tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius.This term is often mistakenly used to describe various related/proximal conditions, including Anterior Shin Splints. It is important to distinguish between the two, as shin splints rarely causes serious health problems, while Anterior Compartment Syndrome can lead to irreversible damage.The true compartment syndrome arises due to increased pressure within the unyielding anterior compartment of the leg. The pressure obstructs venous outflow, which causes further swelling and increased pressure. The resultant ischemia leads to necrosis (death of tissue) of the muscles and nerves. The process can begin with swelling of the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and/or the peroneus tertius muscles in response to strong eccentric contractions sufficient to produce postexercise soreness. Diagnosis If these symptoms are observed/experienced it is important to contact a physician specializing in sports medicine (MD/DO), a doctor of podiatric medicine (DPM), or other qualified health care professional immediately so as to get the appropriate advice/treatment before serious damage occurs.The 5 Ps of Anterior Compartment Syndrome: Pain Pallor Paresthesia Pulselessness Paralysis (If not treated) Treatment The only option to treat acute compartment syndrome is surgery. The procedure, called a fasciotomy, involves a surgeon cutting open the skin and the fascia to relieve the pressure. Options to treat chronic compartment syndrome include physiotherapy, shoe inserts, and anti-inflammatory medications. References ADAM Health Illustrated Encyclopedia Article, 8/3/2004 == External links ==

External cause

In medicine, an external cause is a reason for the existence of a medical condition which can be associated with a specific object or acute process that was caused by something outside the body. Such causes are classified as "E codes" in ICD 9.External Cause of Injury Codes (E codes) are ICD-9-CM codes or ICD-10 codes that are used to define the mechanism of death or injury, along with the place of occurrence of the event. [1] E codes are assigned on death certificates based on the manner of death. ICD-10 codes in the range V01–X59 refer to unintentional injuries. Codes in the range X60–X84 refer to intentional self-harm. Codes in the range Y85–Y09 refer to assault, and codes in the range Y10–Y34 refer to events of undetermined intent.E codes are well-collected on death certificate data, but less so on hospital discharge data. Numerous initiatives have increased the percentage of records coded (CDC, MMWR March 28, 2008 / Vol. 57 / No. RR-1). == References ==

Acute myelomonocytic leukemia

Acute myelomonocytic leukemia (AMML) is a form of acute myeloid leukemia that involves a proliferation of CFU-GM myeloblasts and monoblasts. AMML occurs with a rapid increase amount in white blood cell count and is defined by more than 20% of myeloblast in the bone marrow. It is classified under "M4" in the French-American-British classification (FAB). It is classified under "AML, not otherwise classified" in the WHO classification.Translocations have been observed. Progression from myelodysplastic syndrome has been reported. Signs and symptoms Some patients may experience: Fatigue Easy Bruising Abnormal Bleeding Anemia Thrombocytopenia DyspneaIf the blast count gets too high and clog up blood vessels, some patients may experience: Slurred Speech Headache Confusion Weakness on one side of the body Sleepiness Cause The cause has not yet been determined. It has been said that acute myeloid leukemia can occur from a progression of chronic myelomonocytic leukemia type 1 and 2. Normal red blood cells decrease and a rapid proliferation of the abnormal myeloblasts occur. Apoptosis functional ability decreases which causes a back up of myeloblasts in the bone marrow and blood. AML with a translocation or inversion is seen in different chromosomes. Specifically, AML with inversion in chromosome 16 also known as inv(16) is commonly seen in children. Mechanism AMML does not have an exact mechanism. The underlying pathophysiology of acute myeloid leukemia consist of maturational arrest of the bone marrow cell during the early stages of development. A myeloblast is an immature precursor cell that will change into a monocyte, healthy white blood cell. In AML, Myeloblast do not mature but grow and multiply with regulation. The abnormal cells build up in the bone marrow and prevent the development of other healthy cells. This type of arrest is still under study but in most cases, a gene inactivation or activation has occurred due to chromosome translocations or inversion. AML-M4 with an inversion of chromosome 16 is caused by breakage and rearrangement within itself. Diagnosis Criteria for AMML is confirmed if the myeloblasts and promonocytes in the bone marrow are greater than 20 percent. It can also be confirmed if the blood monocytes is 5x109/L or higher. Testing available to diagnosis AML includes a complete blood count which is characterized by blood that is taken from the vein in the arm to test for leukemia, a peripheral blood smear and a bone marrow test. During a peripheral blood smear, a sample of blood is checked for blast cells, white blood cell count and changes in shape of blood cells. During a bone marrow test, bone marrow is taken from the hip bone in a search for leukemia cells. Aspiration and biopsy are two types of testing that can be done in order to obtain bone marrow. Further classification can be done for the type of AML by examining the cells shape and size. Generally youll find immature cells which lack normal features of a cell. Treatment AMML can be treated depending on the degree of disease, age of patient, and current patients health status. Treatment consists of a multi-drug chemotherapy regimen. Chemotherapy drugs often used to treat AML are cytarabine and an anthracycline drug. Chemotherapy is broken down into 2 phases: Induction therapy: first short and invasive phase of treatment with the goal to the blood of blasts and reduce the number of blasts in the bone marrow back to normal. Consolidation therapy: second phase given in cycles that occur after the patient has recovered from induction therapy. Its objective is to kill remaining blasts that cant be seen.In some cases, an allogenic bone marrow transplantation can be performed. If AML with chromosomal abnormalities such as inv(16) are often cured by the standard chemotherapy regimen. Prognosis With AMML being difficult to fully treat, the five-year survival rate is about 38-72% which typically decrease to 35-60% if theres no bone marrow transplantation performed. Generally older patients over 60 have a poor outlook due to prior health status before the diagnosis and the aggressive chemotherapy regimen used. The aggressive chemotherapy regimen can lead to long-term side effects such as prolonged anemia, leukocytopenia, neutropenia, and thrombocytopenia. The use of anthracycline drugs can cause a decrease in cardiac contractility, both short and long term. Those with AML-M4 inv(16) have a favorable prognosis with a five-year overall survival rate of 61%. Epidemiology AML is commonly seen in pediatric patients with higher pediatric incidence in Hispanics and Asians as compared to non-Hispanic Caucasian and African Americans in the USA. Predisposition to AML includes but not limited to:Down syndrome, Klinefelters syndrome, and Fanconis anemia. Acquired predisposing factors include: aplastic anemia, chemotherapy, prenatal exposure to tobacco, marihuana, and alcohol. Research directions Considering the disease is rare, not much research is being done specifically for the AML-M4 subtype. Research regarding the production of granulocyte colony stimulating factor (G-CSF) is being conducted to investigate AMML ability to secrete and synthesize G-CSF. Multiple chemotherapy drugs and its effects are being research in comparison to its treatment success in AML not specifically AML-M4. See also Juvenile myelomonocytic leukemia References == External links ==

Acute bronchitis

Acute bronchitis, also known as a chest cold, is short-term bronchitis – inflammation of the bronchi (large and medium-sized airways) of the lungs. The most common symptom is a cough. Other symptoms include coughing up mucus, wheezing, shortness of breath, fever, and chest discomfort. The infection may last from a few to ten days. The cough may persist for several weeks afterward with the total duration of symptoms usually around three weeks. Some have symptoms for up to six weeks.In more than 90% of cases, the cause is a viral infection. These viruses may be spread through the air when people cough or by direct contact. Risk factors include exposure to tobacco smoke, dust, and other air pollution. A small number of cases are due to high levels of air pollution or bacteria such as Mycoplasma pneumoniae or Bordetella pertussis. Diagnosis is typically based on a persons signs and symptom. The color of the sputum does not indicate if the infection is viral or bacterial. Determining the underlying organism is typically not needed. Other causes of similar symptoms include asthma, pneumonia, bronchiolitis, bronchiectasis, and COPD. A chest X-ray may be useful to detect pneumonia.Prevention is by not smoking and avoiding other lung irritants. Frequent hand washing and flu vaccination may also be protective. Treatment of acute bronchitis typically involves rest, paracetamol (acetaminophen), and NSAIDs to help with the fever. Cough medicine has little support for its use and is not recommended in children less than six years of age. Antibiotics should generally not be used. An exception is when acute bronchitis is due to pertussis. Tentative evidence supports honey and pelargonium to help with symptoms.Acute bronchitis is one of the most common diseases. About 5% of adults are affected and about 6% of children have at least one episode a year. It occurs more often in the winter. More than 10 million people in the United States visit a doctor each year for this condition with approximately 70% receiving antibiotics, most of which are not needed. There are efforts to decrease the use of antibiotics in acute bronchitis. Signs and symptoms The primary symptom is cough with sputum that may be purulent. The illness may also cause shortness of breath or wheezing. Upper respiratory tract infections often precede acute bronchitis, with overlapping symptoms including headache, nasal congestion, sore throat. Fever and other systemic symptoms are rare in acute bronchitis; their presence raises suspicion for influenza or pneumonia. Cause Acute bronchitis can be caused by contagious pathogens, most commonly viruses. Typical viruses include respiratory syncytial virus, rhinovirus, influenza, and others. Bacteria are uncommon pathogens but may include Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bordetella pertussis, Streptococcus pneumoniae, and Haemophilus influenzae. Damage caused by irritation of the airways leads to inflammation and leads to neutrophils infiltrating the lung tissue. Mucosal hypersecretion is promoted by a substance released by neutrophils. Further obstruction to the airways is caused by more goblet cells in the small airways. This is typical of chronic bronchitis. Although infection is not the reason or cause of chronic bronchitis, it is seen to aid in sustaining the bronchitis. Diagnosis A physical examination will often reveal decreased intensity of breath sounds, wheezing, rhonchi, and prolonged expiration. During examination for physicians rely on history and the presence of persistent or acute onset of cough, followed by a URTI with no traces of pneumonia. Acute bronchitis is typically a clinical diagnosis that relies on patients history and exam, and should be suspected in patients with an acute onset of cough, which often follows a URTI without traces of pneumonia.Although there is no universally-accepted clinical definition for acute bronchitis, there is a proposed set of practical criteria (Macfarlane, 2001) that include: An acute illness of less than three weeks. Cough as the predominant symptom. At least one other lower respiratory tract symptom, such as sputum production, wheezing, chest pain. No alternative explanation for the symptoms.A variety of tests may be performed in people presenting with cough and shortness of breath: A chest X-ray is useful to exclude pneumonia which is more common in those with a fever, fast heart rate, fast respiratory rate, or who are old. A sputum sample showing neutrophil granulocytes (inflammatory white blood cells) and culture showing that has pathogenic microorganisms such as Streptococcus species. A blood test would indicate inflammation (as indicated by a raised white blood cell count and elevated C-reactive protein).Decreased breath sounds, crackles, wheezing, and rhonchi that clears with coughs may be heard in the chest. Dullness to percussion and pleural rub suggest disease extension beyond the bronchi such as seen with pneumonia. Paroxysms of cough followed by inspiratory whoop and vomiting suggests pertussis. Prevention Prevention is by not smoking and avoiding other lung irritants. Frequent hand washing may also be protective. Furthermore, an oral whole cell nontypeable Haemophilus influenzae vaccine given in the fall has demonstrated short term effectiveness in reducing the frequency and severity of the disease during the winter. Treatment Most cases are self-limited and resolve themselves in a few weeks. Pain medications may help with symptoms. Other recommendations may include rest and keeping well hydrated. Antibiotics Evidence does not support the general use of antibiotics in acute bronchitis. A systematic review found antibiotics reduced cough by an average of 12 hours (out of a total average of about 14–28 days). Antibiotics caused more side effects such as nausea and diarrhoea, and also may promote antibiotic-resistant bacteria. It is possible they are useful in susceptible groups such as the frail and elderly but there was not enough research information to determine this.Calling acute bronchitis with benign-sounding labels such as chest cold or viral infections may reduce antibiotic usage by improving patients satisfaction when antibiotics are not prescribed. Smoking cessation To help the bronchial tree heal faster and not make bronchitis worse, smokers should quit smoking completely. Alternative therapeutic approaches Salbutamol is not effective in children with an acute cough who do not have restricted airways. There is weak evidence that salbutamol may be useful in adults with wheezing due to a restricted airway; however, it may result in nervousness, shakiness or a tremor. Prognosis Acute bronchitis usually lasts a few days or weeks. It may accompany or closely follow a cold or the flu, or may occur on its own. Bronchitis usually begins with a dry cough, including waking the patient at night. After a few days, it progresses to a wetter or productive cough, which may be accompanied by fever, fatigue, and headache. The fever, fatigue, and malaise may last only a few days, but the wet cough may last up to several weeks. Epidemiology Acute bronchitis is one of the most common diseases. About 5% of adults are affected and about 6% of children have at least one episode a year. It occurs more often in the winter.In infants under one year of age, acute bronchitis was the most common reason for admission to the hospital after an emergency department visit in the US in 2011. References External links Acute Bronchitis FamilyDoctor.org (American Academy of Family Physicians) "Acute Bronchitis". MedlinePlus. U.S. National Library of Medicine.

Tract

Tract may refer to: Geography and real estate Housing tract, an area of land that is subdivided into smaller individual lots Land lot or tract, a section of land Census tract, a geographic region defined for the purpose of taking a census Writings Tract (literature), a short written work, usually of a political or religious nature Tract (liturgy), a component of Roman Catholic liturgy Treatise Biology Nerve tract, a bundle of fibers that connects different parts of the central nervous system - analogous to a nerve in the peripheral nervous system A genetic tract, a sequence of repeating nucleotides or amino acids, such as a polyglutamine tract A collection of related anatomic structures, such as: Gastrointestinal tract Genitourinary tract Reproductive tract A grouping of feathers, e.g. primaries, auricular, scapular Businesses Tract (imprint), an imprint of the German group VDM Publishing devoted to the reproduction of Wikipedia content See also Track (disambiguation) All pages with titles beginning with Tract All pages with titles containing Tract

Osteolysis

Osteolysis is an active resorption of bone matrix by osteoclasts and can be interpreted as the reverse of ossification. Although osteoclasts are active during the natural formation of healthy bone the term "osteolysis" specifically refers to a pathological process. Osteolysis often occurs in the proximity of a prosthesis that causes either an immunological response or changes in the bones structural load. Osteolysis may also be caused by pathologies like bone tumors, cysts, or chronic inflammation. Joint replacement While bone resorption is commonly associated with many diseases or joint problems, the term osteolysis generally refers to a problem common to artificial joint replacements such as total hip replacements, total knee replacements and total shoulder replacements. Osteolysis can also be associated with the radiographic changes seen in those with bisphosphonate-related osteonecrosis of the jaw.There are several biological mechanisms which may lead to osteolysis. In total hip replacement, the generally accepted explanation for osteolysis involves wear particles (worn off the contact surface of the artificial ball and socket joint). As the body attempts to clean up these wear particles (typically consisting of plastic or metal), it triggers an autoimmune reaction which causes resorption of living bone tissue. Osteolysis has been reported to occur as early as 12 months after implantation and is usually progressive. This may require a revision surgery (replacement of the prosthesis).Although osteolysis itself is clinically asymptomatic, it can lead to implant loosening or bone breakage, which in turn causes serious medical problems. Distal clavicular osteolysis Distal clavicular osteolysis (DCO) is often associated with problems weightlifters have with their acromioclavicular joints due to high mechanical stresses put on the clavicle as it meets with the acromion. This condition is often referred to as "weight lifters shoulder". Medical ultrasonography readily depicts resorption of the distal clavicle as irregular cortical erosions, whereas the acromion remains intact. Associated findings may include distended joint capsule, soft tissue swelling, and joint instability. A common surgery to treat recalcitrant DCO is resection of distal clavicle by removing a few millimetres of bone from the very end of the bone. See also Osteolytic lesion Biomineralization References == External links ==

Caught

Caught is a method of dismissing a batsman in cricket. A batsman is out caught if the batsman hits the ball, from a legitimate delivery, with the bat, and the ball is caught by the bowler or a fielder before it hits the ground. If the ball hits the stumps after hitting the wicket-keeper, If the wicket-keeper fails to do this, the delivery is a "no ball", and the batsman cannot be stumped (nor run out, unless he attempts to run to the other wicket.) If the catch taken by the wicket-keeper,then informally it is known as caught behind or caught at the wicket. A catch by the bowler is known as caught and bowled. This has nothing to do with the dismissal bowled but is rather a shorthand for saying the catcher and bowler are the same player. (The scorecard annotation is usually c. and b. or c&b followed by the bowlers name.) Caught is the most common method of dismissal at higher levels of competition, accounting for 36,190 Test match dismissals between 1877 and 2012, which is 56.9% of all Test match dismissals in this period.South African wicket-keeper Mark Boucher holds the record for the most Test match catches, with 532, while Rahul Dravid holds the record for the most Test match catches by non-wicket-keepers, with 210. Laws This method of dismissal is covered by Law 33 of the Laws of cricket which reads: The striker is out Caught if a ball delivered by the bowler, not being a No ball, touches his/her bat without having previously been in contact with any fielder, and is subsequently held by a fielder as a fair catch,..., before it touches the wicket and ground.This means that the batsman cannot be out caught if: The ball is called a no-ball or dead ball. The batsman does not hit the ball with his bat or a gloved hand holding the bat. The ball, having been hit, makes contact with the field before a fielder catches the ball. The ball does not remain under the control of the fielder. The ball is hit and lands beyond or on the boundary; (six runs). A fielder taking the catch makes contact with the boundary rope or the area outside the boundary, with any part of his body, equipment, when touching the ball. An airborne fielder taking the catch, having not previously legally touched the ball, had his last contact with the ground not entirely within the boundary.Note that if a batsman could be given out both caught and by another method, caught takes precedence, unless the other method is bowled.If a batsman is out caught, any runs scored off that delivery are voided. If a batsman is caught, the bowler is credited with the batsmans wicket and the catching fielder is credited for the dismissal, there is no catch assists for a saving boundaries before catch, or deflecting the ball to a different fielder in the slips cordon. If the two batsmen cross each other, in attempting to take a run, before the catch was taken, the non-striking batsman at the time remains at the opposite end of the pitch as the new incoming batsman comes to the crease at his former end. This means, unless it is now a new over, he is now on strike and the incoming batsman is not. Adjudication If the catch taken is pronounced or obvious, the players need not appeal to the umpire; the batsman normally chooses to acknowledge the dismissal himself. However, if the ball brushes the edge of the bat, or the catch is taken very close to the ground, or the ball appears to have bounced off the batsmans foot (so it has not touched the ground), or the ball appearing to come off the bat very close to the pitch surface (bump ball), or if the batsman is reluctant to accept that he has been dismissed, then the fielding team has to appeal to the umpire for this decision. In international competition, if neither field umpire can clearly decide if a catch has been made or not, they may refer to the third (television) umpire for a review. The third umpire may also be used if the Umpire Decision Review System is available and a team wishes to dispute a call concerning a possible catch. Celebration Before 2000, the Laws of Cricket defined a catch as being completed when the player had "complete control over the further disposal of the ball". In the very strictest sense, this meant that the player did not finish catching the ball until he threw it away, though the player doesnt have to throw the ball to anyone in particular in so doing. For this reason, even today many cricketers celebrate a catch by lobbing the ball into the air. In a Super Sixes match in the 1999 Cricket World Cup, South African Herschelle Gibbs caught Australian captain Steve Waugh but Waugh was given not out when Gibbs was ruled to not have control of the ball when attempting to throw the ball in celebration. Waugh went on to score a match-winning 120 not out to qualify his team for the semi-finals; Australia went on to win the tournament. Records Test matches The wicket-keepers with the highest number of catches taken in Test matches are as follows. Note this excludes catches made while not fielding as a wicket-keeper. Source: Cricinfo Statsguru. Last updated: 19 April 2019. The non-wicket-keepers with the highest number of catches taken in Test matches are as follows. Note this excludes any catches made while fielding as a wicket-keeper. Source: Cricinfo Statsguru. Last updated: 19 April 2019. One Day Internationals T20 Internationals First Class cricket See also Other sports Catch (baseball) == References ==

