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Would you describe Compartment syndrome, to me Aarogya

Compartment syndrome

Compartment syndrome is a condition in which increased pressure within one of the bodys anatomical compartments results in insufficient blood supply to tissue within that space. There are two main types: acute and chronic. Compartments of the leg or arm are most commonly involved.Symptoms of acute compartment syndrome (ACS) can include severe pain, poor pulses, decreased ability to move, numbness, or a pale color of the affected limb. It is most commonly due to physical trauma such as a bone fracture (up to 75% of cases) or crush injury, but it can also be caused by acute exertion during sport. It can also occur after blood flow returns following a period of poor blood flow. Diagnosis is generally based upon a persons symptoms and may be supported by measurement of intracompartmental pressure before, during, and after activity. Normal compartment pressure should be within 12-18 mmHg; anything greater than that is considered abnormal and would need treatment. Treatment is by surgery to open the compartment, completed in a timely manner. If not treated within six hours, permanent muscle or nerve damage can result.In chronic compartment syndrome (aka chronic exertional compartment syndrome), there is generally pain with exercise but the pain dissipates once activity ceases. Other symptoms may include numbness. Symptoms typically resolve with rest. Common activities that trigger chronic compartment syndrome include running and biking. Generally, this condition does not result in permanent damage. Other conditions that may present similarly include stress fractures and tendinitis. Treatment may include physical therapy or—if that is not effective—surgery.Acute compartment syndrome occurs in about 3% of those who have a midshaft fracture of the forearm. Rates in other areas of the body and for chronic cases are unknown. The condition occurs more often in males and people under the age of 35, in line with the occurrence of trauma. Compartment syndrome was first described in 1881 by German surgeon Richard von Volkmann. Untreated, acute compartment syndrome can result in Volkmanns contracture. Signs and symptoms Compartment syndrome usually presents within a few hours of an inciting event, but may present anytime up to 48 hours after. The limb affected by compartment syndrome is often associated with a firm, wooden feeling or a deep palpation, and is usually described as feeling tight. There may also be decrease pulses in the limb along with associated paresthesia. Usually, the pain cannot be relieved by NSAIDs. Range of motion may be limited while the compartment pressure is high. In acute compartment syndrome, the pain will not be relieved with rest. In chronic exertional compartment syndrome the pain will dissipate with rest. Acute There are five characteristic signs and symptoms related to acute compartment syndrome: pain, paraesthesia (reduced sensation), paralysis, pallor, and pulselessness. Pain and paresthesia are the early symptoms of compartment syndrome. CommonPain – A person may experience pain disproportionate to the findings of the physical examination. This pain may not be relieved by strong analgesic medications. The pain is aggravated by passively stretching the muscle group within the compartment. However, such pain may disappear in the late stages of the compartment syndrome. The role of local anesthesia in delaying the diagnosis of compartment syndrome is still being debated. Paresthesia (altered sensation) – A person may complain of "pins & needles", numbness, and a tingling sensation. This may progress to loss of sensation (anesthesia) if no intervention is made.UncommonParalysis – Paralysis of the limb is a rare, late finding. It may indicate both a nerve or muscular lesion. Pallor and pulselessness – A lack of pulse rarely occurs in patients, as pressures that cause compartment syndrome are often well below arterial pressures. Absent pulses only occur when there is arterial injury or during the late stages of the compartment syndrome, when compartment pressures are very high. Pallor can also result from arterial occlusion. Chronic The symptoms of chronic exertional compartment syndrome, CECS, may involve pain, tightness, cramps, weakness, and diminished sensation. This pain can occur for months, and in some cases over a period of years, and may be relieved by rest. Moderate weakness in the affected region can also be observed. These symptoms are brought on by exercise and consist of a sensation of extreme tightness in the affected muscles followed by a painful burning sensation if exercise is continued. After exercise is ceased, the pressure in the compartment will decrease within a few minutes, relieving painful symptoms. Symptoms will occur at a certain threshold of exercise which varies from person to person but is rather consistent for a given individual. This threshold can range anywhere from 30 seconds of running to 2–3 miles of running. CECS most commonly occurs in the lower leg, with the anterior compartment being the most frequently affected compartment. Foot drop is a common symptom of CECS. Complications Failure to relieve the pressure can result in the death of tissues (necrosis) in the affected anatomical compartment, since the ability of blood to enter the smallest vessels in the compartment (capillary perfusion pressure) will fall. This, in turn, leads to progressively increasing oxygen deprivation of the tissues dependent on this blood supply. Without sufficient oxygen, the tissue will die. On a large scale, this can cause Volkmanns contracture in affected limbs, a permanent and irreversible process. Other reported complications include neurological deficits of the affected limb, gangrene, and chronic regional pain syndrome. Rhabdomyolysis and subsequent kidney failure are also possible complications. In some case series, rhabdomyolysis is reported in 23% of patients with ACS. Causes Acute Acute compartment syndrome (ACS) is a medical emergency that can develop after traumatic injuries, such as in automobile accidents or dynamic sporting activities – for example, a severe crush injury or an open or closed fracture of an extremity. Rarely, ACS can develop after a relatively minor injury, or due to another medical issue. The lower legs and the forearms are the most frequent sites affected by compartment syndrome. Other areas of the body such as thigh, buttock, hand, abdomen, and foot can also be affected. The most common cause of acute compartment syndrome is fracture of a bone, most commonly the tibia. There is no difference between acute compartment syndrome originating from an open or closed fracture. Leg compartment syndrome is found in 2% to 9% of tibial fractures. It is strongly related to fractures involving the tibial diaphysis as well as other sections of the tibia. Direct injury to blood vessels can lead to compartment syndrome by reducing the downstream blood supply to soft tissues. This reduction in blood supply can cause a series of inflammatory reactions that promote the swelling of the soft tissues. Such inflammation can be further worsened by reperfusion therapy. Because the fascia layer that defines the compartment of the limbs does not stretch, a small amount of bleeding into the compartment, or swelling of the muscles within the compartment, can cause the pressure to rise greatly. Intravenous drug injection, casts, prolonged limb compression, crush injuries, anabolic steroid use, vigorous exercise, and eschar from burns can also cause compartment syndrome. Patients on anticoagulant therapy have an increased risk of bleeding into a closed compartment.Abdominal compartment syndrome occurs when the intra-abdominal pressure exceeds 20 mmHg and abdominal perfusion pressure is less than 60 mmHg. This disease process is associated with organ dysfunction and multiple organ failures. There are many causes, which can be broadly grouped into three mechanisms: primary (internal bleeding and swelling); secondary (vigorous fluid replacement as an unintended complication of resuscitative medical treatment, leading to the acute formation of ascites and a rise in intra-abdominal pressure); and recurrent (compartment syndrome that has returned after the initial treatment of secondary compartment syndrome).Compartment syndrome after snake bite is rare. Its incidence varies from 0.2 to 1.36% as recorded in case reports. Compartment syndrome is more common in children possibly due to inadequate volume of the bodily fluid to dilute the snake venom. Increased white blood cell count of more than 1,650/μL and aspartate transaminase (AST) level of more than 33.5 U/L could increase the risk of developing compartment syndrome. Otherwise, those bitten by venomous snake should be observed for 48 hours to exclude the possibility of compartment syndrome.Acute compartment syndrome due to severe/uncontrolled hypothyroidism is rare. Chronic When compartment syndrome is caused by repetitive use of the muscles, it is known as chronic compartment syndrome (CCS). This is usually not an emergency, but the loss of circulation can cause temporary or permanent damage to nearby nerves and muscles. A subset of chronic compartment syndrome is chronic exertional compartment syndrome (CECS), often called exercise-induced compartment syndrome (EICS). Oftentimes, CECS is a diagnosis of exclusion. CECS of the leg is a condition caused by exercise which results in increased tissue pressure within an anatomical compartment due to an acute increase in muscle volume – as much as 20% is possible during exercise. When this happens, pressure builds up in the tissues and muscles causing tissue ischemia. An increase in muscle weight will reduce the compartment volume of the surrounding fascial borders and result in an increased compartment pressure. An increase in the pressure of the tissue can force fluid to leak into the interstitial space (extracellular fluid), leading to a disruption of the micro-circulation of the leg. This condition occurs commonly in the lower leg and various other locations within the body, such as the foot or forearm. CECS can be seen in athletes who train rigorously in activities that involve constant repetitive actions or motions. Pathophysiology In a normal human body, blood flow from the arterial system (higher pressure) to venous system (lower pressure) requires a pressure gradient. When this pressure gradient is diminished, blood flow from the artery to the vein is reduced. This causes a backup of blood and excessive fluid to leak from the capillary wall into spaces between the soft tissues cells, causing swelling of the extracellular space and a rise in intracompartmental pressure. This swelling of the soft tissues surrounding the blood vessels compresses the blood and lymphatic vessels further, causing more fluid to enter the extracellular spaces, leading to additional compression. The pressure continues to increase due to the non-compliant nature of the fascia containing the compartment. This worsening cycle can eventually lead to a lack of sufficient oxygen in the soft tissues (tissue ischemia) and tissue death (necrosis). Tingling and abnormal sensation (paraesthesia) can begin as early as 30 minutes from the start of tissue ischemia and permanent damage can occur as early as 12 hours from the onset of the inciting injury. Diagnosis Compartment syndrome is a clinical diagnosis, meaning that a medical providers examination and the patients history usually give the diagnosis. Apart from the typical signs and symptoms, measurement of intracompartmental pressure can also be important for diagnosis. Using a combination of clinical diagnosis and serial intracompartmental pressure measurements increases both the sensitivity and specificity of diagnosing compartment syndrome. A transducer connected to a catheter is inserted 5 cm into the zone of injury. A compartment pressure no less than 30 mmHg of the diastolic pressure in a conscious or unconscious person is associated with compartment syndrome. Fasciotomy is indicated in that case. For those patients with low blood pressure (hypotension), a pressure of 20 mmHg higher than the intracompartmental pressure is associated with compartmental syndrome. Noninvasive methods of diagnosis such as near-infraredspectroscopy (NIRS) which uses sensors on the skin, shows promise in controlled settings. However, with limited data in uncontrolled settings, clinical presentation and intracompartmental pressure remain the gold standard for diagnosis.Chronic exertional compartment syndrome is usually a diagnosis of exclusion, with the hallmark finding being absence of symptoms at rest. Measurement of intracompartmental pressures during symptom reproduction (usually immediately following running) is the most useful test. Imaging studies (X-ray, CT, MRI) can be useful in ruling out other more common diagnoses instead of confirming the diagnosis of compartment syndrome. Additionally, MRI has been shown to be effective in diagnosing chronic exertional compartment syndrome. The average duration of symptoms prior to diagnosis is 28 months. Treatment Acute Any external compression (tourniquet, orthopedic casts or dressings applied on the affected limb) should be removed. Cutting of the cast will reduce the intracompartmental pressure by 65%, followed by 10 to 20% pressure reduction once padding is cut. After removal of the external compression the limb should be placed at the level of the heart. The vital signs of the patient should be closely monitored. If the clinical condition does not improve, then fasciotomy is indicated to decompress the compartments. An incision large enough to decompress all the compartments is necessary. This surgical procedure is performed inside an operating theater under general or local anesthesia. The timing of the fasciotomy wound closure is debated. Some surgeons suggest wound closure should be done seven days after fasciotomy. Multiple techniques exist for closure of the surgical site including vacuum-assisted and shoelace. Both techniques are acceptable methods for closure, but the vacuum-assisted technique has led to longer hospitalization time. A skin graft may be required to close the wound, which would complicate the treatment with a much longer hospitalization stay. Chronic Treatment for chronic exertional compartment syndrome can include decreasing or subsiding exercise and/or exacerbating activities, massage, non-steroidal anti-inflammatory medication, and physiotherapy. Chronic compartment syndrome in the lower leg can be treated conservatively or surgically. Conservative treatment includes rest, anti-inflammatory medications, and manual decompression. Warming the affected area with a heating pad may help to loosen the fascia prior to exercise. Icing the area may result in further constriction of the fascia and is not recommended before exercise. The use of devices that apply external pressure to the area, such as splints, casts, and tight wound dressings, should be avoided. If symptoms persist after conservative treatment or if an individual does not wish to give up the physical activities which bring on symptoms, compartment syndrome can be treated by a surgery known as a fasciotomy. A US military study conducted in 2012 found that teaching individuals with lower leg chronic exertional compartment syndrome to change their running style to a forefoot running technique abated symptoms in those with symptoms limited to the anterior compartment. Running with a forefoot strike limits use of the tibialis anterior muscle which may explain the relief in symptoms in those with anterior compartment syndrome. Hyperbaric oxygen therapy has been suggested by case reports – though as of 2011 not proven in randomized control trials – to be an effective adjunctive therapy for crush injury, compartment syndrome, and other acute traumatic ischemias, by improving wound healing and reducing the need for repetitive surgery. Prognosis A mortality rate of 47% has been reported for acute compartment syndrome of the thigh. According to one study the rate of fasciotomy for acute compartment syndrome varied from 2% to 24%. This is due to uncertainty and differences in labeling a condition as acute compartment syndrome. The most significant prognostic factor in people with acute compartment syndrome is time to diagnosis and subsequent fasciotomy. In people with a missed or late diagnosis of acute compartment syndrome, limb amputation may be necessary for survival. Following a fasciotomy, some symptoms may be permanent depending on factors such as which compartment, time until fasciotomy, and muscle necrosis. Muscle necrosis can occur quickly, within 3 hours of original injury in some studies. Fasciotomy of the lateral compartment of the leg may lead to symptoms due to the nerves and muscles in that compartment. These may include foot drop, numbness along leg, numbness of big toe, pain, and loss of foot eversion. Epidemiology In one case series of 164 people with acute compartment syndrome, 69% of the cases had an associated fracture. The authors of that article also calculated an annual incidence of acute compartment syndrome of 1 to 7.3 per 100,000. There are significant differences in the incidence of acute compartment syndrome based on age and gender in the setting of trauma. Men are ten times more likely than women to develop ACS. The mean age for ACS in men is 30 years while the mean age is 44 years for women. Acute compartment syndrome may occur more often in individuals less than 35 years old due to increased muscle mass within the compartments . The anterior compartment of the leg is the most common site for ACS. See also Abdominal compartment syndrome Escharotomy Ischemia-reperfusion injury of the appendicular musculoskeletal system References External links Compartment Syndrome of the Forearm – Orthopaedia.com Chronic Exertional Compartment Syndrome detailed at MayoClinic.com Compartment syndrome at the Duke University Health Systems Orthopedics program 05-062a. at Merck Manual of Diagnosis and Therapy Home Edition Compartment syndrome American Association of Orthopaedic Surgeons Compartment Syndrome

Do you know what is Secondary hyperparathyroidism, Aarogya

Secondary hyperparathyroidism

Secondary hyperparathyroidism is the medical condition of excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels), with resultant hyperplasia of these glands. This disorder is primarily seen in patients with chronic kidney failure. It is sometimes abbreviated "SHPT" in medical literature. Signs and symptoms Bone and joint pain are common, as are limb deformities. The elevated PTH has also pleiotropic effects on the blood, immune system, and neurological system. Cause Chronic kidney failure is the most common cause of secondary hyperparathyroidism. Failing kidneys do not convert enough vitamin D to its active form, and they do not adequately excrete phosphate. When this happens, insoluble calcium phosphate forms in the body and removes calcium from the circulation. Both processes lead to hypocalcemia and hence secondary hyperparathyroidism. Secondary hyperparathyroidism can also result from malabsorption (chronic pancreatitis, small bowel disease, malabsorption-dependent bariatric surgery) in that the fat-soluble vitamin D can not get reabsorbed. This leads to hypocalcemia and a subsequent increase in parathyroid hormone secretion in an attempt to increase the serum calcium levels. A few other causes can stem from inadequate dietary intake of calcium, a vitamin D deficiency, or steatorrhea. Diagnosis The PTH is elevated due to decreased levels of calcium or 1,25-dihydroxy-vitamin D3. It is usually seen in cases of chronic kidney disease or defective calcium receptors on the surface of parathyroid glands. Treatment If the underlying cause of the hypocalcemia can be addressed, the hyperparathyroidism will resolve. In people with chronic kidney failure, treatment consists of dietary restriction of phosphorus; supplements containing an active form of vitamin D, such as calcitriol, doxercalciferol, paricalcitol; and phosphate binders, which are either calcium-based and non-calcium based.Extended Release Calcifediol was recently approved by the FDA as a treatment for secondary hyperparathyroidism (SHPT) in adults with stage 3 or 4 chronic kidney disease (CKD) and low vitamin D blood levels (25-hydroxyvitamin D less than 30 ng/mL). It can help treat SHPT by increasing Vitamin D levels and lowering parathyroid hormone or PTH. It is not indicated for people with stage 5 CKD or on dialysis.In the treatment of secondary hyperparathyroidism due to chronic kidney disease on dialysis calcimimetics do not appear to affect the risk of early death. It does decrease the need for a parathyroidectomy but caused more issues with low blood calcium levels and vomiting.Most people with hyperparathyroidism secondary to chronic kidney disease will improve after renal transplantation, but many will continue to have a degree of residual hyperparathyroidism (tertiary hyperparathyroidism) post-transplant with associated risk of bone loss, etc. Prognosis If left untreated, the disease will progress to tertiary hyperparathyroidism, where correction of the underlying cause will not stop excess PTH secretion, i.e. parathyroid gland hypertrophy becomes irreversible. In contrast with secondary hyperparathyroidism, tertiary hyperparathyroidism is associated with hypercalcemia rather than hypocalcemia. See also Primary hyperparathyroidism Tertiary hyperparathyroidism References == External links ==

What does Filariasis mean Aarogya

Filariasis

Filariasis is a parasitic disease caused by an infection with roundworms of the Filarioidea type. These are spread by blood-feeding insects such as black flies and mosquitoes. They belong to the group of diseases called helminthiases. These parasites exist in the wild in subtropical parts of southern Asia, Africa, the South Pacific, and parts of South America. One does not acquire them in temperate areas like Europe or the United States.Eight known filarial worms have humans as a definitive host. These are divided into three groups according to the part of the body they affect: Lymphatic filariasis is caused by the worms Wuchereria bancrofti, Brugia malayi, and Brugia timori. These worms occupy the lymphatic system, including the lymph nodes; in chronic cases, these worms lead to the syndrome of elephantiasis. Subcutaneous filariasis is caused by Loa loa (the eye worm), Mansonella streptocerca, and Onchocerca volvulus. These worms occupy the layer just under the skin. L. loa causes Loa loa filariasis, while O. volvulus causes river blindness. Serous cavity filariasis is caused by the worms Mansonella perstans and Mansonella ozzardi, which occupy the serous cavity of the abdomen. Dirofilaria immitis, the dog heartworm, rarely infects humans.The adult worms, which usually stay in one tissue, release early larval forms known as microfilariae into the persons blood. These circulating microfilariae can be taken up during a blood meal by an insect vector; in the vector, they develop into infective larvae that can be spread to another person. Individuals infected by filarial worms may be described as either "microfilaraemic" or "amicrofilaraemic", depending on whether microfilariae can be found in their peripheral blood. Filariasis is diagnosed in microfilaraemic cases primarily through direct observation of microfilariae in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic cases based on clinical observations and, in some cases, by finding a circulating antigen in the blood. Signs and symptoms The most spectacular symptom of lymphatic filariasis is elephantiasis – edema with thickening of the skin and underlying tissues—which was the first disease discovered to be transmitted by mosquito bites. Elephantiasis results when the parasites lodge in the lymphatic system.Elephantiasis affects mainly the lower extremities, while the ears, mucous membranes, and amputation stumps are affected less frequently. However, different species of filarial worms tend to affect different parts of the body; Wuchereria bancrofti can affect the legs, arms, vulva, breasts, and scrotum (causing hydrocele formation), while Brugia timori rarely affects the genitals. Those who develop the chronic stages of elephantiasis are usually free from microfilariae (amicrofilaraemic), and often have adverse immunological reactions to the microfilariae, as well as the adult worms.The subcutaneous worms present with rashes, urticarial papules, and arthritis, as well as hyper- and hypopigmentation macules. Onchocerca volvulus manifests itself in the eyes, causing "river blindness" (onchocerciasis), one of the leading causes of blindness in the world. Serous cavity filariasis presents with symptoms similar to subcutaneous filariasis, in addition to abdominal pain, because these worms are also deep-tissue dwellers. Cause Human filarial nematode worms have complicated life cycles, which primarily consists of five stages. After the male and female worms mate, the female gives birth to live microfilariae by the thousands. The microfilariae are taken up by the vector insect (intermediate host) during a blood meal. In the intermediate host, the microfilariae molt and develop into third-stage (infective) larvae. Upon taking another blood meal, the vector insect, such as Culex pipiens, injects the infectious larvae into the dermis layer of the skin. After about one year, the larvae molt through two more stages, maturing into the adult worms. Diagnosis Filariasis is usually diagnosed by identifying microfilariae on Giemsa stained, thin and thick blood film smears, using the "gold standard" known as the finger prick test. The finger prick test draws blood from the capillaries of the finger tip; larger veins can be used for blood extraction, but strict windows of the time of day must be observed. Blood must be drawn at appropriate times, which reflect the feeding activities of the vector insects. Examples are W. bancrofti, whose vector is a mosquito; night is the preferred time for blood collection. Loa loas vector is the deer fly; daytime collection is preferred. This method of diagnosis is only relevant to microfilariae that use the blood as transport from the lungs to the skin. Some filarial worms, such as M. streptocerca and O. volvulus, produce microfilariae that do not use the blood; they reside in the skin only. For these worms, diagnosis relies upon skin snips and can be carried out at any time. Concentration methods Various concentration methods are applied: membrane filter, Knotts concentration method, and sedimentation technique.Polymerase chain reaction (PCR) and antigenic assays, which detect circulating filarial antigens, are also available for making the diagnosis. The latter are particularly useful in amicrofilaraemic cases. Spot tests for antigen are far more sensitive, and allow the test to be done anytime, rather in the late hours. Lymph node aspirate and chylous fluid may also yield microfilariae. Medical imaging, such as CT or MRI, may reveal "filarial dance sign" in the chylous fluid; X-ray tests can show calcified adult worms in lymphatics. The DEC provocation test is performed to obtain satisfying numbers of parasites in daytime samples. Xenodiagnosis is now obsolete, and eosinophilia is a nonspecific primary sign. Treatment The recommended treatment for people outside the United States is albendazole combined with ivermectin. A combination of diethylcarbamazine and albendazole is also effective. Side effects of the drugs include nausea, vomiting, and headaches. All of these treatments are microfilaricides; they have no effect on the adult worms. While the drugs are critical for treatment of the individual, proper hygiene is also required. There is good evidence that albendazole alone; or addition of albendazole to diethylcarbamazine or ivermectin, makes minimal difference in clearing microfilaria or adult worms from blood circulation. Diethylcarbamazine-medicated salt is effective in controlling lymphatic filariasis while maintaining its coverage at 90% in the community for six months.Different trials were made to use the known drug at its maximum capacity in absence of new drugs. In a study from India, it was shown that a formulation of albendazole had better anti-filarial efficacy than albendazole itself.In 2003, the common antibiotic doxycycline was suggested for treating elephantiasis. Filarial parasites have symbiotic bacteria in the genus Wolbachia, which live inside the worm and seem to play a major role in both its reproduction and the development of the disease. This drug has shown signs of inhibiting the reproduction of the bacteria, further inducing sterility. Clinical trials in June 2005 by the Liverpool School of Tropical Medicine reported an eight-week course almost eliminated microfilaraemia. Society and culture Research teams In 2015 William C. Campbell and Satoshi Ōmura were co-awarded half of that years Nobel prize in Physiology or Medicine for the discovery of the drug avermectin, which, in the further developed form ivermectin, has decreased the occurrence of lymphatic filariasis. Prospects for elimination Filarial diseases in humans offer prospects for elimination by means of vermicidal treatment. If the human link in the chain of infection can be broken, then notionally the disease could be wiped out in a season. In practice it is not quite so simple, and there are complications in that multiple species overlap in certain regions and double infections are common. This creates difficulties for routine mass treatment because people with onchocerciasis in particular react badly to treatment for lymphatic filariasis. Other animals Filariasis can also affect domesticated animals, such as cattle, sheep, and dogs. Cattle Verminous hemorrhagic dermatitis is a clinical disease in cattle due to Parafilaria bovicola. Intradermal onchocerciasis of cattle results in losses in leather due to Onchocerca dermata, O. ochengi, and O. dukei. O. ochengi is closely related to human O. volvulus (river blindness), sharing the same vector, and could be useful in human medicine research. Stenofilaria assamensis and others cause different diseases in Asia, in cattle and zebu. Horses "Summer bleeding" is hemorrhagic subcutaneous nodules in the head and upper forelimbs, caused by Parafilaria multipapillosa (North Africa, Southern and Eastern Europe, Asia and South America). Dogs Heart filariasis is caused by Dirofilaria immitis. See also Ascariasis Eradication of infectious diseases Helminthiasis List of parasites (human) Neglected tropical diseases References Further reading "Special issue", Indian Journal of Urology, 21 (1), January–June 2005 "Filariasis". Therapeutics in Dermatology. June 2012. Retrieved 24 July 2012. External links Page from the "Merck Veterinary Manual" on "Parafilaria multipapillosa" in horses

Please give me a short description about Papulosquamous disorder , Aarogya

Papulosquamous disorder

A papulosquamous disorder is a condition which presents with both papules and scales, or both scaly papules and plaques.Examples include psoriasis, lichen planus, and pityriasis rosea. See also List of cutaneous conditions References Further reading Norman RA, Blanco PM (2003). "Papulosquamous diseases in the elderly". Dermatologic Therapy. 16 (3): 231–42. doi:10.1046/j.1529-8019.2003.01633.x. PMID 14510880. http://www.emedicine.com/derm/index.shtml#papulosquamous == External links ==

Aarogya, elaborate on Brain ischemia

Brain ischemia

Brain ischemia is a condition in which there is insufficient bloodflow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ischemic stroke. It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage.Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis.There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue. The main symptoms of brain ischemia involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage. An interruption of blood flow to the brain for more than 10 seconds causes unconsciousness, and an interruption in flow for more than a few minutes generally results in irreversible brain damage. In 1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to an hour can be at least partially recovered. Accordingly, this discovery raised the possibility of intervening after brain ischemia before the damage becomes irreversible. Symptoms and signs The symptoms of brain ischemia reflect the anatomical region undergoing blood and oxygen deprivation. Ischemia within the arteries branching from the internal carotid artery may result in symptoms such as blindness in one eye, weakness in one arm or leg, or weakness in one entire side of the body. Ischemia within the arteries branching from the vertebral arteries in the back of the brain may result in symptoms such as dizziness, vertigo, double vision, or weakness on both sides of the body. Other symptoms include difficulty speaking, slurred speech, and the loss of coordination. The symptoms of brain ischemia range from mild to severe. Further, symptoms can last from a few seconds to a few minutes or extended periods of time. If the brain becomes damaged irreversibly and infarction occurs, the symptoms may be permanent.Similar to cerebral hypoxia, severe or prolonged brain ischemia will result in unconsciousness, brain damage or death, mediated by the ischemic cascade.Multiple cerebral ischemic events may lead to subcortical ischemic depression, also known as vascular depression. This condition is most commonly seen in elderly depressed patients. Late onset depression is increasingly seen as a distinct sub-type of depression, and can be detected with an MRI. Causes Brain ischemia has been linked to a variety of diseases or abnormalities. Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison to the average population. Sickle cell anemia may cause brain ischemia associated with the irregularly shaped blood cells. Sickle shaped blood cells clot more easily than normal blood cells, impeding blood flow to the brain.Compression of blood vessels may also lead to brain ischemia, by blocking the arteries that carry oxygen to the brain. Tumors are one cause of blood vessel compression.Ventricular tachycardia represents a series of irregular heartbeats that may cause the heart to completely shut down resulting in cessation of oxygen flow. Further, irregular heartbeats may result in formation of blood clots, thus leading to oxygen deprivation to all organs.Blockage of arteries due to plaque buildup may also result in ischemia. Even a small amount of plaque build up can result in the narrowing of passageways, causing that area to become more prone to blood clots. Large blood clots can also cause ischemia by blocking blood flow.A heart attack can also cause brain ischemia due to the correlation that exists between heart attack and low blood pressure. Extremely low blood pressure usually represents the inadequate oxygenation of tissues. Untreated heart attacks may slow blood flow enough that blood may start to clot and prevent the flow of blood to the brain or other major organs. Extremely low blood pressure can also result from drug overdose and reactions to drugs. Therefore, brain ischemia can result from events other than heart attacks.Congenital heart defects may also cause brain ischemia due to the lack of appropriate artery formation and connection. People with congenital heart defects may also be prone to blood clots.Other pathological events that may result in brain ischemia include cardiorespiratory arrest, stroke, and severe irreversible brain damage.Recently, Moyamoya disease has also been identified as a potential cause for brain ischemia. Moyamoya disease is an extremely rare cerebrovascular condition that limits blood circulation to the brain, consequently leading to oxygen deprivation. Pathophysiology During brain ischemia, the brain cannot perform aerobic metabolism due to the loss of oxygen and substrate. The brain is not able to switch to anaerobic metabolism and, because it does not have any long term energy stored, the levels of adenosine triphosphate (ATP) drop rapidly, approaching zero within 4 minutes. In the absence of biochemical energy, cells begin to lose the ability to maintain electrochemical gradients. Consequently, there is a massive influx of calcium into the cytosol, a massive release of glutamate from synaptic vesicles, lipolysis, calpain activation, and the arrest of protein synthesis. Additionally, removal of metabolic wastes is slowed. The interruption of blood flow to the brain for ten seconds results in the immediate loss of consciousness. The interruption of blood flow for twenty seconds results in the stopping of electrical activity. An area called a penumbra may result, wherein neurons do not receive enough blood to communicate, however do receive sufficient oxygenation to avoid cell death for a short period of time. Diagnosis Classification The broad term, "stroke" can be divided into three categories: brain ischemia, subarachnoid hemorrhage and intracerebral hemorrhage. Brain ischemia can be further subdivided, by cause, into thrombotic, embolic, and hypoperfusion. Thrombotic and embolic are generally focal or multifocal in nature while hypoperfusion affects the brain globally. Focal brain ischemia Focal brain ischemia occurs when a blood clot has occluded a cerebral vessel. Focal brain ischemia reduces blood flow to a specific brain region, increasing the risk of cell death to that particular area. It can be either caused by thrombosis or embolism. Global brain ischemia Global brain ischemia occurs when blood flow to the brain is halted or drastically reduced. This is commonly caused by cardiac arrest. If sufficient circulation is restored within a short period of time, symptoms may be transient. However, if a significant amount of time passes before restoration, brain damage may be permanent. While reperfusion may be essential to protecting as much brain tissue as possible, it may also lead to reperfusion injury. Reperfusion injury is classified as the damage that ensues after restoration of blood supply to ischemic tissue.Due to different susceptibility to ischemia of various brain regions, a global brain ischemia may cause focal brain infarction. The cerebral cortex and striatum are more susceptible than the thalamus, and the thalamus in turn is more sensitive than the brainstem. Partial cerebral cortex infarction from global brain ischemia typically manifests as watershed stroke. Biomarker Use of biomarker is one method that has been evaluated to predict the risk of stroke, diagnose stroke and its causes, predict stroke severity and outcome, and guide prevention therapy. Blood Biomarkers: Many proteins and RNA biomarkers identified are connected to ischemic stroke pathophysiology includes Central Nervous System Tissue Injury Biomarkers- S100B, Glial fibrillary acidic protein, enolase 2,Anti-NMDA receptor encephalitis. Inflammatory Biomarkers - c-reactive protein, Interleukin 6, Tumor necrosis factor α,VCAM-1. Coagulation / Thrombosis Biomarkers - Fibrinogen, D-dimer,Von Willebrand factor Other Biomarkers- PARK7, B-type neurotrophic growth factor. Treatment Alteplase (t-PA) is an effective medication for acute ischemic stroke. When given within 3 hours, treatment with tpa significantly improves the probability of a favourable outcome versus treatment with placebo.The outcome of brain ischemia is influenced by the quality of subsequent supportive care. Systemic blood pressure (or slightly above) should be maintained so that cerebral blood flow is restored. Also, hypoxaemia and hypercapnia should be avoided. Seizures can induce more damage; accordingly, anticonvulsants should be prescribed and should a seizure occur, aggressive treatment should be undertaken. Hyperglycaemia should also be avoided during brain ischemia. Management When someone presents with an ischemic event, treatment of the underlying cause is critical for prevention of further episodes.Anticoagulation with warfarin or heparin may be used if the patient has atrial fibrillation.Operative procedures such as carotid endarterectomy and carotid stenting may be performed if the patient has a significant amount of plaque in the carotid arteries associated with the local ischemic events. Research Therapeutic hypothermia has been attempted to improve results post brain ischemia. This procedure was suggested to be beneficial based on its effects post cardiac arrest. Evidence supporting the use of therapeutic hypothermia after brain ischemia, however, is limited.A closely related disease to brain ischemia is brain hypoxia. Brain hypoxia is the condition in which there is a decrease in the oxygen supply to the brain even in the presence of adequate blood flow. If hypoxia lasts for long periods of time, coma, seizures, and even brain death may occur. Symptoms of brain hypoxia are similar to ischemia and include inattentiveness, poor judgment, memory loss, and a decrease in motor coordination. Potential causes of brain hypoxia are suffocation, carbon monoxide poisoning, severe anemia, and use of drugs such as cocaine and other amphetamines. Other causes associated with brain hypoxia include drowning, strangling, choking, cardiac arrest, head trauma, and complications during general anesthesia. Treatment strategies for brain hypoxia vary depending on the original cause of injury, primary and/or secondary. See also Mechanism of anoxic depolarization in the brain Watershed stroke References Bibliography Gusev, Eugene I.; Skvortsova, Veronica I. (2003). Brain ischemia. New York: Kluwer Academic/Plenum Publishers. ISBN 0-306-47694-0. Further reading Chang, Steven; Doty, James; Skirboll, Stephen; Steinberg, Gary. Cerebral ischemia . cgi.stanford.edu. URL last accessed February 26, 2006. == External links ==

Can you describe Diarrhea, to me Aarogya

Diarrhea

Diarrhea, also spelled diarrhoea, is the condition of having at least three loose, liquid, or watery bowel movements each day. It often lasts for a few days and can result in dehydration due to fluid loss. Signs of dehydration often begin with loss of the normal stretchiness of the skin and irritable behaviour. This can progress to decreased urination, loss of skin color, a fast heart rate, and a decrease in responsiveness as it becomes more severe. Loose but non-watery stools in babies who are exclusively breastfed, however, are normal.The most common cause is an infection of the intestines due to either a virus, bacterium, or parasite—a condition also known as gastroenteritis. These infections are often acquired from food or water that has been contaminated by feces, or directly from another person who is infected. The three types of diarrhea are: short duration watery diarrhea, short duration bloody diarrhea, and persistent diarrhea (lasting more than two weeks, which can be either watery or bloody). The short duration watery diarrhea may be due to cholera, although this is rare in the developed world. If blood is present, it is also known as dysentery. A number of non-infectious causes can result in diarrhea. These include lactose intolerance, irritable bowel syndrome, non-celiac gluten sensitivity, celiac disease, inflammatory bowel disease such as ulcerative colitis, hyperthyroidism, bile acid diarrhea, and a number of medications. In most cases, stool cultures to confirm the exact cause are not required.Diarrhea can be prevented by improved sanitation, clean drinking water, and hand washing with soap. Breastfeeding for at least six months and vaccination against rotavirus is also recommended. Oral rehydration solution (ORS)—clean water with modest amounts of salts and sugar—is the treatment of choice. Zinc tablets are also recommended. These treatments have been estimated to have saved 50 million children in the past 25 years. When people have diarrhea it is recommended that they continue to eat healthy food and babies continue to be breastfed. If commercial ORS is not available, homemade solutions may be used. In those with severe dehydration, intravenous fluids may be required. Most cases, however, can be managed well with fluids by mouth. Antibiotics, while rarely used, may be recommended in a few cases such as those who have bloody diarrhea and a high fever, those with severe diarrhea following travelling, and those who grow specific bacteria or parasites in their stool. Loperamide may help decrease the number of bowel movements but is not recommended in those with severe disease.About 1.7 to 5 billion cases of diarrhea occur per year. It is most common in developing countries, where young children get diarrhea on average three times a year. Total deaths from diarrhea are estimated at 1.53 million in 2019—down from 2.9 million in 1990. In 2012, it was the second most common cause of deaths in children younger than five (0.76 million or 11%). Frequent episodes of diarrhea are also a common cause of malnutrition and the most common cause in those younger than five years of age. Other long term problems that can result include stunted growth and poor intellectual development. Definition Diarrhea is defined by the World Health Organization as having three or more loose or liquid stools per day, or as having more stools than is normal for that person.Acute diarrhea is defined as an abnormally frequent discharge of semisolid or fluid fecal matter from the bowel, lasting less than 14 days, by World Gastroenterology Organization. Acute diarrhea that is watery may be known as AWD (Acute Watery Diarrhoea.) Secretory Secretory diarrhea means that there is an increase in the active secretion, or there is an inhibition of absorption. There is little to no structural damage. The most common cause of this type of diarrhea is a cholera toxin that stimulates the secretion of anions, especially chloride ions (Cl–). Therefore, to maintain a charge balance in the gastrointestinal tract, sodium (Na+) is carried with it, along with water. In this type of diarrhea intestinal fluid secretion is isotonic with plasma even during fasting. It continues even when there is no oral food intake. Osmotic Osmotic diarrhea occurs when too much water is drawn into the bowels. If a person drinks solutions with excessive sugar or excessive salt, these can draw water from the body into the bowel and cause osmotic diarrhea. Osmotic diarrhea can also result from maldigestion, e.g. pancreatic disease or coeliac disease, in which the nutrients are left in the lumen to pull in water. Or it can be caused by osmotic laxatives (which work to alleviate constipation by drawing water into the bowels). In healthy individuals, too much magnesium or vitamin C or undigested lactose can produce osmotic diarrhea and distention of the bowel. A person who has lactose intolerance can have difficulty absorbing lactose after an extraordinarily high intake of dairy products. In persons who have fructose malabsorption, excess fructose intake can also cause diarrhea. High-fructose foods that also have a high glucose content are more absorbable and less likely to cause diarrhea. Sugar alcohols such as sorbitol (often found in sugar-free foods) are difficult for the body to absorb and, in large amounts, may lead to osmotic diarrhea. In most of these cases, osmotic diarrhea stops when the offending agent, e.g. milk or sorbitol, is stopped. Exudative Exudative diarrhea occurs with the presence of blood and pus in the stool. This occurs with inflammatory bowel diseases, such as Crohns disease or ulcerative colitis, and other severe infections such as E. coli or other forms of food poisoning. Inflammatory Inflammatory diarrhea occurs when there is damage to the mucosal lining or brush border, which leads to a passive loss of protein-rich fluids and a decreased ability to absorb these lost fluids. Features of all three of the other types of diarrhea can be found in this type of diarrhea. It can be caused by bacterial infections, viral infections, parasitic infections, or autoimmune problems such as inflammatory bowel diseases. It can also be caused by tuberculosis, colon cancer, and enteritis. Dysentery If there is blood visible in the stools, it is also known as dysentery. The blood is a trace of an invasion of bowel tissue. Dysentery is a symptom of, among others, Shigella, Entamoeba histolytica, and Salmonella. Health effects Diarrheal disease may have a negative impact on both physical fitness and mental development. "Early childhood malnutrition resulting from any cause reduces physical fitness and work productivity in adults," and diarrhea is a primary cause of childhood malnutrition. Further, evidence suggests that diarrheal disease has significant impacts on mental development and health; it has been shown that, even when controlling for helminth infection and early breastfeeding, children who had experienced severe diarrhea had significantly lower scores on a series of tests of intelligence.Diarrhea can cause electrolyte imbalances, kidney impairment, dehydration, and defective immune system responses. When oral drugs are administered, the efficiency of the drug is to produce a therapeutic effect and the lack of this effect may be due to the medication travelling too quickly through the digestive system, limiting the time that it can be absorbed. Clinicians try to treat the diarrheas by reducing the dosage of medication, changing the dosing schedule, discontinuation of the drug, and rehydration. The interventions to control the diarrhea are not often effective. Diarrhea can have a profound effect on the quality of life because fecal incontinence is one of the leading factors for placing older adults in long term care facilities (nursing homes). Causes In the latter stages of human digestion, ingested materials are inundated with water and digestive fluids such as gastric acid, bile, and digestive enzymes in order to break them down into their nutrient components, which are then absorbed into the bloodstream via the intestinal tract in the small intestine. Prior to defecation, the large intestine reabsorbs the water and other digestive solvents in the waste product in order to maintain proper hydration and overall equilibrium. Diarrhea occurs when the large intestine is prevented, for any number of reasons, from sufficiently absorbing the water or other digestive fluids from fecal matter, resulting in a liquid, or "loose", bowel movement.Acute diarrhea is most commonly due to viral gastroenteritis with rotavirus, which accounts for 40% of cases in children under five. In travelers, however, bacterial infections predominate. Various toxins such as mushroom poisoning and drugs can also cause acute diarrhea. Chronic diarrhea can be the part of the presentations of a number of chronic medical conditions affecting the intestine. Common causes include ulcerative colitis, Crohns disease, microscopic colitis, celiac disease, irritable bowel syndrome, and bile acid malabsorption. Infections There are many causes of infectious diarrhea, which include viruses, bacteria and parasites. Infectious diarrhea is frequently referred to as gastroenteritis. Norovirus is the most common cause of viral diarrhea in adults, but rotavirus is the most common cause in children under five years old. Adenovirus types 40 and 41, and astroviruses cause a significant number of infections. Shiga-toxin producing Escherichia coli, such as E coli o157:h7, are the most common cause of infectious bloody diarrhea in the United States.Campylobacter spp. are a common cause of bacterial diarrhea, but infections by Salmonella spp., Shigella spp. and some strains of Escherichia coli are also a frequent cause.In the elderly, particularly those who have been treated with antibiotics for unrelated infections, a toxin produced by Clostridioides difficile often causes severe diarrhea.Parasites, particularly protozoa e.g., Cryptosporidium spp., Giardia spp., Entamoeba histolytica, Blastocystis spp., Cyclospora cayetanensis, are frequently the cause of diarrhea that involves chronic infection. The broad-spectrum antiparasitic agent nitazoxanide has shown efficacy against many diarrhea-causing parasites.Other infectious agents, such as parasites or bacterial toxins, may exacerbate symptoms. In sanitary living conditions where there is ample food and a supply of clean water, an otherwise healthy person usually recovers from viral infections in a few days. However, for ill or malnourished individuals, diarrhea can lead to severe dehydration and can become life-threatening. Sanitation Open defecation is a leading cause of infectious diarrhea leading to death.Poverty is a good indicator of the rate of infectious diarrhea in a population. This association does not stem from poverty itself, but rather from the conditions under which impoverished people live. The absence of certain resources compromises the ability of the poor to defend themselves against infectious diarrhea. "Poverty is associated with poor housing, crowding, dirt floors, lack of access to clean water or to sanitary disposal of fecal waste (sanitation), cohabitation with domestic animals that may carry human pathogens, and a lack of refrigerated storage for food, all of which increase the frequency of diarrhea ... Poverty also restricts the ability to provide age-appropriate, nutritionally balanced diets or to modify diets when diarrhea develops so as to mitigate and repair nutrient losses. The impact is exacerbated by the lack of adequate, available, and affordable medical care."One of the most common causes of infectious diarrhea is a lack of clean water. Often, improper fecal disposal leads to contamination of groundwater. This can lead to widespread infection among a population, especially in the absence of water filtration or purification. Human feces contains a variety of potentially harmful human pathogens. Nutrition Proper nutrition is important for health and functioning, including the prevention of infectious diarrhea. It is especially important to young children who do not have a fully developed immune system. Zinc deficiency, a condition often found in children in developing countries can, even in mild cases, have a significant impact on the development and proper functioning of the human immune system. Indeed, this relationship between zinc deficiency and reduced immune functioning corresponds with an increased severity of infectious diarrhea. Children who have lowered levels of zinc have a greater number of instances of diarrhea, severe diarrhea, and diarrhea associated with fever. Similarly, vitamin A deficiency can cause an increase in the severity of diarrheal episodes. However, there is some discrepancy when it comes to the impact of vitamin A deficiency on the rate of disease. While some argue that a relationship does not exist between the rate of disease and vitamin A status, Others suggest an increase in the rate associated with deficiency. Given that estimates suggest 127 million preschool children worldwide are vitamin A deficient, this population has the potential for increased risk of disease contraction. Malabsorption Malabsorption is the inability to absorb food fully, mostly from disorders in the small bowel, but also due to maldigestion from diseases of the pancreas. Causes include: enzyme deficiencies or mucosal abnormality, as in food allergy and food intolerance, e.g. celiac disease (gluten intolerance), lactose intolerance (intolerance to milk sugar, common in non-Europeans), and fructose malabsorption. pernicious anemia, or impaired bowel function due to the inability to absorb vitamin B12, loss of pancreatic secretions, which may be due to cystic fibrosis or pancreatitis, structural defects, like short bowel syndrome (surgically removed bowel) and radiation fibrosis, such as usually follows cancer treatment and other drugs, including agents used in chemotherapy; and certain drugs, like orlistat, which inhibits the absorption of fat. Inflammatory bowel disease The two overlapping types here are of unknown origin: Ulcerative colitis is marked by chronic bloody diarrhea and inflammation mostly affects the distal colon near the rectum. Crohns disease typically affects fairly well demarcated segments of bowel in the colon and often affects the end of the small bowel. Irritable bowel syndrome Another possible cause of diarrhea is irritable bowel syndrome (IBS), which usually presents with abdominal discomfort relieved by defecation and unusual stool (diarrhea or constipation) for at least three days a week over the previous three months. Symptoms of diarrhea-predominant IBS can be managed through a combination of dietary changes, soluble fiber supplements and medications such as loperamide or codeine. About 30% of patients with diarrhea-predominant IBS have bile acid malabsorption diagnosed with an abnormal SeHCAT test. Other diseases Diarrhea can be caused by other diseases and conditions, namely: Chronic ethanol ingestion Hyperthyroidism Certain medications Bile acid malabsorption Ischemic bowel disease: This usually affects older people and can be due to blocked arteries. Microscopic colitis, a type of inflammatory bowel disease where changes are seen only on histological examination of colonic biopsies. Bile salt malabsorption (primary bile acid diarrhea) where excessive bile acids in the colon produce a secretory diarrhea. Hormone-secreting tumors: some hormones, e.g. serotonin, can cause diarrhea if secreted in excess (usually from a tumor). Chronic mild diarrhea in infants and toddlers may occur with no obvious cause and with no other ill effects; this condition is called toddlers diarrhea. Environmental enteropathy Radiation enteropathy following treatment for pelvic and abdominal cancers. Medications Some medications, such as the penicillin can cause diarrhea. Over 700 medications are known to cause diarrhea. The classes of medications that are known to cause diarrhea are laxatives, antacids, heartburn medications, antibiotics, anti-neoplastic drugs, anti-inflammatories as well as many dietary supplements. Pathophysiology Evolution According to two researchers, Nesse and Williams, diarrhea may function as an evolved expulsion defense mechanism. As a result, if it is stopped, there might be a delay in recovery. They cite in support of this argument research published in 1973 that found that treating Shigella with the anti-diarrhea drug (Co-phenotrope, Lomotil) caused people to stay feverish twice as long as those not so treated. The researchers indeed themselves observed that: "Lomotil may be contraindicated in shigellosis. Diarrhea may represent a defense mechanism". Diagnostic approach The following types of diarrhea may indicate further investigation is needed: In infants Moderate or severe diarrhea in young children Associated with blood Continues for more than two days Associated non-cramping abdominal pain, fever, weight loss, etc. In travelers In food handlers, because of the potential to infect others; In institutions such as hospitals, child care centers, or geriatric and convalescent homes.A severity score is used to aid diagnosis in children. Chronic diarrhea When diarrhea lasts for more than four weeks a number of further tests may be recommended including: Complete blood count and a ferritin if anemia is present Thyroid stimulating hormone Tissue transglutaminase for celiac disease Fecal calprotectin to exclude inflammatory bowel disease Stool tests for ova and parasites as well as for Clostridioides difficile A colonoscopy or fecal immunochemical testing for cancer, including biopsies to detect microscopic colitis Testing for bile acid diarrhea with SeHCAT, 7α-hydroxy-4-cholesten-3-one or fecal bile acids depending on availability Hydrogen breath test looking for lactose intolerance Further tests if immunodeficiency, pelvic radiation disease or small intestinal bacterial overgrowth suspected.A 2019 guideline recommended that testing for ova and parasites was only needed in people who are at high risk though they recommend routine testing for giardia. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were not recommended. Prevention Sanitation Numerous studies have shown that improvements in drinking water and sanitation (WASH) lead to decreased risks of diarrhoea. Such improvements might include for example use of water filters, provision of high-quality piped water and sewer connections.In institutions, communities, and households, interventions that promote hand washing with soap lead to significant reductions in the incidence of diarrhea. The same applies to preventing open defecation at a community-wide level and providing access to improved sanitation. This includes use of toilets and implementation of the entire sanitation chain connected to the toilets (collection, transport, disposal or reuse of human excreta). There is limited evidence that safe disposal of child or adult feces can prevent diarrheal disease. Hand washing Basic sanitation techniques can have a profound effect on the transmission of diarrheal disease. The implementation of hand washing using soap and water, for example, has been experimentally shown to reduce the incidence of disease by approximately 30–48%. Hand washing in developing countries, however, is compromised by poverty as acknowledged by the CDC: "Handwashing is integral to disease prevention in all parts of the world; however, access to soap and water is limited in a number of less developed countries. This lack of access is one of many challenges to proper hygiene in less developed countries." Solutions to this barrier require the implementation of educational programs that encourage sanitary behaviours. Water Given that water contamination is a major means of transmitting diarrheal disease, efforts to provide clean water supply and improved sanitation have the potential to dramatically cut the rate of disease incidence. In fact, it has been proposed that we might expect an 88% reduction in child mortality resulting from diarrheal disease as a result of improved water sanitation and hygiene. Similarly, a meta-analysis of numerous studies on improving water supply and sanitation shows a 22–27% reduction in disease incidence, and a 21–30% reduction in mortality rate associated with diarrheal disease.Chlorine treatment of water, for example, has been shown to reduce both the risk of diarrheal disease, and of contamination of stored water with diarrheal pathogens. Vaccination Immunization against the pathogens that cause diarrheal disease is a viable prevention strategy, however it does require targeting certain pathogens for vaccination. In the case of Rotavirus, which was responsible for around 6% of diarrheal episodes and 20% of diarrheal disease deaths in the children of developing countries, use of a Rotavirus vaccine in trials in 1985 yielded a slight (2–3%) decrease in total diarrheal disease incidence, while reducing overall mortality by 6–10%. Similarly, a Cholera vaccine showed a strong reduction in morbidity and mortality, though the overall impact of vaccination was minimal as Cholera is not one of the major causative pathogens of diarrheal disease. Since this time, more effective vaccines have been developed that have the potential to save many thousands of lives in developing nations, while reducing the overall cost of treatment, and the costs to society.Rotavirus vaccine decrease the rates of diarrhea in a population. New vaccines against rotavirus, Shigella, Enterotoxigenic Escherichia coli (ETEC), and cholera are under development, as well as other causes of infectious diarrhea. Nutrition Dietary deficiencies in developing countries can be combated by promoting better eating practices. Zinc supplementation proved successful showing a significant decrease in the incidence of diarrheal disease compared to a control group. The majority of the literature suggests that vitamin A supplementation is advantageous in reducing disease incidence. Development of a supplementation strategy should take into consideration the fact that vitamin A supplementation was less effective in reducing diarrhea incidence when compared to vitamin A and zinc supplementation, and that the latter strategy was estimated to be significantly more cost effective. Breastfeeding Breastfeeding practices have been shown to have a dramatic effect on the incidence of diarrheal disease in poor populations. Studies across a number of developing nations have shown that those who receive exclusive breastfeeding during their first 6 months of life are better protected against infection with diarrheal diseases. One study in Brazil found that non-breastfed infants were 14 times more likely to die from diarrhea than exclusively breastfed infants. Exclusive breastfeeding is currently recommended for the first six months of an infants life by the WHO, with continued breastfeeding until at least two years of age. Others Probiotics decrease the risk of diarrhea in those taking antibiotics. Insecticide spraying may reduce fly numbers and the risk of diarrhea in children in a setting where there is seasonal variations in fly numbers throughout the year. Management In many cases of diarrhea, replacing lost fluid and salts is the only treatment needed. This is usually by mouth – oral rehydration therapy – or, in severe cases, intravenously. Diet restrictions such as the BRAT diet are no longer recommended. Research does not support the limiting of milk to children as doing so has no effect on duration of diarrhea. To the contrary, WHO recommends that children with diarrhea continue to eat as sufficient nutrients are usually still absorbed to support continued growth and weight gain, and that continuing to eat also speeds up recovery of normal intestinal functioning. CDC recommends that children and adults with cholera also continue to eat. There is no evidence that early refeeding in children can cause an increase in inappropriate use of intravenous fluid, episodes of vomiting, and risk of having persistent diarrhea.Medications such as loperamide (Imodium) and bismuth subsalicylate may be beneficial; however they may be contraindicated in certain situations. Fluids Oral rehydration solution (ORS) (a slightly sweetened and salty water) can be used to prevent dehydration. Standard home solutions such as salted rice water, salted yogurt drinks, vegetable and chicken soups with salt can be given. Home solutions such as water in which cereal has been cooked, unsalted soup, green coconut water, weak tea (unsweetened), and unsweetened fresh fruit juices can have from half a teaspoon to full teaspoon of salt (from one-and-a-half to three grams) added per liter. Clean plain water can also be one of several fluids given. There are commercial solutions such as Pedialyte, and relief agencies such as UNICEF widely distribute packets of salts and sugar. A WHO publication for physicians recommends a homemade ORS consisting of one liter water with one teaspoon salt (3 grams) and two tablespoons sugar (18 grams) added (approximately the "taste of tears"). Rehydration Project recommends adding the same amount of sugar but only one-half a teaspoon of salt, stating that this more dilute approach is less risky with very little loss of effectiveness. Both agree that drinks with too much sugar or salt can make dehydration worse.Appropriate amounts of supplemental zinc and potassium should be added if available. But the availability of these should not delay rehydration. As WHO points out, the most important thing is to begin preventing dehydration as early as possible. In another example of prompt ORS hopefully preventing dehydration, CDC recommends for the treatment of cholera continuing to give Oral Rehydration Solution during travel to medical treatment.Vomiting often occurs during the first hour or two of treatment with ORS, especially if a child drinks the solution too quickly, but this seldom prevents successful rehydration since most of the fluid is still absorbed. WHO recommends that if a child vomits, to wait five or ten minutes and then start to give the solution again more slowly.Drinks especially high in simple sugars, such as soft drinks and fruit juices, are not recommended in children under five as they may increase dehydration. A too rich solution in the gut draws water from the rest of the body, just as if the person were to drink sea water. Plain water may be used if more specific and effective ORT preparations are unavailable or are not palatable. Additionally, a mix of both plain water and drinks perhaps too rich in sugar and salt can alternatively be given to the same person, with the goal of providing a medium amount of sodium overall. A nasogastric tube can be used in young children to administer fluids if warranted. Eating The WHO recommends a child with diarrhea continue to be fed. Continued feeding speeds the recovery of normal intestinal function. In contrast, children whose food is restricted have diarrhea of longer duration and recover intestinal function more slowly. The WHO states "Food should never be withheld and the childs usual foods should not be diluted. Breastfeeding should always be continued." In the specific example of cholera, the CDC makes the same recommendation. Breast-fed infants with diarrhea often choose to breastfeed more, and should be encouraged to do so. In young children who are not breast-fed and live in the developed world, a lactose-free diet may be useful to speed recovery. Eating food containing fibers may help. Medications Antidiarrheal agents can be classified into four different groups: antimotility, antisecretory, adsorbent, and anti-infectious. While antibiotics are beneficial in certain types of acute diarrhea, they are usually not used except in specific situations. There are concerns that antibiotics may increase the risk of hemolytic uremic syndrome in people infected with Escherichia coli O157:H7. In resource-poor countries, treatment with antibiotics may be beneficial. However, some bacteria are developing antibiotic resistance, particularly Shigella. Antibiotics can also cause diarrhea, and antibiotic-associated diarrhea is the most common adverse effect of treatment with general antibiotics. While bismuth compounds (Pepto-Bismol) decreased the number of bowel movements in those with travelers diarrhea, they do not decrease the length of illness. Anti-motility agents like loperamide are also effective at reducing the number of stools but not the duration of disease. These agents should be used only if bloody diarrhea is not present.Diosmectite, a natural aluminomagnesium silicate clay, is effective in alleviating symptoms of acute diarrhea in children, and also has some effects in chronic functional diarrhea, radiation-induced diarrhea, and chemotherapy-induced diarrhea. Another absorbent agent used for the treatment of mild diarrhea is kaopectate. Racecadotril an antisecretory medication may be used to treat diarrhea in children and adults. It has better tolerability than loperamide, as it causes less constipation and flatulence. However, it has little benefit in improving acute diarrhea in children.Bile acid sequestrants such as cholestyramine can be effective in chronic diarrhea due to bile acid malabsorption. Therapeutic trials of these drugs are indicated in chronic diarrhea if bile acid malabsorption cannot be diagnosed with a specific test, such as SeHCAT retention. Alternative therapies Zinc supplementation may benefit children over six months old with diarrhea in areas with high rates of malnourishment or zinc deficiency. This supports the World Health Organization guidelines for zinc, but not in the very young. A Cochrane Review from 2020 concludes that probiotics make little or no difference to people who have diarrhoea lasting 2 days or longer and that there is no proof that they reduce its duration. The probiotic lactobacillus can help prevent antibiotic-associated diarrhea in adults but possibly not children. For those with lactose intolerance, taking digestive enzymes containing lactase when consuming dairy products often improves symptoms. Epidemiology Worldwide in 2004, approximately 2.5 billion cases of diarrhea occurred, which resulted in 1.5 million deaths among children under the age of five. Greater than half of these were in Africa and South Asia. This is down from a death rate of 4.5 million in 1980 for gastroenteritis. Diarrhea remains the second leading cause of infant mortality (16%) after pneumonia (17%) in this age group.The majority of such cases occur in the developing world, with over half of the recorded cases of childhood diarrhea occurring in Africa and Asia, with 696 million and 1.2 billion cases, respectively, compared to only 480 million in the rest of the world.Infectious diarrhea resulted in about 0.7 million deaths in children under five years old in 2011 and 250 million lost school days. In the Americas, diarrheal disease accounts for a total of 10% of deaths among children aged 1–59 months while in South East Asia, it accounts for 31.3% of deaths. It is estimated that around 21% of child mortalities in developing countries are due to diarrheal disease. Terminology The word diarrhea is from the Ancient Greek διάρροια from διά dia "through" and ῥέω rheo "flow". Diarrhea is the spelling in American English, whereas diarrhoea is the spelling in British English. Slang terms for the condition include "the runs", "the squirts" (or "squits" in Britain) and "the trots". See also Dysentery Travelers diarrhea == References ==

Would you describe Tonicity, to me Aarogya

Tonicity

In chemical biology, tonicity is a measure of the effective osmotic pressure gradient; the water potential of two solutions separated by a partially-permeable cell membrane. Tonicity depends on the relative concentration of selective membrane-impermeable solutes across a cell membrane which determine the direction and extent of osmotic flux. It is commonly used when describing the swelling-versus-shrinking response of cells immersed in an external solution. Unlike osmotic pressure, tonicity is influenced only by solutes that cannot cross the membrane, as only these exert an effective osmotic pressure. Solutes able to freely cross the membrane do not affect tonicity because they will always equilibrate with equal concentrations on both sides of the membrane without net solvent movement. It is also a factor affecting imbibition. There are three classifications of tonicity that one solution can have relative to another: hypertonic, hypotonic, and isotonic.A hypotonic solution example is distilled water. Hypertonic solution A hypertonic is when the concentration inside the cell is high and the environment is dilute. In biology, the tonicity of a solution usually refers to its solute concentration relative to that of another solution on the opposite side of a cell membrane; a solution inside of a cell is called hypertonic if it has a greater concentration of solutes than the cytosol inside the cell and its environment is dilute. So when the cell is hypertonic(concentrated) the cell needs more water, so water is forced to enter inside the cell and the cell will swell up and eventually burst. When plant cells lose water they are hypotonic, because their inside is diluted(with more water) and the environment is concentrated so it needs water then the flexible cell membrane pulls away from the rigid cell wall, but remains joined to the cell wall at points called plasmodesmata. The cells often take on the appearance of a pincushion. In plant cells the terms isotonic, hypotonic and hypertonic cannot strictly be used accurately because the pressure exerted by the cell wall significantly affects the osmotic equilibrium point. Hypotonic solution A hypotonic is when the concentration inside of the cell is lower than a solution outside of a cell is called hypotonic. If it has a lower concentration of solutes inside a cell then water is forced to move out. Due to this, water is removed out of the cell causing shrinking of the cell membrane. For cells without a cell wall such as animal cells, they lose water and shrivel. When plant cells are in a hypotonic solution, the central vacuole loses water and the cell membrane sticks against the cell wall. Isotonicity A solution is isotonic when its effective osmole concentration is the same as that of another solution. In biology, the solutions on either side of a cell membrane are isotonic if the concentration of solutes outside the cell is equal to the concentration of solutes inside the cell. In this case the cell neither swells nor shrinks because there is no concentration gradient to induce the diffusion of large amounts of water across the cell membrane. Water molecules freely diffuse through the plasma membrane in both directions, and as the rate of water diffusion is the same in each direction, the cell will neither gain nor lose water. == References ==

Aarogya, elaborate on Bilateral

Bilateral

Bilateral may refer to any concept including two sides, in particular: Bilateria, bilateral animals Bilateralism, the political and cultural relations between two states Bilateral, occurring on both sides of an organism (Anatomical terms of location § Medial and lateral) Bilateral symmetry, symmetry between two sides of an organism Bilateral filter, an image processing algorithm Bilateral amplifier, a type of amplifier Bilateral (album), an album by the band Leprous Bilateral school, see Partially selective school (England)

Hello Aarogya, what is Lymphocytopenia

Lymphocytopenia

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

Hey Aarogya, could you help me understand about Orientation (mental)

Orientation (mental)

Orientation is a function of the mind involving awareness of three dimensions: time, place and person. Problems with orientation lead to disorientation, and can be due to various conditions, from delirium to intoxication. Typically, disorientation is first in time, then in place and finally in person. Assessment In the context of an accident or major trauma, the Emergency Medical Responder performs spiraling (increasingly detailed) assessments which guide the critical first response. Assessment of mental orientation typically lands within the immediate top three priorities: Safety - Assess the area safety (potential traffic, fire, overhead/underfoot objects and collapse risks, rushing water, gunfire, chemical/radiation threats, storm conditions, downed power lines, etc.), wait for the threat to subside, or move the person to safety if and when possible, all without endangering oneself. ABCs - Note conscious or unconscious then assess Airway, Breathing and Circulation factors (with priority to any potential gross or debilitating blood loss.) Orientation - Determine if the person is "awake, alert, and oriented, times three (to person, place, and time)." This is frequently abbreviated AAOx3 which also serves as a mnemonic. The assessment involves asking the patient to repeat his own full name, his present location, and todays date. The assessment is best done right up front, ahead of moving or transporting the victim, because it may illuminate potential internal damage. Event/Situation - A fourth category is now used as well. If the person is oriented to what is going on around them, then they are said to be AAOx4. AAOx3 is not a concerning response since people are sometimes less aware of the situation due to pain, time of day, or lack of significant event.Alternately, the letters in AAOx4 can be documented as COAX4. A person who is COAx4 is said to be "conscious, alert, & oriented to person, place, time and event". When a handoff report is made, anything less than 4 is specifically noted for clarity (e.g., patient is COAx2, oriented to self and place). Mental orientation is closely related, and often intermixed with trauma shock, including physical shock (see: Shock (circulatory)) and mental shock (see: Acute stress reaction, a psychological condition in response to terrifying events.) The exact cerebral region involved in orientation is uncertain, but lesions of the brain stem and the cerebral hemispheres have been reported to cause disorientation, suggesting that they act together in maintaining awareness and its subfunction of orientation. Disorientation Disorientation is the opposite of orientation. It is a cognitive disability in which the senses of time, direction, and recognition of items (things), people and places become difficult to distinguish/identify. Causes of mental disorientation Disorientation can occur in healthy young adults as well as in the elderly or ill person. While exercising, if a person becomes dehydrated as a result of over-exertion, he or she may become disoriented to the time or place. While exercising, the body may not be able to supply enough oxygen to the brain fast enough. Mental disorientation can be the aim of some performance art, as creators with audience disorientation as a goal may work to deliberately augment sensations of time, place, person, purpose. See also Destabilisation Mental confusion Mental status examination Spatial disorientation Up-down cues == References ==

Do you know what is Ventricular flutter, Aarogya

Ventricular flutter

Ventricular flutter is an arrhythmia, more specifically a tachycardia affecting the ventricles with a rate over 250-350 beats/min, and one of the most indiscernible. It is characterized on the ECG by a sinusoidal waveform without clear definition of the QRS and T waves. It has been considered as a possible transition stage between ventricular tachycardia and fibrillation, and is a critically unstable arrhythmia that can result in sudden cardiac death.It can occur in infancy, youth, or as an adult. It can be induced by programmed electrical stimulation. References External links http://www.medscape.com/viewarticle/409172_3

Hello Aarogya , Do you know what is Infarction,

Infarction

Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction. The resulting lesion is referred to as an infarct (from the Latin infarctus, "stuffed into"). Causes Infarction occurs as a result of prolonged ischemia, which is the insufficient supply of oxygen and nutrition to an area of tissue due to a disruption in blood supply. The blood vessel supplying the affected area of tissue may be blocked due to an obstruction in the vessel (e.g., an arterial embolus, thrombus, or atherosclerotic plaque), compressed by something outside of the vessel causing it to narrow (e.g., tumor, volvulus, or hernia), ruptured by trauma causing a loss of blood pressure downstream of the rupture, or vasoconstricted, which is the narrowing of the blood vessel by contraction of the muscle wall rather than an external force (e.g., cocaine vasoconstriction leading to myocardial infarction). Hypertension and atherosclerosis are risk factors for both atherosclerotic plaques and thromboembolism. In atherosclerotic formations, a plaque develops under a fibrous cap. When the fibrous cap is degraded by metalloproteinases released from macrophages or by intravascular shear force from blood flow, subendothelial thrombogenic material (extracellular matrix) is exposed to circulating platelets and thrombus formation occurs on the vessel wall occluding blood flow. Occasionally, the plaque may rupture and form an embolus which travels with the blood-flow downstream to where the vessel narrows and eventually clogs the vessel lumen Classification By histopathology Infarctions are divided into two types according to the amount of blood present: White infarctions (anemic infarcts) affect solid organs such as the spleen, heart and kidneys wherein the solidity of the tissue substantially limits the amount of nutrients (blood/oxygen/glucose/fuel) that can flow into the area of ischaemic necrosis. Similar occlusion to blood flow and consequent necrosis can occur as a result of severe vasoconstriction as illustrated in severe Raynauds phenomenon that can lead to irreversible gangrene. Red infarctions (hemorrhagic infarcts) generally affect the lungs or other loose organs (testis, ovary, small intestines). The occlusion consists more of red blood cells and fibrin strands. Characteristics of red infarcts include: occlusion of a vein loose tissues that allow blood to collect in the infarcted zone tissues with a dual circulatory system (lung, small intestines) tissues previously congested from sluggish venous outflow reperfusion (injury) of previously ischemic tissue that is associated with reperfusion-related diseases, such as myocardial infarction, stroke (cerebral infarction), shock-resuscitation, replantation surgery, frostbite, burns, and organ transplantation. By localization Heart: Myocardial infarction (MI), commonly known as a heart attack, is an infarction of the heart, causing some heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or kill heart muscle tissue (myocardium). Brain: Cerebral infarction is the ischemic kind of stroke due to a disturbance in the blood vessels supplying blood to the brain. It can be atherothrombotic or embolic. Stroke caused by cerebral infarction should be distinguished from two other kinds of stroke: cerebral hemorrhage and subarachnoid hemorrhage. Cerebral infarctions vary in their severity with one third of the cases resulting in death. In response to ischemia, the brain degenerates by the process of liquefactive necrosis. Lung: Pulmonary infarction or lung infarction Spleen: Splenic infarction occurs when the splenic artery or one of its branches are occluded, for example by a blood clot. Although it can occur asymptomatically, the typical symptom is severe pain in the left upper quadrant of the abdomen, sometimes radiating to the left shoulder. Fever and chills develop in some cases. It has to be differentiated from other causes of acute abdomen. Limb: Limb infarction is an infarction of an arm or leg. Causes include arterial embolisms and skeletal muscle infarction as a rare complication of long standing, poorly controlled diabetes mellitus. A major presentation is painful thigh or leg swelling. Bone: Infarction of bone results in avascular necrosis. Without blood, the bone tissue dies and the bone collapses. If avascular necrosis involves the bones of a joint, it often leads to destruction of the joint articular surfaces (see osteochondritis dissecans). Testicle: an infarction of a testicle is commonly caused by testicular torsion and may require removal of the affected testicle(s) if not undone by surgery quickly enough. Eye: an infarction can occur to the central retinal artery which supplies the retina causing sudden visual loss. Bowel: Bowel infarction is generally caused by mesenteric ischemia due to blockages in the arteries or veins that supply the bowel. Associated diseases Diseases commonly associated with infarctions include: Peripheral artery occlusive disease (the most severe form of which is gangrene) Antiphospholipid syndrome Sepsis Giant-cell arteritis (GCA) Hernia Volvulus Sickle-cell disease References External links Media related to Infarction at Wikimedia Commons The dictionary definition of infarction at Wiktionary

Hello Aarogya, explain a situation where Alzheimers disease occurs

Alzheimers disease

Alzheimers disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens. It is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation (including easily getting lost), mood swings, loss of motivation, self-neglect, and behavioral issues. As a persons condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the typical life expectancy following diagnosis is three to nine years.The cause of Alzheimers disease is poorly understood. There are many environmental and genetic risk factors associated with its development. The strongest genetic risk factor is from an allele of APOE. Other risk factors include a history of head injury, clinical depression, and high blood pressure. The disease process is largely associated with amyloid plaques, neurofibrillary tangles, and loss of neuronal connections in the brain. A probable diagnosis is based on the history of the illness and cognitive testing with medical imaging and blood tests to rule out other possible causes. Initial symptoms are often mistaken for normal aging. Examination of brain tissue is needed for a definite diagnosis, but this can only take place after death. Good nutrition, physical activity, and engaging socially are known to be of benefit generally in aging, and these may help in reducing the risk of cognitive decline and Alzheimers; in 2019 clinical trials were underway to look at these possibilities. There are no medications or supplements that have been shown to decrease risk.No treatments stop or reverse its progression, though some may temporarily improve symptoms. Affected people increasingly rely on others for assistance, often placing a burden on the caregiver. The pressures can include social, psychological, physical, and economic elements. Exercise programs may be beneficial with respect to activities of daily living and can potentially improve outcomes. Behavioral problems or psychosis due to dementia are often treated with antipsychotics, but this is not usually recommended, as there is little benefit and an increased risk of early death.As of 2020, there were approximately 50 million people worldwide with Alzheimers disease. It most often begins in people over 65 years of age, although up to 10% of cases are early-onset affecting those in their 30s to mid-60s. It affects about 6% of people 65 years and older, and women more often than men. The disease is named after German psychiatrist and pathologist Alois Alzheimer, who first described it in 1906. Alzheimers financial burden on society is large, with an estimated global annual cost of US$1 trillion. Alzheimers disease is currently ranked as the seventh leading cause of death in the United States. Signs and symptoms The course of Alzheimers is generally described in three stages, with a progressive pattern of cognitive and functional impairment. The three stages are described as early or mild, middle or moderate, and late or severe. The disease is known to target the hippocampus which is associated with memory, and this is responsible for the first symptoms of memory impairment. As the disease progresses so does the degree of memory impairment. First symptoms The first symptoms are often mistakenly attributed to aging or stress. Detailed neuropsychological testing can reveal mild cognitive difficulties up to eight years before a person fulfills the clinical criteria for diagnosis of Alzheimers disease. These early symptoms can affect the most complex activities of daily living. The most noticeable deficit is short term memory loss, which shows up as difficulty in remembering recently learned facts and inability to acquire new information.Subtle problems with the executive functions of attentiveness, planning, flexibility, and abstract thinking, or impairments in semantic memory (memory of meanings, and concept relationships) can also be symptomatic of the early stages of Alzheimers disease. Apathy and depression can be seen at this stage, with apathy remaining as the most persistent symptom throughout the course of the disease. Mild cognitive impairment (MCI) is often found to be a transitional stage between normal aging and dementia. MCI can present with a variety of symptoms, and when memory loss is the predominant symptom, it is termed amnestic MCI and is frequently seen as a prodromal stage of Alzheimers disease. Amnestic MCI has a greater than 90% likelihood of being associated with Alzheimers. Early stage In people with Alzheimers disease, the increasing impairment of learning and memory eventually leads to a definitive diagnosis. In a small percentage, difficulties with language, executive functions, perception (agnosia), or execution of movements (apraxia) are more prominent than memory problems. Alzheimers disease does not affect all memory capacities equally. Older memories of the persons life (episodic memory), facts learned (semantic memory), and implicit memory (the memory of the body on how to do things, such as using a fork to eat or how to drink from a glass) are affected to a lesser degree than new facts or memories.Language problems are mainly characterised by a shrinking vocabulary and decreased word fluency, leading to a general impoverishment of oral and written language. In this stage, the person with Alzheimers is usually capable of communicating basic ideas adequately. While performing fine motor tasks such as writing, drawing, or dressing, certain movement coordination and planning difficulties (apraxia) may be present, but they are commonly unnoticed. As the disease progresses, people with Alzheimers disease can often continue to perform many tasks independently, but may need assistance or supervision with the most cognitively demanding activities. Middle stage Progressive deterioration eventually hinders independence, with subjects being unable to perform most common activities of daily living. Speech difficulties become evident due to an inability to recall vocabulary, which leads to frequent incorrect word substitutions (paraphasias). Reading and writing skills are also progressively lost. Complex motor sequences become less coordinated as time passes and Alzheimers disease progresses, so the risk of falling increases. During this phase, memory problems worsen, and the person may fail to recognise close relatives. Long-term memory, which was previously intact, becomes impaired.Behavioral and neuropsychiatric changes become more prevalent. Common manifestations are wandering, irritability and emotional lability, leading to crying, outbursts of unpremeditated aggression, or resistance to caregiving. Sundowning can also appear. Approximately 30% of people with Alzheimers disease develop illusionary misidentifications and other delusional symptoms. Subjects also lose insight of their disease process and limitations (anosognosia). Urinary incontinence can develop. These symptoms create stress for relatives and caregivers, which can be reduced by moving the person from home care to other long-term care facilities. Late stage During the final stage, known as the late-stage or severe stage, there is complete dependence on caregivers. Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech. Despite the loss of verbal language abilities, people can often understand and return emotional signals. Although aggressiveness can still be present, extreme apathy and exhaustion are much more common symptoms. People with Alzheimers disease will ultimately not be able to perform even the simplest tasks independently; muscle mass and mobility deteriorates to the point where they are bedridden and unable to feed themselves. The cause of death is usually an external factor, such as infection of pressure ulcers or pneumonia, not the disease itself. Causes Proteins fail to function normally. This disrupts the work of the brain cells affected and triggers a toxic cascade, ultimately leading to cell death and later brain shrinkage.Alzheimers disease is believed to occur when abnormal amounts of amyloid beta (Aβ), accumulating extracellularly as amyloid plaques and tau proteins, or intracellularly as neurofibrillary tangles, form in the brain, affecting neuronal functioning and connectivity, resulting in a progressive loss of brain function. This altered protein clearance ability is age-related, regulated by brain cholesterol, and associated with other neurodegenerative diseases.Advances in brain imaging techniques allow researchers to see the development and spread of abnormal amyloid and tau proteins in the living brain, as well as changes in brain structure and function. Beta-amyloid is a fragment of a larger protein. When these fragments cluster together, a toxic effect appears on neurons and disrupt cell-to-cell communication. Larger deposits called amyloid plaques are thus further formed.Tau proteins are responsible in neurons internal support and transport system to carry nutrients and other essential materials. In Alzheimers disease, the shape of tau proteins is altered and thus organize themselves into structures called neurofibrillary tangles. The tangles disrupt the transport system and are toxic to cells. The cause for most Alzheimers cases is still mostly unknown, except for 1–2% of cases where deterministic genetic differences have been identified. Several competing hypotheses attempt to explain the underlying cause; the two predominant hypotheses are the amyloid beta (Aβ) hypothesis and the cholinergic hypothesis.The oldest hypothesis, on which most drug therapies are based, is the cholinergic hypothesis, which proposes that Alzheimers disease is caused by reduced synthesis of the neurotransmitter acetylcholine. The loss of cholinergic neurons noted in the limbic system and cerebral cortex, is a key feature in the progression of Alzheimers. The 1991 amyloid hypothesis postulated that extracellular amyloid beta (Aβ) deposits are the fundamental cause of the disease. Support for this postulate comes from the location of the gene for the amyloid precursor protein (APP) on chromosome 21, together with the fact that people with trisomy 21 (Down syndrome) who have an extra gene copy almost universally exhibit at least the earliest symptoms of Alzheimers disease by 40 years of age. A specific isoform of apolipoprotein, APOE4, is a major genetic risk factor for Alzheimers disease. While apolipoproteins enhance the breakdown of beta amyloid, some isoforms are not very effective at this task (such as APOE4), leading to excess amyloid buildup in the brain. Genetic Only 1–2% of Alzheimers cases are inherited (autosomal dominant). These types are known as early onset familial Alzheimers disease, can have a very early onset, and a faster rate of progression. Early onset familial Alzheimers disease can be attributed to mutations in one of three genes: those encoding amyloid-beta precursor protein (APP) and presenilins PSEN1 and PSEN2. Most mutations in the APP and presenilin genes increase the production of a small protein called amyloid beta (Aβ)42, which is the main component of amyloid plaques. Some of the mutations merely alter the ratio between Aβ42 and the other major forms—particularly Aβ40—without increasing Aβ42 levels. Two other genes associated with autosomal dominant Alzheimers disease are ABCA7 and SORL1.Most cases of Alzheimers are not inherited and are termed sporadic Alzheimers disease, in which environmental and genetic differences may act as risk factors. Most cases of sporadic Alzheimers disease in contrast to familial Alzheimers disease are late-onset Alzheimers disease (LOAD) developing after the age of 65 years. Less than 5% of sporadic Alzheimers disease have an earlier onset. The strongest genetic risk factor for sporadic Alzheimers disease is APOEε4. APOEε4 is one of four alleles of apolipoprotein E (APOE). APOE plays a major role in lipid-binding proteins in lipoprotein particles and the epsilon4 allele disrupts this function. Between 40 and 80% of people with Alzheimers disease possess at least one APOEε4 allele. The APOEε4 allele increases the risk of the disease by three times in heterozygotes and by 15 times in homozygotes. Like many human diseases, environmental effects and genetic modifiers result in incomplete penetrance. For example, certain Nigerian populations do not show the relationship between dose of APOEε4 and incidence or age-of-onset for Alzheimers disease seen in other human populations.Alleles in the TREM2 gene have been associated with a 3 to 5 times higher risk of developing Alzheimers disease.A Japanese pedigree of familial Alzheimers disease was found to be associated with a deletion mutation of codon 693 of APP. This mutation and its association with Alzheimers disease was first reported in 2008, and is known as the Osaka mutation. Only homozygotes with this mutation have an increased risk of developing Alzheimers disease. This mutation accelerates Aβ oligomerization but the proteins do not form the amyloid fibrils that aggregate into amyloid plaques, suggesting that it is the Aβ oligomerization rather than the fibrils that may be the cause of this disease. Mice expressing this mutation have all the usual pathologies of Alzheimers disease. Other hypotheses The tau hypothesis proposes that tau protein abnormalities initiate the disease cascade. In this model, hyperphosphorylated tau begins to pair with other threads of tau as paired helical filaments. Eventually, they form neurofibrillary tangles inside nerve cell bodies. When this occurs, the microtubules disintegrate, destroying the structure of the cells cytoskeleton which collapses the neurons transport system.A number of studies connect the misfolded amyloid beta and tau proteins associated with the pathology of Alzheimers disease, as bringing about oxidative stress that leads to chronic inflammation. Sustained inflammation (neuroinflammation) is also a feature of other neurodegenerative diseases including Parkinsons disease, and ALS. Spirochete infections have also been linked to dementia. DNA damages accumulate in AD brains; reactive oxygen species may be the major source of this DNA damage.Sleep disturbances are seen as a possible risk factor for inflammation in Alzheimers disease. Sleep problems have been seen as a consequence of Alzheimers disease but studies suggest that they may instead be a causal factor. Sleep disturbances are thought to be linked to persistent inflammation. The cellular homeostasis of biometals such as ionic copper, iron, and zinc is disrupted in Alzheimers disease, though it remains unclear whether this is produced by or causes the changes in proteins. Smoking is a significant Alzheimers disease risk factor. Systemic markers of the innate immune system are risk factors for late-onset Alzheimers disease. Exposure to air pollution may be a contributing factor to the development of Alzheimers disease.One hypothesis posits that dysfunction of oligodendrocytes and their associated myelin during aging contributes to axon damage, which then causes amyloid production and tau hyper-phosphorylation as a side effect. Retrogenesis is a medical hypothesis that just as the fetus goes through a process of neurodevelopment beginning with neurulation and ending with myelination, the brains of people with Alzheimers disease go through a reverse neurodegeneration process starting with demyelination and death of axons (white matter) and ending with the death of grey matter. Likewise the hypothesis is, that as infants go through states of cognitive development, people with Alzheimers disease go through the reverse process of progressive cognitive impairment.The association with celiac disease is unclear, with a 2019 study finding no increase in dementia overall in those with CD, while a 2018 review found an association with several types of dementia including Alzheimers disease. Pathophysiology Neuropathology Alzheimers disease is characterised by loss of neurons and synapses in the cerebral cortex and certain subcortical regions. This loss results in gross atrophy of the affected regions, including degeneration in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus. Degeneration is also present in brainstem nuclei particularly the locus coeruleus in the pons. Studies using MRI and PET have documented reductions in the size of specific brain regions in people with Alzheimers disease as they progressed from mild cognitive impairment to Alzheimers disease, and in comparison with similar images from healthy older adults.Both Aβ plaques and neurofibrillary tangles are clearly visible by microscopy in brains of those with Alzheimers disease, especially in the hippocampus. However, Alzheimers disease may occur without neurofibrillary tangles in the neocortex. Plaques are dense, mostly insoluble deposits of beta-amyloid peptide and cellular material outside and around neurons. Tangles (neurofibrillary tangles) are aggregates of the microtubule-associated protein tau which has become hyperphosphorylated and accumulate inside the cells themselves. Although many older individuals develop some plaques and tangles as a consequence of aging, the brains of people with Alzheimers disease have a greater number of them in specific brain regions such as the temporal lobe. Lewy bodies are not rare in the brains of people with Alzheimers disease. Biochemistry Alzheimers disease has been identified as a protein misfolding disease, a proteopathy, caused by the accumulation of abnormally folded amyloid beta protein into amyloid plaques, and tau protein into neurofibrillary tangles in the brain. Plaques are made up of small peptides, 39–43 amino acids in length, called amyloid beta (Aβ). Amyloid beta is a fragment from the larger amyloid-beta precursor protein (APP) a transmembrane protein that penetrates the neurons membrane. APP is critical to neuron growth, survival, and post-injury repair. In Alzheimers disease, gamma secretase and beta secretase act together in a proteolytic process which causes APP to be divided into smaller fragments. One of these fragments gives rise to fibrils of amyloid beta, which then form clumps that deposit outside neurons in dense formations known as amyloid plaques.Alzheimers disease is also considered a tauopathy due to abnormal aggregation of the tau protein. Every neuron has a cytoskeleton, an internal support structure partly made up of structures called microtubules. These microtubules act like tracks, guiding nutrients and molecules from the body of the cell to the ends of the axon and back. A protein called tau stabilises the microtubules when phosphorylated, and is therefore called a microtubule-associated protein. In Alzheimers disease, tau undergoes chemical changes, becoming hyperphosphorylated; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neurons transport system. Pathogenic tau can also cause neuronal death through transposable element dysregulation. Disease mechanism Exactly how disturbances of production and aggregation of the beta-amyloid peptide give rise to the pathology of Alzheimers disease is not known. The amyloid hypothesis traditionally points to the accumulation of beta-amyloid peptides as the central event triggering neuron degeneration. Accumulation of aggregated amyloid fibrils, which are believed to be the toxic form of the protein responsible for disrupting the cells calcium ion homeostasis, induces programmed cell death (apoptosis). It is also known that Aβ selectively builds up in the mitochondria in the cells of Alzheimers-affected brains, and it also inhibits certain enzyme functions and the utilisation of glucose by neurons.Various inflammatory processes and cytokines may also have a role in the pathology of Alzheimers disease. Inflammation is a general marker of tissue damage in any disease, and may be either secondary to tissue damage in Alzheimers disease or a marker of an immunological response. There is increasing evidence of a strong interaction between the neurons and the immunological mechanisms in the brain. Obesity and systemic inflammation may interfere with immunological processes which promote disease progression.Alterations in the distribution of different neurotrophic factors and in the expression of their receptors such as the brain-derived neurotrophic factor (BDNF) have been described in Alzheimers disease. Diagnosis Alzheimers disease can only be definitively diagnosed with autopsy findings; in the absence of autopsy, clinical diagnoses of AD are "possible" or "probable", based on other findings. Up to 23% of those clinically diagnosed with AD may be misdiagnosed and may have pathology suggestive of another condition with symptoms that mimic those of AD.AD is usually clinically diagnosed based on the persons medical history, history from relatives, and behavioral observations. The presence of characteristic neurological and neuropsychological features and the absence of alternative conditions supports the diagnosis. Advanced medical imaging with computed tomography (CT) or magnetic resonance imaging (MRI), and with single-photon emission computed tomography (SPECT) or positron emission tomography (PET), can be used to help exclude other cerebral pathology or subtypes of dementia. Moreover, it may predict conversion from prodromal stages (mild cognitive impairment) to Alzheimers disease. FDA-approved radiopharmaceutical diagnostic agents used in PET for Alzheimers disease are florbetapir (2012), flutemetamol (2013), florbetaben (2014), and flortaucipir (2020). Because many insurance companies in the United States do not cover this procedure, its use in clinical practice is largely limited to clinical trials as of 2018.Assessment of intellectual functioning including memory testing can further characterise the state of the disease. Medical organizations have created diagnostic criteria to ease and standardise the diagnostic process for practising physicians. Definitive diagnosis can only be confirmed with post-mortem evaluations when brain material is available and can be examined histologically for senile plaques and neurofibrillary tangles. Criteria There are three sets of criteria for the clinical diagnoses of the spectrum of Alzheimers disease: the 2013 fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5); the National Institute on Aging-Alzheimers Association (NIA-AA) definition as revised in 2011; and the International Working Group criteria as revised in 2010. Three broad time periods, which can span decades, define the progression of Alzheimers disease from the preclinical phase, to mild cognitive impairment (MCI), followed by Alzheimers disease dementia.Eight intellectual domains are most commonly impaired in AD—memory, language, perceptual skills, attention, motor skills, orientation, problem solving and executive functional abilities, as listed in the fourth text revision of the DSM (DSM-IV-TR).The DSM-5 defines criteria for probable or possible Alzheimers for both major and mild neurocognitive disorder. Major or mild neurocognitive disorder must be present along with at least one cognitive deficit for a diagnosis of either probable or possible AD. For major neurocognitive disorder due to Alzheimers disease, probable Alzheimers disease can be diagnosed if the individual has genetic evidence of Alzheimers or if two or more acquired cognitive deficits, and a functional disability that is not from another disorder, are present. Otherwise, possible Alzheimers disease can be diagnosed as the diagnosis follows an atypical route. For mild neurocognitive disorder due to Alzheimers, probable Alzheimers disease can be diagnosed if there is genetic evidence, whereas possible Alzheimers disease can be met if all of the following are present: no genetic evidence, decline in both learning and memory, two or more cognitive deficits, and a functional disability not from another disorder.The NIA-AA criteria are used mainly in research rather than in clinical assessments. They define Alzheimers disease through three major stages: preclinical, mild cognitive impairment (MCI), and Alzheimers dementia. Diagnosis in the preclinical stage is complex and focuses on asymptomatic individuals; the latter two stages describe individuals experiencing symptoms. The core clinical criteria for MCI is used along with identification of biomarkers, predominantly those for neuronal injury (mainly tau-related) and amyloid beta deposition. The core clinical criteria itself rests on the presence of cognitive impairment without the presence of comorbidities. The third stage is divided into probable and possible Alzheimers disease dementia. In probable Alzheimers disease dementia there is steady impairment of cognition over time and a memory-related or non-memory-related cognitive dysfunction. In possible Alzheimers disease dementia, another causal disease such as cerebrovascular disease is present. Techniques Neuropsychological tests including cognitive tests such as the Mini–Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA) and the Mini-Cog are widely used to aid in diagnosis of the cognitive impairments in AD. These tests may not always be accurate, as they lack sensitivity to mild cognitive impairment, and can be biased by language or attention problems; more comprehensive test arrays are necessary for high reliability of results, particularly in the earliest stages of the disease.Further neurological examinations are crucial in the differential diagnosis of Alzheimers disease and other diseases. Interviews with family members are used in assessment; caregivers can supply important information on daily living abilities and on the decrease in the persons mental function. A caregivers viewpoint is particularly important, since a person with Alzheimers disease is commonly unaware of their deficits. Many times, families have difficulties in the detection of initial dementia symptoms and may not communicate accurate information to a physician.Supplemental testing can rule out other potentially treatable diagnoses and help avoid misdiagnoses. Common supplemental tests include blood tests, thyroid function tests, as well as tests to assess vitamin B12 levels, rule out neurosyphilis and rule out metabolic problems (including tests for kidney function, electrolyte levels and for diabetes). MRI or CT scans might also be used to rule out other potential causes of the symptoms – including tumors or strokes. Delirium and depression can be common among individuals and are important to rule out.Psychological tests for depression are used, since depression can either be concurrent with Alzheimers disease (see Depression of Alzheimer disease), an early sign of cognitive impairment, or even the cause.Due to low accuracy, the C-PIB-PET scan is not recommended as an early diagnostic tool or for predicting the development of Alzheimers disease when people show signs of mild cognitive impairment (MCI). The use of 18F-FDG PET scans, as a single test, to identify people who may develop Alzheimers disease is not supported by evidence. Prevention There are no disease-modifying treatments available to cure Alzheimers disease and because of this, AD research has focused on interventions to prevent the onset and progression. There is no evidence that supports any particular measure in preventing Alzheimers, and studies of measures to prevent the onset or progression have produced inconsistent results. Epidemiological studies have proposed relationships between an individuals likelihood of developing AD and modifiable factors, such as medications, lifestyle, and diet. There are some challenges in determining whether interventions for Alzheimers disease act as a primary prevention method, preventing the disease itself, or a secondary prevention method, identifying the early stages of the disease. These challenges include duration of intervention, different stages of disease at which intervention begins, and lack of standardization of inclusion criteria regarding biomarkers specific for Alzheimers disease. Further research is needed to determine factors that can help prevent Alzheimers disease. Medication Cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes, and smoking, are associated with a higher risk of onset and worsened course of AD. The use of statins to lower cholesterol may be of benefit in Alzheimers. Antihypertensive and antidiabetic medications in individuals without overt cognitive impairment may decrease the risk of dementia by influencing cerebrovascular pathology. More research is needed to examine the relationship with Alzheimers disease specifically; clarification of the direct role medications play versus other concurrent lifestyle changes (diet, exercise, smoking) is needed.Depression is associated with an increased risk for Alzheimers disease; management with antidepressants may provide a preventative measure.Historically, long-term usage of non-steroidal anti-inflammatory drugs (NSAIDs) were thought to be associated with a reduced likelihood of developing Alzheimers disease as it reduces inflammation; however, NSAIDs do not appear to be useful as a treatment. Additionally, because women have a higher incidence of Alzheimers disease than men, it was once thought that estrogen deficiency during menopause was a risk factor. However, there is a lack of evidence to show that hormone replacement therapy (HRT) in menopause decreases risk of cognitive decline. Lifestyle Certain lifestyle activities, such as physical and cognitive exercises, higher education and occupational attainment, cigarette smoking, stress, sleep, and the management of other comorbidities, including diabetes and hypertension, may affect the risk of developing Alzheimers.Physical exercise is associated with a decreased rate of dementia, and is effective in reducing symptom severity in those with AD. Memory and cognitive functions can be improved with aerobic exercises including brisk walking three times weekly for forty minutes. It may also induce neuroplasticity of the brain. Participating in mental exercises, such as reading, crossword puzzles, and chess have shown a potential to be preventative. Meeting the WHO recommendations for physical activity is associated with a lower risk of AD.Higher education and occupational attainment, and participation in leisure activities, contribute to a reduced risk of developing Alzheimers, or of delaying the onset of symptoms. This is compatible with the cognitive reserve theory, which states that some life experiences result in more efficient neural functioning providing the individual a cognitive reserve that delays the onset of dementia manifestations. Education delays the onset of Alzheimers disease syndrome without changing the duration of the disease.Cessation in smoking may reduce risk of developing Alzheimers disease, specifically in those who carry APOE ɛ4 allele. The increased oxidative stress caused by smoking results in downstream inflammatory or neurodegenerative processes that may increase risk of developing AD. Avoidance of smoking, counseling and pharmacotherapies to quit smoking are used, and avoidance of environmental tobacco smoke is recommended.Alzheimers disease is associated with sleep disorders but the precise relationship is unclear. It was once thought that as people get older, the risk of developing sleep disorders and AD independently increase, but research is examining whether sleep disorders may increase the prevalence of AD. One theory is that the mechanisms to increase clearance of toxic substances, including Aβ, are active during sleep. With decreased sleep, a person is increasing Aβ production and decreasing Aβ clearance, resulting in Aβ accumulation. Receiving adequate sleep (approximately 7–8 hours) every night has become a potential lifestyle intervention to prevent the development of AD.Stress is a risk factor for the development of Alzheimers. The mechanism by which stress predisposes someone to development of Alzheimers is unclear, but it is suggested that lifetime stressors may affect a persons epigenome, leading to an overexpression or under expression of specific genes. Although the relationship of stress and Alzheimers is unclear, strategies to reduce stress and relax the mind may be helpful strategies in preventing the progression or Alzheimers disease. Meditation, for instance, is a helpful lifestyle change to support cognition and well-being, though further research is needed to assess long-term effects. Management There is no cure for Alzheimers disease; available treatments offer relatively small symptomatic benefits but remain palliative in nature. Treatments can be divided into pharmaceutical, psychosocial, and caregiving. Pharmaceutical Medications used to treat the cognitive problems of Alzheimers disease include: four acetylcholinesterase inhibitors (tacrine, rivastigmine, galantamine, and donepezil) and memantine, an NMDA receptor antagonist. The acetylcholinesterase inhibitors are intended for those with mild to severe Alzheimers, whereas memantine is intended for those with moderate or severe Alzheimers disease. The benefit from their use is small.Reduction in the activity of the cholinergic neurons is a well-known feature of Alzheimers disease. Acetylcholinesterase inhibitors are employed to reduce the rate at which acetylcholine (ACh) is broken down, thereby increasing the concentration of ACh in the brain and combating the loss of ACh caused by the death of cholinergic neurons. There is evidence for the efficacy of these medications in mild to moderate Alzheimers disease, and some evidence for their use in the advanced stage. The use of these drugs in mild cognitive impairment has not shown any effect in a delay of the onset of Alzheimers disease. The most common side effects are nausea and vomiting, both of which are linked to cholinergic excess. These side effects arise in approximately 10–20% of users, are mild to moderate in severity, and can be managed by slowly adjusting medication doses. Less common secondary effects include muscle cramps, decreased heart rate (bradycardia), decreased appetite and weight, and increased gastric acid production.Glutamate is an excitatory neurotransmitter of the nervous system, although excessive amounts in the brain can lead to cell death through a process called excitotoxicity which consists of the overstimulation of glutamate receptors. Excitotoxicity occurs not only in Alzheimers disease, but also in other neurological diseases such as Parkinsons disease and multiple sclerosis. Memantine is a noncompetitive NMDA receptor antagonist first used as an anti-influenza agent. It acts on the glutamatergic system by blocking NMDA receptors and inhibiting their overstimulation by glutamate. Memantine has been shown to have a small benefit in the treatment of moderate to severe Alzheimers disease. Reported adverse events with memantine are infrequent and mild, including hallucinations, confusion, dizziness, headache and fatigue. The combination of memantine and donepezil has been shown to be "of statistically significant but clinically marginal effectiveness".An extract of Ginkgo biloba known as EGb 761 has been used for treating Alzheimers and other neuropsychiatric disorders. Its use is approved throughout Europe. The World Federation of Biological Psychiatry guidelines lists EGb 761 with the same weight of evidence (level B) given to acetylcholinesterase inhibitors and memantine. EGb 761 is the only one that showed improvement of symptoms in both Alzheimers disease and vascular dementia. EGb 761 may have a role either on its own or as an add-on if other therapies prove ineffective. A 2016 review concluded that the quality of evidence from clinical trials on Ginkgo biloba has been insufficient to warrant its use for treating Alzheimers disease.Atypical antipsychotics are modestly useful in reducing aggression and psychosis in people with Alzheimers disease, but their advantages are offset by serious adverse effects, such as stroke, movement difficulties or cognitive decline. When used in the long-term, they have been shown to associate with increased mortality. Stopping antipsychotic use in this group of people appears to be safe. Psychosocial Psychosocial interventions are used as an adjunct to pharmaceutical treatment and can be classified within behavior-, emotion-, cognition- or stimulation-oriented approaches.Behavioral interventions attempt to identify and reduce the antecedents and consequences of problem behaviors. This approach has not shown success in improving overall functioning, but can help to reduce some specific problem behaviors, such as incontinence. There is a lack of high quality data on the effectiveness of these techniques in other behavior problems such as wandering. Music therapy is effective in reducing behavioral and psychological symptoms.Emotion-oriented interventions include reminiscence therapy, validation therapy, supportive psychotherapy, sensory integration, also called snoezelen, and simulated presence therapy. A Cochrane review has found no evidence that this is effective. Reminiscence therapy (RT) involves the discussion of past experiences individually or in group, many times with the aid of photographs, household items, music and sound recordings, or other familiar items from the past. A 2018 review of the effectiveness of RT found that effects were inconsistent, small in size and of doubtful clinical significance, and varied by setting. Simulated presence therapy (SPT) is based on attachment theories and involves playing a recording with voices of the closest relatives of the person with Alzheimers disease. There is partial evidence indicating that SPT may reduce challenging behaviors.The aim of cognition-oriented treatments, which include reality orientation and cognitive retraining, is the reduction of cognitive deficits. Reality orientation consists of the presentation of information about time, place, or person to ease the understanding of the person about its surroundings and his or her place in them. On the other hand, cognitive retraining tries to improve impaired capacities by exercising mental abilities. Both have shown some efficacy improving cognitive capacities.Stimulation-oriented treatments include art, music and pet therapies, exercise, and any other kind of recreational activities. Stimulation has modest support for improving behavior, mood, and, to a lesser extent, function. Nevertheless, as important as these effects are, the main support for the use of stimulation therapies is the change in the persons routine. Caregiving Since Alzheimers has no cure and it gradually renders people incapable of tending to their own needs, caregiving is essentially the treatment and must be carefully managed over the course of the disease. During the early and moderate stages, modifications to the living environment and lifestyle can increase safety and reduce caretaker burden. Examples of such modifications are the adherence to simplified routines, the placing of safety locks, the labeling of household items to cue the person with the disease or the use of modified daily life objects. If eating becomes problematic, food will need to be prepared in smaller pieces or even puréed. When swallowing difficulties arise, the use of feeding tubes may be required. In such cases, the medical efficacy and ethics of continuing feeding is an important consideration of the caregivers and family members. The use of physical restraints is rarely indicated in any stage of the disease, although there are situations when they are necessary to prevent harm to the person with Alzheimers disease or their caregivers.During the final stages of the disease, treatment is centred on relieving discomfort until death, often with the help of hospice. Diet Diet may be a modifiable risk factor for the development of Alzheimers disease. The Mediterranean diet, and the DASH diet are both associated with less cognitive decline. A different approach has been to incorporate elements of both of these diets into one known as the MIND diet. Studies of individual dietary components, minerals and supplements are conflicting as to whether they prevent AD or cognitive decline. Prognosis The early stages of Alzheimers disease are difficult to diagnose. A definitive diagnosis is usually made once cognitive impairment compromises daily living activities, although the person may still be living independently. The symptoms will progress from mild cognitive problems, such as memory loss through increasing stages of cognitive and non-cognitive disturbances, eliminating any possibility of independent living, especially in the late stages of the disease.Life expectancy of people with Alzheimers disease is reduced. The normal life expectancy for 60 to 70 years old is 23 to 15 years; for 90 years old it is 4.5 years. Following Alzheimers disease diagnosis it ranges from 7 to 10 years for those in their 60s and early 70s (a loss of 13 to 8 years), to only about 3 years or less (a loss of 1.5 years) for those in their 90s.Fewer than 3% of people live more than fourteen years. Disease features significantly associated with reduced survival are an increased severity of cognitive impairment, decreased functional level, history of falls, and disturbances in the neurological examination. Other coincident diseases such as heart problems, diabetes, or history of alcohol abuse are also related with shortened survival. While the earlier the age at onset the higher the total survival years, life expectancy is particularly reduced when compared to the healthy population among those who are younger. Men have a less favourable survival prognosis than women.Pneumonia and dehydration are the most frequent immediate causes of death brought by Alzheimers disease, while cancer is a less frequent cause of death than in the general population. Epidemiology Two main measures are used in epidemiological studies: incidence and prevalence. Incidence is the number of new cases per unit of person-time at risk (usually number of new cases per thousand person-years); while prevalence is the total number of cases of the disease in the population at any given time. Regarding incidence, cohort longitudinal studies (studies where a disease-free population is followed over the years) provide rates between 10 and 15 per thousand person-years for all dementias and 5–8 for Alzheimers disease, which means that half of new dementia cases each year are Alzheimers disease. Advancing age is a primary risk factor for the disease and incidence rates are not equal for all ages: every 5 years after the age of 65, the risk of acquiring the disease approximately doubles, increasing from 3 to as much as 69 per thousand person years. Females with Alzheimers disease are more common than males, but this difference is likely due to womens longer life spans. When adjusted for age, both sexes are affected by Alzheimers at equal rates. In the United States, the risk of dying from Alzheimers disease in 2010 was 26% higher among the non-Hispanic white population than among the non-Hispanic black population, and the Hispanic population had a 30% lower risk than the non-Hispanic white population. However, much Alzheimers research remains to be done in minority groups, such as the African American and the Hispanic/Latino populations. Studies have shown that these groups are underrepresented in clinical trials and do not have the same risk of developing Alzheimers when carrying certain genetic risk factors (i.e. APOE4), compared to their caucasian counterparts.The prevalence of Alzheimers disease in populations is dependent upon factors including incidence and survival. Since the incidence of Alzheimers disease increases with age, prevalence depends on the mean age of the population for which prevalence is given. In the United States in 2020, Alzheimers dementia prevalence was estimated to be 5.3% for those in the 60–74 age group, with the rate increasing to 13.8% in the 74–84 group and to 34.6% in those greater than 85. Prevalence rates in some less developed regions around the globe are lower. As the incidence and prevalence are steadily increasing, the prevalence itself is projected to triple by 2050. As of 2020, 50 million people globally have AD, with this number expected to increase to 152 million by 2050. History The ancient Greek and Roman philosophers and physicians associated old age with increasing dementia. It was not until 1901 that German psychiatrist Alois Alzheimer identified the first case of what became known as Alzheimers disease, named after him, in a fifty-year-old woman he called Auguste D. He followed her case until she died in 1906 when he first reported publicly on it. During the next five years, eleven similar cases were reported in the medical literature, some of them already using the term Alzheimers disease. The disease was first described as a distinctive disease by Emil Kraepelin after suppressing some of the clinical (delusions and hallucinations) and pathological features (arteriosclerotic changes) contained in the original report of Auguste D. He included Alzheimers disease, also named presenile dementia by Kraepelin, as a subtype of senile dementia in the eighth edition of his Textbook of Psychiatry, published on 15 July, 1910.For most of the 20th century, the diagnosis of Alzheimers disease was reserved for individuals between the ages of 45 and 65 who developed symptoms of dementia. The terminology changed after 1977 when a conference on Alzheimers disease concluded that the clinical and pathological manifestations of presenile and senile dementia were almost identical, although the authors also added that this did not rule out the possibility that they had different causes. This eventually led to the diagnosis of Alzheimers disease independent of age. The term senile dementia of the Alzheimer type (SDAT) was used for a time to describe the condition in those over 65, with classical Alzheimers disease being used to describe those who were younger. Eventually, the term Alzheimers disease was formally adopted in medical nomenclature to describe individuals of all ages with a characteristic common symptom pattern, disease course, and neuropathology.The National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) and the Alzheimers Disease and Related Disorders Association (ADRDA, now known as the Alzheimers Association) established the most commonly used NINCDS-ADRDA Alzheimers Criteria for diagnosis in 1984, extensively updated in 2007. These criteria require that the presence of cognitive impairment, and a suspected dementia syndrome, be confirmed by neuropsychological testing for a clinical diagnosis of possible or probable Alzheimers disease. A histopathologic confirmation including a microscopic examination of brain tissue is required for a definitive diagnosis. Good statistical reliability and validity have been shown between the diagnostic criteria and definitive histopathological confirmation. Society and culture Social costs Dementia, and specifically Alzheimers disease, may be among the most costly diseases for societies worldwide. As populations age, these costs will probably increase and become an important social problem and economic burden. Costs associated with AD include direct and indirect medical costs, which vary between countries depending on social care for a person with AD. Direct costs include doctor visits, hospital care, medical treatments, nursing home care, specialized equipment, and household expenses. Indirect costs include the cost of informal care and the loss in productivity of informal caregivers.In the United States as of 2019, informal (family) care is estimated to constitute nearly three-fourths of caregiving for people with AD at a cost of US$234 billion per year and approximately 18.5 billion hours of care. The cost to society worldwide to care for individuals with AD is projected to increase nearly ten-fold, and reach about US$9.1 trillion by 2050.Costs for those with more severe dementia or behavioral disturbances are higher and are related to the additional caregiving time to provide physical care. Caregiving burden The role of the main caregiver is often taken by the spouse or a close relative. Alzheimers disease is known for placing a great burden on caregivers which includes social, psychological, physical, or economic aspects. Home care is usually preferred by people with Alzheimers disease and their families. This option also delays or eliminates the need for more professional and costly levels of care. Nevertheless, two-thirds of nursing home residents have dementias.Dementia caregivers are subject to high rates of physical and mental disorders. Factors associated with greater psychosocial problems of the primary caregivers include having an affected person at home, the carer being a spouse, demanding behaviors of the cared person such as depression, behavioral disturbances, hallucinations, sleep problems or walking disruptions and social isolation. Regarding economic problems, family caregivers often give up time from work to spend 47 hours per week on average with the person with Alzheimers disease, while the costs of caring for them are high. Direct and indirect costs of caring for somebody with Alzheimers average between $18,000 and $77,500 per year in the United States, depending on the study.Cognitive behavioral therapy and the teaching of coping strategies either individually or in group have demonstrated their efficacy in improving caregivers psychological health. Media Alzheimers disease has been portrayed in films such as: Iris (2001), based on John Bayleys memoir of his wife Iris Murdoch; The Notebook (2004), based on Nicholas Sparks 1996 novel of the same name; A Moment to Remember (2004); Thanmathra (2005); Memories of Tomorrow (Ashita no Kioku) (2006), based on Hiroshi Ogiwaras novel of the same name; Away from Her (2006), based on Alice Munros short story The Bear Came over the Mountain; Still Alice (2014), about a Columbia University professor who has early onset Alzheimers disease, based on Lisa Genovas 2007 novel of the same name and featuring Julianne Moore in the title role. Documentaries on Alzheimers disease include Malcolm and Barbara: A Love Story (1999) and Malcolm and Barbara: Loves Farewell (2007), both featuring Malcolm Pointon.Alzheimers disease has also been portrayed in music by English musician the Caretaker in releases such as Persistent Repetition of Phrases (2008), An Empty Bliss Beyond This World (2011), and Everywhere at the End of Time (2016–2019). Paintings depicting the disorder include the late works by American artist William Utermohlen, who drew self-portraits from 1995 to 2000 as an experiment of showing his disease through art. Research directions Additional research on the lifestyle effect may provide insight into neuroimaging biomarkers and better understanding of the mechanisms causing both Alzheimers disease and early-onset AD. Treatment and prevention There is ongoing research examining the role of specific medications in reducing the prevalence (primary prevention) and/or progression (secondary prevention) of Alzheimers disease. The research trials investigating medications generally impact Aβ plaques, inflammation, APOE, neurotransmitter receptors, neurogenesis, epigenetic regulators, growth factors and hormones. These studies have led to a better understanding of the disease, but none identified a prevention strategy. Experimental models are commonly used by researchers in order to understand disease mechanisms as well develop and test novel therapeutics aimed at treating Alzheimers disease. Antibodies are being developed that may have the ability to alter the disease course by targeting amyloid beta, such as donanemab and aducanumab. Aducanumab was approved by the FDA in 2021, but its use and effectiveness remain unclear and controversial. Although it received FDA approval, aducanumab failed to show effectiveness in people who already had Alzheimers symptoms. References Further reading External links "Alzheimers Disease Research Timeline - Alzforum". www.alzforum.org. "Alzheimers Disease Brain Cell Atlas- brain-map.org". portal.brain-map.org. Alzheimers disease at Curlie