Coma scale

A coma scale is a system to assess the severity of coma. There are several such systems: Glasgow Coma Scale The Glasgow Coma Scale is neurological scale which aims to give a reliable, objective way of recording the conscious state of a person, for initial as well as continuing assessment. A patient is assessed against the criteria of the scale, and the resulting points give a patient score between 3 (indicating deep unconsciousness) and either 14 (original scale) or 15 (the more widely used modified or revised scale). GCS was initially used to assess level of consciousness after head injury and the scale is now used by first aid, EMS and doctors as being applicable to all acute medical and trauma patients. In hospital it is also used in chronic patient monitoring, in for instance, intensive care. Pediatric Glasgow Coma Scale The Pediatric Glasgow Coma Scale (also known as Pediatric Glasgow Coma Score or simply PGCS) is the equivalent of the Glasgow Coma Scale (GCS) used to assess the mental state of adult patients. As many of the assessments for an adult patient would not be appropriate for infants, the scale was modified slightly. As with the GCS, the PGCS comprises three tests: eye, verbal and motor responses. The three values separately as well as their sum are considered. The lowest possible PGCS (the sum) is 3 (deep coma or death) whilst the highest is 15 (fully awake and aware person). Blantyre Coma Scale The Blantyre Coma Scale is a modification of the Pediatric Glasgow Coma Scale, designed to assess malarial coma in children. It was designed by doctors Terrie Taylor and Malcolm Molyneux in 1987, and named for the Malawian city of Blantyre, site of the Blantyre Malaria Project. Rancho Los Amigos Scale The Rancho Los Amigos Scale is used to assess individuals after a closed head injury based on cognitive and behavioural presentations as they emerge from coma. It is named after the Rancho Los Amigos National Rehabilitation Center, located in Downey, California, United States. FOUR score See also Level of consciousness == References ==

Tuberous sclerosis

Tuberous sclerosis complex (TSC) is a rare multisystem autosomal dominant genetic disease that causes non-cancerous tumours to grow in the brain and on other vital organs such as the kidneys, heart, liver, eyes, lungs and skin. A combination of symptoms may include seizures, intellectual disability, developmental delay, behavioral problems, skin abnormalities, lung disease, and kidney disease.TSC is caused by a mutation of either of two genes, TSC1 and TSC2, which code for the proteins hamartin and tuberin, respectively, with TSC2 mutations accounting for the majority and tending to cause more severe symptoms. These proteins act as tumor growth suppressors, agents that regulate cell proliferation and differentiation.Prognosis is highly variable and depends on the symptoms, but life expectancy is normal for many.The prevalence of the disease is estimated to be 7 to 12 in 100,000. The disease is often abbreviated to tuberous sclerosis, which refers to the hard swellings in the brains of patients, first described by French neurologist Désiré-Magloire Bourneville in 1880. Signs and symptoms The physical manifestations of TSC are due to the formation of hamartia (malformed tissue such as the cortical tubers), hamartomas (benign growths such as facial angiofibroma and subependymal nodules), and very rarely, cancerous hamartoblastomas. The effect of these on the brain leads to neurological symptoms such as seizures, intellectual disability, developmental delay, and behavioral problems. Neurological Three types of brain tumours are associated with TSC: Giant cell astrocytoma: (grows and blocks the cerebrospinal fluid flow, leading to dilatation of ventricles causing headache and vomiting) Cortical tubers: after which the disease is named Subependymal nodules: form in the walls of ventriclesClassic intracranial manifestations of TSC include subependymal nodules and cortical/subcortical tubers.The tubers are typically triangular in configuration, with the apex pointed towards the ventricles, and are thought to represent foci of abnormal neuronal migration. The T2 signal abnormalities may subside in adulthood, but will still be visible on histopathological analysis. On magnetic resonance imaging (MRI), TSC patients can exhibit other signs consistent with abnormal neuron migration such as radial white matter tracts hyperintense on T2WI and heterotopic grey matter.Subependymal nodules are composed of abnormal, swollen glial cells and bizarre multinucleated cells which are indeterminate for glial or neuronal origin. Interposed neural tissue is not present. These nodules have a tendency to calcify as the patient ages. A nodule that markedly enhances and enlarges over time should be considered suspicious for transformation into a subependymal giant cell astrocytoma, which typically develops in the region of the foramen of Monro, in which case it is at risk of developing an obstructive hydrocephalus.A variable degree of ventricular enlargement is seen, either obstructive (e.g. by a subependymal nodule in the region of the foramen of Monro) or idiopathic in nature. Neuropsychiatric About 90% of people with TSC develop a range of neurodevelopmental, behavioural, psychiatric, and psychosocial difficulties. The "TSC‐associated neuropsychiatric disorders" are abbreviated TAND. These difficulties are less frequently identified and thus undertreated when compared with the neurological symptoms. Most problems are associated with more severe intellectual delay or associated with childhood and adolescence, and some (for example depressed mood) may be unreported if the person is unable to communicate. TAND can be investigated and considered at six levels: behavioural, psychiatric, intellectual, academic, neuropsychological, and psychosocial.Behavioural problems most commonly seen include overactivity, impulsivity and sleeping difficulties. Also common are anxiety, mood swings, and severe aggression. Less common are depressed mood, self-injury, and compulsive behaviours.People with TSC are frequently also diagnosed with psychiatric disorders: autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), anxiety disorder and depressive disorder. TSC is one of the most common genetic causes of autism spectrum disorder, which affects nearly half of people with TSC. ASD is more common in TSC2 than TSC1 and more common with earlier and more severe epilepsy, and with lower intellectual ability. ADHD is nearly as frequently seen in TSC as ASD (up to half of all people with TSC). Anxiety and depressive disorders, when they occur, are typically diagnosed in early adulthood and among those intellectually able to express their moods. Schizophrenia (and symptoms like hallucinations or psychosis) is no more common in TSC than the general population.The intellectual ability of people with TSC varies enormously. About 40–50% have a normal IQ. A normal IQ is much more commonly seen in TSC1 than TSC2, and profound intellectual disability seen in 34% of TSC2 compared with 10% of TSC1 in one study. Many studies have examined whether early onset, type and severity of epilepsy associates with intellectual ability. Academic issues occur even in people with TSC who have normal intellectual ability. These are often specific learning disorders such as dyscalculia (understanding mathematics), but also include other aspects affecting school life such as anxiety, lack of social skills or low self-esteem.About half of people with TSC, when assessed for neuropsychological skills, are in the bottom 5th percentile in some areas, which indicates a severe impairment. These include problems with attention (for example, being able to concentrate on two separate things like looking and listening), memory (particularly recall, verbal and spatial working memory) and executive function (for example, planning, self-monitoring, cognitive flexibility).The psychosocial impacts of TSC include low self-esteem and self-efficacy in the individual, and a burden on the family coping with a complex and unpredictable disorder. Kidneys Between 60 and 80% of TSC patients have benign tumors (once thought hamartomatous, but now considered true neoplasms) of the kidneys called angiomyolipomas frequently causing hematuria. These tumors are composed of vascular (angio–), smooth muscle (–myo–), and fat (–lip-) tissue. Although benign, an angiomyolipoma larger than 4 cm is at risk for a potentially catastrophic hemorrhage either spontaneously or with minimal trauma. Angiomyolipomas are found in about one in 300 people without TSC. However, those are usually solitary, whereas in TSC they are commonly multiple and bilateral.About 20-30% of people with TSC have renal cysts, causing few problems. However, 2% may also have autosomal dominant polycystic kidney disease.Very rare (< 1%) problems include renal cell carcinoma and oncocytomas (benign adenomatous hamartoma). Lungs Patients with TSC can develop progressive replacement of the lung parenchyma with multiple cysts, known as lymphangioleiomyomatosis (LAM). Recent genetic analysis has shown that the proliferative bronchiolar smooth muscle in TSC-related lymphangioleiomyomatosis is monoclonal metastasis from a coexisting renal angiomyolipoma. Cases of TSC-related lymphangioleiomyomatosis recurring following lung transplant have been reported. Heart Small tumours of the heart muscle, called cardiac rhabdomyomas, are rare in the general population (perhaps 0.2% of children) but very common in people with TSC. Around 80% of children under two-years-old with TSC have at least one rhabdomyoma, and about 90% of those will have several. The vast majority of children with at least one rhabdomyoma, and nearly all children with multiple rhabdomyomas will be found to have TSC. Prenatal ultrasound, performed by an obstetric sonographer specializing in cardiology, can detect a rhabdomyoma after 20 weeks. Rhabdomyoma vary in size from a few millimetres to several centimetres, and are usually found in the lower chambers (ventricles) and less often in the upper chambers (atria). They grow in size during the second half of pregnancy, but regress after birth, and are seen in only around 20% of children over two years old.Most rhabdomyomas cause no problems but some may cause heart failure in the foetus or first year of life. Rhabdomyomas are believed to be responsible for the development of heart arrhythmia later in life, which is relatively common in TSC. Arrhythmia can be hard to spot in people with TSC, other than by performing routine ECG. For example, arrhythmia may cause fainting that is confused with drop seizures, and symptoms of arrhythmia such as palpitations may not be reported in an individual with developmental delay. Skin Some form of dermatological sign is present in 96% of individuals with TSC. Most cause no problems, but are helpful in diagnosis. Some cases may cause disfigurement, necessitating treatment. The most common skin abnormalities include: Hypomelanic macules ("ash leaf spots") are present in about 90% of people with TSC. These small white or lighter patches of skin may appear anywhere on the body, and are caused by a lack of melanin. They are usually the only visible sign of TSC at birth. In fair-skinned individuals, a Woods lamp (ultraviolet light) may be required to see them. On the scalp, the effect may be a white patch of hair (poliosis). Patches smaller than 3mm are known as "confetti" skin lesions. Facial angiofibromas are present in about 75% of people with TSC. These are a rash of reddish spots or bumps on the nose and cheeks in a butterfly distribution, which consist of blood vessels and fibrous tissue. This potentially socially embarrassing rash starts to appear during childhood. Ungual fibromas: Also known as Koenens tumors, these are small fleshy tumors that grow around and under the toenails or fingernails. These are rare in childhood, but common by middle age. They are generally more common on toes than on fingers, develop at 15–29 years, and are more common in women than in men. Fibrous cephalic plaques are present in about 25% of people with TSC. These are raised, discoloured areas usually found on the forehead, but sometimes on the face or elsewhere on the scalp. Shagreen patches are present in about half of people with TSC, appearing in childhood. They are areas of thick leathery skin that are dimpled like an orange peel, and pigmented, they are usually found on the lower back or nape of the neck, or scattered across the trunk or thighs. The frequency of these lesions rises with age. Dental enamel pits are found in almost all adults with TSC. Intraoral fibromas are small surface-tumours found in the gums, inside the cheeks or tongue. Gum (gingival) fibromas are found in about 20-50% of people with TSC, more commonly in adults. Eyes Retinal lesions, called astrocytic hamartomas (or "phakomas"), which appear as a greyish or yellowish-white lesion in the back of the globe on the ophthalmic examination. Astrocytic hamartomas can calcify, and they are in the differential diagnosis of a calcified globe mass on a CT scan.Nonretinal lesions associated with TSC include: Coloboma Angiofibromas of the eyelids Papilledema (related to hydrocephalus) Pancreas Pancreatic neuroendocrine tumours have been described in rare cases of TSC. Variability Individuals with TSC may experience none or all of the clinical signs discussed above. The following table shows the prevalence of some of the clinical signs in individuals diagnosed with TSC. Genetics TSC is a genetic disorder with an autosomal dominant pattern of inheritance, variable expressivity, and incomplete penetrance. Two-thirds of TSC cases result from sporadic genetic mutations, not inheritance, but their offspring may inherit it from them. Current genetic tests have difficulty locating the mutation in roughly 20% of individuals diagnosed with the disease. So far, it has been mapped to two genetic loci, TSC1 and TSC2.TSC1 encodes for the protein hamartin, is located on chromosome 9 q34, and was discovered in 1997. TSC2 encodes for the protein tuberin, is located on chromosome 16 p13.3, and was discovered in 1993. TSC2 is contiguous with PKD1, the gene involved in one form of polycystic kidney disease (PKD). Gross deletions affecting both genes may account for the 2% of individuals with TSC who also develop polycystic kidney disease in childhood. TSC2 has been associated with a more severe form of TSC. However, the difference is subtle and cannot be used to identify the mutation clinically. Estimates of the proportion of TSC caused by TSC2 range from 55% to 90%.TSC1 and TSC2 are both tumor suppressor genes that function according to Knudsons "two hit" hypothesis. That is, a second random mutation must occur before a tumor can develop. This explains why, despite its high penetrance, TSC has wide expressivity. Pathophysiology Hamartin and tuberin function as a complex which is involved in the control of cell growth and cell division. The complex appears to interact with RHEB GTPase, thus sequestering it from activating mTOR signalling, part of the growth factor (insulin) signalling pathway. Thus, mutations at the TSC1 and TSC2 loci result in a loss of control of cell growth and cell division, and therefore a predisposition to forming tumors. TSC affects tissues from different germ layers. Cutaneous and visceral lesions may occur, including angiofibroma, cardiac rhabdomyomas, and renal angiomyolipomas. The central nervous system lesions seen in this disorder include hamartomas of the cortex, hamartomas of the ventricular walls, and subependymal giant cell tumors, which typically develop in the vicinity of the foramina of Monro.Molecular genetic studies have defined at least two loci for TSC. In TSC1, the abnormality is localized on chromosome 9q34, but the nature of the gene protein, called hamartin, remains unclear. No missense mutations occur in TSC1. In TSC2, the gene abnormalities are on chromosome 16p13. This gene encodes tuberin, a guanosine triphosphatase–activating protein. The specific function of this protein is unknown. In TSC2, all types of mutations have been reported; new mutations occur frequently. Few differences have yet been observed in the clinical phenotypes of patients with mutation of one gene or the other.Cells from individuals with pathogenic mutations in the TSC2 gene display abnormal accumulation of glycogen that is associated with depletion of lysosomes and autophagic impairment. The defective degradation of glycogen by the autophagy-lysosome pathway is, at least in part, independent of impaired regulation of mTORC1 and is restored, in cultured cells, by the combined use of PKB/Akt and mTORC1 pharmacological inhibitors. Diagnosis Tuberous sclerosis complex is diagnosed with clinical and genetic tests. There are many different mutations in the TSC1 and TSC2 genes that have been identified in individuals with TSC. A pathogenic mutation in the gene prevents the proteins from being made or inactivates the proteins. If such a pathogenic mutation is found then this alone is sufficient to diagnose TSC. However, some mutations are less clear in their effect, and so not sufficient alone for diagnosis. Between 1 in 10 and 1 in 4 of individuals with TSC have no mutation that can be identified. Once a particular mutation is identified in someone with TSC, this mutation can be used to make confident diagnoses in other family members.For clinical diagnosis, there isnt one sign that is unique (pathognomonic) to TSC, nor are all signs seen in all individuals. Therefore, several signs are considered together, classed as either major or minor features. An individual with two major features, or one major feature and at least two minor features can be given a definite diagnosis of TSC. If only one major feature or at least two minor features are present, the diagnosis is only regarded as possibly TSC. TSC can be first diagnosed at any stage of life. Prenatal diagnosis is possible by chance if heart tumours are discovered during routine ultrasound. In infancy, epilepsy, particularly infantile spasms, or developmental delay may lead to neurological tests. The white patches on the skin may also first become noticed. In childhood, behavioural problems and autism spectrum disorder may provoke a diagnosis. During adolescence, the skin problems appear. In adulthood, kidney and lung problems may develop. An individual may also be diagnosed at any time as a result of genetic testing of family members of another affected person. Management Tuberous sclerosis complex affects multiple organ systems so a multidisciplinary team of medical professionals is required.In suspected or newly diagnosed TSC, the following tests and procedures are recommended by 2012 International Tuberous Sclerosis Complex Consensus Conference. Take a personal and family history covering three generations. Genetic counselling and tests determine if other individuals are at risk. A magnetic resonance imaging (MRI) of the brain to identify tubers, subependymal nodules (SEN) and sub-ependymal giant cell astrocytomas (SEGA). Children undergo a baseline electroencephalograph (EEG) and family educated to identify seizures if/when they occur. Assess children for behavioural issues, autism spectrum disorder, psychiatric disorders, developmental delay, and neuropsychological problems. Scan the abdomen for tumours in various organs, but most importantly angiomyolipomata in the kidneys. MRI is superior to CT or ultrasound. Take blood pressure and test renal function. In adult women, test pulmonary function and perform a high-resolution computed tomography (HRCT) of the chest. Examine the skin under a Woods lamp (hypomelanotic macules), the fingers and toes (ungual fibroma), the face (angiofibromas), and the mouth (dental pits and gingival fibromas). In infants under three, perform an echocardiogram to spot rhabdomyomas, and electrocardiogram (ECG) for any arrhythmia. Use a fundoscope to spot retinal hamartomas or achromic patches.The various symptoms and complications from TSC may appear throughout life, requiring continued surveillance and adjustment to treatments. The following ongoing tests and procedures are recommended by 2012 International Tuberous Sclerosis Complex Consensus Conference. In children and adults younger than 25 years, a magnetic resonance imaging (MRI) of the brain is performed every one to three years to monitor for subependymal giant cell astrocytoma (SEGA). If a SEGA is large, growing or interfering with ventricles, the MRI is performed more frequently. After 25 years, if there are no SEGAs then periodic scans may no longer be required. A SEGA causing acute symptoms are removed with surgery, otherwise either surgery or drug treatment with an mTOR inhibitor may be indicated. Repeat screening for TSC-associated neuropsychiatric disorders (TAND) at least annually. Sudden behavioural changes may indicate a new physical problem (for example with the kidneys, epilepsy or a SEGA). Routine EEG determined by clinical need. Infantile spasms are best treated with vigabatrin and adrenocorticotropic hormone used as a second-line therapy. Other seizure types have no TSC-specific recommendation, though epilepsy in TSC is typically difficult to treat (medically refractory). Repeat MRI of abdomen every one to three years throughout life. Check renal (kidney) function annually. Should angiomyolipoma bleed, this is best treated with embolisation and then corticosteroids. Removal of the kidney (nephrectomy) is strongly to be avoided. An asymptomatic angiomyolipoma that is growing larger than 3 cm is best treated with an mTOR inhibitor drug. Other renal complications spotted by imaging include polycystic kidney disease and renal cell carcinoma. Repeat chest HRCT in adult women every five to 10 years. Evidence of lymphangioleiomyomatosis (LAM) indicates more frequent testing. An mTOR inhibitor drug can help, though a lung transplant may be required. A 12-lead ECG should be performed every three to five years.The mTOR inhibitor everolimus was approved in the US for treatment of TSC-related tumors in the brain (subependymal giant cell astrocytoma) in 2010 and in the kidneys (renal angiomyolipoma) in 2012. Oral everolimus (rapalog) reduces tumour size, is effective in terms of response to skin lesions and does not increase the risk of adverse events. Everolimus also showed evidence of effectiveness at treating epilepsy in some people with TSC. In 2017, the European Commission approved everolimus for treatment of refractory partial-onset seizures associated with TSC.Neurosurgical intervention may reduce the severity and frequency of seizures in TSC patients. Embolization and other surgical interventions can be used to treat renal angiomyolipoma with acute hemorrhage. Surgical treatments for symptoms of lymphangioleiomyomatosis (LAM) in adult TSC patients include pleurodesis to prevent pneumothorax and lung transplantation in the case of irreversible lung failure.Other treatments that have been used to treat TSC manifestations and symptoms include a ketogenic diet for intractable epilepsy and pulmonary rehabilitation for LAM. Facial angiofibromas can be reduced with laser treatment and the effectiveness of mTOR inhibitor topical treatment is being investigated. Laser therapy is painful, requires anaesthesia, and has risks of scarring and dyspigmentation. Prognosis The prognosis for individuals with TSC depends on the severity of symptoms, which range from mild skin abnormalities to varying degrees of learning disabilities and epilepsy to severe intellectual disability, uncontrollable seizures, and kidney failure. Those individuals with mild symptoms generally do well and live long, productive lives, while individuals with the more severe form may have serious disabilities. However, with appropriate medical care, most individuals with the disorder can look forward to normal life expectancy.A study of 30 TSC patients in Egypt found, "...earlier age of seizures commencement (<6 months) is associated with poor seizure outcome and poor intellectual capabilities. Infantile spasms and severely epileptogenic EEG patterns are related to the poor seizure outcome, poor intellectual capabilities and autistic behavior. Higher tubers numbers is associated with poor seizure outcome and autistic behavior. Left-sided tuber burden is associated with poor intellect, while frontal location is more encountered in ASD [autism spectrum disorders]. So, close follow up for the mental development and early control of seizures are recommended in a trial to reduce the risk factors of poor outcome. Also early diagnosis of autism will allow for earlier treatment and the potential for better outcome for children with TSC."Leading causes of death include renal disease, brain tumour, lymphangioleiomyomatosis of the lung, and status epilepticus or bronchopneumonia in those with severe intellectual disability. Cardiac failure due to rhabdomyomas is a risk in the fetus or neonate but is rarely a problem subsequently. Kidney complications such as angiomyolipoma and cysts are common and more frequent in females than males and in TSC2 than TSC1. Renal cell carcinoma is uncommon. Lymphangioleiomyomatosis is only a risk for females with angiomyolipomas. In the brain, the subependymal nodules occasionally degenerate to subependymal giant cell astrocytomas. These may block the circulation of cerebrospinal fluid around the brain, leading to hydrocephalus.Detection of the disease should be followed by genetic counselling. It is also important to realise that though the disease does not have a cure, symptoms can be treated symptomatically. Hence, awareness regarding different organ manifestations of TSC is important. Epidemiology TSC occurs in all races and ethnic groups, and in both genders. The live-birth prevalence is estimated to be between 10 and 16 cases per 100,000. A 1998 study estimated total population prevalence between about 7 and 12 cases per 100,000, with more than half of these cases undetected. Prior to the invention of CT scanning to identify the nodules and tubers in the brain, the prevalence was thought to be much lower, and the disease associated with those people diagnosed clinically with learning disability, seizures and facial angiofibroma. Whilst still regarded as a rare disease, TSC is common when compared to many other genetic diseases, with at least 1 million individuals affected worldwide. History TSC first came to medical attention when dermatologists described the distinctive facial rash (1835 and 1850). A more complete case was presented by von Recklinghausen (1862), who identified heart and brain tumours in a newborn who had only briefly lived. However, Bourneville (1880) is credited with having first characterized the disease, coining the name "tuberous sclerosis", thus earning the eponym Bournevilles disease. The neurologist Vogt (1908) established a diagnostic triad of epilepsy, idiocy, and adenoma sebaceum (an obsolete term for facial angiofibroma).Symptoms were periodically added to the clinical picture. The disease as presently understood was first fully described by Gomez (1979). The invention of medical ultrasound, CT and MRI has allowed physicians to examine the internal organs of live patients and greatly improved diagnostic ability.In 2002, treatment with rapamycin was found to be effective at shrinking tumours in animals. This has led to human trials of rapamycin as a drug to treat several of the tumors associated with TSC. References External links tuberous-sclerosis at NIH/UW GeneTests GeneReview/NCBI/NIH/UW entry on Tuberous Sclerosis Complex

Agnosia

Agnosia is the inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia only affects a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information. Types Visual agnosia Visual agnosia is a broad category that refers to a deficiency in the ability to recognize visual objects. Visual agnosia can be further subdivided into two different subtypes: apperceptive visual agnosia and associative visual agnosia.Individuals with apperceptive visual agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Apperceptive visual agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere.In contrast, individuals with associative visual agnosia experience difficulty when asked to name objects. Associative agnosia is associated with damage to both the right and left hemispheres at the occipitotemporal border. A specific form of associative visual agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers. However, individuals with prosopagnosia can recognize all other types of visual stimuli. Speech agnosia Speech agnosia, or auditory verbal agnosia, refers to "an inability to comprehend spoken words despite intact hearing, speech production and reading ability". Patients report that they hear sounds being produced, but that the sounds are fundamentally unrecognizable or untranslatable. EXAMINER: What did you eat for breakfast? PATIENT: Breakfast, breakfast, it sounds familiar but it doesnt speak to me. (Obler & Gjerlow 1999:45)Despite an inability to process what the speaker is saying, some patients have been reported to recognize certain characteristic information about the speakers voice (such as being a man or woman). Causes Agnosia can result from strokes, dementia, or other neurological disorders. It may also be trauma-induced by a head injury, brain infection, or hereditary. Additionally, some forms of agnosia may be the result of developmental disorders. Damage causing agnosia usually occurs in either the occipital or parietal lobes of the brain. Although one modality may be affected, cognitive abilities in other areas are preserved.Patients who experience dramatic recovery from blindness experience significant to total agnosia.The effect of damage to the superior temporal sulcus is consistent with several types of neurolinguistic deficiencies, and some contend that agnosia is one of them. The superior temporal sulcus is vital for speech comprehension because the region is highly involved with the lexical interface. According to the 1985 TRACE II Model, the lexical interface associates sound waves (phonemes) with morphological features to produce meaningful words. This association process is accomplished by lateral inhibition/excitement of certain words within an individuals lexicon (vocabulary). For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface: DOG activates 3, and inhibits 0 letters in DOG. – +3 DOG activates 2, and inhibits 1 letters in FOG. – +2 DOG activates 1, and inhibits 2 letters in DAN. – +1The consistency of this model to agnosia is shown by evidence that bilateral lesions to the superior temporal sulcus produces pure word deafness (Kussmaul, 1877), or as it is understood today, speech agnosia. Patients with pure word deafness demonstrate the inability to recognize and process speech sounds with normal auditory processing for non-speech sounds below the level of the cortex. Diagnosis In order to assess an individual for agnosia, it must be verified that the individual does not have a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual has a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual has a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed. Pure alexia Individuals with pure alexia usually have difficulty reading words as well as difficulty with identifying letters. In order to assess whether an individual has pure alexia, tests of copying and recognition must be performed. An individual with pure alexia should be able to copy a set of words, and should be able to recognize letters. Prosopagnosia Individuals are usually shown pictures of human faces that may be familiar to them such as famous actors, singers, politicians or family members. The pictures shown to the patient are selected to be age and culture appropriate. The task involves the examiner asking the individual to name each face. If the individual cannot name whose face appears in the picture, the examiner may ask a question that would help to recognize the face in the picture. Treatment For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies. Verbal strategies Using verbal descriptions may be helpful for individuals with certain types of agnosia. Individuals such as prosopagnosics may find it useful to listen to a description of their friend or family member and recognize them based on this description more easily than through visual cues. Alternate cues Alternate cues may be particularly useful to an individual with environmental agnosia or prosopagnosia. Alternate cues for an individual with environmental agnosia may include color cues or tactile markers to symbolize a new room or to remember an area by. Prosopagnosics may use alternate cues such as a scar on an individuals face or crooked teeth in order to recognize the individual. Hair color and length can be helpful cues as well. Organizational strategies Organizational strategies may be extremely helpful for an individual with visual agnosia. For example, organizing clothes according to different hangers provides tactile cues for the individual, making it easier to identify certain forms of clothing as opposed to relying solely on visual cues. Alternative medicine These strategies elicit the use of an unaffected modality. For example, visual agnosics can use tactile information in replacement of visual information. Alternatively, an individual with prosopagnosia can use auditory information in order to replace visual information. For example, an individual with prosopagnosia can wait for someone to speak, and will usually recognize the individual from their speech. Current research There are clinical trials being done to further research for treatments. At the National Institute of Neurological Disorders and Stroke (NINDS) they support research for rare diseases like agnosia. Some organizations that are recruiting for trials are using clincaltrials.gov and give status updates on the trials. History The term agnosia comes from the Ancient Greek ἀγνωσία (agnosia), "ignorance", "absence of knowledge". It was introduced by Sigmund Freud in 1891: "For disturbances in the recognition of objects, which Finkelnburg classes as asymbolia, I should like to propose the term agnosia." Prior to Freuds introduction of the term, some of the first ideas about agnosia came from Carl Wernicke, who created theories about receptive aphasia in 1874. He noted that individuals with receptive aphasia did not possess the ability to understand speech or repeat words. He believed that receptive aphasia was due to lesions of the posterior third of the left superior temporal gyrus. Due to these lesions, Wernicke believed that individuals with receptive aphasia had a limited deafness for certain sounds and frequencies in speech.After Wernicke, came Kussmaul in 1877 who attempted to explain why auditory verbal agnosia, also known as word deafness, occurs. Contrary to Wernickes explanations, Kussmaul believed auditory verbal agnosia was the result of major destruction to the first left temporal gyrus. Kussmaul also posited about the origins of alexia (acquired dyslexia) also known as word blindness. He believed that word blindness was the result of lesions to the left angular and supramarginal gyri.Heinrich Lissauer shared his ideas about agnosia after Wernicke and Kussmaul. In 1890, he theorized that there were two ways in which object recognition impairment could occur. One way in which impairment could occur was if there was damage to early perceptual processing or if there was damage to the actual object representation. If the actual object representation was damaged, this would not allow the object to be stored in visual memory, and therefore the individual would not be able to recognize the object. During the time of Wernicke, Kussmaul and Lissauer there was little known about the cerebral cortex. Today, with new neuroimaging techniques, we have been able to expand our knowledge on agnosia greatly. References External links Types and brain areas Total Recall: Memory Requires More than the Sum of Its Parts Scientific American (accessdate 2007-06-05)