Hi Aarogya, explain a situation where Female infertility occurs

Female infertility

Female infertility refers to infertility in women. It affects an estimated 48 million women, with the highest prevalence of infertility affecting women in South Asia, Sub-Saharan Africa, North Africa/Middle East, and Central/Eastern Europe and Central Asia. Infertility is caused by many sources, including nutrition, diseases, and other malformations of the uterus. Infertility affects women from around the world, and the cultural and social stigma surrounding it varies. Cause Causes or factors of female infertility can basically be classified regarding whether they are acquired or genetic, or strictly by location. Although factors of female infertility can be classified as either acquired or genetic, female infertility is usually more or less a combination of nature and nurture. Also, the presence of any single risk factor of female infertility (such as smoking, mentioned further below) does not necessarily cause infertility, and even if a woman is definitely infertile, the infertility cannot definitely be blamed on any single risk factor even if the risk factor is (or has been) present. Acquired According to the American Society for Reproductive Medicine (ASRM), age, smoking, sexually transmitted infections, and being overweight or underweight can all affect fertility.In broad sense, acquired factors practically include any factor that is not based on a genetic mutation, including any intrauterine exposure to toxins during fetal development, which may present as infertility many years later as an adult. Age A womans fertility is affected by her age. The average age of a girls first period (menarche) is 12–13 (12.5 years in the United States, 12.72 in Canada, 12.9 in the UK), but, in postmenarchal girls, about 80% of the cycles are anovulatory in the first year after menarche, 50% in the third and 10% in the sixth year. A womans fertility peaks in the early and mid 20s, after which it starts to decline, with this decline being accelerated after age 35. However, the exact estimates of the chances of a woman to conceive after a certain age are not clear, with research giving differing results. The chances of a couple to successfully conceive at an advanced age depend on many factors, including the general health of a woman and the fertility of the male partner. Menopause typically occurs between 44 and 58 years of age. DNA testing is rarely carried out to confirm claims of maternity at advanced ages, but in one large study, among 12,549 African and Middle Eastern immigrant mothers, confirmed by DNA testing, only two mothers were found to be older than fifty; the oldest mother being 52.1 years at conception (and the youngest mother 10.7 years old). Tobacco smoking Tobacco smoking is harmful to the ovaries, and the degree of damage is dependent upon the amount and length of time a woman smokes or is exposed to a smoke-filled environment. Nicotine and other harmful chemicals in cigarettes interfere with the bodys ability to create estrogen, a hormone that regulates folliculogenesis and ovulation. Also, cigarette smoking interferes with folliculogenesis, embryo transport, endometrial receptivity, endometrial angiogenesis, uterine blood flow and the uterine myometrium. Some damage is irreversible, but stopping smoking can prevent further damage. Smokers are 60% more likely to be infertile than non-smokers. Smoking reduces the chances of IVF producing a live birth by 34% and increases the risk of an IVF pregnancy miscarrying by 30%. Also, female smokers have an earlier onset of menopause by approximately 1–4 years. Sexually transmitted infections Sexually transmitted infections are a leading cause of infertility. They often display few, if any visible symptoms, with the risk of failing to seek proper treatment in time to prevent decreased fertility. Body weight and eating disorders Twelve percent of all infertility cases are a result of a woman either being underweight or overweight. Fat cells produce estrogen, in addition to the primary sex organs. Too much body fat causes production of too much estrogen and the body begins to react as if it is on birth control, limiting the odds of getting pregnant. Too little body fat causes insufficient production of estrogen and disruption of the menstrual cycle. Both under and overweight women have irregular cycles in which ovulation does not occur or is inadequate. Proper nutrition in early life is also a major factor for later fertility.A study in the US indicated that approximately 20% of infertile women had a past or current eating disorder, which is five times higher than the general lifetime prevalence rate.A review from 2010 concluded that overweight and obese subfertile women have a reduced probability of successful fertility treatment and their pregnancies are associated with more complications and higher costs. In hypothetical groups of 1,000 women undergoing fertility care, the study counted approximately 800 live births for normal weight and 690 live births for overweight and obese anovulatory women. For ovulatory women, the study counted approximately 700 live births for normal weight, 550 live births for overweight and 530 live births for obese women. The increase in cost per live birth in anovulatory overweight and obese women were, respectively, 54 and 100% higher than their normal weight counterparts, for ovulatory women they were 44 and 70% higher, respectively. Radiation Exposure to radiation poses a high risk of infertility, depending on the frequency, power, and exposure duration. Radiotherapy is reported to cause infertility,. the amount of radiation absorbed by the ovaries will determine if she becomes infertile. High doses can destroy some or all of the eggs in the ovaries and might cause infertility or early menopause. Chemotherapy Chemotherapy poses a high risk of infertility. Chemotherapies with high risk of infertility include procarbazine and other alkylating drugs such as cyclophosphamide, ifosfamide, busulfan, melphalan, chlorambucil and chlormethine. Drugs with medium risk include doxorubicin and platinum analogs such as cisplatin and carboplatin. On the other hand, therapies with low risk of gonadotoxicity include plant derivatives such as vincristine and vinblastine, antibiotics such as bleomycin and dactinomycin and antimetabolites such as methotrexate, mercaptopurine and 5-fluorouracil.Female infertility by chemotherapy appears to be secondary to premature ovarian failure by loss of primordial follicles. This loss is not necessarily a direct effect of the chemotherapeutic agents, but could be due to an increased rate of growth initiation to replace damaged developing follicles. Antral follicle count decreases after three series of chemotherapy, whereas follicle stimulating hormone (FSH) reaches menopausal levels after four series. Other hormonal changes in chemotherapy include decrease in inhibin B and anti-Müllerian hormone levels.Women may choose between several methods of fertility preservation prior to chemotherapy, including cryopreservation of ovarian tissue, oocytes or embryos. Immune infertility Antisperm antibodies (ASA) have been considered as infertility cause in around 10–30% of infertile couples. ASA production are directed against surface antigens on sperm, which can interfere with sperm motility and transport through the female reproductive tract, inhibiting capacitation and acrosome reaction, impaired fertilization, influence on the implantation process, and impaired growth and development of the embryo. Factors contributing to the formation of antisperm antibodies in women are disturbance of normal immunoregulatory mechanisms, infection, violation of the integrity of the mucous membranes, accidental rape and unprotected oral or anal sex. Other acquired factors Adhesions secondary to surgery in the peritoneal cavity is the leading cause of acquired infertility. A meta-analysis in 2012 came to the conclusion that there is only little evidence for the surgical principle that using less invasive techniques, introducing less foreign bodies or causing less ischemia reduces the extent and severity of adhesions. Diabetes mellitus. A review of type 1 diabetes came to the result that, despite modern treatment, women with diabetes are at increased risk of female infertility, such as reflected by delayed puberty and menarche, menstrual irregularities (especially oligomenorrhoea), mild hyperandrogenism, polycystic ovarian syndrome, fewer live born children and possibly earlier menopause. Animal models indicate that abnormalities on the molecular level caused by diabetes include defective leptin, insulin and kisspeptin signalling. Coeliac disease. Non-gastrointestinal symptoms of coeliac disease may include disorders of fertility, such as delayed menarche, amenorrea, infertility or early menopause; and pregnancy complications, such as intrauterine growth restriction (IUGR), small for gestational age (SGA) babies, recurrent abortions, preterm deliveries or low birth weight (LBW) babies. Nevertheless, gluten-free diet reduces the risk. Some authors suggest that physicians should investigate the presence of undiagnosed coeliac disease in women with unexplained infertility, recurrent miscarriage or IUGR. Significant liver or kidney disease Thrombophilia Cannabis smoking, such as of marijuana causes disturbances in the endocannabinoid system, potentially causing infertility Radiation, such as in radiation therapy. The radiation dose to the ovaries that generally causes permanent female infertility is 20.3 Gy at birth, 18.4 Gy at 10 years, 16.5 Gy at 20 years and 14.3 Gy at 30 years. After total body irradiation, recovery of gonadal function occurs in 10−14% of cases, and the number of pregnancies observed after hematopoietic stem cell transplantation involving such as procedure is lower than 2%. Genetic factors There are many genes wherein mutation causes female infertility, as shown in table below. Also, there are additional conditions involving female infertility which are believed to be genetic but where no single gene has been found to be responsible, notably Mayer-Rokitansky-Küstner-Hauser Syndrome (MRKH). Finally, an unknown number of genetic mutations cause a state of subfertility, which in addition to other factors such as environmental ones may manifest as frank infertility. Chromosomal abnormalities causing female infertility include Turner syndrome. Oocyte donation is an alternative for patients with Turner syndrome.Some of these gene or chromosome abnormalities cause intersex conditions, such as androgen insensitivity syndrome. By location Hypothalamic-pituitary factors Hypothalamic dysfunction Hyperprolactinemia Ovarian factors Chemotherapy (as detailed previously) with certain agents have a high risk of toxicity on the ovaries. Many genetic defects (as also detailed previously) also disturb ovarian function. Polycystic ovary syndrome (also see infertility in polycystic ovary syndrome) Anovulation. Female infertility caused by anovulation is called "anovulatory infertility", as opposed to "ovulatory infertility" in which ovulation is present. Diminished ovarian reserve, also see Poor Ovarian Reserve Premature menopause Menopause Luteal dysfunction Gonadal dysgenesis (Turner syndrome) Tubal (ectopic)/peritoneal factors Endometriosis (also see endometriosis and infertility) Pelvic adhesions Pelvic inflammatory disease (PID, usually due to chlamydia) Tubal dysfunction Previous ectopic pregnancy. A randomized study in 2013 came to the result that the rates of intrauterine pregnancy two years after treatment of ectopic pregnancy are approximately 64% with radical surgery, 67% with medication, and 70% with conservative surgery. In comparison, the cumulative pregnancy rate of women under 40 years of age in the general population over two years is over 90%. Hydrosalpinx is the most frequent. This happens when there is a presence of fluid on the tubes. We have some ways to test it: Hysterosalphingography, in which we can see both the uterus (Hystero) and the tubes. Hysterosonosalphingography, in which we see only the uterus. This tests are used to check if the tubes are permeable or if there is any obstacle in the path to the uterus. We have to introduce a liquid contrast via vagina, and we check its path via x-ray. If the tube is blocked, the contrast liquid will be stopped in the tubes, but if its not blocked, it will end in the abdominal cavity. The flow of this contrast needs peristaltic movements. This blockage can be produced by sexually transmitted diseases, previous surgery, peritonitis or endometriosis. Uterine factors Uterine malformations Uterine fibroids Ashermans syndrome Implantation failure without any known primary cause. It results in negative pregnancy test despite having performed e.g. embryo transfer.Previously, a bicornuate uterus was thought to be associated with infertility, but recent studies have not confirmed such an association. Cervical factors Cervical stenosis Antisperm antibodies Non-receptive cervical mucus Vaginal factors Vaginismus Vaginal obstruction Interrupted meiosis Meiosis. a special type of cell division specific to germ cells, produces egg cells in women. During meiosis, accurate segregation of chromosomes must occur during two rounds of division to create, upon fertilisation, a zygote with a proper diploid(euploid) set of chromosomes. About half of all spontaneous abortions are aneuploid, that is, have an improper set of chromosomes. Human genetic variants that likely cause dysregulation of critical meiotic processes have been identified in 14 female infertility associated genes.A major cause of female infertility is premature ovarian insufficiency. This insufficiency is a heterogeneous disease that affects about 1% of women who are under age 40. Some instances of female infertility are caused by DNA repair dysregulation during meiosis. Diagnosis Diagnosis of infertility begins with a medical history and physical exam. The healthcare provider may order tests, including the following: Lab tests Hormone testing, to measure levels of female hormones at certain times during a menstrual cycle. Day 2 or 3 measure of FSH and estrogen, to assess ovarian reserve. Measurements of thyroid function (a thyroid stimulating hormone (TSH) level of between 1 and 2 is considered optimal for conception). Measurement of progesterone in the second half of the cycle to help confirm ovulation. Anti-Müllerian hormone to estimate ovarian reserve. Examination and imaging An endometrial biopsy, to verify ovulation and inspect the lining of the uterus. Laparoscopy, which allows the provider to inspect the pelvic organs. Fertiloscopy, a relatively new surgical technique used for early diagnosis (and immediate treatment). Pap smear, to check for signs of infection. Pelvic exam, to look for abnormalities or infection. A postcoital test, which is done soon after intercourse to check for problems with sperm surviving in cervical mucous (not commonly used now because of test unreliability). Hysterosalpingography or sonosalpingography, to check for tube patency Sonohysterography to check for uterine abnormalities.There are genetic testing techniques under development to detect any mutation in genes associated with female infertility.Initial diagnosis and treatment of infertility is usually made by obstetrician/gynecologists or womens health nurse practitioners. If initial treatments are unsuccessful, referral is usually made to physicians who are fellowship trained as reproductive endocrinologists. Reproductive endocrinologists are usually obstetrician/gynecologists with advanced training in reproductive endocrinology and infertility (in North America). These physicians treat reproductive disorders affecting not only women but also men, children, and teens. Usually reproductive endocrinology & infertility medical practices do not see women for general maternity care. The practice is primarily focused on helping their women to conceive and to correct any issues related to recurring pregnancy loss. Definition There is no unanimous definition of female infertility, because the definition depends on social and physical characteristics which may vary by culture and situation. NICE guidelines state that: "A woman of reproductive age who has not conceived after 1 year of unprotected vaginal sexual intercourse, in the absence of any known cause of infertility, should be offered further clinical assessment and investigation along with her partner." It is recommended that a consultation with a fertility specialist should be made earlier if the woman is aged 36 years or over, or there is a known clinical cause of infertility or a history of predisposing factors for infertility. According to the World Health Organization (WHO), infertility can be described as the inability to become pregnant, maintain a pregnancy, or carry a pregnancy to live birth. A clinical definition of infertility by the WHO and ICMART is "a disease of the reproductive system defined by the failure to achieve a clinical pregnancy after 12 months or more of regular unprotected sexual intercourse." Infertility can further be broken down into primary and secondary infertility. Primary infertility refers to the inability to give birth either because of not being able to become pregnant, or carry a child to live birth, which may include miscarriage or a stillborn child. Secondary infertility refers to the inability to conceive or give birth when there was a previous pregnancy or live birth. Prevention Acquired female infertility may be prevented through identified interventions: Maintaining a healthy lifestyle. Excessive exercise, consumption of caffeine and alcohol, and smoking have all been associated with decreased fertility. Eating a well-balanced, nutritious diet, with plenty of fresh fruits and vegetables, and maintaining a normal weight, on the other hand, have been associated with better fertility prospects. Treating or preventing existing diseases. Identifying and controlling chronic diseases such as diabetes and hypothyroidism increases fertility prospects. Lifelong practice of safer sex reduces the likelihood that sexually transmitted diseases will impair fertility; obtaining prompt treatment for sexually transmitted diseases reduces the likelihood that such infections will do significant damage. Regular physical examinations (including pap smears) help detect early signs of infections or abnormalities. Not delaying parenthood. Fertility does not ultimately cease before menopause, but it starts declining after age 27 and drops at a somewhat greater rate after age 35. Women whose biological mothers had unusual or abnormal issues related to conceiving may be at particular risk for some conditions, such as premature menopause, that can be mitigated by not delaying parenthood. Egg freezing. A woman can freeze her eggs preserve her fertility. By using egg freezing while in the peak reproductive years, a womans oocytes are cryogenically frozen and ready for her use later in life, reducing her chances of female infertility. Treatment There is no method to reverse advanced maternal age, but there are assisted reproductive technologies for many causes of infertility in pre-menopausal women, including: Ovulation induction for anovulation In vitro fertilization in for example tubal abnormalities Epidemiology Female infertility varies widely by geographic location around the world. In 2010, there was an estimated 48.5 million infertile couples worldwide, and from 1990 to 2010 there was little change in levels of infertility in most of the world. In 2010, the countries with the lowest rates of female infertility included the South American countries of Peru, Ecuador and Bolivia, as well as in Poland, Kenya, and Republic of Korea. The highest rate regions included Eastern Europe, North Africa, the Middle East, Oceania, and Sub-Saharan Africa. The prevalence of primary infertility has increased since 1990, but secondary infertility has decreased overall. Rates decreased (although not prevalence) of female infertility in high-income, Central/Eastern Europe, and Central Asia regions. Female infertility is prevalent across the globe. In 2013, the estimated prevalence of female infertility ranged from roughly 3% to 7% depending on the part of globe being followed. [78] Africa Sub-Saharan Africa has had decreasing levels of primary infertility from 1990 to 2010. Within the Sub-Saharan region, rates were lowest in Kenya, Zimbabwe, and Rwanda, while the highest rates were in Guinea, Mozambique, Angola, Gabon, and Cameroon along with Northern Africa near the Middle East. According to a 2004 DHS report, rates in Africa were highest in Middle and Sub-Saharan Africa, with East Africas rates close behind. Asia In Asia, the highest rates of combined secondary and primary infertility was in the South Central region, and then in the Southeast region, with the lowest rates in the Western areas. Latin America and Caribbean The prevalence of female infertility in the Latin America/Caribbean region is typically lower than the global prevalence. However, the greatest rates occurred in Jamaica, Suriname, Haiti, and Trinidad and Tobago. Central and Western Latin America has some of the lowest rates of prevalence. The highest regions in Latin America and the Caribbean was in the Caribbean Islands and in less developed countries. Society and culture Social stigma Social stigma due to infertility is seen in many cultures throughout the world in varying forms. Often, when women cannot conceive, the blame is put on them, even when approximately 50% of infertility issues come from the man . In addition, many societies only tend to value a woman if she is able to produce at least one child, and a marriage can be considered a failure when the couple cannot conceive. The act of conceiving a child can be linked to the couples consummation of marriage, and reflect their social role in society. This is seen in the "African infertility belt", where infertility is prevalent in Africa which includes countries spanning from Tanzania in the east to Gabon in the west. In this region, infertility is highly stigmatized and can be considered a failure of the couple to their societies. This is demonstrated in Uganda and Nigeria where there is a great pressure put on childbearing and its social implications. This is also seen in some Muslim societies including Egypt and Pakistan. In the United States, and all over the world, infertility and women’s infertility at large is an invisible yet debilitating disease that is stigmatized and looked down upon. But, in recent years many have begun to sue organizations for infertility insurance coverage, as the Americans with Disabilities Act (ADA) has recognized infertility as a disability. This however adds another stigmatization to women suffering from infertility as the word disability has a negative connotation in various world societies. [77] Wealth is sometimes measured by the number of children a woman has, as well as inheritance of property. Children can influence financial security in many ways. In Nigeria and Cameroon, land claims are decided by the number of children. Also, in some Sub-Saharan countries women may be denied inheritance if she did not bear any children In some African and Asian countries a husband can deprive his infertile wife of food, shelter and other basic necessities like clothing. In Cameroon, a woman may lose access to land from her husband and left on her own in old age.In many cases, a woman who cannot bear children is excluded from social and cultural events including traditional ceremonies. This stigmatization is seen in Mozambique and Nigeria where infertile women have been treated as outcasts to society. This is a humiliating practice which devalues infertile women in society. In the Makua tradition, pregnancy and birth are considered major life events for a woman, with the ceremonies of nthaara and nthaara no mwana, which can only be attended by women who have been pregnant and have had a baby.The effect of infertility can lead to social shaming from internal and social norms surrounding pregnancy, which affects women around the world. When pregnancy is considered such an important event in life, and considered a "socially unacceptable condition", it can lead to a search for treatment in the form of traditional healers and expensive Western treatments. The limited access to treatment in many areas can lead to extreme and sometimes illegal acts in order to produce a child. Marital role Men in some countries may find another wife when their first cannot produce a child, hoping that by sleeping with more women he will be able to produce his own child. This can be prevalent in some societies, including Cameroon, Nigeria, Mozambique, Egypt, Botswana, and Bangladesh, among many more where polygamy is more common and more socially acceptable. In couples that are unsuccessful in conceiving, divorce rates are roughly 3.5 times higher than those of couples who are fertile. This was based off of those with female infertility. [78] In some cultures, including Botswana and Nigeria, women can select a woman with whom she allows her husband to sleep with in hopes of conceiving a child. Women who are desperate for children may compromise with her husband to select a woman and accept duties of taking care of the children to feel accepted and useful in society.Women may also sleep with other men in hopes of becoming pregnant. This can be done for many reasons including advice from a traditional healer, or finding if another man was "more compatible". In many cases, the husband was not aware of the extra sexual relations and would not be informed if a woman became pregnant by another man. This is not as culturally acceptable however, and can contribute to the gendered suffering of women who have fewer options to become pregnant on their own as opposed to men.Men and women can also turn to divorce in attempt to find a new partner with whom to bear a child. Infertility in many cultures is a reason for divorce, and a way for a man or woman to increase his/her chances of producing an heir. When a woman is divorced, she can lose her security that often comes with land, wealth, and a family. This can ruin marriages and can lead to distrust in the marriage. The increase of sexual partners can potentially result with the spread of disease including HIV/AIDS, and can actually contribute to future generations of infertility. Domestic abuse The emotional strain and stress that comes with infertility in the household can lead to the mistreatment and domestic abuse of a woman. The devaluation of a wife due to her inability to conceive can lead to domestic abuse and emotional trauma such as victim blaming. Women are sometimes or often blamed as the cause of a couples infertility, which can lead to emotional abuse, anxiety, and shame. In addition, blame for not being able to conceive is often put on the female, even if it is the man who is infertile. Women who are not able to conceive can be starved, beaten, and may be neglected financially by her husband as if she had no child bearing use to him. The physical abuse related to infertility may result from this and the emotional stress that comes with it. In some countries, the emotional and physical abuses that come with infertility can potentially lead to assault, murder, and suicide. Mental and psychological impact Many infertile women tend to cope with immense stress and social stigma behind their condition, which can lead to considerable mental distress. The long-term stress involved in attempting to conceive a child and the social pressures behind giving birth can lead to emotional distress that may manifest as mental disease. Women with infertility might deal with psychological stressors such as denial, anger, grief, guilt, and depression. There can be considerable social shaming that can lead to intense feelings of sadness and frustration that potentially contribute to depression and suicide. The implications behind infertility bear huge consequences for the mental health of an infertile woman because of the social pressures and personal grief behind being unable to bear children. The range of psychological issues pertaining to infertility in women is vast and can include inferiority complex, stress with interpersonal relationships, and possibly major depression and or anxiety. With the impacts of infertility on social life, cultural significance, and psychological factors, “infertility has been classified as one of the greatest stressors of life.” [76] Emotional impact of infertility treatment Many women have reported finding treatment for infertility stressful and a cause of relationship difficulties with their partners. The fear of failure was the most important barrier to treatment. Females, in studied cases, typically experience more adverse effects of infertility and treatments than to males. [75]The psychological support is fundamental to limit the possibility to drop-out from infertility treatment and reduce the distress level which is strongly associated with lower pregnancy rates. In addition some medications (in particular clomifene citrate) used in the treatment have several side effects which may be an important risk factor for the development of depression. See also Advanced maternal age Fertility Infertility Male infertility Oncofertility References [75] Raval, H.; Slade, P.; Buck, P.; Lieberman, B. E. (1987-10). "The impact of infertility on emotions and the marital and sexual relationship". Journal of Reproductive and Infant Psychology. 5 (4): 221–234. doi:10.1080/02646838708403497. ISSN 0264-6838. {{cite journal}}: Empty citation (help): Check date values in: |date= (help) [76] Khan, Ambreen Rashid (March 2019). "Impact of Infertility on Mental Health of Women" (PDF). The International Journal of Indian Psychology. 7 (1): 804–809. doi:10.25215/0701.089. [77] Sternke, Elizabeth A.; Abrahamson, Kathleen (2015-03-01). "Perceptions of Women with Infertility on Stigma and Disability". Sexuality and Disability. 33 (1): 3–17. doi:10.1007/s11195-014-9348-6. ISSN 1573-6717. [78] Direkvand-Moghadam, Ashraf; Delpisheh, Ali; Khosravi, A. (2013-12-30). "Epidemiology of Female Infertility; A Review of Literature". Biosciences Biotechnology Research Asia. 10 (2): 559–567. doi:10.13005/bbra/1165. ISSN 0973-1245. == External links ==

Give me a short description about Hymenolepiasis , Aarogya

Hymenolepiasis

Hymenolepiasis is infestation by one of two species of tapeworm: Hymenolepis nana or H. diminuta. Alternative names are dwarf tapeworm infection and rat tapeworm infection. The disease is a type of helminthiasis which is classified as a neglected tropical disease. Symptoms and signs Hymenolepiasis does not always have symptoms, but they usually are described as abdominal pain, loss of appetite, itching around the anus, irritability, and diarrhea. However, in one study of 25 patients conducted in Peru, successful treatment of the infection made no significant difference to symptoms. Some authorities report that heavily infected cases are more likely to be symptomatic.Symptoms in humans are due to allergic responses or systematic toxaemia caused by waste products of the tapeworm. Light infections are usually symptomless, whereas infection with more than 2000 worms can cause enteritis, abdominal pain, diarrhea, loss of appetite, restlessness, irritability, restless sleep, and anal and nasal pruritus. Rare symptoms include increased appetite, vomiting, nausea, bloody diarrhea, hives, extremity pain, headache, dizziness, and behavioral disturbances. Occasionally, epileptic seizures occur in infected children.Examination of the stool for eggs and parasites confirms the diagnosis. The eggs and proglottids of H. nana are smaller than H. diminuta. Proglottids of both are relatively wide and have three testes. Identifying the parasites to the species level is often unnecessary from a medical perspective, as the treatment is the same for both. Complications Abdominal discomfort and, in case of prolonged diarrhea, dehydration are possible complications.In 2015 an unusual complication was noted in a man whose immune system had been compromised by HIV. He developed multiple tumors of malignant cell nests within his body that had originated from a tapeworm in his intestines. Causes Hymenolepis worms live in the intestines of rats and are common in warm climates, and are generally found in the feces of rats, which are consumed by their secondary hosts—beetles. The worms mature into a life form referred to as a "cysticercoid" in the insect; in H. nana, the insect is always a beetle. Humans and other animals become infected when they intentionally or unintentionally eat material contaminated by insects. In an infected person, it is possible for the worms entire lifecycle to be completed in the bowel, so infection can persist for years if left untreated. H. nana infections are much more common than H. diminuta infections in humans because, in addition to being spread by insects, the disease can be spread directly from person to person by eggs in feces. When this happens, H. nana oncosphere larvae encyst in the intestinal wall and develop into cysticercoids and then adults. These infections were previously common in the southeastern USA, and have been described in crowded environments and individuals confined to institutions. However, the disease occurs throughout the world. H. nana infections can grow worse over time because, unlike in most tapeworms, H. nana eggs can hatch and develop without ever leaving the definitive host. H. diminuta The risk of human infection from H. diminuta is very low, since its main host is the rat. Also known as the rat tapeworm, H. diminuta adults live and mate in the bowels of rats. Eggs of H. diminuta are excreted by the rats in droppings, which are frequently consumed by beetles. Once inside the beetle, the eggs mature into a cysticercoid. The juvenile tapeworms claw their way out of the beetle gut into the circulatory system by means of their three pairs of hooks. There, they wait for a rat to ingest the host beetle, where they mature to adult form, lay eggs, and restart the entire cycle. Beetle manipulation H. diminuta has an effective mechanism for interspecies transfection. Beetles prefer to ingest rat droppings infected with tapeworm eggs, because of their odor. It is not known if the odor is produced specifically by the eggs or the droppings. H. diminuta also sterilizes its beetle host, if female. This is so the beetle does not waste energy in its reproductive system, allowing H. diminuta to further exploit the beetles metabolic resources. H. nana H. nana is a tapeworm, belonging to the class Cestoidea, phylum Platyhelminthes. It consists of a linear series of sets of reproductive organs of both sexes; each set is referred to as a genitaluim and the area around it is a proglottid. New proglottids are continuously differentiated near the anterior end in a process called strobilation. Each segment moves toward the posterior end as a new one takes its place and, during the process, becomes sexually mature. The proglottid can copulate with itself, with others in the strobilla, or with those in other worms. When the segment reaches the end of its strobila, it disintegrates en route, releasing eggs in a process called apolysis. Lifecycle H. nana is the only cestode capable of completing its lifecycle without an intermediate host. It can, however, pass through an intermediate host, as well. The most common intermediate hosts for H. nana are arthropods (e.g. flour beetles). When an egg is ingested by the definitive host, it hatches and releases a six-hook larva called the oncosphere (hexacanth) which penetrates the villi of the small intestine and develops into a cysticercoid. Infection Transmission of H.nana occurs by the fecal-oral route. It also occurs by accidental ingestion of an insect containing the cysticercoid. Screening for activity against H. nana H. nana in mice is used because: Human infection is easily maintained in mice. Its armed scolex is similar to other pathogenic tapeworms. It corresponds to other tapeworms in its sensitivity to standard anthelmintics,Method: Mature worms are collected from infected mice. Terminal gravid proglottids are removed, crushed under coverslips, and eggs are removed. Eggs containing hooklets (mature) are counted. 0.2 ml stock soln. containing 1000 eggs/ml given to each mouse. Adult worms develop in 15–17 days. The test drug is given orally; mice are necropsied on the third day after treatment. A standard drug is given. The intestines are examined under a dissecting microscope for worms or scolices. The response is measured bt the number mice cleared. Pathology H. nana lodges itself in the intestines and absorbs nutrients from the intestinal lumen. In human adults, the tapeworm is more of a nuisance than a health problem, but in small children, many H. nana worms can be dangerous. Usually, the larvae of this tapeworm cause the most problem in children; they burrow into the walls of the intestine, and if enough tapeworms are present in the child, severe damage can be inflicted. This is done by absorbing all the nutrients from the food the child eats. Usually, a single tapeworm will not cause health issues. H. nana usually will not cause deaths unless in extreme circumstances and usually in young children or in people who have weakened immune systems. In some parts of the world, individuals who are heavily infected are a result of internal autoinfection. Prevention Good hygiene, public health and sanitation programs, and elimination of infected rats help to prevent the spread of hymenolepiasis. Preventing fecal contamination of food and water in institutions and crowded areas is of primary importance. General sanitation and rodent and insect control (especially control of fleas and grain insects) are also essential for prevention of H. nana infection. Treatment The two drugs that have been well-described for the treatment of hymenolepiasis are praziquantel and niclosamide. Praziquantel, which is parasiticidal in a single dose for all the stages of the parasite, is the drug of choice because it acts very rapidly against H. nana. Although structurally unrelated to other anthelminthics, it kills both adult worms and larvae. In vitro, the drug produces vacuolization and disruption of the tegument in the neck of the worms, but not in more posterior portions of the strobila. Praziquantel is well absorbed when taken orally, and it undergoes first-pass metabolism and 80% of the dose is excreted as metabolites in urine within 24 hours. Repeated treatment is required for H. nana at an interval of 7–10 days.Praziquantel as a single dose (25 mg/kg) is the current treatment of choice for hymenolepiasis and has an efficacy of 96%. Single-dose albendazole (400 mg) is also very efficacious (>95%).A three-day course of nitazoxanide is 75–93% efficacious. The dose is 1 g daily for adults and children over 12; 400 mg daily for children aged 4 to 11 years; and 200 mg daily for children aged 3 years or younger. Prognosis Cure rates are extremely good with modern treatments, but successful cure results may be of no symptomatic benefit to patients. See also List of parasites (human) References Further reading MedlinePlus Encyclopedia: Hymenolepiasis "Hymenolepiasis". CDC - DPDx. 2013-11-29. Retrieved 2015-11-01. == External links ==

Hi Aarogya, explain a situation where Adie syndrome occurs

Adie syndrome

Adie syndrome, also known as Holmes-Adie syndrome, is a neurological disorder characterized by a tonically dilated pupil that reacts slowly to light but shows a more definite response to accommodation (i.e., light-near dissociation). It is frequently seen in females with absent knee or ankle jerks and impaired sweating. The syndrome is caused by damage to the postganglionic fibers of the parasympathetic innervation of the eye, usually by a viral or bacterial infection that causes inflammation, and affects the pupil of the eye and the autonomic nervous system. It is named after the British neurologists William John Adie and Gordon Morgan Holmes, who independently described the same disease in 1931. Signs and symptoms Adie syndrome presents with three hallmark symptoms, namely at least one abnormally dilated pupil (mydriasis) which does not constrict in response to light, loss of deep tendon reflexes, and abnormalities of sweating. Other signs may include hyperopia due to accommodative paresis, photophobia and difficulty reading. Some individuals with Adie syndrome may also have cardiovascular abnormalities. Pathophysiology Pupillary symptoms of Holmes–Adie syndrome are thought to be the result of a viral or bacterial infection that causes inflammation and damage to neurons in the ciliary ganglion, located in the posterior orbit, that provides parasympathetic control of eye constriction. Additionally, patients with Holmes-Adie Syndrome can also experience problems with autonomic control of the body. This second set of symptoms is caused by damage to the dorsal root ganglia of the spinal cord. Adies pupil is supersensitive to ACh so a muscarinic agonist (e.g. pilocarpine) whose dose would not be able to cause pupillary constriction in a normal patient, would cause it in a patient with Adies Syndrome. The circuitry for the pupillary constriction does not descend below the upper midbrain, henceforth impaired pupillary constriction is extremely important to detect as it can be an early sign of brainstem herniation. Diagnosis Clinical exam may reveal sectoral paresis of the iris sphincter or vermiform iris movements. The tonic pupil may become smaller (miotic) over time which is referred to as "little old Adies". Testing with low dose (1/8%) pilocarpine may constrict the tonic pupil due to cholinergic denervation supersensitivity. A normal pupil will not constrict with the dilute dose of pilocarpine. CT scans and MRI scans may be useful in the diagnostic testing of focal hypoactive reflexes. Treatment The usual treatment of a standardised Adie syndrome is to prescribe reading glasses to correct for impairment of the eye(s). Pilocarpine drops may be administered as a treatment as well as a diagnostic measure. Thoracic sympathectomy is the definitive treatment of diaphoresis, if the condition is not treatable by drug therapy. Prognosis Adies syndrome is not life-threatening or disabling. As such, there is no mortality rate relating to the condition; however, loss of deep tendon reflexes is permanent and may progress over time. Epidemiology It most commonly affects younger women (2.6:1 female preponderance) and is unilateral in 80% of cases. Average age of onset is 32 years. See also Ciliary ganglion Ross syndrome References Further reading == External links ==

Can you describe Hidradenitis suppurativa, to me Aarogya

Hidradenitis suppurativa

Hidradenitis suppurativa (HS), sometimes known as acne inversa or Verneuils disease, is a long-term dermatological condition characterized by the occurrence of inflamed and swollen lumps. These are typically painful and break open, releasing fluid or pus. The areas most commonly affected are the underarms, under the breasts, and the groin. Scar tissue remains after healing. HS may significantly limit many everyday activities, for instance, walking, hugging, moving, and sitting down. Sitting disability may occur in patients with lesions in sacral, gluteal, perineal, femoral, groin or genital regions; and prolonged periods of sitting down itself can also worsen the condition of the skin of these patients.The exact cause is usually unclear, but believed to involve a combination of genetic and environmental factors. About a third of people with the disease have an affected family member. Other risk factors include obesity and smoking. The condition is not caused by an infection, poor hygiene, or the use of deodorant. Instead, it is believed to be caused by hair follicles being obstructed, with the nearby apocrine sweat glands being strongly implicated in this obstruction. The sweat glands themselves may or may not be inflamed. Diagnosis is based on the symptoms.No cure is known. Warm baths may be tried in those with mild disease. Cutting open the lesions to allow them to drain does not result in significant benefit. While antibiotics are commonly used, evidence for their use is poor. Immunosuppressive medication may also be tried. In those with more severe disease, laser therapy or surgery to remove the affected skin may be viable. Rarely, a skin lesion may develop into skin cancer.If mild cases of HS are included, then the estimate of its frequency is from 1–4% of the population. Women are three times more likely to be diagnosed with it than men. Onset is typically in young adulthood and may become less common after 50 years old. It was first described between 1833 and 1839 by French anatomist Alfred Velpeau. Causes The exact cause of hidradenitis suppurativa remains unknown, and there has, in the recent past, been notable disagreement among experts in this regard. The condition, however, likely stems from both genetic and environmental causes. Specifically, an immune-mediated pathology has been proposed, although there have been sources that have already contradicted the probable likelihood of such an idea.Lesions will occur in any body areas with hair follicles, although areas such as the axilla, groin, and perineal region are more commonly involved. This theory includes most of these potential indicators: Post-pubescent individuals Blocked hair follicles or blocked apocrine sweat glands Excessive sweating Androgen dysfunction Genetic disorders that alter cell structure Patients with more advanced cases may find exercise intolerably painful, which may increase their rate of obesity.The historical understanding of the disease suggests dysfunctional apocrine glands or dysfunctional hair follicles, possibly triggered by a blocked gland, which creates inflammation, pain, and a swollen lesion. Triggering factors Several triggering factors should be taken into consideration: Obesity is an exacerbating rather than a triggering factor, through mechanical irritation, occlusion, and skin maceration. Tight clothing, and clothing made of heavy, nonbreathable materials Deodorants, depilation products, shaving of the affected area – their association with HS is still an ongoing debate among researchers. Drugs, in particular oral contraceptive pills and lithium. Hot and especially humid climates. Predisposing factors Genetic factors: an autosomal dominant inheritance pattern has been proposed. Endocrine factors: sex hormones, especially an excess of androgens, are thought to be involved, although the apocrine glands are not sensitive to these hormones. Women often have outbreaks before their menstrual period and after pregnancy; HS severity usually decreases during pregnancy and after menopause.Some cases have been found to result from mutations in the NCSTN, PSEN1, or PSENEN genes. The genes produce proteins that are all components of a complex called gamma- (γ-) secretase. This complex cuts apart (cleaves) many different proteins, which is an important step in several chemical signaling pathways. One of these pathways, known as notch signaling, is essential for the normal maturation and division of hair follicle cells and other types of skin cells. Notch signaling is also involved in normal immune system function. Studies suggest that mutations in the NCSTN, PSEN1, or PSENEN gene impair notch signaling in hair follicles. Although little is known about the mechanism, abnormal notch signaling appears to promote the development of nodules and to lead to inflammation in the skin. In addition, the composition of the intestinal microflora and as a consequence dietary patterns appear to play a role. Although dysbiosis of the cutaneous microbiome apparent in HS is not observed, the concurrent existence of inflammatory gut and skin diseases has led to the postulation of a gut-skin axis in which gut microbiota is implicated. Indeed, analysis of bacterial taxa in fecal samples from HS patients support the possibility of a role for intestinal microbial alterations in this chronic inflammatory skin disease. Diagnosis Stages Hidradenitis suppurativa presents itself in three stages. Due to the large spectrum of clinical severity and the severe impact on quality of life, a reliable method for evaluating HS severity is needed. Hurleys staging system Hurleys staging system was the first classification system proposed, and is still in use for the classification of patients with skin diseases (i.e., psoriasis, HS, acne). Hurley separated patients into three groups based largely on the presence and extent of cicatrization and sinuses. It has been used as a basis for clinical trials in the past and is a useful basis to approach therapy for patients. These three stages are based on Hurleys staging system, which is simple and relies on the subjective extent of the diseased tissue the patient has. Hurleys three stages of hidradenitis suppurativa are: Sartorius staging system The Sartorius staging system is more sophisticated than Hurleys. Sartorius et al. suggested that the Hurley system is not sophisticated enough to assess treatment effects in clinical trials during research. This classification allows for better dynamic monitoring of the disease severity in individual patients. The elements of this staging system are: Anatomic regions involved (axilla, groin gluteal, or other region or inframammary region left or right) Number and types of lesions involved (abscesses, nodules, fistulas or sinuses, scars, points for lesions of all regions involved) The distance between lesions, in particular the longest distance between two relevant lesions (i.e., nodules and fistulas in each region or size if only one lesion present) The presence of normal skin in between lesions (i.e., if all lesions are clearly separated by normal skin)Points are accumulated in each of the above categories, and added to give both a regional and total score. In addition, the authors recommend adding a visual analog scale for pain or using the dermatology life quality index (DLQI, or the skindex) when assessing HS. Treatment Treatment depends upon presentation and severity of the disease. Due to the poorly studied nature of the disease, the effectiveness of the drugs and therapies listed below is unclear. Possible treatments include the following: Lifestyle Warm baths may be tried in those with mild disease. Weight loss and the cessation of smoking are also recommended. Medication Antibiotics: taken by mouth, these are used for their anti-inflammatory properties rather than to treat infection. Most effective is a combination of rifampicin and clindamycin given concurrently for 2–3 months. Popular antibiotics also include tetracycline and minocycline. Topical clindamycin has been shown to have an effect in double-blind placebo controlled studies. Corticosteroid injections, also known as intralesional steroids, can be particularly useful for localized disease, if the drug can be prevented from escaping via the sinuses. Antiandrogen therapy, hormonal therapy with antiandrogenic medications such as spironolactone, flutamide, cyproterone acetate, ethinylestradiol, finasteride, dutasteride, and metformin, have been found to be effective in clinical studies. However, the quality of available evidence is low and does not presently allow for robust evidence-based recommendations. Intravenous infusion or subcutaneous injection of anti-inflammatory (TNF inhibitors; anti-TNF-alpha) drugs such as infliximab, and etanercept This use of these drugs is not currently Food and Drug Administration (FDA) approved and is somewhat controversial, so may not be covered by insurance. TNF inhibitor: Studies have supported that various TNF inhibitors have a positive effect on HS lesions. Specifically adalimumab at weekly intervals is useful. Adalimumab is the only medication approved by the FDA for the treatment of HS as of 2021. Topical isotretinoin is usually ineffective in people with HS, and is more commonly known as a medication for the treatment of acne vulgaris. Individuals affected by HS who responded to isotretinoin treatment tended to have milder cases of the condition. Surgery When the process becomes chronic, wide surgical excision is the procedure of choice. Wounds in the affected area do not heal by secondary intention, and immediate or delayed application of a split-thickness skin graft is an option. Another option is covering the defect with a perforator flap. With this technique, the (mostly totally excised) defect is covered with tissue from an area nearby. For example, the axilla with a fully excised defect of 15 × 7 cm can be covered with a thoracodorsal artery perforator flap. Laser hair removal The 1064-nm wavelength laser for hair removal may aid in the treatment of HS. A randomized control study has shown improvement in HS lesions with the use of an Nd:YAG laser. Prognosis In stage III disease, as classified by the Hurleys staging system, fistulae left undiscovered, undiagnosed, or untreated, can rarely lead to the development of squamous cell carcinoma in the anus or other affected areas. Other stage III chronic sequelae may also include anemia, multilocalized infections, amyloidosis, and arthropathy. Stage III complications have been known to lead to sepsis, but clinical data are still uncertain. Potential complications Contractures and reduced mobility of the lower limbs and axillae due to fibrosis and scarring occur. Severe lymphedema may develop in the lower limbs. Local and systemic infections (meningitis, bronchitis, pneumonia, etc.), are seen, which may even progress to sepsis. Interstitial keratitis Anal, rectal, or urethral fistulae Normochromic or hypochromic anemia People with HS may be at increased risk for autoimmune disorders including ankylosing spondylitis, rheumatoid arthritis, and psoriatic arthritis. Squamous cell carcinoma has been found on rare occasions in chronic hidradenitis suppurativa of the anogenital region. The mean time to the onset of this type of lesion is 10 years or more and the tumors are usually highly aggressive. Tumors of the lung and oral cavity, and liver cancer Hypoproteinemia and amyloidosis, which can lead to kidney failure and death Seronegative and usually asymmetric arthropathy: pauciarticular arthritis, polyarthritis/polyarthralgia syndrome History From 1833 to 1839, in a series of three publications, Velpeau identified and described a disease now known as hidradenitis suppurativa. In 1854, Verneuil described hidradenitis suppurativa as hidrosadénite Phlegmoneuse. This is how HS obtained its alternate name "Verneuils disease". In 1922, Schiefferdecker hypothesized a pathogenic link between "acne inversa" and human sweat glands. In 1956, Pillsbury et al. coined the term follicular occlusion triad for the common association of hidradenitis suppurativa, acne conglobata and dissecting cellulitis of the scalp. Modern clinical research still employs Pillsburys terminology for these conditions descriptions. In 1975, Plewig and Kligman, following Pillsburys research path, modified the "acne triad", replacing it with the "acne tetrad: acne triad, plus pilonidal sinus". Plewig and Kligmans research follows in Pillsburys footsteps, offering explanations of the symptoms associated with hidradenitis suppurativa. In 1989, Plewig and Stegers research led them to rename hidradenitis suppurativa, calling it "acne inversa" – which is not still used today in medical terminology, although some individuals still use this outdated term.A surgeon from Paris, Velpeau described an unusual inflammatory process with formation of superficial axillary, submammary, and perianal abscesses, in a series of three publications from 1833 to 1839. One of his colleagues, also located in Paris, named Verneuil, coined the term hidrosadénite phlegmoneuse about 15 years later. This name for the disease reflects the former pathogenetic model of acne inversa, which is considered inflammation of sweat glands as the primary cause of hidradenitis suppurativa. In 1922, Schiefferdecker suspected a pathogenic association between acne inversa and apocrine sweat glands. In 1956, Pillsbury postulated follicular occlusion as the cause of acne inversa, which they grouped together with acne conglobata and perifolliculitis capitis abscendens et suffodiens ("dissecting cellulitis of the scalp") as the "acne triad". Plewig and Kligman added another element to their acne triad, pilonidal sinus. Plewig et al. noted that this new "acne tetrad" includes all the elements found in the original "acne triad", in addition to a fourth element, pilonidal sinus. In 1989, Plewig and Steger introduced the term "acne inversa", indicating a follicular source of the disease and replacing older terms such as "Verneuil disease". Other names Hidradenitis suppurativa has been referred to by multiple names in the literature, as well as in various cultures. Some of these are also used to describe different diseases, or specific instances of this disease. Acne conglobata – not really a synonym – this is a similar process, but in classic acne areas of chest and back Acne inversa – a proposed new term which has not gained widespread favor. Apocrine acne – an outdated term based on the disproven concept that apocrine glands are primarily involved, though many do have apocrine gland infection Apocrinitis – another outdated term based on the same thesis Fox-den disease – a term not used in medical literature, based on the deep fox den–like sinuses Hidradenitis supportiva – a misspelling Pyodermia fistulans significa – now considered archaic Verneuils disease – recognizing the surgeon whose name is most often associated with the disorder as a result of his 1854–1865 studies Histology Terminology Although hidradenitis suppurativa is often referred to as acne inversa, it is not a form of acne, and lacks the core defining features of acne such as the presence of closed comedones and increased sebum production. References External links Medline: What is Hidradenitis Suppurativa? Hidradenitis Suppurativa (2004) Prof J. Revuz Archived 28 February 2005 at the Wayback Machine

Aarogya what is Urinary incontinence

Urinary incontinence

Urinary incontinence (UI), also known as involuntary urination, is any uncontrolled leakage of urine. It is a common and distressing problem, which may have a large impact on quality of life. It has been identified as an important issue in geriatric health care. The term enuresis is often used to refer to urinary incontinence primarily in children, such as nocturnal enuresis (bed wetting). UI is an example of a stigmatized medical condition, which creates barriers to successful management and makes the problem worse. People may be too embarrassed to seek medical help, and attempt to self-manage the symptom in secrecy from others. Pelvic surgery, pregnancy, childbirth, and menopause are major risk factors. Urinary incontinence is often a result of an underlying medical condition but is under-reported to medical practitioners. There are four main types of incontinence: Urge incontinence due to an overactive bladder Stress incontinence due to "a poorly functioning urethral sphincter muscle (intrinsic sphincter deficiency) or to hypermobility of the bladder neck or urethra" Overflow incontinence due to either poor bladder contraction or blockage of the urethra Mixed incontinence involving features of different other typesTreatments include pelvic floor muscle training, bladder training, surgery, and electrical stimulation. Behavioral therapy generally works better than medication for stress and urge incontinence. The benefit of medications is small and long term safety is unclear. Urinary incontinence is more common in older women. Causes Urinary incontinence can result from both urologic and non-urologic causes. Urologic causes can be classified as either bladder dysfunction or urethral sphincter incompetence and may include detrusor overactivity, poor bladder compliance, urethral hypermobility, or intrinsic sphincter deficiency. Non-urologic causes may include infection, medication or drugs, psychological factors, polyuria, hydrocephalus, stool impaction, and restricted mobility. The causes leading to urinary incontinence are usually specific to each sex, however, some causes are common to both men and women. Women The most common types of urinary incontinence in women are stress urinary incontinence and urge urinary incontinence. Women that have symptoms of both types are said to have "mixed" urinary incontinence. After menopause, estrogen production decreases and, in some women, urethral tissue will demonstrate atrophy, becoming weaker and thinner, possibly playing a role in the development of urinary incontinence.Stress urinary incontinence in women is most commonly caused by loss of support of the urethra, which is usually a consequence of damage to pelvic support structures as a result of pregnancy, childbirth, obesity, age, among others. About 33% of all women experience urinary incontinence after giving birth, and women who deliver vaginally are about twice as likely to have urinary incontinence as women who give birth via a Caesarean section. Stress incontinence is characterized by leaking of small amounts of urine with activities that increase abdominal pressure such as coughing, sneezing, laughing and lifting. This happens when the urethral sphincter cannot close completely due to the damage in the sphincter itself, or the surrounding tissue. Additionally, frequent exercise in high-impact activities can cause athletic incontinence to develop. Urge urinary incontinence, is caused by uninhibited contractions of the detrusor muscle, a condition known as overactive bladder syndrome. It is characterized by leaking of large amounts of urine in association with insufficient warning to get to the bathroom in time. Men Urge incontinence is the most common type of incontinence in men. Similar to women, urine leakage happens following a very intense feeling of urination, not allowing enough time to reach the bathroom, a condition called overactive bladder syndrome. In men, the condition is commonly associated with benign prostatic hyperplasia (an enlarged prostate), which causes bladder outlet obstruction, a dysfunction of the detrusor muscle (muscle of the bladder), eventually causing overactive bladder syndrome, and the associated incontinence.Stress urinary incontinence is the other common type of incontinence in men, and it most commonly happens after prostate surgery. Prostatectomy, transurethral resection of the prostate, prostate brachytherapy, and radiotherapy can all damage the urethral sphincter and surrounding tissue, causing it to be incompetent. An incompetent urethral sphincter cannot prevent the urine from leaking out of the urinary bladder during activities that increase the intraabdominal pressure, such as coughing, sneezing, or laughing. Continence usually improves within 6 to 12 months after prostate surgery without any specific interventions, and only 5 to 10% of people report persistent symptoms. Both Age is a risk factor that increases both the severity and prevalence of UI Polyuria (excessive urine production) of which, in turn, the most frequent causes are: uncontrolled diabetes mellitus, primary polydipsia (excessive fluid drinking), central diabetes insipidus and nephrogenic diabetes insipidus. Polyuria generally causes urinary urgency and frequency, but does not necessarily lead to incontinence. Neurogenic disorders like multiple sclerosis, spina bifida, Parkinsons disease, strokes and spinal cord injury can all interfere with nerve function of the bladder. This can lead to neurogenic bladder dysfunction Overactive bladder syndrome. However, the etiology behind this is usually different between men and women, as mentioned above. Other suggested risk factors include smoking, caffeine intake and depression Mechanism Adults The body stores urine — water and wastes removed by the kidneys — in the urinary bladder, a balloon-like organ. The bladder connects to the urethra, the tube through which urine leaves the body.Continence and micturition involve a balance between urethral closure and detrusor muscle activity (the muscle of the bladder). During urination, detrusor muscles in the wall of the bladder contract, forcing urine out of the bladder and into the urethra. At the same time, sphincter muscles surrounding the urethra relax, letting urine pass out of the body. The urethral sphincter is the muscular ring that closes the outlet of the urinary bladder preventing urine to pass outside the body. Urethral pressure normally exceeds bladder pressure, resulting in urine remaining in the bladder, and maintaining continence. The urethra is supported by pelvic floor muscles and tissue, allowing it to close firmly. Any damage to this balance between the detrusor muscle, urethral sphincter, supportive tissue and nerves can lead to some type of incontinence .For example, stress urinary incontinence is usually a result of the incompetent closure of the urethral sphincter. This can be caused by damage to the sphincter itself, the muscles that support it, or nerves that supply it. In men, the damage usually happens after prostate surgery or radiation, and in women, its usually caused by childbirth and pregnancy. The pressure inside the abdomen (from coughing and sneezing) is normally transmitted to both urethra and bladder equally, leaving the pressure difference unchanged, resulting in continence. When the sphincter is incompetent, this increase in pressure will push the urine against it, leading to incontinence.Another example is urge incontinence. This incontinence is associated with sudden forceful contractions of the detrusor muscle (bladder muscle), leading to an intense feeling of urination, and incontinence if the person does not reach the bathroom on time. The syndrome is known as overactive bladder syndrome, and its related to dysfunction of the detrusor muscle. Children Urination, or voiding, is a complex activity. The bladder is a balloon-like muscle that lies in the lowest part of the abdomen. The bladder stores urine then releases it through the urethra, the canal that carries urine to the outside of the body. Controlling this activity involves nerves, muscles, the spinal cord and the brain.The bladder is made of two types of muscles: the detrusor, a muscular sac that stores urine and squeezes to empty, and the sphincter, a circular group of muscles at the bottom or neck of the bladder that automatically stays contracted to hold the urine in and automatically relax when the detrusor contracts to let the urine into the urethra. A third group of muscles below the bladder (pelvic floor muscles) can contract to keep urine back.A babys bladder fills to a set point, then automatically contracts and empties. As the child gets older, the nervous system develops. The childs brain begins to get messages from the filling bladder and begins to send messages to the bladder to keep it from automatically emptying until the child decides it is the time and place to void.Failures in this control mechanism result in incontinence. Reasons for this failure range from the simple to the complex. Diagnosis The pattern of voiding and urine leakage is important as it suggests the type of incontinence. Other points include straining and discomfort, use of drugs, recent surgery, and illness.The physical examination looks for signs of medical conditions causing incontinence, such as tumors that block the urinary tract, stool impaction, and poor reflexes or sensations, which may be evidence of a nerve-related cause.Other tests include: Stress test – the patient relaxes, then coughs vigorously as the doctor watches for loss of urine. Urinalysis – urine is tested for evidence of infection, urinary stones, or other contributing causes. Blood tests – blood is taken, sent to a laboratory, and examined for substances related to causes of incontinence. Ultrasound – sound waves are used to visualize the kidneys and urinary bladder, assess the capacity of the bladder before voiding, and the remaining amount of urine after voiding. This helps know if theres a problem in emptying. Cystoscopy – a thin tube with a tiny camera is inserted in the urethra and used to see the inside of the urethra and bladder. Urodynamics – various techniques measure pressure in the bladder and the flow of urine.People are often asked to keep a diary for a day or more, up to a week, to record the pattern of voiding, noting times and the amounts of urine produced. Research projects that assess the efficacy of anti-incontinence therapies often quantify the extent of urinary incontinence. The methods include the 1-h pad test, measuring leakage volume; using a voiding diary, counting the number of incontinence episodes (leakage episodes) per day; and assessing of the strength of pelvic floor muscles, measuring the maximum vaginal squeeze pressure. Main types There are 4 main types of urinary incontinence: Stress incontinence, also known as effort incontinence, is essentially due to incomplete closure of the urinary sphincter, due to problems in the sphincter itself or insufficient strength of the pelvic floor muscles supporting it. This type of incontinence is when urine leaks during activities that increase intra-abdominal pressure, such as coughing, sneezing or bearing down. Urge incontinence is an involuntary loss of urine occurring while suddenly feeling the need or urge to urinate, usually secondary to overactive bladder syndrome. Overflow incontinence is the incontinence that happens suddenly without feeling an urge to urinate and without necessarily doing any physical activities. It is also known as under-active bladder syndrome. This usually happens with chronic obstruction of the bladder outlet or with diseases damaging the nerves supplying the urinary bladder. The urine stretches the bladder without the person feeling the pressure, and eventually, it overwhelms the ability of the urethral sphincter to hold it back. Mixed incontinence contains symptoms of multiple other types of incontinence. It is not uncommon in the elderly female population and can sometimes be complicated by urinary retention. Other types Functional incontinence occurs when a person recognizes the need to urinate but cannot make it to the bathroom. The loss of urine may be large. There are several causes of functional incontinence including confusion, dementia, poor eyesight, mobility or dexterity, unwillingness to the toilet because of depression or anxiety or inebriation due to alcohol. Functional incontinence can also occur in certain circumstances where no biological or medical problem is present. For example, a person may recognize the need to urinate but may be in a situation where there is no toilet nearby or access to a toilet is restricted. Structural incontinence: Rarely, structural problems can cause incontinence, usually diagnosed in childhood (for example, an ectopic ureter). Fistulas caused by obstetric and gynecologic trauma or injury are commonly known as obstetric fistulas and can lead to incontinence. These types of vaginal fistulas include, most commonly, vesicovaginal fistula and, more rarely, ureterovaginal fistula. These may be difficult to diagnose. The use of standard techniques along with a vaginogram or radiologically viewing the vaginal vault with instillation of contrast media. Nocturnal enuresis is episodic UI while asleep. It is normal in young children. Transient incontinence is temporary incontinence most often seen in pregnant women when it subsequently resolves after the birth of the child. Giggle incontinence is an involuntary response to laughter. It usually affects children. Double incontinence. There is also a related condition for defecation known as fecal incontinence. Due to involvement of the same muscle group (levator ani) in bladder and bowel continence, patients with urinary incontinence are more likely to have fecal incontinence in addition. This is sometimes termed "double incontinence". Post-void dribbling is the phenomenon where urine remaining in the urethra after voiding the bladder slowly leaks out after urination. Coital incontinence (CI) is urinary leakage that occurs during either penetration or orgasm and can occur with a sexual partner or with masturbation. It has been reported to occur in 10% to 24% of sexually active women with pelvic floor disorders. Climacturia is urinary incontinence at the moment of orgasm. It can be a result of radical prostatectomy. Screening Yearly screening is recommended for women by the Womens Preventive Services Initiative. Screening questions should inquire about what symptoms they have experienced, how severe the symptoms are, and if the symptoms affect their daily lives. As of 2018, studies have not shown a change in outcomes with urinary incontinence screenings in women. Management Treatment options range from conservative treatment, behavioral therapy, bladder retraining, pelvic floor therapy, collecting devices (for men), fixer-occluder devices for incontinence (in men), medications and surgery. A 2018 systematic review update showed that both nonpharmacological and pharmacological treatments are effective for treating UI in non-pregnant women. All treatments, except hormones and periurethral bulking agents, are more effective than no treatment in improving or curing UI symptoms or achieving patient satisfaction. The success of treatment depends on the correct diagnoses. Behavioral therapy Behavioral therapy involves the use of both suppressive techniques (distraction, relaxation) and learning to avoid foods that may worsen urinary incontinence. This may involve avoiding or limiting consumption of caffeine and alcohol. Behavioral therapies, including bladder training, biofeedback, and pelvic floor muscle training, are most effective for improving urinary incontinence in women, with a low risk of adverse events. Behavioral therapy is not curative for urinary incontinence, but it can improve a persons quality of life. Behavioral therapy has benefits as both a monotherapy and as an adjunct to medications for symptom reduction.Avoiding heavy lifting and preventing constipation may help with uncontrollable urine leakage. Stopping smoking is also recommended as it is associated with improvements in urinary incontinence in men and women. Weight loss is recommended in those who are obese. Physical therapy and exercise Physical therapy can be effective for women in reducing urinary incontinence.Pelvic floor physical therapists work with patients to identify and treat underlying pelvic muscle dysfunction that can cease urinary incontinence. They may recommend exercises to strengthen the muscles, electrostimulation, or biofeedback treatments. Exercising the muscles of the pelvis such as with Kegel exercises are a first line treatment for women with stress incontinence. Efforts to increase the time between urination, known as bladder training, is recommended in those with urge incontinence. Both these may be used in those with mixed incontinence.Small vaginal cones of increasing weight may be used to help with exercise. They seem to be better than no active treatment in women with stress urinary incontinence, and have similar effects to training of pelvic floor muscles or electrostimulation.Biofeedback uses measuring devices to help the patient become aware of his or her bodys functioning. By using electronic devices or diaries to track when the bladder and urethral muscles contract, the patient can gain control over these muscles. Biofeedback can be used with pelvic muscle exercises and electrical stimulation to relieve stress and urge incontinence.Time voiding while urinating and bladder training are techniques that use biofeedback. In time voiding, the patient fills in a chart of voiding and leaking. From the patterns that appear in the chart, the patient can plan to empty his or her bladder before he or she would otherwise leak. Biofeedback and muscle conditioning, known as bladder training, can alter the bladders schedule for storing and emptying urine. These techniques are effective for urge and overflow incontinenceA 2013 randomized controlled trial found no benefit of adding biofeedback to pelvic floor muscle exercise in stress urinary incontinence, but observing improvements in both groups. In another randomized controlled trial the addition of biofeedback to the training of pelvic floor muscles for the treatment of stress incontinence, improved pelvic floor muscle function, reduced urinary symptoms, and improved the quality of life.Preoperative pelvic floor muscle training (PFMT) in men undergoing radical prostatectomy was not effective in reducing urinary incontinence.Alternative exercises have been studied for stress urinary incontinence in women. Evidence was insufficient to support the use of Paula method, abdominal muscle training, Pilates, Tai Chi, breathing exercises, postural training, and generalized fitness. Devices Individuals who continue to experience urinary incontinence need to find a management solution that matches their individual situation. The use of mechanical devices has not been well studied in women, as of 2014. Collecting systems (for men) – consists of a sheath worn over the penis funneling the urine into a urine bag worn on the leg. These products come in a variety of materials and sizes for individual fit. Studies show that urisheaths and urine bags are preferred over absorbent products – in particular when it comes to ‘limitations to daily activities’. Solutions exist for all levels of incontinence. Advantages with collecting systems are that they are discreet, the skin stays dry all the time, and they are convenient to use both day and night. Disadvantages are that it is necessary to get measured to ensure proper fit, and in some countries, a prescription is needed. Absorbent products (include shields, incontinence pads, undergarments, protective underwear, briefs, diapers, adult diapers and underpants) are the best-known product types to manage incontinence. They are widely available in pharmacies and supermarkets. The advantages of using these are that they barely need any fitting or introduction by a healthcare specialist. The disadvantages with absorbent products are that they can be bulky, leak, have odors and can cause skin breakdown due to the constant dampness. Intermittent catheters are single-use catheters that are inserted into the bladder to empty it, and once the bladder is empty they are removed and discarded. Intermittent catheters are primarily used for urinary retention (inability to empty the bladder), but for some people they can be used to reduce or avoid incontinence. These are prescription-only medical devices. Indwelling catheters (also known as foleys) are often used in hospital settings, or if the user is not able to handle any of the above solutions himself/herself (e.g. severe neurologic injury or neurodegenerative disease). These are also prescription-only medical devices. The indwelling catheter is typically connected to a urine bag that can be worn on the leg or hung on the side of the bed. Indwelling catheters need to be monitored and changed on a regular basis by a healthcare professional. The advantage of indwelling catheters is that because the urine is funneled away from the body, the skin remains dry. However, the disadvantage is that it is very common to incur urinary tract infections when using indwelling catheters. Bladder spasms and other problems can also occur with long-term use of indwelling catheters. Penis clamp (or penis compression device), which is applied to compress the urethra to compensate for the malfunctioning of the natural urinary sphincter, preventing leakage from the bladder. This management solution is only suitable for light or moderate incontinence. Vaginal pessaries for women are devices inserted into the vagina. This device provides support to the urethra which passes right in front of it, allowing it to close more firmly. Medications A number of medications exist to treat urinary incontinence including: fesoterodine, tolterodine and oxybutynin. These medications work by relaxing smooth muscle in the bladder. While some of these medications appear to have a small benefit, the risk of side effects are a concern. Medications are effective for about one in ten people, and all medications have similar efficacy.Medications are not recommended for those with stress incontinence and are only recommended in those with urge incontinence who do not improve with bladder training.Injectable bulking agents may be used to enhance urethral support, however, they are of unclear benefit. Surgery Women and men that have persistent incontinence despite optimal conservative therapy may be candidates for surgery. Surgery may be used to help stress or overflow incontinence. Common surgical techniques for stress incontinence include slings, tension-free vaginal tape, bladder suspension, artificial urinary sphincters, among others.The use of transvaginal mesh implants and bladder slings is controversial due to the risk of debilitating painful side effects such as vaginal erosion. In 2012 transvaginal mesh implants were classified as a high risk device by the US Food and Drug Administration. Urodynamic testing seems to confirm that surgical restoration of vault prolapse can cure motor urge incontinence. Traditional suburethral sling operations are probably slightly better than open abdominal retropubic colposuspension and are probably slightly less effective than mid-urethral sling operations in reducing urinary incontinence in women, but it is still uncertain if any of the different types of traditional suburethral sling operations are better than others. Similarly, there is insufficient evidence to be certain about the effectiveness or safety of single-incision sling operations for urinary incontinence in women. Traditional suburethral slings may have a higher risk of surgical complications than minimally invasive slings but the risk of complications compared with other types of operation is still uncertain.Laparoscopic colposuspension (keyhole surgery through the abdomen) with sutures is as effective as open colposuspension for curing incontinence in women up to 18 months after surgery, but it is unclear whether there are fewer risk of complications during or after surgery. There is probably a higher risk of complications with traditional suburethral slings than with open abdominal retropubic suspension. The artificial urinary sphincter is an implantable device used to treat stress incontinence, mostly in men. The device is made of 2 or 3 parts: The pump, cuff, and balloon reservoir connected to each other by specialized tubes. The cuff wraps around the urethra and closes it. When the person wants to urinate, he presses the pump (implanted in the scrotum), to deflate the cuff, and allow the urine to pass. The cuff regains pressure within a few minutes to regain continence. The European Association of Urology considers the artificial urinary sphincter as the gold standard in surgical management of stress urinary incontinence in men after prostatectomy. Epidemiology Globally, up to 35% of the population over the age of 60 years is estimated to be incontinent. In 2014, urinary leakage affected between 30% and 40% of people over 65 years of age living in their own homes or apartments in the U.S. Twenty-four percent of older adults in the U.S. have moderate or severe urinary incontinence that should be treated medically. People with dementia are three times more likely to have urinary incontinence compared to people of similar ages.Bladder control problems have been found to be associated with higher incidence of many other health problems such as obesity and diabetes. Difficulty with bladder control results in higher rates of depression and limited activity levels.Incontinence is expensive both to individuals in the form of bladder control products and to the health care system and nursing home industry. Injury-related to incontinence is a leading cause of admission to assisted living and nursing care facilities. In 1997 more than 50% of nursing facility admissions were related to incontinence. Women Bladder symptoms affect women of all ages. However, bladder problems are most prevalent among older women. Women over the age of 60 years are twice as likely as men to experience incontinence; one in three women over the age of 60 years are estimated to have bladder control problems. One reason why women are more affected is the weakening of pelvic floor muscles by pregnancy. Men Men tend to experience incontinence less often than women, and the structure of the male urinary tract accounts for this difference. Stress incontinence is common after prostate cancer treatments.While urinary incontinence affects older men more often than younger men, the onset of incontinence can happen at any age. Estimates around 2007 suggested that 17 percent of men over age 60, an estimated 600,000 men in the US, experienced urinary incontinence, with this percentage increasing with age. Children Incontinence happens less often after age 5: About 10 percent of 5-year-olds, 5 percent of 10-year-olds, and 1 percent of 18-year-olds experience episodes of incontinence. It is twice as common in girls as in boys. History The management of urinary incontinence with pads is mentioned in the earliest medical book known, the Ebers Papyrus (1500 BC).Incontinence has historically been a taboo subject in Western culture. However, this situation changed some when Kimberly-Clark aggressively marketed adult diapers in the 1980s with actor June Allyson as spokeswoman. Allyson was initially reticent to participate, but her mother, who had incontinence, convinced her that it was her duty in light of her successful career. The product proved a success. Law The case Hiltibran et al v. Levy et al in the United States District Court for the Western District of Missouri resulted in that court issuing an order in 2011. That order requires incontinence briefs funded by Medicaid to be given by Missouri to adults who would be institutionalized without them. Research The effectiveness of different therapeutic approaches to treating urinary incontinence is not well studied for some medical conditions. For example, for people who experience urinary incontinence due to stroke, treatment approaches such as physical therapy, cognitive therapy, complementary medicine, and specialized interventions with experienced medical professionals are sometimes suggested, however it is not clear how effective these are at improving incontinence and there is no strong medical evidence to guide clinical practice. References External links Urinary incontinence at Curlie Patient-centered information from the European Urological Association Independent continence product advisor

Hello Aarogya , Do you know what is Hypovolemia,

Hypovolemia

Hypovolemia, also known as volume depletion or volume contraction, is a state of abnormally low extracellular fluid in the body. This may be due to either a loss of both salt and water or a decrease in blood volume. Hypovolemia refers to the loss of extracellular fluid and should not be confused with dehydration.Hypovolemia is caused by a variety of events, but these can be simplified into two categories: those that are associated with kidney function and those that are not. The signs and symptoms of hypovolemia worsen as the amount of fluid lost increases. Immediately or shortly after mild fluid loss (from blood donation, diarrhea, vomiting, bleeding from trauma, etc.), one may experience headache, fatigue, weakness, dizziness, or thirst. Untreated hypovolemia or excessive and rapid losses of volume may lead to hypovolemic shock. Signs and symptoms of hypovolemic shock include increased heart rate, low blood pressure, pale or cold skin, and altered mental status. When these signs are seen, immediate action should be taken to restore the lost volume. Signs and symptoms Signs and symptoms of hypovolemia progress with increased loss of fluid volume.Early symptoms of hypovolemia include headache, fatigue, weakness, thirst, and dizziness. The more severe signs and symptoms are often associated with hypovolemic shock. These include oliguria, cyanosis, abdominal and chest pain, hypotension, tachycardia, cold hands and feet, and progressively altering mental status. Causes The causes of hypovolemia can be characterized into two categories: Kidney Loss of body sodium and consequent intravascular water (due to impaired reabsorption of salt and water in the tubules of the kidneys) Osmotic diuresis: the increase in urine production due to an excess of osmotic (namely glucose and urea) load in the tubules of the kidneys Overuse of pharmacologic diuretics Impaired response to hormones controlling salt and water balance (see mineralocorticoids) Impaired kidney function due to tubular injury or other diseases Other Loss of bodily fluids due to:Gastrointestinal losses; e.g. vomiting and diarrhea Skin losses; e.g. excessive sweating and burns Respiratory losses; e.g. hyperventilation (breathing fast) Build up of fluid in empty spaces (third spaces) of the body due to:Acute pancreatitis Intestinal obstruction Increase in vascular permeability Hypoalbuminemia Loss of blood (external or internal bleeding or blood donation) Pathophysiology The signs and symptoms of hypovolemia are primarily due to the consequences of decreased circulating volume and a subsequent reduction in the amount of blood reaching the tissues of the body. In order to properly perform their functions, tissues require the oxygen transported in the blood. A decrease in circulating volume can lead to a decrease in bloodflow to the brain, resulting in headache and dizziness.Baroreceptors in the body (primarily those located in the carotid sinuses and aortic arch) sense the reduction of circulating fluid and send signals to the brain to increase sympathetic response (see also: baroreflex). This sympathetic response is to release epinephrine and norepinephrine, which results in peripheral vasoconstriction (reducing size of blood vessels) in order to conserve the circulating fluids for organs vital to survival (i.e. brain and heart). Peripheral vasoconstriction accounts for the cold extremities (hands and feet), increased heart rate, increased cardiac output (and associated chest pain). Eventually, there will be less perfusion to the kidneys, resulting in decreased urine output. Diagnosis Hypovolemia can be recognized by a fast heart rate, low blood pressure, and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.In children, compensation can result in an artificially high blood pressure despite hypovolemia (a decrease in blood volume). Children typically are able to compensate (maintain blood pressure despite hypovolemia) for a longer period than adults, but deteriorate rapidly and severely once they are unable to compensate (decompensate). Consequently, any possibility of internal bleeding in children should be treated aggressively.Signs of external bleeding should be assessed, noting that individuals can bleed internally without external blood loss or otherwise apparent signs.There should be considered possible mechanisms of injury that may have caused internal bleeding, such as ruptured or bruised internal organs. If trained to do so and if the situation permits, there should be conducted a secondary survey and checked the chest and abdomen for pain, deformity, guarding, discoloration or swelling. Bleeding into the abdominal cavity can cause the classical bruising patterns of Grey Turners sign (bruising along the sides) or Cullens sign (around the navel). Investigation In a hospital, physicians respond to a case of hypovolemic shock by conducting these investigations: Blood tests: U+Es/Chem7, full blood count, glucose, blood type and screen Central venous catheter Arterial line Urine output measurements (via urinary catheter) Blood pressure SpO2 oxygen saturation monitoring Stages Untreated hypovolemia can lead to shock (see also: hypovolemic shock). Most sources state that there are 4 stages of hypovolemia and subsequent shock; however, a number of other systems exist with as many as 6 stages.The 4 stages are sometimes known as the "Tennis" staging of hypovolemic shock, as the stages of blood loss (under 15% of volume, 15–30% of volume, 30–40% of volume and above 40% of volume) mimic the scores in a game of tennis: 15, 15–30, 30–40 and 40. It is basically the same as used in classifying bleeding by blood loss. The signs and symptoms of the major stages of hypovolemic shock include: Treatment Field care The most important step in treatment of hypovolemic shock is to identify and control the source of bleeding.Medical personnel should immediately supply emergency oxygen to increase efficiency of the patients remaining blood supply. This intervention can be life-saving.Also, the respiratory pump is especially important during hypovolemia as spontaneous breathing may help reduce the effect of this loss of blood pressure on stroke volume by increasing venous return.The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen the way blood does—however, researchers are developing blood substitutes that can. Infusing colloid or crystalloid IV fluids also dilutes clotting factors in the blood, increasing the risk of bleeding. Current best practice allow permissive hypotension in patients with hypovolemic shock, both avoid overly diluting clotting factors and avoid artificially raising blood pressure to a point where it "blows off" clots that have formed. Hospital treatment Fluid replacement is beneficial in hypovolemia of stage 2, and is necessary in stage 3 and 4. See also the discussion of shock and the importance of treating reversible shock while it can still be countered. The following interventions are carried out: IV access Oxygen as required Fresh frozen plasma or blood transfusion Surgical repair at sites of bleedingVasopressors (such as dopamine and noradrenaline) should generally be avoided, as they may result in further tissue ischemia and dont correct the primary problem. Fluids are the preferred choice of therapy. History In cases where loss of blood volume is clearly attributable to bleeding (as opposed to, e.g., dehydration), most medical practitioners prefer the term exsanguination for its greater specificity and descriptiveness, with the effect that the latter term is now more common in the relevant context. See also Hypervolemia Non-pneumatic anti-shock garment Polycythemia, an increase of the hematocrit level, with the "relative polycythemia" being a decrease in the volume of plasma Volume status == References ==

Aarogya what is Slipping

Slipping

Slipping is a technique used in boxing that is similar to bobbing. It is considered one of the four basic defensive strategies, along with blocking, holding, and clinching. It is performed by moving the head to either side so that the opponents punches "slip" by the boxer.Slipping punches allows the fighter to recover quicker and counter punches faster than the opponent can reset into proper fighting stance. In boxing, timing is known to be a key factor in the outcome. Timing your slips correctly is essential in protecting yourself and saving energy. Slipping, if done incorrectly, can be dangerous as it exposes you to a counter-punch and an unbalanced stance. Which can lead to an opening for the opponent. Muhammad Ali is considered to be, pound for pound, one of the greatest fighters of all time. But what made him so lethal? Was it his power, speed, or technique of slipping punches? Many fighters and analysts will say it was his slipping capability. How to slip punches There are multiple ways to slip punches in boxing, but the most basic types are slipping the inside jab, and outside jab. When slipping an outside jab, your body weight needs to be centered. And as your opponent throws the jab, rotate your body clockwise and lean slightly to your right. Which would then shift weight to the rear of your leg. Pivot both your feet in the same direction. Now youre on the outside of your opponents jab which gives the ability to counter punch over their jab. For the inside jab, as the opponent throws the jab, rotate your body counter-clockwise, lean slightly to your left putting more weight on your lead leg. Its possible to just lean without rotating, but rotating helps the movement of your guard. Raise your rear hand ready for the opponent to throw a left hook. Common mistakes There are many different mistakes you can make when trying to slip a punch: Slipping too early Slipping too wide Slipping inside the cross Only moving your head Dropping your guard How to master slipping The best method to mastering slipping is practice. Now just saying practice seems simple. But the practice needs to be with a worthy opponent. Preferably someone that is taller than you and has a longer reach. Another method is a slip bag you can hang up and move back and forth. This helps you improve movement, timing, and eye coordination while performing a slip. Repetition and patience is key to mastering slipping. References External links https://www.mightyfighter.com/how-to-slip-punches/ https://lawofthefist.com/complete-guide-to-slipping-punches-in-boxing/

Aarogya, explain a scenario commonly referred as Maxillary hypoplasia

Maxillary hypoplasia

Maxillary hypoplasia, or maxillary deficiency, is an underdevelopment of the bones of the upper jaw. It is associated with Crouzon syndrome, Angelman syndrome, as well as Fetal alcohol syndrome. It can also be associated with Cleft lip and cleft palate. Some people could develop it due to poor dental extractions. Signs and symptoms The underdevelopment of the bones in the upper jaw, which gives the middle of the face a sunken look. This same underdevelopment can make it difficult to eat and can lead to complications such as Nasopharyngeal airway restriction. This restriction causes forward head posture which can then lead to back pain, neck pain, and numbness in the hands and arms. The nasopharyngeal airway restriction can also lead to Sleep apnea and snoring. Sleep apnea can lead to heart problems, endocrine problems, increased weight, and cognition problems, among other issues. Cause Although the exact genetic link for isolated maxillary hypoplasia has not been identified, the structure of the facial bones as a whole relies on genetic inheritance and therefore there is likely an inheritance pattern. Maxillary hypoplasia can be present as part of genetic syndromes such as Angelman syndrome.Fetal alcohol syndrome is associated with maxillary hypoplasia. Injury to facial bones during childhood can lead to atypical growth. Exposure to Phenytoin in the first trimester of pregnancy has also been associated with the development of maxillary hypoplasia. Pathophysiology Abnormal development of the bones of the upper face which is usually a secondary effect of a different developmental abnormality. When associated with cleft lip and palate, the abnormal development can be due to deficiency in the ability to grow because of the cleft lip or palate. The underdevelopment can also be caused by scarring from surgical repair of a cleft lip or palate. Diagnosis Diagnosed mainly on visual inspection. The cheekbones and nose appear flat with thin lips and the lower jaw appears to be protruding even though it is normal in size. Computed tomography scan CT scan can be performed to compare the size of the Maxilla and Mandible. Computed tomography scan. Treatment Corrective surgery is the most common treatment to correct this disorder. It involves the repositioning of the upper jaw to align with the lower jaw, to provide symmetry. It is best performed during childhood, if possible, to allow the jaw to recover and develop. The surgery may be performed in consultation with an Orthodontist who works on repositioning the teeth in the mouth.Severe cases require surgical correction after completing craniofacial growth around age 17-21.Milder forms without obstruction can be corrected for cosmetic reasons using veneers, snap in smiles, and overlay dentures Prognosis When associated with nasopharyngeal occlusion, the person is more likely to spend their days in forward head posture which may lead to back pain, neck pain and numbness in the arms and hands. It can also lead to sleep apnea and snoring.• People can generally live a relatively normal like with maxillary hypoplasia. Normal life expectancy. Recovery The recovery time after the surgery depends on the extent of the surgery itself. Patients are usually advised to eat soft foods for days, or sometimes weeks, to allow their jaw time to heal. They also require regular checkups with the doctor to monitor bone displacement, signs of infection, or other issues. Epidemiology Maxillary hypoplasia is the most common secondary deformity that results from cleft lip and cleft palate. Because of the subjective nature of the diagnosis, the incidence of maxillary hypoplasia in people with cleft lip and palate varies between 15-50%. It is estimated that 25-50% of these patients require surgical intervention. Research directions Research on the topic of maxillary hypoplasia is currently focused on the best way to treat and manage the disorder. A retrospective study was published in January of 2020 that evaluated the accuracy of virtual surgical planning-assisted management of maxillary hypoplasia. The study found that virtual surgical planning was an acceptable alternative to conventional planning and demonstrated to be very accurate. References == External links ==