Death

Death is the irreversible cessation of all biological functions that sustain an organism. For organisms with a brain, death can also be defined as the irreversible cessation of functioning of the whole brain, including brainstem, and brain death is sometimes used as a legal definition of death. The remains of a former organism normally begin to decompose shortly after death. Death is an inevitable process that eventually occurs in almost all organisms. Death is generally applied to whole organisms; the similar process seen in individual components of an organism, such as cells or tissues, is necrosis. Something that is not considered an organism, such as a virus, can be physically destroyed but is not said to die. As of the early 21st century, over 150,000 humans die each day, with ageing being by far the most common cause of death.Many cultures and religions have the idea of an afterlife, and also may hold the idea of judgement of good and bad deeds in ones life (heaven, hell, karma). Diagnosis Problems of definition The concept of death is a key to human understanding of the phenomenon. There are many scientific approaches and various interpretations of the concept. Additionally, the advent of life-sustaining therapy and the numerous criteria for defining death from both a medical and legal standpoint, have made it difficult to create a single unifying definition. One of the challenges in defining death is in distinguishing it from life. As a point in time, death would seem to refer to the moment at which life ends. Determining when death has occurred is difficult, as cessation of life functions is often not simultaneous across organ systems. Such determination, therefore, requires drawing precise conceptual boundaries between life and death. This is difficult, due to there being little consensus on how to define life. It is possible to define life in terms of consciousness. When consciousness ceases, an organism can be said to have died. One of the flaws in this approach is that there are many organisms that are alive but probably not conscious (for example, single-celled organisms). Another problem is in defining consciousness, which has many different definitions given by modern scientists, psychologists and philosophers. Additionally, many religious traditions, including Abrahamic and Dharmic traditions, hold that death does not (or may not) entail the end of consciousness. In certain cultures, death is more of a process than a single event. It implies a slow shift from one spiritual state to another. Other definitions for death focus on the character of cessation of organismic functioning and a human death which refers to irreversible loss of personhood. More specifically, death occurs when a living entity experiences irreversible cessation of all functioning. As it pertains to human life, death is an irreversible process where someone loses their existence as a person.Historically, attempts to define the exact moment of a humans death have been subjective, or imprecise. Death was once defined as the cessation of heartbeat (cardiac arrest) and of breathing, but the development of CPR and prompt defibrillation have rendered that definition inadequate because breathing and heartbeat can sometimes be restarted. This type of death where circulatory and respiratory arrest happens is known as the circulatory definition of death (DCDD). Proponents of the DCDD believe that this definition is reasonable because a person with permanent loss of circulatory and respiratory function should be considered dead. Critics of this definition state that while cessation of these functions may be permanent, it does not mean the situation is irreversible, because if CPR was applied, the person could be revived. Thus, the arguments for and against the DCDD boil down to a matter of defining the actual words "permanent" and "irreversible," which further complicates the challenge of defining death. Furthermore, events which were causally linked to death in the past no longer kill in all circumstances; without a functioning heart or lungs, life can sometimes be sustained with a combination of life support devices, organ transplants and artificial pacemakers. Today, where a definition of the moment of death is required, doctors and coroners usually turn to "brain death" or "biological death" to define a person as being dead; people are considered dead when the electrical activity in their brain ceases. It is presumed that an end of electrical activity indicates the end of consciousness. Suspension of consciousness must be permanent, and not transient, as occurs during certain sleep stages, and especially a coma. In the case of sleep, EEGs can easily tell the difference. The category of "brain death" is seen as problematic by some scholars. For instance, Dr. Franklin Miller, senior faculty member at the Department of Bioethics, National Institutes of Health, notes: "By the late 1990s... the equation of brain death with death of the human being was increasingly challenged by scholars, based on evidence regarding the array of biological functioning displayed by patients correctly diagnosed as having this condition who were maintained on mechanical ventilation for substantial periods of time. These patients maintained the ability to sustain circulation and respiration, control temperature, excrete wastes, heal wounds, fight infections and, most dramatically, to gestate fetuses (in the case of pregnant "brain-dead" women)."While "brain death" is viewed as problematic by some scholars, there are certainly proponents of it that believe this definition of death is the most reasonable for distinguishing life from death. The reasoning behind the support for this definition is that brain death has a set of criteria that is reliable and reproducible. Also, the brain is crucial in determining our identity or who we are as human beings. The distinction should be made that "brain death" cannot be equated with one who is in a vegetative state or coma, in that the former situation describes a state that is beyond recovery.Those people maintaining that only the neo-cortex of the brain is necessary for consciousness sometimes argue that only electrical activity should be considered when defining death. Eventually it is possible that the criterion for death will be the permanent and irreversible loss of cognitive function, as evidenced by the death of the cerebral cortex. All hope of recovering human thought and personality is then gone given current and foreseeable medical technology. At present, in most places the more conservative definition of death – irreversible cessation of electrical activity in the whole brain, as opposed to just in the neo-cortex – has been adopted (for example the Uniform Determination Of Death Act in the United States). In 2005, the Terri Schiavo case brought the question of brain death and artificial sustenance to the front of American politics. Even by whole-brain criteria, the determination of brain death can be complicated. EEGs can detect spurious electrical impulses, while certain drugs, hypoglycemia, hypoxia, or hypothermia can suppress or even stop brain activity on a temporary basis. Because of this, hospitals have protocols for determining brain death involving EEGs at widely separated intervals under defined conditions. In the past, adoption of this whole-brain definition was a conclusion of the Presidents Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research in 1980. They concluded that this approach to defining death sufficed in reaching a uniform definition nationwide. A multitude of reasons were presented to support this definition including: uniformity of standards in law for establishing death; consumption of a familys fiscal resources for artificial life support; and legal establishment for equating brain death with death in order to proceed with organ donation.Aside from the issue of support of or dispute against brain death, there is another inherent problem in this categorical definition: the variability of its application in medical practice. In 1995, the American Academy of Neurology (AAN), established a set of criteria that became the medical standard for diagnosing neurologic death. At that time, three clinical features had to be satisfied in order to determine "irreversible cessation" of the total brain including: coma with clear etiology, cessation of breathing, and lack of brainstem reflexes. This set of criteria was then updated again most recently in 2010, but substantial discrepancies still remain across hospitals and medical specialties.The problem of defining death is especially imperative as it pertains to the dead donor rule, which could be understood as one of the following interpretations of the rule: there must be an official declaration of death in a person before starting organ procurement or that organ procurement cannot result in death of the donor. A great deal of controversy has surrounded the definition of death and the dead donor rule. Advocates of the rule believe the rule is legitimate in protecting organ donors while also countering against any moral or legal objection to organ procurement. Critics, on the other hand, believe that the rule does not uphold the best interests of the donors and that the rule does not effectively promote organ donation. Signs Signs of death or strong indications that a warm-blooded animal is no longer alive are: Respiratory arrest (no breathing) Cardiac arrest (no pulse) Brain death (no neuronal activity)The stages that follow after death are: Pallor mortis, paleness which happens in 15–120 minutes after death Algor mortis, the reduction in body temperature following death. This is generally a steady decline until matching ambient temperature Rigor mortis, the limbs of the corpse become stiff (Latin rigor) and difficult to move or manipulate Livor mortis, a settling of the blood in the lower (dependent) portion of the body Putrefaction, the beginning signs of decomposition Decomposition, the reduction into simpler forms of matter, accompanied by a strong, unpleasant odor. Skeletonization, the end of decomposition, where all soft tissues have decomposed, leaving only the skeleton. Fossilization, the natural preservation of the skeletal remains formed over a very long period Legal The death of a person has legal consequences that may vary between different jurisdictions. A death certificate is issued in most jurisdictions, either by a doctor, or by an administrative office upon presentation of a doctors declaration of death. Misdiagnosed There are many anecdotal references to people being declared dead by physicians and then "coming back to life", sometimes days later in their own coffin, or when embalming procedures are about to begin. From the mid-18th century onwards, there was an upsurge in the publics fear of being mistakenly buried alive, and much debate about the uncertainty of the signs of death. Various suggestions were made to test for signs of life before burial, ranging from pouring vinegar and pepper into the corpses mouth to applying red hot pokers to the feet or into the rectum. Writing in 1895, the physician J.C. Ouseley claimed that as many as 2,700 people were buried prematurely each year in England and Wales, although others estimated the figure to be closer to 800.In cases of electric shock, cardiopulmonary resuscitation (CPR) for an hour or longer can allow stunned nerves to recover, allowing an apparently dead person to survive. People found unconscious under icy water may survive if their faces are kept continuously cold until they arrive at an emergency room. This "diving response", in which metabolic activity and oxygen requirements are minimal, is something humans share with cetaceans called the mammalian diving reflex.As medical technologies advance, ideas about when death occurs may have to be re-evaluated in light of the ability to restore a person to vitality after longer periods of apparent death (as happened when CPR and defibrillation showed that cessation of heartbeat is inadequate as a decisive indicator of death). The lack of electrical brain activity may not be enough to consider someone scientifically dead. Therefore, the concept of information-theoretic death has been suggested as a better means of defining when true death occurs, though the concept has few practical applications outside the field of cryonics. There have been some scientific attempts to bring dead organisms back to life, but with limited success. Causes The leading cause of human death in developing countries is infectious disease. The leading causes in developed countries are atherosclerosis (heart disease and stroke), cancer, and other diseases related to obesity and aging. By an extremely wide margin, the largest unifying cause of death in the developed world is biological aging, leading to various complications known as aging-associated diseases. These conditions cause loss of homeostasis, leading to cardiac arrest, causing loss of oxygen and nutrient supply, causing irreversible deterioration of the brain and other tissues. Of the roughly 150,000 people who die each day across the globe, about two thirds die of age-related causes. In industrialized nations, the proportion is much higher, approaching 90%. With improved medical capability, dying has become a condition to be managed. Home deaths, once commonplace, are now rare in the developed world. In developing nations, inferior sanitary conditions and lack of access to modern medical technology makes death from infectious diseases more common than in developed countries. One such disease is tuberculosis, a bacterial disease which killed 1.8M people in 2015. Malaria causes about 400–900M cases of fever and 1–3M deaths annually. AIDS death toll in Africa may reach 90–100M by 2025.According to Jean Ziegler (United Nations Special Reporter on the Right to Food, 2000 – Mar 2008), mortality due to malnutrition accounted for 58% of the total mortality rate in 2006. Ziegler says worldwide approximately 62M people died from all causes and of those deaths more than 36M died of hunger or diseases due to deficiencies in micronutrients.Tobacco smoking killed 100 million people worldwide in the 20th century and could kill 1 billion people around the world in the 21st century, a World Health Organization report warned.Many leading developed world causes of death can be postponed by diet and physical activity, but the accelerating incidence of disease with age still imposes limits on human longevity. The evolutionary cause of aging is, at best, only just beginning to be understood. It has been suggested that direct intervention in the aging process may now be the most effective intervention against major causes of death. Selye proposed a unified non-specific approach to many causes of death. He demonstrated that stress decreases adaptability of an organism and proposed to describe the adaptability as a special resource, adaptation energy. The animal dies when this resource is exhausted. Selye assumed that the adaptability is a finite supply, presented at birth. Later on, Goldstone proposed the concept of a production or income of adaptation energy which may be stored (up to a limit), as a capital reserve of adaptation. In recent works, adaptation energy is considered as an internal coordinate on the "dominant path" in the model of adaptation. It is demonstrated that oscillations of well-being appear when the reserve of adaptability is almost exhausted.In 2012, suicide overtook car crashes for leading causes of human injury deaths in the U.S., followed by poisoning, falls, and murder. Causes of death are different in different parts of the world. In high-income and middle income countries nearly half up to more than two thirds of all people live beyond the age of 70 and predominantly die of chronic diseases. In low-income countries, where less than one in five of all people reach the age of 70, and more than a third of all deaths are among children under 15, people predominantly die of infectious diseases. Autopsy An autopsy, also known as a postmortem examination or an obduction, is a medical procedure that consists of a thorough examination of a human corpse to determine the cause and manner of a persons death and to evaluate any disease or injury that may be present. It is usually performed by a specialized medical doctor called a pathologist. Autopsies are either performed for legal or medical purposes. A forensic autopsy is carried out when the cause of death may be a criminal matter, while a clinical or academic autopsy is performed to find the medical cause of death and is used in cases of unknown or uncertain death, or for research purposes. Autopsies can be further classified into cases where external examination suffices, and those where the body is dissected and an internal examination is conducted. Permission from next of kin may be required for internal autopsy in some cases. Once an internal autopsy is complete the body is generally reconstituted by sewing it back together. Autopsy is important in a medical environment and may shed light on mistakes and help improve practices. A necropsy, which is not always a medical procedure, was a term previously used to describe an unregulated postmortem examination. In modern times, this term is more commonly associated with the corpses of animals. Senescence Senescence refers to a scenario when a living being is able to survive all calamities, but eventually dies due to causes relating to old age. Animal and plant cells normally reproduce and function during the whole period of natural existence, but the aging process derives from deterioration of cellular activity and ruination of regular functioning. Aptitude of cells for gradual deterioration and mortality means that cells are naturally sentenced to stable and long-term loss of living capacities, even despite continuing metabolic reactions and viability. In the United Kingdom, for example, nine out of ten of all the deaths that occur on a daily basis relates to senescence, while around the world it accounts for two-thirds of 150,000 deaths that take place daily.Almost all animals who survive external hazards to their biological functioning eventually die from biological aging, known in life sciences as "senescence". Some organisms experience negligible senescence, even exhibiting biological immortality. These include the jellyfish Turritopsis dohrnii, the hydra, and the planarian. Unnatural causes of death include suicide and predation. From all causes, roughly 150,000 people die around the world each day. Of these, two thirds die directly or indirectly due to senescence, but in industrialized countries – such as the United States, the United Kingdom, and Germany – the rate approaches 90% (i.e., nearly nine out of ten of all deaths are related to senescence).Physiological death is now seen as a process, more than an event: conditions once considered indicative of death are now reversible. Where in the process a dividing line is drawn between life and death depends on factors beyond the presence or absence of vital signs. In general, clinical death is neither necessary nor sufficient for a determination of legal death. A patient with working heart and lungs determined to be brain dead can be pronounced legally dead without clinical death occurring. Cryonics Cryonics (from Greek κρύος kryos- meaning icy cold) is the low-temperature preservation of animals and humans who cannot be sustained by contemporary medicine, with the hope that healing and resuscitation may be possible in the future.Cryopreservation of people or large animals is not reversible with current technology. The stated rationale for cryonics is that people who are considered dead by current legal or medical definitions may not necessarily be dead according to the more stringent information-theoretic definition of death.Some scientific literature is claimed to support the feasibility of cryonics. Medical science and cryobiologists generally regards cryonics with skepticism. Life extension Life extension refers to an increase in maximum or average lifespan, especially in humans, by slowing down or reversing the processes of aging through anti-aging measures. Despite the fact that aging is by far the most common cause of death worldwide, it is socially mostly ignored as such and seen as "necessary" and "inevitable" anyway, which is why little money is spent on research into anti-aging therapies, a phenomenon known as the pro-aging trance.Average lifespan is determined by vulnerability to accidents and age or lifestyle-related afflictions such as cancer, or cardiovascular disease. Extension of average lifespan can be achieved by good diet, exercise and avoidance of hazards such as smoking. Maximum lifespan is also determined by the rate of aging for a species inherent in its genes. Currently, the only widely recognized method of extending maximum lifespan is calorie restriction. Theoretically, extension of maximum lifespan can be achieved by reducing the rate of aging damage, by periodic replacement of damaged tissues, or by molecular repair or rejuvenation of deteriorated cells and tissues. A United States poll found that religious people and irreligious people, as well as men and women and people of different economic classes have similar rates of support for life extension, while Africans and Hispanics have higher rates of support than white people. 38 percent of the polled said they would desire to have their aging process cured. Researchers of life extension are a subclass of biogerontologists known as "biomedical gerontologists". They try to understand the nature of aging and they develop treatments to reverse aging processes or to at least slow them down, for the improvement of health and the maintenance of youthful vigor at every stage of life. Those who take advantage of life extension findings and seek to apply them upon themselves are called "life extensionists" or "longevists". The primary life extension strategy currently is to apply available anti-aging methods in the hope of living long enough to benefit from a complete cure to aging once it is developed. Location Before about 1930, most people in Western countries died in their own homes, surrounded by family, and comforted by clergy, neighbors, and doctors making house calls. By the mid-20th century, half of all Americans died in a hospital. By the start of the 21st century, only about 20–25% of people in developed countries died outside of a medical institution. The shift away from dying at home towards dying in a professional medical environment has been termed the "Invisible Death". This shift occurred gradually over the years, until most deaths now occur outside the home. Psychology Death studies is a field within psychology. Many people are afraid of dying. Discussing, thinking about, or planning for their own deaths causes them discomfort. This fear may cause them to put off financial planning, preparing a will and testament, or requesting help from a hospice organization. Different people have different responses to the idea of their own deaths. Philosopher Galen Strawson writes that the death that many people wish for is an instant, painless, unexperienced annihilation. In this unlikely scenario, the person dies without realizing it and without being able to fear it. One moment the person is walking, eating, or sleeping, and the next moment, the person is dead. Strawson reasons that this type of death would not take anything away from the person, as he believes that a person cannot have a legitimate claim to ownership in the future. Society and culture In society, the nature of death and humanitys awareness of its own mortality has for millennia been a concern of the worlds religious traditions and of philosophical inquiry. This includes belief in resurrection or an afterlife (associated with Abrahamic religions), reincarnation or rebirth (associated with Dharmic religions), or that consciousness permanently ceases to exist, known as eternal oblivion (associated with Secular humanism).Commemoration ceremonies after death may include various mourning, funeral practices and ceremonies of honouring the deceased. The physical remains of a person, commonly known as a corpse or body, are usually interred whole or cremated, though among the worlds cultures there are a variety of other methods of mortuary disposal. In the English language, blessings directed towards a dead person include rest in peace (originally the Latin requiescat in pace), or its initialism RIP. Death is the center of many traditions and organizations; customs relating to death are a feature of every culture around the world. Much of this revolves around the care of the dead, as well as the afterlife and the disposal of bodies upon the onset of death. The disposal of human corpses does, in general, begin with the last offices before significant time has passed, and ritualistic ceremonies often occur, most commonly interment or cremation. This is not a unified practice; in Tibet, for instance, the body is given a sky burial and left on a mountain top. Proper preparation for death and techniques and ceremonies for producing the ability to transfer ones spiritual attainments into another body (reincarnation) are subjects of detailed study in Tibet. Mummification or embalming is also prevalent in some cultures, to retard the rate of decay. Legal aspects of death are also part of many cultures, particularly the settlement of the deceased estate and the issues of inheritance and in some countries, inheritance taxation. Capital punishment is also a culturally divisive aspect of death. In most jurisdictions where capital punishment is carried out today, the death penalty is reserved for premeditated murder, espionage, treason, or as part of military justice. In some countries, sexual crimes, such as adultery and sodomy, carry the death penalty, as do religious crimes such as apostasy, the formal renunciation of ones religion. In many retentionist countries, drug trafficking is also a capital offense. In China, human trafficking and serious cases of corruption are also punished by the death penalty. In militaries around the world courts-martial have imposed death sentences for offenses such as cowardice, desertion, insubordination, and mutiny.Death in warfare and in suicide attack also have cultural links, and the ideas of dulce et decorum est pro patria mori, mutiny punishable by death, grieving relatives of dead soldiers and death notification are embedded in many cultures. Recently in the western world, with the increase in terrorism following the September 11 attacks, but also further back in time with suicide bombings, kamikaze missions in World War II and suicide missions in a host of other conflicts in history, death for a cause by way of suicide attack, and martyrdom have had significant cultural impacts. Suicide in general, and particularly euthanasia, are also points of cultural debate. Both acts are understood very differently in different cultures. In Japan, for example, ending a life with honor by seppuku was considered a desirable death, whereas according to traditional Christian and Islamic cultures, suicide is viewed as a sin. Death is personified in many cultures, with such symbolic representations as the Grim Reaper, Azrael, the Hindu god Yama and Father Time. In Brazil, a human death is counted officially when it is registered by existing family members at a cartório, a government-authorized registry. Before being able to file for an official death, the deceased must have been registered for an official birth at the cartório. Though a Public Registry Law guarantees all Brazilian citizens the right to register deaths, regardless of their financial means, of their family members (often children), the Brazilian government has not taken away the burden, the hidden costs and fees, of filing for a death. For many impoverished families, the indirect costs and burden of filing for a death lead to a more appealing, unofficial, local, cultural burial, which in turn raises the debate about inaccurate mortality rates.Talking about death and witnessing it is a difficult issue with most cultures. Western societies may like to treat the dead with the utmost material respect, with an official embalmer and associated rites. Eastern societies (like India) may be more open to accepting it as a fait accompli, with a funeral procession of the dead body ending in an open-air burning-to-ashes of the same. Consciousness Much interest and debate surround the question of what happens to ones consciousness as ones body dies. The belief in the permanent loss of consciousness after death is often called eternal oblivion. Belief that the stream of consciousness is preserved after physical death is described by the term afterlife. Neither are likely to ever be confirmed without the ponderer having to actually die. In biology After death, the remains of a former organism become part of the biogeochemical cycle, during which animals may be consumed by a predator or a scavenger. Organic material may then be further decomposed by detritivores, organisms which recycle detritus, returning it to the environment for reuse in the food chain, where these chemicals may eventually end up being consumed and assimilated into the cells of an organism. Examples of detritivores include earthworms, woodlice and dung beetles. Microorganisms also play a vital role, raising the temperature of the decomposing matter as they break it down into yet simpler molecules. Not all materials need to be fully decomposed. Coal, a fossil fuel formed over vast tracts of time in swamp ecosystems, is one example. Natural selection Contemporary evolutionary theory sees death as an important part of the process of natural selection. It is considered that organisms less adapted to their environment are more likely to die having produced fewer offspring, thereby reducing their contribution to the gene pool. Their genes are thus eventually bred out of a population, leading at worst to extinction and, more positively, making the process possible, referred to as speciation. Frequency of reproduction plays an equally important role in determining species survival: an organism that dies young but leaves numerous offspring displays, according to Darwinian criteria, much greater fitness than a long-lived organism leaving only one. Extinction Extinction is the cessation of existence of a species or group of taxa, reducing biodiversity. The moment of extinction is generally considered to be the death of the last individual of that species (although the capacity to breed and recover may have been lost before this point). Because a species potential range may be very large, determining this moment is difficult, and is usually done retrospectively.

Death

This difficulty leads to phenomena such as Lazarus taxa, where species presumed extinct abruptly "reappear" (typically in the fossil record) after a period of apparent absence. New species arise through the process of speciation, an aspect of evolution. New varieties of organisms arise and thrive when they are able to find and exploit an ecological niche – and species become extinct when they are no longer able to survive in changing conditions or against superior competition. Evolution of aging and mortality Inquiry into the evolution of aging aims to explain why so many living things and the vast majority of animals weaken and die with age (exceptions include Hydra and the jellyfish Turritopsis dohrnii, which research shows to be biologically immortal). The evolutionary origin of senescence remains one of the fundamental puzzles of biology. Gerontology specializes in the science of human aging processes. Organisms showing only asexual reproduction (e.g. bacteria, some protists, like the euglenoids and many amoebozoans) and unicellular organisms with sexual reproduction (colonial or not, like the volvocine algae Pandorina and Chlamydomonas) are "immortal" at some extent, dying only due to external hazards, like being eaten or meeting with a fatal accident. In multicellular organisms (and also in multinucleate ciliates), with a Weismannist development, that is, with a division of labor between mortal somatic (body) cells and "immortal" germ (reproductive) cells, death becomes an essential part of life, at least for the somatic line.The Volvox algae are among the simplest organisms to exhibit that division of labor between two completely different cell types, and as a consequence include death of somatic line as a regular, genetically regulated part of its life history. Religious views Buddhism In Buddhist doctrine and practice, death plays an important role. Awareness of death was what motivated Prince Siddhartha to strive to find the "deathless" and finally to attain enlightenment. In Buddhist doctrine, death functions as a reminder of the value of having been born as a human being. Being reborn as a human being is considered the only state in which one can attain enlightenment. Therefore, death helps remind oneself that one should not take life for granted. The belief in rebirth among Buddhists does not necessarily remove death anxiety, since all existence in the cycle of rebirth is considered filled with suffering, and being reborn many times does not necessarily mean that one progresses.Death is part of several key Buddhist tenets, such as the Four Noble Truths and dependent origination. Christianity While there are different sects of Christianity with different branches of belief; the overarching ideology on death grows from the knowledge of afterlife. Meaning after death the individual will undergo a separation from mortality to immortality; their soul leaves the body entering a realm of spirits. Following this separation of body and spirit (i.e. death) resurrection will occur. Representing the same transformation Jesus Christ embodied after his body was placed in the tomb for three days. Like Him, each persons body will be resurrected reuniting the spirit and body in a perfect form. This process allows the individuals soul to withstand death and transform into life after death. Hinduism In Hindu texts, death is described as the individual eternal spiritual jiva-atma (soul or conscious self) exiting the current temporary material body. The soul exits this body when the body can no longer sustain the conscious self (life), which may be due to mental or physical reasons, or more accurately, the inability to act on ones kama (material desires). During conception, the soul enters a compatible new body based on the remaining merits and demerits of ones karma (good/bad material activities based on dharma) and the state of ones mind (impressions or last thoughts) at the time of death. Usually the process of reincarnation (souls transmigration) makes one forget all memories of ones previous life. Because nothing really dies and the temporary material body is always changing, both in this life and the next, death means forgetfulness of ones previous experiences (previous material identity). Material existence is described as being full of miseries arising from birth, disease, old age, death, mind, weather, etc. To conquer samsara (the cycle of death and rebirth) and become eligible for one of the different types of moksha (liberation), one has to first conquer kama (material desires) and become self-realized. The human form of life is most suitable for this spiritual journey, especially with the help of sadhu (self-realized saintly persons), sastra (revealed spiritual scriptures), and guru (self-realized spiritual masters), given all three are in agreement. Islam The Islamic view is that death is the separation of the soul from the body as well as the beginning of the afterlife. The afterlife or akhirah is one of the six main beliefs in Islam. Rather than seeing death as the end of life, Muslims consider death as a continuation of life in another form. In Islam, the life on earth right now is a short, temporary life and a testing period for every soul. The true life begins with the Day of Judgement, when all people will be divided into two groups. The righteous believers will be welcomed to janna (heaven) and the disbelievers and evildoers will be punished in jahannam (hellfire).Muslims believe death to be wholly natural and predetermined by God. Only God knows the exact time of a person’s death. The Quran emphasizes that death is inevitable, no matter how much people try to escape death, it will reach everyone. Life on earth is the one and only chance for people to prepare themselves for the life to come and choose to either believe or not believe in God, and death is the end of that learning opportunity. Judaism There are a variety of beliefs about the afterlife within Judaism, but none of them contradict the preference of life over death. This is partially because death puts a cessation to the possibility of fulfilling any commandments. Language The word "death" comes from Old English dēaþ, which in turn comes from Proto-Germanic *dauþuz (reconstructed by etymological analysis). This comes from the Proto-Indo-European stem *dheu- meaning the "process, act, condition of dying".The concept and symptoms of death, and varying degrees of delicacy used in discussion in public forums, have generated numerous scientific, legal, and socially acceptable terms or euphemisms. When a person has died, it is also said they have "passed away", "passed on", "expired", or "gone", among other socially accepted, religiously specific, slang, and irreverent terms. As a formal reference to a dead person, it has become common practice to use the participle form of "decease", as in "the deceased"; another noun form is "decedent". Bereft of life, the dead person is a "corpse", "cadaver", "body", "set of remains" or, when all flesh is gone, a "skeleton". The terms "carrion" and "carcass" are also used, usually for dead non-human animals. The ashes left after a cremation are lately called "cremains". See also References Bibliography Further reading Cochem, Martin of (1899). "On Death". The four last things: death, judgment, hell, heaven. Benziger Brothers. Daughters of Charity of St. Vincent de Paul. (1856). "Considerations on Death". St. Vincents Manual. John Murphy & Co. Liguori, Alphonsus (1868). Preparation for Death. Rivingtons. Marques, Susana Moreira (13 October 2015). Now and At the Hour of Our Death. Translated by Sanches, Julia. And Other Stories. ISBN 978-1-908276-62-9. Massillon, Jean-Baptiste (1879). "On Death". Sermons by John-Baptist Massillon. Thomas Tegg & Sons. Rosenberg, David (17 August 2014). "How One Photographer Overcame His Fear of Death by Photographing It (Walter Schels Life Before Death)". Slate. Sachs, Jessica Snyder (2001). Corpse: Nature, Forensics, and the Struggle to Pinpoint Time of Death (270 pages). Perseus Publishing. ISBN 978-0-7382-0336-2. Warraich, Haider (2017). Modern Death: How Medicine Changed the End of Life. St. Martins Press. ISBN 978-1250104588. External links Death at Curlie "Death". Stanford Encyclopedia of Philosophy. Metaphysics Research Lab, Stanford University. 2016. "Death". Encyclopædia Britannica. Vol. 7 (11th ed.). 1911. pp. 898–900. Best, Ben. "Causes of Death". BenBest.com. Retrieved 10 June 2016. Schels, Walter; Lakotta, Beate. "Before and After Death". LensCulture.com. Archived from the original on 11 October 2014. Retrieved 19 September 2016. Interviews with people dying in hospices, and portraits of them before, and shortly after, death. U.S. Census. "Causes of Death 1916". AntiqueBooks.net (scanns). Archived from the original on 18 September 2004. Retrieved 19 September 2016. How the medical profession categorized causes of death. Wald, George. "The Origin of Death". ElijahWald.com. A biologist explains life and death in different kinds of organisms, in relation to evolution. "Death" (video; 10:18) by Timothy Ferris, producer of the Voyager Golden Record for NASA. 2021