Aarogya, Please give me a short description about Non-celiac gluten sensitivity

Non-celiac gluten sensitivity

Non-celiac gluten sensitivity (NCGS) or gluten sensitivity is "a clinical entity induced by the ingestion of gluten leading to intestinal and/or extraintestinal symptoms that improve once the gluten-containing foodstuff is removed from the diet, and celiac disease and wheat allergy have been excluded".NCGS is included in the spectrum of gluten-related disorders. The definition and diagnostic criteria of non-celiac gluten sensitivity were debated and established by three consensus conferences. However, as of 2019, there remained much debate in the scientific community as to whether or not NCGS was a distinct clinical disorder.The pathogenesis of NCGS is not well understood, but the activation of the innate immune system, the direct cytotoxic effects of gluten and probably other wheat components, are implicated. There is evidence that not only gliadin (the main cytotoxic antigen of gluten), but also other proteins named ATIs which are present in gluten-containing cereals (wheat, rye, barley, and their derivatives) may have a role in the development of symptoms. ATIs are potent activators of the innate immune system. FODMAPs, especially fructans, are present in small amounts in gluten-containing grains and have been identified as a possible cause of some gastrointestinal symptoms in NCGS patients. As of 2019, reviews have concluded that although FODMAPs may play a role in NCGS, they explain only certain gastrointestinal symptoms, such as bloating, but not the extra-digestive symptoms that people with NCGS may develop, such as neurological disorders, fibromyalgia, psychological disturbances, and dermatitis.For these reasons, NCGS is a controversial clinical condition and some authors still question it. It has been suggested that "non-celiac wheat sensitivity" is a more appropriate term, without forgetting that other gluten-containing cereals are implicated in the development of symptoms.NCGS is the most common syndrome of gluten-related disorders with prevalence rates between 0.5%–13% in the general population. As no biomarker for diagnosing this condition is available, its diagnosis is made by exclusion of other gluten-related disorders such as celiac disease and wheat allergy. Many people have not been diagnosed following strict criteria, and there is a "fad component" to the recent rise in popularity of the gluten-free diet, leading to debate surrounding the evidence for this condition and its relationship to celiac disease and irritable bowel syndrome. People with NCGS are often unrecognized by specialists and lack adequate medical care and treatment. They often have a long history of health complaints and unsuccessful consultations with physicians, and thus many resort to a gluten-free diet and a self-diagnosis of gluten sensitivity. Signs and symptoms Reported symptoms of NCGS are similar to those of celiac disease, with most patients reporting both gastrointestinal and non-gastrointestinal symptoms. In the "classical" presentation of NCGS, gastrointestinal symptoms are similar to those of irritable bowel syndrome, and are also not distinguishable from those of wheat allergy, but there is a different interval between exposure to wheat and onset of symptoms. Wheat allergy has a fast onset (from minutes to hours) after the consumption of food containing wheat and can be anaphylaxic. Gastrointestinal Gastrointestinal symptoms may include any of the following: abdominal pain, bloating, bowel habit abnormalities (either diarrhea or constipation), nausea, aerophagia, flatulence, gastroesophageal reflux disease, and aphthous stomatitis. Extraintestinal NCGS can cause a wide range of extraintestinal symptoms, which can be the only manifestation of NCGS in absence of gastrointestinal symptoms. These include any of the following: headache, migraine, "foggy mind", fatigue, fibromyalgia, joint and muscle pain, leg or arm numbness, tingling of the extremities, dermatitis (eczema or skin rash), atopic disorders such as asthma, rhinitis, other allergies, depression, anxiety, iron-deficiency anemia, folate deficiency, or autoimmune diseases. NCGS is also linked to a wide spectrum of neurological and psychiatric disorders, including ataxia, schizophrenia, epilepsy, peripheral neuropathy, encephalopathy, vascular dementia, eating disorders, autism, attention deficit hyperactivity disorder (ADHD), hallucinations (so-called "gluten psychosis"), and various movement disorders (restless legs syndrome, chorea, parkinsonism, Tourette syndrome, palatal tremor, myoclonus, dystonia, opsoclonus myoclonus syndrome, paroxysms, dyskinesia, myorhythmia, myokymia).Above 20% of people with NCGS have IgE-mediated allergy to one or more inhalants, foods, or metals, among which most common are mites, graminaceae, parietaria, cat or dog hair, shellfish, and nickel. Approximately 35% of patients suffer other food intolerances, mainly lactose intolerance. Causes The pathogenesis of NCGS is not yet well understood, but the activation of the innate immune system, the direct cytotoxic effects of gluten, and probably the cytotoxicity of other wheat molecules are implicated. Besides gluten, other components in wheat, rye, barley, and their derivatives, including amylasetrypsin inhibitors (ATIs) and FODMAPs, may cause symptoms. Gluten It was hypothesized that gluten, as occurs in celiac disease, is the cause of NCGS. In addition to its ability to elicit abnormal responses of the immune system, in vitro studies on cell cultures showed that gluten is cytotoxic and causes direct intestinal damage. Gluten and gliadin promote cell apoptosis (a form of programmed cell death) and reduce the synthesis of nucleic acids (DNA and RNA) and proteins, leading to a reduction in the viability of cells. Gluten alters cellular morphology and motility, cytoskeleton organization, oxidative balance and intercellular contact (tight junction proteins). Other proteins Some people may have a reaction to other proteins (α-amylase/trypsin inhibitors [ATIs]) present in gluten-containing cereals that are able to inhibit amylase and trypsin. They have been identified as the possible activator of the innate immune system in celiac disease and NCGS.ATIs are part of the plants natural defence against insects and may cause toll-like receptor 4 (TLR4)-mediated intestinal inflammation in humans. These TLR4-stimulating activities of ATIs are limited to gluten-containing cereals (wheat, rye, barley, and derivatives) and may induce innate immunity in people with celiac disease or NCGS. ATIs resist proteolytic digestion. ATIs are about 2%–4% of the total protein in modern wheat and are present in commercial gluten. A 2017 study in mice demonstrated that ATIs exacerbate preexisting inflammation and may also worsen it at extraintestinal sites. This may explain why there is an increase of inflammation in people with preexisting diseases upon ingestion of ATI-containing grains.Modern wheat cultivation, by breeding for high ATI content, may play a role in the onset and course of disorders such as celiac disease and gluten sensitivity. However, it has been questioned whether there is sufficient empirical evidence to support this claim, because as of 2018 we lack studies that directly compare modern wheat versus ancient cultivars with low ATI content (such as einkorn wheat) in people with NCGS.Wheat germ agglutinin is also considered to be a possible trigger of NCGS-like symptoms. FODMAPs FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) that are present in gluten-containing grains (mainly fructans) have been identified as a possible cause of gastrointestinal symptoms in people with NCGS, in place of, or in addition to, gluten.The amount of fructans in gluten-containing cereals is relatively small and their role has been controversial. In rye they account for 3.6%–6.6% of dry matter, 0.7%–2.9% in wheat, and barley contains only trace amounts. They are only minor sources of FODMAPs when eaten in the usual standard amounts in the daily diet. Wheat and rye may comprise a major source of fructans when consumed in large amounts. They may cause mild wheat intolerance at most, limited to certain gastrointestinal symptoms, such as bloating, but do not justify the NCGS extradigestive symptoms. A 2018 review concluded that although fructan intolerance may play a role in NCGS, it only explains some gastrointestinal symptoms, but not the extradigestive symptoms that people with NCGS may develop, such as neurological disorders, fibromyalgia, psychological disturbances, and dermatitis. FODMAPs cause digestive symptoms when the person is hypersensitive to luminal distension. A 2019 review concluded that wheat fructans can cause certain IBS-like symptoms, such as bloating, but are unlikely to cause immune activation or extra-digestive symptoms. Many people with NCGS report resolution of their symptoms after removing gluten-containing cereals while continue to eat fruits and vegetables with high FODMAPs content. Diagnosis Absence of reliable biomarkers and the fact that some people do not have digestive symptoms make the recognition and diagnosis of non-celiac gluten sensitivity (NCGS) difficult.Diagnosis is generally performed only by exclusion criteria. NCGS diagnostic recommendations have been established by several consensus conferences. Exclusion of celiac disease and wheat allergy is important because these two conditions also appear in people who experience symptoms similar to those of NCGS, which improve with a gluten withdrawal and worsen after gluten consumption.The onset of NCGS symptoms may be delayed hours to a few days after gluten ingestion, whereas in celiac disease it can take days to weeks. Wheat allergy has a fast onset (from minutes to hours) after the consumption of food containing wheat and can lead to anaphylaxis.The presence of related extraintestinal manifestations has been suggested to be a feature of NCGS. When symptoms are limited to gastrointestinal effects, there may be an overlap with wheat allergy, irritable bowel syndrome (IBS), and (less likely) intolerance to FODMAPs.Proposed criteria for a diagnosis of NCGS suggest an improvement of gastrointestinal symptoms and extra-intestinal manifestations higher than 30% with a gluten-free diet (GFD), assessed through a rating scale, is needed to make a clinical diagnosis of NCGS. To exclude a placebo effect, a double-blind placebo-controlled gluten challenge is a useful tool, although it is expensive and complicated for routine clinical use, and so is usually performed in research studies.These suggestions were incorporated in the Salerno expert consensus on diagnostic criteria for NCGS. These recommend assessment of the response to a 6-week trial of a gluten-free diet using a defined rating scale (Step 1), followed by a double-blind, placebo-controlled challenge of gluten (or placebo) for a week of each (Step 2). A variation of greater than 30% in the main symptoms when challenged by gluten or placebo is needed for a positive result. Further research on possible biomarkers was also identified. Differential diagnosis Examinations evaluating celiac disease and wheat allergy should be performed before patients remove gluten from their diet. It is critical to make a clear distinction between celiac disease and NCGS. Celiac disease The main goal in diagnosing NCGS is to exclude celiac disease. NCGS and celiac disease cannot be separated in diagnosis because many gastrointestinal and non-gastrointestinal symptoms are similar in both diseases, and there are people with celiac disease having negative serology (absence of specific celiac disease antibodies in serum) or without villus atrophy. There is no test capable of eliminating a diagnosis of a celiac disease, but such a diagnosis is unlikely without confirming HLA-DQ2 and/or HLA-DQ8 haplotypes.The prevalence of undiagnosed celiac disease has increased fourfold during the past half-century, with most cases remaining unrecognized, undiagnosed and untreated, leaving celiac patients with the risk of long-term complications. Some people with NCGS may indeed have celiac disease. A 2015 systematic review found that 20% of people with NCGS presenting with HLA-DQ2 and/or HLA-DQ8 haplotypes, negative serology, and normal histology or duodenal lymphocytosis had celiac disease.The presence of autoimmune symptoms in people with NCGS suggests the possibility of undiagnosed celiac disease. Autoimmune diseases typically associated with celiac disease are diabetes mellitus type 1, thyroiditis, gluten ataxia, psoriasis, vitiligo, autoimmune hepatitis, dermatitis herpetiformis, primary sclerosing cholangitis, and others.To evaluate the possible presence of celiac disease, specific serology and duodenal biopsies are required while the person is still on a diet that includes gluten. Serological markers Serological CD markers (IgA tissue transglutaminase [tTGA], IgA endomysial [EmA] and IgG deamidated gliadin peptide [DGP] antibodies) are always negative in those with NCGS; in addition to specific IgA autoantibody levels, it is necessary to determine total IgA levels. IgG tTGA antibodies should be checked in selective IgA deficiency, which can be associated with celiac disease and occurs in as many as one in 40 celiac patients.Nevertheless, the absence of serological markers does not certainly exclude celiac disease. In those with celiac disease before diagnosis (on a gluten-containing diet), celiac disease serological markers are not always present. As the age of diagnosis increases, these antibody titers decrease, and may be low or even negative in older children and adults. The absence of celiac disease-specific antibodies is more common in patients without villous atrophy who only have duodenal lymphocytosis (Marsh 1 lesions) and who respond to a gluten-free diet with histological and symptomatic improvement. Duodenal biopsies According to the diagnostic criteria established by the consensus conferences (2011 and 2013), it is necessary to perform duodenal biopsies to exclude celiac disease in symptomatic people with negative specific celiac disease antibodies. Because of the patchiness of the celiac disease lesions, four or more biopsies are taken from the second and third parts of the duodenum, and at least one from the duodenal bulb. Even in the same biopsy fragments, different degrees of pathology may exist.Duodenal biopsies in people with NCGS are always almost normal – an essential parameter for diagnosis of NCGS, although is generally accepted that a subgroup of people with NGCS may have an increased number of duodenal intraepithelial lymphocytes (IELs) ( ≥25/100 enterocytes), which represent Marsh I lesions. Nevertheless, Marsh I is considered compatible with celiac disease and the most frequent cause of these findings, especially in people positive for HLA DQ2 and/or DQ8 haplotypes, is celiac disease, with a prevalence of 16-43%.In people with duodenal lymphocytosis – following guidelines from the European Society of Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) – a high count of celiac disease cells (or CD/CD3 ratio) in immunohistochemical assessment of biopsies, or the presence of IgA anti-TG2 and/or anti-endomysial intestinal deposits, might be specific markers for celiac disease. Catassi and Fasano proposed in 2010 that in patients without celiac disease antibodies, either lymphocytic infiltration associated with IgA subepithelial deposits or a histological response to a gluten-free diet, could support a diagnosis of celiac disease. Wheat allergy The clinical presentation may be sufficient in most cases to distinguish a wheat allergy from other entities. It is excluded when there are normal levels of serum IgE antibodies to gluten proteins and wheat fractions, and no skin reaction to prick tests for wheat allergy. Nevertheless, these tests are not always completely reliable.If an allergic reaction can not be clearly identified, the diagnosis should be confirmed by food provocation tests, ideally performed in a double-blinded and placebo-controlled manner. Delayed allergic reactions may occur with these type of tests, which have to be negative over time, but there are no international consensus statements on diagnosing delayed wheat/food-related symptoms. Usually, reactions that appear between two hours and five days after the oral challenge are considered delayed. Mucosal challenge followed by confocal endomicroscopy is a complementary diagnostic technique, but this technology is not yet generally available and remains experimental. Other tests Evaluating the presence of antigliadin antibodies (AGA) can be a useful complementary diagnostic test. Up to 50% NCGS patients may have elevated AGA IgG antibodies, but rarely AGA IgA antibodies (only 7% of the cases). In these patients, unlike in those with celiac disease, the IgG AGA became undetectable within six months of following a gluten-free diet. People already on a gluten-free diet Many people remove gluten from their diet after a long history of health complaints and unsuccessful consultations with numerous physicians, who simply consider them to be suffering from irritable bowel syndrome, and some may eliminate gluten before seeking medical attention. This fact can diminish the CD serological markers titers and may attenuate the inflammatory changes found in the duodenal biopsies. In these cases, patients should be tested for the presence of HLA-DQ2/DQ8 genetic markers because a negative HLA-DQ2 and HLA-DQ8 result has a high negative predictive value for celiac disease. If these markers are positive, it is advisable to undertake a gluten challenge under medical supervision, followed by serology and duodenal biopsies. However, gluten challenge protocols have significant limitations, because a symptomatic relapse generally precedes the onset of a serological and histological relapse, and therefore becomes unacceptable for many patients. Gluten challenge is also discouraged before the age of five and during pubertal growth.It remains unclear what daily intake of gluten is adequate and how long the gluten challenge should last. Some protocols recommend eating a maximum of 10 g of gluten per day for six weeks. Nevertheless, recent studies have shown that a two-week challenge of 3 g of gluten per day may induce histological and serological abnormalities in most adults with proven celiac disease. This new proposed protocol has shown higher tolerability and compliance. It has been calculated that its application in secondary-care gastrointestinal practice would identify celiac disease in 7% of patients referred for suspected NCGS, while the remaining 93% would be confirmed as NCGS; this is not yet universally adopted.For people on a gluten-free diet who are unable to perform an oral gluten challenge, an alternative to identify possible celiac disease is an in vitro gliadin challenge of small bowel biopsies, but this test is only available at selected specialized tertiary-care centers. Treatment After exclusion of celiac disease and wheat allergy, the subsequent step for diagnosis and treatment of NCGS is to start a strict gluten-free diet (GFD) to assess if symptoms improve or resolve completely. This may occur within days to weeks of starting a GFD, but improvement may also be due to a non-specific, placebo response. The recovery of the nervous system is slow and sometimes incomplete.Recommendations may resemble those for celiac disease, for the diet to be strict and maintained, with no transgression. The degree of gluten cross contamination tolerated by people with NCGS is not clear but there is some evidence that they can present with symptoms even after consumption of small amounts. Sporadic accidental contaminations with gluten can reactivate movement disorders. A part of people with gluten-related neuropathy or ataxia appears not to be able to tolerate even the traces of gluten allowed in most foods labeled as "gluten-free".Whereas celiac disease requires adherence to a strict lifelong gluten-free diet, it is not yet known whether NCGS is a permanent or a transient condition. The results of a 2017 study suggest that NCGS may be a chronic disorder, as is the case with celiac disease. A trial of gluten reintroduction to observe any reaction after one to two years of strict gluten-free diet might be performed.A strict gluten-free diet is effective in most of the neurological disorders associated with NCGS, ameliorating or even resolving the symptoms. It should be started as soon as possible to improve the prognosis. The death of neurons in the cerebellum in ataxia is the result of gluten exposure and is irreversible. Early treatment with a strict gluten-free diet can improve ataxia symptoms and prevent its progression. When dementia has progressed to an advanced degree, the diet has no beneficial effect. Cortical myoclonus appears to be treatment-resistant on both gluten-free diet and immunosuppression. Persistent symptoms Approximately one third of presumed NCGS patients continue to have symptoms, despite gluten withdrawal. Apart from a possible diagnostic error, there are multiple possible explanations.One reason is poor compliance with gluten withdrawal, whether voluntary and/or involuntary. There may be ingestion of gluten, in the form of cross contamination or food containing hidden sources. In some cases, the amelioration of gastrointestinal symptoms with a gluten-free diet is only partial, and these patients could significantly improve with the addition of a low-FODMAP diet.A subgroup may not improve when eating commercially available gluten-free products, as these can be rich in preservatives and additives such as sulfites, glutamates, nitrates and benzoates, which can also have a role in triggering functional gastrointestinal symptoms. Furthermore, people with NCGS may often present with IgE-mediated allergies to one or more foods. It has been estimated that around 35% suffer other food intolerances, mainly lactose intolerance. History The subject of "food intolerance", including gluten sensitivity and elimination diets, was discussed in 1976.Patients with symptoms including abdominal pain and diarrhea, which improved on gluten withdrawal, and who did not have celiac disease were initially described in 1976 and 1978 with the first series in 1980. Debate regarding the existence of a specific condition has continued since then, but the three consensus conferences held since 2010 produced consistent definitions of NCGS and its diagnostic criteria. Society and culture NCGS has been a topic of popular interest. Gluten has been named "the new diet villain". The gluten-free diet has become popular in the United States and other countries. Clinicians worldwide have been challenged by an increasing number of people who do not have celiac disease nor wheat allergy, with digestive or extra-digestive symptoms which improved after removing wheat / gluten from the diet. Many of these persons began a gluten-free diet on their own, without having been previously evaluated. Another reason that contributed to this trend was the publication of several books that demonize gluten and point to it as a cause of type 2 diabetes, weight gain and obesity, and a broad list of conditions ranging from depression and anxiety to arthritis and autism. The book that has had the most impact is Grain Brain: The Surprising Truth about Wheat, Carbs, and Sugar – Your Brains Silent Killers, by the American neurologist David Perlmutter, published in September 2013. Another book that has had great impact is Wheat Belly: Lose the Wheat, Lose the Weight, and Find Your Path Back to Health, by cardiologist William Davis. The gluten-free diet has been advocated and followed by many celebrities to lose weight, such as Miley Cyrus and Gwyneth Paltrow, and some elite athletes to improve performance.Estimates suggest that in 2014, 30% of people in the US and Australia were consuming gluten-free foods, with estimates that by 2016 approximately 100 million Americans would consume gluten-free products. Data from a 2015 Nielsen survey of 30,000 adults in 60 countries around the world showed that 21% of people prefer to buy gluten-free foods, with interest highest among younger generations. Another school of thought suggests that many people may be unnecessarily avoiding gluten when they do not need to.Debate around NCGS as a genuine clinical condition can be heightened because often patients are self diagnosed, or a diagnosis is made by alternative health practitioners. Many people who are making a gluten-free diet did not previously exclude celiac disease or, when they are fully evaluated, other alternative diagnoses can be found such as fructose intolerance or small intestinal bacterial overgrowth, or a better response to a low-FODMAP diet obtained. Research There are many open questions on gluten sensitivity, emphasized in one review that "it is still to be clarified whether this disorder is permanent or transient and whether it is linked to autoimmunity". It has not yet been established whether innate or adaptive immune responses are involved in NCGS, nor whether the condition relates specifically to gluten or rather relates to other components of grains.Studies indicate that AGA IgG is high in slightly more than half of NCGS patients and that, unlike for celiac disease patients, the IgG AGA decreases strongly over 6 months of gluten-free diet; AGA IgA is usually low or absent in NCGS patients.The need for developing biomarkers for NCGS is frequently emphasized; for example, one review indicated: "There is a desperate need for reliable biomarkers ... that include clinical, biochemical and histopathological findings which support the diagnosis of NCGS."Research has also attempted to discern, by double-blind placebo-controlled trials, between a "fad component" to the recent popularity of the gluten-free diet and an actual sensitivity to gluten or other components of wheat. In a 2013 double-blind, placebo-controlled challenge (DBPC) by Biesiekierski et al. in a few people with IBS, the authors found no difference between gluten or placebo groups and the concept of NCGS as a syndrome was questioned. Nevertheless, this study had design errors and an incorrect selection of participants, and probably the reintroduction of both gluten and whey protein had a nocebo effect similar in all people, and this could have masked the true effect of gluten/wheat reintroduction. In a 2015 double-blind placebo cross-over trial, small amounts of purified wheat gluten triggered gastrointestinal symptoms (such as abdominal bloating and pain) and extra-intestinal manifestations (such as foggy mind, depression and aphthous stomatitis) in self-reported NCGS. Nevertheless, it remains elusive whether these findings specifically implicate gluten or proteins present in gluten-containing cereals. In a 2018 double-blind, crossover research study on 59 persons on a gluten-free diet with challenges of gluten, fructans or placebo, intestinal symptoms (specifically bloating) were borderline significantly higher after challenge with fructans, in comparison with gluten proteins (P = 0.049). Although the differences between the three interventions was very small, the authors concluded that fructans (the specific type of FODMAP found in wheat) are more likely to be the cause of NCGS gastrointestinal symptoms, rather than gluten. In addition, fructans used in the study were extracted from chicory root, so it remains to be seen whether the wheat fructans produce the same effect. See also Gluten-related disorders == References ==

Hey Aarogya, could you help me understand about Omphalocele

Omphalocele

Omphalocele or omphalocoele also called exomphalos, is a rare abdominal wall defect. Beginning at the 6th week of development, rapid elongation of the gut and increased liver size reduces intra abdominal space, which pushes intestinal loops out of the abdominal cavity. Around 10th week, the intestine returns to the abdominal cavity and the process is completed by the 12th week. Persistence of intestine or the presence of other abdominal viscera (e.g. stomach, liver) in the umbilical cord results in an omphalocele. Omphalocele occurs in 1 in 4,000 births and is associated with a high rate of mortality (25%) and severe malformations, such as cardiac anomalies (50%), neural tube defect (40%), exstrophy of the bladder and Beckwith–Wiedemann syndrome. Approximately 15% of live-born infants with omphalocele have chromosomal abnormalities. About 30% of infants with an omphalocele have other congenital abnormalities. Signs and symptoms The sac, which is formed from an outpouching of the peritoneum, protrudes in the midline, through the umbilicus (navel).It is normal for the intestines to protrude from the abdomen, into the umbilical cord, until about the tenth week of pregnancy, after which they return to inside the fetal abdomen. The omphalocele can be mild, with only a small loop of intestines present outside the abdomen, or severe, containing most of the abdominal organs. In severe cases surgical treatment is made more difficult because the infants abdomen is abnormally small, having had no need to expand to accommodate the developing organs. Larger omphaloceles are associated with a higher risk of cardiac defects. Complications Complications may occur prenatally, during birth, management, treatment or after surgery. Both prenatally and during birth, the exomphalos can rupture. During birth there may be trauma to the liver for giant omphaloceles. During management exomphalos can act as a metabolic drain affecting nitrogen balance which can lead to failure to thrive, as well as hypothermia. Use of a non-absorbent patch during surgery can lead to wound sepsis post-surgery. Herniation from the patch is also a possibility. Intestinal dysfunction for a few weeks after the surgery is common, therefore parenteral feeding is continued post-surgery, however prolonged use of this may lead to hepatomegaly and cholestasis. If intestinal dysfunction persists it can lead to intestinal necrosis. Intestinal atresia can occur, which is where the mucosa and submucosa of the intestine form a web that obstructs the lumen which leads to malabsorption. Obstruction of the bowel can occur which results in short bowel syndrome. For the first few years of life there is a high incidence of gastroesophageal reflux which can be complicated by oesophagitis.Post-surgery the umbilicus (navel) is deficient or abnormally placed that causes dislike amongst many patients. Umbilical reconstruction can be difficult due to scar tissue and lack of extra skin for surgical use, though this can be overcome by using tissue expanders below the skin and umbilicoplasty.Ultimately, prognosis depends on the size of the defect and whether associated abnormalities are present or complications develop. Mortalities and morbidities still occur, with the mortality rate for large omphaloceles with associated abnormalities being higher. Most surviving omphalocele infants have no-long-term problems and grow up to be normal individuals. Causes Omphalocele is caused by malrotation of the bowels while returning to the abdomen during development. Some cases of omphalocele are believed to be due to an underlying genetic disorder, such as Edwards syndrome (trisomy 18) or Patau syndrome (trisomy 13). Beckwith–Wiedemann syndrome is also associated with omphaloceles. Pathophysiology Exomphalos is caused by a failure of the ventral body wall to form and close the naturally occurring umbilical hernia that occurs during embryonic folding which is a process of embryogenesis. The normal process of embryogenesis is that at 2 weeks gestation the human embryo is a flat disc that consists of three layers, the outer ectoderm and inner endoderm separated by a middle layer called the mesoderm. The ectoderm gives rise to skin and the CNS, the mesoderm gives rise to muscle and the endoderm gives rise to organs. The focus areas for exomphalos are that the ectoderm will form the umbilical ring, the mesoderm will form the abdominal muscles and the endoderm will form the gut. After the disc becomes tri-layered, it undergoes growth and folding to transform it from disc to cylinder shaped. The layer of ectoderm and mesoderm in the dorsal axis grow ventrally to meet at the midline. Simultaneously, the cephalic (head) and caudal (tail) ends of these layers of the disc fold ventrally to meet the lateral folds in the center. The meeting of both axis at the center form the umbilical ring. Meanwhile, the endoderm migrates to the center of this cylinder.By the fourth week of gestation the umbilical ring is formed. During the 6th week the midgut rapidly grows from the endoderm which causes a herniation of the gut through the umbilical ring. The gut rotates as it re-enters the abdominal cavity which allows for the small intestine and colon to migrate to their correct anatomical position by the end of the 10th week of development. This process fails to occur normally in cases of exomphalos, resulting in abdominal contents protruding from the umbilical ring.Gut contents fail to return to the abdomen due to a fault in myogenesis (muscle formation and migration during embryogenesis). During embryogenesis the mesoderm that forms muscle divides into several somites that migrate dorso-ventrally towards the midline. The somites develop three parts that are sclerotome which will form bone, dermatome which will form skin of the back and myotome which will form muscle. The somites that remain close to the neural tube at the back of the body have epaxial myotome, whilst the somites that migrate to the midline have hypaxial myotome. The hypaxial myotome forms the abdominal muscles. The myotome cells will give rise to myoblasts (embryonic progenitor cells) which will align to form myotubules and then muscle fibers. Consequently, the myotome will become three muscle sheets that form the layers of abdominal wall muscles. The muscle of concern for exomphalos is the rectus abdominis. In the disease the muscle undergoes normal differentiation but fails to expand ventro-medially and narrow the umbilical ring which causes the natural umbilical hernia that occurs at 6 weeks of gestation to remain external to the body.The location of the folding defect in the embryo determines the ultimate position of the exomphalos. A cephalic folding defect results in an epigastric exomphalos that is positioned high up on the abdomen which can be seen in the chromosomal defect pentalogy of Cantrell. Lateral folding defects result in a typical exomphalos that is positioned in the middle of the abdomen. A caudal folding defect results in a hypogastric exomphalos that is positioned on the lower abdomen. Genetics The genes that cause exomphalos are controversial and subject to research. Exomphalos is greatly associated with chromosomal defects and thus these are being explored to pinpoint the genetic cause of the disease. Studies in mice have indicated that mutations in the fibroblast growth factor receptors 1 and 2 (Fgfr1, Fgfr2) cause exomphalos. Fibroblast growth factor (FBGF) encourages the migration of myotubules during myogenesis. When FBGF runs out myoblasts stop migrating, cease division and differentiate into myotubules that form muscle fibers. Mutations in homeobox genes such as Alx4, that direct the formation of body structures during early embryonic development cause exomphalos in mice. Mutations in the Insulin like growth factor-2 gene (IGF2) and its associated receptor gene IGF2R cause high levels of IGF-2 protein in humans which leads to exomphalos in the associated disease Beckwith Wiedemann syndrome (BWS). IFG2R is responsible for degradation of excess IGF-2 protein. BWS disease is caused by a mutation in chromosome 11 at the locus where the IGF2 gene resides. Observance of the inheritance patterns of the associated anomalies through pedigrees show that exomphalos can be the result of autosomal dominant, autosomal recessive and X-linked inheritance. Environmental factors It is not well known if actions of the mother could predispose or cause the disease. Alcohol use during the first trimester, heavy smoking, use of certain medications like the selective serotonin-reuptake inhibitors and methimazole (anti-thyroid drug) during pregnancy, maternal febrile illness, IVF, parental consanguinity and obesity elevate the risk of a woman giving birth to a baby with exomphalos. Preventive methods that could be utilised by mothers include ingestion of a preconception multivitamin and supplementation with folic acid. Termination of pregnancy may be considered if a large exomphalos with associated congenital abnormalities is confirmed during prenatal diagnosis. Diagnosis Related conditions Gastroschisis is a similar birth defect, but in gastroschisis the umbilical cord is not involved and the intestinal protrusion is usually to the right of the midline. Parts of organs may be free in the amniotic fluid and not enclosed in a membranous (peritoneal) sac. Gastroschisis is less frequently associated with other defects than omphalocele.Omphaloceles occurs more frequently with increased maternal age. Other related syndromes are Shprintzen Goldberg, pentalogy of Cantrell, Beckwith–Wiedemann and OEIS complex (omphalocele, exstrophy of the cloaca, imperforate anus, spinal defects).After surgery a child with omphalocele will have some degree of intestinal malrotation. Due to intestinal malrotation 4.4% of children with omphalocele will experience a midgut volvulus in the days, months, or years after surgery. Parents of children with omphalocele should seek immediate medical attention if their child displays signs and symptoms of an intestinal obstruction at any point in their childhood to avoid the possibility of bowel necrosis or death.Some experts differentiate exomphalos and omphalocele as 2 related conditions, one worse than the other; in this sense, exomphalos involves a stronger covering of the hernia (with fascia and skin), whereas omphalocele involves a weaker covering of only a thin membrane. Others consider the terms synonymous names for any degree of herniation and covering. Screening An omphalocele is often detected through AFP screening or a detailed fetal ultrasound. Genetic counseling and genetic testing such as amniocentesis are usually offered during the pregnancy. Management There is no treatment that is required prenatally unless there is a rupture of the exomphalos within the mother. An intact exomphalos can be delivered safely vaginally and C-sections are also acceptable if obstetrical reasons require it. There appears to be no advantage for delivery by C-section unless it is for a giant exomphalos that contains most of the liver. In this case vaginal delivery may result in dystocia (inability of the baby to exit the pelvis during birth) and liver damage. Immediately after birth a nasogastric tube is required to decompress the intestines and an endotracheal intubation is needed to support respiration. The exomphalos sac is kept warm and covered with a moist saline gauze and plastic transparent bowel bag to prevent fluid loss. The neonate also requires fluid, vitamin K and antibiotic administration intravenously. After management strategies are applied, a baby with an intact sac is medically stable and does not require urgent surgery. This time is used to assess the newborn to rule out associated anomalies prior to surgical closure of the defect. Studies show there is no significant difference in survival between immediate or delayed closure.Surgery can be performed directly for small omphaloceles, which will require a short stay in the nursery department, or in a staged manner for large omphaloceles, which will require several weeks stay. Staged closure requires a temporary artificial holding sac (a silo) to be placed over the abdominal organs and sutured to the abdominal wall. This can be made of non-adhesive dressing. The silo is gradually reduced in size at least once daily until all of the viscera have been returned to the abdominal cavity. This is repeated for several days to a week until surgical closure of the fascia/skin can be done. Closure may require a patch that can be rigid or non-rigid and made of natural biomaterials such as a bovine pericardium or artificial materials. The skin is then closed over the patch and it is re-vascularised by the bodys liver blood vessels post-surgery. The staged surgery is required, as rushed reduction of the exomphalos compromises venous return and ventilation, as it raises intra-abdominal pressure. In some cases, stretching of the abdominal wall to accommodate intestinal contents may be required. Non-operative therapy uses escharotic ointments. This is used for infants with large omphaloceles that have been born prematurely with respiratory insufficiency and associated chromosomal defects, as they would not be able to tolerate surgery. The ointment causes the sac to granulate and epithelialize, which leaves a residual large ventral hernia, which can be repaired later with surgery when the baby is more stable. After surgery, for larger omphaloceles, mechanical ventilation and parenteral nutrition is needed to manage the baby. Society and culture Awareness Day International Omphalocele Awareness Day is celebrated annually in the US on January 31, as part of Birth Defect Awareness Month. Several U.S. states have passed resolutions to officially recognize the date. References Omphalocele Diagnosis and Treatment at SSM Health St. Louis Fetal Care Institute The Brown Fetal Treatment Program - Providence, Rhode Island at Brown University Fetal Treatment Center: Omphalocele at UCSF Gastroschisis Exomphalos Extrophies Parent Support (GEEPS) == External links ==

Hi Aarogya, could you help me understand about Spasm of accommodation

Spasm of accommodation

A spasm of accommodation (also known as a ciliary spasm, an accommodation, or accommodative spasm) is a condition in which the ciliary muscle of the eye remains in a constant state of contraction. Normal accommodation allows the eye to "accommodate" for near-vision. However, in a state of perpetual contraction, the ciliary muscle cannot relax when viewing distant objects. This causes vision to blur when attempting to view objects from a distance. This may cause pseudomyopia or latent hyperopia. Although antimuscarinic drops (homoatropine 5%) can be applied topically to relax the muscle, this leaves the individual without any accommodation and, depending on refractive error, unable to see well at near distances. Also, excessive pupil dilation may occur as an unwanted side effect. This dilation may pose a problem since a larger pupil is less efficient at focusing light (see pupil, aperture, and optical aberration for more.) Patients who have accommodative spasm may benefit from being given glasses or contacts that account for the problem or by using vision therapy techniques to regain control of the accommodative system. Possible clinical findings include: Normal Amplitude of accommodation Normal Near point of convergence Reduced Negative relative accommodation Difficulty clearing plus on facility testing Treatments Cycloplegic Eye Drops (Dilation) Spasm of accommodation is frequently resistant to treatment. However, some patients do find relief through the use of daily eye dilation with cycloplegic drops. One side effect of cycloplegic drops is that they often have BAK as a preservative ingredient, which, with daily use, can erode the tear shield: At each administration of an eye drop containing benzalkonium chloride, its detergent effect disrupts the lipid layer of the tear film. This cannot be regenerated and can no longer protect the aqueous layer of the tear film, which evaporates easily. In these circumstances, the cornea is exposed and eye dryness occurs. In addition, benzalkonium chloride has a cellular toxicity on caliciform cells, entailing a reduction in the amount of mucin, an additional reason for disrupting the tear film. In fact, none of the cycloplegic drops used to treat Spasm of Accommodation in the United States are available without BAK. This unfortunately makes treatment much more difficult as the side effect of dry eyes and corneal damage can occur. France, Australia, Canada, and the United Kingdom do have limited availability of BAK-free eye drops available in unidose, and they must be imported to the United States with a physicians letter to the FDA enclosed with the imported prescription. Due to the high potential of tear shield damage with long-term use and the associated dry eye condition caused by cycloplegic eye drops with BAK (preservative), many physicians do not recommend cycloplegic eye drops. In difficult cases, "cycloplegic agents are highly favored to break spasm quickly and may be more economical compared to other conventional therapies"Cyclopentolate, Atropine, Tropicamide, and Homatropine are the typical cycloplegic eye drops used once daily to treat spasm of accommodation by relaxing the ciliary muscle. One side effect is blurred vision since these induce dilation. Vision Training Vision therapy administered by a trained optometrist has shown a success rate of over 70%. Surgery Multifocal intraocular lens implantation is a new possible treatment involving clear lens extraction and multifocal intraocular lens implantation but it may not be appropriate for patients who have had resistant spasm of accommodation for a long period of time. Research Experimental Nitroglycerin and Nitric Oxide Animal studies have found nitroglycerin, a vasodilator used to treat angina, relaxes the ciliary muscle and may hold hope for those suffering from spasm of accommodation. Nitroglycerin is currently being investigated as a treatment for glaucoma, and has shown to decrease intraocular pressure and relax the ciliary muscle. According to Investigative Ophthalmology & Visual Science Journal. "In a nonhuman primate study, topical administration of nitroglycerin at a dose of 0.1% significantly decreased IOP in normotensive animals after 90 minutes". Further, according to Wiederholt, Sturm, and Lepple-Wienhues, "The data indicate (indicates [sic]) that an increase of intracellular cGMP by application of cGMP and organic nitrate or non-nitrate vasodilators induces relaxation of the bovine trabecular meshwork and ciliary muscle". Experimental Perilla frutescens Since spasm of accommodation is a result of contraction of the ciliary muscle, the goal would be to relax the ciliary muscle. New studies conducted on rats using perilla frutescens aqueous extract have shown to relax the ciliary muscle. Since there are no known drugs to treat this eye condition, perilla frutescens in an aqueous extract form may result in the relaxation of the ciliary muscle in humans as well. Perilla frutescens is currently used in traditional medicine in Korea, Japan, and China and a clinical study "showed that PFA (perilla frutescens extract) attenuates eye fatigue by improving visual accommodation" Prognosis For routine cases of spasm of accommodation, the American Optometric Association says the prognosis is fair and on average, the number of visits a patient needs will be 1-2 for evaluation and 10 follow up visits. Additionally, the AOA recommends the following management plan for spasm of accommodation: "Begin with plus lenses and VT; if VT fails, use cycloplegic agent temporarily; educate patient".For more chronic and acute cases that do not respond to vision training and cycloplegic drops, the eye muscles should weaken with advancing age providing intermittent or permanent relief from this condition. See also Miosis Cycloplegia Pseudomyopia == References ==

Aarogya, give me a short description about Nasal polyp

Nasal polyp

Nasal polyps (NP) are noncancerous growths within the nose or sinuses. Symptoms include trouble breathing through the nose, loss of smell, decreased taste, post nasal drip, and a runny nose. The growths are sac-like, movable, and nontender, though face pain may occasionally occur. They typically occur in both nostrils in those who are affected. Complications may include sinusitis and broadening of the nose.The exact cause is unclear. They may be related to chronic inflammation of the lining of the sinuses. They occur more commonly among people who have allergies, cystic fibrosis, aspirin sensitivity, or certain infections. The polyp itself represents an overgrowth of the mucous membranes. Diagnosis may be accomplished by looking up the nose. A CT scan may be used to determine the number of polyps and help plan surgery.Treatment is typically with steroids, often in the form of a nasal spray. If this is not effective, surgery may be considered. The condition often recurs following surgery; thus, continued use of a steroid nasal spray is often recommended. Antihistamines may help with symptoms but do not change the underlying disease. Antibiotics are not required for treatment unless an infection occurs.About 4% of people currently have nasal polyps while up to 40% of people develop them at some point in their life. They most often occur after the age of 20 and are more frequent in males than females. Nasal polyps have been described since the time of the Ancient Egyptians. Signs and symptoms Symptoms of polyps include nasal congestion, sinusitis, loss of smell, thick nasal discharge, facial pressure, nasal speech, and mouth breathing. Recurrent sinusitis can result from polyps. Long-term, nasal polyps can cause destruction of the nasal bones and widening of the nose.As polyps grow larger, they eventually prolapse into the nasal cavity, resulting in symptoms. The most prominent symptoms of nasal polyps is blockage of the nasal passage. People with nasal polyps due to aspirin intolerance often have symptoms known as Samters triad, which consists of asthma worse with aspirin, a skin rash caused by aspirin, and chronic nasal polyps. Causes The exact cause of nasal polyps is unclear. They are, however, commonly associated with conditions that cause long term inflammation of the sinuses. This includes chronic rhinosinusitis, asthma, aspirin sensitivity, and cystic fibrosis.Various additional diseases associated with polyp formation include: Chronic rhinosinusitis is a common medical condition characterized by symptoms of sinus inflammation lasting at least 12 weeks. The cause is unknown and the role of microorganisms remains unclear. It can be classified as either with or without nasal polyposis.Cystic fibrosis (CF) is the most common cause of nasal polyps in children. Therefore, any child under 12 to 20 years old with nasal polyps should be tested for CF. Half of people with CF will experience extensive polyps leading to nasal obstruction and requiring aggressive management. Pathophysiology The true cause of nasal polyps is unknown, but they are thought to be due to recurrent infection or inflammation. Polyps arise from the lining of the sinuses. Nasal mucosa, particularly in the region of middle meatus becomes swollen due to collection of extracellular fluid. This extracellular fluid collection causes polyp formation and protrusion into the nasal cavity or sinuses. Polyps which are sessile in the beginning become pedunculated due to gravity.In people with nasal polyps due to aspirin or NSAID sensitivity, the underlying mechanism is due to disorders in the metabolism of arachidonic acid. Exposure to cycloxygenase inhibitors such as aspirin and NSAIDs leads to shunting of products through the lipoxygenase pathway leading to an increased production of products that cause inflammation. In the airway, these inflammatory products lead to symptoms of asthma such as wheezing as well as nasal polyp formation. Diagnosis Nasal polyps can be seen on physical examination inside of the nose and are often detected during the evaluation of symptoms. On examination, a polyp will appear as a visible mass in the nostril. Some polyps may be seen with anterior rhinoscopy (looking in the nose with a nasal speculum and a light), but frequently, they are farther back in the nose and must be seen by nasal endoscopy. Nasal endoscopy involves passing a small, rigid camera with a light source into the nose. An image is projected onto a screen in the office so the doctor can examine the nasal passages and sinuses in greater detail. The procedure is not generally painful, but the person can be given a spray decongestant and local anesthetic to minimize discomfort.Attempts have been made to develop scoring systems to determine the severity of nasal polyps. Proposed staging systems take into account the extent of polyps seen on endoscopic exam and the number of sinuses affected on CT imaging. This staging system is only partially validated, but in the future, may be useful for communicating the severity of disease, assessing treatment response, and planning treatment. Types There are two primary types of nasal polyps: ethmoidal and antrochoanal. Ethmoidal polyps arise from the ethmoid sinuses and extend through the middle meatus into the nasal cavity. Antrochoanal polyps usually arise in the maxillary sinus and extend into the nasopharynx and represent only 4–6% of all nasal polyps.However, antrochoanal polyps are more common in children comprising one-third of all polyps in this population. Ethmoidal polyps are usually smaller and multiple while antrochoanal polyps are usually single and larger. CT scan CT scan can show the full extent of the polyp, which may not be fully appreciated with physical examination alone. Imaging is also required for planning surgical treatment. On a CT scan, a nasal polyp generally has an attenuation of 10–18 Hounsfield units, which is similar to that of mucus. Nasal polyps may have calcification. Histology On histologic examination, nasal polyps consist of hyperplastic edematous (excess fluid) connective tissue with some seromucous glands and cells representing inflammation (mostly neutrophils and eosinophils). Polyps have virtually no neurons. Therefore, the tissue that makes up the polyp does not have any tissue sensation and the polyp itself will not be painful. In early stages, the surface of the nasal polyp is covered by normal respiratory epithelium, but later it undergoes metaplastic change to squamous type epithelium with the constant irritation and inflammation. The submucosa shows large intercellular spaces filled with serous fluid. Differential diagnosis Other disorders can mimic the appearance of nasal polyps and should be considered if a mass is seen on exam. Examples include encephalocele, glioma, inverted papilloma, and cancer. Early biopsy is recommended for unilateral nasal polyps to rule out more serious conditions such as cancer, inverted papilloma, or fungal sinusitis. Treatment The first line of treatment for nasal polyps is topical steroids. Steroids decrease the inflammation of the sinus mucosa to decrease the size of the polyps and improve symptoms. Topical preparations are preferred in the form of a nasal spray but are often ineffective for people with many polyps. Steroids by mouth often provide drastic symptom relief, but should not be taken for long periods of time due to their side effects. Because steroids only shrink the size and swelling of the polyp, people often have recurrence of symptoms once the steroids are stopped. Decongestants do not shrink the polyps, but can decrease swelling and provide some relief. Antibiotics are only recommended if the person has a co-occurring bacterial infection.In people with nasal polyps caused by aspirin or NSAIDs, avoidance of these medications will help with symptoms. Aspirin desensitization has also been shown to be beneficial. Surgery Endoscopic sinus surgery, advocated and popularized by Professor Stammberger, is often very effective for most people, providing rapid symptom relief. Endoscopic sinus surgery is minimally-invasive and is done entirely through the nostril with the help of a camera. Surgery should be considered for those with complete nasal obstruction, uncontrolled runny nose, nasal deformity caused by polyps or continued symptoms despite medical management. Surgery serves to remove the polyps as well as the surrounding inflamed mucosa, open obstructed nasal passages, and clear the sinuses. This not only removes the obstruction caused by the polyps themselves, but allows medications such as saline irrigations and topical steroids to become more effective. It has been suggested that one of the main objectives in sinus surgery for polyps is to allow delivery of the steroids into those areas of the sinuses where polyps develop, namely, the ethmoid sinuses. Specially designed long nozzles had been developed to use postoperatively to deliver steroids into those areas after sinus surgery for polyps.Surgery lasts approximately 45 minutes to 1 hour and can be done under general or local anesthesia. Most people tolerate the surgery without much pain, though this can vary from person to person. The person should expect some discomfort, congestion, and drainage from the nose in the first few days after surgery, but this should be mild. Complications from endoscopic sinus surgery are rare, but can include bleeding and damage to other structures in the area including the eye or brain.Many physicians recommend a course of oral steroids prior to surgery to reduce mucosal inflammation, decrease bleeding during surgery, and help with visualization of the polyps. Nasal steroid sprays should be used preventatively after surgery to delay or prevent recurrence. People often have recurrence of polyps even following surgery. Therefore, continued follow up with a combination of medical and surgical management is preferred for the treatment of nasal polyps. Epidemiology Nasal polyps resulting from chronic rhinosinusitis affect approximately 4.3% of the population. Nasal polyps occur more frequently in men than women and are more common as people get older, increasing drastically after the age of 40.Of people with chronic rhinosinusitis, 10% to 54% also have allergies. An estimated 40% to 80% of people with sensitivity to aspirin will develop nasal polyposis. In people with cystic fibrosis, nasal polyps are noted in 37% to 48%. References == External links ==

Hey Aarogya, explain a situation where Peripheral T-cell lymphoma occurs

Peripheral T-cell lymphoma

Peripheral T-cell lymphoma refers to a group of T-cell lymphomas that develop away from the thymus or bone marrow.Examples include: Cutaneous T-cell lymphomas Angioimmunoblastic T-cell lymphoma Extranodal natural killer/T-cell lymphoma, nasal type Enteropathy type T-cell lymphoma Subcutaneous panniculitis-like T-cell lymphoma Anaplastic large cell lymphoma Peripheral T-cell lymphoma-Not-Otherwise-SpecifiedIn ICD-10, cutaneous T-cell lymphomas are classified separately. References == External links ==

Hey Aarogya!, what is Confusional arousals

Confusional arousals

Confusional arousals are classified as “partial awakenings in which the state of consciousness remains impaired for several minutes without any accompanying major behavioural disorders or severe autonomic responses”. Complete or partial amnesia of the episodes may be present. Signs and symptoms Confusional arousals are accompanied by mental confusion and disorientation, relative lack of response to environmental stimuli, and difficulty of awakening the subject. Vocalisation accompanied with coherent speech is common. Patients may appear upset, and some of them become aggressive or agitated. As well as for children, attempting to awaken or console an adult patient may increase agitation. Confusional arousals can occur during or following an arousal of deep sleep (see slow-wave sleep) and upon an attempt of awakening the subject from sleep in the morning.In children, confusional arousals can often be reproduced artificially by awakening the child during deep sleep. However, it doesn’t have any clinical significance without deeper investigation. Children living an episode of confusional arousal typically sit up in bed, whimper, cry, moan, and may utter words like “no” or “go away”. They remain distressed and inconsolable despite all parental efforts. Paradoxically, parental efforts can rather increase agitation of the child. The onset of symptoms is usually within 2 and 3 hours of sleep onset (at the time of transition from slow-wave sleep to a lighter sleep stage) and those events can last from 10 to 30 minutes. Patients generally wake up without any recollection of the event. It is necessary to distinguish confusional arousals in adults from children. Neurological symptomatology Confusional arousals are associated with behavioural awakening with persistent slow-wave electroencephalographic activity (see slow-wave sleep) during Non-rapid eye movement sleep (NREM). It suggests that sensorimotor network is activated while non sensorimotor areas are still "asleep". The altered state of consciousness may be explained by a hypersynchronous delta activity (see delta wave) in network involving the frontoparietal cortices (suggesting to be "asleep"), and higher frequency activities in sensorimotor, orbitofrontal, and temporal lateral cortices (suggesting an "awakening"). Sleep-related violence and abnormal sexual behaviours Confusional arousals have often been linked to sleep-related violence (self-injury or injury to the bed partner). The latter highlights important medical and legal issues when such behaviours are suspected and purported to have caused a criminal offense. The first documented case of homicide as a result of confusional arousal was reported in medieval times by the case of the Silesian woodcutter Bernard Schedmaizig. Sleep-related abnormal sexual behaviours (also called sexsomnia or sleep sex) are mainly classified as confusional arousals and more rarely associated to sleepwalking (also known as somnambulism). Even if sleep-related violence may occur during an episode of confusional arousal, it remains extremely rare and there are no specific predisposition to aggression during these episodes. Distinction between sleepwalking and night terrors Violent behaviours in confusional arousals slightly differ from those in sleepwalking or night terrors. Above all, during an episode of confusional arousal the patient never leaves the bed unlike sleepwalking. A bed partner or parent who tries to calm or restrain the patient by grabbing him or her may trigger a violent reaction as with sleepwalkers. In case of a confusional arousal triggered by an attempt of awakening the patient, violent behaviours may occur almost spontaneously. Unlike confusional arousals and sleep walking, patients experiencing night terrors seem to react to some type of frightening image. Therefore, the violent reaction may occur if another individual is encountered or is in proximity. Classification International Classification of Sleep Disorders (ICSD) According to the 2nd edition of the International Classification of Sleep Disorders (ICSD-2), confusional arousals are classified in NREM parasomnias embedded in the non-epileptic paroxysmal motor events during sleep, which include (1) Parasomnia, (2) Sleep-related movement disorders and (3) Isolated symptoms, apparently normal variants and unresolved issues. NREM parasomnias (or disorders of arousal) also include sleep terrors (see night terror) and sleepwalking. Confusional arousals are characterised by more or less complex movements without leaving bed with whimpering, sitting up in bed and some articulation without walking or terror. In comparison of other arousal parasomnias the age onset of sleep walking is generally between 5 and 10 years whereas confusional arousals and sleep terror may occur 3 years earlier. Sleep terrors are mainly characterised by screaming, agitation, flushed face, sweating and only share the inconsolability with confusional arousals. The current 3rd edition of the International Classification of Sleep Disorders (ICSD-3) added the sleep-related eating disorders in the disorders of arousal from NREM sleep. Diagnostic and Statistical Manual of Mental Disorders (DSM) Confusional arousals are at the time not considered as a disorder in the current 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V). This absence may be explained by the fact that confusional arousals have been understudied by the scientific community. Diagnosis The evaluation "should include a comprehensive medical history, a physical, neurological, and developmental examination, and a detailed description of the nocturnal events, sleep-wake schedules, and daytime behaviour”. However, the episodes have a long duration and a low rate of same-night recurrence. Even if amnesia usually follows episodes of confusional arousal, it is not a distinct trait related to severity.A video-polysomnography (see polysomnography) might be required if life history is untypical. In case of suspicion parents are encouraged to use infrared camera to record the behaviour of their child during sleep. Association of video recordings of nocturnal episodes with historical features is an important tool for both understanding and correctly diagnosing the disorder differently from other episodes of parasomnia. Confusional arousals as well as arousal parasomnias in general must be distinguished from epileptic seizure on the basis of clinical and electroencephalographic features (see electroencephalography). Management Children mostly outgrow the condition by late adolescence if not sooner. Management includes mainly non-pharmacological treatments and daily behaviours guidelines, but may include safety measures and/or medications if the patient is in danger from his or her behaviour: Ensure regular and adequate sleep routines in order to prevent sleep-wake cycle to be disrupted. Use of safety measures for the patient and family by clearing the bedroom from obstacles, securing the windows, or installing locks or alarms. Medications are necessary if the patient is in danger from his or her behaviour. In this case, Imipramine or low-dose Clonazepam is beneficial. Epidemiology The current prevalence of confusional arousals varies according to the year and the sample population and is approximately 4% (4.2% in 1999 in UK sample population, 6.1% (15–24 years old), 3.3% (25–34 y.o.) and 2% (35+ y.o.) in 2000 in UK, Germany and Italy sample population, 6.9% in 2010 in Norway sample population with a lifetime prevalence of 18.5%). The current prevalence of confusional arousals in children (3–13 y.o.) is higher and around 17.3%. Confusional arousals without a known cause or associated condition is uncommon (for about 1% of cases ).The contribution of genetics and family link is strong and episodes of confusional arousals can occur in several members of the same family. Risk factors Some independent risk factors associated with confusional arousals have been identified. According to studies, they are shift work, hypnagogic hallucinations (also known as hypnagogia), excessive daytime sleepiness, insomnia and hypersomnia disorder, circadian rhythm sleep disorder, restless legs syndrome, obstructive sleep apnea syndrome (OSAS), bipolar disorder, daily smoking, and age of 15–24 years. These risk factors of confusional arousals are somehow related to mental disorders and medical conditions and affecting mostly younger subjects regardless of gender. Precipitating factors include sleep deprivation, use of hypnotics or tranquilisers before bedtime, and sudden awakening from sleep (e.g., telephone ringing, alarm clock).In the ICSD-2 alcohol intake had been considered as a precipitating factor of confusional arousals. In the ICSD-3 the relation between alcohol use and disorder or arousal have been excluded. Moreover, the alcohol blackout has been added as a differential diagnosis. These changes have important implications for forensic cases. == References ==

What does General paresis of the insane mean Aarogya

General paresis of the insane

General paresis, also known as general paralysis of the insane (GPI), paralytic dementia, or syphilitic paresis is a severe neuropsychiatric disorder, classified as an organic mental disorder and is caused by late-stage syphilis and the chronic meningoencephalitis and cerebral atrophy that are associated with this late stage of the disease when left untreated. GPI differs from mere paresis, as mere paresis can result from multiple other causes and usually does not affect cognitive function. Degenerative changes caused by GPI are associated primarily with the frontal and temporal lobar cortex. The disease affects approximately 7% of individuals infected with syphilis, and is far more common in third world countries where fewer options for timely treatment are available. It is more common among men. GPI was originally considered to be a type of madness due to a dissolute character, when first identified in the early 19th century. The conditions connection with syphilis was discovered in the late 1880s. Progressively, with the discovery of organic arsenicals such as Salvarsan and Neosalvarsan (1910s), the development of pyrotherapy (1920s), and the widespread availability and use of penicillin in the treatment of syphilis (1940s), the condition was rendered avoidable and curable. Prior to this, GPI was inevitably fatal, and it accounted for as much as 25% of the primary diagnoses for residents in public psychiatric hospitals. Signs and symptoms Symptoms of the disease first appear from 10 to 30 years after infection. Incipient GPI is usually manifested by neurasthenic difficulties, such as fatigue, headaches, insomnia, dizziness, etc. As the disease progresses, mental deterioration and personality changes occur. Typical symptoms include loss of social inhibitions, asocial behavior, gradual impairment of judgment, concentration and short-term memory, euphoria, mania, depression, or apathy. Subtle shivering, minor defects in speech and Argyll Robertson pupil may become noticeable. Delusions, common as the illness progresses, tend to be poorly systematized and absurd. They can be grandiose, melancholic, or paranoid. These delusions include ideas of great wealth, immortality, thousands of lovers, unfathomable power, apocalypsis, nihilism, self-guilt, self-blame, or bizarre hypochondriacal complaints. Later, the patient experiences dysarthria, intention tremors, hyperreflexia, myoclonic jerks, confusion, seizures and severe muscular deterioration. Eventually, the paretic dies bedridden, cachectic and completely disoriented, frequently in a state of status epilepticus. Diagnosis The diagnosis could be differentiated from other known psychoses and dementias by a characteristic abnormality in eye pupil reflexes (Argyll Robertson pupil), and, eventually, the development of muscular reflex abnormalities, seizures, memory impairment (dementia) and other signs of relatively pervasive neurocerebral deterioration. Definitive diagnosis is based on the analysis of cerebrospinal fluid and tests for syphilis. Prognosis Although there were recorded cases of remission of the symptoms, especially if they had not passed beyond the stage of psychosis, these individuals almost invariably experienced relapse within a few months to a few years. Otherwise, the patient was seldom able to return home because of the complexity, severity and unmanageability of the evolving symptom picture. Eventually, the patient would become completely incapacitated, bed ridden, and would die, the process taking about three to five years on average. History While retrospective studies have found earlier instances of what may have been the same disorder, the first clearly identified examples of paresis among the insane were described in Paris after the Napoleonic Wars. General paresis of the insane was first described as a distinct disease in 1822 by Antoine Laurent Jesse Bayle. General paresis most often struck people (men far more frequently than women) between 20 and 40 years of age. By 1877, for example, the superintendent of an asylum for men in New York reported that in his institution this disorder accounted for more than 12% of admissions and more than 2% of deaths. Originally, the cause was believed to be an inherent weakness of character or constitution. While Friedrich von Esmarch and the psychiatrist Peter Willers Jessen (junior) had asserted as early as 1857 that syphilis caused general paresis (progressive Paralyse), progress toward the general acceptance by the medical community of this idea was only accomplished later by the eminent 19th Century syphilographer Jean Alfred Fournier (1832—1914). In 1913 all doubt about the syphilitic nature of paresis was finally eliminated when Hideyo Noguchi and J. W. Moore demonstrated the syphilitic spirochaetes in the brains of paretics. In 1917 Julius Wagner-Jauregg discovered that malaria therapy (in this case, medical induction of a fever) involving infecting paretic patients with malaria could halt the progression of general paresis. He won a Nobel Prize for this discovery in 1927. After World War II the use of penicillin to treat syphilis made general paresis a rarity: even patients manifesting early symptoms of actual general paresis were capable of full recovery with a course of penicillin. The disorder is now virtually unknown outside developing countries, and even there the epidemiology is substantially reduced. Some notable cases of general paresis: General Ranald S. Mackenzie was retired from the US Army in 1884 for "general paresis of the insane" 5 years before his death in 1889. Theo Van Gogh, brother of painter Vincent van Gogh, died six months after Vincent in 1891 from "dementia parylitica" or what is now called syphilitic paresis.The Chicago gangster Al Capone died of syphilitic paresis, having contracted syphilis in a brothel in 1919, and not having been properly treated for it in time to prevent his later onset of syphilitic paresis. See also Karolina Olsson Neurosyphilis Tabes dorsalis Tuskegee experiment References == External links ==

Hello Aarogya, explain a situation where Complex regional pain syndrome occurs

Complex regional pain syndrome

Complex regional pain syndrome (CRPS) is any of several painful conditions that are characterized by a continuing (spontaneous and/or evoked) regional pain that is seemingly disproportionate in time or degree to the usual course of any known trauma or other lesion. Usually starting in a limb, it manifests as extreme pain, swelling, limited range of motion, and changes to the skin and bones. It may initially affect one limb and then spread throughout the body; 35% of affected people report symptoms throughout their whole bodies. Two types exist: reflex sympathetic dystrophy (RSD) and causalgia. Having both types is possible. Classification The classification system in use by the International Association for the Study of Pain (IASP) divides CRPS into two types. It is recognised that people may exhibit both types of CRPS. Signs and symptoms Clinical features of CRPS have been found to be inflammation resulting from the release of certain proinflammatory chemical signals from the nerves, sensitized nerve receptors that send pain signals to the brain, dysfunction of the local blood vessels ability to constrict and dilate appropriately, and maladaptive neuroplasticity.The signs and symptoms of CRPS usually manifest near the injury site. The most common symptoms are extreme pain, including burning, stabbing, grinding, and throbbing. The pain is out of proportion to the severity of the initial injury. Moving or touching the limb is often intolerable. With diagnosis of either CRPS types I or II, patients may develop burning pain and allodynia. Both syndromes are also characterized by autonomic dysfunction, which presents with temperature changes (usually localized, but can be global), cyanosis, and/or edema.The patient may also experience localized swelling; extreme sensitivity to nonpainful stimuli such as wind, water, noise, and vibrations; extreme sensitivity to touch (by themselves, other people, and even light clothing or bedding/blankets); abnormally increased sweating (or absent sweating); changes in skin temperature (alternating between overly warm and cold); changes in skin colouring (from white and mottled to bright red or reddish-violet); changes in skin texture (waxy, shiny, thin, tight skin); softening and thinning of bones; joint tenderness or stiffness; changes in nails and hair (delayed or increased growth, brittle nails/hair that easily break); muscle spasms; muscle loss (atrophy); tremors; dystonia; allodynia; hyperalgesia; and decreased/restricted ability and painful movement of affected body part. Drop attacks (falls), almost fainting, and fainting spells are infrequently reported, as are visual problems.The symptoms of CRPS vary in severity and duration. Since CRPS is a systemic problem, potentially any organ can be affected. Symptoms may change over time, and they can vary from person to person. The more dynamic symptoms, especially vascular aspects (edema, temperature) and location of pain, can change numerous times a day.Previously, CRPS was considered to have three stages however more recent studies suggest people affected by CRPS do not progress through sequential stages and the staging system is no longer in wide use. Growing evidence instead points towards distinct sub-types of CRPS. Cause Complex regional pain syndrome is uncommon, and its cause is not clearly understood. CRPS typically develops after an injury, surgery, heart attack, or stroke. Investigators estimate that 2–5% of those with peripheral nerve injury, and 13-70% of those with hemiplegia (paralysis of one side of the body) will develop CRPS. In addition, some studies have indicated that cigarette smoking was strikingly present in patients and is statistically linked to RSD. This may be involved in its pathology by enhancing sympathetic activity, vasoconstriction, or by some other unknown neurotransmitter-related mechanism. This hypothesis was based on a retrospective analysis of 53 patients with RSD, which showed that 68% of patients and only 37% of controls were smokers. The results are preliminary and are limited by their retrospective nature. 7% of people who have CRPS in one limb later develop it in another limb. Pathophysiology Inflammation and alteration of pain perception in the central nervous system are proposed to play important roles. The persistent pain and the perception of nonpainful stimuli as painful are thought to be caused by inflammatory molecules (IL-1, IL2, TNF-alpha) and neuropeptides (substance P) released from peripheral nerves. This release may be caused by inappropriate cross-talk between sensory and motor fibers at the affected site. CRPS is not a psychological illness, yet pain can cause psychological problems, such as anxiety and depression. Often, impaired social and occupational function occur.Complex regional pain syndrome is a multifactorial disorder with clinical features of neurogenic inflammation (swelling in the central nervous system), nociceptive sensitisation (which causes extreme sensitivity or allodynia), vasomotor dysfunction (blood flow problems which cause swelling and discolouration) and maladaptive neuroplasticity (where the brain changes and adapts with constant pain signals); CRPS is the result of an "aberrant [inappropriate] response to tissue injury". The "underlying neuronal matrix" of CRPS is seen to involve cognitive and motor as well as nociceptive processing; pinprick stimulation of a CRPS affected limb was painful (mechanical hyperalgesia) and showed a "significantly increased activation" of not just the S1 cortex (contralateral), S2 (bilateral) areas, and insula (bilateral) but also the associative-somatosensory cortices (contralateral), frontal cortices, and parts of the anterior cingulate cortex. In contrast to previous thoughts reflected in the name RSD, it appears that there is reduced sympathetic nervous system outflow, at least in the affected region (although there may be sympatho-afferent coupling). Wind-up (the increased sensation of pain with time) and central nervous system (CNS) sensitization are key neurologic processes that appear to be involved in the induction and maintenance of CRPS.Compelling evidence shows that the N-methyl-D-aspartate (NMDA) receptor has significant involvement in the CNS sensitization process. It is also hypothesized that elevated CNS glutamate levels promote wind-up and CNS sensitization. In addition, there exists experimental evidence demonstrating the presence of NMDA receptors in peripheral nerves. Because immunological functions can modulate CNS physiology, a variety of immune processes have also been hypothesized to contribute to the initial development and maintenance of peripheral and central sensitization. Furthermore, trauma-related cytokine release, exaggerated neurogenic inflammation, sympathetic afferent coupling, adrenoreceptor pathology, glial cell activation, cortical reorganisation, and oxidative damage (e.g., by free radicals) are all factors which have been implicated in the pathophysiology of CRPS. In addition, autoantibodies are present in a wide number of CRPS patients and IgG has been recognized as one of the causes of hypersensitivity that stimulates A and C nociceptors, attributing to the inflammation.The mechanisms leading to reduced bone mineral density (up to overt osteoporosis) are still unknown. Potential explanations include a dysbalance of the activities of sympathetic and parasympathetic autonomic nervous system and mild secondary hyperparathyroidism. However, the trigger of secondary hyperparathyroidism has not yet been identified.In summary, the pathophysiology of complex regional pain syndrome has not yet been defined; CRPS, with its variable manifestations, could be the result of multiple pathophysiological processes. Diagnosis Diagnosis is primarily based on clinical findings. The original diagnostic criteria for CRPS adopted by the International Association for the Study of Pain (IASP) in 1994 have now been superseded in both clinical practice and research by the "Budapest Criteria" which were created in 2003 and have been found to be more sensitive and specific. They have since been adopted by the IASP. The criteria require there to be pain as well as a history and clinical evidence of Sensory, Vasomotor, Sudomotor and Motor or Trophic changes. It is also stated that it is a diagnosis of exclusion.To make a clinical diagnosis all four of the following criteria must be met: Continuing pain, which is disproportionate to any inciting event Must report at least one symptom in three of the four following categories.. Sensory: Reports of hyperesthesia Vasomotor: Reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry Sudomotor/Edema: Reports of edema and/or sweating changes and/or sweating asymmetry Motor/Trophic: Reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin) Must display at least one sign at time of evaluation in two or more of the following categories Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or temperature sensation and/or deep somatic pressure and/or joint movement) Vasomotor: Evidence of temperature asymmetry (>1 °C) and/or skin color changes and/or asymmetry Sudomotor/Edema: Evidence of edema and/or sweating changes and/or sweating asymmetry Motor/Trophic: Evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin) There is no other diagnosis that better explains the signs and symptoms Diagnostic adjuncts No specific test is available for CRPS, which is diagnosed primarily through observation of the symptoms. However, thermography, sweat testing, X-rays, electrodiagnostics, and sympathetic blocks can be used to build up a picture of the disorder. Diagnosis is complicated by the fact that some patients improve without treatment. A delay in diagnosis and/or treatment for this syndrome can result in severe physical and psychological problems. Early recognition and prompt treatment provide the greatest opportunity for recovery. Thermography Presently, established empirical evidence suggests against thermographys efficacy as a reliable tool for diagnosing CRPS. Although CRPS may, in some cases, lead to measurably altered blood flow throughout an affected region, many other factors can also contribute to an altered thermographic reading, including the patients smoking habits, use of certain skin lotions, recent physical activity, and prior history of trauma to the region. Also, not all patients diagnosed with CRPS demonstrate such "vasomotor instability" — particularly those in the later stages of the disease. Thus, thermography alone cannot be used as conclusive evidence for—or against—a diagnosis of CRPS and must be interpreted in light of the patients larger medical history and prior diagnostic studies.In order to minimise the confounding influence of external factors, patients undergoing infrared thermographic testing must conform to special restrictions regarding the use of certain vasoconstrictors (namely, nicotine and caffeine), skin lotions, physical therapy, and other diagnostic procedures in the days prior to testing. Patients may also be required to discontinue certain pain medications and sympathetic blockers. After a patient arrives at a thermographic laboratory, he or she is allowed to reach thermal equilibrium in a 16–20 °C, draft-free, steady-state room wearing a loose fitting cotton hospital gown for approximately twenty minutes. A technician then takes infrared images of both the patients affected and unaffected limbs, as well as reference images of other parts of the patients body, including his or her face, upper back, and lower back. After capturing a set of baseline images, some labs further require the patient to undergo cold-water autonomic-functional-stress-testing to evaluate the function of their autonomic nervous systems peripheral vasoconstrictor reflex. This is performed by placing a patients unaffected limb in a cold water bath (approximately 20 °C) for five minutes while collecting images. In a normal, intact, functioning autonomic nervous system, a patients affected extremity will become colder. Conversely, warming of an affected extremity may indicate a disruption of the bodys normal thermoregulatory vasoconstrictor function, which may sometimes indicate underlying CRPS. Radiography Scintigraphy, plain radiographs, and magnetic resonance imaging may all be useful diagnostically. Patchy osteoporosis (post-traumatic osteoporosis), which may be due to disuse of the affected extremity, can be detected through X-ray imagery as early as two weeks after the onset of CRPS. A bone scan of the affected limb may detect these changes even sooner and can almost confirm the disease. Bone densitometry can also be used to detect changes in bone mineral density. It can also be used to monitor the results of treatment since bone densitometry parameters improve with treatment. Ultrasound Ultrasound-based osteodensitometry (ultrasonometry) may be potential future radiation-free technique to identify reduced bone mineral density in CRPS. Additionally, this method promises to quantify the bone architecture in the periphery of affected limbs. This method is still under experimental development. Electrodiagnostic testing Electromyography (EMG) and nerve conduction studies (NCS) are important ancillary tests in CRPS because they are among the most reliable methods of detecting nerve injury. They can be used as one of the primary methods to distinguish between CRPS types I and II, which differ based on evidence of actual nerve damage. EMG and NCS are also among the best tests for ruling in or out alternative diagnoses. CRPS is a "diagnosis of exclusion", which requires that no other diagnosis can explain the patients symptoms. This is very important to emphasise because patients otherwise can be given a wrong diagnosis of CRPS when they actually have a treatable condition that better accounts for their symptoms. An example is severe carpal tunnel syndrome (CTS), which can often present in a very similar way to CRPS. Unlike CRPS, CTS can often be corrected with surgery to alleviate the pain and avoid permanent nerve damage and malformation.Both EMG and NCS involve some measure of discomfort. EMG involves the use of a tiny needle inserted into specific muscles to test the associated muscle and nerve function. Both EMG and NCS involve very mild shocks that in normal patients are comparable to a rubber band snapping on the skin. Although these tests can be very useful in CRPS, thorough informed consent must be obtained prior to the procedure, particularly in patients experiencing severe allodynia. In spite of the utility of the test, these patients may wish to decline the procedure to avoid discomfort. Classification Type I, formerly known as reflex sympathetic dystrophy (RSD), Sudecks atrophy, or algoneurodystrophy, does not exhibit demonstrable nerve lesions. As the vast majority of patients diagnosed with CRPS have this type, it is most commonly referred to in medical literature as type I. Type II, formerly known as causalgia, has evidence of obvious nerve damage. Despite evidence of nerve injury, the cause or the mechanisms of CRPS type II are as unknown, as the mechanisms of type I.Patients are frequently classified into two groups based upon temperature: "warm" or "hot" CRPS in one group and "cold" CRPS in the other group. The majority of patients (about 70%) have the "hot" type, which is said to be an acute form of CRPS. Cold CRPS is said to be indicative of a more chronic CRPS and is associated with poorer McGill Pain Questionnaire scores, increased central nervous system involvement, and a higher prevalence of dystonia. Prognosis is not favourable for cold CRPS patients; longitudinal studies suggest these patients have "poorer clinical pain outcomes and show persistent signs of central sensitisation correlating with disease progression". Prevention Vitamin C may be useful in prevention of the syndrome following fracture of the forearm or foot and ankle. Treatment Treatment of CRPS often involves a number of modalities. Therapy Physical and occupational therapy have low-quality evidence to support their use. Physical therapy interventions may include transcutaneous electrical nerve stimulation, progressive weight bearing, graded tactile desensitization, massage, and contrast bath therapy. In a retrospective cohort (unblinded, non-randomised and with intention-to-treat) of fifty patients diagnosed with CRPS, the subjective pain and body perception scores of patients decreased after engagement with a two-week multidisciplinary rehabilitation programme. The authors call for randomised controlled trials to probe the true value of multidisciplinary programs for CRPS patients. Mirror box therapy Mirror box therapy uses a mirror box, or a stand-alone mirror, to create a reflection of the normal limb such that the patient thinks they are looking at the affected limb. Movement of this reflected normal limb is then performed so that it looks to the patient as though they are performing movement with the affected limb. Mirror box therapy appears to be beneficial at least in early CRPS. However, beneficial effects of mirror therapy in the long term is still unproven. Graded motor imagery Graded motor imagery appears to be useful for people with CRPS-1. Graded motor imagery is a sequential process that consists of (a) laterality reconstruction, (b) motor imagery, and (c) mirror therapy.Transcutaneous Electrical Nerve Stimulation (TENS) Transcutaneous Electrical Nerve Stimulation (TENS) is a therapy that uses low voltage electrical signals to provide pain relief through electrodes that are placed on the surface of the skin. Evidence supports its use in treating pain and edema associated with CRPS although it does not seem to increase functional ability in CRPS patients. Medications Tentative evidence supports the use of bisphosphonates, calcitonin, and ketamine. Nerve blocks with guanethidine appear to be harmful. Evidence for sympathetic nerve blocks generally is insufficient to support their use. Intramuscular botulinum injections may benefit people with symptoms localized to one extremity. Ketamine Ketamine, a dissociative anesthetic, appears promising as a treatment for CRPS. It may be used in low doses if other treatments have not worked. No benefit on either function or depression, however, has been seen. Bisphosphonate treatment As of 2013, high-quality evidence supports the use of bisphosphonates (either orally or via IV infusion) in the treatment of CRPS. Bisphosphonates inhibit osteoclasts which are cells involved in the resorption of bone. Bone remodeling, via osteoclast activity in resorption of bone, is thought to sometimes be hyperactive in CRPS. It is hypothesized that bone resorption causes acidification of the intercellular milieu and this activates nerves involved in nociception that densely innervate bone causing pain; therefore inhibiting bone resorption and remodeling is thought to help with regards to pain in CRPS. CRPS involving high levels of bone resorption, as seen on bone scan, is more likely to respond to bisphosphonate therapy. Opioids Opioids such as oxycodone, morphine, hydrocodone, and fentanyl have a controversial place in treatment of CRPS. These drugs must be prescribed and monitored under close supervision of a physician, as these drugs will lead to physical dependence and can lead to addiction. Thus far, no long-term studies of oral opioid use in treating neuropathic pain, including CRPS, have been performed. The consensus among experts is that opioids should not be a first line therapy and should only be considered after all other modalities (non-opioid medications, physical therapy, and procedures) have been trialed. Surgery Spinal cord stimulators Spinal cord stimulator appears to be an effective therapy in the management of patients with CRPS type I (level A evidence) and type II (level D evidence). While they improve pain and quality of life, evidence is unclear regarding effects on mental health and general functioning.Dorsal root ganglion stimulation is type of neurostimulation that is effective in the management of focal neuropathic pain. The FDA approved its use in February 2016. The ACCURATE Study demonstrated superiority of dorsal root ganglion stimulation over spinal (dorsal column) stimulation in the management of CRPS and causalgia. Sympathectomy Surgical, chemical, or radiofrequency sympathectomy — interruption of the affected portion of the sympathetic nervous system — can be used as a last resort in patients with impending tissue loss, edema, recurrent infection, or ischemic necrosis. However, little evidence supports these permanent interventions to alter the pain symptoms of the affected patients, and in addition to the normal risks of surgery, such as bleeding and infection, sympathectomy has several specific risks, such as adverse changes in how nerves function. Amputation No randomized study in medical literature has studied the response with amputation of patients who have failed the above-mentioned therapies and who continue to be miserable. Nonetheless, on average, about half of the patients will have resolution of their pain, while half will develop phantom limb pain and/or pain at the amputation site. As in any other chronic pain syndrome, the brain likely becomes chronically stimulated with pain, and late amputation may not work as well as it might be expected. In a survey of 15 patients with CRPS type 1, 11 responded that their lives were better after amputation. Since this is the ultimate treatment of a painful extremity, it should be left as a last resort. Prognosis The prognosis in CRPS is improved with early and aggressive treatment; with the risk of chronic, debilitating pain being reduced with the early treatment. If treatment is delayed, however, the disorder can quickly spread to the entire limb, and changes in bone, nerve, and muscle may become irreversible. The prognosis is worse with the chronic "cold" form of CRPS and with CRPS affecting the upper extremities. Disuse of the limb after an injury or psychological distress related to an injury are also associated with a poorer prognosis in CRPS. Some cases of CRPS may resolve spontaneously (with 74% of patients undergoing complete resolution of symptoms (often spontaneously) in a population based study in Minnesota), but others may develop chronic pain for many years. Once one is diagnosed with CRPS, should it go into remission, the likelihood of it resurfacing after going into remission is significant. Taking precautions and seeking immediate treatment upon any injury is important. Epidemiology CRPS can occur at any age, with the average age at diagnosis being 42. It affects both men and women; however, CRPS is three times more frequent in females than males.CRPS affects both adults and children, and the number of reported CRPS cases among adolescents and young adults has been increasing, with a recent observational study finding an incidence of 1.16/100,000 among children in Scotland. History The condition currently known as CRPS was originally described during the American Civil War by Silas Weir Mitchell, who is sometimes also credited with inventing the name "causalgia". However, this term was actually coined by Mitchells friend Robley Dunglison from the Greek words for heat and for pain. Contrary to what is commonly accepted, it emerges that these causalgias were certainly major by the importance of the vasomotor and sudomotor symptoms but stemmed from minor neurological lesions. In the 1940s, the term reflex sympathetic dystrophy came into use to describe this condition, based on the theory that sympathetic hyperactivity was involved in the pathophysiology. In 1959, Noordenbos observed in causalgia patients that "the damage of the nerve is always partial." Misuse of the terms, as well as doubts about the underlying pathophysiology, led to calls for better nomenclature. In 1993, a special consensus workshop held in Orlando, Florida, provided the umbrella term "complex regional pain syndrome", with causalgia and RSD as subtypes. Research The National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health, supports and conducts research on the brain and central nervous system, including research relevant to RSDS, through grants to major medical institutions across the country. NINDS-supported scientists are working to develop effective treatments for neurological conditions and ultimately, to find ways of preventing them. Investigators are studying new approaches to treat CRPS and intervene more aggressively after traumatic injury to lower the patients chances of developing the disorder. In addition, NINDS-supported scientists are studying how signals of the sympathetic nervous system cause pain in CRPS patients. Using a technique called microneurography, these investigators are able to record and measure neural activity in single nerve fibers of affected patients. By testing various hypotheses, these researchers hope to discover the unique mechanism that causes the spontaneous pain of CRPS, and that discovery may lead to new ways of blocking pain. Other studies to overcome chronic pain syndromes are discussed in the pamphlet "Chronic Pain: Hope Through Research", published by the NINDS.Research into treating the condition with mirror visual feedback is being undertaken at the Royal National Hospital for Rheumatic Disease in Bath. Patients are taught how to desensitize in the most effective way, then progress to using mirrors to rewrite the faulty signals in the brain that appear responsible for this condition. However, while CRPS can go into remission, the chance of it reoccurring is significant.The Netherlands has the most comprehensive program of research into CRPS, as part of a multimillion-Euro initiative called TREND. German and Australian research teams are also pursuing better understanding and treatments for CRPS. In other animal species CRPS has also been described in animals, such as cattle. Notable cases Nia Frazier, Dance Moms star Paula Abdul, singer, actor, TV personality Jill Kinmont Boothe, US ski slalom champion Gemma Collis-McCann, British paralympic fencer Shin Dong-wook, South Korean actor and model Howard Hughes, American business tycoon, aviator, inventor, filmmaker, and philanthropist Rachel Morris, British paralympic cyclist. Cynthia Toussaint, author and media personality Danielle Brown, British paralympic archer Radene Marie Cook, former Los Angeles radio broadcaster, artist, and advocate Marieke Vervoort, Belgian Paralympic athlete Bruno Soriano, Spanish footballer References External links Complex regional pain syndrome at Curlie Reflex sympathetic dystrophy at Curlie

Aarogya , Do you know what is Horners syndrome,

Horners syndrome

Horners syndrome, also known as oculosympathetic paresis, is a combination of symptoms that arises when a group of nerves known as the sympathetic trunk is damaged. The signs and symptoms occur on the same side (ipsilateral) as it is a lesion of the sympathetic trunk. It is characterized by miosis (a constricted pupil), partial ptosis (a weak, droopy eyelid), apparent anhidrosis (decreased sweating), with apparent enophthalmos (inset eyeball).The nerves of the sympathetic trunk arise from the spinal cord in the chest, and from there ascend to the neck and face. The nerves are part of the sympathetic nervous system, a division of the autonomic (or involuntary) nervous system. Once the syndrome has been recognized, medical imaging and response to particular eye drops may be required to identify the location of the problem and the underlying cause. Signs and symptoms Signs that are found in people with Horners syndrome on the affected side of the face include the following: ptosis (drooping of the upper eyelid) anhidrosis (decreased sweating) miosis (constriction of the pupil) Enophthalmos (sinking of the eyeball into the face) inability to completely close or open the eyelid facial flushing headaches loss of ciliospinal reflex bloodshot conjunctiva, depending on the site of lesion. unilateral straight hair (in congenital Horners syndrome); the hair on the affected side may be straight in some cases. heterochromia iridum (in congenital Horners syndrome)Interruption of sympathetic pathways leads to several implications. It inactivates the dilator muscle and thereby produces miosis. It inactivates the superior tarsal muscle which produces ptosis. It reduces sweat secretion in the face. Patients may have apparent enophthalmos (affected eye looks to be slightly sunken in) but this is not always the case. The ptosis from inactivation of the superior tarsal muscle causes the eye to appear sunken in, but when actually measured, enophthalmos is not present. The phenomenon of enophthalmos is seen in Horners syndrome in cats, rats, and dogs.Sometimes there is flushing on the affected side of the face due to dilation of blood vessels under the skin. The pupils light reflex is maintained as this is controlled via the parasympathetic nervous system.In children, Horners syndrome sometimes leads to heterochromia, a difference in eye color between the two eyes. This happens because a lack of sympathetic stimulation in childhood interferes with melanin pigmentation of the melanocytes in the superficial stroma of the iris.In veterinary medicine, signs can include partial closure of the third eyelid, or nictitating membrane. Causes Horners syndrome is usually acquired as a result of disease, but may also be congenital (inborn, associated with heterochromatic iris) or iatrogenic (caused by medical treatment). In rare cases, Horners syndrome may be the result of repeated, minor head trauma, such as being hit with a soccer ball. Although most causes are relatively benign, Horners syndrome may reflect serious disease in the neck or chest (such as a Pancoast tumor (tumor in the apex of the lung) or thyrocervical venous dilatation).Causes can be divided according to the presence and location of anhidrosis: Central (anhidrosis of face, arm and trunk) Syringomyelia Multiple sclerosis Encephalitis Brain tumors Lateral medullary syndrome Preganglionic (anhidrosis of face) Cervical rib traction on stellate ganglion Thyroid carcinoma Thyroidectomy Goiter Bronchogenic carcinoma of the superior fissure (Pancoast tumor) on apex of lung Klumpke paralysis Trauma - base of neck, usually blunt trauma, sometimes surgery. As a complication of tube thoracostomy Thoracic aortic aneurysm Postganglionic (no anhidrosis) Cluster headache - combination termed Hortons headache An episode of Horners syndrome may occur during a migraine attack and be relieved afterwards Carotid artery dissection/carotid artery aneurysm/trauma Cavernous sinus thrombosis Middle ear infection Sympathectomy Nerve blocks, such as cervical plexus block, stellate ganglion or interscalene block Pathophysiology Horner syndrome is due to a deficiency of sympathetic activity. The site of lesion to the sympathetic outflow is on the ipsilateral side of the symptoms. The following are examples of conditions that cause the clinical appearance of Horners syndrome: First-order neuron disorder: Central lesions that involve the hypothalamospinal tract (e.g. transection of the cervical spinal cord). Second-order neuron disorder: Preganglionic lesions (e.g. compression of the sympathetic chain by a lung tumor) that releases acetylcholine. Third-order neuron disorder: Postganglionic lesions at the level of the internal carotid artery (e.g. a tumor in the cavernous sinus or a carotid artery dissection) that releases norepinephrine. Partial Horners syndrome: In case of a third-neuron disorder, anhidrosis is limited to the middle part of the forehead or can be absent, resulting in a partial Horners syndrome.If patients have impaired sweating above the waist affecting only one side of the body, and they do not have clinically apparent Horners syndrome, then their lesions are just below the stellate ganglion in the sympathetic chain. Diagnosis Three tests are useful in confirming the presence and severity of Horner syndrome: Cocaine drop test: Cocaine eyedrops block the reuptake of post-ganglionic norepinephrine resulting in the dilation of a normal pupil from retention of norepinephrine in the synapse. However, in Horners syndrome the lack of norepinephrine in the synaptic cleft causes mydriatic failure. A more recently introduced approach that is more dependable and obviates the difficulties in obtaining cocaine is to apply the alpha-agonist apraclonidine to both eyes and observe the increased mydriatic effect (due to hypersensitivity) on the affected side of Horner syndrome (the opposite effect to what the cocaine test would produce in the presence of Horners). Paredrine test: This test helps to localize the cause of the miosis. If the third order neuron (the last of three neurons in the pathway which ultimately discharges norepinephrine into the synaptic cleft) is intact, then the amphetamine causes neurotransmitter vesicle release, thus releasing norepinephrine into the synaptic cleft and resulting in robust mydriasis of the affected pupil. If the lesion itself is of the third order neuron, then the amphetamine will have no effect and the pupil remains constricted. There is no pharmacological test to differentiate between a first and second order neuron lesion. Dilation lag testIt is important to distinguish the ptosis caused by Horners syndrome from the ptosis caused by a lesion to the oculomotor nerve. In the former, the ptosis occurs with a constricted pupil (due to a loss of sympathetics to the eye), whereas in the latter, the ptosis occurs with a dilated pupil (due to a loss of innervation to the sphincter pupillae). In a clinical setting, these two ptoses are fairly easy to distinguish. In addition to the blown pupil in a CNIII (oculomotor nerve) lesion, this ptosis is much more severe, occasionally occluding the whole eye. The ptosis of Horner syndrome can be quite mild or barely noticeable (partial ptosis).When anisocoria occurs and the examiner is unsure whether the abnormal pupil is the constricted or dilated one, if a one-sided ptosis is present then the abnormally sized pupil can be presumed to be on the side of the ptosis. History The syndrome is named after Johann Friedrich Horner, the Swiss ophthalmologist who first described the syndrome in 1869. Several others had previously described cases, but "Horners syndrome" is most prevalent. In France and Italy, Claude Bernard is also eponymized with the condition (Claude Bernard–Horner syndrome, abbreviated CBH). In France, Francois Pourfour du Petit is also credited with describing this syndrome. Children The most common causes in young children are birth trauma and a type of cancer called neuroblastoma. The cause of about a third of cases in children is unknown. See also Anisocoria Harlequin syndrome References == External links ==

Aarogya what is Cutaneous amoebiasis

Cutaneous amoebiasis

Cutaneous amoebiasis, refers to a form of amoebiasis that presents primarily in the skin. It can be caused by Acanthamoeba or Entamoeba histolytica.: 421  When associated with Acanthamoeba, it is also known as "cutaneous acanthamoebiasis". Balamuthia mandrillaris can also cause cutaneous amoebiasis, but can prove fatal if the amoeba enters the bloodstream Diagnosis It is characterized by ulcers. Diagnosis of amebiasis cutis calls for high degree of clinical suspicion. This needs to be backed with demonstration of trophozoites from lesions. Unless an early diagnosis can be made such patients can develop significant morbidity. See also Skin lesion References == External links ==

Please give me a short description about Ehrlichiosis ewingii infection , Aarogya

Ehrlichiosis ewingii infection

Ehrlichiosis ewingii infection is an infectious disease caused by an intracellular bacteria, Ehrlichia ewingii. The infection is transmitted to humans by the tick, Amblyomma americanum. This tick can also transmit Ehrlichia chaffeensis, the bacteria that causes human monocytic ehrlichiosis (HME). Symptoms and signs Patients can present with fever, headache, myalgias, and malaise. Laboratory tests may reveal thrombocytopenia, leukopenia, and evidence of liver damage. Mechanism Humans contract the disease after a bite by an infected tick of the species Amblyomma americanum. Those with an underlying immunodeficiency (such as HIV) appear to be at greater risk of contracting the disease. Compared to HME, ewingii ehrlichiosis has a decreased incidence of complications.Like Anaplasma phagocytophilum, the causative agent of human granulocytic ehrlichiosis, Ehrlichia ewingii infects neutrophils. Infection with E. ewingii may delay neutrophil apoptosis. Diagnosis In endemic areas, a high index of suspicion is warranted, especially with a known exposure to ticks. The diagnosis can be confirmed by using PCR. A peripheral blood smear can also be examined for intracytoplasmic inclusions called morulae. Treatment The treatment of choice is doxycycline. See also Human monocytic ehrlichiosis Human granulocytic ehrlichiosis Ehrlichiosis (canine) References == External links ==

Aarogya, explain a scenario commonly referred as Dust storm

Dust storm

A dust storm, also called a sandstorm, is a meteorological phenomenon common in arid and semi-arid regions. Dust storms arise when a gust front or other strong wind blows loose sand and dirt from a dry surface. Fine particles are transported by saltation and suspension, a process that moves soil from one place and deposits it in another. The arid regions of North Africa, the Arabian peninsula, Central Asia and China are the main terrestrial sources of airborne dust. It has been argued that poor management of Earths drylands, such as neglecting the fallow system, are increasing the size and frequency of dust storms from desert margins and changing both the local and global climate, as well as impacting local economies.The term sandstorm is used most often in the context of desert dust storms, especially in the Sahara Desert, or places where sand is a more prevalent soil type than dirt or rock, when, in addition to fine particles obscuring visibility, a considerable amount of larger sand particles are blown closer to the surface. The term dust storm is more likely to be used when finer particles are blown long distances, especially when the dust storm affects urban areas. Causes As the force of dust passing over loosely held particles increases, particles of sand first start to vibrate, then to move across the surface in a process called saltation. As they repeatedly strike the ground, they loosen and break off smaller particles of dust which then begin to travel in suspension. At wind speeds above that which causes the smallest to suspend, there will be a population of dust grains moving by a range of mechanisms: suspension, saltation and creep.A study from 2008 finds that the initial saltation of sand particles induces a static electric field by friction. Saltating sand acquires a negative charge relative to the ground which in turn loosens more sand particles which then begin saltating. This process has been found to double the number of particles predicted by previous theories.Particles become loosely held mainly due to a prolonged drought or arid conditions, and high wind speeds. Gust fronts may be produced by the outflow of rain-cooled air from an intense thunderstorm. Or, the wind gusts may be produced by a dry cold front: that is, a cold front that is moving into a dry air mass and is producing no precipitation—the type of dust storm which was common during the Dust Bowl years in the U.S. Following the passage of a dry cold front, convective instability resulting from cooler air riding over heated ground can maintain the dust storm initiated at the front. In desert areas, dust and sand storms are most commonly caused by either thunderstorm outflows, or by strong pressure gradients which cause an increase in wind velocity over a wide area. The vertical extent of the dust or sand that is raised is largely determined by the stability of the atmosphere above the ground as well as by the weight of the particulates. In some cases, dust and sand may be confined to a relatively-shallow layer by a low-lying temperature inversion. In other instances, dust (but not sand) may be lifted as high as 6,000 m (20,000 ft). Drought and wind contribute to the emergence of dust storms, as do poor farming and grazing practices by exposing the dust and sand to the wind. One poor farming practice which contributes to dust storms is dryland farming. Particularly poor dryland farming techniques are intensive tillage or not having established crops or cover crops when storms strike at particularly vulnerable times prior to revegetation. In a semi-arid climate, these practices increase susceptibility to dust storms. However, soil conservation practices may be implemented to control wind erosion. Physical and environmental effects A sandstorm can transport and carry large volumes of sand unexpectedly. Dust storms can carry large amounts of dust, with the leading edge being composed of a wall of thick dust as much as 1.6 km (5,200 ft) high. Dust and sand storms which come off the Sahara Desert are locally known as a simoom or simoon (sîmūm, sîmūn). The haboob (həbūb) is a sandstorm prevalent in the region of Sudan around Khartoum, with occurrences being most common in the summer. The Sahara desert is a key source of dust storms, particularly the Bodélé Depression and an area covering the confluence of Mauritania, Mali, and Algeria. Sahara dust is frequently emitted into the Mediterranean atmosphere and transported by the winds sometimes as far north as central Europe and Great Britain.Saharan dust storms have increased approximately 10-fold during the half-century since the 1950s, causing topsoil loss in Niger, Chad, northern Nigeria, and Burkina Faso. In Mauritania there were just two dust storms a year in the early 1960s; there are about 80 a year since 2007, according to English geographer Andrew Goudie, professor at the University of Oxford. Levels of Saharan dust coming off the east coast of Africa in June 2007 were five times those observed in June 2006, and were the highest observed since at least 1999, which may have cooled Atlantic waters enough to slightly reduce hurricane activity in late 2007. Dust storms have also been shown to increase the spread of disease across the globe. Virus spores in the ground are blown into the atmosphere by the storms with the minute particles and interact with urban air pollution.Short-term effects of exposure to desert dust include immediate increased symptoms and worsening of the lung function in individuals with asthma, increased mortality and morbidity from long-transported dust from both Saharan and Asian dust storms suggesting that long-transported dust storm particles adversely affects the circulatory system. Dust pneumonia is the result of large amounts of dust being inhaled. Prolonged and unprotected exposure of the respiratory system in a dust storm can also cause silicosis, which, if left untreated, will lead to asphyxiation; silicosis is an incurable condition that may also lead to lung cancer. There is also the danger of keratoconjunctivitis sicca ("dry eyes") which, in severe cases without immediate and proper treatment, can lead to blindness. Economic impact Dust storms cause soil loss from the drylands, and worse, they preferentially remove organic matter and the nutrient-rich lightest particles, thereby reducing agricultural productivity. Also, the abrasive effect of the storm damages young crop plants. Dust storms also reduce visibility, affecting aircraft and road transportation. Dust can also have beneficial effects where it deposits: Central and South American rainforests get most of their mineral nutrients from the Sahara; iron-poor ocean regions get iron; and dust in Hawaii increases plantain growth. In northern China as well as the mid-western U.S., ancient dust storm deposits known as loess are highly fertile soils, but they are also a significant source of contemporary dust storms when soil-securing vegetation is disturbed. On Mars Dust storms are not limited to Earth and have been known to form on other planets such as Mars. These dust storms can extend over larger areas than those on Earth, sometimes encircling the planet, with wind speeds as high as 25 m/s (60 mph). However, given Mars much lower atmospheric pressure (roughly 1% that of Earths), the intensity of Mars storms could never reach the kind of hurricane-force winds that are experienced on Earth. Martian dust storms are formed when solar heating warms the Martian atmosphere and causes the air to move, lifting dust off the ground. The chance for storms is increased when there are great temperature variations like those seen at the equator during the Martian summer. See also Coccidioidomycosis Dry line Dust storm warning Haboob Iberulites List of dust storms Mineral dust Saharan Air Layer Shamal (wind) Sirocco References External links 12-hour U.S. map of surface dust concentrations Mouse-over an hour block on the row for Surface Dust Concentrations Dust in the Wind Archived 2020-04-16 at the Wayback Machine Photos of the April 14 1935 and September 2 1934 dust storms in the Texas Panhandle hosted by the Portal to Texas History. University of Arizona Dust Model Page Photos of a sandstorm in Riyadh in 2009 from the BBC Newsbeat website Dust storm in Phoenix Arizona via YouTube

Hi Aarogya, explain a situation where Gnathostomiasis occurs

Gnathostomiasis

Gnathostomiasis (also known as larva migrans profundus: 436 ) is the human infection caused by the nematode (roundworm) Gnathostoma spinigerum and/or Gnathostoma hispidum, which infects vertebrates. Symptoms and signs A few days after ingestion epigastric pain, fever, vomiting, and loss of appetite resulting from migration of larvae through intestinal wall to the abdominal cavity will appear in the patient. Migration in the subcutaneous tissues (under the skin) causes intermittent, migratory, painful, pruritic swellings (cutaneous larva migrans). Patches of edema appear after the above symptoms clear and are usually found on the abdomen. These lesions vary in size and can be accompanied by pruritus (itchy anus), rash, and stabbing pain. Swellings may last for 1 to 4 weeks in a given area and then reappear in a different location. Migration to other tissues (visceral larva migrans), can result in cough, hematuria (blood in urine), ocular (eye) involvement, meningitis, encephalitis and eosinophilia. Eosinophilic myeloencephalitis may also result from invasion of the central nervous system by the larvae. Causes Human gnathostomiasis is infection by the migrating third-stage larvae of any of five species of Gnathostoma, which is type of worm (more specifically a type of nematode). The most common cause in Asia is G. spinigerum, and the most common cause in the Americas is G. binucleatum. G. hispidium and G. doloresi occur in East and Southeast Asia; the former has also been found in Eastern Europe. G. nipponicum occurs only in Japan and China. There is one unconfirmed report of G. malaysiae causing disease in humans. Transmission Gnathostomiasis is transmitted by the ingestion of raw or insufficiently cooked definitive hosts such as fresh water fish, poultry, or frogs.In Thailand and Vietnam, the most common cause appears to be consumption of undercooked Asian swamp eels (Monopterus albus, also called Fluta alba) which transmit G. spinigerum. Monopterus albus is an invasive species in North America, but no Gnathostoma infections in humans have yet been conclusively identified in the US. Hosts Intermediate host The primary intermediate host is the minute crustaceans of the genus Cyclops. These crustaceans are then ingested by a second intermediate host, such as frogs. Definitive host The definitive hosts for gnathostomiasis include cats, dogs, tigers, leopards, lions, mink, opossums, raccoons, poultry, frogs, freshwater fish, snakes or birds. Incubation period The incubation period for gnathostomiasis is 3–4 weeks when the larvae begin to migrate through the subcutaneous tissue of the body. Morphology The adult parasite is reddish-brown in color and has a globular cephalic dome that is separated from the rest of the body by constriction. The posterior portion of the nematode is smooth while the anterior half is covered with fine leaf-like spines. The head is round and contains 4 to 8 transverse rows of hooklets that are protected by a pair of fleshy lips . The males are shorter than the females, 11–25 mm (0.43–0.98 in) compared to 25–54 mm (0.98–2.13 in) respectively. Eggs are oval and have a mucoid plug at one end. Life cycle Life cycle in definitive hosts Adult worms are found in a tumor located in the gastric wall of the definitive hosts and release eggs into the hosts digestive tract. The eggs are then released with feces and in about a week hatch in water to develop into first stage larva. Larvae are then ingested by minute copepods of the genus Cyclops. Once entering the copepod, the larvae penetrate the gastric wall of their intermediate host and begin to develop into second-stage and even early third-stage larvae. The copepods are then ingested by a second intermediate host such as fish, frogs, or snakes. Within this second intermediate or definitive host the larva repeat a similar pattern of penetrating the gastric wall, but then continue to migrate to muscular tissue and develop into advanced third-stage larvae. These larvae then encyst within the musculature of the new host. If the cyst containing flesh of these hosts is ingested by a definitive host, such as dogs, and cats, the cysts are ingested and the larvae escape the cysts and penetrate the gastric wall. These released larvae travel to the connective tissue and muscle as observed before and after 4 weeks they return to the gastric wall as adults. Here they form a tumor and continue to mature into adults for the next 6–8 months. Worms mate and females begin to excrete fertilized eggs with feces 8–12 months after ingestion of cysts. They are passed out in the feces and eaten by another fish. Life cycle in humans Infection of humans by gnathostomiasis is accidental because humans are not one of the definitive hosts of the parasite and do not allow the parasite to complete its life cycle. Infection in humans follows ingestion of raw or insufficiently cooked infected intermediate hosts. The ingested third stage larva migrates from the gastric wall and its migration results in the symptoms associated with infection by gnathostomiasis. The third stage larvae dont return to the gastric wall preventing it from maturing into adult worms, leaving the life cycle incomplete. Instead the larvae continue to migrate unpredictably unable to develop into adults, so eggs are seldom found in diagnostic tests. This also means the number of worms present in humans is a reflection of the number of third stage larvae ingested. Diagnosis Diagnosis of gnathostomiasis is possible (with microscopy) after removal of the worm. The primary form of diagnosis of gnathostomiasis is the identification of larva in the tissue. Serological testing such as enzyme-linked immunosorbent assay (ELISA) or the Western blot are also reliable but may not be easily accessible in endemic areas.CT scanning or MRI can be used to help identify a soft tissue worm and when looking at CNS disease it can be used to reveal the presence of the worm. The presence of haemorrhagic tracks on gradient-echo T2-weighted MRI is characteristic and possibly diagnostic. Prevention The best strategies for preventing accidental infection of humans is to educate those living in endemic areas to only consume fully cooked meat. The inability of the parasite to complete its life cycle within humans means that transmission can easily be contained by adequate preparation of meat from intermediate hosts. This is especially useful because of the difficulty and lack of feasibility inherent in eliminating all intermediate hosts of gnathostomiasis. So instead, individuals in endemic areas should avoid eating raw and undercooked meat in endemic areas, but this may be difficult in these areas. The dish ceviche is native to Peru and a favorite of Mexico. It consists of onion, cubed fish, lime or lemon juice and Andean spices including salt and chili. The ingredients are mixed together and they are allowed to marinate several hours before being served at room temperature. Then in endemic areas in Southeast Asia there are traditional dishes associated with these areas that also include raw uncooked fish, such as koipla in Thailand, goi ca song in Vietnam, sashimi and sushi in Japan.Acknowledging these cultural traditions, individuals in these cultural can be educated on methods of adapting their food preparation activities in order to remove the larvae without greatly altering these traditional dishes. For instance, meat should be marinated in vinegar for six hours or in soy sauce for 12 hours in order to successfully kill the larvae. In areas with reliable electricity, meat can be frozen at -20 degrees Celsius for 3–5 days to achieve the same results of killing the larvae present. Treatment Surgical removal or treatment with albendazole or ivermectin is recommended. The most prescribed treatment for gnathostomiasis is surgical removal of the larvae but this is only effective when the worms are located in an accessible location. In addition to surgical excision, albendazole and ivermectin have been noted in their ability to eliminate the parasite. Albendazole is recommended to be administered at 400 mg daily for 21 days as an adjunct to surgical excision, while ivermectin is better tolerated as a single dose. Ivermectin can also serve as a replacement for those that cant handle albendazole 200 ug/kg p.o. as a single dose. However, ivermectin has been shown to be less effective than albendazole. Epidemiology Endemic areas include Asia, Mexico, India and parts of South Africa. Originally believed to be confined to Asia, in the 1970s gnathostomiasis was discovered in Mexico, and found in Australia in 2011. Even though it is endemic in areas of Southeast Asia and Latin America, it is an uncommon disease. However, researchers have noticed recently an increase in incidence. This disease is most common in both Thailand and Japan, but in Thailand it is responsible for most of the observed parasitic CNS infection. It has long been recognised in China, but reports have only recently appeared in the English literature. History The first case of Gnathostoma infection was identified by Sir Richard Owen when inspecting the stomach of a young tiger that had died at London Zoo from a ruptured aorta. However it was not until 1889 that the first human case was described by Levinson when he found the Gnathostoma larva in an infested Thai woman. The lifecycle of G. spinigerum was described by Svasti Daengsvang and Chalerm Prommas from Thailand in 1933 and 1936. This delay in identification of the parasite in humans is due to the fact that humans are not a definitive host for this parasite making infection from this parasite rare. Gnathostomiasis infection is rare because the parasite must be digested when it has reached its third larvae stage, providing only a short time frame in which the parasite is capable of infecting humans. It is uncommon for the larvae to penetrate the skin of individuals exposed to contaminated food or water without ingestion. See also List of parasites (human) List of migrating cutaneous conditions References External links Gnathostomiasis Archived 2013-02-15 at the Wayback Machine at CDC Gnathostomiasis at eMedicine

Hello Aarogya, what is Restless legs syndrome

Restless legs syndrome

Restless legs syndrome (RLS), also known as Willis-Ekbom disease (WED), is generally a long-term disorder that causes a strong urge to move ones legs. There is often an unpleasant feeling in the legs that improves somewhat by moving them. This is often described as aching, tingling, or crawling in nature. Occasionally, arms may also be affected. The feelings generally happen when at rest and therefore can make it hard to sleep. Due to the disturbance in sleep, people with RLS may have daytime sleepiness, low energy, irritability and a depressed mood. Additionally, many have limb twitching during sleep. RLS is not the same as habitual foot tapping or leg rocking.Risk factors for RLS include low iron levels, kidney failure, Parkinsons disease, diabetes mellitus, rheumatoid arthritis, pregnancy and celiac disease. A number of medications may also trigger the disorder including antidepressants, antipsychotics, antihistamines, and calcium channel blockers. There are two main types. One is early onset RLS which starts before age 45, runs in families and worsens over time. The other is late onset RLS which begins after age 45, starts suddenly, and does not worsen. Diagnosis is generally based on a persons symptoms after ruling out other potential causes.Restless legs syndrome may resolve if the underlying problem is addressed. Otherwise treatment includes lifestyle changes and medication. Lifestyle changes that may help include stopping alcohol and tobacco use, and sleep hygiene. Medications used include a dopamine agonist such as pramipexole. RLS affects an estimated 2.5–15% of the American population. Females are more commonly affected than males, and it becomes increasingly common with age. Signs and symptoms RLS sensations range from pain or an aching in the muscles, to "an itch you cant scratch", a "buzzing sensation", an unpleasant "tickle that wont stop", a "crawling" feeling, or limbs jerking while awake. The sensations typically begin or intensify during quiet wakefulness, such as when relaxing, reading, studying, or trying to sleep.It is a "spectrum" disease with some people experiencing only a minor annoyance and others having major disruption of sleep and impairments in quality of life.The sensations—and the need to move—may return immediately after ceasing movement or at a later time. RLS may start at any age, including childhood, and is a progressive disease for some, while the symptoms may remit in others. In a survey among members of the Restless Legs Syndrome Foundation, it was found that up to 45% of patients had their first symptoms before the age of 20 years. "An urge to move, usually due to uncomfortable sensations that occur primarily in the legs, but occasionally in the arms or elsewhere."The sensations are unusual and unlike other common sensations. Those with RLS have a hard time describing them, using words or phrases such as uncomfortable, painful, antsy, electrical, creeping, itching, pins and needles, pulling, crawling, buzzing, and numbness. It is sometimes described similar to a limb falling asleep or an exaggerated sense of positional awareness of the affected area. The sensation and the urge can occur in any body part; the most cited location is legs, followed by arms. Some people have little or no sensation, yet still, have a strong urge to move."Motor restlessness, expressed as activity, which relieves the urge to move."Movement usually brings immediate relief, although temporary and partial. Walking is most common; however, stretching, yoga, biking, or other physical activity may relieve the symptoms. Continuous, fast up-and-down movements of the leg, and/or rapidly moving the legs toward then away from each other, may keep sensations at bay without having to walk. Specific movements may be unique to each person."Worsening of symptoms by relaxation."Sitting or lying down (reading, plane ride, watching TV) can trigger the sensations and urge to move. Severity depends on the severity of the persons RLS, the degree of restfulness, duration of the inactivity, etc."Variability over the course of the day-night cycle, with symptoms worse in the evening and early in the night."Some experience RLS only at bedtime, while others experience it throughout the day and night. Most people experience the worst symptoms in the evening and the least in the morning."restless legs feel similar to the urge to yawn, situated in the legs or arms."These symptoms of RLS can make sleeping difficult for many patients and a 2005 National Sleep Foundation poll shows the presence of significant daytime difficulties resulting from this condition. These problems range from being late for work to missing work or events because of drowsiness. Patients with RLS who responded reported driving while drowsy more than patients without RLS. These daytime difficulties can translate into safety, social and economic issues for the patient and for society.RLS may contribute to higher rates of depression and anxiety disorders in RLS patients. Primary and secondary RLS is categorized as either primary or secondary. Primary RLS is considered idiopathic or with no known cause. Primary RLS usually begins slowly, before approximately 40–45 years of age and may disappear for months or even years. It is often progressive and gets worse with age. RLS in children is often misdiagnosed as growing pains. Secondary RLS often has a sudden onset after age 40, and may be daily from the beginning. It is most associated with specific medical conditions or the use of certain drugs (see below). Causes While the cause is generally unknown, it is believed to be caused by changes in the nerve transmitter dopamine resulting in an abnormal use of iron by the brain. RLS is often due to iron deficiency (low total body iron status). Other associated conditions may include end-stage kidney disease and hemodialysis, folate deficiency, magnesium deficiency, sleep apnea, diabetes, peripheral neuropathy, Parkinsons disease, and certain autoimmune diseases, such as multiple sclerosis. RLS can worsen in pregnancy, possibly due to elevated estrogen levels. Use of alcohol, nicotine products, and caffeine may be associated with RLS. A 2014 study from the American Academy of Neurology also found that reduced leg oxygen levels were strongly associated with restless legs Syndrome symptom severity in untreated patients. ADHD An association has been observed between attention deficit hyperactivity disorder (ADHD) and RLS or periodic limb movement disorder. Both conditions appear to have links to dysfunctions related to the neurotransmitter dopamine, and common medications for both conditions among other systems, affect dopamine levels in the brain. A 2005 study suggested that up to 44% of people with ADHD had comorbid (i.e. coexisting) RLS, and up to 26% of people with RLS had confirmed ADHD or symptoms of the condition. Medications Certain medications may cause or worsen RLS, or cause it secondarily, including: certain antiemetics (antidopaminergic ones) certain antihistamines (especially the sedating, first generation H1 antihistamines often in over-the-counter cold medications) many antidepressants (both older TCAs and newer SSRIs) antipsychotics and certain anticonvulsants a rebound effect of sedative-hypnotic drugs such as a benzodiazepine withdrawal syndrome from discontinuing benzodiazepine tranquilizers or sleeping pills alcohol withdrawal can also cause restless legs syndrome and other movement disorders such as akathisia and parkinsonism usually associated with antipsychotics opioid withdrawal is associated with causing and worsening RLSBoth primary and secondary RLS can be worsened by surgery of any kind; however, back surgery or injury can be associated with causing RLS.The cause vs. effect of certain conditions and behaviors observed in some patients (ex. excess weight, lack of exercise, depression or other mental illnesses) is not well established. Loss of sleep due to RLS could cause the conditions, or medication used to treat a condition could cause RLS. Genetics More than 60% of cases of RLS are familial and are inherited in an autosomal dominant fashion with variable penetrance.Research and brain autopsies have implicated both dopaminergic system and iron insufficiency in the substantia nigra. Iron is well understood to be an essential cofactor for the formation of L-dopa, the precursor of dopamine. Six genetic loci found by linkage are known and listed below. Other than the first one, all of the linkage loci were discovered using an autosomal dominant model of inheritance. The first genetic locus was discovered in one large French Canadian family and maps to chromosome 12q. This locus was discovered using an autosomal recessive inheritance model. Evidence for this locus was also found using a transmission disequilibrium test (TDT) in 12 Bavarian families. The second RLS locus maps to chromosome 14q and was discovered in one Italian family. Evidence for this locus was found in one French Canadian family. Also, an association study in a large sample 159 trios of European descent showed some evidence for this locus. This locus maps to chromosome 9p and was discovered in two unrelated American families. Evidence for this locus was also found by the TDT in a large Bavarian family, in which significant linkage to this locus was found. This locus maps to chromosome 20p and was discovered in a large French Canadian family with RLS. This locus maps to chromosome 2p and was found in three related families from population isolated in South Tyrol. The sixth locus is located on chromosome 16p12.1 and was discovered by Levchenko et al. in 2008.Three genes, MEIS1, BTBD9 and MAP2K5, were found to be associated to RLS. Their role in RLS pathogenesis is still unclear. More recently, a fourth gene, PTPRD was found to be associated with RLS.There is also some evidence that periodic limb movements in sleep (PLMS) are associated with BTBD9 on chromosome 6p21.2, MEIS1, MAP2K5/SKOR1, and PTPRD. The presence of a positive family history suggests that there may be a genetic involvement in the etiology of RLS. Mechanism Although it is only partly understood, pathophysiology of restless legs syndrome may involve dopamine and iron system anomalies. There is also a commonly acknowledged circadian rhythm explanatory mechanism associated with it, clinically shown simply by biomarkers of circadian rhythm, such as body temperature. The interactions between impaired neuronal iron uptake and the functions of the neuromelanin-containing and dopamine-producing cells have roles in RLS development, indicating that iron deficiency might affect the brain dopaminergic transmissions in different ways.Medial thalamic nuclei may also have a role in RLS as part as the limbic system modulated by the dopaminergic system which may affect pain perception. Improvement of RLS symptoms occurs in people receiving low-dose dopamine agonists. Diagnosis There are no specific tests for RLS, but non-specific laboratory tests are used to rule out other causes such as vitamin deficiencies. Five symptoms are used to confirm the diagnosis: A strong urge to move the limbs, usually associated with unpleasant or uncomfortable sensations. It starts or worsens during inactivity or rest. It improves or disappears (at least temporarily) with activity. It worsens in the evening or night. These symptoms are not caused by any medical or behavioral condition.These symptoms are not essential, like the ones above, but occur commonly in RLS patients: genetic component or family history with RLS good response to dopaminergic therapy periodic leg movements during day or sleep most strongly affected are people who are middle-aged or older other sleep disturbances are experienced decreased iron stores can be a risk factor and should be assessedAccording to the International Classification of Sleep Disorders (ICSD-3), the main symptoms have to be associated with a sleep disturbance or impairment in order to support RLS diagnosis. As stated by this classification, RLS symptoms should begin or worsen when being inactive, be relieved when moving, should happen exclusively or mostly in the evening and at night, not be triggered by other medical or behavioral conditions, and should impair ones quality of life. Generally, both legs are affected, but in some cases there is an asymmetry. Differential diagnosis The most common conditions that should be differentiated with RLS include leg cramps, positional discomfort, local leg injury, arthritis, leg edema, venous stasis, peripheral neuropathy, radiculopathy, habitual foot tapping/leg rocking, anxiety, myalgia, and drug-induced akathisia.Peripheral artery disease and arthritis can also cause leg pain but this usually gets worse with movement.There are less common differential diagnostic conditions included myelopathy, myopathy, vascular or neurogenic claudication, hypotensive akathisia, orthostatic tremor, painful legs, and moving toes. Treatment If RLS is not linked to an underlying cause, its frequency may be reduced by lifestyle modifications such as adopting improving sleep hygiene, regular exercise, and stopping smoking. Medications used may include dopamine agonists or gabapentin in those with daily restless legs syndrome, and opioids for treatment of resistant cases.Treatment of RLS should not be considered until possible medical causes are ruled out. Secondary RLS may be cured if precipitating medical conditions (anemia) are managed effectively. Physical measures Stretching the leg muscles can bring temporary relief. Walking and moving the legs, as the name "restless legs" implies, brings temporary relief. In fact, those with RLS often have an almost uncontrollable need to walk and therefore relieve the symptoms while they are moving. Unfortunately, the symptoms usually return immediately after the moving and walking ceases. A vibratory counter-stimulation device has been found to help some people with primary RLS to improve their sleep. Iron There is some evidence that intravenous iron supplementation moderately improves restlessness for people with RLS. Medications For those whose RLS disrupts or prevents sleep or regular daily activities, medication may be useful. Evidence supports the use of dopamine agonists including: pramipexole, ropinirole, rotigotine, and cabergoline. They reduce symptoms, improve sleep quality and quality of life. Levodopa is also effective. However, pergolide and cabergoline are less recommended due to their association with increased risk of valvular heart disease. Ropinirole has a faster onset with shorter duration. Rotigotine is commonly used as a transdermal patch which continuously provides stable plasma drug concentrations, resulting in its particular therapeutic effect on patients with symptoms throughout the day. One 2008 review found pramipexole to be better than ropinirole.There are, however, issues with the use of dopamine agonists including augmentation. This is a medical condition where the drug itself causes symptoms to increase in severity and/or occur earlier in the day. Dopamine agonists may also cause rebound when symptoms increase as the drug wears off. In many cases, the longer dopamine agonists have been used the higher the risk of augmentation and rebound as well as the severity of the symptoms. Also, a recent study indicated that dopamine agonists used in restless legs syndrome can lead to an increase in compulsive gambling. Gabapentin or pregabalin, a non-dopaminergic treatment for moderate to severe primary RLS Opioids are only indicated in severe cases that do not respond to other measures due to their very high abuse liability and high rate of side effects, which may include constipation, fatigue and headache.One possible treatment for RLS is dopamine agonists, unfortunately patients can develop dopamine dysregulation syndrome, meaning that they can experience an addictive pattern of dopamine replacement therapy. Additionally, they can exhibit some behavioral disturbances such as impulse control disorders like pathologic gambling, compulsive purchasing and compulsive eating. There are some indications that stopping the dopamine agonist treatment has an impact on the resolution or at least improvement of the impulse control disorder, even though some people can be particularly exposed to dopamine agonist withdrawal syndrome.Benzodiazepines, such as diazepam or clonazepam, are not generally recommended, and their effectiveness is unknown. They however are sometimes still used as a second line, as add on agents. Quinine is not recommended due to its risk of serious side effects involving the blood. Prognosis RLS symptoms may gradually worsen with age, although more slowly for those with the idiopathic form of RLS than for people who also have an associated medical condition. Current therapies can control the disorder, minimizing symptoms and increasing periods of restful sleep. In addition, some people have remissions, periods in which symptoms decrease or disappear for days, weeks, or months, although symptoms usually eventually reappear. Being diagnosed with RLS does not indicate or foreshadow another neurological disease, such as Parkinsons disease. RLS symptoms can worsen over time when dopamine-related drugs are used for therapy, an effect called "augmentation" which may represent symptoms occurring throughout the day and affect movements of all limbs. There is no cure for RLS. Epidemiology RLS affects an estimated 2.5–15% of the American population. A minority (around 2.7% of the population) experience daily or severe symptoms. RLS is twice as common in women as in men, and Caucasians are more prone to RLS than people of African descent. RLS occurs in 3% of individuals from the Mediterranean or Middle Eastern regions, and in 1–5% of those from East Asia, indicating that different genetic or environmental factors, including diet, may play a role in the prevalence of this syndrome. RLS diagnosed at an older age runs a more severe course. RLS is even more common in individuals with iron deficiency, pregnancy, or end-stage kidney disease. The National Sleep Foundations 1998 Sleep in America poll showed that up to 25 percent of pregnant women developed RLS during the third trimester. Poor general health is also linked.There are several risk factors for RLS, including old age, family history, and uremia. The prevalence of RLS tends to increase with age, as well as its severity and longer duration of symptoms. People with uremia receiving renal dialysis have a prevalence from 20% to 57%, while those having kidney transplant improve compared to those treated with dialysis.RLS can occur at all ages, although it typically begins in the third or fourth decade. Genome‐wide association studies have now identified 19 risk loci associated with RLS. Neurological conditions linked to RLS include Parkinsons disease, spinal cerebellar atrophy, spinal stenosis, lumbosacral radiculopathy and Charcot–Marie–Tooth disease type 2. History The first known medical description of RLS was by Sir Thomas Willis in 1672. Willis emphasized the sleep disruption and limb movements experienced by people with RLS. Initially published in Latin (De Anima Brutorum, 1672) but later translated to English (The London Practice of Physick, 1685), Willis wrote: Wherefore to some, when being abed they betake themselves to sleep, presently in the arms and legs, leapings and contractions on the tendons, and so great a restlessness and tossings of other members ensue, that the diseased are no more able to sleep, than if they were in a place of the greatest torture. The term "fidgets in the legs" has also been used as early as the early nineteenth century.Subsequently, other descriptions of RLS were published, including those by François Boissier de Sauvages (1763), Magnus Huss (1849), Theodur Wittmaack (1861), George Miller Beard (1880), Georges Gilles de la Tourette (1898), Hermann Oppenheim (1923) and Frederick Gerard Allison (1943). However, it was not until almost three centuries after Willis, in 1945, that Karl-Axel Ekbom (1907–1977) provided a detailed and comprehensive report of this condition in his doctoral thesis, restless legs: clinical study of hitherto overlooked disease. Ekbom coined the term "restless legs" and continued work on this disorder throughout his career. He described the essential diagnostic symptoms, differential diagnosis from other conditions, prevalence, relation to anemia, and common occurrence during pregnancy.Ekboms work was largely ignored until it was rediscovered by Arthur S. Walters and Wayne A. Hening in the 1980s. Subsequent landmark publications include 1995 and 2003 papers, which revised and updated the diagnostic criteria. Journal of Parkinsonism and RLS is the first peer-reviewed, online, open access journal dedicated to publishing research about Parkinsons disease and was founded by a Canadian neurologist Dr. Abdul Qayyum Rana. Nomenclature In 2013, the Restless Legs Syndrome Foundation renamed itself the Willis–Ekbom Disease Foundation; however, it reverted to its original name in 2015 “to better support its mission”.A point of confusion is that RLS and delusional parasitosis are entirely different conditions that have both been called "Ekbom syndrome", as both syndromes were described by the same person, Karl-Axel Ekbom. Today, calling WED/RLS "Ekbom syndrome" is outdated usage, as the unambiguous names (WED or RLS) are preferred for clarity. Controversy Some doctors express the view that the incidence of restless legs syndrome is exaggerated by manufacturers of drugs used to treat it. Others believe it is an underrecognized and undertreated disorder. Further, GlaxoSmithKline (GSK) ran advertisements that, while not promoting off-licence use of their drug (ropinirole) for treatment of RLS, did link to the Ekbom Support Group website. That website contained statements advocating the use of ropinirole to treat RLS. The Association of the British Pharmaceutical Industry (ABPI) ruled against GSK in this case. Research Different measurements have been used to evaluate treatments in RLS. Most of them are based on subjective rating scores, such as IRLS rating scale (IRLS), Clinical Global Impression (CGI), Patient Global Impression (PGI), and Quality of life (QoL). These questionnaires provide information about the severity and progress of the disease, as well as the persons quality of life and sleep. Polysomnography (PSG) and actigraphy (both related to sleep parameters) are more objective resources that provide evidences of sleep disturbances associated with RLS symptoms. See also Periodic limb movement disorder References External links Restless legs syndrome at Curlie

Aarogya, What does Elsewhere mean

Elsewhere

Elsewhere may refer to: Film Elsewhere (2001 film), a 2001 Austrian documentary by Nikolaus Geyrhalter Elsewhere (2009 film), an American thriller starring Anna Kendrick Elsewhere (2019 film), an American comedy-drama directed by Hernán Jiménez Literature Elsewhere, a 1991 novel by Will Shetterly Elsewhere (anthology), a 2003 Australian speculative-fiction anthology Elsewhere (Blatty novel), a 2009 novel by William Peter Blatty "Elsewhere" (short story), a 1941 science-fiction short story by Robert Heinlein Elsewhere (Zevin novel), a 2005 novel by Gabrielle Zevin Elsewhere: A Memoir, a 2012 memoir by novelist Richard Russo Music Elsewhere, an EP by Gretta Ray, 2016 Elsewhere (Scott Matthews album) Elsewhere (Joe Morris album) Elsewhere (Pinegrove album), 2017 "Elsewhere", a song by Sarah McLachlan from Fumbling Towards Ecstasy Places Elsewhere, a museum and artist residency in Greensboro, North Carolina The name of a town in Calloway County, Kentucky Elsewhere (music venue), music venue in Bushwick, Brooklyn Other Elsewhere (website), a music, arts and travel website run by New Zealand journalist Graham Reid Elsewhere, the stage name of dancer David Bernal In special relativity, the region of spacetime outside a light cone Elsweyr, a fictional nation in the Elder Scrolls videogame series See also St. Elsewhere, an American television drama series St. Elsewhere (album), a 2006 album by Gnarls Barkley Dispatches from Elsewhere, a 2020 American television drama series Somewhere Else (disambiguation)

Could you describe Alcoholic beverage, to me Aarogya

Alcoholic beverage

An alcoholic beverage (also called an alcoholic drink, adult beverage, or a drink) is a drink that contains ethanol, a type of alcohol that acts as a drug and is produced by fermentation of grains, fruits, or other sources of sugar. The consumption of alcoholic drinks, often referred to as "drinking", plays an important social role in many cultures. Most countries have laws regulating the production, sale, and consumption of alcoholic beverages. Regulations may require the labeling of the percentage alcohol content (as ABV or proof) and the use of a warning label. Some countries ban such activities entirely, but alcoholic drinks are legal in most parts of the world. The global alcoholic drink industry exceeded $1 trillion in 2018.Alcohol is a depressant, which in low doses causes euphoria, reduces anxiety, and increases sociability. In higher doses, it causes drunkenness, stupor, unconsciousness, or death. Long-term use can lead to an alcohol use disorder, an increased risk of developing several types of cancer, cardiovascular disease, and physical dependence. Alcohol is one of the most widely used recreational drugs in the world, and about 33% of all humans currently drink alcohol. In 2015, among Americans, 86% of adults had consumed alcohol at some point, with 70% drinking it in the last year and 56% in the last month. Alcoholic drinks are typically divided into three classes—beers, wines, and spirits—and typically their alcohol content is between 3% and 50%. Discovery of late Stone Age jugs suggest that intentionally fermented drinks existed at least as early as the Neolithic period (c. 10,000 BC). Several other animals are affected by alcohol similarly to humans and, once they consume it, will consume it again if given the opportunity, though humans are the only species known to produce alcoholic drinks intentionally. Fermented drinks Beer Beer is a beverage fermented from grain mash. It is typically made from barley or a blend of several grains and flavored with hops. Most beer is naturally carbonated as part of the fermentation process. If the fermented mash is distilled, then the drink becomes a spirit. Beer is the most consumed alcoholic beverage in the world. Cider Cider or cyder ( SY-dər) is a fermented alcoholic drink made from any fruit juice; apple juice (traditional and most common), peaches, pears ("Perry" cider) or other fruit. Cider alcohol content varies from 1.2% ABV to 8.5% or more in traditional English ciders. In some regions, cider may be called "apple wine". Fermented tea Fermented tea (also known as post-fermented tea or dark tea) is a class of tea that has undergone microbial fermentation, from several months to many years. The tea leaves and the liquor made from them become darker with oxidation. Thus, the various kinds of fermented teas produced across China are also referred to as dark tea, not be confused with black tea. The most famous fermented tea is kombucha which is often homebrewed, pu-erh, produced in Yunnan Province, and the Anhua dark tea produced in Anhua County of Hunan Province. The majority of kombucha on the market are under 0.5% ABV. Fermented water Fermented water is an ethanol-based water solution with approximately 15-17% ABV without sweet reserve. Fermented water is exclusively fermented with white sugar, yeast, and water. Fermented water is clarified after the fermentation to produce a colorless or off-white liquid with no discernible taste other than that of ethanol. Fermented sugar water Fermented sugar water is fermented water with added refined sugar. Mead Mead () is an alcoholic drink made by fermenting honey with water, sometimes with various fruits, spices, grains, or hops. The alcoholic content of mead may range from as low as 3% ABV to more than 20%. The defining characteristic of mead is that the majority of the drinks fermentable sugar is derived from honey. Mead can also be referred to as "honeywine." Pulque Pulque is the Mesoamerican fermented drink made from the "honey water" of maguey, Agave americana. The drink distilled from pulque is tequila or mescal Mezcal. Rice wine Sake, huangjiu, mijiu, and cheongju are popular examples of East Asian rice wine. Wine Wine is a fermented beverage produced from grapes and sometimes other fruits. Wine involves a longer fermentation process than beer and a long aging process (months or years), resulting in an alcohol content of 9%–16% ABV. Others Fruit wines are made from fruits other than grapes, such as plums, cherries, or apples. Sparkling wine like French Champagne, Catalan Cava or Italian Prosecco can be made by means of a secondary fermentation. Distilled beverages Distilled beverages (also called liquors or spirit drinks) are alcoholic drinks produced by distilling (i.e., concentrating by distillation) ethanol produced by means of fermenting grain, fruit, or vegetables. Unsweetened, distilled, alcoholic drinks that have an alcohol content of at least 20% ABV are called spirits. For the most common distilled drinks, such as whiskey and vodka, the alcohol content is around 40%. The term hard liquor is used in North America to distinguish distilled drinks from undistilled ones (implicitly weaker). Vodka, gin, baijiu, shōchū, soju, tequila, whiskey, brandy and rum are examples of distilled drinks. Distilling concentrates the alcohol and eliminates some of the congeners. Freeze distillation concentrates ethanol along with methanol and fusel alcohols (fermentation by-products partially removed by distillation) in applejack. Fortified wine is wine, such as port or sherry, to which a distilled beverage (usually brandy) has been added. Fortified wine is distinguished from spirits made from wine in that spirits are produced by means of distillation, while fortified wine is wine that has had a spirit added to it. Many different styles of fortified wine have been developed, including port, sherry, madeira, marsala, commandaria, and the aromatized wine vermouth. Rectified spirit Rectified spirit, also called "neutral grain spirit", is alcohol which has been purified by means of "rectification" (i.e. repeated distillation). The term neutral refers to the spirits lack of flavor that would have been present if the mash ingredients had been distilled to a lower level of alcoholic purity. Rectified spirit also lacks any flavoring added to it after distillation (as is done, for example, with gin). Other kinds of spirits, such as whiskey, are distilled to a lower alcohol percentage to preserve the flavor of the mash. Rectified spirit is a clear, colorless, flammable liquid that may contain as much as 95% ABV. It is often used for medicinal purposes. It may be a grain spirit or it may be made from other plants. It is used in mixed drinks, liqueurs, and tinctures, and also as a household solvent. Congeners In the alcoholic drinks industry, congeners are substances produced during fermentation. These substances include small amounts of chemicals such as occasionally desired other alcohols, like propanol and 3-methyl-1-butanol, but also compounds that are never desired such as acetone, acetaldehyde and glycols. Congeners are responsible for most of the taste and aroma of distilled alcoholic drinks, and contribute to the taste of non-distilled drinks. It has been suggested that these substances contribute to the symptoms of a hangover. Tannins are congeners found in wine in the presence of phenolic compounds. Wine tannins add bitterness, have a drying sensation, taste herbaceous and are often described as astringent. Wine tannins adds balance, complexity, structure and makes a wine last longer, so they play an important role in the aging of wine. Amount of use The average number of people who drink as of 2016 was 39% for males and 25% for females (2.4 billion people in total). Females on average drink 0.7 drinks per day while males drink 1.7 drinks per day. The rates of drinking varies significantly in different areas of the world. Reasons for use Apéritifs and digestifs An apéritif is any alcoholic beverage usually served before a meal to stimulate the appetite, while a digestif is any alcoholic beverage served after a meal for the stated purpose of improving digestion. Fortified wine, liqueurs, and dry champagne are common apéritifs. Because apéritifs are served before dining, they are usually dry rather than sweet. One example is Cinzano, a brand of vermouth. Digestifs include brandy, fortified wines and herb-infused spirits (Drambuie). Caloric content The USDA uses a figure of 6.93 kilocalories (29.0 kJ) per gram of alcohol (5.47 kcal or 22.9 kJ per ml) for calculating food energy. For distilled spirits, a standard serving in the United States is 44 ml (1.5 US fl oz), which at 40% ethanol (80 proof), would be 14 grams and 98 calories. For other than distille spirits, many alcoholic drinks contain carbohydrates, which adds to the calories per serving.Alcoholic drinks are considered empty calorie foods because other than food energy they contribute no essential nutrients. According to the U.S. Department of Agriculture, based on NHANES 2013–2014 surveys, women in the US ages 20 and up consume on average 6.8 grams/day and men consume on average 15.5 grams/day.Alcohol is known to potentiate the insulin response of the human body to glucose, which, in essence, "instructs" the body to convert consumed carbohydrates into fat and to suppress carbohydrate and fat oxidation. Ethanol is directly processed in the liver to acetyl CoA, the same intermediate product as in glucose metabolism. Because ethanol is mostly metabolized and consumed by the liver, chronic excessive use can lead to fatty liver. This leads to a chronic inflammation of the liver and eventually alcoholic liver disease. Flavoring Pure ethanol tastes bitter to humans; some people also describe it as sweet. However, ethanol is also a moderately good solvent for many fatty substances and essential oils. This facilitates the use of flavoring and coloring compounds in alcoholic drinks as a taste mask, especially in distilled drinks. Some flavors may be naturally present in the beverages raw material. Beer and wine may also be flavored before fermentation, and spirits may be flavored before, during, or after distillation. Sometimes flavor is obtained by allowing the beverage to stand for months or years in oak barrels, usually made of American or French oak. A few brands of spirits may also have fruit or herbs inserted into the bottle at the time of bottling. Wine is important in cuisine not just for its value as an accompanying beverage, but as a flavor agent, primarily in stocks and braising, since its acidity lends balance to rich savory or sweet dishes. Wine sauce is an example of a culinary sauce that uses wine as a primary ingredient. Natural wines may exhibit a broad range of alcohol content, from below 9% to above 16% ABV, with most wines being in the 12.5–14.5% range. Fortified wines (usually with brandy) may contain 20% alcohol or more. Alcohol measurement Alcohol concentration The concentration of alcohol in a beverage is usually stated as the percentage of alcohol by volume (ABV, the number of milliliters (ml) of pure ethanol in 100 ml of beverage) or as proof. In the United States, proof is twice the percentage of alcohol by volume at 60 degrees Fahrenheit (e.g. 80 proof = 40% ABV). Degrees proof were formerly used in the United Kingdom, where 100 degrees proof was equivalent to 57.1% ABV. Historically, this was the most dilute spirit that would sustain the combustion of gunpowder. Ordinary distillation cannot produce alcohol of more than 95.6% by weight, which is about 97.2% ABV (194.4 proof) because at that point alcohol is an azeotrope with water. A spirit which contains a very high level of alcohol and does not contain any added flavoring is commonly called a neutral spirit. Generally, any distilled alcoholic beverage of 170 US proof or higher is considered to be a neutral spirit.Most yeasts cannot reproduce when the concentration of alcohol is higher than about 18%, so that is the practical limit for the strength of fermented drinks such as wine, beer, and sake. However, some strains of yeast have been developed that can reproduce in solutions of up to 25% ABV. Serving measures Shot sizes Shot sizes vary significantly from country to country. In the United Kingdom, serving size in licensed premises is regulated under the Weights and Measures Act (1985). A single serving size of spirits (gin, whisky, rum, and vodka) are sold in 25 ml or 35 ml quantities or multiples thereof. Beer is typically served in pints (568 ml), but is also served in half-pints or third-pints. In Israel, a single serving size of spirits is about twice as much, 50 or 60 mL. The shape of a glass can have a significant effect on how much one pours. A Cornell University study of students and bartenders pouring showed both groups pour more into short, wide glasses than into tall, slender glasses. Aiming to pour one shot of alcohol (1.5 ounces or 44.3 ml), students on average poured 45.5 ml & 59.6 ml (30% more) respectively into the tall and short glasses. The bartenders scored similarly, on average pouring 20.5% more into the short glasses. More experienced bartenders were more accurate, pouring 10.3% less alcohol than less experienced bartenders. Practice reduced the tendency of both groups to over pour for tall, slender glasses but not for short, wide glasses. These misperceptions are attributed to two perceptual biases: (1) Estimating that tall, slender glasses have more volume than shorter, wider glasses; and (2) Over focusing on the height of the liquid and disregarding the width. Standard drinks There is no single standard, but a standard drink of 10g alcohol, which is used in the WHO AUDIT (Alcohol Use Disorders Identification Test)s questionnaire form example, have been adopted by more countries than any other amount. 10 grams is equivalent to 12.7 millilitres. A standard drink is a notional drink that contains a specified amount of pure alcohol. The standard drink is used in many countries to quantify alcohol intake. It is usually expressed as a measure of beer, wine, or spirits. One standard drink always contains the same amount of alcohol regardless of serving size or the type of alcoholic beverage. The standard drink varies significantly from country to country. For example, it is 7.62 ml (6 grams) of alcohol in Austria, but in Japan it is 25 ml (19.75 grams). In the United Kingdom, there is a system of units of alcohol which serves as a guideline for alcohol consumption. A single unit of alcohol is defined as 10 ml. The number of units present in a typical drink is sometimes printed on bottles. The system is intended as an aid to people who are regulating the amount of alcohol they drink; it is not used to determine serving sizes. In the United States, the standard drink contains 0.6 US fluid ounces (18 ml) of alcohol. This is approximately the amount of alcohol in a 12-US-fluid-ounce (350 ml) glass of beer, a 5-US-fluid-ounce (150 ml) glass of wine, or a 1.5-US-fluid-ounce (44 ml) glass of a 40% ABV (80 US proof) spirit. Laws Alcohol laws regulate the manufacture, packaging, labelling, distribution, sale, consumption, blood alcohol content of motor vehicle drivers, open containers, and transportation of alcoholic drinks. Such laws generally seek to reduce the adverse health and social impacts of alcohol consumption. In particular, alcohol laws set the legal drinking age, which usually varies between 15 and 21 years old, sometimes depending upon the type of alcoholic drink (e.g., beer vs wine vs hard liquor or distillates). Some countries do not have a legal drinking or purchasing age, but most countries set the minimum age at 18 years. Some countries, such as the U.S., have the drinking age higher than the legal age of majority (18), at age 21 in all 50 states. Such laws may take the form of permitting distribution only to licensed stores, monopoly stores, or pubs and they are often combined with taxation, which serves to reduce the demand for alcohol (by raising its price) and it is a form of revenue for governments. These laws also often limit the hours or days (e.g., "blue laws") on which alcohol may be sold or served, as can also be seen in the "last call" ritual in US and Canadian bars, where bartenders and servers ask patrons to place their last orders for alcohol, due to serving hour cutoff laws. In some countries, alcohol cannot be sold to a person who is already intoxicated. Alcohol laws in many countries prohibit drunk driving. In some jurisdictions, alcoholic drinks are totally prohibited for reasons of religion (e.g., Islamic countries with sharia law) or for reasons of local option, public health, and morals (e.g., Prohibition in the United States from 1920 to 1933). In jurisdictions which enforce sharia law, the consumption of alcoholic drinks is an illegal offense, although such laws may exempt non-Muslims. History 10,000–5000 BC: Discovery of late Stone Age jugs suggests that intentionally fermented drinks existed at least as early as the Neolithic period. 7000–5600 BC: Examination and analysis of ancient pottery jars from the neolithic village of Jiahu in the Henan province of northern China revealed residue left behind by the alcoholic drinks they had once contained. According to a study published in the Proceedings of the National Academy of Sciences, chemical analysis of the residue confirmed that a fermented drink made of grape and hawthorn fruit wine, honey mead and rice beer was being produced in 7000–5600 BC (McGovern et al., 2005; McGovern 2009). The results of this analysis were published in December 2004. 9th–10th centuries AD: Medieval Muslim chemists such as Jābir ibn Ḥayyān (Latin: Geber, ninth century) and Abū Bakr al-Rāzī (Latin: Rhazes, c. 865–925) experimented extensively with the distillation of various substances. The distillation of wine is attested in Arabic works attributed to al-Kindī (c. 801–873 CE) and to al-Fārābī (c. 872–950), and in the 28th book of al-Zahrāwīs (Latin: Abulcasis, 936–1013) Kitāb al-Taṣrīf (later translated into Latin as Liber servatoris). 12th century: The process of distillation spread from the Middle East to Italy, where distilled alcoholic drinks were recorded in the mid-12th century. In China, archaeological evidence indicates that the true distillation of alcohol began during the 12th century Jin or Southern Song dynasties. A still has been found at an archaeological site in Qinglong, Hebei, dating to the 12th century. 14th century: In India, the true distillation of alcohol was introduced from the Middle East, and was in wide use in the Delhi Sultanate by the 14th century. By the early 14th century, distilled alcoholic drinks had spread throughout the European continent. See also Alcohol (drug) Alcoholic drinks in China Beer and breweries by region Cooking with alcohol Holiday heart syndrome Homebrewing Liquor List of alcoholic drinks List of countries by alcohol consumption per capita List of national drinks Mixed drink References External links About 37 percent of college students could now be considered alcoholics, Daily Emerald Alcohol, Health-EU Portal, Health-EU Portal What Is a Standard Drink?, National Institute on Alcohol Abuse and Alcoholism

Aarogya, can you share information about a health condition involving Anosmia

Anosmia

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

Hello Aarogya, could you help me understand about Microcheilia

Microcheilia

Microcheilia is a congenital disorder where ones lips are unusually small. References == External links ==

Aarogya what is Field

Field

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

Hey Aarogya, explain a situation where Paragonimiasis occurs

Paragonimiasis

Paragonimiasis is a food-borne parasitic disease caused by several species of lung flukes belonging to genus Paragonimus. Infection is acquired by eating crustaceans such as crabs and crayfishes which host the infective forms called metacercariae, or by eating raw or undercooked meat of mammals harboring the metacercariae from crustaceans.More than 40 species of Paragonimus have been identified; 10 of these are known to cause disease in humans. The most common cause of human paragonimiasis is P. westermani, the oriental lung fluke.About 22 million people are estimated to be affected yearly worldwide. It is particularly common in East Asia. Paragonimiasis is easily mistaken for other diseases with which it shares clinical symptoms, such as tuberculosis and lung cancer. Life cycle Not all Paragonimus species infect humans. However, all of them target mammals as their final (definitive) hosts. In mammalian lung tissue, the adult flukes live as encapsulated pairs. As hermaphrodites, they produce and fertilise their own eggs that are released through the respiratory tract. The eggs are excreted to the environment either through the sputum or swallowed and passed out along the faeces.In the external environment, the eggs remain unembryonated until ideal conditions of temperature and humidity are encountered. Then, they embryonate and develop into ciliated larvae called miracidia. As the egg shells disintegrate, the motile miracidia hatch and swim to seek the first intermediate host, a snail, and penetrate its soft tissues. Each miracidium goes through several developmental stages inside the snail: firstly into a series of daughter cells called sporocysts and then into rediae, which give rise to many worm-like larvae called cercariae. The cercariae penetrate through the body of the snail, emerging into the water. Development in the snail takes about 9 to 13 weeks.The cercariae then infect the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. Encystment occurs in the liver, gills, intestine, skeletal muscles and sometimes in the heart. These cysts are the infective stage for the mammalian host. Freshwater crab species of genera Potamiscus, Potamon, Paratelphusa, Eriocheir, Geothelphusa, Barytelphusa, crayfish species of genus Camberoides and shrimps of genera Acrohrachium and Caridina commonly serve as the secondary intermediate hosts. The secondary intermediate hosts are infected either by directly eating the snail or penetration of the body by free-swimming cercariae.Human infection with P. westermani — the best understood species — occurs by eating inadequately cooked or pickled crab or crayfish that harbour metacercariae of the parasite. The metacercariae excyst in the duodenum, penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5 to 12 mm by 4 to 6 mm). Unlike most other trematodes, after they migrate from the intestine, they remain in the peritoneal cavity until they find a suitable partner. Only then do the couples enter the lung tissues to form capsules. The flukes can also reach other organs and tissues, such as the brain and skeletal muscles. However, when this takes place completion of the life cycles is not achieved, because the eggs laid cannot exit these sites. Time from infection to laying of eggs is 65 to 90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani. For other species, rodents and deer are also additional (paratenic) hosts. By consuming infected animals of these reservoir species, even animals and humans that do not eat crustaceans directly can become infected. Background The first human case was seen in 1879 in Taiwan. An autopsy was done and adult trematodes were found in the lungs. The adult flukes have a reddish-brown in color with an ovoid shape. They have two muscular suckers, the first an oral sucker located anteriorly and the second a ventral sucker located mid-body. The adult flukes can live up to 20 years. The eggs are golden brown in color and are asymmetrically ovoid. They have a very thick shell. As seen above, these trematodes have a very complex life cycle with seven distinct phases involving intermediate hosts and humans. These seven phases are outlined as follows: eggs reach fresh water where they develop into miracidia. These penetrate many species of aquatic snails (first intermediate host) where they go through three distinct stages: first sporocysts, then rediae, and finally cercariae, also referred to as the larvae. These larvae released into water and penetrate crabs, crayfish and other crustaceans (second intermediate host). The cercariae situate themselves into the gills, liver and muscles where they further develop into metacercariae. When the parasite-filled crustacean is eaten, the metacercariae hatch in the intestine. These young worms penetrate intestinal wall, peritoneum, the diaphragm and the pleura where they finally reach the lungs. Here they live in pairs, lay eggs that are coughed up in sputum to restart the cycle. Geographic distribution There are more than 30 known species of Paragonimus. Species of Paragonimus are widely distributed in Asia, Africa, and North and South America. P. westermani is found in southeast Asia and Japan, while P. kellicotti is endemic to North America. P. africanus is found in Africa and P. mexicanus is found in central and South America. Just as the species names imply, paragonimiasis is more prominent in Asians, Africans and Hispanics because of their habitats and cultures. Prominence increases with age from older children to young adults then decreases with age. It is also higher among the female populations. This is a very common parasite of crustacean-eating mammals. Symptoms and diagnosis Paragonimiasis causes pneumonia with characteristic symptoms including prolonged cough, chest pain, shortness of breath, and hemoptysis. Owing to the diverse symptoms it presents, the disease is variously known as endemic haemoptysis, oriental lung fluke infection, pulmonary distomiasis, parasitical haemoptysis, and parasitare haemopte. Pulmonary paragonimiasis is the most common clinical manifestation, accounting for 76 to 90% of all infections. It has the classic symptoms of pneumonia. Extra-pulmonary infection is due to migration of the young worms away from the normal route to the lungs. In such case, any other part of the body can be infected. Cutaneous paragonimiasis is common in children and is generally indicated by skin nodules that move from one place to another. Cerebral paragonimias is most severe extra-pulmonary symptoms that affect the brain and leads to seizure, headache, visual disturbance, and motor and sensory disturbances.The acute phase (invasion and migration) may be marked by diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia. During the chronic phase, pulmonary manifestations include cough, expectoration of discolored sputum containing clumps of eggs, hemoptysis, and chest radiographic abnormalities. Extrapulmonary locations of the adult worms result in more severe manifestations, especially when the brain is involved. Diagnosis is based on microscopic demonstration of eggs in stool or sputum, but these are not present until 2 to 3 months after infection. (Eggs are also occasionally encountered in effusion fluid or biopsy material.) Concentration techniques may be necessary in patients with light infections. Biopsy may allow diagnostic confirmation and species identification when an adult or developing fluke is recovered.Diagnosis is done by microscopic examination of sputum and stool samples, and presence of the eggs is a confirmation. However, eggs are not always to be found. In such case, serological tests based on antibody detection using ELISA is a better method. A more arduous method like immunoblotting is also used. For brain infection, radiological examinations including plain skull x-rays, brain CT, and MR scans are used. A rapid antibody detection kit, dot-immunogold filtration assay (DIGFA), was developed for P. Wertermani in China in 2005.Misdiagnosis is a serious issue in paragonimiasis. It is commonly misdiagnosed as tuberculosis because it presents similar symptoms. In China, there were between 69 and 89% of misdiagnostic cases in 10 ten years, from 2009 to 2019. It is also frequently misidentified as malignancy or chronic obstructive pulmonary disease. Treatment The drug of choice to treat paragonimiasis is praziquantel, although bithionol may also be used. Triclabendazole is useful in P. uterobilateralis, P. mexicanus, and P. skrjabini infections but not in P. westermani infection. See also Drunken shrimp Eating live seafood Odori ebi References == External links ==

Aarogya, elaborate on Ganglion

Ganglion

A ganglion is a group of neuron cell bodies in the peripheral nervous system. In the somatic nervous system this includes dorsal root ganglia and trigeminal ganglia among a few others. In the autonomic nervous system there are both sympathetic and parasympathetic ganglia which contain the cell bodies of postganglionic sympathetic and parasympathetic neurons respectively. A pseudoganglion looks like a ganglion, but only has nerve fibers and has no nerve cell bodies. Structure Ganglia are primarily made up of somata and dendritic structures which are bundled or connected. Ganglia often interconnect with other ganglia to form a complex system of ganglia known as a plexus. Ganglia provide relay points and intermediary connections between different neurological structures in the body, such as the peripheral and central nervous systems. Among vertebrates there are three major groups of ganglia: Dorsal root ganglia (also known as the spinal ganglia) contain the cell bodies of sensory (afferent) neurons. Cranial nerve ganglia contain the cell bodies of cranial nerve neurons. Autonomic ganglia contain the cell bodies of autonomic nerves.In the autonomic nervous system, fibers from the central nervous system to the ganglia are known as preganglionic fibers, while those from the ganglia to the effector organ are called postganglionic fibers. Basal ganglia The term "ganglion" refers to the peripheral nervous system.However, in the brain (part of the central nervous system), the "basal ganglia" is a group of nuclei interconnected with the cerebral cortex, thalamus, and brainstem, associated with a variety of functions: motor control, cognition, emotions, and learning. Partly due to this ambiguity, the Terminologia Anatomica recommends using the term basal nuclei instead of basal ganglia; however, this usage has not been generally adopted. Pseudoganglion A pseudoganglion is a localized thickening of the main part or trunk of a nerve that has the appearance of a ganglion but has only nerve fibers and no nerve cell bodies. Pseudoganglia are found in the teres minor muscle and radial nerve. See also Sympathetic ganglion Ganglion cyst Nervous system Neuron Chiasm References External links Media related to Ganglia at Wikimedia Commons

Aarogya, Please give me a short description about Subacute thyroiditis

Subacute thyroiditis

Subacute thyroiditis is a form of thyroiditis that can be a cause of both thyrotoxicosis and hypothyroidism. It is uncommon and can affect individuals of both sexes, occurring three times as often in women than in men. and people of all ages. The most common form, subacute granulomatous, or de Quervains, thyroiditis manifests as a sudden and painful enlargement of the thyroid gland accompanied with fever, malaise and muscle aches. Indirect evidence has implicated viral infection in the etiology of subacute thyroiditis. This evidence is limited to preceding upper respiratory tract infection, elevated viral antibody levels, and both seasonal and geographical clustering of cases. There may be a genetic predisposition. Nishihara and coworkers studied the clinical features of subacute thyroiditis in 852 mostly 40- to 50-year-old women in Japan. They noted seasonal clusters (summer to early autumn) and most subjects presented with neck pain. Fever and symptoms of thyrotoxicosis were present in two thirds of subjects. Upper respiratory tract infections in the month preceding presentation were reported in only 1 in 5 subjects. Recurrent episodes following resolution of the initial episode were rare, occurring in just 1.6% of cases. Laboratory markers for thyroid inflammation and dysfunction typically peaked within one week of onset of illness. Types Subacute granulomatous thyroiditis (De Quervain thyroiditis) Subacute lymphocytic thyroiditis Postpartum thyroiditis Palpation thyroiditis References == External links ==

Aarogya, could you share information about a health condition involving Periodic fever syndrome

Periodic fever syndrome

Periodic fever syndromes are a set of disorders characterized by recurrent episodes of systemic and organ-specific inflammation. Unlike autoimmune disorders such as systemic lupus erythematosus, in which the disease is caused by abnormalities of the adaptive immune system, people with autoinflammatory diseases do not produce autoantibodies or antigen-specific T or B cells. Instead, the autoinflammatory diseases are characterized by errors in the innate immune system.The syndromes are diverse, but tend to cause episodes of fever, joint pains, skin rashes, abdominal pains and may lead to chronic complications such as amyloidosis.Most autoinflammatory diseases are genetic and present during childhood. The most common genetic autoinflammatory syndrome is familial Mediterranean fever, which causes short episodes of fever, abdominal pain, serositis, lasting less than 72 hours. It is caused by mutations in the MEFV gene, which codes for the protein pyrin.Pyrin is a protein normally present in the inflammasome. The mutated pyrin protein is thought to cause inappropriate activation of the inflammasome, leading to release of the pro-inflammatory cytokine IL-1β. Most other autoinflammatory diseases also cause disease by inappropriate release of IL-1β. Thus, IL-1β has become a common therapeutic target, and medications such as anakinra, rilonacept, and canakinumab have revolutionized the treatment of autoinflammatory diseases.However, there are some autoinflammatory diseases that are not known to have a clear genetic cause. This includes PFAPA, which is the most common autoinflammatory disease seen in children, characterized by episodes of fever, aphthous stomatitis, pharyngitis, and cervical adenitis. Other autoinflammatory diseases that do not have clear genetic causes include adult-onset Stills disease, systemic-onset juvenile idiopathic arthritis, Schnitzler syndrome, and chronic recurrent multifocal osteomyelitis. It is likely that these diseases are multifactorial, with genes that make people susceptible to these diseases, but they require an additional environmental factor to trigger the disease. Individual periodic fever syndromes See also Kawasaki disease - possible autoinflammatory mechanism Multisystem inflammatory syndrome in children List of cutaneous conditions Further reading Hobart A. Reimann, Periodic Disease: a probable syndrome including periodic fever, benign paroxysmal peritonitis, cyclic neutropenia and intermittent arthralgia. JAMA, 1948. Hobart A Reimann, Periodic Disease: periodic fever, periodic abdominalgia, cyclic neutropenia, intermittent arthralgia, angioneurotic edema, anaphylactoid purpura and periodic paralysis. JAMA, 1949. Hobart A Reimann, Moadié, J; Semerdjian, S; Sahyoun, PF, Periodic Peritonitis—Heredity & Pathology: report of seventy-two cases. JAMA, 1954. Hobart A Reimann, Periodic fever, an entity: A collection of 52 cases. AmJMedSci, 1962. References External links Understanding Autoinflammatory Diseases - US National Institute of Arthritis and Musculoskeletal and Skin Diseases

Hi Aarogya , Do you know what is Idiopathic interstitial pneumonia,

Idiopathic interstitial pneumonia

Idiopathic interstitial pneumonia (IIP), or noninfectious pneumonia are a class of diffuse lung diseases. These diseases typically affect the pulmonary interstitium, although some also have a component affecting the airways (for instance, cryptogenic organizing pneumonitis). There are seven recognized distinct subtypes of IIP. Diagnosis Classification can be complex, and the combined efforts of clinicians, radiologists, and pathologists can help in the generation of a more specific diagnosis.Idiopathic interstitial pneumonia can be subclassified based on histologic appearance into the following patterns: Usual interstitial pneumonia is the most common type. Development Table 1: Development of the (histologic) idiopathic interstitial pneumonia classification UIP=usual interstitial pneumonia; DAD=diffuse alveolar damage; NSIP=non-specific interstitial pneumonia; DIP=desquamative interstitial pneumonia; RB=respiratory bronchiolitis; BIP=bronchiolitis obliterans interstitial pneumonia; OP=organizing pneumonia; LIP=lymphoid interstitial pneumonia; LPD=lymphoproliferative disease (not considered a diffuse lung disease); GIP=giant cell interstitial pneumonia; HMF=heavy metal fibrosis, no longer grouped with diffuse lung disease Lymphoid interstitial pneumonia was originally included in this category, then excluded, then included again. References == External links ==

Hey Aarogya, explain a scenario commonly referred as Avascular necrosis

Avascular necrosis

Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply. Early on, there may be no symptoms. Gradually joint pain may develop which may limit the ability to move. Complications may include collapse of the bone or nearby joint surface.Risk factors include bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids. The condition may also occur without any clear reason. The most commonly affected bone is the femur. Other relatively common sites include the upper arm bone, knee, shoulder, and ankle. Diagnosis is typically by medical imaging such as X-ray, CT scan, or MRI. Rarely biopsy may be used.Treatments may include medication, not walking on the affected leg, stretching, and surgery. Most of the time surgery is eventually required and may include core decompression, osteotomy, bone grafts, or joint replacement. About 15,000 cases occur per year in the United States. People 30 to 50 years old are most commonly affected. Males are more commonly affected than females. Signs and symptoms In many cases, there is pain and discomfort in a joint which increases over time. While it can affect any bone, about half of cases show multiple sites of damage.Avascular necrosis most commonly affects the ends of long bones such as the femur. Other common sites include the humerus, knees, shoulders, ankles and the jaw. Causes The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids. Other risk factors include radiation therapy, chemotherapy, and organ transplantation. Osteonecrosis is also associated with cancer, lupus, sickle cell disease, HIV infection, Gauchers disease, and Caisson disease (dysbaric osteonecrosis). The condition may also occur without any clear reason.Bisphosphonates are associated with osteonecrosis of the mandible. Prolonged, repeated exposure to high pressures (as experienced by commercial and military divers) has been linked to AVN, though the relationship is not well understood.In children, avascular osteonecrosis can have several causes. It can occur in the hip as part of Legg–Calvé–Perthes syndrome, and it can also occur as a result after malignancy treatment such as acute lymphoblastic leukemia and allotransplantation. Pathophysiology The hematopoietic cells are most sensitive to low oxygen and are the first to die after reduction or removal of the blood supply, usually within 12 hours. Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 12–48 hours, and that bone marrow fat cells die within 5 days.Upon reperfusion, repair of bone occurs in 2 phases. First, there is angiogenesis and movement of undifferentiated mesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry of macrophages that degrade dead cellular and fat debris. Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts. Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue. Diagnosis In the early stages, bone scintigraphy and MRI are the preferred diagnostic tools.X-ray images of avascular necrosis in the early stages usually appear normal. In later stages it appears relatively more radio-opaque due to the nearby living bone becoming resorbed secondary to reactive hyperemia. The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by living osteoclasts. Late radiographic signs also include a radiolucency area following the collapse of subchondral bone (crescent sign) and ringed regions of radiodensity resulting from saponification and calcification of marrow fat following medullary infarcts. Types When AVN affects the scaphoid bone, it is known as Preiser disease. Another named form of AVN is Köhler disease, which affects the navicular bone of the foot, primarily in children. Yet another form of AVN is Kienböcks disease, which affects the lunate bone in the wrist. Treatment A variety of methods may be used to treat the most common being the total hip replacement (THR). However, THRs have a number of downsides including long recovery times and short life spans of the hip joints. THRs are an effective means of treatment in the older population; however, in younger people, they may wear out before the end of a persons life.Other techniques such as metal on metal resurfacing may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage has occurred to the femoral head. Bisphosphonates which reduce the rate of bone breakdown may prevent collapse (specifically of the hip) due to AVN. Core decompression Other treatments include core decompression, where internal bone pressure is relieved by drilling a hole into the bone, and a living bone chip and an electrical device to stimulate new vascular growth are implanted; and the free vascular fibular graft (FVFG), in which a portion of the fibula, along with its blood supply, is removed and transplanted into the femoral head. A 2016 Cochrane review found no clear improvement between people who have had hip core decompression and participate in physical therapy, versus physical therapy alone. There is additionally no strong research on the effectiveness of hip core decompression for people with sickle cell disease.Progression of the disease could possibly be halted by transplanting nucleated cells from bone marrow into avascular necrosis lesions after core decompression, although much further research is needed to establish this technique. Prognosis The amount of disability that results from avascular necrosis depends on what part of the bone is affected, how large an area is involved, and how effectively the bone rebuilds itself. The process of bone rebuilding takes place after an injury as well as during normal growth. Normally, bone continuously breaks down and rebuilds—old bone is resorbed and replaced with new bone. The process keeps the skeleton strong and helps it to maintain a balance of minerals. In the course of avascular necrosis, however, the healing process is usually ineffective and the bone tissues break down faster than the body can repair them. If left untreated, the disease progresses, the bone collapses, and the joint surface breaks down, leading to pain and arthritis. Epidemiology Avascular necrosis usually affects people between 30 and 50 years of age; about 10,000 to 20,000 people develop avascular necrosis of the head of the femur in the US each year. Society and culture Cases of avascular necrosis have been identified in a few high-profile athletes. It abruptly ended the career of American football running-back Bo Jackson in 1991. Doctors discovered Jackson to have lost all of the cartilage supporting his hip while he was undergoing tests following a hip-injury he had on the field during a 1991 NFL Playoff game. Avascular necrosis of the hip was also identified in a routine medical check-up on quarterback Brett Favre following his trade to the Green Bay Packers in 1991. However, Favre would go on to have a long career at the Packers.Another high-profile athlete was American road racing cyclist Floyd Landis, winner of the 2006 Tour de France, the title being subsequently stripped from his record by cyclings governing bodies after his blood samples tested positive for banned substances. During that tour, Landis was allowed cortisone shots to help manage his ailment, despite cortisone also being a banned substance in professional cycling at the time. Rafael Nadal successfully continued his tennis career after having surgery for Mueller-Weiss syndrome (osteonecrosis of the navicular.) References External links Osteonecrosis / Avascular Necrosis at the National Institute of Health Osteonecrosis / Avascular necrosis at Merck Manual for patients Osteonecrosis / Avascular necrosis at Merck Manual for medical professionals

Hello Aarogya, could you help me understand about Side

Side

Side or Sides may refer to: Geometry Edge (geometry) of a polygon (two-dimensional shape) Face (geometry) of a polyhedron (three-dimensional shape) Places Side (Ainis), a town of Ainis, ancient Thessaly, Greece Side (Caria), a town of ancient Caria, Anatolia Side (Laconia), a town of ancient Laconia, Greece Side (Pontus), a town of ancient Pontus, Anatolia Side, Turkey, a city in Turkey Side, Iran, a village in Iran Side, Gloucestershire, or Syde, a village in England Music Side (recording), the A-side or B-side of a record The Side, a Scottish rock band Sides (album), a 1979 album by Anthony Phillips Sides, a 2020 album by Emily King "Side" (song), a 2001 song by Travis "Sides", a song by Flobots from the album The Circle in the Square, 2012 "Sides", a song by Allday from the album Speeding, 2017 Teams Side (cue sports technique) Side, a team, in particular: Sports team Other uses Side (mythology), one of three mythological figures Side, a Morris dance team Sideboard (cards), known as a "side" in some collectible card games Sides (surname), a surname Side dish, a food item accompanying a main course School of Isolated and Distance Education, a public school in Perth, Western Australia Secretaría de Inteligencia, the premier intelligence agency of the Argentine Republic Social identity model of deindividuation effects, in social psychology Side (gay sex), a term describes gay men who are not interested in anal sex See also All pages with titles beginning with Side All pages with titles containing side Cide (disambiguation) Relative direction, left and right Sidle (disambiguation)

Would you describe Farmers lung, to me Aarogya

Farmers lung

Farmers lung (not to be confused with silo-fillers disease) is a hypersensitivity pneumonitis induced by the inhalation of biologic dusts coming from hay dust or mold spores or any other agricultural products. It results in a type III hypersensitivity inflammatory response and can progress to become a chronic condition which is considered potentially dangerous. Signs and symptoms Acute Stage: Appears four to eight hours after exposure. Symptoms such as headache, irritating cough, and shortness of breath upon physical exertion. Subacute Stage: Symptoms persist without further exposure, and increase in severity. Symptoms include: shortness of breath upon exertion, chronic coughing, physical weakness, occasional fever and sweating, decrease in appetite, aches and pains. Chronic Stage: Debilitating effects are now considered long-term. Symptoms include: severe shortness of breath, chronic coughing, physical weakness, occasional fever and sweating at night, decrease in appetite, and general aches and pains.These symptoms develop between four and eight hours after exposure to the antigens. In acute attacks, the symptoms mimic pneumonia or flu. In chronic attacks, there is a possibility of the victim going into shock and dying from the attack. Causes Permanent lung damage can arise due to ones inability to recognize the cause of symptoms. Farmers lung occurs because repeated exposure to antigens, found in the mold spores of hay, crops, and animal feed, triggers an allergic reaction within the farmers immune system. The defense mechanisms of the body present as cold and flu-like symptoms that occur in individuals who experience either acute or chronic reactions.The mold spores are inhaled and provoke the creation of IgE antibodies that circulate in the bloodstream, these types of immune response are most often initiated by exposure to thermophilic actinomycetes (most commonly Saccharopolyspora rectivirgula), which generate IgG-type antibodies. Following a subsequent exposure, IgG antibodies combined with the inhaled allergen to form immune complexes in the walls of the alveoli in the lungs. This causes fluid, protein, and cells to accumulate in the alveolar wall which slows blood-gas interchange and compromises the function of the lung. After multiple exposures, it takes less and less of the antigens to set off the reaction in the lung. Prevention Farmers lung disease (FLD) is permanent and cannot be reversed, therefore in order to prevent the onset of further stages, farmers should inform their doctor of their occupation and if they have mold in their work environment. Prevention of this respiratory illness can be facilitated through the ventilation of work areas, drying of materials, and the use of a mask when working in confined areas with moldy hay or crops. Diagnosis Diagnoses of Farmers lung is difficult due to its similarity to cold and flu-like symptoms. Doctors diagnose patients with Farmers lung under the following conditions: A clinical history of symptoms such as cough, fever, and labored breathing when exposed to mold in work environment. The presence of diffuse lung disease in chronic cases. Presentation of antibodies when exposed to thermophilic Actinomyces.Examination procedures may include: • taking a blood test• taking a chest x-ray• administering a breathing capacity test• administering an inhalation challenge• examining lung tissue• performing an immunological investigation• performing a lung function test• reviewing the clinical history Treatment Depending on the severity of the symptoms, FLD can last from one to two weeks, or it can last for the rest of ones life. Acute FLD has the ability to be treated because hypersensitivity to the antigens has not yet developed. The main treatment options are: rest and reducing the exposure to the antigens through masks and increased airflow in confined spaces where the antigens are present. Any exposure to the antigens once hypersensitivity has occurred can set off another chronic reaction. For chronic FLD, there are no true treatments because the patient has developed hypersensitivity meaning that their condition will last the rest of their life. Epidemiology The growth of mold spores occurs when hay is not dried properly. The growth of these mold spores accumulates over time and will infect the host upon release from the source. When in the air, the farmer may inhale the particles and induce an allergic reaction. The hay at risk for increased volumes of spores is found at the bottom of the pile. The presence of Farmers Lung Disease peaks during late winter and early spring and is mostly seen after the harvest season when symptoms have set in. This disease is most prevalent in damp climates. See also Organic dust toxic syndrome == References ==

Aarogya, What does Megaureter mean

Megaureter

Megaureter is a medical anomaly whereby the ureter is abnormally dilated. Congenital megaureter is an uncommon condition which is more common in males, may be bilateral, and is often associated with other congenital anomalies. The cause is thought to be aperistalsis of the distal ureter, leading to dilatation.The cutoff value for megaureter is when it is wider than 6 or 7 mm.A functional obstruction at the lower end of the ureter leads to progressive dilatation and a tendency to infection. The ureteric orifice appears normal and a ureteric catheter passes easily.Definitive surgical treatment involves refashioning the lower end of the affected ureter so that a tunnelled reimplantation into the bladder can be done to prevent reflux. References Bailey and Loves Short Practice of Surgery == External links ==

Hi Aarogya, explain a situation where Decompression sickness occurs

Decompression sickness

Decompression sickness (abbreviated DCS; also called divers disease, the bends, aerobullosis, and caisson disease) is a medical condition caused by dissolved gases emerging from solution as bubbles inside the body tissues during decompression. DCS most commonly occurs during or soon after a decompression ascent from underwater diving, but can also result from other causes of depressurisation, such as emerging from a caisson, decompression from saturation, flying in an unpressurised aircraft at high altitude, and extravehicular activity from spacecraft. DCS and arterial gas embolism are collectively referred to as decompression illness. Since bubbles can form in or migrate to any part of the body, DCS can produce many symptoms, and its effects may vary from joint pain and rashes to paralysis and death. DCS often causes air bubbles to settle in major joints like knees or elbows, causing individuals to bend over in excruciating pain, hence its common name, the bends. Individual susceptibility can vary from day to day, and different individuals under the same conditions may be affected differently or not at all. The classification of types of DCS according to symptoms has evolved since its original description in the 19th century. The severity of symptoms varies from barely noticeable to rapidly fatal. The risk of DCS caused by diving can be managed through proper decompression procedures, and contracting the condition has become uncommon. Its potential severity has driven much research to prevent it, and divers almost universally use dive tables or dive computers to limit their exposure and to monitor their ascent speed. If DCS is suspected, it is treated by hyperbaric oxygen therapy in a recompression chamber. Where a chamber is not accessible within a reasonable time frame, in-water recompression may be indicated for a narrow range of presentations, if there are suitably skilled personnel and appropriate equipment available on site. Diagnosis is confirmed by a positive response to the treatment. Early treatment results in a significantly higher chance of successful recovery. Classification DCS is classified by symptoms. The earliest descriptions of DCS used the terms: "bends" for joint or skeletal pain; "chokes" for breathing problems; and "staggers" for neurological problems. In 1960, Golding et al. introduced a simpler classification using the term "Type I (simple)" for symptoms involving only the skin, musculoskeletal system, or lymphatic system, and "Type II (serious)" for symptoms where other organs (such as the central nervous system) are involved. Type II DCS is considered more serious and usually has worse outcomes. This system, with minor modifications, may still be used today. Following changes to treatment methods, this classification is now much less useful in diagnosis, since neurological symptoms may develop after the initial presentation, and both Type I and Type II DCS have the same initial management. Decompression illness and dysbarism The term dysbarism encompasses decompression sickness, arterial gas embolism, and barotrauma, whereas decompression sickness and arterial gas embolism are commonly classified together as decompression illness when a precise diagnosis cannot be made. DCS and arterial gas embolism are treated very similarly because they are both the result of gas bubbles in the body. The U.S. Navy prescribes identical treatment for Type II DCS and arterial gas embolism. Their spectra of symptoms also overlap, although the symptoms from arterial gas embolism are generally more severe because they often arise from an infarction (blockage of blood supply and tissue death). Signs and symptoms While bubbles can form anywhere in the body, DCS is most frequently observed in the shoulders, elbows, knees, and ankles. Joint pain ("the bends") accounts for about 60% to 70% of all altitude DCS cases, with the shoulder being the most common site for altitude and bounce diving, and the knees and hip joints for saturation and compressed air work. Neurological symptoms are present in 10% to 15% of DCS cases with headache and visual disturbances being the most common symptom. Skin manifestations are present in about 10% to 15% of cases. Pulmonary DCS ("the chokes") is very rare in divers and has been observed much less frequently in aviators since the introduction of oxygen pre-breathing protocols. The table below shows symptoms for different DCS types. Frequency The relative frequencies of different symptoms of DCS observed by the U.S. Navy are as follows: Onset Although onset of DCS can occur rapidly after a dive, in more than half of all cases symptoms do not begin to appear for at least an hour. In extreme cases, symptoms may occur before the dive has been completed. The U.S. Navy and Technical Diving International, a leading technical diver training organization, have published a table that documents time to onset of first symptoms. The table does not differentiate between types of DCS, or types of symptom. Causes DCS is caused by a reduction in ambient pressure that results in the formation of bubbles of inert gases within tissues of the body. It may happen when leaving a high-pressure environment, ascending from depth, or ascending to altitude. A closely related condition of bubble formation in body tissues due to isobaric counterdiffusion can occur with no change of pressure. Ascent from depth DCS is best known as a diving disorder that affects divers having breathed gas that is at a higher pressure than the surface pressure, owing to the pressure of the surrounding water. The risk of DCS increases when diving for extended periods or at greater depth, without ascending gradually and making the decompression stops needed to slowly reduce the excess pressure of inert gases dissolved in the body. The specific risk factors are not well understood and some divers may be more susceptible than others under identical conditions. DCS has been confirmed in rare cases of breath-holding divers who have made a sequence of many deep dives with short surface intervals, and may be the cause of the disease called taravana by South Pacific island natives who for centuries have dived by breath-holding for food and pearls.Two principal factors control the risk of a diver developing DCS: the rate and duration of gas absorption under pressure – the deeper or longer the dive the more gas is absorbed into body tissue in higher concentrations than normal (Henrys Law); the rate and duration of outgassing on depressurization – the faster the ascent and the shorter the interval between dives the less time there is for absorbed gas to be offloaded safely through the lungs, causing these gases to come out of solution and form "micro bubbles" in the blood.Even when the change in pressure causes no immediate symptoms, rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis (DON). DON can develop from a single exposure to rapid decompression. Leaving a high-pressure environment When workers leave a pressurized caisson or a mine that has been pressurized to keep water out, they will experience a significant reduction in ambient pressure. A similar pressure reduction occurs when astronauts exit a space vehicle to perform a space-walk or extra-vehicular activity, where the pressure in their spacesuit is lower than the pressure in the vehicle.The original name for DCS was "caisson disease". This term was introduced in the 19th century, when caissons under pressure were used to keep water from flooding large engineering excavations below the water table, such as bridge supports and tunnels. Workers spending time in high ambient pressure conditions are at risk when they return to the lower pressure outside the caisson if the pressure is not reduced slowly. DCS was a major factor during construction of Eads Bridge, when 15 workers died from what was then a mysterious illness, and later during construction of the Brooklyn Bridge, where it incapacitated the project leader Washington Roebling. On the other side of the Manhattan island during construction of the Hudson River Tunnel contractors agent Ernest William Moir noted in 1889 that workers were dying due to decompression sickness and pioneered the use of an airlock chamber for treatment. Ascent to altitude The most common health risk on ascent to altitude is not decompression sickness but altitude sickness, or acute mountain sickness (AMS), which has an entirely different and unrelated set of causes and symptoms. AMS results not from the formation of bubbles from dissolved gasses in the body but from exposure to a low partial pressure of oxygen and alkalosis. However, passengers in unpressurized aircraft at high altitude may also be at some risk of DCS.Altitude DCS became a problem in the 1930s with the development of high-altitude balloon and aircraft flights but not as great a problem as AMS, which drove the development of pressurized cabins, which coincidentally controlled DCS. Commercial aircraft are now required to maintain the cabin at or below a pressure altitude of 2,400 m (7,900 ft) even when flying above 12,000 m (39,000 ft). Symptoms of DCS in healthy individuals are subsequently very rare unless there is a loss of pressurization or the individual has been diving recently. Divers who drive up a mountain or fly shortly after diving are at particular risk even in a pressurized aircraft because the regulatory cabin altitude of 2,400 m (7,900 ft) represents only 73% of sea level pressure.Generally, the higher the altitude the greater the risk of altitude DCS but there is no specific, maximum, safe altitude below which it never occurs. There are very few symptoms at or below 5,500 m (18,000 ft) unless patients had predisposing medical conditions or had dived recently. There is a correlation between increased altitudes above 5,500 m (18,000 ft) and the frequency of altitude DCS but there is no direct relationship with the severity of the various types of DCS. A US Air Force study reports that there are few occurrences between 5,500 m (18,000 ft) and 7,500 m (24,600 ft) and 87% of incidents occurred at or above 7,500 m (24,600 ft). High-altitude parachutists may reduce the risk of altitude DCS if they flush nitrogen from the body by pre-breathing pure oxygen. Predisposing factors Although the occurrence of DCS is not easily predictable, many predisposing factors are known. They may be considered as either environmental or individual. Decompression sickness and arterial gas embolism in recreational diving are associated with certain demographic, environmental, and dive style factors. A statistical study published in 2005 tested potential risk factors: age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous decompression illness, years since certification, dives in the last year, number of diving days, number of dives in a repetitive series, last dive depth, nitrox use, and drysuit use. No significant associations with risk of decompression sickness or arterial gas embolism were found for asthma, diabetes, cardiovascular disease, smoking, or body mass index. Increased depth, previous DCI, larger number of consecutive days diving, and being male were associated with higher risk for decompression sickness and arterial gas embolism. Nitrox and drysuit use, greater frequency of diving in the past year, increasing age, and years since certification were associated with lower risk, possibly as indicators of more extensive training and experience. Environmental The following environmental factors have been shown to increase the risk of DCS: the magnitude of the pressure reduction ratio – a large pressure reduction ratio is more likely to cause DCS than a small one. repetitive exposures – repetitive dives within a short period of time (a few hours) increase the risk of developing DCS. Repetitive ascents to altitudes above 5,500 metres (18,000 ft) within similar short periods increase the risk of developing altitude DCS. the rate of ascent – the faster the ascent the greater the risk of developing DCS. The U.S. Navy Diving Manual indicates that ascent rates greater than about 20 m/min (66 ft/min) when diving increase the chance of DCS, while recreational dive tables such as the Bühlmann tables require an ascent rate of 10 m/min (33 ft/min) with the last 6 m (20 ft) taking at least one minute. An individual exposed to a rapid decompression (high rate of ascent) above 5,500 metres (18,000 ft) has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent. the duration of exposure – the longer the duration of the dive, the greater is the risk of DCS. Longer flights, especially to altitudes of 5,500 m (18,000 ft) and above, carry a greater risk of altitude DCS. underwater diving before flying – divers who ascend to altitude soon after a dive increase their risk of developing DCS even if the dive itself was within the dive table safe limits. Dive tables make provisions for post-dive time at surface level before flying to allow any residual excess nitrogen to outgas. However, the pressure maintained inside even a pressurized aircraft may be as low as the pressure equivalent to an altitude of 2,400 m (7,900 ft) above sea level. Therefore, the assumption that the dive table surface interval occurs at normal atmospheric pressure is invalidated by flying during that surface interval, and an otherwise-safe dive may then exceed the dive table limits. diving before travelling to altitude – DCS can occur without flying if the person moves to a high-altitude location on land immediately after diving, for example, scuba divers in Eritrea who drive from the coast to the Asmara plateau at 2,400 m (7,900 ft) increase their risk of DCS. diving at altitude – diving in water whose surface pressure is significantly below sea level pressure — for example, Lake Titicaca is at 3,800 m (12,500 ft). Versions of decompression tables for altitudes exceeding 300 m (980 ft), or dive computers with high-altitude settings or surface pressure sensors may be used to reduce this risk. Individual The following individual factors have been identified as possibly contributing to increased risk of DCS: dehydration – Studies by Walder concluded that decompression sickness could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline, and the high surface tension of water is generally regarded as helpful in controlling bubble size. Maintaining proper hydration is recommended. There is no convincing evidence that overhydration has any benefits, and it is implicated in immersion pulmonary oedema. patent foramen ovale – a hole between the atrial chambers of the heart in the fetus is normally closed by a flap with the first breaths at birth. In about 20% of adults the flap does not completely seal, however, allowing blood through the hole when coughing or during activities that raise chest pressure. In diving, this can allow venous blood with microbubbles of inert gas to bypass the lungs, where the bubbles would otherwise be filtered out by the lung capillary system, and return directly to the arterial system (including arteries to the brain, spinal cord and heart). In the arterial system, bubbles (arterial gas embolism) are far more dangerous because they block circulation and cause infarction (tissue death, due to local loss of blood flow). In the brain, infarction results in stroke, and in the spinal cord it may result in paralysis. a persons age – there are some reports indicating a higher risk of altitude DCS with increasing age. previous injury – there is some indication that recent joint or limb injuries may predispose individuals to developing decompression-related bubbles. ambient temperature – there is some evidence suggesting that individual exposure to very cold ambient temperatures may increase the risk of altitude DCS. Decompression sickness risk can be reduced by increased ambient temperature during decompression following dives in cold water. body type – typically, a person who has a high body fat content is at greater risk of DCS. This is due to nitrogens five times greater solubility in fat than in water, leading to greater amounts of total body dissolved nitrogen during time at pressure. Fat represents about 15–25 percent of a healthy adults body, but stores about half of the total amount of nitrogen (about 1 litre) at normal pressures. alcohol consumption – although alcohol consumption increases dehydration and therefore may increase susceptibility to DCS, a 2005 study found no evidence that alcohol consumption increases the incidence of DCS. Mechanism Depressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body. These bubbles produce the symptoms of decompression sickness. Bubbles may form whenever the body experiences a reduction in pressure, but not all bubbles result in DCS. The amount of gas dissolved in a liquid is described by Henrys Law, which indicates that when the pressure of a gas in contact with a liquid is decreased, the amount of that gas dissolved in the liquid will also decrease proportionately. On ascent from a dive, inert gas comes out of solution in a process called "outgassing" or "offgassing". Under normal conditions, most offgassing occurs by gas exchange in the lungs. If inert gas comes out of solution too quickly to allow outgassing in the lungs then bubbles may form in the blood or within the solid tissues of the body. The formation of bubbles in the skin or joints results in milder symptoms, while large numbers of bubbles in the venous blood can cause lung damage. The most severe types of DCS interrupt — and ultimately damage — spinal cord function, leading to paralysis, sensory dysfunction, or death. In the presence of a right-to-left shunt of the heart, such as a patent foramen ovale, venous bubbles may enter the arterial system, resulting in an arterial gas embolism. A similar effect, known as ebullism, may occur during explosive decompression, when water vapour forms bubbles in body fluids due to a dramatic reduction in environmental pressure. Inert gases The main inert gas in air is nitrogen, but nitrogen is not the only gas that can cause DCS. Breathing gas mixtures such as trimix and heliox include helium, which can also cause decompression sickness. Helium both enters and leaves the body faster than nitrogen, so different decompression schedules are required, but, since helium does not cause narcosis, it is preferred over nitrogen in gas mixtures for deep diving. There is some debate as to the decompression requirements for helium during short-duration dives. Most divers do longer decompressions; however, some groups like the WKPP have been experimenting with the use of shorter decompression times by including deep stops. The balance of evidence as of 2020 does not indicate that deep stops increase decompression efficiency. Any inert gas that is breathed under pressure can form bubbles when the ambient pressure decreases. Very deep dives have been made using hydrogen-oxygen mixtures (hydrox), but controlled decompression is still required to avoid DCS. Isobaric counterdiffusion DCS can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of inert gas. This is known as isobaric counterdiffusion, and presents a problem for very deep dives. For example, after using a very helium-rich trimix at the deepest part of the dive, a diver will switch to mixtures containing progressively less helium and more oxygen and nitrogen during the ascent. Nitrogen diffuses into tissues 2.65 times slower than helium but is about 4.5 times more soluble. Switching between gas mixtures that have very different fractions of nitrogen and helium can result in "fast" tissues (those tissues that have a good blood supply) actually increasing their total inert gas loading. This is often found to provoke inner ear decompression sickness, as the ear seems particularly sensitive to this effect. Bubble formation The location of micronuclei or where bubbles initially form is not known. The most likely mechanisms for bubble formation are tribonucleation, when two surfaces make and break contact (such as in joints), and heterogeneous nucleation, where bubbles are created at a site based on a surface in contact with the liquid. Homogeneous nucleation, where bubbles form within the liquid itself is less likely because it requires much greater pressure differences than experienced in decompression. The spontaneous formation of nanobubbles on hydrophobic surfaces is a possible source of micronuclei, but it is not yet clear if these can grow large enough to cause symptoms as they are very stable.Once microbubbles have formed, they can grow by either a reduction in pressure or by diffusion of gas into the gas from its surroundings. In the body, bubbles may be located within tissues or carried along with the bloodstream. The speed of blood flow within a blood vessel and the rate of delivery of blood to capillaries (perfusion) are the main factors that determine whether dissolved gas is taken up by tissue bubbles or circulation bubbles for bubble growth. Pathophysiology The primary provoking agent in decompression sickness is bubble formation from excess dissolved gases. Various hypotheses have been put forward for the nucleation and growth of bubbles in tissues, and for the level of supersaturation which will support bubble growth. The earliest bubble formation detected is subclinical intravascular bubbles detectable by doppler ultrasound in the venous systemic circulation. The presence of these "silent" bubbles is no guarantee that they will persist and grow to be symptomatic.Vascular bubbles formed in the systemic capillaries may be trapped in the lung capillaries, temporarily blocking them. If this is severe, the symptom called "chokes" may occur. If the diver has a patent foramen ovale (or a shunt in the pulmonary circulation), bubbles may pass through it and bypass the pulmonary circulation to enter the arterial blood. If these bubbles are not absorbed in the arterial plasma and lodge in systemic capillaries they will block the flow of oxygenated blood to the tissues supplied by those capillaries, and those tissues will be starved of oxygen. Moon and Kisslo (1988) concluded that "the evidence suggests that the risk of serious neurological DCI or early onset DCI is increased in divers with a resting right-to-left shunt through a PFO. There is, at present, no evidence that PFO is related to mild or late onset bends. Bubbles form within other tissues as well as the blood vessels. Inert gas can diffuse into bubble nuclei between tissues. In this case, the bubbles can distort and permanently damage the tissue. As they grow, the bubbles may also compress nerves, causing pain. Extravascular or autochthonous bubbles usually form in slow tissues such as joints, tendons and muscle sheaths. Direct expansion causes tissue damage, with the release of histamines and their associated affects. Biochemical damage may be as important as, or more important than mechanical effects.Bubble size and growth may be affected by several factors - gas exchange with adjacent tissues, the presence of surfactants, coalescence and disintegration by collision. Vascular bubbles may cause direct blockage, aggregate platelets and red blood cells, and trigger the coagulation process, causing local and downstream clotting.Arteries may be blocked by intravascular fat aggregation. Platelets accumulate in the vicinity of bubbles. Endothelial damage may be a mechanical effect of bubble pressure on the vessel walls, a toxic effect of stabilised platelet aggregates and possibly toxic effects due to the association of lipids with the air bubbles. Protein molecules may be denatured by reorientation of the secondary and tertiary structure when non-polar groups protrude into the bubble gas and hydrophilic groups remain in the surrounding blood, which may generate a cascade of pathophysiological events with consequent production of clinical signs of decompression sickness.The physiological effects of a reduction in environmental pressure depend on the rate of bubble growth, the site, and surface activity. A sudden release of sufficient pressure in saturated tissue results in a complete disruption of cellular organelles, while a more gradual reduction in pressure may allow accumulation of a smaller number of larger bubbles, some of which may not produce clinical signs, but still cause physiological effects typical of a blood/gas interface and mechanical effects. Gas is dissolved in all tissues, but decompression sickness is only clinically recognised in the central nervous system, bone, ears, teeth, skin and lungs.Necrosis has frequently been reported in the lower cervical, thoracic, and upper lumbar regions of the spinal cord. A catastrophic pressure reduction from saturation produces explosive mechanical disruption of cells by local effervescence, while a more gradual pressure loss tends to produce discrete bubbles accumulated in the white matter, surrounded by a protein layer. Typical acute spinal decompression injury occurs in the columns of white matter. Infarcts are characterised by a region of oedema, haemorrhage and early myelin degeneration, and are typically centred on small blood vessels. The lesions are generally discrete. Oedema usually extends to the adjacent grey matter. Microthrombi are found in the blood vessels associated with the infarcts.Following the acute changes there is an invasion of lipid phagocytes and degeneration of adjacent neural fibres with vascular hyperplasia at the edges of the infarcts. The lipid phagocytes are later replaced by a cellular reaction of astrocytes. Vessels in surrounding areas remain patent but are collagenised. Distribution of spinal cord lesions may be related to vascular supply. There is still uncertainty regarding the aetiology of decompression sickness damage to the spinal cord.Dysbaric osteonecrosis lesions are typically bilateral and usually occur at both ends of the femur and at the proximal end of the humerus Symptoms are usually only present when a joint surface is involved, which typically does not occur until a long time after the causative exposure to a hyperbaric environment. The initial damage is attributed to the formation of bubbles, and one episode can be sufficient, however incidence is sporadic and generally associated with relatively long periods of hyperbaric exposure and aetiology is uncertain. Early identification of lesions by radiography is not possible, but over time areas of radiographic opacity develop in association with the damaged bone. Diagnosis Diagnosis of decompression sickness relies almost entirely on clinical presentation, as there are no laboratory tests that can incontrovertibly confirm or reject the diagnosis. Various blood tests have been proposed, but they are not specific for decompression sickness, they are of uncertain utility and are not in general use.Decompression sickness should be suspected if any of the symptoms associated with the condition occurs following a drop in pressure, in particular, within 24 hours of diving. In 1995, 95% of all cases reported to Divers Alert Network had shown symptoms within 24 hours. This window can be extended to 36 hours for ascent to altitude and 48 hours for prolonged exposure to altitude following diving. An alternative diagnosis should be suspected if severe symptoms begin more than six hours following decompression without an altitude exposure or if any symptom occurs more than 24 hours after surfacing. The diagnosis is confirmed if the symptoms are relieved by recompression. Although MRI or CT can frequently identify bubbles in DCS, they are not as good at determining the diagnosis as a proper history of the event and description of the symptoms. Test of pressure There is no gold standard for diagnosis, and DCI experts are rare. Most of the chambers open to treatment of recreational divers and reporting to Divers Alert Network see fewer than 10 cases per year, making it difficult for the attending doctors to develop experience in diagnosis. A method used by commercial diving supervisors when considering whether to recompress as first aid when they have a chamber on site, is known as the test of pressure. The diver is checked for contraindications to recompression, and if none are present, recompressed. If the symptoms resolve or reduce during recompression, it is considered likely that a treatment schedule will be effective. The test is not entirely reliable, and both false positives and false negatives are possible, however in the commercial diving environment it is often considered worth treating when there is doubt, and very early recompression has a history of very high success rates and reduced number of treatments needed for complete resolution and minimal sequelae. Differential diagnosis Symptoms of DCS and arterial gas embolism can be virtually indistinguishable. The most reliable way to tell the difference is based on the dive profile followed, as the probability of DCS depends on duration of exposure and magnitude of pressure, whereas AGE depends entirely on the performance of the ascent. In many cases it is not possible to distinguish between the two, but as the treatment is the same in such cases it does not usually matter.Other conditions which may be confused with DCS include skin symptoms cutis marmorata due to DCS and skin barotrauma due to dry suit squeeze, for which no treatment is necessary. Dry suit squeeze produces lines of redness with possible bruising where the skin was pinched between folds of the suit, while the mottled effect of cutis marmorata is usually on skin where there is subcutaneous fat, and has no linear pattern.Transient episodes of severe neurological incapacitation with rapid spontaneous recovery shortly after a dive may be attributed to hypothermia, but may be symptomatic of short term CNS involvement, which may have residual problems or relapses. These cases are thought to be under-diagnosed.Inner ear decompression sickness (IEDCS) can be confused with inner ear barotrauma (IEBt), alternobaric vertigo, caloric vertigo and reverse squeeze. A history of difficulty in equalising the ears during the dive makes ear barotrauma more likely, but does not always eliminate the possibility of inner ear DCS, which is usually associated with deep, mixed gas dives with decompression stops. Both conditions may exist concurrently, and it can be difficult to distinguish whether a person has IEDCS, IEBt, or both. Numbness and tingling are associated with spinal DCS, but can also be caused by pressure on nerves (compression neurapraxia). In DCS the numbness or tingling is generally confined to one or a series of dermatomes, while pressure on a nerve tends to produce characteristic areas of numbness associated with the specific nerve on only one side of the body distal to the pressure point. A loss of strength or function is likely to be a medical emergency. A loss of feeling that lasts more than a minute or two indicates a need for immediate medical attention. It is only partial sensory changes, or paraesthesias, where this distinction between trivial and more serious injuries applies.Large areas of numbness with associated weakness or paralysis, especially if a whole limb is affected, are indicative of probable brain involvement and require urgent medical attention. Paraesthesias or weakness involving a dermatome indicate probable spinal cord or spinal nerve root involvement. Although it is possible that this may have other causes, such as an injured intervertebral disk, these symptoms indicate an urgent need for medical assessment. In combination with weakness, paralysis or loss of bowel or bladder control, they indicate a medical emergency. Prevention Underwater diving To prevent the excess formation of bubbles that can lead to decompression sickness, divers limit their ascent rate—the recommended ascent rate used by popular decompression models is about 10 metres (33 ft) per minute—and follow a decompression schedule as necessary. This schedule may require the diver to ascend to a particular depth, and remain at that depth until sufficient inert gas has been eliminated from the body to allow further ascent. Each of these is termed a "decompression stop", and a schedule for a given bottom time and depth may contain one or more stops, or none at all. Dives that contain no decompression stops are called "no-stop dives", but divers usually schedule a short "safety stop" at 3 to 6 m (10 to 20 ft), depending on the training agency or dive computer.The decompression schedule may be derived from decompression tables, decompression software, or from dive computers, and these are generally based upon a mathematical model of the bodys uptake and release of inert gas as pressure changes. These models, such as the Bühlmann decompression algorithm, are modified to fit empirical data and provide a decompression schedule for a given depth and dive duration using a specified breathing gas mixture.Since divers on the surface after a dive may still have excess inert gas in their bodies, decompression from any subsequent dive before this excess is eliminated needs to modify the schedule to take account of the residual gas load from the previous dive. This will result in a shorter allowable time under water without obligatory decompression stops, or an increased decompression time during the subsequent dive. The total elimination of excess gas may take many hours, and tables will indicate the time at normal pressures that is required, which may be up to 18 hours.Decompression time can be significantly shortened by breathing mixtures containing much less inert gas during the decompression phase of the dive (or pure oxygen at stops in 6 metres (20 ft) of water or less). The reason is that the inert gas outgases at a rate proportional to the difference between the partial pressure of inert gas in the divers body and its partial pressure in the breathing gas; whereas the likelihood of bubble formation depends on the difference between the inert gas partial pressure in the divers body and the ambient pressure. Reduction in decompression requirements can also be gained by breathing a nitrox mix during the dive, since less nitrogen will be taken into the body than during the same dive done on air.Following a decompression schedule does not completely protect against DCS. The algorithms used are designed to reduce the probability of DCS to a very low level, but do not reduce it to zero. The mathematical implications of all current decompression models are that provided that no tissue is ingassing, longer decompression stops will decrease decompression risk, or at worst not increase it. Efficient decompression requires the diver to ascend fast enough to establish as high a decompression gradient, in as many tissues, as safely possible, without provoking the development of symptomatic bubbles. This is facilitated by the highest acceptably safe oxygen partial pressure in the breathing gas, and avoiding gas changes that could cause counterdiffusion bubble formation or growth. The development of schedules that are both safe and efficient has been complicated by the large number of variables and uncertainties, including personal variation in response under varying environmental conditions and workload, attributed to variations of body type, fitness and other risk factors. Exposure to altitude One of the most significant breakthroughs in the prevention of altitude DCS is oxygen pre-breathing. Breathing pure oxygen significantly reduces the nitrogen loads in body tissues by reducing the partial pressure of nitrogen in the lungs, which induces diffusion of nitrogen from the blood into the breathing gas, and this effect eventually lowers the concentration of nitrogen in the other tissues of the body. If continued for long enough, and without interruption, this provides effective protection upon exposure to low-barometric pressure environments. However, breathing pure oxygen during flight alone (ascent, en route, descent) does not decrease the risk of altitude DCS as the time required for ascent is generally not sufficient to significantly desaturate the slower tissues.Pure aviator oxygen which has moisture removed to prevent freezing of valves at altitude is readily available and routinely used in general aviation mountain flying and at high altitudes. Most small general aviation aircraft are not pressurized, therefore oxygen use is an FAA requirement at higher altitudes. Although pure oxygen pre-breathing is an effective method to protect against altitude DCS, it is logistically complicated and expensive for the protection of civil aviation flyers, either commercial or private. Therefore, it is currently used only by military flight crews and astronauts for protection during high-altitude and space operations. It is also used by flight test crews involved with certifying aircraft, and may also be used for high-altitude parachute jumps. Astronauts aboard the International Space Station preparing for extra-vehicular activity (EVA) "camp out" at low atmospheric pressure, 10.2 psi (0.70 bar), spending eight sleeping hours in the Quest airlock chamber before their spacewalk. During the EVA they breathe 100% oxygen in their spacesuits, which operate at 4.3 psi (0.30 bar), although research has examined the possibility of using 100% O2 at 9.5 psi (0.66 bar) in the suits to lessen the pressure reduction, and hence the risk of DCS. Treatment Recompression on air was shown to be an effective treatment for minor DCS symptoms by Keays in 1909. Evidence of the effectiveness of recompression therapy utilizing oxygen was first shown by Yarbrough and Behnke, and has since become the standard of care for treatment of DCS. Recompression is normally carried out in a recompression chamber. At a dive site, a riskier alternative is in-water recompression.Oxygen first aid has been used as an emergency treatment for diving injuries for years. Particularly if given within the first four hours of surfacing, it increases the success of recompression therapy as well as decreasing the number of recompression treatments required. Most fully closed-circuit diving rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as a means of supplying oxygen if dedicated equipment is not available.It is beneficial to give fluids, as this helps reduce dehydration. It is no longer recommended to administer aspirin, unless advised to do so by medical personnel, as analgesics may mask symptoms. People should be made comfortable and placed in the supine position (horizontal), or the recovery position if vomiting occurs. In the past, both the Trendelenburg position and the left lateral decubitus position (Durants maneuver) have been suggested as beneficial where air emboli are suspected, but are no longer recommended for extended periods, owing to concerns regarding cerebral edema. First aid All cases of decompression sickness should be treated initially with the highest available concentration of oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a hyperbaric chamber) can be provided. Mild cases of the "bends" and some skin symptoms may disappear during descent from high altitude; however, it is recommended that these cases still be evaluated. Neurological symptoms, pulmonary symptoms, and mottled or marbled skin lesions should be treated with hyperbaric oxygen therapy if seen within 10 to 14 days of development. Early recompression has a history of better outcomes and less treatment being needed.Normobaric oxygen administered at as close to 100% as practicable is known to be beneficial based on observed bubble reduction and symptom resolution. For this reason diver training in oxygen administration, and a system for administering a high percentage of inspired oxygen at quantities sufficient for plausible evacuation scenarios is desirable. Where oxygenation may be compromised the administration rate should be adjusted to ensure that the best practicable supplementation is maintained until supplies can be replenished.A horizontal position is preferable during evacuation if possible, with the recovery position recommended for unconscious divers, as there is evidence that inert gas washout is improved in horizontal subjects, and that large arterial bubbles tend to distribute towards the head in upright positions. A head down position is thought to be harmful in DCS.Oral hydration is recommended in fully conscious persons, and fluids should ideally be isotonic, without alcohol, carbonation or caffeine, as diving is known to cause dehydration, and rehydration is known to reduce post-dive venous gas emboli.Intravascular rehydration is recommended if suitably competent responders are present. Glucose free isotonic crystalloid solutions are preferred. Case evidence shows that aggressive rehydration can be life-saving in severe cases.If there are no contraindications, a non-steroidal anti-inflammatory drug along with hyperbatic oxygen is likely to improve rate of recovery. Corticosteroids, pentoxyphylline, aspirin, lidocaine and nicergoline have been used in early management of DCS, but there is insufficient evidence on their effectiveness.Divers should be kept comfortably warm, but not overheated, as warm subjects are known to eliminate gas more quickly, but overheating aggravates neurological injury. Delay of recompression Observational evidence shows that outcomes after recompression are likely to be better after immediate recompression, which is only possible when on-site recompression is possible, although the 2004 workshop on decompression came to the conclusion that for cases with mild symptoms, a delay before recompression is unlikely to cause any worsening of long-term outcomes.In more serious cases recompression should be done as soon as safely possible. There is some evidence that delays longer than six hours result in slower or less complete recovery, and the number of treatments required may be increased. Transport of a symptomatic diver Exposing a case of decompression sickness to reduced ambient pressure will cause the bubbles to expand if not constrained by a rigid local tissue environment. This can aggravate the symptoms, and should be avoided if reasonably practicable. If a diver with DCS is transported by air, cabin pressure should be kept as close to sea level atmospheric pressure as possible, preferably not more than 150 m, either by cabin pressurisation or by remaining at low altitude throughout the flight. The risk of deterioration at higher altitudes must be considered against the risk of deterioration if not transported. Some divers with symptoms or signs of mild decompression sickness may be evacuated by pressurised commercial airliner for further treatment after a surface interval of at least 24 hours. The 2004 workshop considered it unlikely for this to cause a worse outcome. Most experience has been for short flights of less than two hours. There is little known about the effects of longer flights. Where possible, pre-flight and in-flight oxygen breathing at the highest available percentage is considered best practice. Similar precautions apply to surface transport through higher altitudes. In-water recompression Recompression and hyperbaric oxygen administered in a recompression chamber is recognised as the definitive treatment for DCI, but when there is no readily available access to a suitable hyperbaric chamber, and if symptoms are significant or progressing, in-water recompression (IWR) with oxygen is a medically recognised option where a group of divers including the symptomatic diver already have relevant training and equipment that provides a sufficient understanding of the associated risks and allows the involved parties to collectively accept responsibility for a decision to proceed with IWR.In-water recompression (IWR) or underwater oxygen treatment is the emergency treatment of decompression sickness by returning the diver underwater to help the gas bubbles in the tissues, which are causing the symptoms, to resolve. It is a procedure that exposes the diver to significant risk which should be compared with the risk associated with the other available options. Some authorities recommend that it is only to be used when the time to travel to the nearest recompression chamber is too long to save the victims life, others take a more pragmatic approach, and accept that in some circumstances IWR is the best available option. The risks may not be justified for case of mild symptoms likely to resolve spontaneously, or for cases where the diver is likely to be unsafe in the water, but in-water recompression may be justified in cases where severe outcomes are likely, if conducted by a competent and suitably equipped team.Carrying out in-water recompression when there is a nearby recompression chamber or without suitable equipment and training is never a desirable option. The risk of the procedure is due to the diver suffering from DCS being seriously ill and may become paralysed, unconscious or stop breathing while under water. Any one of these events is likely to result in the diver drowning or asphyxiating or suffering further injury during a subsequent rescue to the surface. This risk can be reduced by improving airway security by using surface supplied gas and a helmet or full-face mask.Several schedules have been published for in-water recompression treatment, but little data on their efficacy is available.The decision of whether or not to attempt IWR is dependent on identifying the diver whose condition is serious enough to justify the risk, but whose clinical condition does not indicate that the risk is unacceptable. The risk may not be justified for mild DCI, if spontaneous recovery is probable whether the diver is recompressed or not, and surface oxygen is indicated for these cases. However, in these cases the risk of the recompression is also low, and early abandonment is also unlikely to cause further harm. Contraindications Some signs of decompression illness which suggest a risk of permanent injury are nevertheless considered contraindications for IWR. Hearing loss and vertigo displayed in isolation with no other symptoms of DCI can have been caused by inner ear barotrauma rather than DCI, and inner ear barotrauma is generally considered a contraindication for recompression. Even when caused by DCI, vertigo can make in-water treatment hazardous if accompanied by nausea and vomiting. A diver with a deteriorating level of consciousness or with a persisting reduced level of consciousness should also not be recompressed in-water nor should a diver who does not want to go back down, or with a history of oxygen toxicity in the preceding dives, or any physical injury or incapacitation which may make the procedure unsafe. Definitive treatment The duration of recompression treatment depends on the severity of symptoms, the dive history, the type of recompression therapy used and the patients response to the treatment. One of the more frequently used treatment schedules is the US Navy Table 6, which provides hyperbaric oxygen therapy with a maximum pressure equivalent to 60 feet (18 m) of seawater (2.8 bar PO2) for a total time under pressure of 288 minutes, of which 240 minutes are on oxygen and the balance are air breaks to minimise the possibility of oxygen toxicity.A multiplace chamber is the preferred facility for treatment of decompression sickness as it allows direct physical access to the patient by medical personnel, but monoplace chambers are more widely available and should be used for treatment if a multiplace chamber is not available or transportation would cause significant delay in treatment, as the interval between onset of symptoms and recompression is important to the quality of recovery. It may be necessary to modify the optimum treatment schedule to allow use of a monoplace chamber, but this is usually better than delaying treatment. A US Navy treatment table 5 can be safely performed without air breaks if a built-in breathing system is not available. In most cases the patient can be adequately treated in a monoplace chamber at the receiving hospital. Altitude decompression sickness Treatment and management may vary depending on the grade or form of decompression sickness and the treating facility or organization. First aid at altitude is oxygen at the highest practicable concentration and earliest and largest practicable reduction in cabin altitude. Ground-level 100% oxygen therapy is suggested for 2 hours following type-1 decompression sickness that occurs at altitude, if it resolves upon descent. In more severe cases, hyperbaric oxygen therapy following standard recompression protocols is indicated. Decompression sickness in aviation most commonly follows flights in non-pressurized aircraft, flights with cabin pressure fluctuations, or in individuals who fly after diving. Cases have also been reported after the use of altitude chambers. These are relatively rare clinical events. Prognosis Immediate treatment with 100% oxygen, followed by recompression in a hyperbaric chamber, will in most cases result in no long-term effects. However, permanent long-term injury from DCS is possible. Three-month follow-ups on diving accidents reported to DAN in 1987 showed 14.3% of the 268 divers surveyed had ongoing symptoms of Type II DCS, and 7% from Type I DCS. Long-term follow-ups showed similar results, with 16% having permanent neurological sequelae.Long term effects are dependent on both initial injury, and treatment. While almost all cases will resolve more quickly with treatment, milder cases may resolve adequately over time without recompression, where the damage is minor and the damage is not significantly aggravated by lack of treatment. In some cases the cost, inconvenience, and risk to the patient may make it appropriate not to evacuate to a hyperbaric treatment facility. These cases should be assessed by a specialist in diving medicine, which can generally be done remotely by telephone or internet.For joint pain, the likely tissues affected depend on the symptoms, and the urgency of hyperbaric treatment will depend largely on the tissues involved. Sharp, localised pain that is affected by movement suggests tendon or muscle injury, both of which will usually fully resolve with oxygen and anti-inflammatory medication. Sharp, localised pain that is not affected by movement suggests local inflammation, which will also usually fully resolve with oxygen and anti-inflammatory medication. Deep, non-localised pain affected by movement suggests joint capsule tension, which is likely to fully resolve with oxygen and anti-inflammatory medication, though recompression will help it to resolve faster. Deep, non-localised pain not affected by movement suggests bone medulla involvement, with ischaemia due to blood vessel blockage and swelling inside the bone, which is mechanistically associated with osteonecrosis, and therefore it has been strongly recommended that these symptoms are treated with hyperbaric oxygen. Epidemiology The incidence of decompression sickness is rare, estimated at 2.8 to 4 cases per 10,000 dives, with the risk 2.6 times greater for males than females. DCS affects approximately 1,000 U.S. scuba divers per year. In 1999, the Divers Alert Network (DAN) created "Project Dive Exploration" to collect data on dive profiles and incidents. From 1998 to 2002, they recorded 50,150 dives, from which 28 recompressions were required — although these will almost certainly contain incidents of arterial gas embolism (AGE) — a rate of about 0.05%.Around 2013, Honduras had the highest number of decompression-related deaths and disabilities in the world, caused by unsafe practices in lobster diving among the indigenous Miskito people, who face great economic pressures. At that time it was estimated that in the country over 2000 divers had been injured and 300 others had died since the 1970s. Timeline 1670: Robert Boyle demonstrated that a reduction in ambient pressure could lead to bubble formation in living tissue. This description of a bubble forming in the eye of a viper subjected to a near vacuum was the first recorded description of decompression sickness. 1769: Giovanni Morgagni described the post mortem findings of air in cerebral circulation and surmised that this was the cause of death. 1840: Charles Pasley, who was involved in the recovery of the sunken warship HMS Royal George, commented that, of those having made frequent dives, "not a man escaped the repeated attacks of rheumatism and cold". 1841: First documented case of decompression sickness, reported by a mining engineer who observed pain and muscle cramps among coal miners working in mine shafts air-pressurized to keep water out. 1854: Decompression sickness reported and one resulting death of caisson workers on the Royal Albert Bridge. 1867: Panamanian pearl divers using the revolutionary Sub Marine Explorer submersible repeatedly experienced "fever" due to rapid ascents. Continued sickness led to the vessels abandonment in 1869. 1870: Bauer published outcomes of 25 paralyzed caisson workers. From 1870 to 1910, all prominent features were established. Explanations at the time included: cold or exhaustion causing reflex spinal cord damage; electricity cause by friction on compression; or organ congestion; and vascular stasis caused by decompression. 1871: The Eads Bridge in St Louis employed 352 compressed air workers including Alphonse Jaminet as the physician in charge. There were 30 seriously injured and 12 fatalities. Jaminet himself developed decompression sickness and his personal description was the first such recorded. According to Divers Alert Network, in its Inert Gas Exchange, Bubbles and Decompression Theory course, this is where "bends" was first used to refer to DCS. 1872: The similarity between decompression sickness and iatrogenic air embolism as well as the relationship between inadequate decompression and decompression sickness was noted by Friedburg. He suggested that intravascular gas was released by rapid decompression and recommended: slow compression and decompression; four-hour working shifts; limit to maximum pressure of 44.1 psig (4 atm); using only healthy workers; and recompression treatment for severe cases. 1873: Andrew Smith first used the term "caisson disease" describing 110 cases of decompression sickness as the physician in charge during construction of the Brooklyn Bridge. The project employed 600 compressed air workers. Recompression treatment was not used. The project chief engineer Washington Roebling had caisson disease, and endured the after-effects of the disease for the rest of his life. During this project, decompression sickness became known as "The Grecian Bends" or simply "the bends" because affected individuals characteristically bent forward at the hips: this is possibly reminiscent of a then popular womens fashion and dance maneuver known as the Grecian Bend. 1890 During construction of the Hudson River Tunnel contractors agent Ernest William Moir pioneered the use of an airlock chamber for treatment. 1900: Leonard Hill used a frog model to prove that decompression causes bubbles and that recompression resolves them. Hill advocated linear or uniform decompression profiles. This type of decompression is used today by saturation divers. His work was financed by Augustus Siebe and the Siebe Gorman Company. 1904: Tunnel building to and from Manhattan Island caused over 3,000 injuries and over 30 deaths which led to laws requiring PSI limits and decompression rules for "sandhogs" in the United States. 1904: Siebe and Gorman in conjunction with Leonard Hill developed and produced a closed bell in which a diver can be decompressed at the surface. 1908: "The Prevention of Compressed Air Illness" was published by JS Haldane, Boycott and Damant recommending staged decompression. These tables were accepted for use by the Royal Navy. 1914–16: Experimental decompression chambers were in use on land and aboard ship. 1924: The US Navy published the first standardized recompression procedure. 1930s: Albert R Behnke separated the symptoms of Arterial Gas Embolism (AGE) from those of DCS. 1935: Behnke et al. experimented with oxygen for recompression therapy. 1937: Behnke introduced the "no-stop" decompression tables. 1941: Altitude DCS is treated with hyperbaric oxygen for the first time. 1944: US Navy published hyperbaric treatment tables "Long Air Recompression Table with Oxygen" and "Short Oxygen Recompression Table", both using 100% oxygen below 60 fsw (18 msw) 1945: Field results showed that the 1944 oxygen treatment table was not yet satisfactory, so a series of tests were conducted by staff from the Navy Medical Research Institute and the Navy Experimental Diving Unit using human subjects to verify and modify the treatment tables. Tests were conducted using the 100-foot air-oxygen treatment table and the 100-foot air treatment table, which were found to be satisfactory. Other tables were extended until they produced satisfactory results. The resulting tables were used as the standard treatment for the next 20 years, and these tables and slight modifications were adopted by other navies and industry. Over time, evidence accumulated that the success of these table for severe decompression sickness was not very good. 1957: Robert Workman established a new method for calculation of decompression requirements (M-values). 1959: The "SOS Decompression Meter", a submersible mechanical device that simulated nitrogen uptake and release, was introduced. 1960: FC Golding et al. split the classification of DCS into Type 1 and 2. 1965: Low success rates of the existing US Navy treatment tables led to the development of the oxygen treatment table by Goodman and Workman in 1965, variations of which are still in general use as the definitive treatment for most cases of decompression sickness. 1965: LeMessurier and Hills published a paper on A thermodynamic approach arising from a study on Torres Strait diving techniques which suggests that decompression by conventional models results in bubble formation which is then eliminated by re-dissolving at the decompression stops. 1976 – M.P. Spencer showed that the sensitivity of decompression testing is increased by the use of ultrasonic methods which can detect mobile venous bubbles before symptoms of DCS emerge. 1982: Paul K Weathersby, Louis D Homer and Edward T Flynn introduce survival analysis into the study of decompression sickness. 1983: Orca produced the "EDGE", a personal dive computer, using a microprocessor to calculate nitrogen absorption for twelve tissue compartments. 1984: Albert A Bühlmann released his book "Decompression–Decompression Sickness", which detailed his deterministic model for calculation of decompression schedules. Bt 1989: The advent of dive computers had not been widely acceped, but after the 1989 AAUS Dive computer workshop published a group consensus list of recommendations for the use of dive computers in scientific diving, most opposition to dive computers dissipated, numerous new models were introduced, the technology dramatically improved and dive computers became standard scuba diving equipment. Over time, some of the recommendations became irrelevant as the technology improved. c2000: HydroSpace Engineering developed the HS Explorer, a Trimix computer with optional PO2 monitoring and twin decompression algorithms, Buhlmann, and the first full real time RGBM implementation. 2001: The US Navy approved the use of Cochran NAVY decompression computer with the VVAL 18 Thalmann algorithm for Special Warfare operations. By 2010: The use of dive computers for decompression status tracking was virtually ubiquitous among recreational divers and widespread in scientific diving. 2018: A group of diving medical experts issued a consensus guideline on pre-hospital decompression sickness management and concluded that in-water recompression is a valid and effective emergency treatment where a chamber is not available, but is only appropriate in groups that have been trained and are competent in the skills required for IWR and have appropriate equipment. Society and culture Economics In the United States, it is common for medical insurance not to cover treatment for the bends that is the result of recreational diving. This is because scuba diving is considered an elective and "high-risk" activity and treatment for decompression sickness is expensive. A typical stay in a recompression chamber will easily cost several thousand dollars, even before emergency transportation is included. As a result, groups such as Divers Alert Network (DAN) offer medical insurance policies that specifically cover all aspects of treatment for decompression sickness at rates of less than $100 per year.In the United Kingdom, treatment of DCS is provided by the National Health Service. This may occur either at a specialised facility or at a hyperbaric centre based within a general hospital. Other animals Animals may also contract DCS, especially those caught in nets and rapidly brought to the surface. It has been documented in loggerhead turtles and likely in prehistoric marine animals as well. Modern reptiles are susceptible to DCS, and there is some evidence that marine mammals such as cetaceans and seals may also be affected. AW Carlsen has suggested that the presence of a right-left shunt in the reptilian heart may account for the predisposition in the same way as a patent foramen ovale does in humans. Footnotes See also Decompression (diving) – Adjusting to pressure changes in ascents Decompression illness – Disorders arising from ambient pressure reduction Decompression theory – Theoretical modelling of decompression physiology Diving disorders – Physiological disorders resulting from underwater diving Inner ear decompression sickness – Medical condition caused by inert gas bubbles forming out of solution Taravana – Decompression sickness after breath-hold diving Notes 1. ^a autochthonous: formed or originating in the place where found. References Bibliography External links Divers Alert Network: diving medicine articles Archived 8 December 2005 at the Wayback Machine Dive Tables from the NOAA CDC – Decompression Sickness and Tunnel Workers – NIOSH Workplace Safety and Health Topic Pathophysiology of decompression and acute dysbaric disorders "Decompression Sickness" on Medscape