Melena

Melena or melaena refers to the dark black, tarry feces that are associated with upper gastrointestinal bleeding. The black color and characteristic strong odor are caused by hemoglobin in the blood being altered by digestive enzymes and intestinal bacteria.Iron supplements may cause a grayish-black stool that should be distinguished from melena, as should black coloration caused by a number of medications, such as bismuth subsalicylate (the active ingredient in Pepto-Bismol), or by foods such as beetroot, black liquorice, or blueberries. Causes The most common cause of melena is peptic ulcer disease. However, any bleeding within the upper gastrointestinal tract or the ascending colon can lead to melena. Melena may also be a complication of anticoagulant medications, such as warfarin.Causes of upper gastrointestinal bleeding that may result in melena include malignant tumors affecting the esophagus, stomach or small intestine, hemorrhagic blood diseases, such as thrombocytopenia and hemophilia, gastritis, Stomach cancer, esophageal varices, Meckels diverticulum and Mallory-Weiss syndrome.Causes of "false" melena include iron supplements, Pepto-Bismol, Maalox, and lead, blood swallowed as a result of a nose bleed (epistaxis), and blood ingested as part of the diet, as with consumption of black pudding (blood sausage), or with the traditional African Maasai diet, which includes much blood drained from cattle.Melena is considered a medical emergency as it arises from a significant amount of bleeding. Urgent care is required to rule out serious causes and prevent potentially life-threatening emergencies.A less serious, self-limiting case of melena can occur in newborns two to three days after delivery, due to swallowed maternal blood. Diagnosis In acute cases, with a large amount of blood loss, patients may present with anemia or low blood pressure. However, aside from the melena itself, many patients may present with few symptoms. Often, the first approach is to use endoscopy to look for obvious signs of a bleed. In cases where the source of the bleed is unclear, but melena is present, an upper endoscopy is recommended, to try to ascertain the source of the bleed.Lower gastrointestinal bleeding sources usually present with hematochezia or frank blood. A test with poor sensitivity/specificity that may detect the source of bleeding is the tagged red blood cell scan. This is especially used for slow bleeding (<0.5 ml/min). However, for rapid bleeding (>0.5 ml/min), mesenteric angiogram ± embolization is the gold standard. Colonoscopy is often first line, however. Melena versus hematochezia Bleeds that originate from the lower gastrointestinal tract (such as the sigmoid colon and rectum) are generally associated with the passage of bright red blood, or hematochezia, particularly when brisk. Only blood that originates from a more proximal source (such as the small intestine), or bleeding from a lower source that occurs slowly enough to allow for enzymatic breakdown, is associated with melena. For this reason, melena is often associated with blood in the stomach or duodenum (upper gastrointestinal bleeding), for example by a peptic ulcer. A rough estimate is that it takes about 14 hours for blood to be broken down within the intestinal lumen; therefore if transit time is less than 14 hours the patient will have hematochezia, and if greater than 14 hours the patient will exhibit melena.: 322  One often-stated rule of thumb is that melena only occurs if the source of bleeding is above the ligament of Treitz although, as noted below, exceptions occur with enough frequency to render it unreliable. Etymology The origin of melena is dated to the early 19th century via modern Latin, via Greek melaina (feminine of melas, black). See also Blood in stool Dieulafoys lesion Hematemesis References == External links ==

Myxedema coma

Myxedema coma is an extreme or decompensated form of hypothyroidism and while uncommon, is potentially lethal. A person may have laboratory values identical to a "normal" hypothyroid state, but a stressful event (such as an infection, myocardial infarction, or stroke) precipitates the myxedema coma state, usually in the elderly. Primary symptoms of myxedema coma are altered mental status and low body temperature. Low blood sugar, low blood pressure, hyponatremia, hypercapnia, hypoxia, slowed heart rate, and hypoventilation may also occur. Myxedema, although included in the name, is not necessarily seen in myxedema coma. Coma is also not necessarily seen in myxedema coma.According to newer theories, myxedema coma could result from allostatic overload in a situation where the effects of hypothyroidism are amplified by nonthyroidal illness syndrome. Causes Myxedema coma represents an extreme or decompensated form of hypothyroidism. Most cases occur in patients who have been previously diagnosed with hypothyroidism, yet in some cases, hypothyroidism may not have been previously identified. Common precipitating factors of myxedema coma include: Hypothermia, especially during winter months Metabolic disruption including hypoglycemia, hyponatremia, acidosis, and hypercalcemia Respiratory compromise including hypoxemia and hypercapnia Infections including pneumonia, cellulitis, and urosepsis Congestive heart failure Cerebrovascular accidents Gastrointestinal bleeding Trauma, motor vehicle accidents, and fractures Medications including anesthetics, sedatives, tranquilizers, narcotics, amiodarone, and lithium Withdrawal of thyroid supplements, especially in relation to a hospitalizationOther precipitating factors include: Other medications including beta-blockers, diuretics, phenothiazines, phenytoin, rifampin, anti-TNF therapy Burns Influenza Surgery Consumption of raw bok choy Diabetic ketoacidosis after total thyroidectomy Pathophysiology The thyroid gland is responsible for regulating whole-body metabolism through the production of two major hormones: thyroxine (T4) and triiodothyronine (T3). Of the metabolically active thyroid hormones, 93% is T4 and 7% is T3. T3 is four times more potent than T4 and most T4 is converted to T3 in the tissues. Iodine is necessary for adequate hormone production. Thyroid-stimulating hormone (TSH) is a circulating or serum hormone from the pituitary gland that stimulates the thyroid gland to produce T3 and T4. Hypothyroidism occurs when the thyroid gland does not produce enough T3 and T4.The most common cause of hypothyroidism worldwide is too little dietary iodine. Hashimotos thyroiditis is the most common cause of hypothyroidism in countries with sufficient dietary iodine. With the cessation of the production of thyroid hormone, the thyroid gland contains enough reserve T3 and T4 to last 2 to 3 months.The thyroid hormones T3 and T4 influence the production by virtually all cells in the body of hundreds of new intracellular proteins and enzymes. This influence includes the expression of the calcium ATPase, regulation of ion channels, oxidative phosphorylation, increased Na-K-ATPase activity, increased carbohydrate metabolism, increased free fatty acids, increased vitamin requirements, and increased overall metabolism. The absence of the thyroid hormones T3 and T4 are responsible for many bodily functions at the genetic and cellular level and an absence of these thyroid hormones as seen in myxedema coma has very serious consequences including a broad spectrum of symptoms and a high mortality rate. Diagnosis Clinical features of myxedema coma: Cardiovascular Bradycardia Bundle branch blocks Complete heart block and arrhythmias Cardiomegaly Elevated diastolic blood pressure—early Hypotension—late Low cardiac output Non-specific ECG findings Pericardial effusion Polymorphic ventricular tachycardia (torsades de pointes) Prolonged QT interval Respiratory Hypoxia Hypercapnia Hyperventilation Myxedema of the larynx Pleural effusion Gastrointestinal Abdominal distention Abdominal pain Anasarca Anorexia and nausea Decreased motility Fecal impaction and constipation Gastrointestinal atony or ileus Myxedema or toxic megacolon—late Neurogenic oropharyngeal dysphagia ileus Neurological Altered mentation Coma Confusion and obtundation Delayed tendon reflexes Depression Poor cognitive function Psychosis Seizures Renal and urinary function Bladder dystonia and distension Fluid retention Appearance and dermatological Alopecia Coarse, sparse hair Dry, cool, doughy skin Myxedematous face Generalized swelling Goiter Macroglossia Non-pitting edema Ptosis Periorbital edema Surgical scar from prior thyroidectomy HypothermiaLaboratory features in myxedema coma: Anemia Elevated creatine kinase (CPK) Elevated creatinine Elevated transaminases Hypercapnia Hypercholesterolemia (elevated LDL) Hyperlipidemia Hypoglycemia Hyponatremia Hypoxia Leukopenia Respiratory acidosis Epidemiology Hypothyroidism is four times more common in women than men. The incidence of myxedema coma has been reported to be 0.22 per 1000000 per year but the data is limited and especially lacking in countries outside the western world and countries along the equator. Myxedema coma is most common in people 60 years old and older and is most common in the winter months when hypothermia is more common. See also Thyroid storm Euthyroid sick syndrome References == External links ==

Site

Site most often refers to: Archaeological site Campsite, a place used for overnight stay in an outdoor area Construction site Location, a point or an area on the Earths surface or elsewhere Website, a set of related web pages, typically with a common domain nameIt may also refer to: Site, a National Register of Historic Places property type SITE (originally known as Sculpture in the Environment), an American architecture and design firm Site (mathematics), a category C together with a Grothendieck topology on C The Site, a 1990s TV series that aired on MSNBC SITE Intelligence Group, a for-profit organization tracking jihadist and white supremacist organizations SITE Institute, a terrorism-tracking organization, precursor to the SITE Intelligence Group Sindh Industrial and Trading Estate, a company in Sindh, Pakistan SITE Centers, American commercial real estate company SITE Town, a densely populated town in Karachi, Pakistan S.I.T.E Industrial Area, an area in Karachi, Pakistan Satellite Instructional Television Experiment, an experimental satellite communications project launched in India in 1975 Google Sites, web based website editor See also Sites, California All pages with titles beginning with Site All pages with titles containing Site

Hyperesthesia

Hyperesthesia is a condition that involves an abnormal increase in sensitivity to stimuli of the sense. Stimuli of the senses can include sound that one hears, foods that one tastes, textures that one feels, and so forth. Increased touch sensitivity is referred to as "tactile hyperesthesia", and increased sound sensitivity is called "auditory hyperesthesia". In the context of pain hyperaesthesia can refer to an increase in sensitivity where there is both allodynia and hyperalgesia.In psychology, Jeanne Siaud-Facchin uses the term by defining it as an "exacerbation des sens": 37  that characterizes gifted individuals: for them, the sensory information reaches the brain much faster than the average, and the information is processed in a significantly shorter time. Other animals Feline hyperesthesia syndrome is an uncommon but recognized condition in cats, particularly Siamese, Burmese, Himalayan, and Abyssinian cats. It can affect cats of all ages, though it is most prevalent during maturity. Detection can be somewhat difficult as it is characterized by brief bursts of abnormal behavior, lasting around a minute or two. One of its symptoms is also found in dogs that have canine distemper disease (CD) caused by canine distemper virus (CDV). See also Auditory processing disorder Hyperacusis Multisensory integration Sensory overload Sensory processing Sensory processing disorder Sensory processing sensitivity References == External links ==