Aarogya, What does Auditory hallucination mean

Auditory hallucination

An auditory hallucination, or paracusia, is a form of hallucination that involves perceiving sounds without auditory stimulus. While experiencing an auditory hallucination, the affected person would hear a sound or sounds which did not come from the natural environment. A common form of auditory hallucination involves hearing one or more voices without a speaker present, known as an auditory verbal hallucination. This may be associated with psychotic disorders, most notably schizophrenia, and this phenomenon is often used to diagnose these conditions. However, individuals without any psychiatric disease whatsoever may hear voices, including those under the influence of mind-altering substances, such as cannabis, cocaine, amphetamines, and PCP. There are three main categories into which the hearing of talking voices often fall: a person hearing a voice speak ones thoughts, a person hearing one or more voices arguing, or a person hearing a voice narrating their own actions. These three categories do not account for all types of auditory hallucinations. Hallucinations of music also occur. In these, people more often hear snippets of songs that they know, or the music they hear may be original. They may occur in mentally sound people and with no known cause. Other types of auditory hallucinations include exploding head syndrome and musical ear syndrome. In the latter, people will hear music playing in their mind, usually songs they are familiar with. These hallucinations can be caused by: lesions on the brain stem (often resulting from a stroke), sleep disorders such as narcolepsy, tumors, encephalitis, or abscesses. This should be distinguished from the commonly experienced phenomenon of getting a song stuck in ones head. Reports have also mentioned that it is also possible to get musical hallucinations from listening to music for long periods of time. Other causes include hearing loss and epileptic activity.In the past, the cause of auditory hallucinations was attributed to cognitive suppression by way of executive function failure of the frontoparietal sulcus. Newer research has found that they coincide with the left superior temporal gyrus, suggesting that they are better attributed to speech misrepresentations. It is assumed through research that the neural pathways involved in normal speech perception and production, which are lateralized to the left temporal lobe, also underlie auditory hallucinations. Auditory hallucinations correspond with spontaneous neural activity of the left temporal lobe, and the subsequent primary auditory cortex. The perception of auditory hallucinations corresponds to the experience of actual external hearing, despite the absence of any sound itself. Causes In 2015 a small survey reported voice hearing in persons with a wide variety of DSM-5 diagnoses, including: Bipolar disorder Borderline personality disorder Depression (mixed) Dissociative identity disorder Generalized anxiety disorder Major depression Obsessive compulsive disorder Post-traumatic stress disorder Psychosis (NOS) Schizoaffective disorder Schizophrenia Substance-induced psychosisHowever, numerous persons surveyed reported no diagnosis. In his popular 2012 book Hallucinations, neurologist Oliver Sacks describes voice hearing in patients with a wide variety of medical conditions, as well as his own personal experience of hearing voices. Genetic correlations have been identified with auditory hallucinations, but most work with non-psychotic causes of auditory hallucinations is still ongoing. Schizophrenia In people with psychosis, the premier cause of auditory hallucinations is schizophrenia, and these are known as auditory verbal hallucinations (AVHs). In schizophrenia, people show a consistent increase in activity of the thalamic and striatal subcortical nuclei, hypothalamus, and paralimbic regions; confirmed by PET and fMRI scans. Other research shows an enlargement of temporal white matter, frontal gray matter, and temporal gray matter volumes (those areas crucial to both inner and outer speech) when compared to control groups. This implies that functional and structural abnormalities in the brain, both of which may have a genetic component, can induce auditory hallucinations.Auditory verbal hallucinations attributed to an external source, rather than internal, are considered the defining factor for the diagnosis of schizophrenia. The voices heard are generally destructive and emotive, adding to the state of artificial reality and disorientation seen in psychotic patients. The causal basis of hallucinations has been explored on the cellular receptor level. The glutamate hypothesis, proposed as a possible cause for schizophrenia, may also have implications in auditory hallucinations, which are suspected to be triggered by altered glutamatergic transmission.Studies using dichotic listening methods suggest that people with schizophrenia have major deficits in the functioning of the left temporal lobe by showing that patients do not generally exhibit what is a functionally normal right ear advantage. Inhibitory control of hallucinations in patients has been shown to involve failure of top-down regulation of resting-state networks and up-regulation of effort networks, further impeding normal cognitive functioning.Not all who experience hallucinations find them to be distressing. The relationship between an individual and their hallucinations is personal, and everyone interacts with their troubles in different ways. There are those who hear solely malevolent voices, solely benevolent voices, those that hear a mix of the two, and those that see them as either malevolent or benevolent and not believing the voice. Mood disorders and dementias Mood disorders such as bipolar disorder and major depression have also been known to correlate with auditory hallucinations, but tend to be milder than their psychosis-induced counterpart. Auditory hallucinations are a relatively common sequelae of major neurocognitive disorders (formerly dementia) such as Alzheimers disease. Transient causes Auditory hallucinations have been known to manifest as a result of intense stress, sleep deprivation, and drug use. Auditory hallucinations can also occur in mentally healthy individuals during the altered state of consciousness while falling asleep (hypnagogic hallucinations) and waking up (hypnopompic hallucinations).High caffeine consumption has been linked to an increase in the likelihood of experiencing auditory hallucinations. A study conducted by the La Trobe University School of Psychological Sciences revealed that as few as five cups of coffee a day could trigger the phenomenon. Intoxication of psychoactive drugs such as PCP, amphetamines, cocaine, marijuana and other substances can produce hallucinations in general, especially in high doses. Withdrawal from certain drugs such as alcohol, sedatives, hypnotics, anxiolytics, and opioids can also produce hallucinations, including auditory. Pathophysiology The following areas of the brain have been found to be active during auditory hallucinations, through the use of fMRIs. Transverse temporal gyri (Heschls gyri): found within the primary auditory cortex. Left temporal lobe: processes semantics in speech and vision, including primary auditory cortex. Brocas area: speech and language comprehension. Superior temporal gyrus: contains primary auditory cortex. Primary auditory cortex: processes hearing and speech perception. Globus pallidus: Regulation of voluntary movement. Treatments Medication The primary means of treating auditory hallucinations is antipsychotic medications which affect dopamine metabolism. If the primary diagnosis is a mood disorder (with psychotic features), adjunctive medications are often used (e.g., antidepressants or mood stabilizers). These medical approaches may allow the person to function normally but are not a cure as they do not eradicate the underlying thought disorder. Therapy Cognitive behavioral therapy has been shown to help decrease the frequency and distressfulness of auditory hallucinations, particularly when other psychotic symptoms were presenting. Enhanced supportive therapy has been shown to reduce the frequency of auditory hallucinations, the violent resistance the patient displayed towards said hallucinations, and an overall decrease in the perceived malignancy of the hallucinations. Other cognitive and behavioural therapies have been used with mixed success.Another key to therapy is to help patients see that they do not need to obey the voices that they are hearing. It has been seen in patients with schizophrenia and auditory hallucinations that therapy might help confer insight into recognising and choosing to not obey the voices that they hear. Others Between 25% and 30% of schizophrenia patients do not respond to antipsychotic medication which has led researchers to look for alternate sources to help them. Two common methods to help are electroconvulsive therapy and repetitive transcranial magnetic stimulation (rTMS). Electroconvulsive therapy or ECT has been shown to reduce psychotic symptoms associated with schizophrenia, mania, and depression, and is often used in psychiatric hospitals. Transcranial magnetic stimulation when used to treat auditory hallucinations in patients with schizophrenia is done at a low frequency of 1 Hertz to the left temporoparietal cortex. History Ancient history Presentation In the ancient world, auditory hallucinations were often viewed as either a gift or curse by God or the gods (depending on the specific culture). According to the Greek historian Plutarch, during the reign of Tiberius (A.D. 14–37), a sailor named Thamus heard a voice cry out to him from across the water, "Thamus, are you there? When you reach Palodes, take care to proclaim that the great god Pan is dead."The oracles of ancient Greece were known to experience auditory hallucinations while breathing in certain neurologically active vapors (such as the smoke from bay leaves), while the more pervasive delusions and symptomatology were often viewed as possession by demonic forces as punishment for misdeeds. Treatments Treatment in the ancient world is ill-documented, but there are some cases of therapeutics being used to attempt treatment, while the common treatment was sacrifice and prayer in an attempt to placate the gods. During the Middle Ages, those with auditory hallucinations were sometimes subjected to trepanning or trial as a witch. In other cases of extreme symptomatology, individuals were seen as being reduced to animals by a curse; these individuals were either left on the streets or imprisoned in insane asylums. It was the latter response that eventually led to modern psychiatric hospitals. Pre-modern Presentation Auditory hallucinations were rethought during the enlightenment. As a result, the predominant theory in the western world beginning in the late 18th century was that auditory hallucinations were the result of a disease in the brain (e.g., mania), and treated as such. Treatments There were no effective treatments for hallucinations at this time. Conventional thought was that clean food, water, and air would allow the body to heal itself (sanatorium). Beginning in the 16th century insane asylums were first introduced in order to remove "the mad dogs" from the streets. These asylums acted as prisons until the late 18th century. This is when doctors began the attempt to treat patients. Often attending doctors would douse patients in cold water, starve them, or spin patients on a wheel. Soon, this gave way to brain-specific treatments with the most famous examples including lobotomy, shock therapy, and branding the skull with a hot iron. Society and culture Notable cases Robert Schumann, a famous music composer, spent the end of his life experiencing auditory hallucinations. Schumanns diaries state that he suffered perpetually from imagining that he had the note A5 sounding in his ears. The musical hallucinations became increasingly complex. One night he claimed to have been visited by the ghost of Schubert and wrote down the music that he was hearing. Thereafter, he began making claims that he could hear an angelic choir singing to him. As his condition worsened, the angelic voices developed into demonic ones.Brian Wilson, songwriter and co-founder of the Beach Boys, has schizoaffective disorder that presents itself in the form of disembodied voices. They formed a major component of Bill Pohlads Love & Mercy (2014), a biographical film which depicts Wilsons hallucinations as a source of musical inspiration, constructing songs that were partly designed to converse with them. Wilson has said of the voices: "Mostly [theyre] derogatory. Some of its cheerful. Most of it isnt." To combat them, his psychiatrist advised that he "talk humorously to them", which he says has helped "a little bit".The onset of delusional thinking is most often described as being gradual and insidious. Patients have described an interest in psychic phenomena progressing to increasingly unusual preoccupations and then to bizarre beliefs "in which I believed wholeheartedly". One author wrote of their hallucinations: "they deceive, derange and force me into a world of crippling paranoia". In many cases, the delusional beliefs could be seen as fairly rational explanations for abnormal experiences: "I increasingly heard voices (which Id always call loud thoughts)... I concluded that other people were putting these loud thoughts into my head". Some cases have been described as an "auditory ransom note". Cultural effects According to research on hallucinations, both with participants from the general population and people diagnosed with schizophrenia, psychosis and related mental illnesses, there is a relationship between culture and hallucinations. In relation to hallucinations, the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) states that "transient hallucinatory experiences may occur without a mental disorder"; put differently, short or temporary hallucinations are not exclusive to being diagnosed with a mental disorder.In a study of 1,080 people with a schizophrenia diagnosis from seven countries of origin: Austria, Poland, Lithuania, Georgia, Pakistan, Nigeria and Ghana, researchers found that 74.8% of the total participants (n = 1,080) disclosed having experienced more auditory hallucinations in the last year than any other hallucinations from the date of the interview. Further, the study found the highest rates of both auditory hallucinations and visual hallucinations in both of the West African countries, Ghana and Nigeria. In the Ghana sample, n = 76, auditory hallucinations were reported by 90.8% and visual hallucinations were reported by 53.9% of participants. In the Nigeria sample, n = 324, auditory hallucinations were reported by 85.4%, and visual hallucinations were reported by 50.8% of participants. These findings are in line with other studies that have found that visual hallucinations were reported more in traditional cultures. A 2015 published study, "Hearing Voices in Different Cultures: A Social Kindling Hypothesis" compared the experiences of three groups of 20 participants who met the criteria for schizophrenia (n = 60) from three places, including San Mateo, California (USA), Accra, Ghana (Africa), and Chennai, India (South Asia). In this study, researchers found distinct differences among the participants experience with voices. In the San Mateo, CA sample all but three of the participants referred to their experience of hearing voices with "diagnostic labels, and even [used] diagnostic criteria readily", they also connected "hearing voices" with being "crazy". For the Accra, Ghana sample, almost no participants referenced a diagnosis and instead they spoke about voices as having "a spiritual meaning and as well as a psychiatric one". In the Chennai, India sample, similarly to the Ghana interviewees, most of the participants did not reference a diagnosis and for many of these participants, the voices they heard were of people they knew and people they were related to, "voices of kin". Another key finding that was identified in this research study is that "voice-hearing experience outside the West may be less harsh". Finally, researchers found that "different cultural expectations about the mind, or about the way people expect thoughts and feelings to be private or accessible to spirits or persons" could be attributed to the differences they found across the participants. In a qualitative study of 57 self-identified Māori participants subcategorized within one or more of the following groups including: "tangata Māori (people seeking wellness/service users), Kaumatua/Kuia (elders), Kai mahi (cultural support workers), Managers of mental health services, clinicians (psychiatrists, nurses, and psychologists) and students (undergraduate and postgraduate psychology students)", researchers interviewed participants and asked them about "[1] their understanding of experiences that could be considered to be psychotic or labelled schizophrenic, [2] what questions they would ask someone who came seeking help and [3] they we asked about their understanding of the terms schizophrenia and psychosis". The participants were also people who either had worked with psychosis or schizophrenia or had experienced psychosis or schizophrenia. In this study, researchers found that the participants understood these experiences labelled "psychotic" or "schizophrenic" through multiple models. Taken directly from the article, the researchers wrote that there is "no one Māori way of understanding psychotic experiences". Instead, as part of understanding these experiences, the participants combined both "biological explanations and Māori spiritual beliefs", with a preference for cultural and psychosocial explanations. For example, 19 participants spoke about psychotic experiences as sometimes being a sign of matakite (giftedness). One of the Kaumatua/Kuia (elders) was quoted as saying:"I never wanted to accept it, I said no it isnt, it isnt [matakite] but it wouldnt stop and in truth I knew what I had to do, help my people, I didnt want the responsibility but here I am. They helped me understand it and told me what to do with it."An important finding highlighted in this study is that studies done by the World Health Organization (WHO) have found that "developing countries (non-Western) experience far higher rates of recovery from schizophrenia than Western countries". The researchers further articulate that these findings may be due to culturally specific meaning created about the experience of schizophrenia, psychosis, and hearing voices as well as "positive expectations around recovery". Research has found that auditory hallucinations and hallucinations more broadly are not necessarily a symptom of "severe mental health" and instead might be more commonplace than assumed and also experienced by people in the general population. According to a literature review, "The prevalence of voice-hearers in the general population: A literature review", which compared 17 studies on auditory hallucinations in participants from nine countries, found that "differences in the prevalence of [voice-hearing in the adult general population] can be attributed to true variations based on gender, ethnicity and environmental context". The studies took place from 1894 to 2007 and the nine countries in which the studies took place were the United Kingdom, Philippines, United States, Sweden, France, Germany, Italy, Netherlands, and New Zealand. The same literature review highlighted that "studies that [analyzed] their data by gender report[ed] a higher frequency of women reporting hallucinatory experiences of some kind". Although generally speaking hallucinations (including auditory) are strongly related to psychotic diagnoses and schizophrenia, the presence of hallucinations does not exclusively mean that someone has a psychotic or schizophrenic episode or diagnosis. Audible thoughts General information Audible thoughts, also called thought sonorisation, is a kind of auditory verbal hallucination. People with this hallucination constantly hear a voice narrating ones own thoughts out loud. This idea was first defined by Kurt Schneider, who included this symptom as one of the "first-rank symptoms" in diagnosing schizophrenia. Although the diagnostic reliability of "first-rank symptoms" has long been questioned, this idea remains important for its historical and descriptive value in psychiatry. Audible thoughts is a positive symptom of schizophrenia according to DSM-5, however, this hallucination is not exclusively found among people with schizophrenia, but also among patients of bipolar disorder in their manic phase. Types Patients who experience audible thoughts will hear the voice repeating their own thoughts either as or after the thought comes into their minds. The first kind of audible thought, the voice and the thought appear simultaneously, was named by German psychiatry August Cramer as Gedankenlautwerden, a German word stands for "thoughts become aloud".Example of Gedankenlautwerden: A 35-year-old painter heard a quiet voice with an Oxford accent. The volume was slightly lower than that of normal conversation and could be heard equally well with either ear. The voice would say, I cant stand that man, the way he holds his brush he looks like a poof. He immediately experienced whatever the voice was saying as his own thoughts, to the exclusion of all other thoughts.And the second kind in which the voice comes after the thought appears is called echo de la pensée in French, namely thought echo.Example of thought echo: A 32-year-old housewife complained of a mans voice. The voice would repeat almost all the patients goal-directed thinking, even banalest thoughts. The patient would think I must put the kettle on, and after a pause of not more than one second the voice would say I must put the kettle on.If categorized by patients subjective feelings about where the voices come from, audible thoughts can be either external or internal. Patients reporting an internal origin of the hallucination claim that the voices are coming from somewhere inside their body, mainly in their own heads, while those reporting an external origin feel the voice as coming from the environment. The external origins vary in the patients description: some hear the voice in front of their ears, some attribute the ambient surrounding noise, like running water or wind, as the source. This sometimes influences patients behaviours as they believe people around them can also hear these audible thoughts, therefore they may avoid social events and public places to prevent others from hearing their thoughts. Besides, study suggests that the locus of the voice may change as the patients hallucinations develop. Theres a trend of internalization of external perceptions, which means patients will locate the source of their hallucination from external objects to internal subjectivity over time. Phenomenological study According to the study conducted by Tony Nayani and Anthony David in 1996, about half of the patients(46%) with audible thoughts claimed that the hallucination has somehow taken the place of their conscience in making decisions and judgement. They tend to follow the voices instructions when confronting dilemmas in their daily lives. The study also suggests that a majority of the patients, both male and female, labeled the sounds they heard as male voices. However, younger patients tend to hear younger voices, which suggests that the voices in the hallucination may share age with the patients but not gender. Whats more, voices in the hallucination usually differ from the patients own voices in accents. They reported the voices they heard as coming from different regions or social classes with them.Some patients may develop skills to control their hallucinations to a certain extent through some kind of cognitive focusing. They cant eliminate the voices, but through cognitive focusing or suggestive behaviours (e.g. swallowing), they can control the onset and offset of their hallucination. Pathophysiology Studies have suggested that damage to specific brain areas may relate to the formation of audible thought. Patients who attribute the hallucination to an external locus are more likely to report the voice coming from the right. This unilateral characteristic can be explained by either contralateral temporal lobe disease or ipsilateral ear disease. Researchers also came up with hypotheses that audible thought may result from damage in the right hemisphere, which causes the malfunction of prosodic construction. If this happens, the left hemisphere may misinterpret the patients own thoughts as alien, leading the patients to misconceive their thoughts as coming from another voice. Research A good amount of the research done has focused primarily on patients with schizophrenia, and beyond that drug-resistant auditory hallucinations. Auditory verbal hallucinations as symptoms of disordered speech There is now substantial evidence that auditory verbal hallucinations (AVHs) in psychotic patients are manifestations of disorganized speech capacity at least as much as, and even more than, being genuinely auditory phenomena. Such evidence comes mainly from research carried out on the neuroimaging of AVHs, on the so-called "inner" and "subvocal" speech, on "voices" experienced by deaf patients, and on the phenomenology of AVHs. Interestingly, this evidence is in line with clinical insights of the classical psychiatric school (de Clérambault) as well as of (Lacanian) psychoanalysis. According to the latter, the experience of the voice is linked more to speech as a chain of articulated signifying elements than to sensorium itself. Non-psychotic symptomatology There is on-going research that supports the prevalence of auditory hallucinations, with a lack of other conventional psychotic symptoms (such as delusions, or paranoia), particularly in pre-pubertal children. These studies indicate a remarkably high percentage of children (up to 14% of the population sampled) experienced sounds or voices without any external cause, although "sounds" are not considered by psychiatrists to be examples of auditory hallucinations. Differentiating actual auditory hallucinations from "sounds" or a normal internal dialogue is important since the latter phenomena are not indicative of mental illness. Methods To explore the auditory hallucinations in schizophrenia, experimental neurocognitive use approaches such as dichotic listening, structural fMRI, and functional fMRI. Together, they allow insight into how the brain reacts to auditory stimuli, be they external or internal. Such methods allowed researchers to find a correlation between a decreased gray matter of the left temporal lobe and difficulties in processing external sound stimuli in hallucinating patients.Functional neuroimaging has shown increased blood and oxygen flow to speech-related areas of the left temporal lobe, including Brocas area and the thalamus. Causes The causes of auditory hallucinations are unclear. It is suspected that deficits in the left temporal lobe attribute that lead to spontaneous neural activity cause speech misrepresentations that account for auditory hallucinations.Charles Fernyhough, of the University of Durham, poses one theory among many but stands as a reasonable example of the literature. Given standing evidence towards the involvement of the inner voice in auditory hallucinations, he proposes two alternative hypotheses on the origins of auditory hallucinations in the non-psychotic. They both rely on an understanding of the internalization process of the inner voice. Internalization of the inner voice The internalization process of the inner voice is the process of creating an inner voice during early childhood and can be separated into four distinct levels.Level one (external dialogue) involves the capacity to maintain an external dialogue with another person, i.e. a toddler talking with their parent(s). Level two (private speech) involves the capacity to maintain a private external dialogue, as seen in children voicing the actions of play using dolls or other toys, or someone talking to themselves while repeating something they had written down. Level three (expanded inner speech) is the first internal level in speech. This involves the capacity to carry out internal monologues, as seen in reading to oneself or going over a list silently. Level four (condensed inner speech) is the final level in the internalization process. It involves the capacity to think in terms of pure meaning without the need to put thoughts into words in order to grasp the meaning of the thought. Disruption to internalization A disruption could occur during the normal process of internalizing ones inner voice, where the individual would not interpret their own voice as belonging to them; a problem that would be interpreted as a level one to level four error. Re-expansion Alternatively, the disruption could occur during the process of re-externalizing ones inner voice, resulting in an apparent second voice that seems alien to the individual; a problem that would be interpreted as a level four to level one error. Treatments Psychopharmacological treatments include antipsychotic medications. Meta-analyses show that cognitive behavioral therapy and metacognitive training also reduce the severity of hallucinations. Psychology research shows that the first step in treatment is for the patient to realize that the voices they hear are a creation of their own mind. This realization allows patients to reclaim a measure of control over their lives. See also Auditory imagery Earworm Hearing Voices Network Hypnagogic hallucinations Intrusive thought Microwave auditory effect Speech synthesis Tinnitus References Further reading Johnson FH (1978). The anatomy of hallucinations. Chicago: Nelson-Hall Co. ISBN 978-0-88229-155-0. Bentall RP, Slade PD (1988). Sensory deception: a scientific analysis of hallucination. London: Croom Helm. ISBN 978-0-7099-3961-0. Larøi F, Aleman A (2008). Hallucinations: The Science of Idiosyncratic Perception. American Psychological Association (APA). ISBN 978-1-4338-0311-6. Archived from the original on 2008-12-21. Retrieved 2009-10-27. External links "Anthropology and Hallucinations", chapter from The Making of Religion "The voice inside: A practical guide to coping with hearing voices" A salience dysregulation syndrome, from Jim van Os. The British Journal of Psychiatry, 2009.

Hey Aarogya, explain a situation where Egg allergy occurs

Egg allergy

Egg allergy is an immune hypersensitivity to proteins found in chicken eggs, and possibly goose, duck, or turkey eggs. Symptoms can be either rapid or gradual in onset. The latter can take hours to days to appear. The former may include anaphylaxis, a potentially life-threatening condition which requires treatment with epinephrine. Other presentations may include atopic dermatitis or inflammation of the esophagus.In the United States, 90% of allergic responses to foods are caused by cows milk, eggs, wheat, shellfish, peanuts, tree nuts, fish, and soy beans. The declaration of the presence of trace amounts of allergens in foods is not mandatory in any country, with the exception of Brazil.Prevention is by avoiding eating eggs and foods that may contain eggs, such as cake or cookies. It is unclear if the early introduction of the eggs to the diet of babies aged 4–6 months decreases the risk of egg allergies.Egg allergy appears mainly in children but can persist into adulthood. In the United States, it is the second most common food allergy in children after cows milk. Most children outgrow egg allergy by the age of five, but some people remain allergic for a lifetime. In North America and Western Europe, egg allergy occurs in 0.5% to 2.5% of children under the age of five years. The majority grow out of it by school age, but for roughly one-third, the allergy persists into adulthood. Strong predictors for adult-persistence are anaphylaxis, high egg-specific serum immunoglobulin E (IgE), robust response to the skin prick test and absence of tolerance to egg-containing baked foods. Signs and symptoms Food allergies usually have an onset from minutes to one to two hours. Symptoms may include: rash, hives, itching of mouth, lips, tongue, throat, eyes, skin, or other areas, swelling of lips, tongue, eyelids, or the whole face, difficulty swallowing, runny or congested nose, hoarse voice, wheezing, shortness of breath, diarrhea, abdominal pain, lightheadedness, fainting, nausea, or vomiting. Symptoms of allergies vary from person to person and may vary from incident to incident. Serious danger regarding allergies can begin when the respiratory tract or blood circulation is affected. The former can be indicated by wheezing, a blocked airway and cyanosis, the latter by weak pulse, pale skin, and fainting. When these symptoms occur the allergic reaction is called anaphylaxis. Anaphylaxis occurs when IgE antibodies are involved, and areas of the body that are not in direct contact with the food become affected and show severe symptoms. Untreated, this can proceed to vasodilation and a low blood pressure situation called anaphylactic shock.Young children may exhibit dermatitis/eczema on face, scalp and other parts of the body, in older children knees and elbows are more commonly affected. Children with dermatitis are at greater than expected risk of also exhibiting asthma and allergic rhinitis. Causes Eating egg The cause is typically the eating of eggs or foods that contain eggs. Briefly, the immune system over-reacts to proteins found in eggs. This allergic reaction may be triggered by small amounts of egg, even egg incorporated into cooked foods, such as cake. People with an allergy to chicken eggs may also be reactive to goose, duck, or turkey eggs. Vaccines Influenza vaccines are created by injecting a live virus into fertilized chicken eggs. The viruses are harvested, killed and purified, but a residual amount of egg white protein remains. For adults ages 18 and older there is an option to receive recombinant flu vaccines (RIV3 or RIV4) which are grown on mammalian cell cultures instead of in eggs, and so are no risk for people with severe egg allergy. Recommendations are that for people with a history of mild egg allergy should receive any IIV or RIV vaccine. People with a more severe allergic reaction may also receive any IIV or RIV, but in an inpatient or outpatient medical setting, administered by a healthcare provider. People with a known severe allergic reaction to influenza vaccine (which could be egg protein or the gelatin or the neomycin components of the vaccine) should not receive a flu vaccine.Each year the American Academy of Pediatrics (AAP) publishes recommendations for prevention and control of influenza in children. In the 2016-2017 guidelines a change was made, that children with a history of egg allergy may receive the IIV3 or IIV4 vaccine without special precautions. It did, however, state that "Standard vaccination practice should include the ability to respond to acute hypersensitivity reactions." Prior to this, AAP recommended precautions based on egg allergy history: if no history, immunize; if a history of mild reaction, i.e., hives, immunize in a medical setting with healthcare professionals and resuscitative equipment available; if a history of severe reactions, refer to an allergist.The measles and mumps parts of the "MMR vaccine" (for measles, mumps, and rubella) are cultured on chick embryo cell culture and contain trace amounts of egg protein. The amount of egg protein is lower than in influenza vaccines and the risk of an allergic reaction is much lower. One guideline stated that all infants and children should get the two MMR vaccinations, mentioning that "Studies on large numbers of egg-allergic children show there is no increased risk of severe allergic reactions to the vaccines." Another guideline recommended that if a child has a known medical history of severe anaphylaxis reaction to eggs, then the vaccination should be done in a hospital center, and the child be kept for observation for 60 minutes before being allowed to leave. The second guideline also stated that if there was a severe reaction to the first vaccination - which could have been to egg protein or the gelatin and neomycin components of the vaccine - the second is contraindicated. Exercise as a contributing factor There is a condition called food-dependent, exercise-induced anaphylaxis (FDEIAn). Exercise can trigger hives and more severe symptoms of an allergic reaction. For some people with this condition, exercise alone is not sufficient, nor consumption of a food to which they are mildly allergic sufficient, but when the food in question is consumed within a few hours before high intensity exercise, the result can be anaphylaxis. Egg are specifically mentioned as a causative food. One theory is that exercise is stimulating the release of mediators such as histamine from IgE-activated mast cells. Two of the reviews postulate that exercise is not essential for the development of symptoms, but rather that it is one of several augmentation factors, citing evidence that the culprit food in combination with alcohol or aspirin will result in a respiratory anaphylactic reaction. Mechanisms Conditions caused by food allergies are classified into three groups according to the mechanism of the allergic response: IgE-mediated (classic) – the most common type, manifesting acute changes that occur shortly after eating, and may progress to anaphylaxis Non-IgE mediated – characterized by an immune response not involving immunoglobulin E; may occur hours to days after eating, complicating diagnosis IgE and non-IgE-mediated – a hybrid of the above two typesAllergic reactions are hyperactive responses of the immune system to generally innocuous substances, such as proteins in the foods we eat. Why some proteins trigger allergic reactions while others do not is not entirely clear, although in part thought to be due to resistance to digestion. Because of this, intact or largely intact proteins reach the small intestine, which has a large presence of white blood cells involved in immune reactions. The heat of cooking structurally degrades protein molecules, potentially making them less allergenic.The pathophysiology of allergic responses can be divided into two phases. The first is an acute response that occurs within minutes to an hour or two exposure to an allergen. This phase can either subside or progress into a "late-phase reaction" which can substantially prolong the symptoms of a response, and result in more tissue damage. In the early stages of acute allergic reaction, lymphocytes previously sensitized to a specific protein or protein fraction react by quickly producing a particular type of antibody known as secreted IgE (sIgE), which circulates in the blood and binds to IgE-specific receptors on the surface of other kinds of immune cells called mast cells and basophils. Both of these are involved in the acute inflammatory response. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators called (cytokines, interleukins, leukotrienes, and prostaglandins) into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth-muscle contraction. This results in runny nose, itchiness, shortness of breath, and potentially anaphylaxis. Depending on the individual, the allergen, and the mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system while eczema is localized to the skin.After the chemical mediators of the acute response subside, late-phase responses can often occur due to the migration of other white blood cells such as neutrophils, lymphocytes, eosinophils, and macrophages to the initial reaction sites. This is usually seen 2–24 hours after the original reaction. Cytokines from mast cells may also play a role in the persistence of long-term effects. Late-phase responses seen in asthma are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils.Five major allergenic proteins from the egg of the domestic chicken (Gallus domesticus) have been identified; these are designated Gal d 1–5. Four of these are in egg white: ovomucoid (Gal d 1), ovalbumin (Gal d 2), ovotransferrin (Gal d 3) and lysozyme (Gal d 4). Of these, ovomucoid is the dominant allergen, and one that is less likely to be outgrown as children get older. Ingestion of under-cooked egg may trigger more severe clinical reactions than well-cooked egg. In egg yolk, alpha-livetin (Gal d 5) is the major allergen, but various vitellins may also trigger a reaction. People allergic to alpha-livetin may experience respiratory symptoms such as rhinitis and/or asthma when exposed to chickens, because the yolk protein is also found in live birds. In addition to IgE-mediated responses, egg allergy can manifest as atopic dermatitis, especially in infants and young children. Some will display both, so that a child could react to an oral food challenge with allergic symptoms, followed a day or two later with a flare up of atopic dermatitis and/or gastrointestinal symptoms, including allergic eosinophilic esophagitis. Non-allergic intolerance Egg whites, which are potentially histamine liberators, also provoke a nonallergic response in some people. In this situation, proteins in egg white directly trigger the release of histamine from mast cells. Because this mechanism is classified as a pharmacological reaction, or "pseudoallergy", the condition is considered a food intolerance instead of a true immunoglobulin E (IgE) based allergic reaction. The response is usually localized, typically in the gastrointestinal tract. Symptoms may include abdominal pain, diarrhea, or any other symptoms typical to histamine release. If sufficiently strong, it can result in an anaphylactoid reaction, which is clinically indistinguishable from true anaphylaxis. Some people with this condition tolerate small quantities of egg whites. They are more often able to tolerate well-cooked eggs, such as found in cake or dried egg-based pasta, than incompletely cooked eggs, such as fried eggs or meringues, or uncooked eggs. Diagnosis Diagnosis of egg allergy is based on the persons history of allergic reactions, skin prick test (SPT), patch test and measurement of egg-specific serum immunoglobulin E (IgE or sIgE). Confirmation is by double-blind, placebo-controlled food challenges. SPT and sIgE have sensitivity greater than 90% but specificity in the 50-60% range, meaning these tests will detect an egg sensitivity, but will also be positive for other allergens. For young children, attempts have been made to identify SPT and sIgE responses strong enough to avoid the need for a confirming oral food challenge. Prevention When eggs are introduced to a babys diet is thought to affect risk of developing allergy, but there are contradictory recommendations. A 2016 review acknowledged that introducing peanuts early appears to have a benefit, but stated "The effect of early introduction of egg on egg allergy are controversial." A meta-analysis published the same year supported the theory that early introduction of eggs into an infants diet lowers risk, and a review of allergens in general stated that introducing solid foods at 4–6 months may result in the lowest subsequent allergy risk. However, an older consensus document from the American College of Allergy, Asthma and Immunology recommended that introduction of chicken eggs be delayed to 24 months of age. Treatment The mainstay of treatment is total avoidance of egg protein intake. This is complicated because the declaration of the presence of trace amounts of allergens in foods is not mandatory (see regulation of labelling). Treatment for accidental ingestion of egg products by allergic individuals varies depending on the sensitivity of the person. An antihistamine such as diphenhydramine (Benadryl) may be prescribed. Sometimes prednisone will be prescribed to prevent a possible late phase Type I hypersensitivity reaction. Severe allergic reactions (anaphalaxis) may require treatment with an epinephrine pen, an injection device designed to be used by a non-healthcare professional when emergency treatment is warranted. Immunotherapy There is active research on trying oral immunotherapy (OIT) to desensitize people to egg allergens. A Cochrane Review concluded that OIT can desensitize people, but it remains unclear whether long-term tolerance develops after treatment ceases, and 69% of the people enrolled in the trials had adverse effects. They concluded there was a need for standardized protocols and guidelines prior to incorporating OIT into clinical practice. A second review noted that allergic reactions, up to anaphylaxis, can occur during OIT, and recommends this treatment not be routine medical practice. A third review limited its scope to trials of baked egg-containing goods such as bread or cake as a means of resolving egg allergy. Again, there were some successes, but also some severe allergic reactions, and the authors came down on the side of not recommending this as treatment. Avoiding eggs Prevention of egg-allergic reactions means avoiding eggs and egg-containing foods. People with an allergy to chicken eggs may also be allergic to other types of eggs, such as goose, duck, or turkey eggs. In cooking, eggs are multifunctional: they may act as an emulsifier to reduce oil/water separation (mayonnaise), a binder (water binding and particle adhesion, as in meatloaf), or an aerator (cakes, especially angel food). Some commercial egg substitutes can substitute for particular functions (potato starch and tapioca for water binding, whey protein or bean water for aeration or particle binding, or soy lecithin or avocado for emulsification). Food companies produce egg-free mayonnaise and other replacement foods. Alfred Bird invented egg-free Birds Custard, the original version of what is known generically as custard powder today.Most people find it necessary to strictly avoid any item containing eggs, including: Ingredients that sometimes include egg protein include: artificial flavoring, natural flavoring, lecithin and nougat candy. Probiotic products have been tested, and some found to contain milk and egg proteins which were not always indicated on the labels. Prognosis The majority of children outgrow egg allergy. One review reported that 70% of children will outgrow this allergy by 16 years. In subsequently published longitudinal studies, one reported that for 140 infants who had challenge-confirmed egg allergy, 44% had resolved by two years. A second reported that for 203 infants with confirmed IgE-mediated egg allergy, 45% resolved by two years of age, 66% by four years, and 71% by six years. Children will be able to tolerate eggs as an ingredient in baked goods and well-cooked eggs sooner than under-cooked eggs. Resolution was more likely if baseline serum IgE was lower, and if the baseline symptoms did not include anaphylaxis. Epidemiology In countries in North America and western Europe, where use of cows milk based infant formula is common, chicken egg allergy is the second most common food allergy in infants and young children after cows milk. However, in Japan, egg allergy is first and cows milk second, followed by wheat and then the other common allergenic foods. A review from South Africa reported egg and peanut as the two most common allergenic foods.Incidence and prevalence are terms commonly used in describing disease epidemiology. Incidence is newly diagnosed cases, which can be expressed as new cases per year per million people. Prevalence is the number of cases alive, expressible as existing cases per million people during a period of time. Egg allergies are usually observed in infants and young children, and often disappear with age (see Prognosis), so prevalence of egg allergy may be expressed as a percentage of children under a set age. One review estimates that in North American and western European populations the prevalence of egg allergy in children under the age of five years is 1.8-2.0%. A second described the range in young children as 0.5-2.5%. Although the majority of children develop tolerance as they age into school age years, for roughly one-third the allergy persists into adulthood. Strong predictors for adult-persistent allergy are anaphylactic symptoms as a child, high egg-specific serum IgE, robust response to the skin prick test and absence of tolerance to egg-containing baked foods. Self-reported allergy prevalence is always higher than food-challenge confirmed allergy. For all age groups, a review of fifty studies conducted in Europe estimated 2.5% for self-reported egg allergy and 0.2% for confirmed. National survey data in the United States collected in 2005 and 2006 showed that from age six and older, the prevalence of serum IgE confirmed egg allergy was under 0.2%.Adult-onset of egg allergy is rare, but there is confirmation of cases. Some were described as having started in late teenage years; another group were workers in the baking industry who were exposed to powdered egg dust. Regulation Whether food allergy prevalence is increasing or not, food allergy awareness has definitely increased, with impacts on the quality of life for children, their parents and their immediate caregivers. In the United States, the Food Allergen Labeling and Consumer Protection Act of 2004 (FALCPA) causes people to be reminded of allergy problems every time they handle a food package, and restaurants have added allergen warnings to menus. The Culinary Institute of America, a premier school for chef training, has courses in allergen-free cooking and a separate teaching kitchen. School systems have protocols about what foods can be brought into the school. Despite all these precautions, people with serious allergies are aware that accidental exposure can easily occur at other peoples houses, at school or in restaurants. Regulation of labelling In response to the risk that certain foods pose to those with food allergies, some countries have responded by instituting labeling laws that require food products to clearly inform consumers if their products contain major allergens or byproducts of major allergens among the ingredients intentionally added to foods. Nevertheless, there are no labeling laws to mandatory declare the presence of trace amounts in the final product as a consequence of cross-contamination, except in Brazil. Ingredients intentionally added FALCPA became effective 1 January 2006, requiring companies selling foods in the United States to disclose on labels whether a packaged food product contains any of these eight major food allergens, added intentionally: cows milk, peanuts, eggs, shellfish, fish, tree nuts, soy and wheat. This list originated in 1999 from the World Health Organisation Codex Alimentarius Commission. To meet FALCPA labeling requirements, if an ingredient is derived from one of the required-label allergens, then it must either have its "food sourced name" in parentheses, for example "Casein (milk)," or as an alternative, there must be a statement separate but adjacent to the ingredients list: "Contains milk" (and any other of the allergens with mandatory labeling).FALCPA applies to packaged foods regulated by the FDA, which does not include poultry, most meats, certain egg products, and most alcoholic beverages. However, some meat, poultry, and egg processed products may contain allergenic ingredients. These products are regulated by the Food Safety and Inspection Service (FSIS), which requires that any ingredient be declared in the labeling only by its common or usual name. Neither the identification of the source of a specific ingredient in a parenthetical statement nor the use of statements to alert for the presence of specific ingredients, like "Contains: milk", are mandatory according to FSIS. FALCPA also does not apply to food prepared in restaurants. The EU Food Information for Consumers Regulation 1169/2011 – requires food businesses to provide allergy information on food sold unpackaged, for example, in catering outlets, deli counters, bakeries and sandwich bars. Trace amounts as a result of cross-contamination The value of allergen labeling other than for intentional ingredients is controversial. This concerns labeling for ingredients present unintentionally as a consequence of cross-contact or cross-contamination at any point along the food chain (during raw material transportation, storage or handling, due to shared equipment for processing and packaging, etc.). Experts in this field propose that if allergen labeling is to be useful to consumers, and healthcare professionals who advise and treat those consumers, ideally there should be agreement on which foods require labeling, threshold quantities below which labeling may be of no purpose, and validation of allergen detection methods to test and potentially recall foods that were deliberately or inadvertently contaminated.Labeling regulations have been modified to provide for mandatory labeling of ingredients plus voluntary labeling, termed precautionary allergen labeling (PAL), also known as "may contain" statements, for possible, inadvertent, trace amount, cross-contamination during production. PAL labeling can be confusing to consumers, especially as there can be many variations on the wording of the warning. As of 2014 PAL is regulated only in Switzerland, Japan, Argentina, and South Africa. Argentina decided to prohibit precautionary allergen labeling since 2010, and instead puts the onus on the manufacturer to control the manufacturing process and label only those allergenic ingredients known to be in the products. South Africa does not permit the use of PAL, except when manufacturers demonstrate the potential presence of allergen due to cross-contamination through a documented risk assessment and despite adherence to Good Manufacturing Practice. In Australia and New Zealand there is a recommendation that PAL be replaced by guidance from VITAL 2.0 (Vital Incidental Trace Allergen Labeling). A review identified "the eliciting dose for an allergic reaction in 1% of the population" as ED01. This threshold reference dose for foods such as cows milk, egg, peanut and other proteins) will provide food manufacturers with guidance for developing precautionary labeling and give consumers a better idea of might be accidentally in a food product beyond "may contain." VITAL 2.0 was developed by the Allergen Bureau, a food industry sponsored, non-government organization. The European Union has initiated a process to create labeling regulations for unintentional contamination but is not expected to publish such before 2024.In Brazil since April 2016, the declaration of the possibility of cross-contamination is mandatory when the product does not intentionally add any allergenic food or its derivatives but the Good Manufacturing Practices and allergen control measures adopted are not sufficient to prevent the presence of accidental trace amounts. These allergens include wheat, rye, barley, oats and their hybrids, crustaceans, eggs, fish, peanuts, soybean, milk of all species of mammalians, almonds, hazelnuts, cashew nuts, Brazil nuts, macadamia nuts, walnuts, pecan nuts, pistaches, pine nuts, and chestnuts. Society and culture Food fear has a significant impact on quality of life. For children with allergies, their quality of life is also affected by actions of their peers. There is an increased occurrence of bullying, which can include threats or acts of deliberately being touched with foods they need to avoid, also having their allergen-free food deliberately contaminated. See also List of allergens (food and non-food) References == External links ==

Hello Aarogya, explain a situation where Dermatopolymyositis occurs

Dermatopolymyositis

Dermatopolymyositis is a family of myositis disorders that includes polymyositis and dermatomyositis. As such, it includes both a distinctive skin rash and progressive muscular weakness. It is a rare disease. References == External links ==

Aarogya, give me a short description about Gapeworm

Gapeworm

A gapeworm (Syngamus trachea), also known as a red worm and forked worm, is a parasitic nematode worm that infects the tracheas of certain birds. The resulting disease, known as "gape" occurs when the worms clog and obstruct the airway. The worms are also known as "red worms" or "forked worms" due to their red color and the permanent procreative conjunction of males and females. Gapeworms are common in young, domesticated chickens and turkeys. When the female gapeworm lays her eggs in the trachea of an infected bird, the eggs are coughed up, swallowed, then defecated. Birds are infected with the parasite when they consume the eggs found in the feces, or by consuming a transport host such as earthworms, snails (Planorbarius corneus, Bithynia tentaculata and others) Morphology Males and females are joined together in a state of permanent copulation forming, a Y shape (forked worms). They are also known as the red worms because of their color. Females (up to 20mm long) are much longer than males (up to 6mm long). The life cycle of the gapeworm is peculiar in that transmission from bird to bird may be successfully accomplished either directly (by ingesting embryonated eggs or infective larvae) or indirectly (by ingestion of earthworms containing free or encysted gapeworm larvae they had obtained by feeding on contaminated soil). Life cycle and pathogenesis In the preparasitic phase, third stage infective larvae (L3) develop inside the eggs at which time they may hatch. Earthworms serve as transport (paratenic) hosts. Larvae have been shown to remain viable for more than three years encapsulated in earthworm muscles. Other invertebrates may also serve as paratenic hosts, including terrestrial snails and slugs. The parasitic phase involves substantial migration in the definitive host to reach the predilection site. Young birds are most severely affected with migration of larvae and adults through the lungs causing a severe pneumonia. Lymphoid nodules form at the point of attachment of the worms in the bronchi and trachea. Adult worms also appear to feed on blood. Worms in the bronchi and trachea provoke a hemorrhagic tracheitis and bronchitis, forming large quantities of mucus, plugging the air passages and, in severe cases, causing asphyxiation. Pheasants appear to be particularly susceptible to infections resulting in mortality rates as high as 25% during outbreaks. The rapidly growing worms soon obstruct the lumen of the trachea, causing suffocation. Turkey poults, baby chicks and pheasant chicks are most susceptible to infection. Turkey poults usually develop gapeworm signs earlier and begin to die sooner after infection than young chickens. Lesions are usually found in the trachea of turkeys and pheasants but seldom if ever in the tracheas of young chickens and guinea fowl. The male worm, in the form of lesions, remains permanently attached to the tracheal wall throughout the duration of its life. The female worms apparently detach and reattach from time to time in order to obtain a more abundant supply of food. Epidemiology Earthworm transport hosts are important factors in the transmission of Syngamus trachea when poultry and game birds are reared on soil. The longevity of L3s in earthworms (up to 3 years) is particularly important in perpetuating the infection from year to year. Wild birds may serve as reservoirs of infection and have been implicated as the sources of infections in outbreaks on game-bird farms as well as poultry farms. Wild reservoir hosts may include pheasants, ruffed grouse, partridges, wild turkeys, magpies, meadowlarks, American robins, grackles, jays, jackdaws, rooks, starlings and crows. There is also evidence to suggest that strains of Syngamus trachea from wild bird reservoir hosts may be less effective in domestic birds; if they have an earthworm transport host rather than direct infections via ingestion of L3s, or eggs containing L3s. Clinical signs Blockage of the bronchi and trachea with worms and mucus will cause infected birds to gasp for air. They stretch out their necks, open their mouths and gasp for air producing a hissing noise as they do so. This "gaping" posture has given rise to the common term "gapeworm" to describe Syngamus trachea. These clinical signs first appear approximately 1–2 weeks after infection. Birds infected with gapeworms show signs of weakness and emaciation, usually spending much of their time with eyes closed and head drawn back against the body. An infected bird may give its head a convulsive shake in an attempt to remove the obstruction from the trachea so that normal breathing may be resumed. Severely affected birds, particularly young ones, will deteriorate rapidly; they stop drinking and become anorexic. At this stage, death is the usual outcome. Adult birds are usually less severely affected and may only show an occasional cough or even no obvious clinical signs. Diagnosis A diagnosis is usually made on the basis of the classical clinical signs of "gaping". Subclinical infections with few worms may be confirmed at necropsy by finding copulating worms in the trachea and also by finding the characteristic eggs in the feces of infected birds. Examination of the tracheas of infected birds shows that the mucous membrane is extensively irritated and inflamed. Coughing is apparently the result of this irritation to the mucous lining. Control and treatment Prevention In the artificial rearing of pheasants, gapes are a serious menace. Confinement rearing of young birds has reduced the problem in chickens compared to a few years ago. However, this parasite continues to present an occasional problem with turkeys raised on range. Confinement rearing of broilers/pullets and caging of laying hens, have significantly influenced the quantity and variety of nematode infections in poultry. For most nematodes, control measures consist of sanitation and breaking the life cycle rather than chemotherapy. Confinement rearing on litter largely prevents infections with nematodes using intermediate hosts such as earthworms or grasshoppers, which are not normally found in poultry houses. Conversely, nematodes with direct life cycles or those that utilize intermediate hosts such as beetles, which are common in poultry houses, may prosper. Treatment of the soil or litter to kill intermediate hosts may be beneficial. Insecticides suitable for litter treatment include carbaryl, tetrachlorvinphos (stirofos). However, treatment is usually done only between grow-outs. Extreme care should be taken to ensure that feed and water are not contaminated. Treatment of range soil to kill ova is only partially successful. Changing litter can reduce infections, but treating floors with oil is not very effective. Raising different species or different ages of birds together or in close proximity is a dangerous procedure as regards parasitism. Adult turkeys, which are carriers of gapeworms, can transmit the disease to young chicks or pheasants, although older chickens are almost resistant to infection. Treatment Flubendazole (Flubenvet) is the only licensed anthelmintic for use in poultry and game birds. Continuous medication of pen-reared birds has been recommended, but is not economical and increases the possibility of drug resistance. Several other compounds have been shown effective against S. trachea under experimental conditions. Methyl 5-benzoyl-2-benzimidazole was 100% efficacious when fed prophylactically to turkey poults. 5-Isopropoxycarbonylamino-2-(4-thizolyl)-benzimidazole was found to be more efficacious than thiabendazole or disophenol. The level of control with three treatments of cambendazole on days 3–4, 6–7, and 16-17 post-infection was 94.9% in chickens and 99.1% in turkeys. Levamisole (Ergamisol), fed at a level of 0.04% for 2 days or 2 g/gal drinking water for 1 day each month, has proven effective in game birds. Fenbendazole (Panacur) at 20 mg/kg for 3–4 days is also effective. Ivermectin injections may be effective in treating resistant strains. Sources https://web.archive.org/web/20100703145151/http://cal.vet.upenn.edu/projects/merial/Strongls/strong_4.htm https://web.archive.org/web/20110717194656/http://www.vetsweb.com/diseases/syngamus-trachea-d75.html#effects

Hello Aarogya , Do you know what is Eclampsia,

Eclampsia

Eclampsia is the onset of seizures (convulsions) in a woman with pre-eclampsia. Pre-eclampsia is one of the hypertensive disorders of pregnancy that presents with three main features: new onset of high blood pressure, large amounts of protein in the urine or other organ dysfunction, and edema. The diagnostic criteria for pre-eclampsia is high blood pressure occurring after 20 weeks gestation or during the second half of pregnancy. Most often it occurs during the 3rd trimester of pregnancy and may occur before, during, or after delivery. The seizures are of the tonic–clonic type and typically last about a minute. Following the seizure, there is either a period of confusion or coma. Other complications include aspiration pneumonia, cerebral hemorrhage, kidney failure, pulmonary edema, HELLP syndrome, coagulopathy, placental abruption and cardiac arrest.Low dose aspirin is recommended to prevent pre-eclampsia and eclampsia in those at high risk. Other preventative recommendation include calcium supplementation in areas with low calcium intake and treatment of prior hypertension with anti-hypertensive medications. Exercise during pregnancy may also be useful. The use of intravenous or intramuscular magnesium sulfate improves outcomes in those with severe pre-eclampsia and eclampsia and is generally safe. Treatment options include blood pressure medications such as hydralazine and emergency delivery of the baby either vaginally or by cesarean section.Pre-eclampsia is estimated to globally affect about 5% of deliveries while eclampsia affects about 1.4% of deliveries. In the developed world eclampsia rates are about 1 in 2,000 deliveries due to improved medical care whereas in developing countries it can impact 10-30 times as many women. Hypertensive disorders of pregnancy are one of the most common causes of death in pregnancy. They resulted in 46,900 deaths in 2015. Around one percent of women with eclampsia die. The word eclampsia is from the Greek term for lightning. The first known description of the condition was by Hippocrates in the 5th century BC. Signs and symptoms Eclampsia is a disorder of pregnancy characterized by seizures in the setting of pre-eclampsia. Most women have premonitory signs/symptoms in the hours before the initial seizure. Typically the woman develops hypertension before the onset of a convulsion (seizure). Other signs and symptoms to looks out for include: Long-lasting (persistent) frontal or occipital headaches or thunderclap headaches) Visual disturbance (blurred vision, photophobia, diplopopia) Photophobia (i.e. bright light causes discomfort) Abdominal pain Either in the epigastric region (the center of the abdomen above the navel, or belly-button) And/or in the right upper quadrant of the abdomen (below the right side of the rib cage) Altered mental status (confusion)Any of these symptoms may be present before or after the seizure. It is also possible for the woman to be asymptomatic prior to the onset of the seizure. Other cerebral signs that may precede the convulsion include nausea, vomiting, headaches, and cortical blindness. If the complication of multi-organ failure ensues, signs and symptoms of those failing organs will appear, such as abdominal pain, jaundice, shortness of breath, and diminished urine output. Onset The seizures of eclampsia typically present during pregnancy and prior to delivery (the antepartum period), but may also occur during labor and delivery (the intrapartum period) or after the baby has been delivered (the postpartum period). If postpartum seizures develop, it is most likely to occur within the first 48 hours after delivery. However, late postpartum seizures of eclampsia may occur as late as 4 weeks after delivery. Characteristics Eclamptic seizure is typically described as a tonic–clonic seizure which may cause an abrupt loss of consciousness at onset. This is often associated with a shriek or scream followed by stiffness of the muscles of the arms, legs, back and chest. During the tonic phase, the mother may begin to appear cyanotic. This presentation lasts for about a minute, after which the muscles begin in jerk and twitch for an additional one to two minutes. Other signs include tongue biting, frothy and bloody sputum coming out of the mouth. Complications There are risks to both the mother and the fetus when eclampsia occurs. The fetus may grow more slowly than normal within the womb (uterus) of a woman with eclampsia, which is termed intrauterine growth restriction and may result in the child appearing small for gestational age or being born with low birth weight. Eclampsia may also cause problems with the placenta. The placenta may bleed (hemorrhage) or begin to separate early from the wall of the uterus. It is normal for the placenta to separate from the uterine wall during delivery, but it is abnormal for it to separate prior to delivery; this condition is called placental abruption and can be dangerous for the fetus. Placental insufficiency may also occur, a state in which the placenta fails to support appropriate fetal development because it cannot deliver the necessary amount of oxygen or nutrients to the fetus. During an eclamptic seizure, the beating of the fetal heart may become slower than normal (bradycardia). If any of these complications occurs, fetal distress may develop. Treatment of the mothers seizures may also manage fetal bradycardia. If the risk to the health of the fetus or the mother is high, the definitive treatment for eclampsia is delivery of the baby. Delivery by cesarean section may be necessary, especially if the instance of fetal bradycardia does not resolve after 10 to 15 minutes of resuscitative interventions. It may be safer to deliver the infant preterm than to wait for the full 40 weeks of fetal development to finish, and as a result prematurity is also a potential complication of eclampsia.In the mother, changes in vision may occur as a result of eclampsia, and these changes may include blurry vision, one-sided blindness (either temporary due to amaurosis fugax or potentially permanent due to retinal detachment), or cortical blindness, which affects the vision from both eyes. There are also potential complications in the lungs. The woman may have fluid slowly collecting in the lungs in a process known as pulmonary edema. During an eclamptic seizure, it is possible for a person to vomit the contents of the stomach and to inhale some of this material in a process known as aspiration. If aspiration occurs, the woman may experience difficulty breathing immediately or could develop an infection in the lungs later, called aspiration pneumonia. It is also possible that during a seizure breathing will stop temporarily or become inefficient, and the amount of oxygen reaching the womans body and brain will be decreased (in a state known as hypoxia). If it becomes difficult for the woman to breathe, she may need to have her breathing temporarily supported by an assistive device in a process called mechanical ventilation. In some severe eclampsia cases, the mother may become weak and sluggish (lethargy) or even comatose. These may be signs that the brain is swelling (cerebral edema) or bleeding (intracerebral hemorrhage). Risk factors Eclampsia, like pre-eclampsia, tends to occur more commonly in first pregnancies than subsequent pregnancies. Women who have long term high blood pressure before becoming pregnant have a greater risk of pre-eclampsia. Patients who have gestational hypertension and pre-eclampsia have an increased risk of eclampsia. Furthermore, women with other pre-existing vascular diseases (diabetes or nephropathy) or thrombophilia disease such as the antiphospholipid syndrome are at higher risk to develop pre-eclampsia and eclampsia. Having a placenta that is enlarged by multiple gestation or hydatidiform mole also increases risk of eclampsia. In addition, there is a genetic component: a woman whose mother or sister had the condition is at higher risk than otherwise. Patients who have experienced eclampsia are at increased risk for pre-eclampsia/eclampsia in a later pregnancy. The occurrence of pre-eclampsia was 5% in white, 9% in Hispanic, and 11% in African American patients and this may reflect disproportionate risk of developing pre-eclampsia among ethnic groups. Additionally, black patients were also shown to have a disproportionately higher risk of dying from eclampsia. Mechanism The mechanisms of eclampsia and preeclampsia are not definitively understood, but following provides some insight. The presence of a placenta is required, and eclampsia resolves if it is removed. Reduced blood flow to the placenta (placental hypoperfusion) may be a key feature of the process. It is typically accompanied by increased sensitivity of the maternal vasculature to agents which cause constriction of the small arteries, leading to reduced blood flow to multiple organs. Vascular dysfunction-associated maternal conditions such as Lupus, hypertension, and renal disease, or obstetric conditions that increase placental volume without an increase in placental blood flow (such as multifetal gestation) may increase risk for pre-eclampsia. Also, activation of the coagulation cascade can lead to microthrombi formation, which may further impair blood flow. Thirdly, increased vascular permeability results in the shift of extracellular fluid from the blood to the interstitial space which reduces blood flow and causes edema. These events can lead to hypertension, renal dysfunction, pulmonary dysfunction, hepatic dysfunction, and cerebral edema with cerebral dysfunction and convulsions. In clinical context, increased platelet and endothelial activation may be detected before symptoms appear.Hypoperfusion of the placenta is associated with abnormal modelling of the fetal–maternal placental interface that may be immunologically mediated. The pathogenesis of pre-eclampsia is poorly understood and may be attributed to factors related to the woman and placenta since pre-eclampsia is seen in molar pregnancies absent of a fetus or fetal tissue. The placenta normally produces the potent vasodilator adrenomedullin but it is reduced in pre-eclampsia and eclampsia. Other vasodilators, including prostacyclin, thromboxane A2, nitric oxide, and endothelins, are reduced in eclampsia and may lead to vasoconstriction.Eclampsia is associated with hypertensive encephalopathy in which cerebral vascular resistance is reduced, leading to increased blood flow to the brain, cerebral edema and resultant convulsions. An eclamptic convulsion usually does not cause chronic brain damage unless intracranial haemorrhage occurs. Diagnosis If a pregnant woman has already been diagnosed with pre-eclampsia during the current pregnancy and then develops a seizure, she may be assigned a clinical diagnosis of eclampsia without further workup. While seizures are most common in the third trimester, they may occur any time from 20 weeks of pregnancy until 6 weeks after birth. Because pre-eclampsia and eclampsia are common conditions in women, eclampsia can be assumed to be the correct diagnosis until proven otherwise in pregnant or postpartum women who experience seizures. However, if a woman has a seizure and it is unknown whether or not they have pre-eclampsia, testing can help make the diagnosis clear. Pre-eclampsia is diagnosed when repeated blood pressure measurements are greater or equal to 140/90mmHg, in addition to any signs of organ dysfunction, including: proteinuria, thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, cerebral symptoms, or abdominal pain. Vital signs One of the core features of pre-eclampsia is the new onset of high blood pressure. Blood pressure is a measurement of two numbers: systolic blood pressure and diastolic blood pressure. A systolic blood pressure (the top number) of greater than 140 mmHg and/or a diastolic blood pressure (the bottom number) of greater than 90 mmHg is higher than the normal range. If the blood pressure is high on at least two separate occasions after the first 20 weeks of pregnancy and the woman has signs of organ dysfunction (e.g. proteinuria), then they meet the criteria for a diagnosis of pre-eclampsia. If the systolic blood pressure is greater than 160 or the diastolic pressure is greater than 110, the hypertension is considered to be severe. Laboratory testing Another common feature of pre-eclampsia is proteinuria, which is the presence of excess protein in the urine. To determine if proteinuria is present, the urine can be collected and tested for protein; if there is 0.3 grams of protein or more in the urine of a pregnant woman collected over 24 hours, this is one of the diagnostic criteria for pre-eclampsia and raises the suspicion that a seizure is due to eclampsia.In cases of severe eclampsia or pre-eclampsia, the woman can have low levels of platelets in the blood, a condition termed thrombocytopenia. A complete blood count, or CBC, is a test of the blood that can be performed to check platelet levels. Other investigations include: kidney function test, liver function tests (LFT), coagulation screen, 24-hour urine creatinine, and fetal/placental ultrasound. Differential diagnosis Convulsions during pregnancy that are unrelated to pre-eclampsia need to be distinguished from eclampsia. Such disorders include seizure disorders as well as brain tumor, aneurysm of the brain, and medication- or drug-related seizures. Usually, the presence of the signs of severe pre-eclampsia precede and accompany eclampsia, facilitating the diagnosis. Prevention Detection and management of pre-eclampsia is critical to reduce the risk of eclampsia. The USPSTF recommends regular checking of blood pressure through pregnancy in order to detect preeclampsia. Appropriate management of a woman with pre-eclampsia generally involves the use of magnesium sulfate to prevent eclamptic seizures. In some cases, low-dose aspirin has been shown to decrease the risk of pre-eclampsia in women, especially when taken in the late first trimester. Treatment The four goals of the treatment of eclampsia are to stop and prevent further convulsions, to control the elevated blood pressure, to deliver the baby as promptly as possible, and to monitor closely for the onset of multi-organ failure. Convulsions Convulsions are prevented and treated using magnesium sulfate. The study demonstrating the effectiveness of magnesium sulfate for the management of eclampsia was first published in 1955. Effective anticonvulsant serum levels range from 2.5 to 7.5 mEq/L.With intravenous administration, the onset of anticonvulsant action is fast and lasts about 30 minutes. Following intramuscular administration the onset of action is about one hour and lasts for three to four hours. Magnesium is excreted solely by the kidneys at a rate proportional to the plasma concentration (concentration in the blood) and glomerular filtration (rate at which the blood is filtered through the kidneys). Magnesium sulfate is associated with several minor side effects; serious side effects are uncommon, occurring at elevated magnesium serum concentrations greater than 7.0 mEq/L. Serious toxicity can be counteracted with calcium gluconate.Even with therapeutic serum magnesium concentrations, recurrent convulsions may occur, and additional magnesium may be needed, but with close monitoring for respiratory, cardiac, and neurological depression. If magnesium administration with resultant high serum concentrations fails to control convulsions, the addition of other intravenous anticonvulsants may be used and intubation and mechanical ventilation may be initiated. It is important to avoid magnesium toxicity, including thoracic muscle paralysis, which could cause respiratory failure and death. Magnesium sulfate results in better outcomes than diazepam, phenytoin or a combination of chlorpromazine, promethazine, and pethidine. Blood pressure management Blood pressure control is used to prevent stroke, which accounts for 15 to 20 percent of deaths in women with eclampsia. The agents of choice for blood pressure control during eclampsia are hydralazine or labetalol. This is because of their effectiveness, lack of negative effects on the fetus, and mechanism of action. Blood pressure management is indicated with a diastolic blood pressure above 105–110 mm Hg. Delivery If the baby has not yet been delivered, steps need to be taken to stabilize the woman and deliver her speedily. This needs to be done even if the baby is immature, as the eclamptic condition is unsafe for both baby and mother. As eclampsia is a manifestation of a type of non-infectious multiorgan dysfunction or failure, other organs (liver, kidney, lungs, cardiovascular system, and coagulation system) need to be assessed in preparation for a delivery (often a caesarean section), unless the woman is already in advanced labor. Regional anesthesia for caesarean section is contraindicated when a coagulopathy has developed. There is limited to no evidence in favor of a particular delivery method for women with eclampsia. Therefore, the delivery method of choice is an individualized decision. Monitoring Invasive hemodynamic monitoring may be elected in an eclamptic woman at risk for or with heart disease, kidney disease, refractory hypertension, pulmonary edema, or poor urine output. Etymology The Greek noun ἐκλαμψία, eklampsía, denotes a "light burst"; metaphorically, in this context, "sudden occurrence." The New Latin term first appeared in Johannes Varandaeus’ 1620 treatise on gynaecology Tractatus de affectibus Renum et Vesicae. The term toxemia of pregnancy is no longer recommended: placental toxins are not the cause of eclampsia occurrences, as previously believed. Popular culture In Downton Abbey, a historical drama television series, the character Lady Sybil dies (in series 3, episode 5) of eclampsia shortly after child birth. In Call the Midwife, a medical drama television series set in London in the 1950s and 1960s, the character (in series 1, episode 4) named Margaret Jones is struck with pre-eclampsia, ultimately proceeding from a comatose condition to death. The term "toxemia" was also used for the condition, in the dialogue. In House M.D., a medical drama television series set in the U.S., Dr. Cuddy, the hospital director, adopts a baby whose teenage mother dies from eclampsia and had no other parental figures available. In The Lemon Drop Kid, the main characters wife dies of eclampsia shortly after giving birth to a boy. References External links Eclampsia at Curlie

Please give me a short description about Anxiety disorder , Aarogya

Anxiety disorder

Anxiety disorders are a cluster of mental disorders characterized by significant and uncontrollable feelings of anxiety and fear such that a persons social, occupational, and personal function are significantly impaired. Anxiety may cause physical and cognitive symptoms, such as restlessness, irritability, easy fatiguability, difficulty concentrating, increased heart rate, chest pain, abdominal pain, and a variety of other symptoms that may vary based on the individual.In casual discourse, the words anxiety and fear are often used interchangeably. In clinical usage, they have distinct meanings: anxiety is defined as an unpleasant emotional state for which the cause is either not readily identified or perceived to be uncontrollable or unavoidable, whereas fear is an emotional and physiological response to a recognized external threat. The umbrella term anxiety disorder refers to a number of specific disorders that include fears (phobias) or anxiety symptoms. There are several types of anxiety disorders, including generalized anxiety disorder, specific phobia, social anxiety disorder, separation anxiety disorder, agoraphobia, panic disorder, and selective mutism. The individual disorder can be diagnosed using the specific and unique symptoms, triggering events, and timing. If a person is diagnosed with an anxiety disorder, a medical professional must have evaluated the person to ensure the anxiety cannot be attributed to another medical illness or mental disorder. It is possible for an individual to have more than one anxiety disorder during their life or at the same time and anxiety disorders are marked by a typical persistent course. Anxiety disorders are the most common of mental disorders and affect nearly 30% of adults at some point in their lives. However, anxiety disorders are treatable and a number of effective treatments are available. Treatment helps most people lead normal productive lives. Sub-types Generalized anxiety disorder Generalized anxiety disorder (GAD) is a common disorder, characterized by long-lasting anxiety which is not focused on any one object or situation. Those with generalized anxiety disorder experience non-specific persistent fear and worry, and become overly concerned with everyday matters. Generalized anxiety disorder is "characterized by chronic excessive worry accompanied by three or more of the following symptoms: restlessness, fatigue, concentration problems, irritability, muscle tension, and sleep disturbance". Generalized anxiety disorder is the most common anxiety disorder to affect older adults. Anxiety can be a symptom of a medical or substance use disorder problem, and medical professionals must be aware of this. A diagnosis of GAD is made when a person has been excessively worried about an everyday problem for six months or more. These stresses can include family life, work, social life, or their own health. A person may find that they have problems making daily decisions and remembering commitments as a result of lack of concentration and/or preoccupation with worry. A symptom can be a strained appearance, with increased sweating from the hands, feet, and axillae, and they may be tearful, which can suggest depression. Before a diagnosis of anxiety disorder is made, physicians must rule out drug-induced anxiety and other medical causes.In children, GAD may be associated with headaches, restlessness, abdominal pain, and heart palpitations. Typically it begins around 8 to 9 years of age. Specific phobias The single largest category of anxiety disorders is that of specific phobias, which includes all cases in which fear and anxiety are triggered by a specific stimulus or situation. Between 5% and 12% of the population worldwide have specific phobias. According to the National Institute of Mental Health, a phobia is an intense fear of or aversion to specific objects or situations. Individuals with a phobia typically anticipate terrifying consequences from encountering the object of their fear, which can be anything from an animal to a location to a bodily fluid to a particular situation. Common phobias are flying, blood, water, highway driving, and tunnels. When people are exposed to their phobia, they may experience trembling, shortness of breath, or rapid heartbeat. Thus meaning that people with specific phobias often go out of their way to avoid encountering their phobia. People understand that their fear is not proportional to the actual potential danger but still are overwhelmed by it. Panic disorder With panic disorder, a person has brief attacks of intense terror and apprehension, often marked by trembling, shaking, confusion, dizziness, nausea, and/or difficulty breathing. These panic attacks, defined by the APA as fear or discomfort that abruptly arises and peaks in less than ten minutes, can last for several hours. Attacks can be triggered by stress, irrational thoughts, general fear or fear of the unknown, or even exercise. However, sometimes the trigger is unclear and the attacks can arise without warning. To help prevent an attack, one can avoid the trigger. This can mean avoiding places, people, types of behaviors, or certain situations that have been known to cause a panic attack. This being said, not all attacks can be prevented. In addition to recurrent unexpected panic attacks, a diagnosis of panic disorder requires that said attacks have chronic consequences: either worry over the attacks potential implications, persistent fear of future attacks, or significant changes in behavior related to the attacks. As such, those with panic disorder experience symptoms even outside specific panic episodes. Often, normal changes in heartbeat are noticed, leading them to think something is wrong with their heart or they are about to have another panic attack. In some cases, a heightened awareness (hypervigilance) of body functioning occurs during panic attacks, wherein any perceived physiological change is interpreted as a possible life-threatening illness (i.e., extreme hypochondriasis). Agoraphobia Agoraphobia is the specific anxiety about being in a place or situation where escape is difficult or embarrassing or where help may be unavailable. Agoraphobia is strongly linked with panic disorder and is often precipitated by the fear of having a panic attack. A common manifestation involves needing to be in constant view of a door or other escape route. In addition to the fears themselves, the term agoraphobia is often used to refer to avoidance behaviors that individuals often develop. For example, following a panic attack while driving, someone with agoraphobia may develop anxiety over driving and will therefore avoid driving. These avoidance behaviors can have serious consequences and often reinforce the fear they are caused by. In a severe case of agoraphobia, the person may never leave their home. Social anxiety disorder Social anxiety disorder (SAD; also known as social phobia) describes an intense fear and avoidance of negative public scrutiny, public embarrassment, humiliation, or social interaction. This fear can be specific to particular social situations (such as public speaking) or, more typically, is experienced in most (or all) social interactions. Roughly 7% of American adults have social anxiety disorder, and more than 75% of people experience their first symptoms in their childhood or early teenage years. Social anxiety often manifests specific physical symptoms, including blushing, sweating, rapid heart rate, and difficulty speaking. As with all phobic disorders, those with social anxiety often will attempt to avoid the source of their anxiety; in the case of social anxiety this is particularly problematic, and in severe cases can lead to complete social isolation. Children are also affected by social anxiety disorder, although their associated symptoms are different than that of teenagers and adults. They may experience difficulty processing or retrieving information, sleep deprivation, disruptive behaviors in class, and irregular class participation.Social physique anxiety (SPA) is a subtype of social anxiety, involving concern over the evaluation of ones body by others. SPA is common among adolescents, especially females. Post-traumatic stress disorder Post-traumatic stress disorder (PTSD) was once an anxiety disorder (now moved to trauma- and stressor-related disorders in DSM-V) that results from a traumatic experience. PTSD affects approximately 3.5% of U.S. adults every year, and an estimated one in eleven people will be diagnosed with PTSD in their lifetime. Post-traumatic stress can result from an extreme situation, such as combat, natural disaster, rape, hostage situations, child abuse, bullying, or even a serious accident. It can also result from long-term (chronic) exposure to a severe stressor— for example, soldiers who endure individual battles but cannot cope with continuous combat. Common symptoms include hypervigilance, flashbacks, avoidant behaviors, anxiety, anger and depression. In addition, individuals may experience sleep disturbances. People who have PTSD often try to detach themselves from their friends and family, and have difficulty maintaining these close relationships. There are a number of treatments that form the basis of the care plan for those with PTSD. Such treatments include cognitive behavioral therapy (CBT), prolonged exposure therapy, stress inoculation therapy, medication, and psychotherapy and support from family and friends.Post-traumatic stress disorder (PTSD) research began with Vietnam veterans, as well as natural and non-natural disaster victims. Studies have found the degree of exposure to a disaster has been found to be the best predictor of PTSD. Separation anxiety disorder Separation anxiety disorder (SepAD) is the feeling of excessive and inappropriate levels of anxiety over being separated from a person or place. Separation anxiety is a normal part of development in babies or children, and it is only when this feeling is excessive or inappropriate that it can be considered a disorder. Separation anxiety disorder affects roughly 7% of adults and 4% of children, but the childhood cases tend to be more severe; in some instances, even a brief separation can produce panic. Treating a child earlier may prevent problems. This may include training the parents and family on how to deal with it. Often, the parents will reinforce the anxiety because they do not know how to properly work through it with the child. In addition to parent training and family therapy, medication, such as SSRIs, can be used to treat separation anxiety. Obsessive–compulsive disorder Obsessive–compulsive disorder (OCD) is not classified as an anxiety disorder by the DSM-5, but is by the ICD-10. It was previously classified as an anxiety disorder in the DSM-IV. It is a condition where the person has obsessions (distressing, persistent, and intrusive thoughts or images) and compulsions (urges to repeatedly perform specific acts or rituals), that are not caused by drugs or physical disorder, and which cause distress or social dysfunction. The compulsive rituals are personal rules followed to relieve the feeling of discomfort. OCD affects roughly 1–⁠2% of adults (somewhat more women than men), and under 3% of children and adolescents.A person with OCD knows that the symptoms are unreasonable and struggles against both the thoughts and the behavior. Their symptoms could be related to external events they fear (such as their home burning down because they forget to turn off the stove) or worry that they will behave inappropriately.It is not certain why some people have OCD, but behavioral, cognitive, genetic, and neurobiological factors may be involved. Risk factors include family history, being single (although that may result from the disorder), and higher socioeconomic class or not being in paid employment. Of those with OCD about 20% of people will overcome it, and symptoms will at least reduce over time for most people (a further 50%). Selective mutism Selective mutism (SM) is a disorder in which a person who is normally capable of speech does not speak in specific situations or to specific people. Selective mutism usually co-exists with shyness or social anxiety. People with selective mutism stay silent even when the consequences of their silence include shame, social ostracism or even punishment. Selective mutism affects about 0.8% of people at some point in their life.Testing for selective mutism is important because doctors must determine if it is an issue associated with the childs hearing, movements associated with the jaw or tongue, and if the child can understand when others are speaking to them. Diagnosis The diagnosis of anxiety disorders is made by symptoms, triggers, and a persons personal and family histories. There are no objective biomarkers or laboratory tests that can diagnose anxiety. It is important for a medical professional to evaluate a person for other medical and mental causes for prolonged anxiety because treatments will vary considerably.Numerous questionnaires have been developed for clinical use and can be used for an objective scoring system. Symptoms may be vary between each subtype of generalized anxiety disorder. Generally, symptoms must be present for at least six months, occur more days than not, and significantly impair a persons ability to function in daily life. Symptoms may include: feeling nervous, anxious, or on edge; worrying excessively; difficulty concentrating; restlessness; irritability.Questionnaires developed for clinical use include the State-Trait Anxiety Inventory (STAI), the Generalized Anxiety Disorder 7 (GAD-7), the Beck Anxiety Inventory (BAI), the Zung Self-Rating Anxiety Scale, and the Taylor Manifest Anxiety Scale. Other questionnaires combine anxiety and depression measurement, such as the Hamilton Anxiety Rating Scale, the Hospital Anxiety and Depression Scale (HADS), the Patient Health Questionnaire (PHQ), and the Patient-Reported Outcomes Measurement Information System (PROMIS). Examples of specific anxiety questionnaires include the Liebowitz Social Anxiety Scale (LSAS), the Social Interaction Anxiety Scale (SIAS), the Social Phobia Inventory (SPIN), the Social Phobia Scale (SPS), and the Social Anxiety Questionnaire (SAQ-A30). Differential diagnosis Anxiety disorders differ from developmentally normal fear or anxiety by being excessive or persisting beyond developmentally appropriate periods. They differ from transient fear or anxiety, often stress-induced, by being persistent (e.g., typically lasting 6 months or more), although the criterion for duration is intended as a general guide with allowance for some degree of flexibility and is sometimes of shorter duration in children.The diagnosis of an anxiety disorder requires first ruling out an underlying medical cause. Diseases that may present similar to an anxiety disorder, including certain endocrine diseases (hypo- and hyperthyroidism, hyperprolactinemia), metabolic disorders (diabetes), deficiency states (low levels of vitamin D, B2, B12, folic acid), gastrointestinal diseases (celiac disease, non-celiac gluten sensitivity, inflammatory bowel disease), heart diseases, blood diseases (anemia), and brain degenerative diseases (Parkinsons disease, dementia, multiple sclerosis, Huntingtons disease).Several drugs can also cause or worsen anxiety, whether in intoxication, withdrawal, or from chronic use. These include alcohol, tobacco, cannabis, sedatives (including prescription benzodiazepines), opioids (including prescription painkillers and illicit drugs like heroin), stimulants (such as caffeine, cocaine and amphetamines), hallucinogens, and inhalants. Prevention Focus is increasing on prevention of anxiety disorders. There is tentative evidence to support the use of cognitive behavioral therapy and mindfulness therapy. A 2013 review found no effective measures to prevent GAD in adults. A 2017 review found that psychological and educational interventions had a small benefit for the prevention of anxiety. Research indicates that predictors of the emergence of anxiety disorders partly differ from the factors that predict their persistence. Perception and Discrimination Stigma People with an anxiety disorder may be challenged by prejudices and stereotypes that the world believes, most likely as a result of misconception around anxiety and anxiety disorders. Misconceptions found in a data analysis from the National Survey of Mental Health Literacy and Stigma include (1) many people believe anxiety is not a real medical illness; and (2) many people believe that people with anxiety could turn it off if they wanted to. For people experiencing the physical and mental symptoms of an anxiety disorder, stigma and negative social perception can make an individual less likely to seek treatment.There are two prevalent types of stigmas that surround anxiety disorders: Public and Self-Stigma. Public stigma in this context is the reaction that the general population has to people with an anxiety disorder. Self-Stigma is described as the prejudice which people with mental illness turn against themselves.There is no explicit evidence that announces the exact cause of stigma towards anxiety, however there are three highlighted perspectives. The macro, intermediate, and micro levels. The macro level marks society as whole with the influence from mass media. The intermediate level includes health care professionals and their perspective. The micro level details the individuals contributions to the process through self-stigmatization.Stigma can be described in three conceptual ways: cognitive, emotional, and behavioural. This allows for differentiation between stereotypes, prejudice, and discrimination. Treatment Treatment options include lifestyle changes, therapy, and medications. There is no clear evidence as to whether therapy or medication is most effective; the specific medication decision can be made by a doctor and patient with consideration to the patients specific circumstances and symptoms. If while on treatment with a chosen medication, the persons anxiety does not improve, another medication may be offered. Specific treatments will vary by subtype of anxiety disorder, a persons other medical conditions, and medications. Lifestyle and diet Lifestyle changes include exercise, for which there is moderate evidence for some improvement, regularizing sleep patterns, reducing caffeine intake, and stopping smoking. Stopping smoking has benefits in anxiety as large as or larger than those of medications. Omega-3 polyunsaturated fatty acids, such as fish oil, may reduce anxiety, particularly in those with more significant symptoms. Psychotherapy Cognitive behavioral therapy (CBT) is effective for anxiety disorders and is a first-line treatment. CBT appears to be equally effective when carried out via the internet compared to sessions completed face to face.Mindfulness-based programs also appear to be effective for managing anxiety disorders. It is unclear if meditation has an effect on anxiety and transcendental meditation appears to be no different than other types of meditation.A 2015 Cochrane review of Morita therapy for anxiety disorder in adults found not enough evidence to draw a conclusion.Adventure-based counseling can be an effective way to anxiety. Using rock-climbing as an example, climbing can often bring on fear or frustration, and tackling these negative feelings in a nurturing environment can help people develop coping mechanisms necessary to deal with these negative feelings. Medications First-line choices for medications include SSRIs or SNRIs to treat generalized anxiety disorder. For adults there is no good evidence supporting which specific medication in the SSRI or SNRI class is best for treating anxiety, so cost often drives drug choice. Fluvoxamine is effective in treating a range of anxiety disorders in children and adolescents. Fluoxetine, sertraline and paroxetine can also help with some forms of anxiety in children and adolescents. If the chosen medicine is effective, it is recommended that it is continued for at least a year. Stopping medication results in a greater risk of relapse.Buspirone and pregabalin are second-line treatments for people who do not respond to SSRIs or SNRIs; there is also evidence that benzodiazepines, including diazepam and clonazepam, are effective. Pregabalin and gabapentin are effective in treating some anxiety disorders but there is concern regarding their off-label use due to the lack of strong scientific evidence for their efficacy in multiple conditions and their proven side effects.Medications need to be used with care among older adults, who are more likely to have side effects because of coexisting physical disorders. Adherence problems are more likely among older people, who may have difficulty understanding, seeing, or remembering instructions.In general, medications are not seen as helpful in specific phobia, but a benzodiazepine is sometimes used to help resolve acute episodes. In 2007, data were sparse for efficacy of any drug. Cannabis As of 2019, there is little evidence for cannabis in treating anxiety disorders. Children Both therapy and a number of medications have been found to be useful for treating childhood anxiety disorders. Therapy is generally preferred to medication.Cognitive behavioral therapy (CBT) is a good first therapy approach. Studies have gathered substantial evidence for treatments that are not CBT-based as being effective forms of treatment, expanding treatment options for those who do not respond to CBT. Although studies have demonstrated the effectiveness of CBT for anxiety disorders in children and adolescents, evidence that it is more effective than treatment as usual, medication, or wait list controls is inconclusive. Like adults, children may undergo psychotherapy, cognitive-behavioral therapy, or counseling. Family therapy is a form of treatment in which the child meets with a therapist together with the primary guardians and siblings. Each family member may attend individual therapy, but family therapy is typically a form of group therapy. Art and play therapy are also used. Art therapy is most commonly used when the child will not or cannot verbally communicate, due to trauma or a disability in which they are nonverbal. Participating in art activities allows the child to express what they otherwise may not be able to communicate to others. In play therapy, the child is allowed to play however they please as a therapist observes them. The therapist may intercede from time to time with a question, comment, or suggestion. This is often most effective when the family of the child plays a role in the treatment.If a medication option is warranted, antidepressants such as SSRIs and SNRIs can be effective. Fluvoxamine is effective in treating a range of anxiety disorders in children and adolescents. Minor side effects with medications, however, are common. Epidemiology Globally, as of 2010, approximately 273 million (4.5% of the population) had an anxiety disorder. It is more common in females (5.2%) than males (2.8%).In Europe, Africa and Asia, lifetime rates of anxiety disorders are between 9 and 16%, and yearly rates are between 4 and 7%. In the United States, the lifetime prevalence of anxiety disorders is about 29% and between 11 and 18% of adults have the condition in a given year. This difference is affected by the range of ways in which different cultures interpret anxiety symptoms and what they consider to be normative behavior. In general, anxiety disorders represent the most prevalent psychiatric condition in the United States, outside of substance use disorder.Like adults, children can experience anxiety disorders; between 10 and 20 percent of all children will develop a full-fledged anxiety disorder prior to the age of 18, making anxiety the most common mental health issue in young people. Anxiety disorders in children are often more challenging to identify than their adult counterparts, owing to the difficulty many parents face in discerning them from normal childhood fears. Likewise, anxiety in children is sometimes misdiagnosed as attention deficit hyperactivity disorder or, due to the tendency of children to interpret their emotions physically (as stomachaches, headaches, etc.), anxiety disorders may initially be confused with physical ailments.Anxiety in children has a variety of causes; sometimes anxiety is rooted in biology, and may be a product of another existing condition, such as autism spectrum disorder. Gifted children are also often more prone to excessive anxiety than non-gifted children. Other cases of anxiety arise from the child having experienced a traumatic event of some kind, and in some cases, the cause of the childs anxiety cannot be pinpointed.Anxiety in children tends to manifest along age-appropriate themes, such as fear of going to school (not related to bullying) or not performing well enough at school, fear of social rejection, fear of something happening to loved ones, etc. What separates disordered anxiety from normal childhood anxiety is the duration and intensity of the fears involved. See also List of people with an anxiety disorder Exposure Therapy Mixed anxiety–depressive disorder References External links Support Group Providers for Anxiety disorder at Curlie

What does Seizure mean Aarogya

Seizure

An epileptic seizure, informally known as a seizure, is a period of symptoms due to abnormally excessive or synchronous neuronal activity in the brain. Outward effects vary from uncontrolled shaking movements involving much of the body with loss of consciousness (tonic-clonic seizure), to shaking movements involving only part of the body with variable levels of consciousness (focal seizure), to a subtle momentary loss of awareness (absence seizure). Most of the time these episodes last less than two minutes and it takes some time to return to normal. Loss of bladder control may occur.Seizures may be provoked and unprovoked. Provoked seizures are due to a temporary event such as low blood sugar, alcohol withdrawal, abusing alcohol together with prescription medication, low blood sodium, fever, brain infection, or concussion. Unprovoked seizures occur without a known or fixable cause such that ongoing seizures are likely. Unprovoked seizures may be exacerbated by stress or sleep deprivation. Epilepsy describes brain disease in which there has been at least one unprovoked seizure and where there is a high risk of additional seizures in the future. Conditions that look like epileptic seizures but are not include: fainting, nonepileptic psychogenic seizure and tremor.A seizure that lasts for more than a brief period is a medical emergency. Any seizure lasting longer than five minutes should be treated as status epilepticus. A first seizure generally does not require long-term treatment with anti-seizure medications unless a specific problem is found on electroencephalogram (EEG) or brain imaging. Typically it is safe to complete the work-up following a single seizure as an outpatient. In many, with what appears to be a first seizure, other minor seizures have previously occurred.Up to 10% of people have at least one epileptic seizure. Provoked seizures occur in about 3.5 per 10,000 people a year while unprovoked seizures occur in about 4.2 per 10,000 people a year. After one seizure, the chance of experiencing a second is about 50%. Epilepsy affects about 1% of the population at any given time with about 4% of the population affected at some point in time. Many places require people to stop driving until they have not had a seizure for a specific period. Signs and symptoms The signs and symptoms of seizures vary depending on the type. The most common and stereotypical type of seizure is convulsive (60%), typically called a tonic-clonic seizure. Two-thirds of these begin as focal seizures prior to developing into tonic-clonic seizures. The remaining 40% of seizures are non-convulsive, an example of which is absence seizure. When EEG monitoring shows evidence of a seizure, but no symptoms are present, it is referred to as a subclinical seizure. Focal seizures Focal seizures often begin with certain experiences, known as an aura. These may include sensory (including visual, auditory, etc.), cognitive, autonomic, olfactory or motor phenomena.In a complex partial seizure a person may appear confused or dazed and cannot respond to questions or direction.Jerking activity may start in a specific muscle group and spread to surrounding muscle groups—known as a Jacksonian march. Unusual activities that are not consciously created may occur. These are known as automatisms and include simple activities like smacking of the lips or more complex activities such as attempts to pick something up. Generalized seizures There are six main types of generalized seizures: tonic-clonic, tonic, clonic, myoclonic, absence, and atonic seizures. They all involve a loss of consciousness and typically happen without warning. Tonic-clonic seizures present with a contraction of the limbs followed by their extension, along with arching of the back for 10–30 seconds. A cry may be heard due to contraction of the chest muscles. The limbs then begin to shake in unison. After the shaking has stopped it may take 10–30 minutes for the person to return to normal. Tonic seizures produce constant contractions of the muscles. The person may turn blue if breathing is impaired. Clonic seizures involve shaking of the limbs in unison. Myoclonic seizures involve spasms of muscles in either a few areas or generalized through the body. Absence seizures can be subtle, with only a slight turn of the head or eye blinking. The person often does not fall over and may return to normal right after the seizure ends, though there may also be a period of post-ictal disorientation. Atonic seizures involve the loss of muscle activity for greater than one second. This typically occurs bilaterally (on both sides of the body). Duration A seizure can last from a few seconds to more than five minutes, at which point it is known as status epilepticus. Most tonic-clonic seizures last less than two or three minutes. Absence seizures are usually around 10 seconds in duration. Postictal After the active portion of a seizure, there is typically a period of confusion called the postictal period before a normal level of consciousness returns. This usually lasts 3 to 15 minutes but may last for hours. Other common symptoms include: feeling tired, headache, difficulty speaking, and abnormal behavior. Psychosis after a seizure is relatively common, occurring in between 6 and 10% of people. Often people do not remember what occurred during this time. Causes Seizures have a number of causes. Of those who have a seizure, about 25% have epilepsy. A number of conditions are associated with seizures but are not epilepsy including: most febrile seizures and those that occur around an acute infection, stroke, or toxicity. These seizures are known as "acute symptomatic" or "provoked" seizures and are part of the seizure-related disorders. In many the cause is unknown. Different causes of seizures are common in certain age groups. Seizures in babies are most commonly caused by hypoxic ischemic encephalopathy, central nervous system (CNS) infections, trauma, congenital CNS abnormalities, and metabolic disorders. The most frequent cause of seizures in children is febrile seizures, which happen in 2–5% of children between the ages of six months and five years. During childhood, well-defined epilepsy syndromes are generally seen. In adolescence and young adulthood, non-compliance with the medication regimen and sleep deprivation are potential triggers. Pregnancy and labor and childbirth, and the post-partum, or post-natal period (after birth) can be at-risk times, especially if there are certain complications like pre-eclampsia. During adulthood, the likely causes are alcohol related, strokes, trauma, CNS infections, and brain tumors. In older adults, cerebrovascular disease is a very common cause. Other causes are CNS tumors, head trauma, and other degenerative diseases that are common in the older age group, such as dementia. Metabolic Dehydration can trigger epileptic seizures if it is severe enough. A number of disorders including: low blood sugar, low blood sodium, hyperosmolar nonketotic hyperglycemia, high blood sodium, low blood calcium and high blood urea levels may cause seizures. As may hepatic encephalopathy and the genetic disorder porphyria. Structural Cavernoma or cavernous malformation is a treatable medical condition that can cause seizures, headaches, and brain hemorrhages. Arteriovenous malformation (AVM) is a treatable medical condition that can cause seizures, headaches, and brain hemorrhages. Space-occupying lesions in the brain (abscesses, tumours). In people with brain tumours, the frequency of epilepsy depends on the location of the tumor in the cortical region. Medications Both medication and drug overdoses can result in seizures, as may certain medication and drug withdrawal. Common drugs involved include: antidepressants, antipsychotics, cocaine, insulin, and the local anaesthetic lidocaine. Difficulties with withdrawal seizures commonly occurs after prolonged alcohol or sedative use, a condition known as delirium tremens. In people who are at risk of developing epileptic seizures, common herbal medicines such as ephedra, ginkgo biloba and wormwood can provoke seizures. Infections Infection with the pork tapeworm, which can cause neurocysticercosis, is the cause of up to half of epilepsy cases in areas of the world where the parasite is common. Parasitic infections such as cerebral malaria. In Nigeria this is one of the most common causes of seizures among children under five years of age. Infection, such as encephalitis or meningitis Stress Stress can induce seizures in people with epilepsy, and is a risk factor for developing epilepsy. Severity, duration, and time at which stress occurs during development all contribute to frequency and susceptibility to developing epilepsy. It is one of the most frequently self-reported triggers in patients with epilepsy.Stress exposure results in hormone release that mediates its effects in the brain. These hormones act on both excitatory and inhibitory neural synapses, resulting in hyper-excitability of neurons in the brain. The hippocampus is known to be a region that is highly sensitive to stress and prone to seizures. This is where mediators of stress interact with their target receptors to produce effects. Other Seizures may occur as a result of high blood pressure, known as hypertensive encephalopathy, or in pregnancy as eclampsia when accompanied by either seizures or a decreased level of consciousness. Very high body temperatures may also be a cause. Typically this requires a temperature greater than 42 °C (107.6 °F). Head injury may cause non-epileptic post-traumatic seizures or post-traumatic epilepsy About 3.5 to 5.5% of people with celiac disease also have seizures. Seizures in a person with a shunt may indicate failure Hemorrhagic stroke can occasionally present with seizures, embolic strokes generally do not (though epilepsy is a common later complication); cerebral venous sinus thrombosis, a rare type of stroke, is more likely to be accompanied by seizures than other types of stroke Multiple sclerosis may cause seizures Electroconvulsive therapy (ECT) deliberately sets out to induce a seizure for the treatment of major depression. Reflex seizure induced by a specific stimulus or trigger (extrinsic or intrinsic stimuli) Mechanism Normally, brain electrical activity is non-synchronous. In epileptic seizures, due to problems within the brain, a group of neurons begin firing in an abnormal, excessive, and synchronized manner. This results in a wave of depolarization known as a paroxysmal depolarizing shift.Normally after an excitatory neuron fires it becomes more resistant to firing for a period of time. This is due in part from the effect of inhibitory neurons, electrical changes within the excitatory neuron, and the negative effects of adenosine. In epilepsy the resistance of excitatory neurons to fire during this period is decreased. This may occur due to changes in ion channels or inhibitory neurons not functioning properly. Forty-one ion-channel genes and over 1,600 ion-channel mutations have been implicated in the development of epileptic seizure. These ion channel mutations tend to confer a depolarized resting state to neurons resulting in pathological hyper-excitability. This long-lasting depolarization in individual neurons is due to an influx of Ca2+ from outside of the cell and leads to extended opening of Na+ channels and repetitive action potentials. The following hyperpolarization is facilitated by γ-aminobutyric acid (GABA) receptors or potassium (K+) channels, depending on the type of cell. Equally important in epileptic neuronal hyper-excitability, is the reduction in the activity of inhibitory GABAergic neurons, an effect known as disinhibition. Disinhibition may result from inhibitory neuron loss, dysregulation of axonal sprouting from the inhibitory neurons in regions of neuronal damage, or abnormal GABAergic signaling within the inhibitory neuron. Neuronal hyper-excitability results in a specific area from which seizures may develop, known as a "seizure focus". Following an injury to the brain, another mechanism of epilepsy may be the up regulation of excitatory circuits or down regulation of inhibitory circuits. These secondary epilepsies occur through processes known as epileptogenesis. Failure of the blood–brain barrier may also be a causal mechanism. While blood-brain barrier disruption alone does appear to cause epileptogenesis, it has been correlated to increased seizure activity. Furthermore, it has been implicated in chronic epileptic conditions through experiments inducing barrier permeability with chemical compounds. Disruption may lead to fluid leaking out of the blood vessels into the area between cells and driving epileptic seizures. Preliminary findings of blood proteins in the brain after a seizure support this theory.Focal seizures begin in one hemisphere of the brain while generalized seizures begin in both hemispheres. Some types of seizures may change brain structure, while others appear to have little effect. Gliosis, neuronal loss, and atrophy of specific areas of the brain are linked to epilepsy but it is unclear if epilepsy causes these changes or if these changes result in epilepsy.Seizure activity may be propagated through the brains endogenous electrical fields. Proposed mechanisms that may cause the spread and recruitment of neurons include an increase in K+ from outside the cell, and increase of Ca2+ in the presynaptic terminals. These mechanisms blunt hyperpolarization and depolarizes nearby neurons, as well as increasing neurotransmitter release. Diagnosis Seizures may be divided into provoked and unprovoked. Provoked seizures may also be known as "acute symptomatic seizures" or "reactive seizures". Unprovoked seizures may also be known as "reflex seizures". Depending on the presumed cause blood tests and lumbar puncture may be useful. Hypoglycemia may cause seizures and should be ruled out. An electroencephalogram and brain imaging with CT scan or MRI scan is recommended in the work-up of seizures not associated with a fever. Classification Seizure types are organized by whether the source of the seizure is localized (focal seizures) or distributed (generalized seizures) within the brain. Generalized seizures are divided according to the effect on the body and include tonic-clonic (grand mal), absence (petit mal), myoclonic, clonic, tonic, and atonic seizures. Some seizures such as epileptic spasms are of an unknown type.Focal seizures (previously called partial seizures) are divided into simple partial or complex partial seizure. Current practice no longer recommends this, and instead prefers to describe what occurs during a seizure.The classification of seizures can also be made according to dynamical criteria, observable in electrophysiological measurements. It is a classification according to their type of onset and offset. Physical examination Most people are in a postictal state (drowsy or confused) following a seizure. They may show signs of other injuries. A bite mark on the side of the tongue helps confirm a seizure when present, but only a third of people who have had a seizure have such a bite. When present in people thought to have had a seizure, this physical sign tentatively increases the likelihood that a seizure was the cause. Tests An electroencephalography is only recommended in those who likely had an epileptic seizure and may help determine the type of seizure or syndrome present. In children it is typically only needed after a second seizure. It cannot be used to rule out the diagnosis and may be falsely positive in those without the disease. In certain situations it may be useful to prefer the EEG while sleeping or sleep deprived.Diagnostic imaging by CT scan and MRI is recommended after a first non-febrile seizure to detect structural problems inside the brain. MRI is generally a better imaging test except when intracranial bleeding is suspected. Imaging may be done at a later point in time in those who return to their normal selves while in the emergency room. If a person has a previous diagnosis of epilepsy with previous imaging repeat imaging is not usually needed with subsequent seizures.In adults, testing electrolytes, blood glucose and calcium levels is important to rule these out as causes, as is an electrocardiogram. A lumbar puncture may be useful to diagnose a central nervous system infection but is not routinely needed. Routine antiseizure medical levels in the blood are not required in adults or children. In children additional tests may be required.A high blood prolactin level within the first 20 minutes following a seizure may be useful to confirm an epileptic seizure as opposed to psychogenic non-epileptic seizure. Serum prolactin level is less useful for detecting partial seizures. If it is normal an epileptic seizure is still possible and a serum prolactin does not separate epileptic seizures from syncope. It is not recommended as a routine part of diagnosis epilepsy. Differential diagnosis Differentiating an epileptic seizure from other conditions such as syncope can be difficult. Other possible conditions that can mimic a seizure include: decerebrate posturing, psychogenic seizures, tetanus, dystonia, migraine headaches, and strychnine poisoning. In addition, 5% of people with a positive tilt table test may have seizure-like activity that seems due to cerebral hypoxia. Convulsions may occur due to psychological reasons and this is known as a psychogenic non-epileptic seizure. Non-epileptic seizures may also occur due to a number of other reasons. Prevention A number of measures have been attempted to prevent seizures in those at risk. Following traumatic brain injury anticonvulsants decrease the risk of early seizures but not late seizures.In those with a history of febrile seizures, some medications (both antipyretics and anticonvulsants) have been found effective for reducing reoccurrence, however due to the frequency of adverse effects and the benign nature of febrile seizures the decision to use medication should be weighted carefully against potential negative effects.There is no clear evidence that antiepileptic drugs are effective or not effective at preventing seizures following a craniotomy, following subdural hematoma, after a stroke, or after subarachnoid haemorrhage, for both people who have had a previous seizure, and those who have not. Management Potentially sharp or dangerous objects should be moved from the area around a person experiencing a seizure so that the individual is not hurt. After the seizure, if the person is not fully conscious and alert, they should be placed in the recovery position. A seizure longer than five minutes, or two or more seizures occurring within the time of five minutes is a medical emergency known as status epilepticus. Contrary to a common misconception, bystanders should not attempt to force objects into the mouth of the person having a seizure, as doing so may cause injury to the teeth and gums.Treatments of a person that is actively seizing follows a progression from initial response, through first line, second line, and third line treatments. The initial response involves ensuring the person is protected from potential harms (such as nearby objects) and managing their airway, breathing, and circulation. Airway management should include placing the person on their side, known as the recovery position, to prevent them from choking. If they are unable to breathe because something is blocking their airway, they may require treatments to open their airway. Medication The first line medication for an actively seizing person is a benzodiazepine, with most guidelines recommending lorazepam. Diazepam and midazolam are alternatives. This may be repeated if there is no effect after 10 minutes. If there is no effect after two doses, barbiturates or propofol may be used.Second-line therapy for adults is phenytoin or fosphenytoin and phenobarbital for children. Third-line medications include phenytoin for children and phenobarbital for adults.Ongoing anti-epileptic medications are not typically recommended after a first seizure except in those with structural lesions in the brain. They are generally recommended after a second one has occurred. Approximately 70% of people can obtain full control with continuous use of medication. Typically one type of anticonvulsant is preferred. Following a first seizure, while immediate treatment with an anti-seizure drug lowers the probability of seizure recurrence up to five years it does not change the risk of death and there are potential side effects.In seizures related to toxins, up to two doses of benzodiazepines should be used. If this is not effective pyridoxine is recommended. Phenytoin should generally not be used.There is a lack of evidence for preventive anti-epileptic medications in the management of seizures related to intracranial venous thrombosis. Other Helmets may be used to provide protection to the head during a seizure. Some claim that seizure response dogs, a form of service dog, can predict seizures. Evidence for this, however, is poor. At present there is not enough evidence to support the use of cannabis for the management of seizures, although this is an ongoing area of research. There is low quality evidence that a ketogenic diet may help in those who have epilepsy and is reasonable in those who do not improve following typical treatments. Prognosis Following a first seizure, the risk of more seizures in the next two years is 40–50%. The greatest predictors of more seizures are problems either on the electroencephalogram or on imaging of the brain. In adults, after 6 months of being seizure-free after a first seizure, the risk of a subsequent seizure in the next year is less than 20% regardless of treatment. Up to 7% of seizures that present to the emergency department (ER) are in status epilepticus. In those with a status epilepticus, mortality is between 10% and 40%. Those who have a seizure that is provoked (occurring close in time to an acute brain event or toxic exposure) have a low risk of re-occurrence, but have a higher risk of death compared to those with epilepsy. Epidemiology Approximately 8–10% of people will experience an epileptic seizure during their lifetime. In adults, the risk of seizure recurrence within the five years following a new-onset seizure is 35%; the risk rises to 75% in persons who have had a second seizure. In children, the risk of seizure recurrence within the five years following a single unprovoked seizure is about 50%; the risk rises to about 80% after two unprovoked seizures. In the United States in 2011, seizures resulted in an estimated 1.6 million emergency department visits; approximately 400,000 of these visits were for new-onset seizures. The exact incidence of epileptic seizures in low-income and middle-income countries is unknown, however it probably exceeds that in high-income countries. This may be due to increased risks of traffic accidents, birth injuries, and malaria and other parasitic infections. History Epileptic seizures were first described in an Akkadian text from 2000 B.C. Early reports of epilepsy often saw seizures and convulsions as the work of "evil spirits". The perception of epilepsy, however, began to change in the time of Ancient Greek medicine. The term "epilepsy" itself is a Greek word, which is derived from the verb "epilambanein", meaning "to seize, possess, or afflict". Although the Ancient Greeks referred to epilepsy as the "sacred disease", this perception of epilepsy as a "spiritual" disease was challenged by Hippocrates in his work On the Sacred Disease, who proposed that the source of epilepsy was from natural causes rather than supernatural ones.Early surgical treatment of epilepsy was primitive in Ancient Greek, Roman and Egyptian medicine. The 19th century saw the rise of targeted surgery for the treatment of epileptic seizures, beginning in 1886 with localized resections performed by Sir Victor Horsley, a neurosurgeon in London. Another advancement was that of the development by the Montreal procedure by Canadian neurosurgeon Wilder Penfield, which involved use of electrical stimulation among conscious patients to more accurately identify and resect the epileptic areas in the brain. Society and culture Economics Seizures result in direct economic costs of about one billion dollars in the United States. Epilepsy results in economic costs in Europe of around €15.5 billion in 2004. In India, epilepsy is estimated to result in costs of US$1.7 billion or 0.5% of the GDP. They make up about 1% of emergency department visits (2% for emergency departments for children) in the United States. Driving Many areas of the world require a minimum of six months from the last seizure before people can drive a vehicle. Research Scientific work into the prediction of epileptic seizures began in the 1970s. Several techniques and methods have been proposed, but evidence regarding their usefulness is still lacking.Two promising areas include gene therapy, and seizure detection and seizure prediction.Gene therapy for epilepsy consists of employing vectors to deliver pieces of genetic material to areas of the brain involved in seizure onset.Seizure prediction is a special case of seizure detection in which the developed systems is able to issue a warning before the clinical onset of the epileptic seizure.Computational neuroscience has been able to bring a new point of view on the seizures by considering the dynamical aspects. References External links Seizure at Curlie

Hi Aarogya, explain a situation where Localized hypertrichosis occurs

Localized hypertrichosis

Localized hypertrichosis may refer to: Localized acquired hypertrichosis Localized congenital hypertrichosisSee also: Hypertrichosis

Aarogya, can you share information about a health condition involving Bacteriuria

Bacteriuria

Bacteriuria is the presence of bacteria in urine. Bacteriuria accompanied by symptoms is a urinary tract infection while that without is known as asymptomatic bacteriuria. Diagnosis is by urinalysis or urine culture. Escherichia coli is the most common bacterium found. People without symptoms should generally not be tested for the condition. Differential diagnosis include contamination.If symptoms are present treatment is generally with antibiotics. Bacteriuria without symptoms generally does not require treatment. Exceptions may include pregnant women, those who have had a recent kidney transplant, young children with significant vesicoureteral reflux, and those undergoing surgery of the urinary tract.Bacteriuria without symptoms is present in about 3% of otherwise healthy middle aged women. In nursing homes rates are as high as 50% among women and 40% in men. In those with a long term indwelling urinary catheter rates are 100%. Up to 10% of women have a urinary tract infection in a given year and half of all women have at least one infection at some point in their lives. There is an increased risk of asymptomatic or symptomatic bacteriuria in pregnancy due to physiological changes that occur in a pregnant women which promotes unwanted pathogen growth in the urinary tract. Signs and symptoms Asymptomatic Asymptomatic bacteriuria is bacteriuria without accompanying symptoms of a urinary tract infection and is commonly caused by the bacterium Escherichia coli. Other potential pathogens are Klebsiella spp., and group B streptococci. It is more common in women, in the elderly, in residents of long-term care facilities, and in people with diabetes, bladder catheters, and spinal cord injuries. People with a long-term Foley catheter always show bacteriuria. Chronic asymptomatic bacteriuria occurs in as many as 50% of the population in long-term care.There is an association between asymptomatic bacteriuria in pregnant women with low birth weight, preterm delivery, cystitis, infection of the newborn and fetus death. However, most of these studies were graded as poor quality. Bacteriuria in pregnancy also increases the risk of preeclampsia. Symptomatic Symptomatic bacteriuria is bacteriuria with the accompanying symptoms of a urinary tract infection (such as frequent urination, painful urination, fever, back pain, abdominal pain and blood in the urine) and includes pyelonephritis or cystitis. The most common cause of urinary tract infections is Escherichia coli. Diagnosis Testing for bacteriuria is usually performed in people with symptoms of a urinary tract infection. Certain populations that cannot feel or express symptoms of infection are also tested when showing nonspecific symptoms. For example, confusion or other changes in behaviour can be a sign of an infection in the elderly. Screening for asymptomatic bacteriuria in pregnancy is a common routine in many countries, but controversial. The gold standard for detecting bacteriuria is a bacterial culture which identifies the concentration of bacterial cells in the urine. The culture is usually combined with subsequent testing using biochemical methods or MALDI-TOF, which allows to identify the causal bacterial species, and antibiotic susceptibility testing. Urine culture is quantitative and very reliable, but can take at least one day to obtain a result and it is expensive.Miniaturization of bacterial culture within dipstick format, Digital Dipstick, allows bacterial detection, identification and quantification for bacteriuria within 10–12 hours at the point-of-care. Clinicians will often treat symptomatic bacteriuria based on the results of the urine dipstick test while waiting for the culture results. Bacteriuria can usually be detected using a urine dipstick test. The nitrite test detects nitrate-reducing bacteria if growing in high numbers in urine. A negative dipstick test does not exclude bacteriuria, as not all bacteria which can colonise the urinary tract are nitrate-reducing. The leukocyte esterase test indirectly detects the presence of leukocytes (white blood cells) in urine which can be associated with a urinary tract infection. In the elderly, the leukocyte esterase test is often positive even in the absence of an infection. The urine dipstick test is readily available and provides fast, but often unreliable results. Microscopy can also be used to detect bacteriuria. It is rarely used in clinical routine since it requires more time and equipment and does not allow reliable identification or quantification of the causal bacterial species.Bacteriuria is assumed if a single bacterial species is isolated in a concentration greater than 100,000 colony forming units per millilitre of urine in clean-catch midstream urine specimens. In urine samples obtained from women, there is a risk for bacterial contamination from the vaginal flora. Therefore, in research, usually a second specimen is analysed to confirm asymptomatic bacteriuria in women. For urine collected via bladder catheterization in men and women, a single urine specimen with greater than 100,000 colony forming units of a single species per millilitre is considered diagnostic. The threshold for women displaying UTI symptoms can be as low as 100 colony forming units of a single species per millilitre. However, bacteria below a threshold of 10000 colony forming units per millilitre are usually reported as "no growth" by clinical laboratories.Using special techniques certain non-disease causing bacteria have also been found in the urine of healthy people. These are part of the resident microbiota. Screening Although controversial, many countries including the United States recommend a one time screening for bacteriuria during mid pregnancy. The screening method is by urine culture. Screening non-pregnant adults is recommended against by the United States Preventive Task Force. Treatment The decision to treat bacteriuria depends on the presence of accompanying symptoms and comorbidities. Asymptomatic Asymptomatic bacteriuria generally does not require treatment. Exceptions include those undergoing surgery of the urinary tract, children with vesicoureteral reflux or others with structural abnormalities of the urinary tract. In many countries, regional guidelines recommend treatment of pregnant women.There is no indication to treat asymptomatic bacteriuria in diabetics, renal transplant recipients, and in those with spinal cord injuries.The overuse of antibiotics to treat asymptomatic bacteriuria has many adverse effects such as an increased risk of diarrhea, the spread of antimicrobial resistance, and infection due to Clostridium difficile. Symptomatic Symptomatic bacteriuria is synonymous with urinary tract infection and typically treated with antibiotics. Common choices include nitrofurantoin and trimethoprim/sulfamethoxazole. Epidemiology References == External links ==

Hi Aarogya , Do you know what is Justifiable homicide,

Justifiable homicide

The concept of justifiable homicide in criminal law is a defense to culpable homicide (criminal or negligent homicide). Generally, there is a burden of production of exculpatory evidence in the legal defense of justification. In most countries, a homicide is justified when there is sufficient evidence to disprove (under the "beyond a reasonable doubt" standard for criminal charges, and "preponderance of evidence" standard for claims of wrongdoing, i.e. civil liability) the alleged criminal act or wrongdoing. The key to this legal defense is that it was reasonable for the subject to believe that there was an imminent and otherwise unavoidable danger of death or grave bodily harm to the innocent by the deceased when they committed the homicide. A homicide in this instance is blameless. Common excusing conditions Potentially excusing conditions common to multiple jurisdictions include the following. Capital punishment in places that it is legal. Where a state is engaged in a war with a legitimate casus belli, a combatant may lawfully kill an enemy combatant so long as that combatant is not hors de combat. This principle is embedded in public international law and has been respected by most states around the world. In most countries, it is lawful for a citizen to repel violence with violence to protect someones life or destruction of property.The scope of self-defense varies; some jurisdictions have a duty to retreat rule that disallows this defense if it was safe to flee from potential violence. In some jurisdictions, the castle doctrine allows the use of deadly force in self-defense against an intruder in ones home. Other jurisdictions have stand-your-ground laws that allow use of deadly force in self-defense in a vehicle or in public, without a duty to retreat. Where the persons death is inflicted by the effecting of lawful arrest or prevention of lawfully detained persons escape, quelling riot or insurrection when the use of force is "no more than absolutely necessary". The doctrine of necessity allows, for example, a surgeon to separate conjoined twins, killing the weaker twin to allow the stronger twin to survive. (This is not recognized, for example, in England and Wales). In the United States, the 2005 Unborn Victims of Violence Act changed the legal definition of human fetuses to "unborn children", formally defining feticide as murder (under USC §1111). However, the law retains explicit exceptions which prohibit the prosecution "of any person for conduct relating to an abortion," "of any person for any medical treatment," or "of any woman with respect to her unborn child," thereby preserving the right to an abortion stemming from Roe v. Wade. However, Roe v. Wade was overturned in 2022 by Dobbs v. Jackson Womens Health Organization. Several countries, such as the Netherlands, Belgium, Switzerland, Japan, Canada, and the U.S. states of Oregon and Washington allow both active and passive euthanasia by law, if justified. The "heat of the moment" defense for crimes of passion: death results from a situation where the defendant is deemed to have lost control. This may be considered a part of the defense of provocation against charges of murder. Based on the idea that all individuals may suddenly and unexpectedly lose control when words are spoken or events occur, jurisdictions differ on whether this should be allowed to excuse liability or merely mitigate to a lesser offense such as manslaughter, and under which circumstances this defense can be used. In many common law jurisdictions, provocation is a partial defense that converts what would have been murder into manslaughter. A few jurisdictions do not prosecute (Iran, Iraq) or have a lesser penalty (Kuwait, Egypt) for honor killings. European Convention on Human Rights Article 2 Paragraph 2 of the European Convention On Human Rights provides that death resulted from defending oneself or others, arresting a suspect or fugitive, or suppressing riots or insurrections, will not contravene the Article when the use of force involved is "no more than absolutely necessary": 2. Deprivation of life shall not be regarded as inflicted in contravention of this Article when it results from the use of force which is no more than absolutely necessary: (a) in defence of any person from unlawful violence; (b) in order to effect a lawful arrest or to prevent the escape of a person lawfully detained; (c) in action lawfully taken for the purpose of quelling a riot or insurrection. Example of Criminal Procedure Act in South Africa In South Africa, §49 Criminal Procedure Act used to provide: (2) Where the person concerned is to be arrested for an offense referred to in Schedule 1 or is to be arrested on the ground of having committed such an offense, and the person authorized under this Act to arrest or to assist in arresting him cannot arrest him or prevent him from fleeing by other means than killing him, the killing shall be deemed to be justifiable homicide. This has now been amended by §7 Judicial Matters Second Amendment Act 122 of 1998: (2) If any arrestor attempts to arrest a suspect and the suspect resists the attempt, or flees, or resists the attempt and flees, when it is clear that an attempt to arrest him or her is being made, and the suspect cannot be arrested without the use of force, the arrestor may, in order to effect the arrest, use such force as may be reasonably necessary and proportional in the circumstances to overcome resistance or to prevent the suspect from fleeing: Provided that the arrester is justified in terms of this section in using deadly force that is intended or is likely to cause death or grievous bodily harm to a suspect, only if he believes on reasonable grounds- (a) that the force is immediately necessary for the purpose of protecting the arrestor, any person lawfully assisting the arrestor or any other person from imminent or future death or grievous bodily harm; (b) that there is a substantial risk that the suspect will cause imminent or future death or grievous bodily harm if the arrest is delayed; or (c) that the offence for which the arrest is sought is in progress and is of a forcible and serious nature and involves the use of life threatening violence or a strong likelihood that it will cause grievous bodily harm. Circumstances which justify homicide in the United States A non-criminal homicide ruling, usually committed in self-defense or in defense of another, exists under United States law. A homicide may be considered justified if it is done to prevent a very serious crime, such as rape, armed robbery, manslaughter or murder. The victim must reasonably believe, under the totality of the circumstances, that the assailant intended to commit a criminal act that would likely result in the death or life-threatening injury of an innocent person. A homicide performed out of vengeance, or retribution for action in the past, or in pursuit of a "fleeing felon" (except under specific circumstances) would not be considered justifiable. In many states, given a case of self-defense, the defendant is expected to obey a duty to retreat if it is possible to do so. In the states of Alabama, Alaska, Arizona, California, Colorado, Connecticut, Florida, Georgia, Hawaii, Indiana, Kansas, Kentucky, Louisiana, Maine, Maryland, Massachusetts, Michigan, Mississippi, Missouri, Montana, New Jersey, North Carolina, Ohio, Oklahoma, Oregon, Pennsylvania, Rhode Island, South Carolina, Tennessee, Texas, West Virginia, Washington, Wyoming and other Castle Doctrine states, there is no duty to retreat in certain situations (depending on the state, this may apply to ones home, business, or vehicle, or to any public place where a person is lawfully present). Preemptive self-defense, in which one kills another on suspicion that the victim might eventually become dangerous, is not justifiable. In the U.S. Supreme Court ruling of District of Columbia v. Heller, the majority held that the Constitution protected the right to the possession of firearms for the purpose of self-defense "and to use that arm for traditionally lawful purposes, such as self-defense within the home".Two other forms of justifiable homicide are unique to the prison system: the death penalty and preventing prisoners from escaping. To quote the California State Penal Code (state law) that covers justifiable homicide: 196. Homicide is justifiable when committed by public officers and those acting by their command in their aid and assistance, either--1. In obedience to any judgment of a competent Court; or,2. When necessarily committed in overcoming actual resistance to the execution of some legal process, or in the discharge of any other legal duty; or3. When necessarily committed in retaking felons who have been rescued or have escaped, or when necessarily committed in arresting persons charged with felony, and who are fleeing from justice or resisting such arrest.Although the above text is from California law, many other jurisdictions, like Florida, have similar laws to prevent escapes from custody. Examples include self defense, prevention of criminal act, trespassers, and defense of another person. Notable cases involving justifiable homicide Killing of MaKhia Bryant. Her shooting, which prevented her from stabbing another girl, was later deemed a justifiable homicide with prosecutors noting "Under Ohio law the use of deadly force by a police officer is justified when there exists an immediate or imminent threat of death or serious bodily injury to the officer or another." Sam Cooke. After an inquest and investigation, the courts ruled Cookes death to be a justifiable homicide. John Dillinger. When BOI agents moved to arrest Dillinger as he exited the theater, he tried to flee. He was shot in the back; the deadly shot was ruled justifiable homicide. Fred Hampton. In January 1970, the Cook County Coroner held an inquest; the jury concluded that Hamptons and Clarks deaths were justifiable homicides. George Jackson (activist). Miller had not been charged with any crime, as a grand jury ruled his actions during the prison fight justifiable homicide. Don King. In 1954, King shot a man in the back after spotting him trying to rob one of his gambling houses; this incident was ruled a justifiable homicide. Killing of Sara-Nicole Morales. In 2021 Morales confronted several motorists who had followed her to her Florida home following a road rage incident. After she brandished a pistol at them from her front lawn, a motorcyclist she had deliberately struck with her vehicle during the road-range incident drew his own legally carried weapon and shot her several times; she died shortly after arrival at a local hospital. Police declined to file charges several months later. Eadweard Muybridge. In 1874, Muybridge shot and killed Major Harry Larkyns, his wifes lover, but was acquitted in a controversial jury trial, on the grounds of justifiable homicide. Johnny Stompanato homicide. After four hours of testimony and approximately 25 minutes of deliberation, the jury deemed Stompanatos killing a justifiable homicide. Further reading Omphemetse S. "Use of Deadly Force by the South African Police Services Re-visited". == References ==

Hey Aarogya, explain a scenario commonly referred as Birth injury

Birth injury

Birth injury refers to damage or injury to the child before, during, or just after the birthing process. "Birth trauma" refers specifically to mechanical damage sustained during delivery (such as nerve damage and broken bones).The term "birth injury" may be used in two different ways: the ICD-10 uses "birth injury" and "birth trauma" interchangeably to refer to mechanical injuries sustained during delivery; the legal community uses "birth injury" to refer to any damage or injury sustained during pregnancy, during delivery, or just after delivery, including injuries caused by trauma.Birth injuries must be distinguished from birth defects. "Birth defect" refers to damage that occurs while the fetus is in the womb, which may be caused by genetic mutations, infections, or exposure to toxins. There are more than 4,000 types of birth defects. Causes Difficult labor (dystocia) Difficult labor, also known as dystocia or obstructed labor, occurs when the child cannot easily pass through the birth canal. This can result in fetal distress or physical trauma to the child, especially broken clavicles and damage to the brachial plexus nerves. It can also deprive the child of oxygen as the umbilical cord is pinched, potentially causing brain damage or death.Difficult labor may occur because the baby is abnormally large (macrosomia), because the mothers pelvis or birth canal is small or deformed, or because the baby is in an abnormal presentation for the birth (such as breech or transverse presentation). External causes Fetal malformations and birth injuries may occur as a result of exposure to environmental toxins such as mercury or lead. Many medications can also affect the development of the fetus, as can alcohol, tobacco, and illicit drugs.See Environmental toxins and fetal development. See Drugs in pregnancy. Genetic mutations Genetic mutations can cause a wide variety of fetal malformations, ranging from relatively mild cleft lips to severe and even fatal deformities. Infection Maternal infection may be transmitted to the fetus; this is called a vertically transmitted infection. The fetus has a weak immune system, so infections that are relatively minor in adults can be very serious in a developing fetus. In addition, some studies suggest that maternal infections increase the risk of neurodevelopmental disorders, including schizophrenia, in the child. Intrauterine hypoxia Intrauterine hypoxia, or oxygen deprivation in the womb, can cause serious brain damage in the fetus. It most commonly occurs because of damage to or malformation of the umbilical cord or placenta. Intrauterine hypoxia can cause brain damage, including cerebral palsy and other neurological and psychiatric disorders. Maternal health issues Certain maternal health issues can cause birth injuries. Gestational diabetes can cause premature birth, macrosomia, or stillbirth. Pregnancy complications Complications such as placenta previa, placental abruption, Placenta accreta, Retained placenta, Placental insufficiency, Placental infarcts, anemia, and preeclampsia can limit the supply of oxygen and nutrients to the fetus, increasing the risk of birth defects. Severe cases may be fatal to the fetus. Common types of birth injury Brachial plexus injury The brachial plexus is the plexus of nerves that lies between the neck and axilla and controls the motion of the arm and hand. The brachial plexus may be stretched and damaged during a difficult delivery. In minor cases, the nerves heal and full use of the hand and arm is recovered. In more severe cases, the child may sustain permanent nerve damage and may not have full use of the shoulder, arm, or hand. Brachial plexus injuries occur in 1-3 children per 1,000 live births.See Erbs palsy and Klumpkes palsy. Brain damage Brain damage may be caused by a number of factors, including fetal malformation due to genetic mutation or exposure to toxins, intrauterine hypoxia, or physical trauma during delivery.Cerebral palsy is one example of brain damage incurred before or during delivery; about 10,000 children are diagnosed with cerebral palsy every year. Bruising A difficult delivery may lead to bruising, especially on the head and face, from pressure against the mothers pelvis or pressure caused by forceps or a vacuum device (see ventouse) used in delivery. Bone fractures Bone fractures can occur during a difficult delivery. Fracture of the clavicle is the most common birth injury. Meconium aspiration syndrome Meconium is a sticky substance that usually makes up the childs first bowel movement. If the fetus is stressed before or during delivery, the meconium may be released and may mix with the amniotic fluid. If it gets into the childs airways or lungs, it can cause meconium aspiration syndrome. Serious cases may result in pneumonia or a collapsed lung. Legal issues Birth injuries may be unavoidable or they may be attributable to medical malpractice. When a legal claim results, birth injury cases are a subset of medical malpractice cases. Legal claims from birth injury cases typically seek compensation for the medical costs associated with the injury, including ongoing therapeutic and medical support for the child.In order to prevail in a birth injury malpractice case, the plaintiff must show (1) that the medical care provider owed a duty to the child, (2) that the medical care provider breached that duty by failing to meet the accepted standard of care, (3) that the child sustained an injury that was caused by the medical care providers breach of duty to the child, and (4) the child sustained damages as a result of the injury. All four elements must be present in order for the plaintiff to win. == References ==

Aarogya, share information about a health condition involving Fasciolopsiasis

Fasciolopsiasis

Fasciolopsiasis results from an infection by the trematode Fasciolopsis buski, the largest intestinal fluke of humans (up to 7.5 cm in length). Signs and symptoms Most infections are light, almost asymptomatic. In heavy infections, symptoms can include abdominal pain, chronic diarrhea, anemia, ascites, toxemia, allergic responses, sensitization caused by the absorption of the worms allergenic metabolites can lead to intestinal obstruction and may eventually cause death of the patient. Cause The parasite infects an amphibic snail (Segmentina nitidella, Segmentina hemisphaerula, Hippeutis schmackerie, Gyraulus, Lymnaea, Pila, Planorbis (Indoplanorbis)) after being released by infected mammalian feces; metacercaria released from this intermediate host encyst on aquatic plants like water spinach, which are eaten raw by pigs and humans. Water itself can also be infective when drunk unboiled ("Encysted cercariae exist not only on aquatic plants, but also on the surface of the water.") Diagnosis Microscopic identification of eggs, or more rarely of the adult flukes, in the stool or vomitus is the basis of specific diagnosis. The eggs are indistinguishable from those of the very closely related Fasciola hepatica liver fluke, but that is largely inconsequential since treatment is essentially identical for both. Prevention Infection can be prevented by immersing vegetables in boiling water for a few seconds to kill the infective metacercariae, avoiding the use of untreated feces ("nightsoil") as a fertilizer, and maintenance of proper sanitation and good hygiene. Additionally, snail control should be attempted. Treatment Praziquantel is the drug of choice for treatment. Treatment is effective in early or light infections. Heavy infections are more difficult to treat. Studies of the effectiveness of various drugs for treatment of children with F. buski have shown tetrachloroethylene as capable of reducing faecal egg counts by up to 99%. Other anthelmintics that can be used include thiabendazole, mebendazole, levamisole and pyrantel pamoate. Oxyclozanide, hexachlorophene and nitroxynil are also highly effective. Epidemiology F. buski is endemic in Asia including China, Taiwan, Southeast Asia, Indonesia, Malaysia, and India. It has an up to 60% prevalence in worst-affected communities in southern and eastern India and mainland China and has an estimated 10 million human infections. Infections occur most often in school-aged children or in impoverished areas with a lack of proper sanitation systems.A study from 1950s found that F. buski was endemic in central Thailand, affecting about 2,936 people due to infected aquatic plants called water caltrops and the snail hosts which were associated with them. The infection, or the eggs which hatch in the aquatic environment, were correlated with the water pollution in different districts of Thailand such as Ayuthaya Province. The high incidence of infection was prevalent in females and children ages 10–14 years of age. References Further reading Graczyk TK, Gilman RH, Fried B (2001). "Fasciolopsiasis: is it a controllable food-borne disease?". Parasitol. Res. 87 (1): 80–3. doi:10.1007/s004360000299. PMID 11199855. S2CID 19075125. Mas-Coma S, Bargues MD, Valero MA (2005). "Fascioliasis and other plant-borne trematode zoonoses". Int. J. Parasitol. 35 (11–12): 1255–78. doi:10.1016/j.ijpara.2005.07.010. PMID 16150452. http://www.ijmm.org/text.asp?2017/35/4/551/224440 Fasciolopsiasis in children: Clinical, Sociodemographic Profile and outcome. Indian Journal of Medical Microbiology2017 vol 35, issue 4 page 551-554DOI:10.4103/ijmm.IJMM_17_7 == External links ==

Hi Aarogya, could you help me understand about Sneeze

Sneeze

A sneeze (also known as sternutation) is a semi-autonomous, convulsive expulsion of air from the lungs through the nose and mouth, usually caused by foreign particles irritating the nasal mucosa. A sneeze expels air forcibly from the mouth and nose in an explosive, spasmodic involuntary action. This action allows for mucus to escape through the nasal cavity. Sneezing is possibly linked to sudden exposure to bright light, sudden change (fall) in temperature, breeze of cold air, a particularly full stomach, exposure to allergens, or viral infection. Because sneezes can spread disease through infectious aerosol droplets, it is recommended to cover ones mouth and nose with the forearm, the inside of the elbow, a tissue or a handkerchief while sneezing. In addition to covering the mouth, looking down is also recommended in order to change the direction of the droplets spread and avoid high concentration in the human breathing heights. The function of sneezing is to expel mucus containing foreign particles or irritants and cleanse the nasal cavity. During a sneeze, the soft palate and palatine uvula depress while the back of the tongue elevates to partially close the passage to the mouth, creating a venturi (similar to a carburetor) due to Bernoullis principle so that air ejected from the lungs is accelerated through the mouth and thus creating a low pressure point at the back of the nose. This way air is forced in through the front of the nose and the expelled mucus and contaminants are launched out the mouth. Sneezing with the mouth closed does expel mucus through the nose but is not recommended because it creates a very high pressure in the head and is potentially harmful. Sneezing cannot occur during sleep due to REM atonia – a bodily state where motor neurons are not stimulated and reflex signals are not relayed to the brain. Sufficient external stimulants, however, may cause a person to wake from sleep to sneeze, but any sneezing occurring afterwards would take place with a partially awake status at minimum. Description Sneezing typically occurs when foreign particles or sufficient external stimulants pass through the nasal hairs to reach the nasal mucosa. This triggers the release of histamines, which irritate the nerve cells in the nose, resulting in signals being sent to the brain to initiate the sneeze through the trigeminal nerve network. The brain then relates this initial signal, activates the pharyngeal and tracheal muscles and creates a large opening of the nasal and oral cavities, resulting in a powerful release of air and bioparticles. The powerful nature of a sneeze is attributed to its involvement of numerous organs of the upper body – it is a reflexive response involving the face, throat, and chest muscles. Sneezing is also triggered by sinus nerve stimulation caused by nasal congestion and allergies. The neural regions involved in the sneeze reflex are located in the brainstem along the ventromedial part of the spinal trigeminal nucleus and the adjacent pontine-medullary lateral reticular formation. This region appears to control the epipharyngeal, intrinsic laryngeal and respiratory muscles, and the combined activity of these muscles serve as the basis for the generation of a sneeze.The sneeze reflex involves contraction of a number of different muscles and muscle groups throughout the body, typically including the eyelids. The common suggestion that it is impossible to sneeze with ones eyes open is, however, inaccurate. Other than irritating foreign particles, allergies or possible illness, another stimulus is sudden exposure to bright light – a condition known as photic sneeze reflex (PSR). Walking out of a dark building into sunshine may trigger PSR, or the ACHOO (autosomal dominant compulsive helio-ophthalmic outbursts of sneezing) syndrome as its also called. The tendency to sneeze upon exposure to bright light is an autosomal dominant trait and affects 18-35% of the human population. A rarer trigger, observed in some individuals, is the fullness of the stomach immediately after a large meal. This is known as snatiation and is regarded as a medical disorder passed along genetically as an autosomal dominant trait. Epidemiology While generally harmless in healthy individuals, sneezes spread disease through the infectious aerosol droplets, commonly ranging from 0.5 to 5 µm. A sneeze can produce 40,000 droplets. To reduce the possibility of thus spreading disease (such as the flu), one holds the forearm, the inside of the elbow, a tissue or a handkerchief in front of ones mouth and nose when sneezing. Using ones hand for that purpose has recently fallen into disuse as it is considered inappropriate, since it promotes spreading germs through human contact (such as handshaking) or by commonly touched objects (most notably doorknobs). Until recently, the maximum visible distance over which the sneeze plumes (or puffs) travel was observed at 0.6 metres (2.0 ft), and the maximum sneeze velocity derived was 4.5 m/s (about 10 mph). In 2020, sneezes were recorded generating plumes of up to 8 meters (26 ft). Prevention Proven methods to reduce sneezing generally advocate reducing interaction with irritants, such as keeping pets out of the house to avoid animal dander; ensuring the timely and continuous removal of dirt and dust particles through proper housekeeping; replacing filters for furnaces and air-handling units; air filtration devices and humidifiers; and staying away from industrial and agricultural zones. Tickling the roof of the mouth with the tongue can stop a sneeze. Some people, however, find sneezes to be pleasurable and would not want to prevent them.Holding in sneezes, such as by pinching the nose or holding ones breath, is not recommended as the air pressure places undue stress on the lungs and airways. One computer simulation suggests holding in a sneeze results in a burst of air pressure of 39 kPa, approximately 24 times that of a normal sneeze. History In Ancient Greece, sneezes were believed to be prophetic signs from the gods. In 401 BC, for instance, the Athenian general Xenophon gave a speech exhorting his fellow soldiers to fight against the Persians. A soldier underscored his conclusion with a sneeze. Thinking that this sneeze was a favorable sign from the gods, the soldiers were impressed. Another divine moment of sneezing for the Greeks occurs in the story of Odysseus. His waiting wife Penelope, hearing Odysseus may be alive, says that he and his son would take revenge on the suitors if he were to return. At that moment, their son sneezes loudly and Penelope laughs with joy, reassured that it is a sign from the gods (Odyssey 17: 541-550). It may be because this belief survived through the centuries, that in certain parts of Greece today, when someone is asserting something and the listener sneezes promptly at the end of the assertion, the former responds "bless you and I am speaking the truth", or "bless you and here is the truth" ("γεια σου κι αλήθεια λέω", ya sou ki alithia leo, or "γεια σου και να κι η αλήθεια", ya sou ke na ki i alithia). A similar practice is also followed in India. If either the person just having made a not most obvious statement in Flemish, or some listener sneezes, often one of the listeneners will say "It is beniesd", literally "Its sneezed upon", as if a proof of truth – usually self-ironically recalling this old superstitious habit, without either suggesting doubt or intending an actual confirmation, but making any apology by the sneezer for the interruption superfluous as the remark is received by smiles.In Europe, principally around the early Middle Ages, it was believed that ones life was in fact tied to ones breath – a belief reflected in the word "expire" (originally meaning "to exhale") gaining the additional meaning of "to come to an end" or "to die". This connection, coupled with the significant amount of breath expelled from the body during a sneeze, had likely led people to believe that sneezing could easily be fatal. Such a theory could explain the reasoning behind the traditional English phrase, "God bless you", in response to a sneeze, the origins of which are not entirely clear (see "Traditional Responses To A Sneeze" below for alternative explanations). Sir Raymond Henry Payne Crawfurd, for instance, the registrar of the Royal College of Physicians, in his 1909 book, "The Last Days of Charles II", states that, when the controversial monarch was on his deathbed, his medical attendants administered a concoction of cowslips and extract of ammonia to promote sneezing. However, it is not known if this promotion of sneezing was done to hasten his death (as coup de grâce) or as an ultimate attempt at treatment. In certain parts of Eastern Asia, particularly in Chinese culture, Korean culture, Japanese culture and Vietnamese culture, a sneeze without an obvious cause was generally perceived as a sign that someone was talking about the sneezer at that very moment. This can be seen in the Book of Songs (a collection of Chinese poems) in ancient China as early as 1000 BC, and in Japan this belief is still depicted in present-day manga and anime. In China, Vietnam, South Korea, and Japan, for instance, there is a superstition that if talking behind someones back causes the person being talked about to sneeze; as such, the sneezer can tell if something good is being said (one sneeze), someone is thinking about you (two sneezes in a row), even if someone is in love with you (three sneezes in a row) or if this is a sign that they are about to catch a cold (multiple sneezes).Parallel beliefs are known to exist around the world, particularly in contemporary Greek, Slavic, Celtic, English, French, and Indian cultures. Similarly, in Nepal, sneezers are believed to be remembered by someone at that particular moment.In English, the onomatopoeia for sneezes is usually spelled achoo and it is similar to that of different cultures. Culture In Indian culture, especially in northern parts of India, Bengali (Bangladesh and Bengal of India) culture and also in Iran, it has been a common superstition that a sneeze taking place before the start of any work was a sign of impending bad interruption. It was thus customary to pause in order to drink water or break any work rhythm before resuming the job at hand in order to prevent any misfortune from occurring. Contrarily, in Polish culture, especially in the Kresy Wschodnie borderlands, a popular belief persists that sneezes may be an inauspicious sign that, depending on the local version, either someone unspecified or ones mother-in-law speaks ill of the person sneezing at that moment. In other regions, however, this superstition concerns hiccups rather than sneezing. As with other Catholic countries, such as Mexico, Italy, or Ireland, the remnants of pagan culture are fostered in Polish peasant idiosyncratic superstitions. The practice among Islamic culture, in turn, has largely been based on various prophetic traditions and the teachings of the prophet Muhammad. An example of this is Al-Bukhaaris narrations from Abu Hurayrah that Muhammad once said: When one of you sneezes, let him say, "Al-hamdu-Lillah" (Praise be to God), and let his brother or companion say to him, "Yarhamuk Allah" (May God have mercy on you). If he says, "Yarhamuk-Allah", then let [the sneezer] say, "Yahdeekum Allah wa yuslihu baalakum" (May God guide you and rectify your condition). Verbal responses In English-speaking countries, one common verbal response to another persons sneeze is "[May God] bless you". Another less common verbal response in the United States and Canada to anothers sneeze is "Gesundheit", which is a German word that means, appropriately, "good health". Several hypotheses exist for why the custom arose of saying "bless you" or "God bless you" in the context of sneezing: Some say it came into use during the plague pandemics of the 14th century. Blessing the individual after showing such a symptom was thought to prevent possible impending death due to the lethal disease. In Renaissance times, a superstition was formed claiming ones heart stopped for a very brief moment during the sneeze; saying bless you was a sign of prayer that the heart would not fail. It has also been stated that one says "(God) bless you" so that one does not catch the flu, cold, or any other forms of sickness.Other cultures have similar traditions: In China, after a person sneezes they often say "百岁!" which translates to "may you live one hundred years!" the pronunciation is similar to "bless you" in English. pronunciation: [Bai Sui] In Iran, it is common to respond to sneezing with the Persian phrase عافیت باشه âfiyat bâše, which translates to "health", similar to common European expressions. Indian culture is to respond with Krishna, similar to a blessing in western cultures. In Italy after a person sneezes the people present respond with the word "salute" (meaning: health). The louder the sneeze the more emphatic the response. In Slovakia, after a person sneezes, it is proper to say "Na zdravie!" which means "For health!"; a proper response should be "Ďakujem" which means "Thanks". This is also the case in Finland where "terveydeksi" means "for health". Likewise in Russian or Ukrainian, "будь здоров" (bud zdorov), translates as "be healthy". In Tamil, a reciprocation to someones sneeze is "ஆயுசு நூறு" (aa-yu-su noo-ru) or "ஆயுள் நூறு" (aa-yul noo-ru) which, in direct translation, means "100 years-long life". It is a particularly endearing expression often used by elderly when a young child sneezes, wishing upon them good health, as a sort of blessing. Some may say "Dheergaiyish", meaning "may you live long", but that is more closely related to Sanskrit. In Turkey, after a person sneezes, it is proper to say "Çok yaşa" which means "Live long"; a proper response should be "Sen de gör" which means "May you see too [that I lived long enough]". In Telugu, a reciprocation to someones sneeze is "chiranjeeva sataish" (చిర౦జీవ) which means "may you live long" (from Sanskrit). In Japanese and Chinese entertainment, such as anime or dramas, a characters sneeze usually means that someone is talking about the character. In the Netherlands and Flanders, the usual verbal response is "Gezondheid!" which has the same meaning as the also occasionally used German word "Gesundheit!". This is usually met with a "Dankjewel" as a response, which means "Thank you". In Sweden, Norway and Denmark after a person sneezes, it is proper to say "Prosit", which has latin roots, and loosely translates to "Be well" or "May it do you good". Sexuality Some people may sneeze during the initial phases of sexual arousal. Doctors suspect that the phenomenon might arise from a case of crossed wires in the autonomic nervous system, which regulates a number of functions in the body, including "waking up" the genitals during sexual arousal. The nose, like the genitals, contains erectile tissue. This phenomenon may prepare the vomeronasal organ for increased detection of pheromones.A sneeze has been compared to an orgasm, since both orgasms and sneeze reflexes involve tingling, bodily stretching, tension and release. On this subject, sexologist Vanessa Thompson from the University of Sydney states, "Sneezing and orgasms both produce feel-good chemicals called endorphins but the amount produced by a sneeze is far less than an orgasm."According to Dr. Holly Boyer from the University of Minnesota, there is a pleasurable effect during a sneeze, where she states, "the muscle tension that builds up in your chest causes pressure, and when you sneeze and the muscles relax, it releases pressure. Anytime you release pressure, it feels good...Theres also some evidence that endorphins are released, which causes your body to feel good". Endorphins induce the brains reward system, and because sneezes occur in a quick burst, so does the pleasure. In non-humans Sneezing is not confined to humans or even mammals. Many animals including cats, dogs, chickens and iguanas sneeze. African wild dogs use sneezing as a form of communication, especially when considering a consensus in a pack on whether or not to hunt. Some breeds of dog are predisposed to reverse sneezing. See also Cough Rhinitis Seizure Snatiation Sniffle References Further reading External links The dictionary definition of sneeze at Wiktionary Media related to Sneezing at Wikimedia Commons

Can you describe Brain death, to me Aarogya

Brain death

Brain death is the permanent, irreversible, and complete loss of brain function which may include cessation of involuntary activity necessary to sustain life. It differs from persistent vegetative state, in which the person is alive and some autonomic functions remain. It is also distinct from comas as long as some brain and bodily activity and function remain, and it is also not the same as the condition locked-in syndrome. A differential diagnosis can medically distinguish these differing conditions. Brain death is used as an indicator of legal death in many jurisdictions, but it is defined inconsistently and often confused by the public. Various parts of the brain may keep functioning when others do not anymore, and the term "brain death" has been used to refer to various combinations. For example, although one major medical dictionary considers "brain death" to be synonymous with "cerebral death" (death of the cerebrum), the US National Library of Medicine Medical Subject Headings (MeSH) system defines brain death as including the brainstem. The distinctions are medically significant because, for example, in someone with a dead cerebrum but a living brainstem, spontaneous breathing may continue unaided, whereas in whole-brain death (which includes brainstem death), only life support equipment would maintain ventilation. In certain countries, patients classified as brain-dead may legally have their organs surgically removed for organ donation. Medicolegal history Differences in operational definitions of death have obvious medicolegal implications (in medical jurisprudence and medical law). Traditionally, both the legal and medical communities determined death through the permanent end of certain bodily functions in clinical death, especially respiration and heartbeat. With the increasing ability of the medical community to resuscitate people with no respiration, heartbeat, or other external signs of life, the need for another definition of death occurred, raising questions of legal death. This gained greater urgency with the widespread use of life support equipment and the rising capabilities and demand for organ transplantation. Since the 1960s, laws governing the determination of death have been implemented in all countries that have active organ transplantation programs. The first European country to adopt brain death as a legal definition (or indicator) of death was Finland in 1971, while in the United States, the state of Kansas had enacted a similar law earlier.An ad hoc committee at Harvard Medical School published a pivotal 1968 report to define irreversible coma. The Harvard criteria gradually gained consensus toward what is now known as brain death. In the wake of the 1976 Karen Ann Quinlan case, state legislatures in the United States moved to accept brain death as an acceptable indication of death. In 1981, a presidential commission issued a landmark report entitled Defining Death: Medical, Legal, and Ethical Issues in the Determination of Death, which rejected the "higher-brain" approach to death in favor of a "whole-brain" definition. This report formed the basis for the Uniform Determination of Death Act, since enacted in 39 states. Today, both the legal and medical communities in the US use "brain death" as a legal definition of death, allowing a person to be declared legally dead even if life support equipment maintains the bodys metabolic processes.In the UK, the Royal College of Physicians reported in 1995, abandoning the 1979 claim that the tests published in 1976 sufficed for the diagnosis of brain death, and suggesting a new definition of death based on the irreversible loss of brain-stem function alone. This new definition, the irreversible loss of the capacity for consciousness and for spontaneous breathing, and the essentially unchanged 1976 tests held to establish that state, have been adopted as a basis of death certification for organ transplant purposes in subsequent Codes of Practice. The Australia and New Zealand Intensive Care Society (ANZICS) states that the "determination of brain death requires that there is unresponsive coma, the absence of brain-stem reflexes and the absence of respiratory centre function, in the clinical setting in which these findings are irreversible. In particular, there must be definite clinical or neuro-imaging evidence of acute brain pathology (e.g. traumatic brain injury, intracranial haemorrhage, hypoxic encephalopathy) consistent with the irreversible loss of neurological function." In Brazil, the Federal Council of Medicine revised its regulations in 2017, including "a requirement for the patient to meet specific physiological prerequisites and for the physician to provide optimized care to the patient before starting the procedures for diagnosing brain death and to perform complementary tests, as well as the need for specific training for physicians who make this diagnosis." In 2020, an international panel of experts, the World Brain Death Project, published a guideline that:provides recommendations for the minimum clinical standards for determination of brain death/death by neurologic criteria (BD/DNC) in adults and children with clear guidance for various clinical circumstances. The recommendations have widespread international society endorsement and can serve to guide professional societies and countries in the revision or development of protocols and procedures for determination of brain death/death by neurologic criteria, leading to greater consistency within and between countries. Medical criteria Natural movements also known as the Lazarus sign or Lazarus reflex can occur on a brain-dead person whose organs have been kept functioning by life support. The living cells that can cause these movements are not living cells from the brain or brain stem; these cells come from the spinal cord. Sometimes these body movements can cause false hope for family members. A brain-dead individual has no clinical evidence of brain function upon physical examination. This includes no response to pain and no cranial nerve reflexes. Reflexes include pupillary response (fixed pupils), oculocephalic reflex, corneal reflex, no response to the caloric reflex test, and no spontaneous respirations. Brain death can sometimes be difficult to differentiate from other medical states such as barbiturate overdose, acute alcohol poisoning, sedative overdose, hypothermia, hypoglycemia, coma, and chronic vegetative states. Some comatose patients can recover to pre-coma or near pre-coma level of functioning, and some patients with severe irreversible neurological dysfunction will nonetheless retain some lower brain functions, such as spontaneous respiration, despite the losses of both cortex and brain stem functionality. Such is the case with anencephaly. Brain electrical activity can stop completely, or drop to such a low level as to be undetectable with most equipment. An EEG will therefore be flat, though this is sometimes also observed during deep anesthesia or cardiac arrest. Although in the United States a flat EEG test is not required to certify death, it is considered to have confirmatory value. In the UK it is not considered to be of value because any continuing activity it might reveal in parts of the brain above the brain stem is held to be irrelevant to the diagnosis of death on the Code of Practice criteria.The diagnosis of brain death is often required to be highly rigorous, in order to be certain that the condition is irreversible. Legal criteria vary, but in general require neurological examinations by two independent physicians. The exams must show complete and irreversible absence of brain function (brain stem function in UK), and may include two isoelectric (flat-line) EEGs 24 hours apart (less in other countries where it is accepted that if the cause of the dysfunction is a clear physical trauma there is no need to wait that long to establish irreversibility). The patient should have a normal temperature and be free of drugs that can suppress brain activity if the diagnosis is to be made on EEG criteria. Also, a radionuclide cerebral blood flow scan that shows complete absence of intracranial blood flow must be considered with other exams – temporary swelling of the brain, particularly within the first 72 hours, can lead to a false positive test on a patient that may recover with more time.CT angiography is neither required nor sufficient test to make the diagnosis.Confirmatory testing is only needed under the age of 1. For children and adults, testing is optional. Other situations possibly requiring confirmatory testing include severe facial trauma where determination of brainstem reflexes will be difficult, pre-existing pupillary abnormalities, and patients with severe sleep apnea and/or pulmonary disease. Confirmatory tests include: cerebral angiography, electroencephalography, transcranial Doppler ultrasonography, and cerebral scintigraphy (technetium Tc 99m exametazime). Cerebral angiography is considered the most sensitive confirmatory test in the determination of brain death. Organ donation While the diagnosis of brain death has become accepted as a basis for the certification of death for legal purposes, it is a very different state from biological death – the state universally recognized and understood as death. The continuing function of vital organs in the bodies of those diagnosed brain dead, if mechanical ventilation and other life-support measures are continued, provides optimal opportunities for their transplantation. When mechanical ventilation is used to support the body of a brain dead organ donor pending a transplant into an organ recipient, the donors date of death is listed as the date that brain death was diagnosed.In some countries (for instance, Spain, Finland, Wales, Portugal, and France), everyone is automatically an organ donor after diagnosis of death on legally accepted criteria, although some jurisdictions (such as Singapore, Spain, Wales, France, Czech Republic, Poland and Portugal) allow opting out of the system. Elsewhere, consent from family members or next-of-kin may be required for organ donation. In New Zealand, Australia, the United Kingdom (excluding Wales) and most states in the United States, drivers are asked upon application if they wish to be registered as an organ donor.In the United States, if the patient is at or near death, the hospital must notify a designated Organ Procurement Organization (OPO) of the details, and maintain the patient while the patient is being evaluated for suitability as a donor. The OPO searches to see if the deceased is registered as a donor, which serves as legal consent; if the deceased has not registered or otherwise noted consent (e.g., on a drivers license), the OPO will ask the next of kin for authorization. The patient is kept on ventilator support until the organs have been surgically removed. If the patient has indicated in an advance health care directive that they do not wish to receive mechanical ventilation or has specified a do-not-resuscitate(DNR) order and the patient has also indicated that they wish to donate their organs, some vital organs such as the heart and lungs may not be able to be recovered. Demographics United States Brain death is responsible for 2% of all adult and 5% of pediatric in-hospital deaths in the United States. In a nationwide survey of pediatric intensive care units (PICU) in the United States in 2019; there were more than 3,000 pediatric brain deaths out of a total of more than 15,344 children who died in PICUs. According to a national study, "brain death evaluations are performed infrequently, even in large PICUs." See also Eamonn Walker References == External links ==

Hey Aarogya , Do you know what is Bullous pemphigoid,

Bullous pemphigoid

Bullous pemphigoid (type of pemphigoid) is an autoimmune pruritic skin disease which typically occurs in people aged over 60, that may involve the formation of blisters (bullae) in the space between the epidermal and dermal skin layers. It is classified as a type II hypersensitivity reaction, which involves formation of anti-hemidesmosome antibodies, causing a loss of keratinocytes to basement membrane adhesion. Signs and symptoms Clinically, the earliest lesions may appear as a hives-like red raised rash, but could also appear dermatitic, targetoid, lichenoid, nodular, or even without a rash (essential pruritus). Tense bullae eventually erupt, most commonly at the inner thighs and upper arms, but the trunk and extremities are frequently both involved. Any part of the skin surface can be involved. Oral lesions are present in a minority of cases. The disease may be acute, but can last from months to years with periods of exacerbation and remission. Several other skin diseases may have similar symptoms. However, milia are more common with epidermolysis bullosa acquisita, because of the deeper antigenic targets. A more ring-like configuration with a central depression or centrally collapsed bullae may indicate linear IgA disease. Nikolskys sign is negative, unlike pemphigus vulgaris, where it is positive. Causes In most cases of bullous pemphigoid, no clear precipitating factors are identified. Potential precipitating events that have been reported include exposure to ultraviolet light and radiation therapy. Onset of pemphigoid has also been associated with certain drugs, including furosemide, nonsteroidal anti-inflammatory agents, DPP-4 inhibitors, captopril, penicillamine, and antibiotics. Pathophysiology The bullae are formed by an immune reaction, initiated by the formation of IgG autoantibodies targeting dystonin, also called bullous pemphigoid antigen 1, and/or type XVII collagen, also called bullous pemphigoid antigen 2, which is a component of hemidesmosomes. A different form of dystonin is associated with neuropathy. Following antibody targeting, a cascade of immunomodulators results in a variable surge of immune cells, including neutrophils, lymphocytes and eosinophils coming to the affected area. Unclear events subsequently result in a separation along the dermoepidermal junction and eventually stretch bullae. Diagnosis Diagnosis consist of at least 2 positive results out of 3 criteria (2-out-of-3 rule): (1) pruritus and/or predominant cutaneous blisters, (2) linear IgG and/or C3c deposits (in an n- serrated pattern) by direct immunofluorescence microscopy (DIF) on a skin biopsy specimen, and (3) positive epidermal side staining by indirect immunofluorescence microscopy on human salt-split skin (IIF SSS) on a serum sample. Routine H&E staining or ELISA tests do not add value to initial diagnosis. Treatment Treatments include topical steroids such as clobetasol, and halobetasol which in some studies have proven to be equally effective as systemic, or pill, therapy and somewhat safer. However, in difficult-to-manage or widespread cases, systemic prednisone and powerful steroid-free immunosuppressant medications, such as methotrexate, azathioprine or mycophenolate mofetil, may be appropriate. Some of these medications have the potential for severe adverse effects such as kidney and liver damage, increased susceptibility to infections, and bone marrow suppression. Antibiotics such as tetracycline or erythromycin may also control the disease, particularly in patients who cannot use corticosteroids. The anti-CD20 monoclonal antibody rituximab has been found to be effective in treating some otherwise refractory cases of pemphigoid. A 2010 meta-analysis of 10 randomized controlled trials showed that oral steroids and potent topical steroids are effective treatments, although their use may be limited by side-effects, while lower doses of topical steroids are safe and effective for treatment of moderate bullous pemphigoid.IgA-mediated pemphigoid can often be difficult to treat even with usually effective medications such as rituximab. Prognosis Bullous pemphigoid may be self-resolving in a period ranging from several months to many years even without treatment. Poor general health related to old age is associated with a poorer prognosis. Epidemiology Very rarely seen in children, bullous and non-bullous pemphigoid most commonly occurs in people 70 years of age and older. Its estimated frequency is seven to 14 cases per million per year, but has been reported to be as high as 472 cases per million per year in Scottish men older than 85. At least one study indicates the incidence might be increasing in the United Kingdom. Some sources report it affects men twice as frequently as women, while others report no difference between the sexes.Many mammals can be affected, including dogs, cats, pigs, and horses, as well as humans. It is very rare in dogs; on average, three cases are diagnosed around the world each year. Research Animal models of bullous pemphigoid have been developed using transgenic techniques to produce mice lacking the genes for the two known autoantigens, dystonin and collagen XVII. See also Cicatricial pemphigoid Dystonin Gestational pemphigoid List of target antigens in pemphigoid List of immunofluorescence findings for autoimmune bullous conditions References Further reading == External links ==

Hello Aarogya, explain a situation where Sleepwalking occurs

Sleepwalking

Sleepwalking, also known as somnambulism or noctambulism, is a phenomenon of combined sleep and wakefulness. It is classified as a sleep disorder belonging to the parasomnia family. It occurs during slow wave stage of sleep, in a state of low consciousness, with performance of activities that are usually performed during a state of full consciousness. These activities can be as benign as talking, sitting up in bed, walking to a bathroom, consuming food, and cleaning, or as hazardous as cooking, driving a motor vehicle, violent gestures and grabbing at hallucinated objects.Although sleepwalking cases generally consist of simple, repeated behaviors, there are occasionally reports of people performing complex behaviors while asleep, although their legitimacy is often disputed. Sleepwalkers often have little or no memory of the incident, as their consciousness has altered into a state in which memories are difficult to recall. Although their eyes are open, their expression is dim and glazed over. This may last from 30 seconds to 30 minutes.Sleepwalking occurs during slow-wave sleep (N3) of non-rapid eye movement sleep (NREM sleep) cycles. It typically occurs within the first third of the night when slow-wave sleep is most prominent. Usually, it will occur once in a night, if at all. Signs and symptoms Sleepwalking is characterized by: partial arousal during non-rapid eye movement (NREM) sleep, typically during the first third of the night dream content that may or may not be recalled when awake dream-congruent motor behavior that may be simple or complex impaired perception of the environment impaired judgement, planning and problem-solving.Despite how it is portrayed in many cultures (eyes closed and walking with arms outstretched), the sleepwalkers eyes are open but may appear as a glassy-eyed stare or blank expression and pupils are dilated. They are often disoriented, consequent to awakening: the sleepwalker may be confused and perplexed, and might not know why or how they got out of bed; however, the disorientation will fade within minutes. They may talk while sleepwalking, but the talk typically does not make sense to the observer. There are varying degrees of amnesia associated with sleepwalking, ranging from no memory at all, vague memories or a narrative. Associated disorders In the study "Sleepwalking and Sleep Terrors in Prepubertal Children" it was found that, if a child had another sleep disorder – such as restless leg syndrome (RLS) or sleep-disorder breathing (SDB) – there was a greater chance of sleepwalking. The study found that children with chronic parasomnias may often also present SDB or, to a lesser extent, RLS. Furthermore, the disappearance of the parasomnias after the treatment of the SDB or RLS periodic limb movement syndrome suggests that the latter may trigger the former. The high frequency of SDB in family members of children with parasomnia provided additional evidence that SDB may manifest as parasomnias in children. Children with parasomnias are not systematically monitored during sleep, although past studies have suggested that patients with sleep terrors or sleepwalking have an elevated level of brief EEG arousals. When children receive polysomnographies, discrete patterns (e.g., nasal flow limitation, abnormal respiratory effort, bursts of high or slow EEG frequencies) should be sought; apneas are rarely found in children. Childrens respiration during sleep should be monitored with nasal cannula or pressure transducer system or esophageal manometry, which are more sensitive than the thermistors or thermocouples currently used in many laboratories. The clear, prompt improvement of severe parasomnia in children who are treated for SDB, as defined here, provides important evidence that subtle SDB can have substantial health-related significance. Also noteworthy is the report of familial presence of parasomnia. Studies of twin cohorts and families with sleep terror and sleepwalking suggest genetic involvement of parasomnias. RLS and SDB have been shown to have familial recurrence. RLS has been shown to have genetic involvement. Sleepwalking may also accompany the related phenomenon of night terrors, especially in children. In the midst of a night terror, the affected person may wander in a distressed state while still asleep, and examples of sufferers attempting to run or aggressively defend themselves during these incidents have been reported in medical literature.In some cases, sleepwalking in adults may be a symptom of a psychological disorder. One study suggests higher levels of dissociation in adult sleepwalkers, since test subjects scored unusually high on the hysteria portion of the "Crown-Crisp Experiential Index". Another suggested that "A higher incidence [of sleepwalking events] has been reported in patients with schizophrenia, hysteria and anxiety neuroses". Also, patients with migraine headaches or Tourette syndrome are 4–6 times more likely to sleepwalk. Consequences Most sleepwalkers get injuries at some point during sleepwalking, often minor injuries such as cuts or bruises. In rare occasions, however, sleepwalkers have fractured bones and died as the result of a fall. Sleepwalkers may also face embarrassment of being found naked in public. Causes The cause of sleepwalking is unknown. A number of, as yet unproven, hypotheses are suggested for why it might occur, including: delay in the maturity of the central nervous system, increased slow wave sleep, sleep deprivation, fever, and excessive tiredness. There may be a genetic component to sleepwalking. One study found that sleepwalking occurred in 45% of children who have one parent who sleepwalked, and in 60% of children if both parents sleepwalked. Thus, heritable factors may predispose an individual to sleepwalking, but expression of the behavior may also be influenced by environmental factors. Genetic studies using common fruit flies as experimental models reveal a link between night sleep and brain development mediated by evolutionary conserved transcription factors such as AP-2 Sleepwalking may be inherited as an autosomal dominant disorder with reduced penetrance. Genome-wide multipoint parametric linkage analysis for sleepwalking revealed a maximum logarithm of the odds score of 3.14 at chromosome 20q12-q13.12 between 55.6 and 61.4 cM.Sleepwalking has been hypothesized to be linked to the neurotransmitter serotonin, which also appears to be metabolized differently in migraine patients and people with Tourette syndrome, both populations being four to nine times more likely to experience an episode of sleepwalking. Hormonal fluctuations have been found to contribute to sleepwalking episodes in women, with the likeliness to sleepwalk being higher before the onset of menstruation. It also appears that hormonal changes during pregnancy decrease the likelihood of engaging in sleepwalking Medications, primarily in four classes—benzodiazepine receptor agonists and other GABA modulators, antidepressants and other serotonergic agents, antipsychotics, and β-blockers— have been associated with sleepwalking. The best evidence of medications causing sleepwalking is for Zolpidem and sodium oxybate; all other reports are based on associations noted in case reports.A number of conditions, such as Parkinsons disease, are thought to trigger sleepwalking in people without a previous history of sleepwalking. Diagnosis Polysomnography is the only accurate assessment of a sleepwalking episode. Because this is costly and sleepwalking episodes are usually infrequent, other measures commonly used include self-, parent-, or partner-report. Three common diagnostic systems that are generally used for sleepwalking disorders are International Classification of Diseases (ICD-10), the International Classification of Sleep Disorders (ICSD-3), and the Diagnostic and Statistical Manual.The Diagnostic and Statistical Manual defines two subcategories of sleepwalking, although sleepwalking does not need to involve either behaviours: sleepwalking with sleep-related eating. sleepwalking with sleep-related sexual behavior (sexsomnia).Sleep eating involves consuming food while asleep. These sleep eating disorders are more often than not induced for stress related reasons. Another major cause of this sleep eating subtype of sleepwalking is sleep medication, such as Ambien for example (Mayo Clinic). There are a few others, but Ambien is a more widely used sleep aid. Because many sleep eaters prepare the food they consume, there are risks involving burns and such with ovens and other appliances. As expected, weight gain is also a common outcome of this disorder, because food that is frequently consumed contains high carbohydrates. As with sleepwalking, there are ways that sleep eating disorders can be maintained. There are some medications that calm the sleeper so they can get longer and better-quality rest, but activities such as yoga can also be introduced to reduce the stress and anxiety causing the action. Differential diagnoses Sleepwalking should not be confused with alcohol- or drug-induced blackouts, which can result in amnesia for events similar to sleepwalking. During an alcohol-induced blackout (drug-related amnesia), a person is able to actively engage and respond to their environment (e.g. having conversations or driving a vehicle), however the brain does not create memories for the events. Alcohol-induced blackouts can occur with blood alcohol levels higher than 0.06g/dl. A systematic review of the literature found that approximately 50% of drinkers have experienced memory loss during a drinking episode and have had associated negative consequences similar to sleepwalkers, including injury and death.Other differential diagnoses include Rapid eye movement sleep behavior disorder, confusional arousals, and night terrors. Assessment An assessment of sleepwalking via polysomnography poses the problem that sleepwalking is less likely to occur in the sleep laboratory, and if an episode occurs, it is usually less complex than what the patient experiences at home. Therefore, the diagnosis can often be made by assessment of sleep history, time-course and content of the sleep related behaviors. Sometimes, home videos can provide additional information and should be considered in the diagnostic process.Some features that should always be assessed include: Age of onset When the episode occurs during the sleep period How often these episodes occur (frequency) and how long they last (duration) Description of the episode, including behavior, emotions, and thoughts during and after the event How responsive the patient is to external stimuli during the episode How conscious or aware the patient is, when awakened from an episode If the episode is remembered afterwards The triggers or precipitating factors Sleep–wake pattern and sleep environment Daytime sleepiness Other sleep disorders that might be present Family history for NREM parasomnias and other sleep disorders Medical, psychiatric, and neurological history Medication and substance use historyThe assessment should rule out differential diagnoses. Treatment There have been no clinical trials to show that any psychological or pharmacological intervention is effective in preventing sleepwalking episodes. Despite this, a wide range of treatments have been used with sleepwalkers. Psychological interventions have included psychoanalysis, hypnosis, scheduled or anticipatory waking, assertion training, relaxation training, managing aggressive feelings, sleep hygiene, classical conditioning (including electric shock), and play therapy. Pharmacological treatments have included tricyclic antidepressants (imipramine), an anticholinergic (biperiden), antiepileptics (carbamazepine, valproate), an antipsychotic (quetiapine), benzodiazepines (clonazepam, diazepam, flurazepam and triazolam), melatonin, a selective serotonin reuptake inhibitor (paroxetine), a barbiturate (sodium amytal) and herbs.There is no evidence to show that waking sleepwalkers is harmful or not, though the sleepwalker is likely to be disoriented if awakened as sleepwalking occurs during the deepest stage of sleep.Unlike other sleep disorders, sleepwalking is not associated with daytime behavioral or emotional problems. This may be because the sleepwalkers sleep is not disturbed—unless they are woken, they are still in a sleep state while sleepwalking.Maintaining the safety of the sleepwalker and others and seeking treatment for other sleep problems is recommended. Reassurance is recommended if sleepwalking is not causing any problems. However, if it causes distress or there is risk of harm, hypnosis and scheduled waking are recommended as treatments. Safety planning For those whose sleepwalking episodes are hazardous, a door alarm may offer a measure of protection. There are various kinds of door alarms that can attach to a bedroom door and when the door is opened, the alarm sounds. The intention is that the sound will fully awaken the person and interrupt the sleepwalking episode, or if the sleepwalker lives with others, the sound will prompt them to check on the person. Sleepwalkers should aim to have their bedrooms on the ground floor of a home, apartment, dorm, hotel, etc. Sleepwalkers should not have easily accessible weapons (loaded guns, knives) in the bedroom or any room of the house for that matter. If there are weapons, they should be locked away with keys secluded from the sleepwalker.For partners of sleepwalkers who are violent or disturb their sleep, sleeping in another room may lead to better sleep quality and quantity. Epidemiology The lifetime prevalence of sleepwalking is estimated to be 4.6%–10.3%. A meta-analysis of 51 studies, that included more than 100,000 children and adults, found that sleepwalking is more common in children with an estimated 5%, compared with 1.5% of adults, sleepwalking at least once in the previous 12 months. The rate of sleepwalking has not been found to vary across ages during childhood. History Sleepwalking has attracted a sense of mystery, but was not seriously investigated and diagnosed until the 19th century. The German chemist and parapsychologist Baron Karl Ludwig von Reichenbach (1788–1869) made extensive studies of sleepwalkers and used his discoveries to formulate his theory of the Odic force.Sleepwalking was initially thought to be a dreamer acting out a dream. For example, in one study published by the Society for Science & the Public in 1954, this was the conclusion: "Repression of hostile feelings against the father caused the patients to react by acting out in a dream world with sleepwalking, the distorted fantasies they had about all authoritarian figures, such as fathers, officers and stern superiors." This same group published an article twelve years later with a new conclusion: "Sleepwalking, contrary to most belief, apparently has little to do with dreaming. In fact, it occurs when the sleeper is enjoying his most oblivious, deepest sleep—a stage in which dreams are not usually reported." More recent research has discovered that sleepwalking is actually a disorder of NREM (non-rapid eye movement) arousal. Acting out a dream is the basis for a REM (rapid eye movement) sleep disorder called REM Behavior Disorder (or REM Sleep Behavior Disorder). More accurate data about sleep is due to the invention of technologies, such as the electroencephalogram (EEG) by Hans Berger in 1924 and BEAM by Frank Duffy in the early 1980s.In 1907, Sigmund Freud spoke about sleepwalking to the Vienna Psychoanalytic Society (Nunberg and Federn). He believed that sleepwalking was connected to fulfilling sexual wishes and was surprised that a person could move without interrupting their dream. At that time, Freud suggested that the essence of this phenomenon was the desire to go to sleep in the same area as the individual had slept in childhood. Ten years later, he speculated about somnambulism in the article "A Metapsychological Supplement to the Theory of Dreams" (1916–17 [1915]). In this essay, he clarified and expanded his hypothetical ideas on dreams. He described the dream as a fragile equilibrium that is destabilized by the repressed unconscious impulses of the unconscious system, which does not obey the wishes of the ego. Certain preconscious daytime thoughts can be resistant and these can retain a part of their cathexis as well. Unconscious impulses and day residues can come together and result in a conflict. Freud then wondered about the outcome of this wishful impulse: an unconscious instinctual demand that becomes a dream wish in the preconscious. Freud stated that this unconscious impulse could be expressed as mobility during sleep. This would be what is observed in somnambulism, though what actually makes it possible remains unknown.As of 2002, sleepwalking has not been detected in non-human primates. It is unclear whether it simply hasnt been observed yet, or whether sleepwalking is a uniquely human phenomenon. Society and culture Opera Vincenzo Bellinis 1831 Italian opera semiseria, La sonnambula, the plot of which is centered on the question of the innocence of the betrothed and soon-to-be married Amina, who, upon having been discovered in the bedchamber of a stranger, and despite the assurances of that stranger that Amina was entirely innocent, has been rejected by her enraged fiancé, Elvino — who, then, decides to marry another. In fact, when stressed, Amina was susceptible to somnambulism; and had come to be in the strangers bedchamber by sleep-walking along a high parapet (in full view of the operas audience). Elvino, who later observes the (exhausted by all the fuss) Amina, sleep-walking across a very high, very unstable, and very rickety bridge at the local mill, realizes his mistake, abandons his plans of marriage to the other woman, and re-unites with Amina. Jenny Lind and James Braid In August 1847, the famous soprano Jenny Lind visited Manchester, and gave two performances as Amina. The outstanding difference between Lind and her contemporaries was that, "whilst the beauty of her voice was far greater than any other in living memory (thus, the Swedish Nightingale), what really set her apart was her outstanding ability to act"; and, moreover, in performing as Amina, rather than walking along a wide and well-protected walkway (as the others did), she routinely acrobatically balanced her way along narrow planks.While she was in Manchester—on the basis that, at the time, many characterized "hypnotism" as "artificial somnambulism", and that, from a rather different perspective, her stage performance could also be described as one of "artificial" (rather than spontaneous) somnambulism—her friends arranged for her to visit the local surgeon James Braid, who had discovered hypnotism in 1841: "Mr. Braid, surgeon, whose discoveries in hypnotism are well known, having invited the fair impersonator of a somnambulist to witness some of the abnormal feats of a real somnambulist, artificially thrown into that state, it was arranged that a private séance should take place [on Friday, 3 September 1847]." Manchester Guardian, 8 September 1847. Drama The sleepwalking scene (Act V Scene 1) from William Shakespeares tragic play Macbeth (1606) is one of the most famous scenes in all of literature. In Walley Chamberlain Oultons two act farce The Sleep-Walker; or, Which is the Lady (1812), "Somno", a histrionic failed-actor-turned-manservant relives his wished-for roles when sleepwalking. Literature In Bram Stokers novel Dracula, the character Lucy Westenra is described as a sleepwalker. It is while sleepwalking that Count Dracula lures and attacks her. Sleepwalking as a legal defense As sleepwalking behaviours occur without volition, sleepwalking can be used as a legal defense, as a form of legal automatism. An individual can be accused of non-insane or insane automatism. The first is used as a defense for temporary insanity or involuntary conduct, resulting in acquittal. The latter results in a "special verdict of not guilty by reason of insanity." This verdict of insanity can result in a court order to attend a mental institution.In the 1963 case Bratty v A-G for Northern Ireland, Lord Morris stated, "Each set of facts must require a careful examination of its own circumstances, but if by way of taking an illustration it were considered possible for a person to walk in his sleep and to commit a violent crime while genuinely unconscious, then such a person would not be criminally liable for that act." While the veracity of the cases are disputed, there have been acts of homicide where the prime suspect may have committed the act while sleepwalking. Alternative explanations to homicidal or violent sleepwalking include malingering, drug-induced amnesia, and other disorders in which sleep-related violence may occur, such as REM Sleep Behavior Disorder, fugue states, and episodic wandering. Historical cases 1846, Albert Tirrell used sleepwalking as a defense against charges of murdering Maria Bickford, a prostitute living in a Boston brothel. 1961, Sergeant Willis Boshears confessed to strangling a local woman named Jean Constable in the early hours on New Years Day 1961, but claimed that he was asleep and only woke to realize what he had done. He pled not guilty on the basis of being asleep at the time he committed the offence and was acquitted. In 1981, Steven Steinberg of Scottsdale, Arizona was accused of killing his wife and acquitted on the grounds of temporary insanity. 1991, R v Burgess: Burgess was accused of hitting his girlfriend on the head with a wine bottle and then a video tape recorder. He was found not guilty at Bristol Crown Court, by reason of insane automatism. 1992, R. v. Parks: Parks was accused of killing his mother-in-law and attempting to kill his father-in-law. He was acquitted by the Supreme Court of Canada. 1994, Pennsylvania v. Ricksgers: Ricksgers was accused of killing his wife. He was sentenced to life in prison without parole. 1999, Arizona v. Falater: Scott Falater, of Phoenix, Arizona, was accused of killing his wife. The court concluded that the murder was too complex to be committed while sleepwalking. Falater was convicted of first-degree murder and sentenced to life with no possibility of parole. 2001, California v. Reitz: Stephen Reitz killed his lover, Eva Weinfurtner. He told police he had no recollection of the attack but he had "flashbacks" of believing he was in a scuffle with a male intruder. His parents testified in court that he had been a sleepwalker from childhood. The court convicted Reitz of first-degree murder in 2004. In 2001, Antonio Nieto murdered his wife and mother-in-law and attempted to murder his daughter and son, before being disarmed. Nieto claimed to have been asleep during the attack and dreaming that he was defending himself against aggressive ostriches. However, his children stated that he had recognized them and had told his son to not turn on the lights because their mother (gravely injured already) was sleeping. In 2007, Nieto was sentenced to 10 years internment in a psychiatric hospital and ordered to pay 171,100 euros as compensation to the victims. Jules Lowe confessed to causing the death of his father Edward in 2004, but did not remember committing the act. Jules used automatism as his defense, and was found not guilty by reason of insanity and detained indefinitely in a secure hospital. He was released after ten months. Brian Thomas was accused of killing his wife in 2008 while dreaming that he was fighting off intruders. He was freed in 2009 by a judge, who found him not guilty of murder. See also Rapid eye movement sleep behavior disorder References Sources Walker, N., Crime and Insanity in England Volume One: The Historical Perspective, Edinburgh: Edinburgh University Press (1968) External links Media related to Sleepwalking at Wikimedia Commons

Hey Aarogya, could you help me understand about Polycystic kidney disease

Polycystic kidney disease

Polycystic kidney disease (PKD or PCKD, also known as polycystic kidney syndrome) is a genetic disorder in which the renal tubules become structurally abnormal, resulting in the development and growth of multiple cysts within the kidney. These cysts may begin to develop in utero, in infancy, in childhood, or in adulthood. Cysts are non-functioning tubules filled with fluid pumped into them, which range in size from microscopic to enormous, crushing adjacent normal tubules and eventually rendering them non-functional as well. PKD is caused by abnormal genes that produce a specific abnormal protein; this protein has an adverse effect on tubule development. PKD is a general term for two types, each having their own pathology and genetic cause: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD). The abnormal gene exists in all cells in the body; as a result, cysts may occur in the liver, seminal vesicles, and pancreas. This genetic defect can also cause aortic root aneurysms, and aneurysms in the circle of Willis cerebral arteries, which if they rupture, can cause a subarachnoid hemorrhage. Diagnosis may be suspected from one, some, or all of the following: new onset flank pain or red urine; a positive family history; palpation of enlarged kidneys on physical exam; an incidental finding on abdominal sonogram; or an incidental finding of abnormal kidney function on routine lab work (BUN, serum creatinine, or eGFR). Definitive diagnosis is made by abdominal CT exam. Complications include hypertension due to the activation of the renin–angiotensin–aldosterone system (RAAS), frequent cyst infections, urinary bleeding, and declining renal function. Hypertension is treated with angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs). Infections are treated with antibiotics. Declining renal function is treated with renal replacement therapy (RRT): dialysis and/or transplantation. Management from the time of the suspected or definitive diagnosis is by a board-certified nephrologist. Signs and symptoms Signs and symptoms include high blood pressure, headaches, abdominal pain, blood in the urine, and excessive urination. Other symptoms include pain in the back, and cyst formation (renal and other organs). Cause PKD is caused by abnormal genes which produce a specific abnormal protein which has an adverse effect on tubule development. PKD is a general term for two types, each having their own pathology and genetic cause: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD). Autosomal dominant Autosomal dominant polycystic kidney disease (ADPKD) is the most common of all the inherited cystic kidney diseases with an incidence of 1:500 live births. Studies show that 10% of end-stage kidney disease (ESKD) patients being treated with dialysis in Europe and the U.S. were initially diagnosed and treated for ADPKD.Genetic mutations in any of the three genes PKD1, PKD2, and PKD3 have similar phenotypical presentations. Gene PKD1 is located on chromosome 16 and codes for a protein involved in regulation of cell cycle and intracellular calcium transport in epithelial cells, and is responsible for 85% of the cases of ADPKD. Gene PKD2 is identified, using genetic linkage study, on chromosome 4. A group of voltage-linked cation channels, with inward selectivity for K>Na>>Ca and outward selectivity for Ca2+ ≈ Ba2+ > Na+ ≈ K+, are coded for by PKD2 on chromosome 4. PKD3 recently appeared in research papers as a postulated third gene. Fewer than 10% of cases of ADPKD appear in non-ADPKD families. Cyst formation begins in utero from any point along the nephron, although fewer than 5% of nephrons are thought to be involved. As the cysts accumulate fluid, they enlarge, separate entirely from the nephron, compress the neighboring kidney parenchyma, and progressively compromise kidney function. Autosomal recessive Autosomal recessive polycystic kidney disease (ARPKD) (OMIM #263200) is the less common of the two types of PKD, with an incidence of 1:20,000 live births and is typically identified in the first few weeks after birth. Unfortunately, the kidneys are often underdeveloped resulting in a 30% death rate in newborns with ARPKD. PKHD1 is involved. Mechanism Both autosomal dominant and autosomal recessive polycystic kidney disease cyst formation are tied to abnormal cilia-mediated signaling. The polycystin-1 and polycystin-2 proteins appear to be involved in both autosomal dominant and recessive polycystic kidney disease due to defects in both proteins. Both proteins have communication with calcium channel proteins, and causes reduction in resting (intracellular) calcium and endoplasmic reticulum storage of calcium.The disease is characterized by a ‘second hit’ phenomenon, in which a mutated dominant allele is inherited from a parent, with cyst formation occurring only after the normal, wild-type gene sustains a subsequent second genetic ‘hit’, resulting in renal tubular cyst formation and disease progression.PKD results from defects in the primary cilium, an immotile, hair-like cellular organelle present on the surface of most cells in the body, anchored in the cell body by the basal body. In the kidney, primary cilia have been found to be present on most cells of the nephron, projecting from the apical surface of the renal epithelium into the tubule lumen. The cilia were believed to bend in the urine flow, leading to changes in signalling, however this has since been shown to be an experimental error (the bending of cilia was an artifact of focal plane compensation, and also the actual effect on micturition by severe hypertension and cardiac arrest) and that bending of cilia does not contribute to alterations in Ca flux. While it is not known how defects in the primary cilium lead to cyst development, it is thought to possibly be related to disruption of one of the many signaling pathways regulated by the primary cilium, including intracellular calcium, Wnt/β-catenin, cyclic adenosine monophosphate (cAMP), or planar cell polarity (PCP). Function of the primary cilium is impaired, resulting in disruption of a number of intracellular signaling cascades which produce differentiation of cystic epithelium, increased cell division, increased apoptosis, and loss of resorptive capacity. Diagnosis Polycystic kidney disease can be ascertained via a CT scan of abdomen, as well as, an MRI and ultrasound of the same area. A physical exam/test can reveal enlarged liver, heart murmurs and elevated blood pressure Natural history Most cases progress to bilateral disease in adulthood. Treatment In 2018, Jynarque (Tolvaptan) was introduced as the first FDA-approved treatment for PKD. In a recent long-term study, patients using Tolvaptan had a 6.4% higher kidney function after 5 years compared to standard of care. In 2019, a team of researchers at UCSB found that a ketogenic diet might be able to halt, or even reverse progression in mice, and the results of a first human case series study are showing potential benefit. The results of a 3-month randomized, prospective dietary intervention clinical trial are pending. In addition, recent research indicates that mild to moderate calorie restriction or time-restricted feeding slow the progression of autosomal dominant polycystic kidney disease (ADPKD) in mice Patient communities have been combining both ketogenic diets and time-restricted feeding with a low-oxalate diet to prevent the formation of stones and early reports show an average of 17% increase in kidney function after approximately one year on a ketogenic, time-restricted dietary regimen. If and when the disease progresses enough in a given case, the nephrologist or other practitioner and the patient will have to decide what form of renal replacement therapy will be used to treat end-stage kidney disease (kidney failure, typically stage 4 or 5 of chronic kidney disease).That will either be some form of dialysis, which can be done at least two different ways at varying frequencies and durations (whether it is done at home or in the clinic depends on the method used and the patients stability and training) and eventually, if they are eligible because of the nature and severity of their condition and if a suitable match can be found, unilateral or bilateral kidney transplantation.A Cochrane Review study of autosomal dominant polycystic kidney disease made note of the fact that it is important at all times, while avoiding antibiotic resistance, to control infections of the cysts in the kidneys, and if affected, the liver, when needed for a certain duration to combat infection, by using, "bacteriostatic and bacteriocidal drugs". Prognosis ADPKD individuals might have a normal life; conversely, ARPKD can cause kidney dysfunction and can lead to kidney failure by the age of 40–60. ADPKD1 and ADPKD2 are very different, in that ADPKD2 is much milder.Currently, there are no therapies proven effective to prevent the progression of ADPKD. Epidemiology PKD is one of the most common hereditary diseases in the United States, affecting more than 600,000 people. It is the cause of nearly 10% of all end-stage renal disease. It equally affects men, women, and all races. PKD occurs in some animals as well as humans. See also Autosomal recessive polycystic kidney disease References Further reading == External links ==

Aarogya what is Dysgeusia

Dysgeusia

Dysgeusia, also known as parageusia, is a distortion of the sense of taste. Dysgeusia is also often associated with ageusia, which is the complete lack of taste, and hypogeusia, which is a decrease in taste sensitivity. An alteration in taste or smell may be a secondary process in various disease states, or it may be the primary symptom. The distortion in the sense of taste is the only symptom, and diagnosis is usually complicated since the sense of taste is tied together with other sensory systems. Common causes of dysgeusia include chemotherapy, asthma treatment with albuterol, and zinc deficiency. Liver disease, hypothyroidism, and rarely certain types of seizures can also lead to dysgeusia. Different drugs could also be responsible for altering taste and resulting in dysgeusia. Due to the variety of causes of dysgeusia, there are many possible treatments that are effective in alleviating or terminating the symptoms of dysgeusia. These include artificial saliva, pilocarpine, zinc supplementation, alterations in drug therapy, and alpha lipoic acid. Signs and symptoms The alterations in the sense of taste, usually a metallic taste, and sometimes smell are the only symptoms. Causes Chemotherapy A major cause of dysgeusia is chemotherapy for cancer. Chemotherapy often induces damage to the oral cavity, resulting in oral mucositis, oral infection, and salivary gland dysfunction. Oral mucositis consists of inflammation of the mouth, along with sores and ulcers in the tissues. Healthy individuals normally have a diverse range of microbial organisms residing in their oral cavities; however, chemotherapy can permit these typically non-pathogenic agents to cause serious infection, which may result in a decrease in saliva. In addition, patients who undergo radiation therapy also lose salivary tissues. Saliva is an important component of the taste mechanism. Saliva both interacts with and protects the taste receptors in the mouth. Saliva mediates sour and sweet tastes through bicarbonate ions and glutamate, respectively. The salt taste is induced when sodium chloride levels surpass the concentration in the saliva. It has been reported that 50% of chemotherapy patients have had either dysgeusia or another form of taste impairment. Examples of chemotherapy treatments that can lead to dysgeusia are cyclophosphamide, cisplatin, vismodegib, and etoposide. The exact mechanism of chemotherapy-induced dysgeusia is unknown. Taste buds Distortions in the taste buds may give rise to dysgeusia. In a study conducted by Masahide Yasuda and Hitoshi Tomita from Nihon University of Japan, it has been observed that patients with this taste disorder have fewer microvilli than normal. In addition, the nucleus and cytoplasm of the taste bud cells have been reduced. Based on their findings, dysgeusia results from loss of microvilli and the reduction of Type III intracellular vesicles, all of which could potentially interfere with the gustatory pathway. Radiation to head and neck also results in direct destruction of taste buds, apart from effects of altered salivary output. Zinc deficiency Another primary cause of dysgeusia is zinc deficiency. While the exact role of zinc in dysgeusia is unknown, it has been cited that zinc is partly responsible for the repair and production of taste buds. Zinc somehow directly or indirectly interacts with carbonic anhydrase VI, influencing the concentration of gustin, which is linked to the production of taste buds. It has also been reported that patients treated with zinc experience an elevation in calcium concentration in the saliva. In order to work properly, taste buds rely on calcium receptors. Zinc “is an important cofactor for alkaline phosphatase, the most abundant enzyme in taste bud membranes; it is also a component of a parotid salivary protein important to the development and maintenance of normal taste buds.” Drugs There are also a wide variety of drugs that can trigger dysgeusia, including zopiclone, H1-antihistamines, such as azelastine and emedastine. Approximately 250 drugs affect taste, including Paxlovid, a drug used to treat COVID-19. Some describe so-called "Paxlovid mouth" as like a "mouthful of dirty pennies and rotten soymilk," according to the Wall Street Journal.The sodium channels linked to taste receptors can be inhibited by amiloride, and the creation of new taste buds and saliva can be impeded by antiproliferative drugs. Saliva can have traces of the drug, giving rise to a metallic flavor in the mouth; examples include lithium carbonate and tetracyclines. Drugs containing sulfhydryl groups, including penicillamine and captopril, may react with zinc and cause deficiency. Metronidazole and chlorhexidine have been found to interact with metal ions that associate with the cell membrane. Drugs that act by blocking the renin - angiotensin - aldosterone system, for example by antagonizing the angiotensin II receptor (as eprosartan does), have been linked to dysgeusia. There are few case reports claiming calcium channel blockers like Amlodipine also cause dysguesia by blocking calcium sensitive taste buds. Pregnancy Changes in hormone levels during pregnancy, such as estrogen, can affect the sense of taste. A study found that 93 percent of pregnant women reported some change in taste during pregnancy. Miscellaneous causes Xerostomia, also known as dry mouth syndrome, can precipitate dysgeusia because normal salivary flow and concentration are necessary for taste. Injury to the glossopharyngeal nerve can result in dysgeusia. In addition, damage done to the pons, thalamus, and midbrain, all of which compose the gustatory pathway, can be potential factors. In a case study, 22% of patients who were experiencing a bladder obstruction were also experiencing dysgeusia. Dysgeusia was eliminated in 100% of these patients once the obstruction was removed. Although it is uncertain what the relationship between bladder relief and dysgeusia entails, it has been observed that the areas responsible for urinary system and taste in the pons and cerebral cortex in the brain are close in proximity.Dysgeusia often occurs for unknown reasons. A wide range of miscellaneous factors may contribute to this taste disorder, such as gastric reflux, lead poisoning, and diabetes mellitus. A minority of pine nuts can apparently cause taste disturbances, for reasons which are not entirely proven. Certain pesticides can have damaging effects on the taste buds and nerves in the mouth. These pesticides include organochloride compounds and carbamate pesticides. Damage to the peripheral nerves, along with injury to the chorda tympani branch of the facial nerve, also cause dysgeusia. A surgical risk for laryngoscopy and tonsillectomy include dysgeusia. Patients with the burning mouth syndrome, most likely menopausal women, often have dysgeusia as well. Normal function The sense of taste is based on the detection of chemicals by specialized taste cells in the mouth. The mouth, throat, larynx, and esophagus all have taste buds, which are replaced every ten days. Each taste bud contains receptor cells. Afferent nerves make contact with the receptor cells at the base of the taste bud. A single taste bud is innervated by several afferent nerves, while a single efferent fiber innervates several taste buds. Fungiform papillae are present on the anterior portion of the tongue while circumvallate papillae and foliate papillae are found on the posterior portion of the tongue. The salivary glands are responsible for keeping the taste buds moist with saliva.A single taste bud is composed of four types of cells, and each taste bud has between 30 and 80 cells. Type I cells are thinly shaped, usually in the periphery of other cells. They also contain high amounts of chromatin. Type II cells have prominent nuclei and nucleoli with much less chromatin than Type I cells. Type III cells have multiple mitochondria and large vesicles. Type I, II, and III cells also contain synapses. Type IV cells are normally rooted at the posterior end of the taste bud. Every cell in the taste bud forms microvilli at the ends. Diagnosis In general, gustatory disorders are challenging to diagnose and evaluate. Because gustatory functions are tied to the sense of smell, the somatosensory system, and the perception of pain (such as in tasting spicy foods), it is difficult to examine sensations mediated through an individual system. In addition, gustatory dysfunction is rare when compared to olfactory disorders.Diagnosis of dysgeusia begins with the patient being questioned about salivation, swallowing, chewing, oral pain, previous ear infections (possibly indicated by hearing or balance problems), oral hygiene, and stomach problems. The initial history assessment also considers the possibility of accompanying diseases such as diabetes mellitus, hypothyroidism, or cancer. A clinical examination is conducted and includes an inspection of the tongue and the oral cavity. Furthermore, the ear canal is inspected, as lesions of the chorda tympani have a predilection for this site. Gustatory testing In order to further classify the extent of dysgeusia and clinically measure the sense of taste, gustatory testing may be performed. Gustatory testing is performed either as a whole-mouth procedure or as a regional test. In both techniques, natural or electrical stimuli can be used. In regional testing, 20 to 50 µL of liquid stimulus is presented to the anterior and posterior tongue using a pipette, soaked filter-paper disks, or cotton swabs. In whole mouth testing, small quantities (2-10 mL) of solution are administered, and the patient is asked to swish the solution around in the mouth.Threshold tests for sucrose (sweet), citric acid (sour), sodium chloride (salty), and quinine or caffeine (bitter) are frequently performed with natural stimuli. One of the most frequently used techniques is the "three-drop test." In this test, three drops of liquid are presented to the subject. One of the drops is of the taste stimulus, and the other two drops are pure water. Threshold is defined as the concentration at which the patient identifies the taste correctly three times in a row.Suprathreshold tests, which provide intensities of taste stimuli above threshold levels, are used to assess the patients ability to differentiate between different intensities of taste and to estimate the magnitude of suprathreshold loss of taste. From these tests, ratings of pleasantness can be obtained using either the direct scaling or magnitude matching method and may be of value in the diagnosis of dysgeusia. Direct scaling tests show the ability to discriminate among different intensities of stimuli and whether a stimulus of one quality (sweet) is stronger or weaker than a stimulus of another quality (sour). Direct scaling cannot be used to determine if a taste stimulus is being perceived at abnormal levels. In this case, magnitude matching is used, in which a patient is asked to rate the intensities of taste stimuli and stimuli of another sensory system, such as the loudness of a tone, on a similar scale. For example, the Connecticut Chemosensory Clinical Research Center asks patients to rate the intensities of NaCl, sucrose, citric acid and quinine-HCl stimuli, and the loudness of 1000 Hz tones.Other tests include identification or discrimination of common taste substances. Topical anesthesia of the tongue has been reported to be of use in the diagnosis of dysgeusia as well, since it has been shown to relieve the symptoms of dysgeusia temporarily. In addition to techniques based on the administration of chemicals to the tongue, electrogustometry is frequently used. It is based on the induction of gustatory sensations by means of an anodal electrical direct current. Patients usually report sour or metallic sensations similar to those associated with touching both poles of a live battery to the tongue. Although electrogustometry is widely used, there seems to be a poor correlation between electrically and chemically induced sensations. Diagnostic tools Certain diagnostic tools can also be used to help determine the extent of dysgeusia. Electrophysiological tests and simple reflex tests may be applied to identify abnormalities in the nerve-to-brainstem pathways. For example, the blink reflex may be used to evaluate the integrity of the trigeminal nerve–pontine brainstem–facial nerve pathway, which may play a role in gustatory function.Structural imaging is routinely used to investigate lesions in the taste pathway. Magnetic resonance imaging allows direct visualization of the cranial nerves. Furthermore, it provides significant information about the type and cause of a lesion. Analysis of mucosal blood flow in the oral cavity in combination with the assessment of autonomous cardiovascular factors appears to be useful in the diagnosis of autonomic nervous system disorders in burning mouth syndrome and in patients with inborn disorders, both of which are associated with gustatory dysfunction. Cell cultures may also be used when fungal or bacterial infections are suspected.In addition, the analysis of saliva should be performed, as it constitutes the environment of taste receptors, including transport of tastes to the receptor and protection of the taste receptor. Typical clinical investigations involve sialometry and sialochemistry. Studies have shown that electron micrographs of taste receptors obtained from saliva samples indicate pathological changes in the taste buds of patients with dysgeusia and other gustatory disorders. Treatments Artificial saliva and pilocarpine Because medications have been linked to approximately 22% to 28% of all cases of dysgeusia, researching a treatment for this particular cause has been important. Xerostomia, or a decrease in saliva flow, can be a side effect of many drugs, which, in turn, can lead to the development of taste disturbances such as dysgeusia. Patients can lessen the effects of xerostomia with breath mints, sugarless gum, or lozenges, or physicians can increase saliva flow with artificial saliva or oral pilocarpine. Artificial saliva mimics the characteristics of natural saliva by lubricating and protecting the mouth but does not provide any digestive or enzymatic benefits. Pilocarpine is a cholinergic drug meaning it has the same effects as the neurotransmitter acetylcholine. Acetylcholine has the function of stimulating the salivary glands to actively produce saliva. The increase in saliva flow is effective in improving the movement of tastants to the taste buds. Zinc deficiency Zinc supplementation Approximately one half of drug-related taste distortions are caused by a zinc deficiency. Many medications are known to chelate, or bind, zinc, preventing the element from functioning properly. Due to the causal relationship of insufficient zinc levels to taste disorders, research has been conducted to test the efficacy of zinc supplementation as a possible treatment for dysgeusia. In a randomized clinical trial, fifty patients with idiopathic dysgeusia were given either zinc or a lactose placebo. The patients prescribed the zinc reported experiencing improved taste function and less severe symptoms compared to the control group, suggesting that zinc may be a beneficial treatment. The efficacy of zinc, however, has been ambiguous in the past. In a second study, 94% of patients who were provided with zinc supplementation did not experience any improvement in their condition. This ambiguity is most likely due to small sample sizes and the wide range of causes of dysgeusia. A recommended daily oral dose of 25–100 mg, as zinc gluconate, appears to be an effective treatment for taste dysfunction provided that there are low levels of zinc in the blood serum. There is not a sufficient amount of evidence to determine whether or not zinc supplementation is able to treat dysgeusia when low zinc concentrations are not detected in the blood.A Cochrane Review in 2017 assessed the effects of different interventions for the management of taste disturbances. There was very low-quality evidence to support the role of zinc supplementation in the improvement of taste acuity and taste discrimination in patients with zinc deficiency or idiopathic taste disorders. Further research is required to improve the quality of evidence for zinc supplementation as an effective intervention for the management of dysgeusia. Zinc infusion in chemotherapy It has been reported that approximately 68% of cancer patients undergoing chemotherapy experience disturbances in sensory perception such as dysgeusia. In a pilot study involving twelve lung cancer patients, chemotherapy drugs were infused with zinc in order to test its potential as a treatment. The results indicated that, after two weeks, no taste disturbances were reported by the patients who received the zinc-supplemented treatment while most of the patients in the control group who did not receive the zinc reported taste alterations. A multi-institutional study involving a larger sample size of 169 patients, however, indicated that zinc-infused chemotherapy did not have an effect on the development of taste disorders in cancer patients. An excess amount of zinc in the body can have negative effects on the immune system, and physicians must use caution when administering zinc to immunocompromised cancer patients. Because taste disorders can have detrimental effects on a patients quality of life, more research needs to be conducted concerning possible treatments such as zinc supplementation. Altering drug therapy The effects of drug-related dysgeusia can often be reversed by stopping the patients regimen of the taste altering medication. In one case, a forty-eight-year-old woman who had hypertension was being treated with valsartan. Due to this drugs inability to treat her condition, she began taking a regimen of eprosartan, an angiotensin II receptor antagonist. Within three weeks, she began experiencing a metallic taste and a burning sensation in her mouth that ceased when she stopped taking the medication. When she began taking eprosartan on a second occasion, her dysgeusia returned. In a second case, a fifty-nine-year-old man was prescribed amlodipine in order to treat his hypertension. After eight years of taking the drug, he developed a loss of taste sensation and numbness in his tongue. When he ran out of his medication, he decided not to obtain a refill and stopped taking amlodipine. Following this self-removal, he reported experiencing a return of his taste sensation. Once he refilled his prescription and began taking amlodipine a second time, his taste disturbance reoccurred. These two cases suggest that there is an association between these drugs and taste disorders. This link is supported by the "de-challenge" and "re-challenge" that took place in both instances. It appears that drug-induced dysgeusia can be alleviated by reducing the drugs dose or by substituting a second drug from the same class. Alpha lipoic acid Alpha lipoic acid (ALA) is an antioxidant that is made naturally by human cells. It can also be administered in capsules or can be found in foods such as red meat, organ meats, and yeast. Like other antioxidants, it functions by ridding the body of harmful free radicals that can cause damage to tissues and organs. It has an important role in the Krebs cycle as a coenzyme leading to the production of antioxidants, intracellular glutathione, and nerve-growth factors. Animal research has also uncovered the ability of ALA to improve nerve conduction velocity. Because flavors are perceived by differences in electric potential through specific nerves innervating the tongue, idiopathic dysgeusia may be a form of a neuropathy. ALA has proven to be an effective treatment for burning mouth syndrome spurring studies in its potential to treat dysgeusia. In a study of forty-four patients diagnosed with the disorder, one half was treated with the drug for two months while the other half, the control group, was given a placebo for two months followed by a two-month treatment of ALA. The results reported show that 91% of the group initially treated with ALA reported an improvement in their condition compared to only 36% of the control group. After the control group was treated with ALA, 72% reported an improvement. This study suggests that ALA may be a potential treatment for patients and supports that full double blind randomized studies should be performed. Managing dysgeusia In addition to the aforementioned treatments, there are also many management approaches that can alleviate the symptoms of dysgeusia. These include using non-metallic silverware, avoiding metallic or bitter tasting foods, increasing the consumption of foods high in protein, flavoring foods with spices and seasonings, serving foods cold in order to reduce any unpleasant taste or odor, frequently brushing ones teeth and utilizing mouthwash, or using sialogogues such as chewing sugar-free gum or sour-tasting drops that stimulate the productivity of saliva. When taste is impeded, the food experience can be improved through means other than taste, such as texture, aroma, temperature, and color. Psychological impacts People with dysgeusia are also forced to manage the impact that the disorder has on their quality of life. An altered taste has effects on food choice and intake and can lead to weight loss, malnutrition, impaired immunity, and a decline in health. Patients diagnosed with dysgeusia must use caution when adding sugar and salt to food and must be sure not to overcompensate for their lack of taste with excess amounts. Since the elderly are often on multiple medications, they are at risk for taste disturbances increasing the chances of developing depression, loss of appetite, and extreme weight loss. This is cause for an evaluation and management of their dysgeusia. In patients undergoing chemotherapy, taste distortions can often be severe and make compliance with cancer treatment difficult. Other problems that may arise include anorexia and behavioral changes that can be misinterpreted as psychiatric delusions regarding food. Symptoms including paranoia, amnesia, cerebellar malfunction, and lethargy can also manifest when undergoing histidine treatment. Future research Every year, more than 200,000 individuals see their physicians concerning chemosensory problems, and many more taste disturbances are never reported. Due to the large number of persons affected by taste disorders, basic and clinical research are receiving support at different institutions and chemosensory research centers across the country. These taste and smell clinics are focusing their research on better understanding the mechanisms involved in gustatory function and taste disorders such as dysgeusia. For example, the National Institute on Deafness and Other Communication Disorders is looking into the mechanisms underlying the key receptors on taste cells and applying this knowledge to the future of medications and artificial food products. Meanwhile, the Taste and Smell Clinic at the University of Connecticut Health Center is integrating behavioral, neurophysiological, and genetic studies involving stimulus concentrations and intensities in order to better understand taste function. See also Anosmia Parosmia References External links Dysgeusia at NIH