Acute myeloid leukemia

Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal cells that build up in the bone marrow and blood and interfere with normal blood cell production. Symptoms may include feeling tired, shortness of breath, easy bruising and bleeding, and increased risk of infection. Occasionally, spread may occur to the brain, skin, or gums. As an acute leukemia, AML progresses rapidly, and is typically fatal within weeks or months if left untreated.Risk factors include smoking, previous chemotherapy or radiation therapy, myelodysplastic syndrome, and exposure to the chemical benzene. The underlying mechanism involves replacement of normal bone marrow with leukemia cells, which results in a drop in red blood cells, platelets, and normal white blood cells. Diagnosis is generally based on bone marrow aspiration and specific blood tests. AML has several subtypes for which treatments and outcomes may vary.The first-line treatment of AML is usually chemotherapy, with the aim of inducing remission. People may then go on to receive additional chemotherapy, radiation therapy, or a stem cell transplant. The specific genetic mutations present within the cancer cells may guide therapy, as well as determine how long that person is likely to survive.In 2015, AML affected about one million people, and resulted in 147,000 deaths globally. It most commonly occurs in older adults. Males are affected more often than females. The five-year survival rate is about 35% in people under 60 years old and 10% in people over 60 years old. Older people whose health is too poor for intensive chemotherapy have a typical survival of five to ten months. It accounts for roughly 1.1% of all cancer cases, and 1.9% of cancer deaths in the United States. Signs and symptoms Most signs and symptoms of AML are caused by the crowding out in bone marrow of space for normal blood cells to develop. A lack of normal white blood cell production makes people more susceptible to infections. A low red blood cell count (anemia) can cause fatigue, paleness, shortness of breath and palpitations. A lack of platelets can lead to easy bruising, bleeding from the nose (epistaxis), small blood vessels on the skin (petechiae) or gums, or bleeding with minor trauma. Other symptoms may include fever, fatigue worse than what can be attributed to anaemia alone, weight loss and loss of appetite.Enlargement of the spleen may occur in AML, but it is typically mild and asymptomatic. Lymph node swelling is rare in most types of AML, except for acute myelomonocytic leukemia (AMML). The skin can be involved in the form of leukemia cutis; Sweets syndrome; or non-specific findings: flat lesions (macules), raised lesion papules), pyoderma gangrenosum and vasculitis.Some people with AML may experience swelling of the gums because of infiltration of leukemic cells into the gum tissue. Involvement of other parts of the body such as the gastrointestinal tract, respiratory tract and other parts is possible but less common. One area which has particular importance for treatment is whether there is involvement of the meninges around the central nervous system. Risk factors Most cases of AML do not have exposure to any identified risk factors. However, a number of risk factors for developing AML have been identified. These include other blood disorders, chemical exposures, ionizing radiation, and genetic risk factors. Where a defined exposure to past chemotherapy, radiotherapy, toxin or hematologic malignancy is known, this is termed secondary AML. Other blood disorders Other blood disorders, particularly myelodysplastic syndrome (MDS) and less commonly myeloproliferative neoplasms (MPN), can evolve into AML; the exact risk depends on the type of MDS/MPN. The presence of asymptomatic clonal hematopoiesis also raises the risk of transformation into AML. Chemical exposure Exposure to anticancer chemotherapy, in particular alkylating agents, can increase the risk of subsequently developing AML. Other chemotherapy agents, including fludarabine, and topoisomerase II inhibitors are also associated with the development of AML; most commonly after 4–6 years and 1–3 years respectively. These are often associated with specific chromosomal abnormalities in the leukemic cells.Other chemical exposures associated with the development of AML include benzene, chloramphenicol and phenylbutazone. Radiation High amounts of ionizing radiation exposure, such as that used for radiotherapy used to treat some forms of cancer, can increase the risk of AML. People treated with ionizing radiation after treatment for prostate cancer, non-Hodgkin lymphoma, lung cancer, and breast cancer have the highest chance of acquiring AML, but this increased risk returns to the background risk observed in the general population after 12 years. Historically, survivors of the atomic bombings of Hiroshima and Nagasaki had an increased rate of AML, as did radiologists exposed to high levels of X-rays prior to the adoption of modern radiation safety practices. Genetics Most cases of AML arise spontaneously, however there are some genetic mutations associated with an increased risk. Several congenital conditions increase the risk of leukemia; the most common is Down syndrome, with other more rare conditions including Fanconi anemia, Bloom syndrome and ataxia-telangiectasia (all characterised by problems with DNA repair), and Kostmann syndrome. Other factors Being overweight and obese increase the risk of developing AML, as does any amount of active smoking. For reasons that may relate to substance or radiation exposure, certain occupations have a higher rate of AML; particularly work in the nuclear power industry, electronics or computer manufacturing, fishing and animal slaughtering and processing. Pathophysiology The malignant cell in AML is the myeloblast. In normal development of blood cells (hematopoiesis), the myeloblast is an immature precursor of myeloid white blood cells; a normal myeloblast will mature into a white blood cell such as an eosinophil, basophil, neutrophil or monocyte. In AML, though, a single myeloblast accumulates genetic changes which stop maturation, increase its proliferation, and protect it from programmed cell death (apoptosis). Much of the diversity and heterogeneity of AML is because leukemic transformation can occur at a number of different steps along the differentiation pathway. Genetic abnormalities or the stage at which differentiation was halted form part of modern classification systems.Specific cytogenetic abnormalities can be found in many people with AML; the types of chromosomal abnormalities often have prognostic significance. The chromosomal translocations encode abnormal fusion proteins, usually transcription factors whose altered properties may cause the "differentiation arrest". For example, in APL, the t(15;17) translocation produces a PML-RARA fusion protein which binds to the retinoic acid receptor element in the promoters of several myeloid-specific genes and inhibits myeloid differentiation.The clinical signs and symptoms of AML result from the growth of leukemic clone cells, which tends to interfere with the development of normal blood cells in the bone marrow. This leads to neutropenia, anemia, and thrombocytopenia. Other symptoms can arise from the infiltration of malignant cells into parts of the body, such as the gingiva and skin.Many cells develop mutations in genes that affect epigenetics, such as DNA methylation. When these mutations occur, it is likely in the early stages of AML. Such mutations include in the DNA demethylase TET2 and the metabolic enzymes IDH1 and IDH2, which lead to the generation of a novel oncometabolite, D-2-hydroxyglutarate, which inhibits the activity of epigenetic enzymes such as TET2. Epigenetic mutations may lead to the silencing of tumor suppressor genes and/or the activation of proto-oncogenes. Diagnosis A complete blood count, which is a blood test, is one of the initial steps in the diagnosis of AML. It may reveal both an excess of white blood cells (leukocytosis) or a decrease (leukopenia), and a low red blood cell count (anemia) and low platelets (thrombocytopenia) can also be commonly seen. A blood film may show leukemic blast cells. Inclusions within the cells called Auer rods, when seen, make the diagnosis highly likely. A definitive diagnosis requires a bone marrow aspiration and biopsy.Bone marrow is examined under light microscopy, as well as flow cytometry, to diagnose the presence of leukemia, to differentiate AML from other types of leukemia (e.g. acute lymphoblastic leukemia), and to provide information about how mature or immature the affected cells are that can assist in classifying the subtype of disease. A sample of marrow or blood is typically also tested for chromosomal abnormalities by routine cytogenetics or fluorescent in situ hybridization. Genetic studies may also be performed to look for specific mutations in genes such as FLT3, nucleophosmin, and KIT, which may influence the outcome of the disease.Cytochemical stains on blood and bone marrow smears are helpful in the distinction of AML from ALL, and in subclassification of AML. The combination of a myeloperoxidase or Sudan black stain and a nonspecific esterase stain will provide the desired information in most cases. The myeloperoxidase or Sudan black reactions are most useful in establishing the identity of AML and distinguishing it from ALL. The nonspecific esterase stain is used to identify a monocytic component in AMLs and to distinguish a poorly differentiated monoblastic leukemia from ALL.The standard classification scheme for AML is the World Health Organization (WHO) system. According to the WHO criteria, the diagnosis of AML is established by demonstrating involvement of more than 20% of the blood and/or bone marrow by leukemic myeloblasts, except in three forms of acute myeloid leukemia with recurrent genetic abnormalities: t(8;21), inv(16) or t(16;16), and acute promyelocytic leukemia with PML-RARA, in which the presence of the genetic abnormality is diagnostic irrespective of blast percent. Myeloid sarcoma is also considered a subtype of AML independently of the blast count. The older French-American-British (FAB) classification, which is no longer widely used, is a bit more stringent, requiring a blast percentage of at least 30% in bone marrow or peripheral blood for the diagnosis of AML.Because acute promyelocytic leukemia has the highest curability and requires a unique form of treatment, it is important to quickly establish or exclude the diagnosis of this subtype of leukemia. Fluorescent in situ hybridization performed on blood or bone marrow is often used for this purpose, as it readily identifies the chromosomal translocation [t(15;17)(q22;q12);] that characterizes APL. There is also a need to molecularly detect the presence of PML/RARA fusion protein, which is an oncogenic product of that translocation. World Health Organization The WHO classification of AML attempts to be more clinically useful and to produce more meaningful prognostic information than the FAB criteria. Each of the WHO categories contains numerous descriptive subcategories of interest to the hematopathologist and oncologist; however, most of the clinically significant information in the WHO schema is communicated via categorization into one of the subtypes listed below. The revised fourth edition of the WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues was released in 2016. This classification, which is based on a combination of genetic and immunophenotypic markers and morphology, defines the subtypes of AML and related neoplasms as: In 2022 a new classification has been published. Acute leukemias of ambiguous lineage (also known as mixed phenotype or biphenotypic acute leukemia) occur when the leukemic cells can not be classified as either myeloid or lymphoid cells, or where both types of cells are present. French-American-British The French-American-British (FAB) classification system provides terminology that is still sometimes used, and it remains a valuable diagnostic tool in areas without access to genetic testing, this system has largely become obsolete in favor of the WHO classification, which correlates more strongly with treatment outcomes.The FAB system divides AML into eight subtypes, M0 through to M7, based on the type of cell from which the leukemia developed and its degree of maturity. AML of types M0 to M2 may be called acute myeloblastic leukemia. Classification is done by examining the appearance of the malignant cells with light microscopy and/or by using cytogenetics to characterize any underlying chromosomal abnormalities. The subtypes have varying prognoses and responses to therapy. Six FAB subtypes (M1 through to M6) were initially proposed in 1976, although later revisions added M7 in 1985 and M0 in 1987. The morphologic subtypes of AML also include rare types not included in the FAB system, such as acute basophilic leukemia, which was proposed as a ninth subtype, M8, in 1999. Treatment First-line treatment of AML consists primarily of chemotherapy, and is divided into two phases: induction and consolidation. The goal of induction therapy is to achieve a complete remission by reducing the number of leukemic cells to an undetectable level; the goal of consolidation therapy is to eliminate any residual undetectable disease and achieve a cure. Hematopoietic stem cell transplantation is usually considered if induction chemotherapy fails or after a person relapses, although transplantation is also sometimes used as front-line therapy for people with high-risk disease. Efforts to use tyrosine kinase inhibitors in AML continue. Induction The goal of the induction phase is to reach a complete remission. Complete remission does not mean the disease has been cured; rather, it signifies no disease can be detected with available diagnostic methods. All subtypes except acute promyelocytic leukemia are usually given induction chemotherapy with cytarabine and an anthracycline such as daunorubicin or idarubicin. This induction chemotherapy regimen is known as "7+3" (or "3+7"), because the cytarabine is given as a continuous IV infusion for seven consecutive days while the anthracycline is given for three consecutive days as an IV push. Response to this treatment varies with age, with people aged less than 60 years having better remission rates between 60% and 80%, while older people having lower remission rates between 33% and 60%. Because of the toxic effects of therapy and a greater chance of AML resistance to this induction therapy, different treatment, such as that in clinical trials might be offered to people 60–65 years or older.Acute promyelocytic leukemia is treated with all-trans-retinoic acid (ATRA) and either arsenic trioxide (ATO) monotherapy or an anthracycline. A syndrome similar to disseminated intravascular coagulation can develop during the initial few days of treatment or at the time the leukemia is diagnosed, and treatment can be complicated by a differentiation syndrome characterised by fever, fluid overload and low oxygen levels. Acute promyelocytic leukemia is considered curable. There is insufficient evidence to determine if prescribing ATRA in addition to chemotherapy to adults who have other subtypes of acute myeloid leukaemia is helpful. Consolidation Even after complete remission is achieved, leukemic cells likely remain in numbers too small to be detected with current diagnostic techniques. If no consolidation therapy or further postremission is given, almost all people with AML will eventually relapse.The specific type of postremission therapy is individualized based on a persons prognostic factors (see above) and general health. For good-prognosis leukemias (i.e. inv(16), t(8;21), and t(15;17)), people will typically undergo an additional three to five courses of intensive chemotherapy, known as consolidation chemotherapy. This generally involves cytarabine, with the doses administered being higher in younger patients, who are less likely to develop toxicity related to this treatment. Stem cell transplantation Stem cell transplantation from a donor, called allogenic stem cell transplantation, is usually pursued if the prognosis is not considered favourable, a person can tolerate a transplant and has a suitable donor. The basis of allogenic stem cell transplantation is on a graft versus leukemia effect whereby graft cells stimulate an immune response against leukemia cells. Unfortunately this is accompanied by immune responses against other host organs, called a graft versus host disease. Supportive treatment Support is necessary throughout treatment because of problems associated with AML and also arising from treatment. Blood transfusions, including of red blood cells and platelets, are necessary to maintain health levels, preventing complications of anemia (from low red blood cells) and bleeding (from low platelets). AML leads to an increased risk of infections, particularly drug-resistant strains of bacteria and fungi. Antibiotics and antifungals can be used both to treat and to prevent these infections, particularly quinolones.Adding aerobic physical exercises to the standard of care may result in little to no difference in the mortality, in the quality of life and in the physical functioning. These exercises may result in a slight reduction in depression. Furthermore, aerobic physical exercises probably reduce fatigue.Recent research into the role that epigenetic regulators play in hematopoietic malignancies has yielded new insights in the development of targeted epigenetic therapies as a supportive treatment for AML. The FDA has approved certain epigenetic modifying drugs like ivosidenib and enasidenib, which are used in patients that can no longer receive intensive induction chemotherapy; specifically, they are involved in the therapy of IDH1 and IDH2 mutations. Further research must be done to prove the efficacy of epigenetic treatments, but the development of new epigenetic therapies along with immunotherapies holds potential in the future treatment of AML. In pregnancy AML is rare in pregnancy, affecting about 1 in 75,000 to 100,000 pregnant women. It is diagnosed and treated similarly to AML in non pregnancy, with a recommendation that it is treated urgently. However, treatment has significant implications for the pregnancy. First trimester pregnancy is considered unlikely to be viable; pregnancy during weeks 24 – 36 requires consideration of the benefits of chemotherapy to the mother against the risks to the foetus; and there is a recommendation to consider delaying chemotherapy in very late pregnancy (> 36 weeks). Some elements of supportive care, such as which antibiotics to prevent or treat infections, also change in pregnancy. Medication Olutasidenib (Rezlidhia) was approved for medical use in the United States in December 2022. Prognosis Multiple factors influence prognosis in AML, including the presence of specific mutations, and a person with AMLs age. In the United States between 2011 and 2016, the median survival of a person with AML was 8.5 months, with the 5 year survival being 24%. This declines with age, with the poorer prognosis being associated with an age greater than 65 years, and the poorest prognosis seen in those aged 75–84.As of 2001, cure rates in clinical trials have ranged from 20 to 45%; although clinical trials often include only younger people and those able to tolerate aggressive therapies. The overall cure rate for all people with AML (including the elderly and those unable to tolerate aggressive therapy) is likely lower. Cure rates for APL can be as high as 98%. Subtypes Secondary AML has a worse prognosis, as does treatment-related AML arising after chemotherapy for another previous malignancy. Both of these entities are associated with a high rate of unfavorable genetic mutations. Cytogenetics Different genetic mutations are associated with a difference in outcomes. Certain cytogenetic abnormalities are associated with very good outcomes (for example, the (15;17) translocation in APL). About half of people with AML have "normal" cytogenetics; they fall into an intermediate risk group. A number of other cytogenetic abnormalities are known to associate with a poor prognosis and a high risk of relapse after treatment.A large number of molecular alterations are under study for their prognostic impact in AML. However, only FLT3-ITD, NPM1, CEBPA and c-KIT are currently included in validated international risk stratification schema. These are expected to increase rapidly in the near future. FLT3 internal tandem duplications (ITDs) have been shown to confer a poorer prognosis in AML with normal cytogenetics. Several FLT3 inhibitors have undergone clinical trials, with mixed results. Two other mutations – NPM1 and biallelic CEBPA are associated with improved outcomes, especially in people with normal cytogenetics and are used in current risk stratification algorithms.Researchers are investigating the clinical significance of c-KIT mutations in AML. These are prevalent, and potentially clinically relevant because of the availability of tyrosine kinase inhibitors, such as imatinib and sunitinib that can block the activity of c-KIT pharmacologically. It is expected that additional markers (e.g., RUNX1, ASXL1, and TP53) that have consistently been associated with an inferior outcome will soon be included in these recommendations. The prognostic importance of other mutated genes (e.g., DNMT3A, IDH1, IDH2) is less clear. Other prognostic factors Elevated lactate dehydrogenase level were also associated with poorer outcomes. Use of tobacco is associated with a person having a poorer prognosis, and people who are married and live together have a better prognosis. People who are treated at place with a higher volume of AML have a better prognosis than those who are treated at those in the lowest quartile. As with most forms of cancer, performance status (i.e. the general physical condition and activity level of the person) plays a major role in prognosis as well. Epidemiology AML is a relatively rare cancer. There were 19,950 new cases in the United States in 2016. In 2018, AML accounted for 1.2% of all cancer deaths in the United States.The incidence of AML increases with age and varies between countries. The median age when AML is diagnosed ranges between 63 and 71 years in the UK, Canada, Australia and Sweden, compared with 40 to 45 years in India, Brazil and Algeria.AML accounts for about 90% of all acute leukemias in adults, but is rare in children. The rate of therapy-related AML (AML caused by previous chemotherapy) is expected to rise with an increase in the use of chemotherapy, an ageing population and more patients surviving their initial chemotherapy treatment; therapy-related disease accounts for just under 10% of all cases of AML. AML is slightly more common in men, with a male-to-female ratio of 1.3:1 to 1.4:1. Incidence is also seen to differ by ethnicity, with caucasians having higher recorded incidences and the lowest recorded incidences being in Pacific Islanders and native Alaksans.In the UK, AML accounts for 31% of all leukemia cases, and around 3,100 people were diagnosed with the disease each year in 2016–2018. History The first published description of a case of leukemia in medical literature dates to 1827 when French physician Alfred-Armand-Louis-Marie Velpeau described a 63-year-old florist who developed an illness characterized by fever, weakness, urinary stones, and substantial enlargement of the liver and spleen. Velpeau noted the blood of this person had a consistency "like gruel", and speculated the appearance of the blood was due to white corpuscles. In 1845, a series of people who died with enlarged spleens and changes in the "colors and consistencies of their blood" was reported by the Edinburgh-based pathologist J.H. Bennett; he used the term "leucocythemia" to describe this pathological condition.The term "leukemia" was coined by Rudolf Virchow, the renowned German pathologist, in 1856. As a pioneer in the use of the light microscope in pathology, Virchow was the first to describe the abnormal excess of white blood cells in people with the clinical syndrome described by Velpeau and Bennett. As Virchow was uncertain of the etiology of the white blood cell excess, he used the purely descriptive term "leukemia" (Greek: "white blood") to refer to the condition.Further advances in the understanding of AML occurred rapidly with the development of new technology. In 1877, Paul Ehrlich developed a technique of staining blood films which allowed him to describe in detail normal and abnormal white blood cells. Wilhelm Ebstein introduced the term "acute leukemia" in 1889 to differentiate rapidly progressive and fatal leukemias from the more indolent chronic leukemias. The term "myeloid" was coined by Franz Ernst Christian Neumann in 1869, as he was the first to recognize white blood cells were made in the bone marrow (Greek: μυєλός, myelos, lit. (bone) marrow) as opposed to the spleen. The technique of bone marrow examination to diagnose leukemia was first described in 1879 by Mosler. Finally, in 1900, the myeloblast, which is the malignant cell in AML, was characterized by Otto Naegeli, who divided the leukemias into myeloid and lymphocytic.In 2008, AML became the first cancer genome to be fully sequenced. DNA extracted from leukemic cells were compared to unaffected skin. The leukemic cells contained acquired mutations in several genes that had not previously been associated with the disease. References External links PDQ statement on AML for health professionals at National Cancer Institute

Aneuploidy

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

Chest pain

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

Motion sickness

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

Myelitis

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

Chédiak–Higashi syndrome

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

Sleep state misperception

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

Blizzard

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

Blizzard

07) December 20–29, 2006 Colorado February 2007 North America blizzard February 12–20, 2007 January 2008 North American storm complex January, 2008 West Coast US North American blizzard of 2008 March 6–10, 2008 2009 Midwest Blizzard 6–8 December 2009, a bomb cyclogenesis event that also affected parts of Canada North American blizzard of 2009 December 16–20, 2009 2009 North American Christmas blizzard December 22–28, 2009 2010 to 2019 February 5–6, 2010 North American blizzard February 5–6, 2010 Referred to at the time as Snowmageddon was a Category 3 ("major") noreaster and severe weather event. February 9–10, 2010 North American blizzard February 9–10, 2010 February 25–27, 2010 North American blizzard February 25–27, 2010 October 2010 North American storm complex October 23–28, 2010 December 2010 North American blizzard December 26–29, 2010 January 31 – February 2, 2011 North American blizzard January 31 – February 2, 2011. Groundhog Day Blizzard of 2011 2011 Halloween noreaster October 28 – Nov 1, 2011 Hurricane Sandy October 29–31, 2012. West Virginia, western North Carolina, and southwest Pennsylvania received heavy snowfall and blizzard conditions from this hurricane November 2012 noreaster November 7–10, 2012 December 17–22, 2012 North American blizzard December 17–22, 2012 Late December 2012 North American storm complex December 25–28, 2012 February 2013 noreaster February 7–20, 2013 February 2013 Great Plains blizzard February 19 – March 6, 2013 March 2013 noreaster March 6, 2013 October 2013 North American storm complex October 3–5, 2013 Buffalo, NY blizzard of 2014. Buffalo got over 6 feet (1.8 m) of snow during November 18–20, 2014. January 2015 North American blizzard January 26–27, 2015 Late December 2015 North American storm complex December 26–27, 2015 Was one of the most notorious blizzards in the state of New Mexico and West Texas ever reported. It had sustained winds of over 30 miles per hour (48 km/h) and continuous snow precipitation that lasted over 30 hours. Dozens of vehicles were stranded in small county roads in the areas of Hobbs, Roswell, and Carlsbad New Mexico. Strong sustained winds destroyed various mobile homes. January 2016 United States blizzard January 20–23, 2016 February 2016 North American storm complex February 1–8, 2016 February 2017 North American blizzard February 6–11, 2017 March 2017 North American blizzard March 9–16, 2017 Early January 2018 nor’easter January 3–6, 2018 March 2019 North American blizzard March 8–16, 2019 April 2019 North American blizzard April 10–14, 2019 2020 to present December 5–6, 2020 noreaster December 5–6, 2020 January 31 – February 3, 2021 noreaster January 31 – February 3, 2021 February 13–17, 2021 North American winter storm February 13–17, 2021 March 2021 North American blizzard March 11–14, 2021 January 2022 North American blizzard January 27–30, 2022 Canada The Eastern Canadian Blizzard of 1971 – Dumped a foot and a half (45.7 cm) of snow on Montreal and more than two feet (61 cm) elsewhere in the region. The blizzard caused the cancellation of a Montreal Canadiens hockey game for the first time since 1918. Saskatchewan blizzard of 2007 – January 10, 2007 Canada United Kingdom Great Frost of 1709 Blizzard of January 1881 Winter of 1894–95 in the United Kingdom Winter of 1946–1947 in the United Kingdom Winter of 1962–1963 in the United Kingdom January 1987 Southeast England snowfall Winter of 1990–91 in Western Europe February 2009 Great Britain and Ireland snowfall Winter of 2009–10 in Great Britain and Ireland Winter of 2010–11 in Great Britain and Ireland Early 2012 European cold wave Other locations 1954 Romanian blizzard 1972 Iran blizzard Winter of 1990–1991 in Western Europe 2008 Afghanistan blizzard 2008 Chinese winter storms Winter storms of 2009–2010 in East Asia See also Cold wave Lake-effect snow Noreaster European windstorm Whiteout (weather) Blowing snow advisory Ground blizzard Severe weather terminology (Canada) Snowsquall Blowing snow List of blizzards References External links Digital Snow Museum Photos of historic blizzards and snowstorms. Farmers Almanac List of Worst Blizzards in the United States United States Search and Rescue Task Force: About Blizzards A Historical Review On The Origin and Definition of the Word Blizzard Archived 2012-04-25 at the Wayback Machine Dr Richard Wild