Can you describe Chronic myelomonocytic leukemia, to me Aarogya

Chronic myelomonocytic leukemia

Chronic myelomonocytic leukemia (CMML) is a type of leukemia, which are cancers of the blood-forming cells of the bone marrow. In adults, blood cells are formed in the bone marrow, by a process that is known as haematopoiesis. In CMML, there are increased numbers of monocytes and immature blood cells (blasts) in the peripheral blood and bone marrow, as well as abnormal looking cells (dysplasia) in at least one type of blood cell.CMML shows characteristics of a myelodysplastic syndrome (MDS); a disorder that produces abnormal looking blood cells, and a myeloproliferative neoplasm (MPN); a disorder characterised by the overproduction of blood cells. For this reason, CMML was reclassified as a MDS/MPN overlap disorder in 2002. For a diagnosis of CMML, the World Health Organization (WHO) states that the blood monocyte count must be >1x109/L, no Philadelphia chromosome or mutations in the PDGFRA or PDGFRB gene should be present, the blast count must be <20% and dysplasia of at least one lineage of myeloid blood cell should be present.Azacitidine is a drug used to treat CMML and is approved by the Food and Drug Administration (FDA) and the European Medicines Agency. Stem cell transplant is also used to treat CMML, and involves the transplantation of donor haematopoietic stem cells into the recipient. Blood transfusion and erythropoietin are used to treat disease associated anaemia. Signs and symptoms One of the most common signs of CMML is splenomegaly, found in approximately half of cases. Other less frequent signs and symptoms consist of anaemia, fever, weight loss, night sweats, infection, bleeding, synovitis, lymphadenopathy, skin rashes, pleural effusion, pericardial effusion and peritoneal effusion. Cause Although the cause of CMML is unknown, environmental carcinogens, ionising radiation and cytotoxic agents may have a role in causing disease. Approximately one third of cases of MDS with a monocyte count of >10% and <1x109/L will progress to CMML. Pathogenesis With a high rate of Ras mutation in CMML, deregulation of this signalling pathway has been linked to the pathogenesis of the disease. Tumour necrosis factor, GM-CSF, interleukin-3, interleukin-4, interleukin-6, and interleukin-10 may have a role in hyperproliferative CMML cells. These cytokines can stimulate the growth of CMML in vitro. Hypermethylation of cytosine residues (usually in the promoter regions of genes) occurs in many malignancies to regulate gene expression. One commonly hypermethylated gene in CMML is p15INK4b, a gene involved in cell cycle regulation. Genetic mutations Clonal genetic abnormalities are common in CMML but they are not specific for diagnosis of the disease. The most common found are the 8+, −7/del (7q) and structural 12p abnormalities. KRAS and NRAS are mutated in 25–40% of the cases of CMML. The Jak2 V617F mutation is found in 10% of cases. Mutations in transcription factors such as RUNX1, CEBPA, NPM1 and WT1 have been found in up to 30% of cases. Mutations of CBL are found in approximately 5–18% of cases. Mutations in the TET2 gene are found in approximately 40–50% of CMML. Inactivating mutations in one of the two parental GATA2 genes lead to a reduction, i.e. a haploinsufficiency, in the cellular levels of the genes product, the GATA2 transcription factor, and thereby to a rare autosomal dominant genetic disease, GATA2 deficiency. This disease is associated with a highly variable set of disorders including the myelodysplastic syndrome, acute myeloid leukemia, and CMML. GATA2-deficiency-induced CMML, like other types of CMML, is commonly preceded by monocytosis. Diagnosis Blood films display a range of abnormalities. A monocyte count of >1x109/L is essential for a diagnosis of CMML. Other features may include; leukocytosis (50% of cases); left shift and dysplasia of monocytes and granulocytes; presence of metamyelocytes, myelocytes and promonocytes; monocytes with hypersegmented/abnormal shaped nuclei, increased cytoplasmic basophilia and/or the presence of cytoplasmic granules; eosinophilia (in cases of CMML with eosinophilia); and spherocytosis (in cases of direct Coombs test, DCT, positive haemolytic anaemia). Platelet counts may be reduced, increased or normal. Haemoglobin levels are usually reduced with normocytic and normochromic red blood cells. Autoantibodies and cold agglutinins may be present and 10% of CMML is DCT positive.Bone marrow aspirates will display hypercellularity with increased counts of granulocytic and monocytic cells. Bone marrow core biopsies may show a predominance of myelocytic and monocytic cells, abnormal localisation of immature precursors and dysplastic megakaryocytes. Monocytic nodules are a common feature in biopsies.The phenotypical characteristics of CMML are; CD11b, CD11c, CD14, CD33, CD45 and CD64 seen in 100% of cases; CD13 found in 95% of cases; CD4 found in 76% of cases; HLA-DR found in 71% of cases; CD56 found in 53% of cases; CD2 found in 34% of cases; CD16 found in 29% of cases; CD10 found in 28% of cases; CD23 and CD7 found in 9% of cases; and CD117 found in 5% of cases. Classification Leukemia subtypes are categorised into single clinical entities so that they can be diagnosed and treated appropriately. Leukaemias are subdivided into lymphoid and myeloid neoplasms, depending on which bone marrow cells are cancerous. The myeloid neoplasms contain acute and chronic leukemias, myelodysplastic syndromes (MDSs) and myeloproliferative neoplasms (MPNs). MPNs are characterised by increased production of myeloid blood cells, with a higher than normal number of mature cells. Unlike MPNs, MDSs have a dysfunctional production of myeloid cells with a reduced number of mature cells. Many of the cells produced in MDS are abnormal looking, known as dysplasia. CMML shows characteristics of both groups and thus is a difficult disease to categorise. FAB classification The French-American-British (FAB) classification system was published in 1976 to classify the leukaemias. It placed CMML into the category of MDS, along with the refractory anaemia, refractory anaemia with ring sideroblasts, refractory anaemia with excess blasts and refractory anaemia with excess blasts in transformation. The system does have clinical utility; however factors such as cytogenetic status are not within the remit of the classification. For this reason, many disease entities in these groups show a great deal of heterogeneity. WHO classification In 2001, the WHO Classification of Myeloid Neoplasms was published, classifying CMML into a new group of diseases, the myelodysplastic/myeloproliferative neoplasms (MDS/MPN), reflecting the diseases neoplastic nature. Other diseases in this category are juvenile myelomonocytic leukaemia, atypical CML; BCR-ABL1 negative and MDS/MPD unclassifiable. These MDS/MPN overlap syndromes have effective production of some lineages of blood cells, but show ineffective proliferation of other lineages. The 2008 revision of the classification moved cases of CMML with PDGFR gene translocations to a new group, myeloid/lymphoid neoplasms with eosinophilia with abnormalities of PDGFRA, PDGFRB or FGFR1. Diagnostic criteria FAB criteria The FAB criteria for diagnosis are as follows: Monocyte count >1x109/L 0–19% blasts in bone marrow <5% blasts in peripheral bloodThe FAB also arbitrarily categorises CMML into myelodysplastic-like and myeloproliferative-like groups. A white blood count of 13x109 is used as a cut-off to differentiate the two. WHO criteria The WHO criteria for diagnosis are as follows: Persistent peripheral blood monocytosis with counts >1x109/L No Philadelphia chromosome or BCR-ABL1 fusion gene No rearrangement of PDGFRA or PDGFRB gene <20% myeloblasts, monoblasts and promonocytes in peripheral blood or bone marrow Dysplasia in one or more of the myeloid lineages; if myelodysplasia is absent or minimal then a diagnosis of CMML can be made if other requirements are met and: A molecular genetic abnormality is present in haematopoietic cells, or Monocytosis present for ≥3 months and other causes of monocytosis have been ruled outWHO defined CMML has two main subsets, CMML-1 and CMML-2. CMML-1 is diagnosed if myeloblasts, monoblasts and promonocytes are <5% of peripheral blood and <10% of bone marrow. CMML-2 is diagnosed if: Myeloblasts, monoblasts or promonocytes are 5-19% in blood, or Myeloblasts, monoblasts or promonocytes are 10-19% in bone marrow, or Auer rods are presentCMML-1 and CMML-2 can be additionally grouped as CMML-1 or CMML-2 with eosinophilia. These are diagnosed if the above criteria are met and the blood eosinophil count is >1.5x109/L.Presence of two or more phenotypic abnormalities can aid a diagnosis of CMML in the absence of identifying cytogenetic or dysplastic features. These can include the expression of CD56 and/or CD2, or under-expression of HLA-DR. Prognosis Factors affecting prognosis CMML-2 has a reduced overall survival as compared with CMML-1, with median survivals of 15 and 20 months, respectively. Myeloproliferative CMML (>13x109 monocytes/L) has a reduced survival compared with myelodysplastic CMML. A platelet count of <100 x109/L reduces overall survival. A haemoglobin level of <10g/dL has a reduced overall survival. Some cytogenetic abnormalities have implications on the prognosis of CMML. Normal karyotypes or the single loss of the Y chromosome have low risk prognoses. Trisomy 8, chromosome 7 abnormalities and complex karyotypes comprise a high risk group. Other cytogenetic abnormalities have intermediate prognoses. Somatic mutations in genes such as ASXL1 and EZH2 are associated with a poor prognosis.CMML has a 20–30% chance of transformation to AML, a lower rate than other similar diseases. The CMML-2 subtype is associated with increased risk of transformation and ASXL1 and RUNX1 mutations also increase the risk of transition to AML. Scoring systems IPSS The International Prognostic Scoring System (IPSS) was developed in the mid-1990s to assess the prognosis of MDS patients. This system stratifies cases into 2 groups; a lower-risk group (sub divided into low and intermediate-1) and a higher risk (subdivided into intermediate-2 and high). It uses the blast percentage, number of cytopenias and bone marrow cytogenetics data to place cases of CMML into these groups. Due to the scoring system being developed for MDS, the more myeloproliferative cases of CMML (WBC >13x109) are excluded from the scoring system. Although the IPSS scoring system is used clinically, there is a high variability in each group. For this reason, new modalities for assessing prognosis in MDS (and CMML) are being developed. MD Anderson Prognostic Scoring System A new method developed using data from the M.D. Anderson Cancer Center found that a haemoglobin level of <12g/dL, total circulating lymphocyte count of >2.5 x 109/L, >0% immature myeloid cells, >10% bone marrow blasts causes a reduced overall survival. This data allows cases of CMML to be stratified into low, intermediate-1, intermediate-2 and high risk groups. These groups have median survival times of 24, 15, 8 and 5 months respectively. The Düsseldorf score The Düsseldorf score stratifies cases using four categories, giving one point for each; bone marrow blasts ≥5%, LDH >200U/L, haemoglobin ≤9g/dL and a platelet count ≤100,000/uL. A score of 0 indicates a low risk group 1-2 indicates an intermediate risk group and 3-4 indicates a high risk group. The cumulative 2 year survival of scores 0, 1-2 and 3-4 is 91%, 52% and 9%; and risk of AML transformation is 0%, 19% and 54% respectively. Treatment The treatment of CMML remains challenging due to the lack of clinical trials investigating the disease as its own clinical entity. It is often grouped with MDS in clinical trials, and for this reason the treatment of CMML is very similar to that of MDS. Most cases are dealt with as supportive rather than curative because most therapies do not effectively increase survival. Indications for treatment include the presence of B symptoms, symptomatic organ involvement, increasing blood counts, hyperleukocytosis, leukostasis and/or worsening cytopenias.Blood transfusions and erythropoietin administration are used to raise haemoglobin levels in cases with anemia.Azacitidine is a drug approved by the U.S. Food and Drug Administration (FDA) for the treatment of CMML and by the European Medicines Agency (EMA) for high risk non-proliferative CMML with 10–19% marrow blasts. It is a cytidine analogue that causes hypomethylation of DNA by inhibition of DNA methyltransferase. Decitabine is a similar drug to azacitidine and is approved by the FDA for treatments of all subtypes of MDS, including CMML. Hydroxyurea is a chemotherapy that is used in the myeloproliferative form of CMML to reduce cell numbers. Decitabine/cedazuridine (Inqovi) is a fixed-dosed combination medication for the treatment of adults with myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML) that was approved for use in the United States in July 2020.Hematopoietic stem cell transplantation remains the only curative treatment for CMML. However, due to the late age of onset and presence of other illnesses, this form of treatment is often not possible. Epidemiology There have been few individual epidemiological studies of CMML, due to the difficulty in the disease classification. CMML has an estimated incidence of less than 1 per 100,000 persons per year. The median age of diagnosis is 65–75. CMML has a propensity for males rather than females, at a ratio of 1.5–3:1. References == External links ==

Aarogya, give me a short description about Anhedonia

Anhedonia

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

Hello Aarogya, could you help me understand about Pulled elbow

Pulled elbow

A pulled elbow, also known as a radial head subluxation, is when the ligament that wraps around the radial head slips off. Often a child will hold their arm against their body with the elbow slightly bent. They will not move the arm as this results in pain. Touching the arm, without moving the elbow, is usually not painful.A pulled elbow typically results from a sudden pull on an extended arm. This may occur when lifting or swinging a child by the arms. The underlying mechanism involves slippage of the annular ligament off of the head of the radius followed by the ligament getting stuck between the radius and humerus. Diagnosis is often based on symptoms. X-rays may be done to rule out other problems.Prevention is by avoiding potential causes. Treatment is by reduction. Moving the forearm into a palms down position with straightening at the elbow appears to be more effective than moving it into a palms up position followed by bending at the elbow. Following a successful reduction the child should return to normal within a few minutes. A pulled elbow is common. It generally occurs in children between the ages of 1 and 4 years old, though it can happen up to 7 years old. Signs and symptoms Symptoms include: The child stops using the arm, which is held in extension (or slightly bent) and palm down. Minimal swelling. All movements are permitted except supination. Caused by longitudinal traction with the wrist in pronation, although in a series only 51% of people were reported to have this mechanism, with 22% reporting falls, and patients less than 6 months of age noted to have the injury after rolling over in bed. Cause This injury has also been reported in babies younger than six months and in older children up to the preteen years. There is a slight predilection for this injury to occur in girls and in the left arm. The classic mechanism of injury is longitudinal traction on the arm with the wrist in pronation, as occurs when the child is lifted up by the wrist. There is no support for the common assumption that a relatively small head of the radius as compared to the neck of the radius predisposes the young to this injury. Pathophysiology The distal attachment of the annular ligament covering the radial head is weaker in children than in adults, allowing it to be more easily torn. The older child will usually point to the dorsal aspect of the proximal forearm when asked where it hurts. This may mislead one to suspect a buckle fracture of the proximal radius. There is no tear in the soft tissue (probably due to the pliability of young connective tissues).The forearm contains two bones: the radius and the ulna. These bones are attached to each other both at the proximal, or elbow, end and also at the distal, or wrist, end. Among other movements, the forearm is capable of pronation and supination, which is to say rotation about the long axis of the forearm. In this movement the ulna, which is connected to the humerus by a simple hinge-joint, remains stationary, while the radius rotates, carrying the wrist and hand with it. To allow this rotation, the proximal (elbow) end of the radius is held in proximity to the ulna by a ligament known as the annular ligament. This is a circular ligamentous structure within which the radius is free, with constraints existing elsewhere in the forearm, to rotate. The proximal end of the radius in young children is conical, with the wider end of the cone nearest the elbow. With the passage of time the shape of this bone changes, becoming more cylindrical but with the proximal end being widened.If the forearm of a young child is pulled, it is possible for this traction to pull the radius into the annular ligament with enough force to cause it to be jammed therein. This causes significant pain, partial limitation of flexion/extension of the elbow and total loss of pronation/supination in the affected arm. The situation is rare in adults, or in older children, because the changing shape of the radius associated with growth prevents it. Diagnosis Diagnosis is often based on symptoms. X-rays may be done to rule out other problems. Treatment To resolve the problem, the affected arm is moved in a way that causes the joint to move back into a normal position. The two main methods are hyperpronation and a combination of supination and flexion. Hyperpronation has a higher success rate and is less painful than a supination-flexion maneuver. References == External links ==

Aarogya, What does Nevus mean

Nevus

Nevus (plural nevi) is a nonspecific medical term for a visible, circumscribed, chronic lesion of the skin or mucosa. The term originates from nævus, which is Latin for "birthmark"; however, a nevus can be either congenital (present at birth) or acquired. Common terms, including mole, birthmark, and beauty mark, are used to describe nevi, but these terms do not distinguish specific types of nevi from one another. Classification The term nevus is applied to a number of conditions caused by neoplasias and hyperplasias of melanocytes, as well as a number of pigmentation disorders, both hypermelanotic (containing increased melanin, the pigment responsible for skin color) and hypomelanotic (containing decreased melanin). Suspicious skin moles which are multi-colored or pink may be a finding in skin cancer. Increased melanin Usually acquired Melanocytic nevus Melanocytic nevi can be categorized based on the location of melanocytic cellsJunctional: epidermis Intradermal: dermis Compound: epidermis and dermis Atypical (dysplastic) nevus: This type of nevus must be diagnosed based on histological features. Clinically, atypical nevi are characterized by variable pigmentation and irregular borders. Beckers nevus Blue nevus (rarely congenital): A classic blue nevus is usually smaller than 1 cm, flat, and blue-black in color. Horis nevus Nevus spilus (speckled lentiginous nevus): This lesion includes dark speckles within a tan-brown background. Pigmented spindle cell nevus Spitz nevus Zosteriform lentiginous nevus Usually congenital Congenital melanocytic nevus These nevi are often categorized based on size, however, the lesions usually grow in proportion to the body over time, so the category may change over an individuals life. This categorization is important because large congenital melanocytic nevi are associated with an increased risk of melanoma, a serious type of skin cancer.Small: <1.5 cm Medium: 1.5–19.9 cm Large: ≥ 20 cm Nevus of Ito Nevus of Ota Decreased melanin Acquired Nevus anemicus Congenital Nevus depigmentosus Additional types of nevi do not involve disorders of pigmentation or melanocytes. These additional nevi represent hamartomatous proliferations of the epithelium, connective tissue, and vascular malformations. Epidermal nevi These nevi represent excess growth of specific cells types found in the skin, including those that make up oil and sweat glands. Verrucous epidermal nevus Nevus sebaceous Nevus comedonicus Eccrine nevus Apocrine nevus Connective tissue nevi Connective tissue nevi represent abnormalities of collagen in the dermis, the deep layer of the skin. Collagenoma Elastoma Vascular nevi These nevi represent excess growth of blood vessels, including capillaries. Nevus simplex (nevus flammeus nuchae), also known as a stork bite or salmon patch. Intramucosal nevi An intramucosal nevus is a nevus within the mucosa as found in for example the mouth and genital areas. In the mouth, they are found most frequently on the hard palate. They are typically light brown and dome-shaped. Intramucosal nevi account for 64% of all reported case of oral nevi. Diagnosis Nevi are typically diagnosed clinically with the naked eye or using dermatoscopy. More advanced imaging tests are available for distinguishing melanocytic nevi from melanoma, including computerized dermoscopy and image analysis. The management of nevi depends on the type of nevus and the degree of diagnostic uncertainty. Some nevi are known to be benign, and may simply be monitored over time. Others may warrant more thorough examination and biopsy for histopathological examination (looking at a sample of skin under a microscope to detect unique cellular features). For example, a clinician may want to determine whether a pigmented nevus is a type of melanocytic nevus, dysplastic nevus, or melanoma as some of these skin lesions pose a risk for malignancy. The ABCDE criteria (asymmetry, border irregularity, color variegation, diameter > 6 mm, and evolution) are often used to distinguish nevi from melanomas in adults, while modified criteria (amelanosis, bleeding or bumps, uniform color, small diameter or de novo, and evolution) can be used when evaluating suspicious lesions in children. In addition to histopathological examination, some lesions may also warrant additional tests to aid in diagnosis, including special stains, immunohistochemistry, and electron microscopy. Typically, the nevi that exist since childhood are harmless. Differential diagnoses Hypermelanotic nevi must be differentiated from other types of pigmented skin lesions, including: Lentigo simplex Solar lentigo Café au lait macule Ink-spot lentigo Mucosal melanotic macule Mongolian spot (dermal melanocytosis) Management The management of a nevus depends on the specific diagnosis, however, the options for treatment generally include the following modalities: Observation Destruction Chemical peels Cryotherapy Dermabrasion Electrodessication Laser ablation Surgery The decision to observe or treat a nevus may depend on a number of factors, including cosmetic concerns, irritative symptoms (e.g., pruritus), ulceration, infection, and concern for potential malignancy. Syndromes The term nevus is included in the names of multiple dermatologic syndromes: Basal cell nevus syndrome Blue rubber bleb nevus syndrome Dysplastic nevus syndrome Epidermal nevus syndrome Linear nevus sebaceous syndrome Etymology A naevus may also be spelled nevus. The plural is nevi or naevi. The word is from nævus, Latin for "birthmark" and is correctly pronounced Nye-voos. See also Skin lesion References == External links ==

Give me a short description about Proteinuria , Aarogya

Proteinuria

Proteinuria is the presence of excess proteins in the urine. In healthy persons, urine contains very little protein; an excess is suggestive of illness. Excess protein in the urine often causes the urine to become foamy (although this symptom may also be caused by other conditions). Severe proteinuria can cause nephrotic syndrome in which there is worsening swelling of the body. Signs and symptoms Proteinuria often causes no symptoms and it may only be discovered incidentally.Foamy urine is considered a cardinal sign of proteinuria, but only a third of people with foamy urine have proteinuria as the underlying cause. It may also be caused by bilirubin in the urine (bilirubinuria), retrograde ejaculation, pneumaturia (air bubbles in the urine) due to a fistula, or drugs such as pyridium. Causes There are three main mechanisms to cause proteinuria: Due to disease in the glomerulus Because of increased quantity of proteins in serum (overflow proteinuria) Due to low reabsorption at proximal tubule (Fanconi syndrome)Proteinuria can also be caused by certain biological agents, such as bevacizumab (Avastin) used in cancer treatment. Excessive fluid intake (drinking in excess of 4 litres of water per day) is another cause.Proteinuria may be a sign of renal (kidney) damage. Since serum proteins are readily reabsorbed from urine, the presence of excess protein indicates either an insufficiency of absorption or impaired filtration. People with diabetes may have damaged nephrons and develop proteinuria. The most common cause of proteinuria is diabetes, and in any person with proteinuria and diabetes, the cause of the underlying proteinuria should be separated into two categories: diabetic proteinuria versus the field. With severe proteinuria, general hypoproteinemia can develop which results in diminished oncotic pressure. Symptoms of diminished oncotic pressure may include ascites, edema and hydrothorax. Conditions with proteinuria Proteinuria may be a feature of the following conditions: Nephrotic syndromes (i.e. intrinsic kidney failure) Pre-eclampsia Eclampsia Toxic lesions of kidneys Amyloidosis Collagen vascular diseases (e.g. systemic lupus erythematosus) Dehydration Glomerular diseases, such as membranous glomerulonephritis, focal segmental glomerulonephritis, minimal change disease (lipoid nephrosis) Strenuous exercise Stress Benign orthostatic (postural) proteinuria Focal segmental glomerulosclerosis (FSGS) IgA nephropathy (i.e. Bergers disease) IgM nephropathy Membranoproliferative glomerulonephritis Membranous nephropathy Minimal change disease Sarcoidosis Alport syndrome Diabetes mellitus (diabetic nephropathy) Drugs (e.g. NSAIDs, nicotine, penicillamine, lithium carbonate, gold and other heavy metals, ACE inhibitors, antibiotics, or opiates (especially heroin) Fabry disease Infections (e.g. HIV, syphilis, hepatitis, poststreptococcal infection, urinary schistosomiasis) Aminoaciduria Fanconi syndrome in association with Wilson disease Hypertensive nephrosclerosis Interstitial nephritis Sickle cell disease Hemoglobinuria Multiple myeloma Myoglobinuria Organ rejection: Ebola virus disease Nail–patella syndrome Familial Mediterranean fever HELLP syndrome Systemic lupus erythematosus Granulomatosis with polyangiitis Rheumatoid arthritis Glycogen storage disease type 1 Goodpasture syndrome Henoch–Schönlein purpura A urinary tract infection which has spread to the kidney(s) Sjögren syndrome Post-infectious glomerulonephritis Living kidney donor Polycystic kidney disease Bence–Jones proteinuria Amyloidosis Pre-malignant plasma cell dyscrasias: Monoclonal gammopathy of undetermined significance Smoldering multiple myeloma Malignant plasma cell dyscrasias Multiple myeloma Waldenströms macroglobulinemia Other malignancies Chronic lymphocytic leukemia Rare cases of other Lymphoid leukemias Rare cases of Lymphomas Pathophysiology Protein is the building block of all living organisms. When kidneys are functioning properly by filtering the blood, they distinguish the proteins from the wastes which were previously present together in the blood. Thereafter, kidneys retain or reabsorb the filtered proteins and return them to the circulating blood while removing wastes by excreting them in the urine. Whenever the kidney is compromised, their ability to filter the blood by differentiating protein from the waste, or retaining the filtered protein then returning which back to the body, is damaged. As a result, there is a significant amount of protein to be discharged along with waste in the urine that makes the concentration of proteins in urine high enough to be detected by medical machine.Medical testing equipment has improved over time, and as a result tests are better able to detect smaller quantities of protein. Protein in urine is considered normal as long as the value remains within the normal reference range. Variation exists between healthy patients, and it is generally considered harmless for the kidney to fail to retain a few proteins in the blood, letting those protein discharge from the body through urine. Albumin and immunoglobins Albumin is a protein produced by the liver which makes up roughly 50%-60% of the proteins in the blood while the other 40%-50% are proteins other than albumin, such as immunoglobins. This is why the concentration of albumin in the urine is one of the single sensitive indicators of kidney disease, particularly for those with diabetes or hypertension, compared to routine proteinuria examination.As the loss of proteins from the body progresses, the suffering will gradually become symptomatic.The exception applies to the scenario when theres an overproduction of proteins in the body, in which the kidney is not to blame. Diagnosis Conventionally, proteinuria is diagnosed by a simple dipstick test, although it is possible for the test to give a false negative reading, even with nephrotic range proteinuria if the urine is dilute. False negatives may also occur if the protein in the urine is composed mainly of globulins or Bence Jones proteins because the reagent on the test strips, bromophenol blue, is highly specific for albumin. Traditionally, dipstick protein tests would be quantified by measuring the total quantity of protein in a 24-hour urine collection test, and abnormal globulins by specific requests for protein electrophoresis. Trace results may be produced in response to excretion of Tamm–Horsfall mucoprotein. More recently developed technology detects human serum albumin (HSA) through the use of liquid crystals (LCs). The presence of HSA molecules disrupts the LCs supported on the AHSA-decorated slides thereby producing bright optical signals which are easily distinguishable. Using this assay, concentrations of HSA as low as 15 µg/mL can be detected.Alternatively, the concentration of protein in the urine may be compared to the creatinine level in a spot urine sample. This is termed the protein/creatinine ratio. The 2005 UK Chronic Kidney Disease guidelines state that protein/creatinine ratio is a better test than 24-hour urinary protein measurement. Proteinuria is defined as a protein/creatinine ratio greater than 45 mg/mmol (which is equivalent to albumin/creatinine ratio of greater than 30 mg/mmol or approximately 300 mg/g) with very high levels of proteinuria having a ratio greater than 100 mg/mmol.Protein dipstick measurements should not be confused with the amount of protein detected on a test for microalbuminuria which denotes values for protein for urine in mg/day versus urine protein dipstick values which denote values for protein in mg/dL. That is, there is a basal level of proteinuria that can occur below 30 mg/day which is considered non-pathology. Values between 30 and 300 mg/day are termed microalbuminuria which is considered pathologic. Urine protein lab values for microalbumin of >30 mg/day correspond to a detection level within the "trace" to "1+" range of a urine dipstick protein assay. Therefore, positive indication of any protein detected on a urine dipstick assay obviates any need to perform a urine microalbumin test as the upper limit for microalbuminuria has already been exceeded. Analysis It is possible to analyze urine samples in determining albumin, hemoglobin and myoglobin with an optimized MEKC method. Treatment Treating proteinuria mainly needs proper diagnosis of the cause. The most common cause is diabetic nephropathy; in this case, proper glycemic control may slow the progression. Medical management consists of angiotensin converting enzyme (ACE) inhibitors, which are typically first-line therapy for proteinuria. In patients whose proteinuria is not controlled with ACE inhibitors, the addition of an aldosterone antagonist (i.e., spironolactone) or angiotensin receptor blocker (ARB) may further reduce protein loss. Caution must be used if these agents are added to ACE inhibitor therapy due to the risk of hyperkalemia. Proteinuria secondary to autoimmune disease should be treated with steroids or steroid-sparing agent plus the use of ACE inhibitors. See also Albuminuria Microalbuminuria List of terms associated with diabetes Protein toxicity Major urinary proteins UPCR References == External links ==

Aarogya, explain a scenario commonly referred as Dysfunction

Dysfunction

Dysfunction can refer to: Abnormality (behavior) Dysfunctional family Sexual dysfunction Dysfunction (album), an album by the rock band Staind Manifest and latent functions and dysfunctions (sociological theory) Measurement dysfunction See also Malfunction (disambiguation)

Would you describe Onycholysis, to me Aarogya

Onycholysis

Onycholysis is a common medical condition characterized by the painless detachment of the nail from the nail bed, usually starting at the tip and/or sides. On the hands, it occurs particularly on the ring finger but can occur on any of the fingernails. It may also happen to toenails. Onycholysis can occur in many conditions, including psoriasis. In thyrotoxicosis, it is thought to be due to sympathetic overactivity. It may also be seen in infections or trauma. Causes Unknown Trauma, excessive manicuring Infection: especially fungal Skin disease: psoriasis, dermatitis Impaired peripheral circulation, e.g. Raynauds syndrome Systemic disease: hyperthyroidism, hypothyroidism, reactive arthritis, porphyria cutanea tarda Reaction to detergents (e.g. washing dishes with bare hands, using detergent-based shampoos or soaps). Patients with hepatocellular dysfunction may develop hair-thinning or hair loss and nail changes such as clubbing, leukonychia (whitening), or onycholysis, affecting the nails of the hands and feet. Onychomycosis (tinea) It is common in ballet dancers Chemotherapy (cytotoxic agents like taxanes, vinca alkaloids and others) Chronic Renal Failure Treatment Most instances of onycholysis without a clear cause will heal spontaneously within a few weeks. The most commonly recommended treatment is to keep the nail dry as much as possible and allow the nail to slowly reattach. Trimming away as much loose nail as can be done comfortably will prevent the nail from being pried upwards. Cleaning under the nail is not recommended as this only serves to separate the nail further. Bandages are also to be avoided. When kept dry and away from further trauma, the nail will reattach from the base upward (i.e., from proximal to distal).The aim of treatement is also to eliminate onychomycosis that is a major cause of onycholysis .Anti-biotics like Terbinafin and itraconazole in the form of oral pills should be given for 6 to 8 weeks. If the underlying cause of the condition is not found and the nail continues to detach despite conservative treatment, the nail bed may begin to form a granular layer of abnormal cells on its surface. After six months of detachment, this layer is likely to prevent the adhesion of any new nail tissue, possibly leading to permanent deformity. Etymology The word onycholysis comes from onycho-, from Ancient Greek ὄνυξ ónuks nail, and Ancient Greek λύσις lúsis lysis/disintegration. See also List of cutaneous conditions Plummers nail References == External links ==

Aarogya, give me a short description about Agoraphobia

Agoraphobia

Agoraphobia is a mental and behavioral disorder, specifically an anxiety disorder characterized by symptoms of anxiety in situations where the person perceives their environment to be unsafe with no easy way to escape. These situations can include open spaces, public transit, shopping centers, crowds and queues, or simply being outside their home on their own. Being in these situations may result in a panic attack. Those affected will go to great lengths to avoid these situations. In severe cases people may become completely unable to leave their homes.Agoraphobia is believed to be due to a combination of genetic and environmental factors. The condition often runs in families, and stressful or traumatic events such as the death of a parent or being attacked may be a trigger. In the DSM-5 agoraphobia is classified as a phobia along with specific phobias and social phobia. Other conditions that can produce similar symptoms include separation anxiety, post-traumatic stress disorder, and major depressive disorder. The diagnosis of agoraphobia has been shown to be comorbid with depression, substance abuse, and suicide ideation.Without treatment it is uncommon for agoraphobia to resolve. Treatment is typically with a type of counselling called cognitive behavioral therapy (CBT). CBT results in resolution for about half of people. In some instances those with a diagnosis of agoraphobia have reported taking benzodiazepines and antipsychotics augmentation. Agoraphobia affects about 1.7% of adults. Women are affected about twice as often as men. The condition often begins in early adulthood and becomes less common in old age. It is rare in children. Etymology The term "agoraphobia" was coined in German in 1871 by pioneering German psychologist Karl Friedrich Otto Westphal, 1833–1890, in his article "Die Agoraphobie, eine neuropathische Erscheinung." Archiv für Psychiatrie und Nervenkrankheiten, Berlin, 1871–72; 3: 138–161. It is derived from Greek ἀγορά, agorā́, meaning a "place of assembly" or "market-place" and -φοβία, -phobía, meaning "fear". Signs and symptoms Agoraphobia is a condition where individuals become anxious in unfamiliar environments or where they perceive that they have little control. Triggers for this anxiety may include wide-open spaces, crowds (social anxiety), or traveling (even short distances). Agoraphobia is often, but not always, compounded by a fear of social embarrassment, as the agoraphobic fears the onset of a panic attack and appearing distraught in public. Most of the time they avoid these areas and stay in the comfort of their haven, usually their home.Agoraphobia is also defined as "a fear, sometimes terrifying, by those who have experienced one or more panic attacks". In these cases, the patient is fearful of a particular place because they have experienced a panic attack at the same location at a previous time. Fearing the onset of another panic attack, the patient is fearful or even avoids a location. Some refuse to leave their homes even in medical emergencies because the fear of being outside of their comfort areas is too great.The person with this condition can sometimes go to great lengths to avoid the locations where they have experienced the onset of a panic attack. Agoraphobia, as described in this manner, is actually a symptom professionals check when making a diagnosis of panic disorder. Other syndromes like obsessive compulsive disorder or post-traumatic stress disorder can also cause agoraphobia. Essentially, any irrational fear that keeps one from going outside can cause the syndrome.People with agoraphobia may experience temporary separation anxiety disorder when certain other individuals of the household depart from the residence temporarily, such as a parent or spouse, or when they are left home alone. Such temporary conditions can result in an increase in anxiety or a panic attack or feeling the need to separate themselves from family or maybe friends.People with agoraphobia sometimes fear waiting outside for long periods of time; that symptom can be called "macrophobia". Panic attacks Agoraphobia patients can experience sudden panic attacks when traveling to places where they fear they are out of control, help would be difficult to obtain, or they could be embarrassed. During a panic attack, epinephrine is released in large amounts, triggering the bodys natural fight-or-flight response. A panic attack typically has an abrupt onset, building to maximum intensity within 10 to 15 minutes, and rarely lasts longer than 30 minutes. Symptoms of a panic attack include palpitations, rapid heartbeat, sweating, trembling, nausea, vomiting, dizziness, tightness in the throat, and shortness of breath. Many patients report a fear of dying, fear of losing control of emotions, or fear of losing control of behaviors. Causes Agoraphobia is believed to be due to a combination of genetic and environmental factors. The condition often runs in families, and stressful or traumatic events such as the death of a parent or being attacked may be a trigger.Research has uncovered a link between agoraphobia and difficulties with spatial orientation. Individuals without agoraphobia are able to maintain balance by combining information from their vestibular system, their visual system, and their proprioceptive sense. A disproportionate number of agoraphobics have weak vestibular function and consequently rely more on visual or tactile signals. They may become disoriented when visual cues are sparse (as in wide-open spaces) or overwhelming (as in crowds). Likewise, they may be confused by sloping or irregular surfaces. In a virtual reality study, agoraphobics showed impaired processing of changing audiovisual data in comparison with subjects without agoraphobia. Substance-induced Chronic use of tranquilizers and sleeping pills such as benzodiazepines has been linked to onset of agoraphobia. In 10 patients who had developed agoraphobia during benzodiazepine dependence, symptoms abated within the first year of assisted withdrawal. Similarly, alcohol use disorders are associated with panic with or without agoraphobia; this association may be due to the long-term effects of alcohol consumption causing a distortion in brain chemistry. Tobacco smoking has also been associated with the development and emergence of agoraphobia, often with panic disorder; it is uncertain how tobacco smoking results in anxiety-panic with or without agoraphobia symptoms, but the direct effects of nicotine dependence or the effects of tobacco smoke on breathing have been suggested as possible causes. Self-medication or a combination of factors may also explain the association between tobacco smoking and agoraphobia and panic. Attachment theory Some scholars have explained agoraphobia as an attachment deficit, i.e., the temporary loss of the ability to tolerate spatial separations from a secure base. Recent empirical research has also linked attachment and spatial theories of agoraphobia. Spatial theory In the social sciences, a perceived clinical bias exists in agoraphobia research. Branches of the social sciences, especially geography, have increasingly become interested in what may be thought of as a spatial phenomenon. One such approach links the development of agoraphobia with modernity. Factors considered contributing to agoraphobia within modernity are the ubiquity of cars and urbanization. These have helped develop the expansion of public space and the contraction of private space, thus creating in the minds of agoraphobia-prone people a tense, unbridgeable gulf between the two. Evolutionary psychology An evolutionary psychology view is that the more unusual primary agoraphobia without panic attacks may be due to a different mechanism from agoraphobia with panic attacks. Primary agoraphobia without panic attacks may be a specific phobia explained by it once having been evolutionarily advantageous to avoid exposed, large, open spaces without cover or concealment. Agoraphobia with panic attacks may be an avoidance response secondary to the panic attacks, due to fear of the situations in which the panic attacks occurred. Diagnosis Most people who present to mental health specialists develop agoraphobia after the onset of panic disorder. Agoraphobia is best understood as an adverse behavioral outcome of repeated panic attacks and subsequent anxiety and preoccupation with these attacks that leads to an avoidance of situations where a panic attack could occur. Early treatment of panic disorder can often prevent agoraphobia. Agoraphobia is typically determined when symptoms are worse than panic disorder, but also do not meet the criteria for other anxiety disorders such as depression. In rare cases where agoraphobics do not meet the criteria used to diagnose panic disorder, the formal diagnosis of agoraphobia without history of panic disorder is used (primary agoraphobia). Treatments Therapy Systematic desensitization can provide lasting relief to the majority of patients with panic disorder and agoraphobia. The disappearance of residual and sub-clinical agoraphobic avoidance, and not simply of panic attacks, should be the aim of exposure therapy. Many patients can deal with exposure easier if they are in the company of a friend on whom they can rely. Patients must remain in the situation until anxiety has abated because if they leave the situation, the phobic response will not decrease and it may even rise.A related exposure treatment is in vivo exposure, a cognitive behavioral therapy method, that gradually exposes patients to the feared situations or objects. This treatment was largely effective with an effect size from d = 0.78 to d = 1.34, and these effects were shown to increase over time, proving that the treatment had long-term efficacy (up to 12 months after treatment).Psychological interventions in combination with pharmaceutical treatments were overall more effective than treatments simply involving either CBT or pharmaceuticals. Further research showed there was no significant effect between using group CBT versus individual CBT.Cognitive restructuring has also proved useful in treating agoraphobia. This treatment involves coaching a participant through a dianoetic discussion, with the intent of replacing irrational, counterproductive beliefs with more factual and beneficial ones. Relaxation techniques are often useful skills for the agoraphobic to develop, as they can be used to stop or prevent symptoms of anxiety and panic.Videoconferencing psychotherapy (VCP) is an emerging modality used to treat various disorders in a remote method. Similar to traditional face-to-face interventions, VCP can be used to administer CBT. The use of VCP has been shown to be equally effective as face-to-face interventions at treating panic disorder and agoraphobia (PDA) and motivating the client to continue treatment. Medications Antidepressant medications most commonly used to treat anxiety disorders are mainly selective serotonin reuptake inhibitors. Benzodiazepines, monoamine oxidase inhibitor, and tricyclic antidepressants are also sometimes prescribed for treatment of agoraphobia. Antidepressants are important because some have anxiolytic effects. Antidepressants should be used in conjunction with exposure as a form of self-help or with cognitive behaviour therapy. A combination of medication and cognitive behaviour therapy is sometimes the most effective treatment for agoraphobia.Benzodiazepines and other anxiolytic medications such as alprazolam and clonazepam are used to treat anxiety and can also help control the symptoms of a panic attack. Alternative medicine Eye movement desensitization and reprocessing (EMDR) has been studied as a possible treatment for agoraphobia, with poor results. As such, EMDR is only recommended in cases where cognitive-behavioral approaches have proven ineffective or in cases where agoraphobia has developed following trauma.Many people with anxiety disorders benefit from joining a self-help or support group (telephone conference-call support groups or online support groups being of particular help for completely housebound individuals). Sharing problems and achievements with others, as well as sharing various self-help tools, are common activities in these groups. In particular, stress management techniques and various kinds of meditation practices and visualization techniques can help people with anxiety disorders calm themselves and may enhance the effects of therapy, as can service to others, which can distract from the self-absorption that tends to go with anxiety problems. Also, preliminary evidence suggests aerobic exercise may have a calming effect. Since caffeine, certain illicit drugs, and even some over-the-counter cold medications can aggravate the symptoms of anxiety disorders, they should be avoided. Epidemiology Agoraphobia occurs about twice as commonly among women as it does in men.Panic disorder with or without agoraphobia affects roughly 5.1% of Americans, and about 1/3 of this population with panic disorder have co-morbid agoraphobia. It is uncommon to have agoraphobia without panic attacks, with only 0.17% of people with agoraphobia not presenting panic disorders as well. Society and culture Notable cases See also Hikikomori List of phobias Phobia References This article incorporates public domain material from websites or documents of the National Institute of Mental Health. External links Agoraphobia at Curlie

Hi Aarogya , Do you know what is Immunodeficiency,

Immunodeficiency

Immunodeficiency, also known as immunocompromisation, is a state in which the immune systems ability to fight infectious diseases and cancer is compromised or entirely absent. Most cases are acquired ("secondary") due to extrinsic factors that affect the patients immune system. Examples of these extrinsic factors include HIV infection and environmental factors, such as nutrition. Immunocompromisation may also be due to genetic diseases/flaws such as SCID. In clinical settings, immunosuppression by some drugs, such as steroids, can either be an adverse effect or the intended purpose of the treatment. Examples of such use is in organ transplant surgery as an anti-rejection measure and in patients with an overactive immune system, as in autoimmune diseases. Some people are born with intrinsic defects in their immune system, or primary immunodeficiency.A person who has an immunodeficiency of any kind is said to be immunocompromised. An immunocompromised individual may particularly be vulnerable to opportunistic infections, in addition to normal infections that could affect anyone. It also decreases cancer immunosurveillance, in which the immune system scans the bodys cells and kills neoplastic ones. They are also more susceptible to infectious diseases owing to reduced protection afforded by vaccines. Types By affected component Humoral immune deficiency (including B cell deficiency or dysfunction), with signs or symptoms depending on the cause, but generally include signs of hypogammaglobulinemia (decrease of one or more types of antibodies) with presentations including repeated mild respiratory infections, and/or agammaglobulinemia (lack of all or most antibody production) which results in frequent severe infections and is often fatal. T cell deficiency, often causes secondary disorders such as acquired immune deficiency syndrome (AIDS). Granulocyte deficiency, including decreased numbers of granulocytes (called as granulocytopenia or, if absent, agranulocytosis) such as of neutrophil granulocytes (termed neutropenia). Granulocyte deficiencies also include decreased function of individual granulocytes, such as in chronic granulomatous disease. Asplenia, where there is no function of the spleen Complement deficiency is where the function of the complement system is deficientIn reality, immunodeficiency often affects multiple components, with notable examples including severe combined immunodeficiency (which is primary) and acquired immune deficiency syndrome (which is secondary). Primary or secondary The distinction between primary versus secondary immunodeficiencies is based on, respectively, whether the cause originates in the immune system itself or is, in turn, due to insufficiency of a supporting component of it or an external decreasing factor of it. Primary immunodeficiency A number of rare diseases feature a heightened susceptibility to infections from childhood onward. Primary Immunodeficiency is also known as congenital immunodeficiencies. Many of these disorders are hereditary and are autosomal recessive or X-linked. There are over 95 recognised primary immunodeficiency syndromes; they are generally grouped by the part of the immune system that is malfunctioning, such as lymphocytes or granulocytes.The treatment of primary immunodeficiencies depends on the nature of the defect, and may involve antibody infusions, long-term antibiotics and (in some cases) stem cell transplantation. The characteristics of lacking and/or impaired antibody functions can be related to illnesses such as X-Linked Agammaglobulinemia and Common Variable Immune Deficiency Secondary immunodeficiencies Secondary immunodeficiencies, also known as acquired immunodeficiencies, can result from various immunosuppressive agents, for example, malnutrition, aging, particular medications (e.g., chemotherapy, disease-modifying antirheumatic drugs, immunosuppressive drugs after organ transplants, glucocorticoids) and environmental toxins like mercury and other heavy metals, pesticides and petrochemicals like styrene, dichlorobenzene, xylene, and ethylphenol. For medications, the term immunosuppression generally refers to both beneficial and potential adverse effects of decreasing the function of the immune system, while the term immunodeficiency generally refers solely to the adverse effect of increased risk for infection. Many specific diseases directly or indirectly cause immunosuppression. This includes many types of cancer, particularly those of the bone marrow and blood cells (leukemia, lymphoma, multiple myeloma), and certain chronic infections. Immunodeficiency is also the hallmark of acquired immunodeficiency syndrome (AIDS), caused by the human immunodeficiency virus (HIV). HIV directly infects a small number of T helper cells, and also impairs other immune system responses indirectly. Various hormonal and metabolic disorders can also result in immune deficiency including anemia, hypothyroidism and hyperglycemia. Smoking, alcoholism and drug abuse also depress immune response. Heavy schedules of training and competition in athletes increases their risk of immune deficiencies. Diagnosis Patients with immune deficiencies can present with variable clinical phenotypes. This often translates into a significant delay in their diagnosis, and resultant patient morbidity. A structured approach on when to suspect an immunodeficiency and the initial investigations pathway is given in the publication by Grammatikos et al. Immunodeficiency and autoimmunity There are a large number of immunodeficiency syndromes that present clinical and laboratory characteristics of autoimmunity. The decreased ability of the immune system to clear infections in these patients may be responsible for causing autoimmunity through perpetual immune system activation. One example is common variable immunodeficiency (CVID) where multiple autoimmune diseases are seen, e.g., inflammatory bowel disease, autoimmune thrombocytopenia, and autoimmune thyroid disease. Familial hemophagocytic lymphohistiocytosis, an autosomal recessive primary immunodeficiency, is another example. Low blood levels of red blood cells, white blood cells, and platelets, rashes, lymph node enlargement, and enlargement of the liver and spleen are commonly seen in these patients. Presence of multiple uncleared viral infections due to lack of perforin are thought to be responsible. In addition to chronic and/or recurrent infections many autoimmune diseases including arthritis, autoimmune hemolytic anemia, scleroderma and type 1 diabetes are also seen in X-linked agammaglobulinemia (XLA). Recurrent bacterial and fungal infections and chronic inflammation of the gut and lungs are seen in chronic granulomatous disease (CGD) as well. CGD is caused by a decreased production of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase by neutrophils. Hypomorphic RAG mutations are seen in patients with midline granulomatous disease; an autoimmune disorder that is commonly seen in patients with granulomatosis with polyangiitis and NK/T cell lymphomas. Wiskott–Aldrich syndrome (WAS) patients also present with eczema, autoimmune manifestations, recurrent bacterial infections and lymphoma. In autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) also autoimmunity and infections coexist: organ-specific autoimmune manifestations (e.g., hypoparathyroidism and adrenocortical failure) and chronic mucocutaneous candidiasis. Finally, IgA deficiency is also sometimes associated with the development of autoimmune and atopic phenomena. Causes The cause of immunodeficiency varies depending on the nature of the disorder. The cause can be either genetic or acquired by malnutrition and poor sanitary conditions. Only for some genetic causes, the exact genes are known. Treatment Available treatment falls into two modalities: treating infections and boosting the immune system. Prevention of Pneumocystis pneumonia using trimethoprim/sulfamethoxazole is useful in those who are immunocompromised. In the early 1950s Immunoglobulin(Ig) was used by doctors to treat patients with primary immunodeficiency through intramuscular injection. Ig replacement therapy are infusions that can be either subcutaneous or intravenously administrated, resulting in higher Ig levels for about three to four weeks, although this varies with each patient. Prognosis Prognosis depends greatly on the nature and severity of the condition. Some deficiencies cause early mortality (before age one), others with or even without treatment are lifelong conditions that cause little mortality or morbidity. Newer stem cell transplant technologies may lead to gene based treatments of debilitating and fatal genetic immune deficiencies. Prognosis of acquired immune deficiencies depends on avoiding or treating the causative agent or condition (like AIDS). See also Acquired immune deficiency syndrome (AIDS) Immune disorder Autoimmune disease, immune response to self-proteins Allergy, immune response to harmless non-self proteins Histamine Immunosenescence, age-associated immune deficiency Steroids, commonly administered drugs like prednisone that suppress the immune system Human genetic enhancement Immune system Immunology References External links Immune Deficiency Foundation The European Society of Immunodeficiencies

Aarogya , Do you know what is Angiostrongyliasis,

Angiostrongyliasis

Angiostrongyliasis is an infection by a roundworm of the Angiostrongylus type. Symptoms may vary from none, to mild, to meningitis.Infection with Angiostrongylus cantonensis (rat lungworm) can occur after ingestion of raw or undercooked snails or slugs, and less likely unwashed fruits and vegetables. In humans, A. cantonensis is the most common cause of eosinophilic meningitis or meningoencephalitis. Frequently the infection will resolve without treatment or serious consequences, but in cases with a heavy load of parasites the infection can be so severe it can cause permanent damage to the central nervous system or death. Symptoms Infection first presents with severe abdominal pain, nausea, vomiting, and weakness, which gradually lessens and progresses to fever, and then to central nervous system (CNS) symptoms and severe headache and stiffness of the neck. CNS infection CNS symptoms begin with mild cognitive impairment and slowed reactions, and in a very severe form often progress to unconsciousness. Patients may present with neuropathic pain early in the infection. Eventually, severe infection will lead to ascending weakness, quadriparesis, areflexia, respiratory failure, and muscle atrophy, and will lead to death if not treated. Occasionally patients present with cranial nerve palsies, usually in nerves 7 and 8, and rarely larvae will enter ocular structures. Even with treatment, damage to the CNS may be permanent and result in a variety of negative outcomes depending on the location of the infection, and the patient may experience chronic pain as a result of infection. Eye invasion Symptoms of eye invasion include visual impairment, pain, keratitis, and retinal edema. Worms usually appear in the anterior chamber and vitreous and can sometimes be removed surgically. Incubation period The incubation period in humans is usually from 1 week to 1 month after infection, and can be as long as 47 days. This interval varies, since humans are accidental hosts and the life cycle does not continue predictably as it would in a rat. Cause Transmission Transmission of the parasite is usually from eating raw or undercooked snails or other vectors. Infection is also frequent from ingestion of contaminated water or unwashed salad that may contain small snails and slugs, or have been contaminated by them. Reservoirs Rats are the definitive host and the main reservoir for A. cantonensis, though other small mammals may also become infected. While Angiostrongylus can infect humans, humans do not act as reservoirs since the worm cannot reproduce in humans and therefore humans cannot contribute to their life cycle. Vectors Angiostrongylus cantonensis has many vectors among invertebrates, with the most common being several species of snails, including the giant African land snail (Achatina) in the Pacific islands and apple snails of the genus Pila in Thailand and Malaysia. The golden apple snail, Pomacea canaliculata, is the most important vector in areas of China. Freshwater prawns, crabs, or other paratenic, or transport, hosts can also act as vectors. Organism Morphology A. cantonensis is a nematode roundworm with 3 outer protective collagen layers, and a simple stomal opening or mouth with no lips or buccal cavity leading to a fully developed gastrointestinal tract. Males have a small copulatory bursa at the posterior. Females have a "barber pole" shape down the middle of the body, which is created by the twisting together of the intestine and uterine tubules. The worms are long and slender - males are 15.9–19 mm in length, and females are 21–25 mm in length. Life cycle The adult form of A. cantonensis resides in the pulmonary arteries of rodents, where it reproduces. After the eggs hatch in the arteries, larvae migrate up the pharynx and are then swallowed again by the rodent and passed in the stool. These first stage larvae then penetrate or are swallowed by snail intermediate hosts, where they transform into second stage larvae and then into third stage infective larvae. Humans and rats acquire the infection when they ingest contaminated snails or paratenic (transport) hosts including prawns, crabs, and frogs, or raw vegetables containing material from these intermediate and paratenic hosts. After passing through the gastrointestinal tract, the worms enter circulation. In rats, the larvae then migrate to the meninges and develop for about a month before migrating to the pulmonary arteries, where they fully develop into adults.Humans are incidental hosts; the larvae cannot reproduce in humans and therefore humans do not contribute to the A. cantonensis life cycle. In humans, the circulating larvae migrate to the meninges, but do not move on to the lungs. Sometimes the larvae will develop into the adult form in the brain and CSF, but they quickly die, inciting the inflammatory reaction that causes symptoms of infection. Diagnosis Diagnosis of Angiostrongyliasis is complicated due to the difficulty of presenting the angiostrongylus larvae themselves, and will usually be made based on the presence of eosinophilic meningitis and history of exposure to snail hosts. Eosinophilic meningitis is generally characterized as a meningitis with >10 eosinophils/μL in the CSF or at least 10% eosinophils in the total CSF leukocyte count. Occasionally worms found in the cerebrospinal fluid or surgically removed from the eye can be identified in order to diagnose Angiostrongyliasis. Lumbar puncture Lumbar puncture should always be done in cases of suspected meningitis. In cases of eosinophilc meningitis it will rarely produce worms even when they are present in the CSF, because they tend to cling to the end of nerves. Larvae are present in the CSF in only 1.9-10% of cases. However, as a case of eosinophilic meningitis progresses, intracranial pressure and eosinophil counts should rise. Increased levels of eosinophils in the CSF is a hallmark of the eosinophilic meningitis. Brain imaging Brain lesions, with invasion of both gray and white matter, can be seen on a CT or MRI. However MRI findings tend to be inconclusive, and usually include nonspecific lesions and ventricular enlargement. Sometimes a hemorrhage, probably produced by migrating worms, is present and of diagnostic value. Serology In patients with elevated eosinophils, serology can be used to confirm a diagnosis of angiostrongyliasis rather than infection with another parasite. There are a number of immunoassays that can aid in diagnosis, however serologic testing is available in few labs in the endemic area, and is frequently too non-specific. Some cross reactivity has been reported between A. cantonensis and trichinosis, making diagnosis less specific. The most definitive diagnosis always arises from the identification of larvae found in the CSF or eye, however due to this rarity a clinical diagnosis based on the above tests is most likely. Prevention There are public health strategies that can limit the transmission of A. cantonensis by limiting contact with infected vectors. Vector control may be possible, but has not been very successful in the past. Education to prevent the introduction of rats or snail vectors outside endemic areas is important to limit the spread of the disease. There are no vaccines in development for angiostrongyliasis. Recommendations for individuals To avoid infection when in endemic areas, travelers should: Avoid consumption of uncooked vectors, such as snails and freshwater prawns Avoid drinking water from open sources, which may have been contaminated by vectors Prevent young children from playing with or eating live snails Treatment Treatment of angiostrongyliasis is not well defined, but most strategies include a combination of anti-parasitics to kill the worms, steroids to limit inflammation as the worms die, and pain medication to manage the symptoms of meningitis. Anthelmintics Anthelmintics are often used to kill off the worms, however in some cases this may cause patients to worsen due to toxins released by the dying worms. Albendazole, ivermectin, mebendazole, and pyrantel are all commonly used, though albendazole is usually the drug of choice. Studies have shown that anthelmintic drugs may shorten the course of the disease and relieve symptoms. Therefore, anthelmintics are generally recommended, but should be administered gradually so as to limit the inflammatory reaction. Anti-inflammatories Anthelmintics should generally be paired with corticosteroids in severe infections to limit the inflammatory reaction to the dying parasites. Studies suggest that a two-week regimen of a combination of mebendazole and prednisolone significantly shortened the course of the disease and length of associated headaches without observed harmful side effects. Other studies suggest that albendazole may be more favorable, because it may be less like to incite an inflammatory reaction. Symptomatic treatment Symptomatic treatment is indicated for symptoms such as nausea, vomiting, headache, and in some cases, chronic pain due to nerve damage or muscle atrophy. Epidemiology A. cantonensis and its vectors are endemic to Southeast Asia and the Pacific Basin. The infection is becoming increasingly important as globalization allows it to spread to more locations, and as more travelers encounter the parasites. The parasites probably travel effectively through rats traveling as stowaways on ships, and through the introduction of snail vectors outside endemic areas.Although mostly found in Asia and the Pacific where asymptomatic infection can be as high as 88%, human cases have been reported in the Caribbean, where as much as 25% of the population may be infected. In the United States, cases have been reported in Hawaii, which is in the endemic area. The infection is now endemic in wildlife and a few human cases have also been reported in areas where the parasite was not originally endemic, such as New Orleans and Egypt. The disease has also arrived in Brazil, where there were 34 confirmed cases from 2006 to 2014, including one death. The giant African land snail, which can be a vector of the parasite, has been introduced to Brazil as an invasive species and is spreading the disease. There may be more undiagnosed cases, as Brazilian physicians are not familiar with the eosinophilic meningitis associated to angiostrongyliasis and misdiagnose it as bacterial or viral.The parasite is rarely seen outside of endemic areas, and in these cases patients generally have a history of travel to an endemic area. See also Schistosomiasis, a parasitic disease also spread by snails List of unusual deaths – lists Australian man Sam Ballard as dying from Angiostrongyliasis in 2018, as a result of eating a garden slug eight years earlier on a dare References Further reading "Parasites - Angiostrongyliasis (also known as Angiostrongylus Infection)". CDC. 2015-12-28. Retrieved 2017-04-04. "DPDx - Angiostrongyliasis". CDC. 2016-10-17. Retrieved 2017-04-04. Tabs for Parasite Biology, Image Gallery, Laboratory Diagnosis, and Treatment Information. == External links ==

Aarogya, elaborate on Calcaneal spur

Calcaneal spur

A calcaneal spur (also known as a heel spur) is a bony outgrowth from the calcaneal tuberosity (heel bone). Calcaneal spurs are typically detected by x-ray examination. It is a form of exostosis. When a foot is exposed to constant stress, calcium deposits build up on the bottom of the heel bone. Generally, this has no effect on a persons daily life. However, repeated damage can cause these deposits to pile up on each other, causing a spur-shaped deformity, called a calcaneal (or heel) spur.An inferior calcaneal spur is located on the inferior aspect of the calcaneus and is typically a response to plantar fasciitis over a period, but may also be associated with ankylosing spondylitis (typically in children). A posterior calcaneal spur develops on the back of the heel at the insertion of the Achilles tendon.An inferior calcaneal spur consists of a calcification of the calcaneus, which lies superior to the plantar fascia at the insertion of the plantar fascia. A posterior calcaneal spur is often large and palpable through the skin and may need to be removed as part of the treatment of insertional Achilles tendonitis. Signs and symptoms Major symptoms consist of pain in the region surrounding the spur, which typically increases in intensity after prolonged periods of rest. Patients may report heel pain to be more severe when waking up in the morning. Patients may not be able to bear weight on the affected heel comfortably. Running, walking, or lifting heavy weight may exacerbate the issue. Causes Plantar fasciitis is a common cause of calcaneal spurs. When stress is put on the plantar fascia ligament, it does not cause only plantar fasciitis, but causes a heel spur where the plantar fascia attaches to the heel bone. The considerations that affect plantar heel pain are the alignment of the foot with lower leg, foot and ankle mobility, strength and endurance of muscle. External influences on plantar heel pain are the amount of time spent on feet while exercising or standing, type of footwear used and type of floor surfaces.Calcaneal spur develops when proper care is not given to the foot and heels. People who are obese, have flat feet, or who often wear high-heeled shoes are most susceptible to heel spurs. Flat feet can potentially be attributed to the minimal amount of ankle dorsiflexion during stance phase of the gait cycle causing more tension on the plantar fascia. Diagnosis Spur outgrowths can be detected through physical exam followed by a lateral foot x-ray. Treatment It is often seen as a repetitive stress injury, and thus lifestyle modification is typically the basic course of management strategies. For example, a person should begin doing foot and calf workouts. Strong muscles in the calves and lower legs will help take the stress off the bone and prevent heel spurs. Icing the area is an effective way to get immediate pain relief. There are several means to get pain relief from plantar heel pain. Plantar heel pain can be a precursor to many pathologies of the foot. There is evidence that corticosteroid injections may reduce pain for up to one month after the injection, which can have an impact on the formation of calcaneal spurs. Side effects of corticosteroid injections includes peripheral nerve injury, plantar fascia rupture, and post injection flare, among others. Laser therapy, dry needling, and calcaneal taping are also utilized in treating plantar heel pain, however, there is not high quality evidence supporting the clinical usage of such modalities in reduction of pain. References External links Calcaneal spur at Curlie

Aarogya what is Male infertility

Male infertility

Male infertility refers to a sexually mature males inability to impregnate a fertile female. In humans it accounts for 40–50% of infertility. It affects approximately 7% of all men. Male infertility is commonly due to deficiencies in the semen, and semen quality is used as a surrogate measure of male fecundity. More recently, advance sperm analyses that examine intracellular sperm components are being developed. Age considerations There is a decrease in sperm concentration as men age: 90% of seminiferous tubules in men in their 20s and 30s contain spermatids, whereas men in their 40s and 50s have spermatids in 50% of their seminiferous tubules, and only 10% of seminiferous tubules from men aged > 80 years contain spermatids. In a random international sample of 11,548 men confirmed to be biological fathers by DNA paternity testing, the oldest father was found to be 66 years old at the birth of his child; the ratio of DNA-confirmed versus DNA-rejected paternity tests around that age is in agreement with the notion of general male infertility above age 65–66. Causes Factors relating to male infertility include: Immune infertility Antisperm antibodies (ASA) have been considered as infertility cause in around 10–30% of infertile couples. ASA production are directed against surface antigens on sperm, which can interfere with sperm motility and transport through the female reproductive tract, inhibiting capacitation and acrosome reaction, impaired fertilization, influence on the implantation process, and impaired growth and development of the embryo. Risk factors for the formation of antisperm antibodies in men include the breakdown of the blood‑testis barrier, trauma and surgery, orchitis, varicocele, infections, prostatitis, testicular cancer, failure of immunosuppression and unprotected receptive anal or oral sex with men. Genetics Chromosomal anomalies and genetic mutations account for nearly 10–15% of all male infertility cases. Klinefelter syndrome One of the most commonly known causes of infertility is Klinefelter syndrome, which affects one in 500–1000 newborn males. Klinefelter syndrome is a chromosomal defect that occurs during gamete formation due to a non-disjunction error during cell division. Resulting in males having smaller testes, reducing the amount of testosterone and sperm production. Males with this syndrome carry an extra X chromosome (XXY), meaning they have 47 chromosomes compared to the normal 46 in each cell. This extra chromosome directly affects sexual development before birth and during puberty. A variation of Klinefelter syndrome is when some cells in an individual have the extra X chromosome but others do not, referred to as mosaic Klinefelter syndrome. The reduction of testosterone in the male body normally results in an overall decrease in the production of viable sperm for these individuals thereby forcing them to turn to fertility treatments to father children. Y chromosome deletions Y chromosomal infertility is a direct cause of male infertility due to its effects on sperm production, occurring in approximately one in 2000 males. Usually, affected men show no symptoms, although they may have smaller testes. Men with this condition may exhibit azoospermia (no sperm production), oligozoospermia (small number of sperm production), or they may produce abnormally shaped sperm (teratozoospermia). This case of infertility occurs during the development of gametes in the male. Where a normal healthy male will have both an X and a Y chromosome, affected males have genetic deletions in the Y chromosome. These deletions affect protein production that is vital for spermatogenesis. Studies have shown that this is an inherited trait; if a male is fathered by a man who also exhibited Y chromosome deletions then this trait will be passed down. These individuals are thereby "Y-linked". Daughters are not affected and cannot be carriers due to their lack of a Y chromosome. Other Age group 12–49 (Paternal age effect) Aneuploidy, an abnormal number of chromosomes Centriole Neoplasm, e.g. seminoma Idiopathic failure Cryptorchidism Trauma Hydrocele, particularly hydrocele testis Hypopituitarism in adults, and hypopituitarism untreated in children (resulting in growth hormone deficiency and proportionate dwarfism.) Mumps Malaria Testicular cancer Defects in USP26 in some cases Acrosomal defects affecting egg penetration Idiopathic oligospermia – unexplained sperm deficiencies account for 30% of male infertility. Pre-testicular causes Pre-testicular factors refer to conditions that impede adequate support of the testes and include situations of poor hormonal support and poor general health including: Varicocele Varicocele is a condition of swollen testicle veins.It is present in 15% of normal men and in about 40% of infertile men. It is present in up to 35% of cases of primary infertility and 69–81% of secondary infertility. Hypogonadotropic hypogonadism due to various causes Obesity increases the risk of hypogonadotropic hypogonadism. Animal models indicate that obesity causes leptin insensitivity in the hypothalamus, leading to decreased Kiss1 expression, which, in turn, alters the release of gonadotropin-releasing hormone (GnRH). Undiagnosed and untreated coeliac disease (CD). Coeliac men may have reversible infertility. Nevertheless, CD can present with several non-gastrointestinal symptoms that can involve nearly any organ system, even in the absence of gastrointestinal symptoms. Thus, the diagnosis may be missed, leading to a risk of long-term complications. In men, CD can reduce semen quality and cause immature secondary sex characteristics, hypogonadism and hyperprolactinaemia, which causes impotence and loss of libido. The giving of gluten free diet and correction of deficient dietary elements can lead to a return of fertility. It is likely that an effective evaluation for infertility would best include assessment for underlying celiac disease, both in men and women. Drugs, alcohol Strenuous riding (bicycle riding, horseback riding) Medications, including those that affect spermatogenesis such as chemotherapy, fluoxetine, anabolic steroids, cimetidine, spironolactone; those that decrease FSH levels such as phenytoin; those that decrease sperm motility such as sulfasalazine and nitrofurantoin Genetic abnormalities such as a Robertsonian translocation Tobacco smoking There is increasing evidence that the harmful products of tobacco smoking may damage the testicles and kill sperm, but their effect on male fertility is not clear. Some governments require manufacturers to put warnings on packets. Smoking tobacco increases intake of cadmium, because the tobacco plant absorbs the metal. Cadmium, being chemically similar to zinc, may replace zinc in the DNA polymerase, which plays a critical role in sperm production. Zinc replaced by cadmium in DNA polymerase can be particularly damaging to the testes. DNA damage Common inherited variants in genes that encode enzymes employed in DNA mismatch repair are associated with increased risk of sperm DNA damage and male infertility. As men age there is a consistent decline in semen quality, and this decline appears to be due to DNA damage. The damage manifests by DNA fragmentation and by the increased susceptibility to denaturation upon exposure to heat or acid, the features characteristic of apoptosis of somatic cells. These findings suggest that DNA damage is an important factor in male infertility. Epigenetic An increasing amount of recent evidence has been recorded documenting abnormal sperm DNA methylation in association with abnormal semen parameters and male infertility. Until recently, scientists have thought that epigenetic markers only affect the individual and are not passed down due to not changing the DNA. New studies suggest that environmental factors that changed an individuals epigenetic markers can be seen in their grandchildren, one such study demonstrating this through rats and fertility disruptors. Another study bred rats exposed to an endocrine disruptor, observing effects up to generation F5 including decreased sperm motility and decreased sperm count. These studies suggest that environmental factors that influence fertility can be felt for generations even without changing the DNA. Post-testicular causes Post-testicular factors decrease male fertility due to conditions that affect the male genital system after testicular sperm production and include defects of the genital tract as well as problems in ejaculation: Vas deferens obstruction Lack of Vas deferens, often related to genetic markers for cystic fibrosis Infection, e.g. prostatitis, male accessory gland infection Retrograde ejaculation Ejaculatory duct obstruction Hypospadias Impotence Diagnostic evaluations The diagnosis of infertility begins with a medical history and physical exam by a physician, physician assistant, or nurse practitioner. Typically two separate semen analyses will be required. The provider may order blood tests to look for hormone imbalances, medical conditions, or genetic issues. Medical history The history should include prior testicular or penile insults (torsion, cryptorchidism, trauma), infections (mumps orchitis, epididymitis), environmental factors, excessive heat, radiation, medications, and drug use (anabolic steroids, alcohol, smoking).Sexual habits, frequency and timing of intercourse, use of lubricants, and each partners previous fertility experiences are important.Loss of libido and headaches or visual disturbances may indicate a pituitary tumor.The past medical or surgical history may reveal thyroid or liver disease (abnormalities of spermatogenesis), diabetic neuropathy (retrograde ejaculation), radical pelvic or retroperitoneal surgery (absent seminal emission secondary to sympathetic nerve injury), or hernia repair (damage to the vas deferens or testicular blood supply).A family history may reveal genetic problems. Physical examination Usually, the patient disrobes completely and puts on a gown. The physician, physician assistant, or nurse practitioner will perform a thorough examination of the penis, scrotum, testicles, I vas deferens, spermatic cords, ejaculatory ducts, urethra, urinary bladder, anus and rectum. An orchidometer can measure testicular volume, which in turn is tightly associated with both sperm and hormonal parameters. A physical exam of the scrotum can reveal a varicocele, but the impact of detecting and surgically correct a varicocele on sperm parameters or overall male fertility is debated. Sperm sample Semen sample obtaining Semen sample obtaining is the first step in spermiogram. The optimal sexual abstinence for semen sample obtaining is of 2–7 days. The first way to obtain the semen sample is through masturbation, and the best place to obtain it is in the same clinic, as this way temperature changes during transport can be avoided, which can be lethal for some spermatozoa. A single semen sample is not determining for disease diagnosis, so two different samples have to be analyzed with an interval between them of seven days to three months, as sperm production is a cyclic process. It is prudent to ask about possible sample loss, as that could mask true results of spermiogram. To obtain the sample, a sterile plastic recipient is put directly inside, always no more than one hour before being studied. Conventional preservatives shouldnt be used, as they have chemical substances as lubricants or spermicides that could damage the sample. If preservatives have to be used, for cases of religious ethics in which masturbation is forbidden, a preservative with holes is used. In case of paraplegia it is possible to use mechanic tools or electroejaculation. The sample should never be obtained through coitus interruptus for several reasons: Some part of ejaculation could be lost. Bacterial contamination could happen. The acid vaginal pH could be deleterious for sperm motility.Also is very important to label the sample correctly the recipient with patient identification, date, hour, abstinence days, among other data required to be known. The volume of the semen sample (must be more than 1.5 ml), approximate number of total sperm cells, sperm motility/forward progression, and % of sperm with normal morphology are measured. It is possible to have hyperspermia (high volume more than 6 ml) or Hypospermia (low volume less than 0.5 ml). This is the most common type of fertility testing. Semen deficiencies are often labeled as follows: Oligospermia or oligozoospermia – decreased number of spermatozoa in semen Aspermia – complete lack of semen Hypospermia – reduced seminal volume Azoospermia – absence of sperm cells in semen Teratospermia – increase in sperm with abnormal morphology Asthenozoospermia – reduced sperm motility Necrozoospermia – all sperm in the ejaculate are dead Leucospermia – a high level of white blood cells in semen Normozoospermia or normospermia – It is a result of semen analysis that shows normal values of all ejaculate parameters by WHO but still there are chances of being infertile. This is also called as unexplained InfertilityThere are various combinations of these as well, e.g. Teratoasthenozoospermia, which is reduced sperm morphology and motility. Low sperm counts are often associated with decreased sperm motility and increased abnormal morphology, thus the terms "oligoasthenoteratozoospermia" or "oligospermia" can be used as a catch-all. Special obtaining Psychological inhibition– Psychotherapy – Intercourses with special preservatives without lubricants or spermicides. In case of religion limitations we should use a SCD, or Seminal Collection Device, such as preservatives with holes. – Drug stimulation – Percutaneous spermatozoa obtaining directly from epididymis, testes, etc. Neurological injury– Vibro-stimulation – Electro-stimulation Retrograde ejaculationThis type of ejaculation happens when there is a defect on prostate, so the sample is not ejaculated outside but to the bladder. So, in that case, what we have to do to obtain the sample is: – Intake bicarbonate, about 25 grams, the night before and the morning of the sample obtaining. This will neutralize acidic urine and will turn it alkaline, near semens pH, so spermatozoa can survive. – Before masturbation we have to urinate to empty the bladder. This must go to the first recipient. – Just after that, the subject has to masturbate and ejaculate, obtaining then a new urine sample with ejaculation that will be stored on the second recipient. – Finally we have to obtain the next urine, 2nd urine, for potential ejaculation fraction, which will be stored in the third recipient. This may contain the most important fraction. Blood sample Common hormonal test include determination of FSH and testosterone levels. A blood sample can reveal genetic causes of infertility, e.g. Klinefelter syndrome, a Y chromosome microdeletion, or cystic fibrosis. Ultrasonography Scrotal ultrasonography is useful when there is a suspicion of some particular diseases. It may detect signs of testicular dysgenesis, which is often related to an impaired spermatogenesis and to a higher risk of testicular cancer. Scrotum ultrasonography may also detect testicular lesions suggestive of malignancy. A decreased testicular vascularization is characteristic of testicular torsion, whereas hyperemia is often observed in epididymo-orchitis or in some malignant conditions such as lymphoma and leukemia. Doppler ultrasonography useful in assessing venous reflux in case of a varicocele, when palpation is unreliable or in detecting recurrence or persistence after surgery, although the impact of its detection and surgical correction on sperm parameters and overall fertility is debated.Dilation of the head or tail of the epididymis is suggestive of obstruction or inflammation of the male reproductive tract. Such abnormalities are associated with abnormalities in sperm parameters, as are abnormalities in the texture of the epididymis. Scrotal and transrectal ultrasonography (TRUS) are useful in detecting uni- or bilateral congenital absence of the vas deferens (CBAVD), which may be associated with abnormalities or agenesis of the epididymis, seminal vesicles or kidneys, and indicate the need for testicular sperm extraction. TRUS plays a key role in assessing azoospermia caused by obstruction, and detecting distal CBAVD or anomalies related to obstruction of the ejaculatory duct, such as abnormalities within the duct itself, a median cyst of the prostate (indicating a need for cyst aspiration), or an impairment of the seminal vesicles to become enlarged or emptied. Prevention Some strategies suggested or proposed for avoiding male infertility include the following: Avoiding smoking as it damages sperm DNA Avoiding heavy marijuana and alcohol use. Avoiding excessive heat to the testes. Maintaining optimal frequency of coital activity: sperm counts can be depressed by daily coital activity and sperm motility may be depressed by coital activity that takes place too infrequently (abstinence 10–14 days or more). Wearing a protective cup and jockstrap to protect the testicles, in any sport such as baseball, football, cricket, lacrosse, hockey, softball, paintball, rodeo, motorcross, wrestling, soccer, karate or other martial arts or any sport where a ball, foot, arm, knee or bat can come into contact with the groin. Diet: Healthy diets (i.e. the Mediterranean diet) rich in such nutrients as omega-3 fatty acids, some antioxidants and vitamins, and low in saturated fatty acids (SFAs) and trans-fatty acids (TFAs) are inversely associated with low semen quality parameters. In terms of food groups, fish, shellfish and seafood, poultry, cereals, vegetables and fruits, and low-fat dairy products have been positively related to sperm quality. However, diets rich in processed meat, soy foods, potatoes, full-fat dairy products, coffee, alcohol and sugar-sweetened beverages and sweets have been inversely associated with the quality of semen in some studies. The few studies relating male nutrient or food intake and fecundability also suggest that diets rich in red meat, processed meat, tea and caffeine are associated with a lower rate of fecundability. This association is only controversial in the case of alcohol. The potential biological mechanisms linking diet with sperm function and fertility are largely unknown and require further study. Treatment Treatments vary according to the underlying disease and the degree of the impairment of the males fertility. Further, in an infertility situation, the fertility of the female needs to be considered.Pre-testicular conditions can often be addressed by medical means or interventions. Testicular-based male infertility tends to be resistant to medication. Usual approaches include using the sperm for intrauterine insemination (IUI), in vitro fertilization (IVF), or IVF with intracytoplasmatic sperm injection (ICSI). With IVF-ICSI even with a few sperm pregnancies can be achieved. Obstructive causes of post-testicular infertility can be overcome with either surgery or IVF-ICSI. Ejaculatory factors may be treatable by medication, or by IUI therapy or IVF. Vitamin E helps counter oxidative stress, which is associated with sperm DNA damage and reduced sperm motility. A hormone-antioxidant combination may improve sperm count and motility. Giving oral antioxidants to men in couples undergoing in vitro fertilisation for male factor or unexplained subfertility may lead to an increase in the live birth rate but overall the risk of adverse effects is unclear. Hormonal therapy Administration of luteinizing hormone (LH) (or human chorionic gonadotropin) and follicle-stimulating hormone (FSH) is very effective in the treatment of male infertility due to hypogonadotropic hypogonadism. Although controversial, off-label clomiphene citrate, an antiestrogen, may also be effective by elevating gonadotropin levels.Though androgens are absolutely essential for spermatogenesis and therefore male fertility, exogenous testosterone therapy has been found to be ineffective in benefiting men with low sperm count. This is thought to be because very high local levels of testosterone in the testes (concentrations in the seminiferous tubules are 20- to 100-fold greater than circulating levels) are required to mediate spermatogenesis, and exogenous testosterone therapy (which is administered systemically) cannot achieve these required high local concentrations (at least not without extremely supraphysiological dosages). Moreover, exogenous androgen therapy can actually impair or abolish male fertility by suppressing gonadotropin secretion from the pituitary gland, as seen in users of androgens/anabolic steroids (who often have partially or completely suppressed sperm production). This is because suppression of gonadotropin levels results in decreased testicular androgen production (causing diminished local concentrations in the testes) and because FSH is independently critical for spermatogenesis. In contrast to FSH, LH has little role in male fertility outside of inducing gonadal testosterone production.Estrogen, at some concentration, has been found to be essential for male fertility/spermatogenesis. However, estrogen levels that are too high can impair male fertility by suppressing gonadotropin secretion and thereby diminishing intratesticular androgen levels. As such, clomiphene citrate (an antiestrogen) and aromatase inhibitors such as testolactone or anastrozole have shown effectiveness in benefiting spermatogenesis.Low-dose estrogen and testosterone combination therapy may improve sperm count and motility in some men, including in men with severe oligospermia. Research Researchers at Münster University developed in vitro culture conditions using a three-dimensional agar culture system which induces mouse testicular germ cells to reach the final stages of spermatogenesis, including spermatozoa generation. If reproduced in humans, this could potentially enable infertile men to father children with their own sperm.Researchers from Montana State University developed precursors of sperm from skin cells of infertile men.Sharpe et al. comment on the success of intracytoplasmic sperm injection (ICSI) in women saying, "[t]hus, the woman carries the treatment burden for male infertility, a fairly unique scenario in medical practice. Ironically, ICSIs success has effectively diverted attention from identifying what causes male infertility and focused research onto the female, to optimize the provision of eggs and a receptive endometrium, on which ICSIs success depends." Prevalence Currently, there are no solid numbers on how many couples worldwide experience infertility, but the World Health Organization estimates between 60 and 80 million couples are affected. The population in different regions have varying amounts of infertility. Starting in the late 20th century, scientists have expressed concerns about the declining semen quality in men. A study was done in 1992 with men who had never experienced infertility showed that the amount of sperm in semen had declined by 1% per year since 1938. Further research a few years later also confirmed the decline in sperm count and also seminal volume. Various studies in Finland, Southern Tunisia, and Argentina also showed a decline in sperm count, motility, morphology, and seminal volume. Males from India had a 30.3% decline in sperm count, 22.9% decline in sperm motility, and a 51% decrease in morphology over a span of a decade. Doctors in India disclosed that the sperm count of a fertile Indian male had decreased by a third over a span of three decades. Some factors may include exposure to high temperatures at places such as factories. A 1 degree increase in temperature will reduce 14% of spermatogenesis.Researchers in Calcutta conducted a study between 1981 and 1985 that also showed a decrease in sperm motility and seminal volume, but no change in sperm concentration. Society and culture There are a variety of social stigmas that surround male infertility throughout the world. A lot of research has pointed to the relationship between infertility and emasculation. This association has led to infertility being less studied and diagnosed in men over time. In places like Egypt, Zimbabwe, and Mexico, erectile dysfunction also known as impotence, is considered a determinant of infertility. When stereotypical ideals of manhood are virility and strength, men sharing problems of infertility can face feelings of inadequacy, unworthiness, and have thoughts of suicide. In many cases, a variety of socio-economic interventions come in play to determine penile activity. For the Shona people, since impotence is linked to infertility, an examination to check on the penile function spans from infancy to post marriage. At infancy, there are daily check-ups by the mothers on the sons erection and urine quality. When the son reaches puberty, they are asked to ejaculate in river banks and for their male elders to examine sperm quality. The traditions last until post-marriage, when the family of the bride take part to check on consummation and the grooms sperm quality. Crisis See also Female infertility Fertility preservation Fertility testing Infertility Male accessory gland infection (MAGI) Meiosis Oncofertility Paternal age effect Spermatogenesis Vasectomy References == External links ==

Hey Aarogya, could you help me understand about Circadian rhythm sleep disorder

Circadian rhythm sleep disorder

Circadian rhythm sleep disorders (CRSD), also known as circadian rhythm sleep-wake disorders (CRSWD), are a family of sleep disorders which affect the timing of sleep. CRSDs arise from a persistent pattern of sleep/wake disturbances that can be caused either by dysfunction in ones biological clock system, or by misalignment between ones endogenous oscillator and externally imposed cues. As a result of this mismatch, those affected by circadian rhythm sleep disorders have a tendency to fall asleep at unconventional time points in the day. These occurrences often lead to recurring instances of disturbed rest, where individuals affected by the disorder are unable to go to sleep and awaken at "normal" times for work, school, and other social obligations. Delayed sleep phase disorder, advanced sleep phase disorder, non-24-hour sleep–wake disorder and irregular sleep–wake rhythm disorder represents the four main types of CRSD. Overview Humans, like most living organisms, have various biological rhythms. These biological clocks control processes that fluctuate daily (e.g., body temperature, alertness, hormone secretion), generating circadian rhythms. Among these physiological characteristics, the sleep-wake propensity can also be considered one of the daily rhythms regulated by the biological clock system. Humans sleeping cycles are tightly regulated by a series of circadian processes working in tandem, allowing for the experience of moments of consolidated sleep during the night and a long wakeful moment during the day. Conversely, disruptions to these processes and the communication pathways between them can lead to problems in sleeping patterns, which are collectively referred to as circadian rhythm sleep disorders. Normal rhythm A circadian rhythm is an entrainable, endogenous, biological activity that has a period of roughly twenty-four hours. This internal time-keeping mechanism is centralized in the suprachiasmatic nucleus (SCN) of humans, and allows for the internal physiological mechanisms underlying sleep and alertness to become synchronized to external environmental cues, like the light-dark cycle. The SCN also sends signals to peripheral clocks in other organs, like the liver, to control processes such as glucose metabolism. Although these rhythms will persist in constant light or dark conditions, different Zeitgebers (time givers such as the light-dark cycle) give context to the clock and allow it to entrain and regulate expression of physiological processes to adjust to the changing environment. Genes that help control light-induced entrainment include positive regulators BMAL1 and CLOCK and negative regulators PER1 and CRY. A full circadian cycle can be described as a twenty-four hour circadian day, where circadian time zero (CT 0) marks the beginning of a subjective day for an organism and CT 12 marks the start of subjective night.Humans with regular circadian function have been shown to maintain regular sleep schedules, regulate daily rhythms in hormone secretion, and sustain oscillations in core body temperature. Even in the absence of Zeitgebers, humans will continue to maintain a roughly 24-hour rhythm in these biological activities. Regarding sleep, normal circadian function allows people to maintain balance rest and wakefulness that allows people to work and maintain alertness during the days activities, and rest at night.Some misconceptions regarding circadian rhythms and sleep commonly mislabel irregular sleep as a circadian rhythm sleep disorder. In order to be diagnosed with CRSD, there must be either a misalignment between the timing of the circadian oscillator and the surrounding environment, or failure in the clock entrainment pathway. Among people with typical circadian clock function, there is variation in chronotypes, or preferred wake and sleep times, of individuals. Although chronotype varies from individual to individual, as determined by rhythmic expression of clock genes, people with typical circadian clock function will be able to entrain to environmental cues. For example, if a person wishes to shift the onset of a biological activity, like waking time, light exposure during the late subjective night or early subjective morning can help advance ones circadian cycle earlier in the day, leading to an earlier wake time. Diagnosis The International Classification of Sleep Disorders classifies Circadian Rhythm Sleep Disorder as a type of sleep dyssomnia. Although studies suggest that 3% of the adult population has a CRSD, many people are often misdiagnosed with insomnia instead of a CRSD. Of adults diagnosed with sleep disorders, an estimated 10% have a CRSD and of adolescents with sleep disorders, an estimated 16% may have a CRSD. Patients diagnosed with circadian rhythm sleep disorders typically express a pattern of disturbed sleep, whether that be excessive sleep that intrudes on working schedules and daily functions, or insomnia at desired times of sleep. Note that having a preference for extreme early or late wake times are not related to a circadian rhythm sleep disorder diagnosis. There must be distinct impairment of biological rhythms that affects the persons desired work and daily behavior. For a CRSD diagnosis, a sleep specialist gathers the history of a patients sleep and wake habits, body temperature patterns, and dim-light melatonin onset (DLMO). Gathering this data gives insight into the patients current schedule, as well as the physiological phase markers of the patients biological clock.The start of the CRSD diagnostic process is a thorough sleep history assessment. A standard questionnaire is used to record the sleep habits of the patient, including typical bedtime, sleep duration, sleep latency, and instances of waking up. The professional will further inquire about other external factors that may impact sleep. Prescription drugs that treat mood disorders like tricyclic antidepressants, selective serotonin reuptake inhibitors and other antidepressants are associated with abnormal sleep behaviors. Other daily habits like work schedule and timing of exercise are also recorded—because they may impact an individuals sleep and wake patterns. To measure sleep variables candidly, patients wear actigraphy watches that record sleep onset, wake time, and many other physiological variables. Patients are similarly asked to self-report their sleep habits with a week-long sleep diary to document when they go to bed, when they wake up, etc. to supplement the actigraphy data. Collecting this data allows sleep professionals to carefully document and measure patients sleep habits and confirm patterns described in their sleep history.Other additional ways to classify the nature of a patients sleep and biological clock are the morningness-eveningness questionnaire (MEQ) and the Munich ChronoType Questionnaire, both of which have fairly strong correlations with accurately reporting phase advanced or delayed sleep. Questionnaires like the Pittsburgh Sleep Quality Index (PSQI) and the Insomnia Severity Index (ISI) help gauge the severity of sleep disruption. Specifically, these questionnaires can help the professional assess the patients problems with sleep latency, undesired early-morning wakefulness, and problems with falling or staying asleep.Tayside childrens sleep questionnaire is a ten-item questionnaire for sleep disorders in children aged between one and five years old. Types Currently, the International Classification of Sleep Disorders (ICSD-3) lists 6 disorders under the category of circadian rhythm sleep disorders.CRSDs can be categorized into two groups based on their underlying mechanisms: The first category is composed of disorders where the endogenous oscillator has been altered, known as intrinsic type disorders. The second category consists of disorders in which the external environment and the endogenous circadian clock are misaligned, called extrinsic type CRSDs. Intrinsic Delayed sleep phase disorder (DSPD): Individuals who have been diagnosed with delayed sleep phase disorder have sleep-wake times which are delayed when compared to normal functioning individuals. People with DSPD typically have very long periods of sleep latency when they attempt to go to sleep during conventional sleeping times. Similarly, they also have trouble waking up at conventional times. Advanced sleep phase disorder (ASPD): People with advanced sleep phase disorder exhibit characteristics opposite to those with delayed sleep phase disorder. These individuals have advanced sleep wake times, so they tend to go to bed and wake up much earlier as compared to normal individuals. ASPD is less common than DSPD, and is most prevalent within older populations.Familial Advanced Sleep Phase Syndrome (FASPS) is linked to an autosomal dominant mode of inheritance. It is associated with a missense mutation in human PER2 that replaces Serine for a Glycine at position 662 (S662G). Families that have this mutation in PER2 experience extreme phase advances in sleep, waking up around 2 AM and going to bed around 7 PM. Irregular sleep–wake rhythm disorder (ISWRD) is characterized by a normal 24-hr sleeping period. However, individuals with this disorder experience fragmented and highly disorganized sleep that can manifest in the form of waking frequently during the night and taking naps during the day, yet still maintaining sufficient total time asleep. People with ISWRD often experience a range of symptoms from insomnia to excessive daytime sleepiness. Non-24-hour sleep–wake disorder (N24SWD): Most common in individuals that are blind and unable to detect light, is characterized by chronic patterns of sleep/wake cycles which are not entrained to the 24-hr light-dark environmental cycle. As a result of this, individuals with this disorder will usually experience a gradual yet predictable delay of sleep onset and waking times. Patients with DSPD may develop this disorder if their condition is untreated. Extrinsic Shift work sleep disorder (SWSD): Approximately 9% of Americans who work night or irregular work shifts are believed to experience shift work sleep disorder. Night shift work directly opposes the environmental cues that entrain our biological clock, so this disorder arises when an individuals clock is unable to adjust to the socially imposed work schedule. Shift work sleep disorder can lead to severe cases of insomnia as well as excessive daytime sleepiness. Jet lag: Jet lag is best characterized by difficulty falling asleep or staying asleep as a result of misalignment between ones internal circadian system and external, or environmental cues. It is typically associated with rapid travel across multiple time zones. Alzheimers disease CRSD has been frequently associated with excessive daytime sleepiness and nighttime insomnia in patients diagnosed with Alzheimers disease (AD), representing a common characteristic among AD patients as well as a risk factor of progressive functional impairments. On one hand, it has been stated that people with AD have melatonin alteration and high irregularity in their circadian rhythm that lead to a disrupted sleep-wake cycle, probably due to damage on hypothalamic SCN regions typically observed in AD. On the other hand, disturbed sleep and wakefulness states have been related to worsening of an AD patients cognitive abilities, emotional state and quality of life. Moreover, the abnormal behavioural symptoms of the disease negatively contribute to overwhelming patients relatives and caregivers as well.However, the impact of sleep-wake disturbances on the subjective experience of a person with AD is not yet fully understood. Therefore, further studies exploring this field have been highly recommended, mainly considering the increasing life expectancy and significance of neurodegenerative diseases in clinical practices. Treatment Possible treatments for circadian rhythm sleep disorders include: Chronotherapy, best shown to effectively treat delayed sleep phase disorder, acts by systematically delaying an individuals bedtime until their sleep-wake times coincide with the conventional 24-hr day. Light therapy utilizes bright light exposure to induce phase advances and delays in sleep and wake times. This therapy requires 30–60 minutes of exposure to a bright (5,000–10,000 lux) white, blue, or natural light at a set time until the circadian clock is aligned with the desired schedule. Treatment is initially administered either upon awakening or before sleeping, and if successful may be continued indefinitely or performed less frequently. Though proven very effective in the treatment of individuals with DSPD and ASPD, the benefits of light therapy on N24SWD, shift work disorder, and jet lag have not been studied as extensively. Hypnotics have also been used clinically alongside bright light exposure therapy and pharmacotherapy for the treatment of CRSDs such as Advanced Sleep Phase Disorder. Additionally, in conjunction with cognitive behavioral therapy, short-acting hypnotics also present an avenue for treating co-morbid insomnia in patients with circadian sleep disorders. Melatonin, a naturally occurring biological hormone with circadian rhythmicity, has been shown to promote sleep and entrainment to external cues when administered in drug form (0.5–5.0 mg). Melatonin administered in the evening causes phase advances in sleep-wake times while maintaining duration and quality of sleep. Similarly, when administered in the early morning, melatonin can cause phase delays. It has been shown most effective in cases of shift work sleep disorder and delayed phase sleep disorder, but has not been proven particularly useful in cases of jet lag. Dark therapy, for example, the use of blue-blocking goggles, is used to block blue and blue-green wavelength light from reaching the eye during evening hours so as not to hinder melatonin production. See also References External links Circadian Sleep Disorders Network An American Academy of Sleep Medicine Review: Circadian Rhythm Sleep Disorders: Part I, Basic Principles, Shift Work and Jet Lag Disorders. PDF, 24 pages. November 2007. An American Academy of Sleep Medicine Review: Circadian Rhythm Sleep Disorders: Part II, Advanced Sleep Phase Disorder, Delayed Sleep Phase Disorder, Free-Running Disorder, and Irregular Sleep–Wake Rhythm. PDF, 18 pages. November 2007. An American Academy of Sleep Medicine Report: Practice Parameters for the Clinical Evaluation and Treatment of Circadian Rhythm Sleep Disorders, November 1, 2007 NASA Sleep–Wake Actigraphy and Light Exposure During Spaceflight-Long Experiment