Ophthalmia nodosa

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

Myalgia

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

Hyperglycemia

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

Laryngocele

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

Long QT syndrome

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

Nausea

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

Polyarthritis

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

Persistent pupillary membrane

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

Synovial bursa

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

Trimester

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

Hypermagnesemia

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

Lymphocytosis

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

Thrombosis

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

Nasal fracture

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

Diffuse idiopathic skeletal hyperostosis

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

Premature ejaculation

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

Incidents

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

Ketonuria

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

Hereditary fructose intolerance

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

Aphasia

Aphasia is an inability to comprehend or formulate language because of damage to specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine but aphasia due to stroke is estimated to be 0.1–0.4% in the Global North. Aphasia can also be the result of brain tumors, brain infections, or neurodegenerative diseases (such as dementias).To be diagnosed with aphasia, a persons speech or language must be significantly impaired in one (or more) of the four aspects of communication following acquired brain injury. Alternatively, in the case of progressive aphasia, it must have significantly declined over a short period of time. The four aspects of communication are auditory comprehension, verbal expression, reading and writing, and functional communication. The difficulties of people with aphasia can range from occasional trouble finding words, to losing the ability to speak, read, or write; intelligence, however, is unaffected. Expressive language and receptive language can both be affected as well. Aphasia also affects visual language such as sign language. In contrast, the use of formulaic expressions in everyday communication is often preserved. For example, while a person with aphasia, particularly expressive aphasia (Brocas aphasia), may not be able to ask a loved one when their birthday is, they may still be able to sing "Happy Birthday". One prevalent deficit in the aphasias is anomia, which is a difficulty in finding the correct word.: 72 With aphasia, one or more modes of communication in the brain have been damaged and are therefore functioning incorrectly. Aphasia is not caused by damage to the brain that results in motor or sensory deficits, which produces abnormal speech; that is, aphasia is not related to the mechanics of speech but rather the individuals language cognition (although a person can have both problems, as an example, if they have a haemorrhage that damaged a large area of the brain). An individuals language is the socially shared set of rules, as well as the thought processes that go behind communication (as it affects both verbal and nonverbal language). It is not a result of a more peripheral motor or sensory difficulty, such as paralysis affecting the speech muscles or a general hearing impairment. Neurodevelopmental forms of auditory processing disorder are differentiable from aphasia in that aphasia is by definition caused by acquired brain injury, but acquired epileptic aphasia has been viewed as a form of APD. Prevalence Aphasia affects about two million people in the U.S. and 250,000 people in Great Britain. Nearly 180,000 people acquire the disorder every year in the U.S., 170,000 due to stroke. Any person of any age can develop aphasia, given that it is often caused by a traumatic injury. However, people who are middle aged and older are the most likely to acquire aphasia, as the other etiologies are more likely at older ages. For example, approximately 75% of all strokes occur in individuals over the age of 65. Strokes account for most documented cases of aphasia: 25% to 40% of people who survive a stroke develop aphasia as a result of damage to the language-processing regions of the brain. Aphasia and dysphasia Technically, dysphasia means impaired language and aphasia means lack of language. There have been calls to use the term aphasia regardless of severity. Reasons for doing so include dysphasia being easily confused with the swallowing disorder dysphagia, consumers and speech pathologists preferring the term aphasia, and many languages other than English using a word similar to aphasia. The term "aphasia" is more commonly used in North America, while "dysphasia" is more frequently used elsewhere. Signs and symptoms People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems, such as dysarthria or apraxia, and not primarily due to aphasia. Aphasia symptoms can vary based on the location of damage in the brain. Signs and symptoms may or may not be present in individuals with aphasia and may vary in severity and level of disruption to communication. Often those with aphasia may have a difficulty with naming objects, so they might use words such as thing or point at the objects. When asked to name a pencil they may say it is a “thing used to write”. Related behaviors Given the previously stated signs and symptoms, the following behaviors are often seen in people with aphasia as a result of attempted compensation for incurred speech and language deficits: Self-repairs: Further disruptions in fluent speech as a result of mis-attempts to repair erred speech production. Struggle in non-fluent aphasias: A severe increase in expelled effort to speak after a life where talking and communicating was an ability that came so easily can cause visible frustration. Preserved and automatic language: A behavior in which some language or language sequences that were used so frequently prior to onset are still produced with more ease than other language post onset. Subcortical Subcortical aphasias characteristics and symptoms depend upon the site and size of subcortical lesion. Possible sites of lesions include the thalamus, internal capsule, and basal ganglia. Causes Aphasia is most often caused by stroke, where about a quarter of patients who experience an acute stroke develop aphasia. However, any disease or damage to the parts of the brain that control language can cause aphasia. Some of these can include brain tumors, traumatic brain injury, and progressive neurological disorders. In rare cases, aphasia may also result from herpesviral encephalitis. The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia. In acute disorders, such as head injury or stroke, aphasia usually develops quickly. When caused by brain tumor, infection, or dementia, it develops more slowly.Substantial damage to tissue anywhere within the region shown in blue (on the figure in the infobox above) can potentially result in aphasia. Aphasia can also sometimes be caused by damage to subcortical structures deep within the left hemisphere, including the thalamus, the internal and external capsules, and the caudate nucleus of the basal ganglia. The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms. A very small number of people can experience aphasia after damage to the right hemisphere only. It has been suggested that these individuals may have had an unusual brain organization prior to their illness or injury, with perhaps greater overall reliance on the right hemisphere for language skills than in the general population.Primary progressive aphasia (PPA), while its name can be misleading, is actually a form of dementia that has some symptoms closely related to several forms of aphasia. It is characterized by a gradual loss in language functioning while other cognitive domains are mostly preserved, such as memory and personality. PPA usually initiates with sudden word-finding difficulties in an individual and progresses to a reduced ability to formulate grammatically correct sentences (syntax) and impaired comprehension. The etiology of PPA is not due to a stroke, traumatic brain injury (TBI), or infectious disease; it is still uncertain what initiates the onset of PPA in those affected by it.Epilepsy can also include transient aphasia as a prodromal or episodic symptom. Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain. Classification Aphasia is best thought of as a collection of different disorders, rather than a single problem. Each individual with aphasia will present with their own particular combination of language strengths and weaknesses. Consequently, it is a major challenge just to document the various difficulties that can occur in different people, let alone decide how they might best be treated. Most classifications of the aphasias tend to divide the various symptoms into broad classes. A common approach is to distinguish between the fluent aphasias (where speech remains fluent, but content may be lacking, and the person may have difficulties understanding others), and the nonfluent aphasias (where speech is very halting and effortful, and may consist of just one or two words at a time).However, no such broad-based grouping has proven fully adequate. There is wide variation among people even within the same broad grouping, and aphasias can be highly selective. For instance, people with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors.It is important to note that there are typical difficulties with speech and language that come with normal aging as well. As we age, language can become more difficult to process resulting in a slowing of verbal comprehension, reading abilities and more likely word finding difficulties. With each of these though, unlike some aphasias, functionality within daily life remains intact.: 7 Boston classification Individuals with receptive aphasia (Wernickes aphasia), also referred to as fluent aphasia, may speak in long sentences that have no meaning, add unnecessary words, and even create new "words" (neologisms). For example, someone with receptive aphasia may say, "delicious taco", meaning "The dog needs to go out so I will take him for a walk". They have poor auditory and reading comprehension, and fluent, but nonsensical, oral and written expression. Individuals with receptive aphasia usually have great difficulty understanding the speech of both themselves and others and are, therefore, often unaware of their mistakes. Receptive language deficits usually arise from lesions in the posterior portion of the left hemisphere at or near Wernickes area.: 71  It is often the result of trauma to the temporal region of the brain, specifically damage to Wernickes area. Trauma can be the result from an array of problems, however it is most commonly seen as a result of stroke Individuals with expressive aphasia (Brocas aphasia) frequently speak short, meaningful phrases that are produced with great effort. It is thus characterized as a nonfluent aphasia. Affected people often omit small words such as "is", "and", and "the". For example, a person with expressive aphasia may say, "walk dog", which could mean "I will take the dog for a walk", "you take the dog for a walk" or even "the dog walked out of the yard." Individuals with expressive aphasia are able to understand the speech of others to varying degrees. Because of this, they are often aware of their difficulties and can become easily frustrated by their speaking problems. While Brocas aphasia may appear to be solely an issue with language production, evidence suggests that it may be rooted in an inability to process syntactical information. Individuals with expressive aphasia may have a speech automatism (also called recurring or recurrent utterance). These speech automatisms can be repeated lexical speech automatisms; e.g., modalisations (I cant..., I cant...), expletives/swearwords, numbers (one two, one two) or non-lexical utterances made up of repeated, legal but meaningless, consonant-vowel syllables (e.g.., /tan tan/, /bi bi/). In severe cases, the individual may be able to utter only the same speech automatism each time they attempt speech. Individuals with anomic aphasia have difficulty with naming. People with this aphasia may have difficulties naming certain words, linked by their grammatical type (e.g., difficulty naming verbs and not nouns) or by their semantic category (e.g., difficulty naming words relating to photography but nothing else) or a more general naming difficulty. People tend to produce grammatic, yet empty, speech. Auditory comprehension tends to be preserved. Anomic aphasia is the aphasial presentation of tumors in the language zone; it is the aphasial presentation of Alzheimers disease. Anomic aphasia is the mildest form of aphasia, indicating a likely possibility for better recovery. Individuals with transcortical sensory aphasia, in principle the most general and potentially among the most complex forms of aphasia, may have similar deficits as in receptive aphasia, but their repetition ability may remain intact. Global aphasia is considered a severe impairment in many language aspects since it impacts expressive and receptive language, reading, and writing. Despite these many deficits, there is evidence that has shown individuals benefited from speech language therapy. Even though individuals with global aphasia will not become competent speakers, listeners, writers, or readers, goals can be created to improve the individuals quality of life. Individuals with global aphasia usually respond well to treatment that includes personally relevant information, which is also important to consider for therapy. Individuals with conduction aphasia have deficits in the connections between the speech-comprehension and speech-production areas. This might be caused by damage to the arcuate fasciculus, the structure that transmits information between Wernickes area and Brocas area. Similar symptoms, however, can be present after damage to the insula or to the auditory cortex. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Paraphasic errors include phonemic/literal or semantic/verbal. Repetition ability is poor. Conduction and transcortical aphasias are caused by damage to the white matter tracts. These aphasias spare the cortex of the language centers but instead create a disconnection between them. Conduction aphasia is caused by damage to the arcuate fasciculus. The arcuate fasciculus is a white matter tract that connects Brocas and Wernickes areas. People with conduction aphasia typically have good language comprehension, but poor speech repetition and mild difficulty with word retrieval and speech production. People with conduction aphasia are typically aware of their errors. Two forms of conduction aphasia have been described: reproduction conduction aphasia (repetition of a single relatively unfamiliar multisyllabic word) and repetition conduction aphasia (repetition of unconnected short familiar words. Transcortical aphasias include transcortical motor aphasia, transcortical sensory aphasia, and mixed transcortical aphasia. People with transcortical motor aphasia typically have intact comprehension and awareness of their errors, but poor word finding and speech production. People with transcortical sensory and mixed transcortical aphasia have poor comprehension and unawareness of their errors. Despite poor comprehension and more severe deficits in some transcortical aphasias, small studies have indicated that full recovery is possible for all types of transcortical aphasia. Classical-localizationist approaches Localizationist approaches aim to classify the aphasias according to their major presenting characteristics and the regions of the brain that most probably gave rise to them. Inspired by the early work of nineteenth-century neurologists Paul Broca and Carl Wernicke, these approaches identify two major subtypes of aphasia and several more minor subtypes: Expressive aphasia (also known as "motor aphasia" or "Brocas aphasia"), which is characterized by halted, fragmented, effortful speech, but well-preserved comprehension relative to expression. Damage is typically in the anterior portion of the left hemisphere, most notably Brocas area. Individuals with Brocas aphasia often have right-sided weakness or paralysis of the arm and leg, because the left frontal lobe is also important for body movement, particularly on the right side. Receptive aphasia (also known as "sensory aphasia" or "Wernickes aphasia"), which is characterized by fluent speech, but marked difficulties understanding words and sentences. Although fluent, the speech may lack in key substantive words (nouns, verbs, adjectives), and may contain incorrect words or even nonsense words. This subtype has been associated with damage to the posterior left temporal cortex, most notably Wernickes area. These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement. Conduction aphasia, where speech remains fluent, and comprehension is preserved, but the person may have disproportionate difficulty repeating words or sentences. Damage typically involves the arcuate fasciculus and the left parietal region. Transcortical motor aphasia and transcortical sensory aphasia, which are similar to Brocas and Wernickes aphasia respectively, but the ability to repeat words and sentences is disproportionately preserved.Recent classification schemes adopting this approach, such as the Boston-Neoclassical Model, also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Brocas aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernickes aphasia, conduction aphasia and transcortical sensory aphasia). These schemes also identify several further aphasia subtypes, including: anomic aphasia, which is characterized by a selective difficulty finding the names for things; and global aphasia, where both expression and comprehension of speech are severely compromised. Many localizationist approaches also recognize the existence of additional, more "pure" forms of language disorder that may affect only a single language skill. For example, in pure alexia, a person may be able to write but not read, and in pure word deafness, they may be able to produce speech and to read, but not understand speech when it is spoken to them. Cognitive neuropsychological approaches Although localizationist approaches provide a useful way of classifying the different patterns of language difficulty into broad groups, one problem is that a sizeable number of individuals do not fit neatly into one category or another. Another problem is that the categories, particularly the major ones such as Brocas and Wernickes aphasia, still remain quite broad. Consequently, even amongst those who meet the criteria for classification into a subtype, there can be enormous variability in the types of difficulties they experience.Instead of categorizing every individual into a specific subtype, cognitive neuropsychological approaches aim to identify the key language skills or "modules" that are not functioning properly in each individual. A person could potentially have difficulty with just one module, or with a number of modules. This type of approach requires a framework or theory as to what skills/modules are needed to perform different kinds of language tasks. For example, the model of Max Coltheart identifies a module that recognizes phonemes as they are spoken, which is essential for any task involving recognition of words. Similarly, there is a module that stores phonemes that the person is planning to produce in speech, and this module is critical for any task involving the production of long words or long strings of speech. Once a theoretical framework has been established, the functioning of each module can then be assessed using a specific test or set of tests. In the clinical setting, use of this model usually involves conducting a battery of assessments, each of which tests one or a number of these modules. Once a diagnosis is reached as to the skills/modules where the most significant impairment lies, therapy can proceed to treat these skills. Progressive aphasias Primary progressive aphasia (PPA) is a neurodegenerative focal dementia that can be associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimers disease, which is the gradual process of progressively losing the ability to think. Gradual loss of language function occurs in the context of relatively well-preserved memory, visual processing, and personality until the advanced stages. Symptoms usually begin with word-finding problems (naming) and progress to impaired grammar (syntax) and comprehension (sentence processing and semantics). The loss of language before the loss of memory differentiates PPA from typical dementias. People with PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence. There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA).Progressive Jargon Aphasia is a fluent or receptive aphasia in which the persons speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the person has problems with the selection of nouns. Either they will replace the desired word with another that sounds or looks like the original one or has some other connection or they will replace it with sounds. As such, people with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they cannot find with sounds. Substitutions commonly involve picking another (actual) word starting with the same sound (e.g., clocktower – colander), picking another semantically related to the first (e.g., letter – scroll), or picking one phonetically similar to the intended one (e.g., lane – late). Deaf aphasia There have been many instances showing that there is a form of aphasia among deaf individuals. Sign languages are, after all, forms of language that have been shown to use the same areas of the brain as verbal forms of language. Mirror neurons become activated when an animal is acting in a particular way or watching another individual act in the same manner. These mirror neurons are important in giving an individual the ability to mimic movements of hands. Brocas area of speech production has been shown to contain several of these mirror neurons resulting in significant similarities of brain activity between sign language and vocal speech communication. Facial communication is a significant portion of how animals interact with each other. Humans use facial movements to create, what other humans perceive, to be faces of emotions. While combining these facial movements with speech, a more full form of language is created which enables the species to interact with a much more complex and detailed form of communication. Sign language also uses these facial movements and emotions along with the primary hand movement way of communicating. These facial movement forms of communication come from the same areas of the brain. When dealing with damages to certain areas of the brain, vocal forms of communication are in jeopardy of severe forms of aphasia. Since these same areas of the brain are being used for sign language, these same, at least very similar, forms of aphasia can show in the Deaf community. Individuals can show a form of Wernickes aphasia with sign language and they show deficits in their abilities in being able to produce any form of expressions. Brocas aphasia shows up in some people, as well. These individuals find tremendous difficulty in being able to actually sign the linguistic concepts they are trying to express. Severity The severity of the type of aphasia varies depending on the size of the stroke. However, there is much variance between how often one type of severity occurs in certain types of aphasia. For instance, any type of aphasia can range from mild to profound. Regardless of the severity of aphasia, people can make improvements due to spontaneous recovery and treatment in the acute stages of recovery. Additionally, while most studies propose that the greatest outcomes occur in people with severe aphasia when treatment is provided in the acute stages of recovery, Robey (1998) also found that those with severe aphasia are capable of making strong language gains in the chronic stage of recovery as well. This finding implies that persons with aphasia have the potential to have functional outcomes regardless of how severe their aphasia may be. While there is no distinct pattern of the outcomes of aphasia based on severity alone, global aphasia typically makes functional language gains, but may be gradual since global aphasia affects many language areas. Cognitive deficits in aphasia While aphasia has traditionally been described in terms of language deficits, there is increasing evidence that many people with aphasia commonly experience co-occurring non-linguistic cognitive deficits in areas such as attention, memory, executive functions and learning. By some accounts, cognitive deficits, such as attention and working memory constitute the underlying cause of language impairment in people with aphasia. Others suggest that cognitive deficits often co-occur but are comparable to cognitive deficits in stroke patients without aphasia and reflect general brain dysfunction following injury. The degree to which deficits in attention and other cognitive domains underlie language deficits in aphasia is still unclear.In particular, people with aphasia often demonstrate short-term and working memory deficits. These deficits can occur in both the verbal domain as well as the visuospatial domain. Furthermore, these deficits are often associated with performance on language specific tasks such as naming, lexical processing, and sentence comprehension, and discourse production. Other studies have found that most, but not all people with aphasia demonstrate performance deficits on tasks of attention, and their performance on these tasks correlate with language performance and cognitive ability in other domains. Even patients with mild aphasia, who score near the ceiling on tests of language often demonstrate slower response times and interference effects in non-verbal attention abilities.In addition to deficits in short-term memory, working memory, and attention, people with aphasia can also demonstrate deficits in executive function. For instance, people with aphasia may demonstrate deficits in initiation, planning, self-monitoring, and cognitive flexibility. Other studies have found that people with aphasia demonstrate reduced speed and efficiency during completion executive function assessments.Regardless of their role in the underlying nature of aphasia, cognitive deficits have a clear role in the study and rehabilitation of aphasia. For instance, the severity of cognitive deficits in people with aphasia has been associated with lower quality of life, even more so than the severity of language deficits. Furthermore, cognitive deficits may influence the learning process of rehabilitation and language treatment outcomes in aphasia. Non-linguistic cognitive deficits have also been the target of interventions directed at improving language ability, though outcomes are not definitive. While some studies have demonstrated language improvement secondary to cognitively-focused treatment, others have found little evidence that the treatment of cognitive deficits in people with aphasia has an influence on language outcomes.One important caveat in the measurement and treatment of cognitive deficits in people with aphasia is the degree to which assessments of cognition rely on language abilities for successful performance. Most studies have attempted to circumvent this challenge by utilizing non-verbal cognitive assessments to evaluate cognitive ability in people with aphasia. However, the degree to which these tasks are truly non-verbal and not mediated by language in unclear. For instance, Wall et al. found that language and non-linguistic performance was related, except when non-linguistic performance was measured by real life cognitive tasks. Prevention of aphasia Aphasia is largely caused by unavoidable instances. However, some precautions can be taken to decrease risk for experiencing one of the two major causes of aphasia: stroke and traumatic brain injury (TBI). To decrease the probability of having an ischemic or hemorrhagic stroke, one should take the following precautions: Exercising regularly Eating a healthy diet, avoiding cholesterol in particular Keeping alcohol consumption low and avoiding tobacco use Controlling blood pressure Going to the emergency room immediately if you begin to experience unilateral extremity (especially leg) swelling, warmth, redness, and/or tenderness as these are symptoms of a deep vein thrombosis which can lead to a strokeTo prevent aphasia due to traumatic injury, one should take precautionary measures when engaging in dangerous activities such as: Wearing a helmet when operating a bicycle, motor cycle, ATV, or any other moving vehicle that could potentially be involved in an accident Wearing a seatbelt when driving or riding in a car Wearing proper protective gear when playing contact sports, especially American football, rugby, and hockey, or refraining from such activities Minimizing anticoagulant use (including aspirin) if at all possible as they increase the risk of hemorrhage after a head injuryAdditionally, one should always seek medical attention after sustaining head trauma due to a fall or accident. The sooner that one receives medical attention for a traumatic brain injury, the less likely one is to experience long-term or severe effects. Management When addressing Wernickes aphasia, according to Bakheit et al. (2007), the lack of awareness of the language impairments, a common characteristic of Wernickes aphasia, may affect the rate and extent of therapy outcomes. Robey (1998) determined that at least 2 hours of treatment per week is recommended for making significant language gains. Spontaneous recovery may cause some language gains, but without speech-language therapy, the outcomes can be half as strong as those with therapy.When addressing Brocas aphasia, better outcomes occur when the person participates in therapy, and treatment is more effective than no treatment for people in the acute period. Two or more hours of therapy per week in acute and post-acute stages produced the greatest results. High-intensity therapy was most effective, and low-intensity therapy was almost equivalent to no therapy.People with global aphasia are sometimes referred to as having irreversible aphasic syndrome, often making limited gains in auditory comprehension, and recovering no functional language modality with therapy. With this said, people with global aphasia may retain gestural communication

Aphasia

skills that may enable success when communicating with conversational partners within familiar conditions. Process-oriented treatment options are limited, and people may not become competent language users as readers, listeners, writers, or speakers no matter how extensive therapy is. However, peoples daily routines and quality of life can be enhanced with reasonable and modest goals. After the first month, there is limited to no healing to language abilities of most people. There is a grim prognosis leaving 83% who were globally aphasic after the first month they will remain globally aphasic at the first year. Some people are so severely impaired that their existing process-oriented treatment approaches offer no signs of progress, and therefore cannot justify the cost of therapy.Perhaps due to the relative rareness of conduction aphasia, few studies have specifically studied the effectiveness of therapy for people with this type of aphasia. From the studies performed, results showed that therapy can help to improve specific language outcomes. One intervention that has had positive results is auditory repetition training. Kohn et al. (1990) reported that drilled auditory repetition training related to improvements in spontaneous speech, Francis et al. (2003) reported improvements in sentence comprehension, and Kalinyak-Fliszar et al. (2011) reported improvements in auditory-visual short-term memory.Most acute cases of aphasia recover some or most skills by working with a speech-language pathologist. Recovery and improvement can continue for years after the stroke. After the onset of Aphasia, there is approximately a six-month period of spontaneous recovery; during this time, the brain is attempting to recover and repair the damaged neurons. Improvement varies widely, depending on the aphasias cause, type, and severity. Recovery also depends on the persons age, health, motivation, handedness, and educational level.There is no one treatment proven to be effective for all types of aphasias. The reason that there is no universal treatment for aphasia is because of the nature of the disorder and the various ways it is presented, as explained in the above sections. Aphasia is rarely exhibited identically, implying that treatment needs to be catered specifically to the individual. Studies have shown that, although there is no consistency on treatment methodology in literature, there is a strong indication that treatment, in general, has positive outcomes. Therapy for aphasia ranges from increasing functional communication to improving speech accuracy, depending on the persons severity, needs and support of family and friends. Group therapy allows individuals to work on their pragmatic and communication skills with other individuals with aphasia, which are skills that may not often be addressed in individual one-on-one therapy sessions. It can also help increase confidence and social skills in a comfortable setting.: 97 Evidence does not support the use of transcranial direct current stimulation (tDCS) for improving aphasia after stroke. Moderate quality evidence does indicate naming performance improvements for nouns but not verbs using tDCSSpecific treatment techniques include the following: Copy and recall therapy (CART) – repetition and recall of targeted words within therapy may strengthen orthographic representations and improve single word reading, writing, and naming Visual communication therapy (VIC) – the use of index cards with symbols to represent various components of speech Visual action therapy (VAT) – typically treats individuals with global aphasia to train the use of hand gestures for specific items Functional communication treatment (FCT) – focuses on improving activities specific to functional tasks, social interaction, and self-expression Promoting aphasics communicative effectiveness (PACE) – a means of encouraging normal interaction between people with aphasia and clinicians. In this kind of therapy, the focus is on pragmatic communication rather than treatment itself. People are asked to communicate a given message to their therapists by means of drawing, making hand gestures or even pointing to an object Melodic intonation therapy (MIT) – aims to use the intact melodic/prosodic processing skills of the right hemisphere to help cue retrieval of words and expressive language: 93  Other – i.e. drawing as a way of communicating, trained conversation partnersSemantic feature analysis (SFA) – a type of aphasia treatment that targets word-finding deficits. It is based on the theory that neural connections can be strengthened by using related words and phrases that are similar to the target word, to eventually activate the target word in the brain. SFA can be implemented in multiple forms such as verbally, written, using picture cards, etc. The SLP provides prompting questions to the individual with aphasia in order for the person to name the picture provided. Studies show that SFA is an effective intervention for improving confrontational naming.Melodic intonation therapy is used to treat non-fluent aphasia and has proved to be effective in some cases. However, there is still no evidence from randomized controlled trials confirming the efficacy of MIT in chronic aphasia. MIT is used to help people with aphasia vocalize themselves through speech song, which is then transferred as a spoken word. Good candidates for this therapy include people who have had left hemisphere strokes, non-fluent aphasias such as Brocas, good auditory comprehension, poor repetition and articulation, and good emotional stability and memory. An alternative explanation is that the efficacy of MIT depends on neural circuits involved in the processing of rhythmicity and formulaic expressions (examples taken from the MIT manual: "I am fine," "how are you?" or "thank you"); while rhythmic features associated with melodic intonation may engage primarily left-hemisphere subcortical areas of the brain, the use of formulaic expressions is known to be supported by right-hemisphere cortical and bilateral subcortical neural networks.Systematic reviews support the effectiveness and importance of partner training. According to the National Institute on Deafness and Other Communication Disorders (NIDCD), involving family with the treatment of an aphasic loved one is ideal for all involved, because while it will no doubt assist in their recovery, it will also make it easier for members of the family to learn how best to communicate with them.When a persons speech is insufficient, different kinds of augmentative and alternative communication could be considered such as alphabet boards, pictorial communication books, specialized software for computers or apps for tablets or smartphones. Intensity of treatment The intensity of aphasia therapy is determined by the length of each session, total hours of therapy per week, and total weeks of therapy provided. There is no consensus about what "intense" aphasia therapy entails, or how intense therapy should be to yield the best outcomes. A 2016 Cochrane review of speech and language therapy for people with aphasia found that treatments that are higher intensity, higher dose or over a long duration of time led to significantly better functional communication but people were more likely to drop out of high intensity treatment (up to 15 hours per week).Intensity of therapy is also dependent on the recency of stroke. People with aphasia react differently to intense treatment in the acute phase (0–3 months post stroke), sub-acute phase (3–6 months post stroke), or chronic phase (6+ months post stroke). Intensive therapy has been found to be effective for people with nonfluent and fluent chronic aphasia, but less effective for people with acute aphasia. People with sub-acute aphasia also respond well to intensive therapy of 100 hours over 62 weeks. This suggests people in the sub-acute phase can improve greatly in language and functional communication measures with intensive therapy compared to regular therapy. Individualized service delivery Intensity of treatment should be individualized based on the recency of stroke, therapy goals, and other specific characteristics such as age, size of lesion, overall health status, and motivation. Each individual reacts differently to treatment intensity and is able to tolerate treatment at different times post-stroke. Intensity of treatment after a stroke should be dependent on the persons motivation, stamina, and tolerance for therapy. Outcomes If the symptoms of aphasia last longer than two or three months after a stroke, a complete recovery is unlikely. However, it is important to note that some people continue to improve over a period of years and even decades. Improvement is a slow process that usually involves both helping the individual and family understand the nature of aphasia and learning compensatory strategies for communicating.After a traumatic brain injury (TBI) or cerebrovascular accident (CVA), the brain undergoes several healing and re-organization processes, which may result in improved language function. This is referred to as spontaneous recovery. Spontaneous recovery is the natural recovery the brain makes without treatment, and the brain begins to reorganize and change in order to recover. There are several factors that contribute to a persons chance of recovery caused by stroke, including stroke size and location. Age, sex, and education have not been found to be very predictive. There is also research pointing to damage in the left hemisphere healing more effectively than the right.Specific to aphasia, spontaneous recovery varies among affected people and may not look the same in everyone, making it difficult to predict recovery.Though some cases of Wernickes aphasia have shown greater improvements than more mild forms of aphasia, people with Wernickes aphasia may not reach as high a level of speech abilities as those with mild forms of aphasia. History The first recorded case of aphasia is from an Egyptian papyrus, the Edwin Smith Papyrus, which details speech problems in a person with a traumatic brain injury to the temporal lobe.During the second half of the 19th century, aphasia was a major focus for scientists and philosophers who were working in the beginning stages of the field of psychology. In medical research, speechlessness was described as an incorrect prognosis, and there was no assumption that underlying language complications existed. Broca and his colleagues were some of the first to write about aphasia, but Wernicke was the first credited to have written extensively about aphasia being a disorder that contained comprehension difficulties. Despite claims of who reported on aphasia first, it was F.J. Gall that gave the first full description of aphasia after studying wounds to the brain, as well as his observation of speech difficulties resulting from vascular lesions. A recent book on the entire history of aphasia is available (Reference: Tesak, J. & Code, C. (2008) Milestones in the History of Aphasia: Theories and Protagonists. Hove, East Sussex: Psychology Press). Etymology Aphasia is from Greek a- ("without", negative prefix) + phásis (φάσις, "speech"). The word aphasia comes from the word ἀφασία aphasia, in Ancient Greek, which means "speechlessness", derived from ἄφατος aphatos, "speechless" from ἀ- a-, "not, un" and φημί phemi, "I speak". Neuroimaging Methods Magnetic resonance imaging (MRI) and functional magnetic resonance imaging (fMRI) are the most common neuroimaging tools used in identifying aphasia and studying the extent of damage in the loss of language abilities. This is done by doing MRI scans and locating the extent of lesions or damage within brain tissue, particularly within areas of the left frontal and temporal regions- where a lot of language related areas lie. In fMRI studies a language related task is often completed and then the BOLD image is analyzed. If there are lower than normal BOLD responses that indicate a lessening of blood flow to the affected area and can show quantitatively that the cognitive task is not being completed. There are limitations to the use of fMRI in aphasic patients particularly. Because a high percentage of aphasic patients develop it because of stroke there can be infarcts present which is the total loss of blood flow. This can be due to the thinning of blood vessels or the complete blockage of it. This is important in fMRI as it relies on the BOLD response (the oxygen levels of the blood vessels), and this can create a false hyporesponse upon fMRI study. Due to the limitations of fMRI such as a lower spatial resolution, it can show that some areas of the brain are not active during a task when they in reality are. Additionally, with stroke being the cause of many cases of aphasia the extent of damage to brain tissue can be difficult to quantify therefore the effects of stroke brain damage on the functionality of the patient can vary. Neural Substrates of Aphasia Subtypes MRI is often used to predict or confirm the subtype of aphasia present. Researchers compared 3 subtypes of aphasia- nonfluent-variant primary progressive aphasia (nfPPA), logopenic-variant primary progressive aphasia (lvPPA), and semantic-variant primary progressive aphasia (svPPA), with primary progressive aphasia (PPA) and Alzheimer’s disease. This was done by analyzing the MRIs of patients with each of the subsets of PPA. Images which compare subtypes of aphasia as well as for finding the extent of lesions are generated by overlapping images of different participants brains (if applicable) and isolating areas of lesions or damage using third party software such as MRIcron. MRI has also been used to study the relationship between the type of aphasia developed and the age of the person with aphasia. It was found that patients with fluent aphasia are on average older than people with non-fluent aphasia. It was also found that among patients with lesions confined to the anterior portion of the brain an unexpected portion of them presented with fluent aphasia and were remarkably older than those with non-fluent aphasia. This effect was not found when the posterior portion of the brain was studied.Associated Conditions In a study on the features associated with different disease trajectories in Alzheimers disease (AD)-related primary progressive aphasia (PPA), it was found that metabolic patterns via PET SPM analysis can help predict progression of total loss of speech and functional autonomy in AD and PPA patients. This was done by comparing an MRI or CT image of the brain and presence of a radioactive biomarker with normal levels in patients without Alzheimer’s Disease. Apraxia is another disorder often correlated with aphasia. This is due to a subset of apraxia which affects speech. Specifically, this subset affects the movement of muscles associated with speech production, apraxia and aphasia are often correlated due to the proximity of neural substrates associated with each of the disorders. Researchers concluded that there were 2 areas of lesion overlap between patients with apraxia and aphasia, the anterior temporal lobe and the left inferior parietal lobe.Treatment and Neuroimaging Evidence for positive treatment outcomes can also be quantified using neuroimaging tools. The use of fMRI and an automatic classifier can help predict language recovery outcomes in stroke patients with 86% accuracy when coupled with age and language test scores. The stimuli tested were sentences both correct and incorrect and the subject had to press a button whenever the sentence was incorrect. The fMRI data collected focused on responses in regions of interest identified by healthy subjects. Recovery from aphasia can also be quantified using diffusion tensor imaging. The accurate fasciculus (AF) connects the right and left superior temporal lobe, premotor regions/posterior inferior frontal gyrus. and the primary motor cortex. In a study which enrolled patients in a speech therapy program, an increase in AF fibers and volume was found in patients after 6-weeks in the program which correlated with long-term improvement in those patients. The results of the experiment are pictured in Figure 2. This implies that DTI can be used to quantify the improvement in patients after speech and language treatment programs are applied. Conclusion Neuroimaging tools serve as a useful method for determining disorder progression, quantification of cortical damage, aphasia subtype, treatment effectiveness, and differentiating diagnosis with correlated disorders. Utilization of neuroimaging tools is necessary for the progression of knowledge of aphasia and its subtypes. Further research Research is currently being done using functional magnetic resonance imaging (fMRI) to witness the difference in how language is processed in normal brains vs aphasic brains. This will help researchers to understand exactly what the brain must go through in order to recover from Traumatic Brain Injury (TBI) and how different areas of the brain respond after such an injury.Another intriguing approach being tested is that of drug therapy. Research is in progress that will hopefully uncover whether or not certain drugs might be used in addition to speech-language therapy in order to facilitate recovery of proper language function. Its possible that the best treatment for Aphasia might involve combining drug treatment with therapy, instead of relying on one over the other.One other method being researched as a potential therapeutic combination with speech-language therapy is brain stimulation. One particular method, Transcranial Magnetic Stimulation (TMS), alters brain activity in whatever area it happens to stimulate, which has recently led scientists to wonder if this shift in brain function caused by TMS might help people re-learn languages. The research being put into Aphasia has only just begun. Researchers appear to have multiple ideas on how Aphasia could be more effectively treated in the future. See also References External links National Aphasia Association Aphasia at Curlie

Thigh

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

Rheumatism

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

Bandemia

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

Peritoneal cavity

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

Polyphagia

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

Arteriovenous fistula

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

Smear

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

Avalanche

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

Avalanche

achieving a speed in the region of 100 km/h (62 mph). It killed 12 people in their chalets under 100,000 tons of snow, 5 meters (16 feet) deep. The mayor of Chamonix was convicted of second-degree murder for not evacuating the area, but received a suspended sentence.The small Austrian village of Galtür was hit by the Galtür avalanche in 1999. The village was thought to be in a safe zone but the avalanche was exceptionally large and flowed into the village. Thirty-one people died. On 1 December 2000, the Glory Bowl Avalanche formed on Mt. Glory which is located within the Teton Mountain Range in Wyoming, United States. Joel Roof was snowboarding recreationally in this backcountry, bowl-shaped run and triggered the avalanche. He was carried nearly 2,000 feet to the base of the mountain and was not successfully rescued. Classification European avalanche risk In Europe, the avalanche risk is widely rated on the following scale, which was adopted in April 1993 to replace the earlier non-standard national schemes. Descriptions were last updated in May 2003 to enhance uniformity.In France, most avalanche deaths occur at risk levels 3 and 4. In Switzerland most occur at levels 2 and 3. It is thought that this may be due to national differences of interpretation when assessing the risks. [1] Stability: Generally described in more detail in the avalanche bulletin (regarding the altitude, aspect, type of terrain etc.)[2] additional load: heavy: two or more skiers or boarders without spacing between them, a single hiker or climber, a grooming machine, avalanche blasting light: a single skier or snowboarder smoothly linking turns and without falling, a group of skiers or snowboarders with a minimum 10 m gap between each person, a single person on snowshoesGradient: gentle slopes: with an incline below about 30° steep slopes: with an incline over 30° very steep slopes: with an incline over 35° extremely steep slopes: extreme in terms of the incline (over 40°), the terrain profile, proximity of the ridge, smoothness of underlying ground European avalanche size table Avalanche size: North American Avalanche Danger Scale In the United States and Canada, the following avalanche danger scale is used. Descriptors vary depending on country. Avalanche Problems There are nine different types of avalanche problems: Storm slab Wind slab Wet slab avalanches Persistent slab Deep persistent slab Loose dry avalanches Loose wet avalanches Glide avalanches Cornice fall Canadian classification for avalanche size The Canadian classification for avalanche size is based upon the consequences of the avalanche. Half sizes are commonly used. United States classification for avalanche size The size of avalanches are classified using two scales; size relative to destructive force or D-scale and size relative to the avalanche path or R-scale. Both size scales range from 1 to 5 with the D size scale half sizes can be used. Rutschblock Test Slab avalanche hazard analysis can be done using the Rutschblock Test. A 2 m wide block of snow is isolated from the rest of the slope and progressively loaded. The result is a rating of slope stability on a seven step scale. (Rutsch means slide in German). Avalanches and climate change Avalanche formation and frequency is highly affected by weather patterns and the local climate. Snowpack layers will form differently depending on whether snow is falling in very cold or very warm conditions, and very dry or very humid conditions. Thus, climate change may affect when, where, and how often avalanches occur, and may also change the type of avalanches that are occurring. Impacts on avalanche type and frequency Overall, a rising seasonal snow line and a decrease in the number of days with snow cover are predicted. Climate change-caused temperature increases and changes in precipitation patterns will likely differ between the different mountain regions, and the impacts of these changes on avalanches will change at different elevations. In the long term, avalanche frequency at lower elevations is expected to decline corresponding to a decrease in snow cover and depth, and a short-term increase in the number of wet avalanches are predicted.Precipitation is expected to increase, meaning more snow or rain depending on the elevation. Higher elevations predicted to remain above the seasonal snow line will likely see an increase in avalanche activity due to the increases in precipitation during the winter season. Storm precipitation intensity is also expected to increase, which is likely to lead to more days with enough snowfall to cause the snowpack to become unstable. Moderate and high elevations may see an increase in volatile swings from one weather extreme to the other. Predictions also show an increase in the number of rain on snow events, and wet avalanche cycles occurring earlier in the spring during the remainder of this century. Impacts on burial survival rate The warm, wet snowpacks that are likely to increase in frequency due to climate change may also make avalanche burials more deadly. Warm snow has a higher moisture content and is therefore denser than colder snow. Denser avalanche debris decreases the ability for a buried person to breath and the amount of time they have before they run out of oxygen. This increases the likelihood of death by asphyxia in the event of a burial. Additionally, the predicted thinner snowpacks may increase the frequency of injuries due to trauma, such as a buried skier striking a rock or tree. Avalanches on the planet Mars See also Related flows Avalanche disasters 1999 Galtür avalanche Montroc 2012 Gayari Sector avalanche References Bibliography McClung, David. Snow Avalanches as a Non-critical, Punctuated Equilibrium System: Chapter 24 in Nonlinear Dynamics in Geosciences, A.A. Tsonsis and J.B. Elsner (Eds.), Springer, 2007 Daffern, Tony: Avalanche Safety for Skiers, Climbers and Snowboarders, Rocky Mountain Books, 1999, ISBN 0-921102-72-0 Billman, John: Mike Elggren on Surviving an Avalanche. Skiing magazine February 2007: 26. McClung, David and Shaerer, Peter: The Avalanche Handbook, The Mountaineers: 2006. 978-0-89886-809-8 Tremper, Bruce: Staying Alive in Avalanche Terrain, The Mountaineers: 2001. ISBN 0-89886-834-3 Munter, Werner: Drei mal drei (3x3) Lawinen. Risikomanagement im Wintersport, Bergverlag Rother, 2002. ISBN 3-7633-2060-1 (in German) (partial English translation included in PowderGuide: Managing Avalanche Risk ISBN 0-9724827-3-3) Michael Falser: Historische Lawinenschutzlandschaften: eine Aufgabe für die Kulturlandschafts- und Denkmalpflege In: kunsttexte 3/2010, unter: Historische Lawinenschutzlandschaften: eine Aufgabe für die Kulturlandschafts- und Denkmalpflege Notes External links Media related to Avalanche chute at Wikimedia Commons The Avalanche Education Project Surviving an Avalanche – A guide for children and youth Avalanche Defense Photographs Avalanche Canada Canadian Avalanche Association Archived 21 October 2020 at the Wayback Machine Colorado Avalanche Information Center Center for Snow and Avalanche Studies EAWS – European Avalanche Warning Services Directory of European avalanche services Avalanches collected news and commentary at The New York Times Swiss Federal Institute for Snow and Avalanche Research Scottish Avalanche Information Service Chisholm, Hugh, ed. (1911). "Avalanche". Encyclopædia Britannica (11th ed.). Cambridge University Press. But note the myths cited above Utah Avalanche Center New Zealand Avalanche Advisory Gulmarg Avalanche Center US Avalanche.org Sierra Avalanche Center (Tahoe National Forest)

Sacroiliitis

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

Cerebral atherosclerosis

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

Pressure

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

Pressure

by Bernoullis equation, where velocity head is zero and comparisons per unit volume in the vessel are p γ + z = c o n s t . {\displaystyle {\frac {p}{\gamma }}+z=\mathrm {const}.} Terms have the same meaning as in section Fluid pressure. Direction of liquid pressure An experimentally determined fact about liquid pressure is that it is exerted equally in all directions. If someone is submerged in water, no matter which way that person tilts their head, the person will feel the same amount of water pressure on their ears. Because a liquid can flow, this pressure isnt only downward. Pressure is seen acting sideways when water spurts sideways from a leak in the side of an upright can. Pressure also acts upward, as demonstrated when someone tries to push a beach ball beneath the surface of the water. The bottom of a boat is pushed upward by water pressure (buoyancy). When a liquid presses against a surface, there is a net force that is perpendicular to the surface. Although pressure doesnt have a specific direction, force does. A submerged triangular block has water forced against each point from many directions, but components of the force that are not perpendicular to the surface cancel each other out, leaving only a net perpendicular point. This is why water spurting from a hole in a bucket initially exits the bucket in a direction at right angles to the surface of the bucket in which the hole is located. Then it curves downward due to gravity. If there are three holes in a bucket (top, bottom, and middle), then the force vectors perpendicular to the inner container surface will increase with increasing depth – that is, a greater pressure at the bottom makes it so that the bottom hole will shoot water out the farthest. The force exerted by a fluid on a smooth surface is always at right angles to the surface. The speed of liquid out of the hole is 2 g h {\displaystyle \scriptstyle {\sqrt {2gh}}} , where h is the depth below the free surface. This is the same speed the water (or anything else) would have if freely falling the same vertical distance h. Kinematic pressure P = p / ρ 0 {\displaystyle P=p/\rho _{0}} is the kinematic pressure, where p {\displaystyle p} is the pressure and ρ 0 {\displaystyle \rho _{0}} constant mass density. The SI unit of P is m2/s2. Kinematic pressure is used in the same manner as kinematic viscosity ν {\displaystyle \nu } in order to compute the Navier–Stokes equation without explicitly showing the density ρ 0 {\displaystyle \rho _{0}} . Navier–Stokes equation with kinematic quantities ∂ u ∂ t + ( u ∇ ) u = − ∇ P + ν ∇ 2 u . {\displaystyle {\frac {\partial u}{\partial t}}+(u\nabla )u=-\nabla P+\nu \nabla ^{2}u.} See also Notes References External links Introduction to Fluid Statics and Dynamics on Project PHYSNET Pressure being a scalar quantity wikiUnits.org - Convert units of pressure

Hypertensive crisis

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

Aphagia

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

Sealpox

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

Tachypnea

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

Bloating

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