Aarogya, can you share information about a health condition involving Hypothalamic disease

Hypothalamic disease

Hypothalamic disease is a disorder presenting primarily in the hypothalamus, which may be caused by damage resulting from malnutrition, including anorexia and bulimia eating disorders, genetic disorders, radiation, surgery, head trauma, lesion, tumour or other physical injury to the hypothalamus. The hypothalamus is the control center for several endocrine functions. Endocrine systems controlled by the hypothalamus are regulated by antidiuretic hormone (ADH), corticotropin-releasing hormone, gonadotropin-releasing hormone, growth hormone-releasing hormone, oxytocin, all of which are secreted by the hypothalamus. Damage to the hypothalamus may impact any of these hormones and the related endocrine systems. Many of these hypothalamic hormones act on the pituitary gland. Hypothalamic disease therefore affects the functioning of the pituitary and the target organs controlled by the pituitary, including the adrenal glands, ovaries and testes, and the thyroid gland.Numerous dysfunctions manifest as a result of hypothalamic disease. Damage to the hypothalamus may cause disruptions in body temperature regulation, growth, weight, sodium and water balance, milk production, emotions, and sleep cycles. Hypopituitarism, neurogenic diabetes insipidus, tertiary hypothyroidism, and developmental disorders are examples of precipitating conditions caused by hypothalamic disease. Hypopituitarism The hypothalamus and pituitary gland are tightly integrated. Damage to the hypothalamus will impact the responsiveness and normal functioning of the pituitary. Hypothalamic disease may cause insufficient or inhibited signalling to the pituitary leading to deficiencies of one or more of the following hormones: thyroid-stimulating hormone, adrenocorticotropic hormone, beta-endorphin, luteinizing hormone, follicle-stimulating hormone, and melanocyte–stimulating hormones. Treatment for hypopituitarism involves hormone replacement therapy. Neurogenic diabetes insipidus Neurogenic diabetes insipidus may occur due to low levels of ADH production from the hypothalamus. Insufficient levels of ADH result in increased thirst and urine output, and prolonged excessive urine excretion increases the risk of dehydration. Tertiary hypothyroidism The thyroid gland is an auxiliary organ to the hypothalamus-pituitary system. Thyrotropin-releasing hormone (TRH) produced by the hypothalamus signals to the pituitary to release thyroid-stimulating hormone (TSH), which then stimulates the thyroid to secrete T4 and T3 thyroid hormones. Secondary hypothyroidism occurs when TSH secretion from the pituitary is impaired, whereas tertiary hypothyroidism is the deficiency or inhibition of TRH.Thyroid hormones are responsible for metabolic activity. Insufficient production of the thyroid hormones result in suppressed metabolic activity and weight gain. Hypothalamic disease may therefore have implications for obesity. Developmental disorders Growth hormone-releasing hormone (GHRH) is another releasing factor secreted by the hypothalamus. GHRH stimulates the pituitary gland to secrete growth hormone (GH), which has various effects on body growth and sexual development. Insufficient GH production may cause poor somatic growth, precocious puberty or gonadotropin deficiency, failure to initiate or complete puberty, and is often associated with rapid weight gain, low T4, and low levels of sex hormones. Sleep disorders Non-24-hour sleep-wake syndrome, a disabling condition in which ones sleep/wake cycle is longer, or rarely, shorter, than the standard 24 hours, is thought to involve or be caused by, at least in some cases, an abnormal functioning of the suprachiasmatic nucleus (SCN) in the hypothalamus. References == External links ==

Aarogya, Please give me a short description about Diffuse large B-cell lymphoma

Diffuse large B-cell lymphoma

Diffuse large B-cell lymphoma (DLBCL) is a cancer of B cells, a type of lymphocyte that is responsible for producing antibodies. It is the most common form of non-Hodgkin lymphoma among adults, with an annual incidence of 7–8 cases per 100,000 people per year in the US and UK. This cancer occurs primarily in older individuals, with a median age of diagnosis at ~70 years, although it can occur in young adults and, in rare cases, children. DLBCL can arise in virtually any part of the body and, depending on various factors, is often a very aggressive malignancy. The first sign of this illness is typically the observation of a rapidly growing mass or tissue infiltration that is sometimes associated with systemic B symptoms, e.g. fever, weight loss, and night sweats.The causes of diffuse large B-cell lymphoma are not well understood. Usually DLBCL arises from normal B cells, but it can also represent a malignant transformation of other types of lymphoma (particularly marginal zone lymphomas) or, in rare cases termed Richters transformation, chronic lymphocytic leukemia. An underlying immunodeficiency is a significant risk factor for development of the disease. Infections with the Epstein–Barr virus (EBV), Kaposis sarcoma-associated herpesvirus, human immunodeficiency virus (i.e. HIV), and the Helicobacter pylori bacterium are also associated with the development of certain subtypes of diffuse large B-cell lymphoma. However, most cases of this disease are associated with the unexplained step-wise acquisition of increasing numbers of gene mutations and changes in gene expression that occur in, and progressively promote the malignant behavior of, certain B-cell types.Diagnosis of DLBCL is made by removing a portion of the tumor through a biopsy, and then examining this tissue using a microscope. Usually a hematopathologist makes this diagnosis. Numerous subtypes of DLBCL have been identified which differ in their clinical presentations, biopsy findings, aggressive characteristics, prognoses, and recommended treatments. However, the usual treatment for most subtypes of DLBCL is chemotherapy combined with a monoclonal antibody drug that targets the diseases cancerous B-cells, usually rituximab. Through these treatments, more than half of all patients with DLBCL can be cured; the overall cure rate for older adults is less than this but their five-year survival rate has been around 58%. Subtypes of diffuse large B-cell lymphoma Diffuse large B-cell lymphoma encompasses a biologically and clinically diverse set of disease subtypes, many of which are difficult to separate from one another based on well-defined and widely accepted criteria. The World Health Organization, 2008, classification system defined more than a dozen subtypes, each of which was identified based on the location of the tumor, the presence of other cell types such as T cells in the tumor, and whether the patient had certain other illnesses related to DLBCL. Based on further research, the World Health Organization, 2016, reclassified DLBCL into its most common subtype, diffuse large B-cell lymphoma, not otherwise specified (DLBCL, NOS). DLBCL, NOS represents 80–85% of all DLBCL. The remaining DLBCL cases consist of relatively rare subtypes that are distinguished by their morphology, (i.e. microscopic appearance), immunophenotype, (i.e. expression of certain marker proteins), clinical findings, and/or association with certain pathogenic viruses. Some cases of DLBCL, NOS, while not included in the 2016 World Health Organizations classification, are clearly associated with, and caused by, chronic infection by the bacterium, Helicobacter pylori. Diffuse large B-cell lymphoma, not otherwise specified DLBCL cases that do not fit the distinctive clinical presentation, tissue morphology, neoplastic cell phenotype, and/or pathogen-associated criteria of other DLBCL subtypes are termed Diffuse large B-cell lymphoma, not otherwise specified: DLBCL, NOS, while representing 80–85% of all DLBCL cases, is a diagnosis of exclusion. In general, DLBCL, NOS is an aggressive disease with an overall long-term survival rate in patients treated with standard chemotherapy regimens of ~65%. However, this disease has many variants that differ not only in the just cited parameters but also in their aggressiveness and responsiveness to treatment. Presenting signs and symptoms About 70% of DLBCL, NOS cases present primarily with lymph node disease. In these cases, the most typical presenting symptom at the time of diagnosis is a mass that is rapidly enlarging and located in a part of the body with multiple lymph nodes such as the groin, arm pits, or neck. In the remaining ~30% of other cases, the disease begins as an extranodal lymphoma, most commonly in the stomach, or, less commonly, in other sites such as the testicles, breasts, uterus, ovaries, kidneys, adrenal glands, thyroid gland, or bone. The presenting signs and symptoms in these cases reflect the presence of a rapidly expanding tumor or infiltrate that produces symptoms specific to the organ of involvement such as increased size, pain, and/or dysfunction. Individuals with nodal or extranodal disease also present with: systemic B symptoms such as weight loss, night sweats, fevers, and/or fatigue in ~33% of cases; unexplained elevations in their blood levels of lactic acid dehydrogenase and beta-2 microglobulin in many cases; malignant cells infiltrating their bone marrow in 10–20% of cases; and/or localized Stage I or II disease in up to 50% of cases and disseminated Stage III or IV disease in the remaining cases. Bone marrow involvement may be due to DLBCL, NOS cells or low grade lymphoma cells; only DLBCL, NOS cell infiltrates indicate a worse prognosis. Uncommonly, DLBCL may arise as a transformation of marginal zone lymphoma (MZL) in individuals who have been diagnosed with this indolent cancer 4–5 years (median times) previously. Prognostic indicators based on clinical presentation The International Prognostic Index and more recently, the Indexs age-adjusted variant use age >60 years, elevated serum lactate dehydrogenase levels, low performance status, and involvement in more than one extranodal site as contributors to a poor prognosis in patients with DLBCL, NOS. In addition, disease that initially involves the testes, breast, or uterus has a relatively high rate of spreading to the central nervous system while disease initially involving the kidneys, adrenal glands, ovaries, or bone marrow has a high rate of spreading to other organs, including the central nervous system. All of these cases as well as cases initially involving the central nervous system have relatively poor to very poor prognoses. Cases initially involving the stomach, thyroid, or a single bone site have relatively good prognoses. Pathophysiology Most cases of DLBCL, NOS appear to result at least in part from the step-wise development of gene changes such as mutations, altered expressions, amplifications (i.e. increases in the number of copies of specific genes), and tranlocations from normal sites to other chromosomal sites. These changes often result in gains or loses in the production or function of the product of these genes and thereby the activity of cell signaling pathways that regulate the maturation, proliferation, survival, spread, evasion of the immune system, and other malignant behaviors of the cells in which they occur. While scores of genes have been reported to be altered in DLBCL, NOS many of these may not contribute to DLBCL, NOS. Changes in the following genes occur frequently in, and are suspected of contributing to, this diseases development and/or progression. BCL2: This gene is a protooncogene, i.e. a normal gene that can become cancer-causing when mutated or overexpressed. Its product, Bcl-2 protein, regulates cellular apoptosis (i.e. survival) by inhibiting the apoptosis-causing proteins, Bcl-2-associated X protein and Bcl-2 homologous antagonist killer. BCL6: This genes product, Bcl-6, is a repressor of transcription that regulates the expression of other genes which control cell maturation, proliferation, and survival. MYC: This protooncogenes product, Myc, encodes a transcription factor which regulates the expression of other genes whose products stimulate cell proliferation and expansion to extra-nodal tissues. EZH2: This genes product, the EZH2 protein, is a histone-lysine N-methyltransferase. It thereby regulates the expression of other genes which control lymphocyte maturation. MYD88: This genes product is a signal transducing adaptor protein essential for the transduction of interleukin-1 and toll-like receptor signaling pathways. It thereby regulates NF-κB and MAPK/ERK signaling pathways that control cell proliferation and survival. CREBBP: This genes product is a transcriptional coactivator; it activates numerous transcription factors, some of which control cell proliferation. CD79A and CD79B: these genes products are critical components of the B-cell receptor. Mutations in either gene can cause uncontrolled cell activation and proliferation. PAX5: this genes product, Pax-5, is a transcription factor that controls the development, maturation, and survival of B-cells; it also controls expression of the MYC gene in these cells.As a consequence of these gene changes and possibly other changes that have not yet been identified, the neoplastic cells in DLBCL, NOS exhibit pathologically overactive NF-κB, PI3K/AKT/mTOR, JAK-STAT0, MAPK/ERK, B-cell receptor, toll-like receptor, and NF-κB signaling pathways and thereby uncontrolled pro-malignant behaviors. Diagnosis Microscopic examinations of involved tissues reveal large neoplastic cells that are typically classified as B-cells based on their expression of B-cell marker proteins (e.g. CD20, CD19, CD22, CD79, PAX5, BOB1, OCT2, an immunoglobulin [usually IgM but occasionally IgG or IgA)], CD30, and in ~20–25% of cases PD-L1 or PD-L2 (PD-L1 and PD-L2 are transmembrane proteins that normally function to suppress attack by the immune system). These cells arrange in a diffuse pattern, efface the tissues architecture, and resemble Centroblast cells (80% of cases), Immunoblast cells (8–10% of cases), or anaplastic cells (9% of cases; anaplastic cells have bizarre nuclei and other features that may mimic the Reed–Sternberg cells of Hodgkin disease or the neoplastic cells of anaplastic large cell lymphoma). Rarely, these neoplastic cells are characterized as having signet ring or spindle shaped nuclei, prominent cytoplasmic granules, multiple microvillus projections, or, when viewed by electron microscopy, tight junctions with other cells. These neoplastic tissue infiltrates are often accompanied by small non-malignant T-cell lymphocytes and histiocytes that have a reactive morphology. Variants of DLBCL, NOS The World Health Organization, 2016, requires that the neoplastic cells in DLBCL, NOS be further defined based on whether they are derived from germinal center B-cells (i.e. GBC) or activated B-cells (i.e. ABC) as identified by gene expression profiling (GEP) or are GBC or non-GBC as identified by immunohistochemical (IHC) analyses. As identified by GEP, which measures all cellular messenger RNAs, GBC and ABC represent about 50 and ~35% of DLBCL, NOS cases, respectively, with ~15% of cases being unclassifiable. IHC analyses measure the cellular expression of specific proteins using a panel of fluorescent antibodies that bind to and therefore stain a set of key proteins. For example, one commercially available panel uses three antibodies to detect CD10, BCL6, and MUM1 proteins; GBC express whereas ABC and unidentified cells do not express these proteins; accordingly, this as well as other IHC panels classify ABC and undetermined neoplastic cell types together as non-GBC. Individuals with the ABC, unclassifiable, and non-GBC variants have significantly worse prognoses than individuals with the GBC variant: respective 5 year progression-free and overall survival rates have been reported to be 73–80% for GBC variants and 31–56% for ABC variants. Clinically, however, most DLBCL, NOS cases are analyzed by IHC and therefore classified as either GBC or non-GBC variants with non-GBC variants having progression-free and overall survival rates similar to those of the ABC variants.Gene and protein markers in the neoplastic cells of DLBCL, NOS that have clinical significance include CD5, MYC, BCL2, BCL6, CD20, CD19, CD22, CD30, PD-L1, and PD-L2. The 5–10% of DLBCL, NOS cases in which the neoplastic cells express CD5 have a very poor prognosis that is not improved by even aggressive treatment regimens. Cases in which fluorescence in situ hybridization analysis show that the neoplastic cells in this disease bear translocations in both the MYC and BCL2 genes or MYC and BCL6 genes (termed double hit lymphomas) or in all three genes (termed triple hit lymphomas) are associated with advanced disease that spreads to the central nervous system. These lymphomas, termed high-grade B-cell lymphoma with MYC, BL2, and/or BL6 rearrangements or, more simply, DH/THL, are regarded as borderline DLBCL,NOS. They represent 6–14% of all DLBCL, NOS and have had long-term survival rates of only 20–25%. Another variant B-cell lymphoma that is also considered to be a borderline DLBCL, NOS is termed high-grade B-cell lymphoma, not otherwise specified (HGBCL, NOS). These two aggressive borderline B-cell lymphomas were previously grouped together as "B-cell lymphoma, unclassifiable with features intermediate between DLBCL and Burkitt lymphoma" (i.e. BCLU) but were separated into DH/THL and HGBC, NOS by the World Health Organization, 2016. The neoplastic cells in a related variant, double expresser lymphoma (i.e. DEL), express the products of MYC and BCL2 genes, i.e. c-Myc and bcl-2 proteins, respectively, but do not have translocations in either of their genes. DEL, which represents about one-third of all DLBCL, NOS cases, has a poorer prognosis than standard DLBCL, NOS but not as poor as DH/THL cases. Cases in which the neoplastic cells have alterations in the MYC gene or its expression without changes in BLC2 or BLC6 also have a poor prognosis, particularly in cases where the MYC gene translocates (i.e. rearranges) with one of the immunoglobulin gene loci. DLBCL that begin in the testicles are a variant of DLBCL, NOS that some authors suggest should be classified as a distinct DLBCL subtype. This variant, termed Primary testicular diffuse large B-cell lymphoma (PT-DLBCL), is a DLBCL, NOS that in >75% of cases involves activated B-cells, i.e. ABC. These cells, which typically have a centroblast-like morphology, infiltrate one or, in ~6% of cases, both testicles. PT-DLBCL is an aggressive disease that often spreads to the central nervous system and has median overall survival and progression-free survival times of 96 and 49 months, respectively.The neoplastic cells in almost all cases of DLBCL, NOS express CD20. Commercially available anti-CD20 antibody agents such as rituximab or Obinutuzumab (which is sometimes used in place of rituximab) kill cells that express high levels of CD20 by binding to this cell-surface protein and thereby targeting them for attack by the hosts adaptive immune system. The addition of one of these immunotherapy agents to chemotherapy protocols has greatly improved the prognosis of most DLBCL, NOS variants. Neoplastic cell expression of CD30, found in 10–15% of DLBCL, NOS cases is a favorable prognostic indicator. As indicated in the following Treatments and prognoses section, expression of the CD20 and CD30 proteins as well as the CD19, CD20 CD22, CD30, CD79A, CD79B, and D-L1 proteins, expression of the MYC, BCL2, MYD88nd, and CREBBP genes, and expression of the PI3K/AKT/mTOR, JAK-STAT, B-cell receptor, toll-like receptor, and NF-κB signaling pathways are being studied as potential therapeutic targets for the individualized treatment of GBC and ABC/non-GBC DLBCL, NOS cases. Treatments and prognoses First-line therapy First-line therapy for patients with the GBC variant of DLBCL, NOS is R-CHOP. R-CHOP consists of rituximab, three chemotherapy drugs (cyclophosphamide, doxorubicin, and vincristine) and a glucocorticoid (either prednisone or prednisolone). The regimen achieves cure, relapse following remission, and unresponsive rates of 60–70%, 30–40% and <10%, respectively, in GBC variant cases. Relapses generally occur within the first 3 years of diagnosis with few cases doing so after 5 years. Patients who are refractory to, relapse within 1 year of diagnosis before starting, relapse within 6 months after completing, or progress within 2 years of starting R-CHOP have poorer prognoses. R-CHOP is less effective and not recommended for patients who have MYC, BL2, and/or BL6 rearrangements regardless of their GBC, ABC, or non-GBC type. One recommendation for treating these DH/THL cases is the DA-R-EPOCH regimen (dose-adjusted rituximab, etoposide, prednisolone, oncovin, cyclophosphamide, and hydroxydaunorubicin). S-R-EPOCH achieves 2 year survival rates of 40–67% compared to a ~25% survival rate for R-CHOP in these cases. DA-R-EPOCH has also been recommended for patients with double expresser lymphoma although some experts recommend treating this variant more like a typical DLCBL, NOS. First-line therapy for patients with the ABC, undetermined, or non-GBC variants has been the DA-R-EPOCH regimen. Patients with these variants (including those with double expresser lymphoma) have had a ~40% cure rate when treated with it. A randomized clinical trial conducted in France reported that a R-ACVBP chemotherapy regimen (rituximab, adriamycin, cyclophosphamide, vindesine, bleomycin, and cytarabine followed by sequential consolidation therapy with systemic methotrexate, ifosfamide, and etoposide, and then cytarabine) achieved significantly better response rates than R-CHOP in ABC/NGC variant cases lymphoma. In DLBCL, NOS variants which trend to spread or to the central nervous system, methotrexate has been recommended to be added to regimens not containing it for use as prophylaxis to reduce the incidence of this complication. The role of Autologous stem-cell transplantation as an addition to first-line therapy in the treatment of DLBCL, NOS, including cases with a poor prognosis, is unclear.A phase I clinical research trial found that the addition of lenalidomide to the R-CHOP regimen produce an ~80% complete response rate in GBC as well as non- GBC DLBCL, NOS variants. Two phase III clinical research trials are underway to confirm these results and determine if the R-CHOP + lenalidomide regimen is superior to R-CHOP in the up-front treatment of GBC and/or non-GBC variants. Treatment of recurrent and refractory DLBCL, NOS Patients with DLBCL, NOS who relapse or progress following first-line therapy have been treated with "salvage regimens" consisting of high-dose (also termed high-intensity) chemotherapy conditioning drugs followed by autologous stem cell transplantation. This regimen has attained 3-year progression-free survival rates of 21–37%. Relapse following this treatment carries a very poor prognosis with median overall survival times of ~10 months. Patients who have failed or because of health issues are ineligible for autologous stem cell transplantation have been treated with low-dose (i.e. low-intensity) chemotherapy conditioning regimens followed by allogeneic stem cell transplantation. This regimen has achieved 3 year progression-free and overall survival rates of 41% and 52%, respectively. Further studies are underway to determine the best treatment regimens for these cases. Patients refractory to first-line therapy or who relapse within 12 months of receiving salvage therapy (including bone marrow transplant) for recurrent disease have had poor prognoses with median overall survival rates of 3.3 and 6.3 months, respectively. The prognosis of these patients appears to be improved by using CAR-T therapy. Chimeric antigen receptor T cell (i.e. CAR-T) adoptive cellular immunotherapy has emerged as a recent advance in treating refractory and relapsed DLBCL, NOS (tisagenlecleucel, axicabtagene ciloleucel, lisocabtagene maraleucel). Chimeric antigen receptor T cells are genetically engineered to express: 1) an artificial T-cell receptor consisting of antigen-recognition and attached hinge domains expressed on their surface membranes; 2) a surface membrane-spanning domain; 3) an intracellular domain which, when the antigen-recognition domain binds its targeted antigen, activates signaling pathways that cause the T-cell to attack and kill cells that bear the recognized antigen on their surface membranes; and 4), in more recently devised second generation CAR-T strategies, an associated intracellular co-stimulating molecule (e.g. CD28 or 4-1BB) which augments activation of the cell-killing signaling pathways. CAR-T therapy, as it pertains to DLBCL, NOS, kills a patients neoplastic B-cells by isolating this patients T-cells; genetically engineering these cells to express an artificial T-cell receptor designed to bind an antigen expressed on the surface of their neoplastic B-cells; and infusing these cells back into the donor patient. The targeted antigen has usually been CD19, a surface membrane protein expressed on virtually all B-cells including the neoplastic cells in DLBCL, NOS. However, design of CARs as well as the antigens chosen to be their targets are constantly being changed in order to improve the efficacy of this therapeutic strategy. CAR-T therapy for DLBCL, NOS has been used on patients who are refractory to and/or have progressed on first-line as well as salvage (including autologous stem cell transplantation) treatment regimens. Patients are treated first with a conditioning chemotherapy regimen, usually cyclophosphamide and fludarabine, and then infused with their own T-cells that have been engineered to attack CD19-bearing or, rarely, CD20-bearing cells. A meta-analysis of 17 studies using this or very similar approaches to treat DLBCL, NOS found the treatments gave complete and partial responses rates of 61% and 43%, respectively. While these studies did not have control groups and were too recent for meaningful estimates of remission durations, the remission rates were higher than expected using other treatment approaches. Significant and potentially lethal therapeutic complications of this therapy included development of the cytokine release syndrome (21% of cases), neurotoxicity, i.e. the CAR-T cell-related encephalopathy syndrome (9% of cases), and the hemophagocytic lymphohistiocytosis/macrophage-activation syndrome (i.e. a form of Hemophagocytic lymphohistiocytosis). Individual studies within and outside of this meta-analysis have reported remissions lasting >2 years but also lethal cytokine release syndrome and neurotoxicity responses to this therapy. As a consequence of these studies, the Committee for Advanced Therapies and the Committee for Medicinal Products for Human Use of the European Medicines Agency recommend granting marketing authorization for tisagenlecleucel (i.e. chimeric antigen receptor T cells directed against CD19) in adult patients with DLBCL, NOS who have relapsed after or are refractory to two or more lines of systemic therapy. The Committee for Orphan Medicinal Products of the European Medicines Agency recommends tisagenlecleucel retain its orphan drug designation. The USA Food and Drug Administration (FDA) has also approved the use of this drug for relapsed or refractory DLBCL of the large B-cell lymphoma subtype in patients who have failed after two or more lines of systemic therapy. Monoclonal antibodies directed against CD19, CD22, CD30, and PD-L1 have been developed for use as immunotherapeutic agents in other hematological malignancies and are being or plan to be tested for their usefulness in DLBCL, NOS. In August 2020, the FDA approved the humanized Fc-modified cytolytic CD19 targeting monoclonal antibody tafasitamab in combination with lenalidomide as a treatment for adult patients with relapsed or refractory DLBCL. In April 2021, the FDA approved the CD19-directed antibody-drug conjugate loncastuximab tesirine as a treatment for adult patients with relapsed or refractory DLBCL after systemic therapy. Emerging therapies Neoplastic cell expression of CD30 in DLBCL, NOS is a favorable prognostic indicator; in these cases, brentuximab vedotin may be a useful addition to chemotherapy treatment protocols. This agent is a CD30-targeting antibody that delivers a toxin, monomethyl auristatin E, to CD30-expressing cells, has therapeutic efficacy against other CD30-expressing lymphomas, and may prove useful in treating the 10–15% of DLBCL, NOS cases expressing this protein. The neoplastic cells in the GBC variant of DLBCL, NOS often have mutations in the EZH2, BCL2 and CREBBP genes and overactive PI3K/AKT/mTOR and JAK-STAT signaling pathways while neoplastic cells in the ABC variant often have mutations in the MYD88, CD79A and CD79B (polatuzumab vedotin) genes and overactive B-cell receptor, toll-like receptor, and NF-κB signaling pathways. These different gene mutations and dysregulated signaling pathways are also being studied as potential therapeutic targets for the individualized treatment of GBC and ABC/non-GBC cases. CUDC-907, an inhibitor of PI3K and histone deacetylases, is being evaluated in two separate clinical trials for the treatment of refractory and/or relapsed DLBCL, NOS including cases with alterations in the MYC gene. GSK525762, an inhibitor of the BET family of proteins, suppresses expression of the MYC gene and is undergoing a phase I clinical trial for the treatment of high-grade B-cell lymphoma with MYC, BL2, and/or BL6 rearrangements (i.e. DH/THL). RO6870810, another BET inhibitor, in combination with Venetoclax, an inhibitor of the Bcl-2 protein, is likewise in a phase I clinical trial for the treatment of DH/THL. Pharmacological inhibition of BCL-2 is effective in most B cell lymphomas, but often leads to acquired resistance due to the expression of other major anti-apoptotic BCL-2 family proteins like BCL-XL and MCL-1. Combined therapy using MCL-1 inhibitor (S63845) or BCL-XL inhibitor (A-1331852) in addition to Venetoclax can be a solution to overcome this issue. Subtypes of diffuse large B-cell lymphoma DLBCL subtypes have been sorted into groups based on their distinctive morphology or immunophenotype, distinctive clinical issues, and distinctive virus-driven etiology. The prognoses and treatment of these subtypes varies with their severity. Most subtypes are aggressive diseases and consequently treated in a manner similar to DLBCL,NOS. Further details on these subtypes, including their treatments, can be found in their respective main article linkages. DLBCL with a distinctive morphology or immunophenotype T cell/histiocyte-rich large B-cell lymphoma T-cell/histiocyte-rich large B-cell lymphoma (THRLBCL) is a DLBCL in which tumors containing small numbers of usually large neoplastic B-cells embedded in a background of reactive T-cells and histiocytes develop in the liver, spleen, bone marrow and/or, rarely other sites. Patients usually present with advanced disease; their overall 3 year survival rates in different studies range between 46% and 72%. ALK+ large B-cell lymphoma ALK+ large B-cell lymphoma (ALK+ LBCL) is a DLBCL in which neoplastic lymphocytes that express the ALK tyrosine kinase receptor protein infiltrate lymph nodes as well as extranodal sites, e.g. the mediastinum, bones, bone marrow, nasopharynx, tongue, stomach, liver, spleen, and skin. About 60% of these individuals present with advanced disease. ALK+ LBCL has an overall 5 year survival rate of ~34%. Plasmablastic lymphoma Plasmablastic lymphoma (PBL) is a DLBCL in which neoplastic immunoblastic or plasmablastic cells embedded in a background of other cell types infiltrate the oral/nasal cavity or much less often the gastrointestinal tract. Some 70% of individuals with PBL are infected with EBV and/or (particularly those with oral/nasal cavity disease) human immunodeficiency virus (HIV). PBL is an aggressive disease with a median survival time of ~15 months. Intravascular large B-cell lymphoma Intravascular large B-cell lymphoma (IVLBCL) is a DLBCL in which medium- to large-sized neoplastic B-cells infiltrate small- to medium-sized blood vessels and sinusoids in the liver, spleen, and/or bone marrow. IVLBCL may be associated with the hemophagic syndrome (i.e. excessive cytokine secretion and systemic inflammation). Patients with the latter syndrome have very short survival times. The poor prognosis of this disease has been significantly improved by rituximab or similar immunochemotherapy drugs but significant proportions of these responding cases relapse, often with central nervous system involvement. Large B-cell lymphoma with IRF4 rearrangement Large B-cell lymphoma with IRF4 rearrangement (LBCL with IRF4 rearrangement) is a DLBCL in which tissue infiltrates containing intermediate- or large-sized neoplastic B-cells strongly express a chromosomal translocation involving the IRF4 gene on the short arm of chromosome 6. These cells form follicular, follicular and diffuse, or entirely diffuse infiltrates in Waldeyers tonsillar ring or other regions of the head and neck. The disease, which represents ~0.05% of all DLBCL, occurs primarily in children and young adults and typically has a good prognoses. Cases with a follicular pattern of tissue infiltrates often have indolent disease and an excellent prognosis following excision and may not need chemotherapy. Cases with a purely diffuse tissue infiltrate pattern, in contrast, often do require chemotherapy. DLBCL with distinctive clinical issues Primary mediastinal large B-cell lymphoma Primary mediastinal large B-cell lymphoma (PMBL), also termed primary mediastinal (thymic) large B-cell lymphoma, is a DLBCL in which neoplastic B-cells infiltrates are commonly located in sclerotic/fibrous tissues of the thymus and mediastinal lymph nodes. The disease represents 6–10% of all DLBCL cases, presents with early stage disease in ~80% of cases, and has an overall survival rate at 5 years of 75–85%. Primary cutaneous diffuse large B-cell lymphoma, leg type Primary cutaneous diffuse large B-cell lymphoma, leg type (PCDLBCL-LT) is a DLBCL in which diffuse patterns of immunoblastic and/or centroblastic B-cells infiltrate the dermis and/or subcutaneous tissue principally, but not exclusively, of the legs. This diseases 5-year overall survival rate is 50–60%. Primary diffuse large B-cell lymphoma of the central nervous system Primary diffuse large B-cell lymphoma of the central nervous system (DLBCL-CNS, also termed primary central nervous system lymphoma [PCNSL]) is a DLBCL in which diffuse patterns of neoplastic B-cells with centroblastic, immunoblastic, or poorly differentiated features infiltrate the brain, spinal cord, leptomeninges, or eye. The disease usually presents as a single lesion with a predilection for the supratentorial region of the brain but may involve the eye in 15–25% of cases, the cerebrospinal fluid in 7–42% of cases, and the spinal cord in ~1% of cases. The disease has a 5-year overall survival rate of ~30%. Diffuse large B-cell lymphoma associated with chronic inflammation Diffuse large B-cell lymphoma associated with chronic inflammation (DLBCL-CI) is an Epstein–Barr virus-associated lymphoproliferative disease arising in persons with a long and persistent history of chronic inflammation. The diseases lesions consist of large, mature-appearing B-cells infiltrating the lungs pleura and nearby tissues. Most cases have occurred in patients who were given a pneumothorax (i.e. therapeutic introduction of air into the chest cavity in order to collapse and thereby "rest" the lung) to treat pulmonary tuberculosis that had progressed to a pyothorax (i.e. pus in the pleural cavity). Fibrin-associated large B-cell lymphoma (FA-DLBCL), often considered a sub-type of DLBCL-CI, is an infiltration of large neoplastic B-cells and fibrin affix to a prosthesis (e.g., cardiac valve, orthopaedic device) or accumulate within a hydrocele, pseudocyst, cardiac myxoma, or chronic subdural hematoma. The B-cells in these lesions are often but not always infected with the Epstein–Barr virus. DLBCL-CI occurring in cases of pleural empyema (sometimes termed pyothorax-associated lymphoma, i.e. PAL) is an aggressive lymphoma with a five-year overall survival rate of 20–35%; FA-DLBCL, when involving the heart (e.g. occurring on myxommas or prosthetic valves) or vasculature structures (e.g. on thrombus-laden vascular grafts), may involve life-threatening cardiovascular complications, particularly strokes. Outside of these complications, however, DLBCL-CI usually has a highly favorable outcome. Lymphomatoid granulomatosis Lymphomatoid granulomatosis (LYG) is a DLBCL in which large, atypical B-cells with immunoblastic or Hodgkin disease-like features that are infected by the Epstein-Barr virus center around and destroy the microvasculature. Lymphomatoid granulomatosis almost always involves the lung but may concurrently involve the brain, peripheral nervous system, skin, kidneys, liver, gastrointestinal tract, and/or upper respiratory tract; LYG has an increased incidence in persons with Wiskott–Aldrich syndrome or HIV or who are immunosuppression due to chemotherapy or organ transplantation. The diseases prognosis is highly variable: patients with low grade disease often require no therapy except watchful waiting while patients with high grade disease usually require chemotherapy. Primary effusion lymphoma Primary effusion lymphoma (PEL) is a DLBCL in which neoplastic B cells that resemble immunoblasts, plasmablasts, or Reed–Sternberg cells infiltrate the pleural, pericardial, or peritoneal membranes that surround the lungs, heart, and abdominal organs, respectively. This infiltration leads to the seeping of fluid into the cavities which are encased by these membranes, i.e. it leads to pleural effusions, pericardial effusions, and abdominal ascites. Some cases of PEL also involve the gastrointestinal tract and lymph nodes. The disease occurs primarily in people who are immunosuppressed or test positive for HIV and are also latently infected with Kaposis sarcoma-associated herpesvirus; PEL is an aggressive disease with an overall 1 year survival rate of ~30%. DLBCL driven by viruses Epstein–Barr virus-positive diffuse large B-cell lymphoma, not otherwise specified Epstein–Barr virus-positive diffuse large B cell lymphoma, not otherwise specified (EBV+ DLBCL, NOS) is a B-cell lymphoma in which neoplastic B-cells that are infected with the Epstein-Barr virus cause a disease that does not fit into other subtypes of DLBCL. In EBV+ DLBCL, small neoplastic B-cells, other lymphocyte typess, plasma cells, histiocytes and epithelioid cells interspersed with Reed–Sternberg-like cells infiltrate, almost exclusively, lymph nodes. Elderly patients with the disease have median survival times of ~2 years while young patients have long-term treatment-related remissions in >80% of cases. HHV8-positive diffuse large B-cell lymphoma, NOS HHV8-positive diffuse large B-cell lymphoma, NOS (HHV8+ DLBCL, NOS; also termed HHV8-positive diffuse large B-cell lymphoma [HHV8+ DLBCL]) is a DLBCL in which Kaposis sarcoma-associated herpesvirus-infected, medium- to large-size neoplastic B-cells that resemble lymphocytes or immunoblasts infiltrate lymph nodes (~80% of cases) and, when disseminated (20% of cases), the liver and spleen. This infiltration usually disrupts the normal architecture of the involved tissues. HHV8+ DLBCL develops in HIV-infected individuals in ~50% of cases, in individuals with multicentric Castleman disease, plasma cell variant in uncommon cases, and in individuals with Kaposi sarcoma in rare cases. HHV8+ DLBCL commonly takes an aggressive course and has a poor prognosis. Related disorders Helicobactor pylori associated diffuse large B-cell lymphoma Rare cases of DLBCL are associated with the presence of the bacterium, Helicobacter pylori, in the neoplastic B-cells. While the histology of Helicobactor pylori-associated diffuse large B-cell lymphoma (H. pylori+ DLBCL) is typical of DLBCL, the disease is sometimes a progression of mantle cell lymphoma, is often restricted to the stomach, is less aggressive that most DLBCL cases, and may respond to a drug regimen consisting of antibiotics and proton pump inhibitors directed at killing the bacterium. Perhaps because of these features of the disease, H. pylori+ DLBCL has not been classified as a DLBCL by the World Health Organization, 2016.Recent studies suggest that localized, early-stage H. pylori+ DLBCL, when limited to the stomach, is successfully treated with H. pylori eradication protocols consisting of two or more antibiotics plus a proton pump inhibitor. However, these studies also agree that patients treated with one of these H. pylori eradication regimes need to be carefully followed: those unresponsive to, or worsening on, these regimens should be switched to a chemotherapy regimen (e.g. R-CHOP) and/or, for complicated bulky disease, surgery and/or local radiotherapy. Epstein–Barr virus-positive mucocutaneous ulcer Epstein-Barr virus-positive mucocutaneous ulcer (EBVMCU) was first described as a lymphoproliferative disorder in which Epstein–Barr virus-infected B-cells proliferate and cause ulcerations in the mucous membranes and skin of immunosuppressed individuals. Its lesions consist of Epstein–Barr virus-positive, variable-sized, atypical B-cells that by conventional histopathologic criteria indicate the lesions are a form of DLBCL. Since these lesions regress spontaneously without anti-cancer treatment, EBVMCU is now considered a pseudo-malignant disorder. Elderly individuals that evidence the disease but have no other cause for immunosuppression may exhibit a relapsing and remitting course with their ulcers worsening but then regressing spontaneously. Persistent and/or severely symptomatic cases have had excellent responses to rituximab. Individuals developing these ulcers as a consequence of immunosuppressive therapy generally have a remission after the dosage of the drugs used in their immunosuppressive treatments are reduced. Most of these patients do not relapse. See also Germinal center B-cell like diffuse large B-cell lymphoma References Sources Swerdlow SH, Campo E, Jaffe ES, Pileri SA, eds. (2008). WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. Lyon: IARC. ISBN 978-92-832-2431-0. Goldman L, Schafer AI (2012). Goldmans Cecil Medicine (24th ed.). ISBN 978-1-4377-1604-7. Turgeon ML (2005). Clinical hematology: theory and procedures. Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 978-0-7817-5007-3. == External links ==

Aarogya, Please give me a short description about Delta-beta thalassemia

Delta-beta thalassemia

Delta-beta thalassemia is a rare form of thalassemia in which there is a reduced production of hemoglobin subunit delta and hemoglobin subunit beta and raised levels of hemoglobin subunit gamma. It is an autosomal recessive disorder. Signs and symptoms An individual with delta-beta thalassemia is usually asymptomatic, however microcytosis can occur where the red blood cells are abnormally small. Mechanism Delta-beta thalassemia is autosomal recessive disorder, which means both parents are affected and two copies of the gene must be present. A carrier gets a normal gene to produce hemoglobin A, from one parent and the other parent supplies a gene which makes no hemoglobin A. Delta-beta thalassemia is considered rare.Delta-beta-thalassemia is caused by deletions of the entire delta and beta genes sequences and only gamma-globin and HbF are formed. Rarely, non-deletional forms have been reported.When two delta0 mutations are inherited, no hemoglobin A2 (alpha2, delta2) are formed. This is innocuous because only 2-3% of normal adult hemoglobin is hemoglobin A2. The individual will have normal hematological parameters (erythrocyte count, total hemoglobin, mean corpuscular volume). The delta-beta thalassemia demonstrates one mutation is at the +69 position. Relation to beta thalassemia Delta-beta thalassemia can mask the diagnosis of beta thalassemia trait. In beta thalassemia, an increase in hemoglobin A2 results, but the co-existence of a delta-beta thalassemia mutation will decrease the value of the hemoglobin A2 into the normal range, thereby obscuring the diagnosis of beta thalassemia trait Diagnosis Following the detection of hypochromic microcytic red blood cells, delta-beta thalassemia is confirmed by high-performance liquid chromatography. Treatment When needed, treatment for anemia, such as blood transfusions are used.Stem cell transplant is another option, but the donor and the individual who will receive the bone marrow transplant must be compatible, the risks involved should be evaluated. See also Alpha thalassemia Beta-thalassemia Hemoglobinopathy References Further reading Verma, S; Bhargava, M; Mittal, SK; Gupta, R (1 January 2013). "Homozygous delta-beta Thalassemia in a Child: a Rare Cause of Elevated Fetal Hemoglobin". Iranian Journal of Pediatric Hematology and Oncology. 3 (1): 222–227. ISSN 2008-8892. PMC 3915439. PMID 24575268. Kumar, B. Vinodh; Choccalingam, Chidambharam; Samuel, Premila (1 March 2016). "Incidental Identification of Possible Delta-Beta Thalassemia Trait in a Family: A Rare Cause of Elevated Hb F." Journal of Clinical and Diagnostic Research. 10 (3): BD01–BD02. doi:10.7860/JCDR/2016/16352.7409. ISSN 2249-782X. PMC 4843246. PMID 27134860. "Public Health Information Network Vocabulary Access and Distribution System (PHIN VADS)". CDC. Centers for Disease Control. Retrieved 17 September 2016. == External links ==

Aarogya, give me a short description about Varus deformity

Varus deformity

A varus deformity is an excessive inward angulation (medial angulation, that is, towards the bodys midline) of the distal segment of a bone or joint. The opposite of varus is called valgus. EX: Varus deformity results in a decreased Q angle of the knee joint. The terms varus and valgus always refer to the direction that the distal segment of the joint points. For example, in a valgus deformity of the knee, the distal part of the leg below the knee is deviated outward, in relation to the femur, resulting in a knock-kneed appearance. Conversely, a varus deformity at the knee results in a bowlegged with the distal part of the leg deviated inward, in relation to the femur. However, in relation to the mid-line of the body, the knee joint is deviated towards the mid-line. EX: Valgus deformity results in an increased Q angle of the knee joint. Terminology The terminology is made confusing by the etymology of these words. The terms varus and valgus are both Latin, but confusingly, their Latin meanings conflict with their current usage. In current usage, as noted above, a varus deformity of the knee describes bowed legs, but in the original Latin, varus meant "knock-kneed." Similarly, while a valgus deformity of the knee would currently describe knocked knees, the original Latin meaning was "bow-legged" Application of these words in adjectival form to other portions of the body by the medical community has resulted in their definitions changing so that they now refer to the angle of the distal segment (i.e. valgus impaction in a Garden I femoral neck fracture). It is correct for a knock-kneed deformity to be called both a varus deformity at the hip (coxa vara) and a valgus deformity at the knee (genu valgum); although the common terminology is to simply refer to it as a valgus knee.When the terminology refers to a bone rather than a joint, the distal segment of the bone is being described. Thus, a varus deformity of the tibia (i.e. a mid-shaft tibial fracture with varus deformity) refers to the distal segment in a varus alignment compared to the proximal segment. Examples Hip: coxa vara — the angle between the head and the shaft of the femur is reduced, resulting in a limp. Knee: genu varum (from Latin genu = knee) — the tibia is turned inward in relation to the femur, resulting in a bowlegged deformity. Ankle: talipes varus (from Latin talus = ankle and pes = foot). A notable subtype is clubfoot or talipes equinovarus, which is where one or both feet are rotated inwards and downwards. Toe: hallux varus (Latin hallux = big toe) — inward deviation of the big toe away from the second toe. Elbows: cubitus varus (Latin cubitus = elbow) — turned inward elbows See also Valgus deformity References External links Canale & Beaty: Campbells Operative Orthopaedics, 11th ed. - 2007 - Mosby, An Imprint of Elsevier

Would you describe Nervous, to me Aarogya

Nervous

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

Do you know what is Animal, Aarogya

Animal

Animals are multicellular, eukaryotic organisms in the biological kingdom Animalia. With few exceptions, animals consume organic material, breathe oxygen, are able to move, can reproduce sexually, and go through an ontogenetic stage in which their body consists of a hollow sphere of cells, the blastula, during embryonic development. Over 1.5 million living animal species have been described—of which around 1 million are insects—but it has been estimated there are over 7 million animal species in total. Animals range in length from 8.5 micrometres (0.00033 in) to 33.6 metres (110 ft). They have complex interactions with each other and their environments, forming intricate food webs. The scientific study of animals is known as zoology. Most living animal species are in Bilateria, a clade whose members have a bilaterally symmetric body plan. The Bilateria include the protostomes, containing animals such as nematodes, arthropods, flatworms, annelids and molluscs, and the deuterostomes, containing the echinoderms and the chordates, the latter including the vertebrates. Life forms interpreted as early animals were present in the Ediacaran biota of the late Precambrian. Many modern animal phyla became clearly established in the fossil record as marine species during the Cambrian explosion, which began around 539 million years ago. 6,331 groups of genes common to all living animals have been identified; these may have arisen from a single common ancestor that lived 650 million years ago. Historically, Aristotle divided animals into those with blood and those without. Carl Linnaeus created the first hierarchical biological classification for animals in 1758 with his Systema Naturae, which Jean-Baptiste Lamarck expanded into 14 phyla by 1809. In 1874, Ernst Haeckel divided the animal kingdom into the multicellular Metazoa (now synonymous for Animalia) and the Protozoa, single-celled organisms no longer considered animals. In modern times, the biological classification of animals relies on advanced techniques, such as molecular phylogenetics, which are effective at demonstrating the evolutionary relationships between taxa. Humans make use of many animal species, such as for food (including meat, milk, and eggs), for materials (such as leather and wool), as pets, and as working animals including for transport. Dogs have been used in hunting, as have birds of prey, while many terrestrial and aquatic animals were hunted for sports. Nonhuman animals have appeared in art from the earliest times and are featured in mythology and religion. Etymology The word "animal" comes from the Latin animalis, meaning having breath, having soul or living being. The biological definition includes all members of the kingdom Animalia. In colloquial usage, the term animal is often used to refer only to nonhuman animals. The term "metazoa" is from Ancient Greek μετα (meta, used to mean "later") and ζῷᾰ (zōia, plural of ζῷον zōion "animal"). Characteristics Animals have several characteristics that set them apart from other living things. Animals are eukaryotic and multicellular. Unlike plants and algae, which produce their own nutrients, animals are heterotrophic, feeding on organic material and digesting it internally. With very few exceptions, animals respire aerobically. All animals are motile (able to spontaneously move their bodies) during at least part of their life cycle, but some animals, such as sponges, corals, mussels, and barnacles, later become sessile. The blastula is a stage in embryonic development that is unique to animals, allowing cells to be differentiated into specialised tissues and organs. Structure All animals are composed of cells, surrounded by a characteristic extracellular matrix composed of collagen and elastic glycoproteins. During development, the animal extracellular matrix forms a relatively flexible framework upon which cells can move about and be reorganised, making the formation of complex structures possible. This may be calcified, forming structures such as shells, bones, and spicules. In contrast, the cells of other multicellular organisms (primarily algae, plants, and fungi) are held in place by cell walls, and so develop by progressive growth. Animal cells uniquely possess the cell junctions called tight junctions, gap junctions, and desmosomes.With few exceptions—in particular, the sponges and placozoans—animal bodies are differentiated into tissues. These include muscles, which enable locomotion, and nerve tissues, which transmit signals and coordinate the body. Typically, there is also an internal digestive chamber with either one opening (in Ctenophora, Cnidaria, and flatworms) or two openings (in most bilaterians). Reproduction and development Nearly all animals make use of some form of sexual reproduction. They produce haploid gametes by meiosis; the smaller, motile gametes are spermatozoa and the larger, non-motile gametes are ova. These fuse to form zygotes, which develop via mitosis into a hollow sphere, called a blastula. In sponges, blastula larvae swim to a new location, attach to the seabed, and develop into a new sponge. In most other groups, the blastula undergoes more complicated rearrangement. It first invaginates to form a gastrula with a digestive chamber and two separate germ layers, an external ectoderm and an internal endoderm. In most cases, a third germ layer, the mesoderm, also develops between them. These germ layers then differentiate to form tissues and organs.Repeated instances of mating with a close relative during sexual reproduction generally leads to inbreeding depression within a population due to the increased prevalence of harmful recessive traits. Animals have evolved numerous mechanisms for avoiding close inbreeding. Some animals are capable of asexual reproduction, which often results in a genetic clone of the parent. This may take place through fragmentation; budding, such as in Hydra and other cnidarians; or parthenogenesis, where fertile eggs are produced without mating, such as in aphids. Ecology Animals are categorised into ecological groups depending on how they obtain or consume organic material, including carnivores, herbivores, omnivores, detritivores, and parasites. Interactions between animals form complex food webs. In carnivorous or omnivorous species, predation is a consumer–resource interaction where a predator feeds on another organism (called its prey). Selective pressures imposed on one another lead to an evolutionary arms race between predator and prey, resulting in various anti-predator adaptations. Almost all multicellular predators are animals. Some consumers use multiple methods; for example, in parasitoid wasps, the larvae feed on the hosts living tissues, killing them in the process, but the adults primarily consume nectar from flowers. Other animals may have very specific feeding behaviours, such as hawksbill sea turtles primarily eating sponges. Most animals rely on the biomass and energy produced by plants through photosynthesis. Herbivores eat plant material directly, while carnivores, and other animals on higher trophic levels typically acquire it indirectly by eating other animals. Animals oxidize carbohydrates, lipids, proteins, and other biomolecules, which allows the animal to grow and to sustain biological processes such as locomotion. Animals living close to hydrothermal vents and cold seeps on the dark sea floor consume organic matter of archaea and bacteria produced in these locations through chemosynthesis (by oxidizing inorganic compounds, such as hydrogen sulfide).Animals originally evolved in the sea. Lineages of arthropods colonised land around the same time as land plants, probably between 510 and 471 million years ago during the Late Cambrian or Early Ordovician. Vertebrates such as the lobe-finned fish Tiktaalik started to move on to land in the late Devonian, about 375 million years ago. Animals occupy virtually all of earths habitats and microhabitats, including salt water, hydrothermal vents, fresh water, hot springs, swamps, forests, pastures, deserts, air, and the interiors of animals, plants, fungi and rocks. Animals are however not particularly heat tolerant; very few of them can survive at constant temperatures above 50 °C (122 °F). Only very few species of animals (mostly nematodes) inhabit the most extreme cold deserts of continental Antarctica. Diversity Size The blue whale (Balaenoptera musculus) is the largest animal that has ever lived, weighing up to 190 tonnes and measuring up to 33.6 metres (110 ft) long. The largest extant terrestrial animal is the African bush elephant (Loxodonta africana), weighing up to 12.25 tonnes and measuring up to 10.67 metres (35.0 ft) long. The largest terrestrial animals that ever lived were titanosaur sauropod dinosaurs such as Argentinosaurus, which may have weighed as much as 73 tonnes. Several animals are microscopic; some Myxozoa (obligate parasites within the Cnidaria) never grow larger than 20 µm, and one of the smallest species (Myxobolus shekel) is no more than 8.5 µm when fully grown. Numbers and habitats The following table lists estimated numbers of described extant species for all the animal groups, along with their principal habitats (terrestrial, fresh water, and marine), and free-living or parasitic ways of life. Species estimates shown here are based on numbers described scientifically; much larger estimates have been calculated based on various means of prediction, and these can vary wildly. For instance, around 25,000–27,000 species of nematodes have been described, while published estimates of the total number of nematode species include 10,000–20,000; 500,000; 10 million; and 100 million. Using patterns within the taxonomic hierarchy, the total number of animal species—including those not yet described—was calculated to be about 7.77 million in 2011. Evolutionary origin Animals are found as long ago as the Ediacaran biota, towards the end of the Precambrian, and possibly somewhat earlier. It had long been doubted whether these life-forms included animals, but the discovery of the animal lipid cholesterol in fossils of Dickinsonia establishes their nature. Animals are thought to have originated under low-oxygen conditions, suggesting that they were capable of living entirely by anaerobic respiration, but as they became specialized for aerobic metabolism they became fully dependent on oxygen in their environments.Many animal phyla first appear in the fossil record during the Cambrian explosion, starting about 539 million years ago, in beds such as the Burgess shale. Extant phyla in these rocks include molluscs, brachiopods, onychophorans, tardigrades, arthropods, echinoderms and hemichordates, along with numerous now-extinct forms such as the predatory Anomalocaris. The apparent suddenness of the event may however be an artefact of the fossil record, rather than showing that all these animals appeared simultaneously. That view is supported by the discovery of Auroralumina attenboroughii, the earliest known Ediacaran crown-group cnidarian (557–562 mya, some 20 million years before the Cambrian explosion) from Charnwood Forest, England. It is thought to be one of the earliest predators, catching small prey with its nematocysts as modern cnidarians do.Some palaeontologists have suggested that animals appeared much earlier than the Cambrian explosion, possibly as early as 1 billion years ago. Early fossils that might represent animals appear for example in the 665-million-year-old rocks of the Trezona Formation of South Australia. These fossils are interpreted as most probably being early sponges.Trace fossils such as tracks and burrows found in the Tonian period (from 1 gya) may indicate the presence of triploblastic worm-like animals, roughly as large (about 5 mm wide) and complex as earthworms. However, similar tracks are produced today by the giant single-celled protist Gromia sphaerica, so the Tonian trace fossils may not indicate early animal evolution. Around the same time, the layered mats of microorganisms called stromatolites decreased in diversity, perhaps due to grazing by newly evolved animals. Objects such as sediment-filled tubes that resemble trace fossils of the burrows of wormlike animals have been found in 1.2 gya rocks in North America, in 1.5 gya rocks in Australia and North America, and in 1.7 gya rocks in Australia. Their interpretation as having an animal origin is disputed, as they might be water-escape or other structures. Phylogeny Animals are monophyletic, meaning they are derived from a common ancestor. Animals are sister to the Choanoflagellata, with which they form the Choanozoa. The most basal animals, the Porifera, Ctenophora, Cnidaria, and Placozoa, have body plans that lack bilateral symmetry. Their relationships are still disputed; the sister group to all other animals could be the Porifera or the Ctenophora, both of which lack hox genes, important in body plan development.These genes are found in the Placozoa and the higher animals, the Bilateria. 6,331 groups of genes common to all living animals have been identified; these may have arisen from a single common ancestor that lived 650 million years ago in the Precambrian. 25 of these are novel core gene groups, found only in animals; of those, 8 are for essential components of the Wnt and TGF-beta signalling pathways which may have enabled animals to become multicellular by providing a pattern for the bodys system of axes (in three dimensions), and another 7 are for transcription factors including homeodomain proteins involved in the control of development.The phylogenetic tree indicates approximately how many millions of years ago (mya) the lineages split. Non-Bilateria Several animal phyla lack bilateral symmetry. Among these, the sponges (Porifera) probably diverged first, representing the oldest animal phylum. Sponges lack the complex organization found in most other animal phyla; their cells are differentiated, but in most cases not organised into distinct tissues. They typically feed by drawing in water through pores.The Ctenophora (comb jellies) and Cnidaria (which includes jellyfish, sea anemones, and corals) are radially symmetric and have digestive chambers with a single opening, which serves as both mouth and anus. They are sometimes placed together in the group Coelenterata because of common traits, not because of close relationships. Animals in both phyla have distinct tissues, but these are not organised into organs. They are diploblastic, having only two main germ layers, ectoderm and endoderm. The tiny placozoans are similar, but they do not have a permanent digestive chamber. Bilateria The remaining animals, the great majority—comprising some 29 phyla and over a million species—form a clade, the Bilateria, which have a bilaterally symmetric body plan. The Bilateria are triploblastic, with three well-developed germ layers, and their tissues form distinct organs. The digestive chamber has two openings, a mouth and an anus, and there is an internal body cavity, a coelom or pseudocoelom. These animals have a head end (anterior) and a tail end (posterior), a back (dorsal) surface and a belly (ventral) surface, and a left and a right side.Having a front end means that this part of the body encounters stimuli, such as food, favouring cephalisation, the development of a head with sense organs and a mouth. Many bilaterians have a combination of circular muscles that constrict the body, making it longer, and an opposing set of longitudinal muscles, that shorten the body; these enable soft-bodied animals with a hydrostatic skeleton to move by peristalsis. They also have a gut that extends through the basically cylindrical body from mouth to anus. Many bilaterian phyla have primary larvae which swim with cilia and have an apical organ containing sensory cells. However, over evolutionary time, descendant spaces have evolved which have lost one or more of each of these characteristics. For example, adult echinoderms are radially symmetric (unlike their larvae), while some parasitic worms have extremely simplified body structures.Genetic studies have considerably changed zoologists understanding of the relationships within the Bilateria. Most appear to belong to two major lineages, the protostomes and the deuterostomes. The basalmost bilaterians are the Xenacoelomorpha. Protostomes and deuterostomes Protostomes and deuterostomes differ in several ways. Early in development, deuterostome embryos undergo radial cleavage during cell division, while many protostomes (the Spiralia) undergo spiral cleavage. Animals from both groups possess a complete digestive tract, but in protostomes the first opening of the embryonic gut develops into the mouth, and the anus forms secondarily. In deuterostomes, the anus forms first while the mouth develops secondarily. Most protostomes have schizocoelous development, where cells simply fill in the interior of the gastrula to form the mesoderm. In deuterostomes, the mesoderm forms by enterocoelic pouching, through invagination of the endoderm.The main deuterostome phyla are the Echinodermata and the Chordata. Echinoderms are exclusively marine and include starfish, sea urchins, and sea cucumbers. The chordates are dominated by the vertebrates (animals with backbones), which consist of fishes, amphibians, reptiles, birds, and mammals. The deuterostomes also include the Hemichordata (acorn worms). Ecdysozoa The Ecdysozoa are protostomes, named after their shared trait of ecdysis, growth by moulting. They include the largest animal phylum, the Arthropoda, which contains insects, spiders, crabs, and their kin. All of these have a body divided into repeating segments, typically with paired appendages. Two smaller phyla, the Onychophora and Tardigrada, are close relatives of the arthropods and share these traits. The ecdysozoans also include the Nematoda or roundworms, perhaps the second largest animal phylum. Roundworms are typically microscopic, and occur in nearly every environment where there is water; some are important parasites. Smaller phyla related to them are the Nematomorpha or horsehair worms, and the Kinorhyncha, Priapulida, and Loricifera. These groups have a reduced coelom, called a pseudocoelom. Spiralia The Spiralia are a large group of protostomes that develop by spiral cleavage in the early embryo. The Spiralias phylogeny has been disputed, but it contains a large clade, the superphylum Lophotrochozoa, and smaller groups of phyla such as the Rouphozoa which includes the gastrotrichs and the flatworms. All of these are grouped as the Platytrochozoa, which has a sister group, the Gnathifera, which includes the rotifers.The Lophotrochozoa includes the molluscs, annelids, brachiopods, nemerteans, bryozoa and entoprocts. The molluscs, the second-largest animal phylum by number of described species, includes snails, clams, and squids, while the annelids are the segmented worms, such as earthworms, lugworms, and leeches. These two groups have long been considered close relatives because they share trochophore larvae. History of classification In the classical era, Aristotle divided animals, based on his own observations, into those with blood (roughly, the vertebrates) and those without. The animals were then arranged on a scale from man (with blood, 2 legs, rational soul) down through the live-bearing tetrapods (with blood, 4 legs, sensitive soul) and other groups such as crustaceans (no blood, many legs, sensitive soul) down to spontaneously generating creatures like sponges (no blood, no legs, vegetable soul). Aristotle was uncertain whether sponges were animals, which in his system ought to have sensation, appetite, and locomotion, or plants, which did not: he knew that sponges could sense touch, and would contract if about to be pulled off their rocks, but that they were rooted like plants and never moved about.In 1758, Carl Linnaeus created the first hierarchical classification in his Systema Naturae. In his original scheme, the animals were one of three kingdoms, divided into the classes of Vermes, Insecta, Pisces, Amphibia, Aves, and Mammalia. Since then the last four have all been subsumed into a single phylum, the Chordata, while his Insecta (which included the crustaceans and arachnids) and Vermes have been renamed or broken up. The process was begun in 1793 by Jean-Baptiste de Lamarck, who called the Vermes une espèce de chaos (a chaotic mess) and split the group into three new phyla: worms, echinoderms, and polyps (which contained corals and jellyfish). By 1809, in his Philosophie Zoologique, Lamarck had created 9 phyla apart from vertebrates (where he still had 4 phyla: mammals, birds, reptiles, and fish) and molluscs, namely cirripedes, annelids, crustaceans, arachnids, insects, worms, radiates, polyps, and infusorians.In his 1817 Le Règne Animal, Georges Cuvier used comparative anatomy to group the animals into four embranchements ("branches" with different body plans, roughly corresponding to phyla), namely vertebrates, molluscs, articulated animals (arthropods and annelids), and zoophytes (radiata) (echinoderms, cnidaria and other forms). This division into four was followed by the embryologist Karl Ernst von Baer in 1828, the zoologist Louis Agassiz in 1857, and the comparative anatomist Richard Owen in 1860.In 1874, Ernst Haeckel divided the animal kingdom into two subkingdoms: Metazoa (multicellular animals, with five phyla: coelenterates, echinoderms, articulates, molluscs, and vertebrates) and Protozoa (single-celled animals), including a sixth animal phylum, sponges. The protozoa were later moved to the former kingdom Protista, leaving only the Metazoa as a synonym of Animalia. In human culture Practical uses The human population exploits a large number of other animal species for food, both of domesticated livestock species in animal husbandry and, mainly at sea, by hunting wild species. Marine fish of many species are caught commercially for food. A smaller number of species are farmed commercially. Humans and their livestock make up more than 90% of the biomass of all terrestrial vertebrates, and almost as much as all insects combined.Invertebrates including cephalopods, crustaceans, and bivalve or gastropod molluscs are hunted or farmed for food. Chickens, cattle, sheep, pigs, and other animals are raised as livestock for meat across the world. Animal fibres such as wool are used to make textiles, while animal sinews have been used as lashings and bindings, and leather is widely used to make shoes and other items. Animals have been hunted and farmed for their fur to make items such as coats and hats. Dyestuffs including carmine (cochineal), shellac, and kermes have been made from the bodies of insects. Working animals including cattle and horses have been used for work and transport from the first days of agriculture.Animals such as the fruit fly Drosophila melanogaster serve a major role in science as experimental models. Animals have been used to create vaccines since their discovery in the 18th century. Some medicines such as the cancer drug Yondelis are based on toxins or other molecules of animal origin. People have used hunting dogs to help chase down and retrieve animals, and birds of prey to catch birds and mammals, while tethered cormorants have been used to catch fish. Poison dart frogs have been used to poison the tips of blowpipe darts. A wide variety of animals are kept as pets, from invertebrates such as tarantulas and octopuses, insects including praying mantises, reptiles such as snakes and chameleons, and birds including canaries, parakeets, and parrots all finding a place. However, the most kept pet species are mammals, namely dogs, cats, and rabbits. There is a tension between the role of animals as companions to humans, and their existence as individuals with rights of their own. A wide variety of terrestrial and aquatic animals are hunted for sport. Symbolic uses Animals have been the subjects of art from the earliest times, both historical, as in Ancient Egypt, and prehistoric, as in the cave paintings at Lascaux. Major animal paintings include Albrecht Dürers 1515 The Rhinoceros, and George Stubbss c. 1762 horse portrait Whistlejacket. Insects, birds and mammals play roles in literature and film, such as in giant bug movies.Animals including insects and mammals feature in mythology and religion. In both Japan and Europe, a butterfly was seen as the personification of a persons soul, while the scarab beetle was sacred in ancient Egypt. Among the mammals, cattle, deer, horses, lions, bats, bears, and wolves are the subjects of myths and worship. The signs of the Western and Chinese zodiacs are based on animals. See also Animal attacks Animal coloration Ethology Fauna List of animal names Lists of organisms by population Notes References External links Tree of Life Project Archived 12 June 2011 at the Wayback Machine Animal Diversity Web – University of Michigans database of animals ARKive – multimedia database of endangered/protected species

Aarogya, Please give me a short description about Diphyllobothriasis

Diphyllobothriasis

Diphyllobothriasis is the infection caused by tapeworms of the genus Diphyllobothrium (commonly D. latum and D. nihonkaiense). Diphyllobothriasis mostly occurs in regions where raw fish is regularly consumed; those who consume raw fish are at risk of infection. The infection is often asymptomatic and usually presents only with mild symptoms, which may include gastrointestinal complaints, weight loss, and fatigue. Rarely, vitamin B12 deficiency (possibly leading to anaemia) and gastrointestinal obstructions may occur. Infection may be long-lasting in absence of treatment. Diphyllobothriasis is generally diagnosed by looking for eggs or tapeworm segments in passed stool. Treatment with antiparasitic medications is straightforward, effective, and safe. Signs and symptoms Most infections (~80%) are asymptomatic. Infections may be long-lasting, persisting for many years or decades (up to 25 years) if untreated. Symptoms (when present) are generally mild. Manifestations may include abdominal pain and discomfort, diarrhea, vomiting, constipation, weight loss, and fatigue. Additional symptoms have been reported/described, including dyspepsia, abdominal distension (commonly as presenting complaint), headache, myalgia, and dizziness. Complications While the infection is generally mild, complications may occur. Complications are predicated on parasite burden, and are generally related to vitamin B12 deficiency and related health conditions. Vitamin B12 deficiency and anaemia Vitamin B12 deficiency with subsequent megaloblastic anaemia (which is indistinguishable from pernicious anaemia) may occur in some instances of the disease. Anaemia may in turn result in subacute combined degeneration of the spinal cord and cognitive decline.D. latum competes with the host for vitamin B12 absorption, absorbing some 80% of dietary intake and causing deficiency and megaloblastic anaemia in some 40% of cases. Vitamin B12 uptake is enabled by the position of the parasite which usually lodges in the jejunum. Vitamin B12 deficiency is - according to research - conversely seldom seen in D. pacificum infection. Gastrointestinal obstructions Rarely, massive infections may result in intestinal obstruction. Migration of proglottids can cause cholecystitis or cholangitis. Cause Diphyllobothriasis is caused by infection by several species of the Diphyllobothrium genus. Transmission Humans are one of the definitive hosts of Diphyllobothrium tapeworms, along with other carnivores; fish-eating mammals (including canids, felids, and bears), marine mammals (dolphins, porpoises, and whales), and (a few) birds (e.g. gulls) may also serve as definitive hosts.Definitive hosts release eggs in faeces; the eggs then mature in ~18–20 days if under favourable conditions. Crustaceans serve as the first intermediate hosts, and Diphyllobothrium larvae develop. The larvae are released when crustaceans are consumed by predators, which serve as second intermediate hosts (these are mostly small fish). Larvae move into deeper tissues in the second intermediate host. Second intermediate hosts do not serve as an important source of infection of humans as these are not regularly consumed raw. Consumption of infected second intermediate hosts by larger predatory fish, which serve as paratenic hosts; the parasites thereupon migrate into the musculature awaiting consumption by definitive hosts in which adult tapeworms will then finally develop in the small intestine to release up to a million immature eggs per day per parasite. Hosts begin to release eggs 5–6 weeks after infection. Pathophysiology Tapeworms develop in the small intestine. Adults attach to the intestinal mucosa. Adult tapeworms may grow to over 10m in length and may constitute of over 3,000 proglottids which contain sets of male and female reproductive organs, allowing for high fecundity. Eggs appear in the faeces 5–6 weeks after infection.D. latum tapeworms are the longest and typically reach a length of 4-15m, but may grow up to 25m in length within the human intestine. Growth rate may exceed 22 cm/day. D. latum tapeworms feature an anterior end (scolex) equipped with attachment grooves on the dorsal and ventral surfaces. Host-parasite interactions Diphyllobothriasis is postulated to cause changes in neuromodulator concentrations in host tissue and serum. D. latum infection has been shown to cause local changes in the host, leading to altered GI function (including motility) via neuroendocrine modulation.Diphyllobothriasis causes mast cell and eosinophil degranulation, leading to pro-inflammatory cytokine release. Diagnosis Infection may be suspected based upon a patients occupation, hobbies, eating habits, and travel history. During diagnostic procedures, standard safety precautions apply. Eggs are not directly infectious to humans (in contrast to some other tapeworm species). Microscopy Diagnosis is usually made by identifying proglottid segments, or characteristic eggs in the faeces. Eggs are usually numerous and can be demonstrated without concentration techniques. Morphologic comparison with other intestinal parasites may be employed as a further diagnostic approach.These simple diagnostic techniques are able to identify the nature of the infection to the genus level, which is usually sufficient in a clinical setting. Though it is difficult to identify the eggs or proglottids to the species level, the distinction is of little clinical importance because - like most adult tapeworms in the intestine - all members of the genus respond to the same treatments. Treatment may distort morphological features of expelled pathogen tissues and complicate subsequent morphological diagnosis attempts. Genetic identification When the exact species need be determined (e.g. in epidemiological studies), restriction fragment length polymorphisms can be effectively used. PCR can be performed on samples of purified eggs, or on native fecal samples following sonication of the eggs to release their contents. Molecular identification is currently generally only used in research. Radiography A potential diagnostic tool and treatment is the contrast medium gastrografin which, when introduced into the duodenum, allows both visualization of the parasite, and has also been shown to cause detachment and passing of the whole parasite. Prevention Ingestion of raw freshwater fish should be avoided. Adequate cooking or freezing of freshwater fish will destroy the encysted fish tapeworm larvae. Fish that is thoroughly cooked, brined, or frozen at -10 °C for 24–48 hours can also be consumed without risk of D. latum infection. Public health information campaigns may be employed to educate the public about the risks of consuming improperly prepared fish. Because human feces are an important mechanism for spreading eggs, proper disposal of sewage can reduce fish (and therefore human) infections. Prevention of water contamination may be achieved both by raising public awareness of the dangers of defecating in recreational bodies of water and by implementation of basic sanitation measures and screening and successful treatment of people infected with the parasite. Treatment Upon diagnosis, treatment is simple and effective.Praziquantel The standard treatment for diphyllobothriasis (as well as many other tapeworm infections) is a single dose of praziquantel, 5–10 mg/kg orally once for both adults and children. Praziquantel is not FDA-approved for this indication. Praziquantel has few side effects, many of which are similar to the symptoms of diphyllobothriasis.Niclosamide An alternative treatment is niclosamide, 2 g orally once for adults or 50 mg/kg (max 2 g) for children. Niclosamide is not available for human or even animal use in the United States. Side effects of niclosamide are very rare due to the fact that the medication is not absorbed in the gastrointestinal tract.Other Reportedly, albendazole can also be effective. Gastrografin may be potentially used both as a diagnostic and therapeutic; when introduced into the duodenum it allows for the visualization of the parasite, and has also been shown to cause detachment and passing of the whole worm. During the 1940s, the preferred treatment was 6 to 8 grams of oleoresin of aspidium, which was introduced into the duodenum via a Rehfuss tube. Epidemiology People at high risk for infection have traditionally been those who regularly consume raw fish. While people of any gender or age may fall sick, the majority of identified cases occurred in middle-aged men. Geographical distribution Diphyllobothriasis occurs in areas where lakes and rivers coexist with human consumption of raw or undercooked freshwater fish. Such areas are found in Europe, newly independent states of the former Soviet Union, North America, Asia, Uganda, Peru (because of ceviche), and Chile. Many regional cuisines include raw or undercooked food, including sushi and sashimi in Japanese cuisine, carpaccio di persico in Italian, tartare maison in French-speaking populations, ceviche in Latin American cuisine and marinated herring in Scandinavia. With emigration and globalization, the practice of eating raw fish in these and other dishes has brought diphyllobothriasis to new parts of the world and created new endemic foci of disease.Infections in Europe and North America were traditionally associated with Jewish women due to the practice of tasting bits of uncooked fish during preparation of the gefilte fish dish, and also occurred in Scandinavian women for the same reason. Diphyllobothriasis was thus also referred to as the "Jewish housewifes disease" or the "Scandinavian housewifes disease". Japan Diphyllobothriasis nihonkaiense was once endemic to coastal provinces of central and northern Japan, where salmon fisheries thrived. In recent decades, regions with endemic diphyllobothriasis nihonkaiense have disappeared from Japan, though cases continue to be reported among urbanites who consume sushi or sashimi. In Kyoto, it is estimated that the average annual incidence in the past 20 years was 0.32/100,000, and that in 2008 was 1.0 case per 100,000 population, suggesting that D. nihonkaiense infection is equally as prevalent in Japan as D. latum is in some European countries. United States The disease is rare in the United States. History The fish tapeworm has a long documented history of infecting people who regularly consume fish and especially those whose customs include the consumption of raw or undercooked fish. In the 1970s, most of the known cases of diphyllobothriasis came from Europe (5 million cases), and Asia (4 million cases) with fewer cases coming from North America and South America, and no reliable data on cases from Africa or Australia. Despite the relatively small number of cases seen today in South America, some of the earliest archeological evidence of diphyllobothriasis comes from sites in South America. Evidence of Diphyllobothrium spp. has been found in 4,000- to 10,000-year-old human remains on the western coast of South America. There is no clear point in time when Diphyllobothrium latum and related species were “discovered” in humans, but it is clear that diphyllobothriasis has been endemic in human populations for a very long time. Due to the changing dietary habits in many parts of the world, autochthonous, or locally acquired, cases of diphyllobothriasis have recently been documented in previously non-endemic areas, such as Brazil. In this way, diphyllobothriasis represents an emerging infectious disease in certain parts of the world where cultural practices involving eating raw or undercooked fish are being introduced. References External links "Diphyllobothriasis". CDC – DPDx – Laboratory Identification of Parasitic Diseases of Public Health Concern. 2013-11-29. Retrieved 2015-09-05.

Hello Aarogya , Do you know what is Sequela,

Sequela

A sequela (UK: , US: ; usually used in the plural, sequelae ) is a pathological condition resulting from a disease, injury, therapy, or other trauma. Derived from the Latin word, meaning “sequel”, it is used in the medical field to mean a complication or condition following a prior illness or disease.A typical sequela is a chronic complication of an acute condition—in other words, a long-term effect of a temporary disease or injury—which follows immediately from the condition. Sequelae differ from late effects, which can appear long after—even several decades after—the original condition has resolved. In general, non-medical usage, the terms sequela and sequelae mean consequence and consequences. Examples and uses Chronic kidney disease, for example, is sometimes a sequela of diabetes; "chronic constipation" or more accurately "obstipation" (that is, inability to pass stool or gas) is a sequela to an intestinal obstruction; and neck pain is a common sequela of whiplash or other trauma to the cervical vertebrae. Post-traumatic stress disorder may be a psychological sequela of rape. Sequelae of traumatic brain injury include headache, dizziness, anxiety, apathy, depression, aggression, cognitive impairments, personality changes, mania, and psychosis. COVID-19 is also known to cause post-acute sequelae, known as long COVID, post-COVID syndrome, or post-acute sequelae of COVID-19 (PASC). This refers to the continuation of COVID-19 symptoms or the development of new ones, four or more weeks after the initial infection; these symptoms may persist for weeks and months. Post-COVID syndrome can occur in individuals who were asymptomatic for COVID, as well as those ranging from mild illness to severe hospitalization. These most commonly reported sequelae include fatigue, shortness of breath, chest pain, loss of smell, and brain fog; symptoms drastically range, from mild illness to severe impairment.Some conditions may be diagnosed retrospectively from their sequelae. An example is pleurisy. Other examples of sequelae include those following neurological injury; including aphasia, ataxia, hemi- and quadriplegia, and any number of other changes that may be caused by neurological trauma. Note that these pathologies can be related to both physical and chemical traumas, as both can cause lingering neuronal damage. The phrase status post, abbreviated in writing as s/p, is used to discuss sequelae with reference to their cause. Clinicians typically use the phrase to refer to acute traumatic conditions. For example: "the patient had neck pain status post a motor vehicle accident". Rheumatic fever is a non-suppurative sequela of a primary infection of group A Streptococcus bacteria. Glomerulonephritis can also be a non-suppurative sequela of Streptococcus pyogenes. References Further reading Lindsay, James (1997). "Chronic Sequelae of Foodborne Disease". Emerging Infectious Diseases. 3 (4): 443–452. doi:10.3201/eid0304.970405. PMC 2640087. PMID 9366595. External links Traumatic causes of Tempormandibular Joints Disorder (dysfunction)

Would you describe Buried penis, to me Aarogya

Buried penis

Buried penis (also known as hidden penis or retractile penis) is a congenital or acquired condition in which the penis is partially or completely hidden below the surface of the skin. A buried penis can lead to urinary difficulties, poor hygiene, infection, and inhibition of normal sexual function.Buried penis is different than micropenis, which is an abnormally small, normally structured penis with a stretched penile length of less than 2.5 standard deviations below the mean for age or stage of sexual development of the patient. History Buried penis was first described by Edward Lawrence Keyes in 1919 as the apparent absence of the penis due to the penis being buried beneath the skin of the abdomen, thigh, or scrotum. Further research was done by Maurice Campbell in 1951, when he reported on the penis being buried beneath subcutaneous fat of the scrotum, perineum, hypogastrium, and thigh. Causes Congenital Congenital causes can include the maldevelopment of the penile shaft with a lack of attachments of the shaft skin to the penile shaft. While rare, it can include an abnormally large pubic fat pad and firm tissue that pulls the penis inward. Acquired Obesity While not every obese male has the buried penis condition, 87% of men that received surgical treatment for buried penis were reported to be obese. Significant overlying abdominal fat can also create an environment that encourages bacterial and fungal growth. Obesity can also increase the likelihood of the development of type II diabetes mellitus, which is characterized by increase susceptibility to infections, making it difficult to successfully and promptly manage the buried penis condition. Such recurring infections can also lead to scar contracture, which can cause the prepubic skin to shift over the shaft and glans, thus invaginating the shafts skin and leading to a buried penis. </ref> Penoscrotal lymphodema While an uncommon cause, penoscrotal lymphodema causes a deformity of the shaft and scrotum, resulting in a buried penis. Overly aggressive circumcision In some cases of circumcision, too much foreskin is removed or the suture line constricts, causing cicatricial scarring, which can trap the penis in the remaining foreskin or push the penis into the suprapubic area and lead to a buried penis. Balanitis xerotica obliterans (BXO) BXO is a chronic inflammatory dermatological process that causes sclerosis of the glans, shaft, prepuce, or urethra. This can result in a cicatrix of the distal penis and its entrapment. Dysgenic dartos Dysgenic dartos is a condition characterized by a lack of dorsal support together with the hypermobility of the ventral skin and the lack of proper attachment between the dartos and the penis. This can enable the penis to "telescope" into the scrotum, thus creating a buried penis. Treatment The condition may resolve itself without any intervention in very young children; however, patients may eventually need definitive reconstructive surgery. Urgent surgery may be necessary if infection is present. Congenitial buried penis can be corrected surgically in childhood by anchoring the corpora cavernosa to dartos bundles at the penile base. While weight loss may be of help to morbidly obese children and adults, it usually does not resolve the problem completely.Surgical options could include the detachment of the ligaments connecting the base of the penis to the pubic bone; the performance of skin grafts to cover areas of the penis requiring additional skin; liposuction using catheters to suck out fat cells under the skin from the area around the penis; an abdominoplasty in which excess fat and skin from the region are removed; an escutheonectomy in which the pad of fat just above the pubic area is removed; or a panniculectomy in which the panniculus, excess tissue, and skin that hangs over the genitals and thighs are removed. In a video demonstrating the use of a panniculectomy in the repair of adult buried penis, Dr. Bryan Voelzke and his colleagues emphasized the need to tack the suprapubic fat pad to the periosteum of the symphysis pubis as well as the importance of not pulling down the peno-scrotal junction and peno-abdominal junction just in order to further expose the penis.King IC, Tahir A, Ramanathan C, and Siddiqui H developed a modified treatment algorithm employing a single surgical technique consisting primarily of scar release and the mobilization of the skin of the penis.An article published in August 2019 by Dr. James J. Elist reported that a procedure involving the insertion of a subcutaneous soft silicone penile implant was successful in reversing the condition of adult acquired buried penis. See also Micropenis Phalloplasty Webbed penis References External links Examples

Aarogya, could you share information about a health condition involving Circumvallate placenta

Circumvallate placenta

Circumvallate placenta is a rare condition affecting about 1-2% of pregnancies, in which the amnion and chorion fetal membranes essentially "double back" on the fetal side around the edges of the placenta. After delivery, a circumvallate placenta has a thick ring of membranes on its fetal surface. Circumvallate placenta is a placental morphological abnormality associated with increased fetal morbidity and mortality due to the restricted availability of nutrients and oxygen to the developing fetus. Physicians may be able to detect a circumvallate placenta during pregnancy by using an ultrasound. However, in other cases, a circumvallate placenta is not identified until delivery of the baby. Circumvallate placenta can increase the risk of associated complications such as preterm delivery and placental abruption. Occasionally, a circumvallate placenta can also increase the risk of neonatal death and emergency caesarean section. Although there is no existing treatment for circumvallate placenta, physicians can attempt to minimize the effects of complications, if they occur, through frequent fetal monitoring and, if necessary, emergency cesarean section.In a circumvallate placenta, the chorionic plate, which forms the fetal surface of the placenta, tends to be smaller than the basal plate, which forms the maternal surface of the placenta. This results in the elevation of the placental margin and the appearance of an annular shape. The fetal surface is divided into a central depressed zone surrounded by a thickened white ring which is incomplete. The ring is situated at varying distances from the margin, or edges, of the placenta. This thick ring of membranes is composed of a double fold of amnion and chorion with degenerated decidua vera and fibrin in between. Blood vessels, supplying nutrients and carrying waste products to and from the developing fetus, radiate from the umbilical cord insertion to as far as the ring of membranes, and then disappears from view. Signs & Symptoms A circumvallate placenta does not always induce associated symptoms during pregnancy, making it extremely difficult to diagnose a circumvallate placenta in asymptomatic mothers. In symptomatic mothers, physicians may be able to detect a circumvallate placenta based on the presentation of the following signs. Vaginal bleeding: A circumvallate placenta can increase the risk of frequent vaginal bleeding during the first trimester of pregnancy. In a study conducted with 92 women with a circumvallate placenta, it was concluded that incidences of vaginal bleeding were significantly higher in women with a circumvallate placenta during all three trimesters when compared to the control group. However, a noted limitation of the study considered by the researchers was that because the study included such a small number of women, the obtained results may not be fully representative of the general population. Because the chorionic plate is much smaller than the basal plate in a circumvallate placenta, vaginal bleeding tends to occur at this site where the placenta is exposed and uncovered. In mothers presenting with vaginal bleeding, circumvallate placenta should be suspected as a possible cause of the vaginal bleeding. Inhibited fetal growth: Fetuses tend to develop more slowly when associated with a circumvallate placenta, largely due to the reduced supply of blood and nutrients from mother to fetus. Physicians will order tests to determine the cause of inhibited fetal growth when a developing fetus does not meet growth expectations during the course of the pregnancy. Premature rupture of membranes (PROM): PROM happens when the protective covering of the amniotic sac ruptures before the onset of labor and delivery. If PROM occurs within the first 37 weeks of pregnancy, it is termed preterm premature rupture of membranes (PPROM). PROM itself has many causes and risk factors. When PROM occurs along with vaginal bleeding in the second trimester of pregnancy, it is suspected that a mother likely has a circumvallate placenta. Complications Circumvallate placenta has also been associated with a higher incidence of complications including placental abruption, low birth weight, premature delivery, perinatal death, and fetal abnormalities. Low birth weight: Lack of proper nutrition and blood flow to the fetus during pregnancy often results in decreased weight of the baby at birth. Placenta abruption: Placenta abruption, in which the placenta divides from the wall of the uterus prior to birth, can have severe outcomes for a mother and her baby. Such consequences include vaginal bleeding, decreased birth weight, preterm delivery, and stillbirth. Significant vaginal bleeding can induce maternal anemia and dangerously low blood pressure. Oligohydramnios: Insufficiency of proper volumes of amniotic fluid, a condition called oligohydramnios, can also occur as a result of a circumvallate placenta. Amniotic fluid is essential to normal fetal movement, fetal organ development, and cushioning of the fetus within the mothers uterus. It is also imperative in preventing umbilical cord compression so that the fetus is able to obtain nourishment and oxygenation from its mother. Premature delivery: Premature birth of the fetus occurs at less than 37 weeks of gestation, compared to full-term delivery at about 40 weeks. Miscarriage: Loss of a fetus prior to birth via miscarriage can transpire if any of the above complications occur without prompt intervention and treatment. Cause Unfortunately, there is no known cause of circumvallate placenta and no major preventative measures that can be taken to minimize the risk of developing a circumvallate placenta. Circumvallate placenta is not a genetic disorder. Some potential causes of circumvallate placenta include reduced amniotic fluid pressure, circumferential hemorrhage, and superficial or deep implantation of the embryo within the uterine wall, although these potential causes are still not well-understood in terms of their relation to circumvallate placenta.High-risk pregnancies are described as pregnancies in which a mother, the fetus, or both are put at a higher risk for developing pregnancy complications before, during, or after birth. Risk factors such as hypertensive medical conditions, maternal age, and substance use are just some of the things that can put a woman at an increased risk for developing circumvallate placenta and/or any other complications. Risk factors Hypertensive disorders Women entering a pregnancy with hypertension are considered to be put at a higher risk for preeclampsia or eclampsia during the course of their pregnancy. Hypertensive disorders, like hypertension, have been found to affect about 10% of pregnancies in the United States and have resulted in about 6.8% of maternal deaths from 2011 to 2015. High blood pressure during pregnancy can potentially damage maternal organ systems such as the liver or the kidneys, which can be life-threatening. To prevent preeclampsia or eclampsia from developing in pregnancy, women with hypertension can be prescribed anti-hypertensive medications during pregnancy and are advised to monitor their blood pressure throughout the course of pregnancy. Maternal age Another risk factor for developing any pregnancy complications is maternal age. Advanced maternal age, considered to be when a woman enters pregnancy at age 35 or above, has also been linked to increased risk of maternal mortality, preeclampsia, restricted fetal growth, fetal distress, and a variety of other pregnancy complications. Conversely, teenage pregnancy is also associated with increased risk of endometriosis, postpartum hemorrhage, and mild preeclampsia, when compared with pregnant mothers in their 20s. Genetically, the long period of time between meiotic arrest of the egg gamete as a fetus and each ovulation cycle occurring after the onset of female puberty in teenage years can potentially contribute to the increased risk for pregnancy complications in mothers who are age 35 or older at time of pregnancy. Substance use Further, yet another factor inducing adverse complications in pregnancy is substance use status. Nicotine, alcohol, and marijuana are the most common substances used during pregnancies. Substance use in pregnancy is concerning because of its alarming association with other risk factors, such as mental illness. Depression alone has been associated within increased risk for preeclampsia, gestational diabetes, hypertension, premature birth, and low birth weight. Women with substance use disorders tend to live in areas that are unable to provide quality prenatal care or proper management of their psychiatric conditions. As a result of improper management of psychiatric illnesses, substances are abused during pregnancy, potentially causing harm to both the mother and the fetus. Some pregnancy complications that can occur as a result of substance use in pregnancy are fetal alcohol syndrome and neonatal abstinence disorder.Women with these risk factors are recommended additional surveillance during pregnancy to monitor fetal development and to be able to detect fetal, placental, or umbilical cord abnormalities as early as possible. Pathophysiology/Mechanism The placenta is a transient organ developed during pregnancy that facilitates nutrient, gas, and waste exchange between a mother and a developing fetus. Placental abnormalities, such as circumvallate placenta, can harm a developing fetus, as normal exchange of materials between a mother and a developing fetus is impaired. With placental abnormalities, a developing fetus is unable to receive the vital materials that it needs for proper development, resulting in the possibility of pregnancy complications, birth defects, and/or death of the fetus. In a normal placenta, there is a smooth transition from the parenchymal villous chorion to the membranous chorion at the border of the placental plate. Fetal blood vessels subdivide from the umbilical cord and spread diagonally throughout the parenchyma towards the edge of the placental plate.In a circumvallate placenta, the membranes often become restrained due to marginal infarct, hemorrhage, or fibrin depositing. This results in the reduction in size of the chorionic plate of the placenta, further causing the membranes on the fetal side to fold backward on themselves. The parenchymal villous chorion continues to proliferate beyond the tethered membranes and appears to protrude outward. The fetal blood vessels are directed downward and then horizontally in order to provide blood flow to the most peripheral parts of the placental plate extending beyond the tethered membranes.Since a portion of the placenta tends to become exposed in a circumvallate placenta, due to the reduced size of the chorionic plate, vaginal bleeding is more likely to occur at this site of exposure. Likewise, inhibited fetal growth can also ensue due to the decreased exchange of nutrients and waste between mother and fetus, since the fetus is unable to sustain necessary nutritional demands for proper fetal development. Premature rupture of membranes often occurs as a result of infection in the uterus, which can be caused by the occurrence vaginal bleeding. Therefore, placental abnormalities such as circumvallate placenta can be extremely detrimental in causing the onset of associated conditions. Diagnosis In some cases, a physician may be able to diagnose a circumvallate placenta via ultrasound during one of many routine ultrasound screenings. In most cases, a circumvallate placenta is not discovered until physical examination of the placenta after delivery of the fetus. For this reason, circumvallate placenta is very difficult to diagnose during pregnancy. On ultrasound, a normal placenta should appear complete and uniform, with the fetal surface of the placenta appearing slightly shiny and translucent. The appearance of a circumvallate placenta on ultrasound may present with irregular edges, uplifted margins, or placental sheets. In a study conducted in 1994, 62 healthy pregnant women were examined with placental sonography for detection of circumvallate placenta. Of the five experienced sonologists who interpreted the placental ultrasounds, all were unable to properly detect and diagnose circumvallate placenta, revealing the difficult nature of circumvallate placenta recognition. Further, these findings indicate that prenatal sonographic criteria used for detection of circumvallate placenta are not reliable enough for screening purposes. Complete circumvallate placenta involves morphological abnormality of the entire dimension of the placenta, while partial circumvallate placenta does not involve the entire placenta but rather a portion of the placenta. Complete circumvallate placenta is very rare, occurring within about 1% of pregnancies, and has been noted to increase the risks of associated complications such as placental abruption, premature childbirth, premature rupture of membranes, perinatal death, and congenital abnormalities. Partial circumvallate placenta is more common but is not found to be as clinically significant as complete circumvallate placenta.The accurate diagnosis of circumvallate placenta during pregnancy can have significant implications in the recognition of patients who are at risk of complications. Although the ability of sonography to accurately diagnosis circumvallate placenta during pregnancy is quite limited, research studies continue to emerge at the possibility of doing so. Treatment/Management Although there is no cure or specific treatment for restoration of the circumvallate placenta, there are ways to decrease the risks of possible complications prior to birth or attempt to manage complications if they develop. If circumvallate placenta is diagnosed during pregnancy, physicians may offer recommendations to reduce the risks of associated complications such as lower birth weight and placental abruption.Decreased birth weight is a major concern associated with circumvallate placenta. Infants born with birth weights that are lower than expected per their gestational age oftentimes end up requiring extra support in the neonatal intensive care unit (NICU). To assist in the monitoring of appropriate fetal growth, a physician may recommend more frequent growth checks during pregnancy if circumvallate placenta is suspected. If a fetus is not growing satisfactorily, premature delivery, via vaginal delivery or caesarean section, may be recommended, with C-section being more favorable compared to vaginal delivery.In women experiencing a placental abruption associated with circumvallate placenta, physicians will normally advocate for frequent growth checks, hospital bed rest, early delivery, and, if necessary, emergency C-section. Likewise, IV fluids and blood transfusions can also be given to patients with a placental abruption in attempts to increase blood pressure and minimize the effects of severe blood loss.If oligohydramnios occurs as a result of a circumvallate placenta, a treatment called amnioinfusion may be considered to replenish the amount of lost amniotic fluid within the amniotic sac. Amnioinfusion may help in preventing underdevelopment of the lungs.If diagnosed with a circumvallate placenta, consistent fetal monitoring by a licensed physician can help to prevent and/or reduce the effects of associated complications that may occur. Additionally, healthy lifestyle choices, a well-balanced and nutritious diet, adequate rest, and cessation of alcohol and tobacco products can also help to prevent the incidence of a circumvallate placenta and its associated complications. If diagnosed with a circumvallate placenta, in association with other threatening pregnancies complications, emergency cesarean section will most likely be suggested by a physician. Prognosis Unfortunately, there is currently not a cure available for circumvallate placenta. While some evidence suggests that a circumvallate placenta can increase the risk of complication during pregnancy, other research suggests this increased risk is marginal. Sadly, circumvallate placenta can occasionally result in infant death depending on the severity of the complications encountered. In other cases, circumvallate placenta can result in premature birth of infants who are otherwise healthy after being monitored in the neonatal intensive care unit for a period of time after birth. Therefore, proper medical care and monitoring are crucial in attempting to minimize the likelihood of complications. In other cases, patients diagnosed with circumvallate placenta are able to carry their babies until term or near-term. Epidemiology Circumvallate placenta is a very rare condition affecting pregnant women. This condition is a placental morphological abnormality, with the placenta being formed during the early periods of pregnancy. Women are able to become pregnant with the onset of ovulation and menstruation in early adolescence, with most women becoming pregnant during adulthood. Circumvallate placenta is currently known to affect about 1-2% of pregnancies. It is not virally transmissible to other individuals, nor can it be transferred through contact or respiration.There are no specific racial or ethnic groups that are more predisposed to acquiring a circumvallate placenta during pregnancy, however, as with all pregnancies, there are general risks factors that can put a pregnant woman at risk for complications, including circumvallate placenta. Notably, certain pregnancy complications, such as preeclampsia, tend to be almost three times as fatal in African American women compared to non-Hispanic white women, even though both groups tend to experience preeclampsia at almost the same rates. This is partially thought to be due to inequalities in accessing quality prenatal care in lower socioeconomic neighborhoods and the effect of structural racism within healthcare systems. Any woman residing in an area with a lower socioeconomic status, regardless of race or age, is predisposed to developing pregnancy complications like circumvallate placenta if quality prenatal care is not available. Women with significant obstetric histories can also be at higher risk for developing any type of pregnancy complication, including circumvallate placenta, and are recommended to be screened for placental abnormalities within their second trimester of pregnancy. Research Directions The placenta plays a dominant role in being responsible for a variety of complications within pregnancy and labor. Placental pathological studies have significantly contributed to recent obstetric literature. Many studies have examined the clinical significance of patients with circumvallate placenta compared to patients with a normal placenta. They have revealed that incidences of preterm birth, oligohydramnios, placental abruption, low birth weight, and fetal death were present in significantly higher rates than when compared to control patients with normal placentas. Because circumvallate placenta is such a rare condition, it is difficult to gain significant evidence and data.A case study reported in 2020 observed the correlation between circumvallate placenta and the occurrence of obstetric complications such as battledore insertion. Battledore insertion, abnormal insertion of the umbilical cord into the placenta, occurs in about 7% of pregnancies and can also result in many of the same pregnancy complications as circumvallate placenta; intrauterine growth restriction, fetal distress, and fetal death. This abnormal insertion of the umbilical cord into the placenta can result in a loss of adequate blood flow to the developing fetus due to restriction. The fetus is unable to obtain normal amounts of required oxygen and nutrition through the placenta, and this can further cause other severe complications. In the study, a 22-year-old woman at 28 weeks and 2 days of gestation, presented for a routine third trimester screening. She was noted to have had 2 prior miscarriages at 17 and 20 weeks. A previous normal second trimester routine screening at 21 weeks of gestation did not identify any structural abnormalities within the placenta, decreased fetal size, or abnormally-appearing umbilical cord insertion. The patient also did not have any episodes of vaginal bleeding during the current pregnancy.Upon presenting for routine screening at 28 weeks and 2 days of gestation, the patient was not exhibiting any signs of active contractions and a cardiotocography was performed as part of routine screening. Cardiotocography is a diagnostic tool used during the third trimester of pregnancy to observe fetal heart rates and presence of uterine contractions. It can also be used to detect signs of any sort of fetal distress. In interpreting the cardiotocography that the 22-year-old pregnant woman had completed, it was noted that the fetus appeared to be much smaller than expected and was exhibiting concerns of decreased amniotic fluid volume, oligohydramnios, and restricted blood flow through the umbilical cord. Cardiotocographic monitoring also noted decreases in fetal heart rate every 25 minutes without contractions. Fetal motion was present, with the placenta appearing enlarged and spherical.Decreases in the fetus heart rate, in addition to the other findings of the cardiotocography, ultimately prompted physicians to deliver the baby via emergency cesarean section without major complications. The newborn, with normal APGAR scores and umbilical cord arterial pH levels, was admitted to the neonatal intensive care unit. Upon examining the placenta after delivery, it was noted that the placenta demonstrated the appearance of a circumvallate placenta, and also showed evidence of abnormal umbilical cord insertion into the placenta. Postpartum, the mother had a good recovery and the newborn was discharged from the neonatal intensive care unit 105 days post-birth.This case study discussed the association of circumvallate placenta and abnormal battledore cord insertion in producing pregnancy complications. Restriction of umbilical cord blood flow from the placenta to the fetus and placental abnormalities like circumvallate placenta may work in conjunction to generate fetal distress. Decreased levels of oxygenation and nutrient absorption resulted in decelerations of fetal heart rate and the decision to deliver the fetus via cesarean section to prevent fetal death by hypoxia. Routine monitoring of fetal growth and development, placental structure, and placental function are recommended with high-risk pregnancies. In patients diagnosed with circumvallate placenta during pregnancy, monthly fetal growth assessments are also recommended. Patients found to have blood flow restrictions to or from the placenta are recommended to undergo weekly ultrasounds with consistent monitoring of fetal heart rate.In a separate case study reported in 2017, a woman at about 35 weeks of gestation presented with preeclampsia and intrauterine fetal demise, or more commonly known as stillbirth. After delivery of the stillborn fetus, examination of the placenta revealed a circumvallate placenta with battledore insertion of the umbilical cord. It was speculated that the combination of circumvallate placenta and battledore insertion had led to the loss of the fetus prior to delivery, as there was no other discernible cause for the stillbirth. While circumvallate placenta and battledore insertion are individually very rare conditions that can result in multiple pregnancy complications, the coexistence of these abnormalities likely resulted in the loss of the fetus. The diminished blood flow and circulation from the placenta to the fetus, as caused by battledore insertion, in combination with the impaired exchange of nutrients and wastes between mother and fetus, as caused by circumvallate placenta, likely contributed to the preeclampsia and this loss of fetal life. Thus, it is highly recommended that if placental or umbilical cord abnormalities, such as circumvallate placental and battledore insertion, are suspected or detected prior to birth, that the pregnancy should be considered high-risk. High-risk pregnancies significantly benefit from frequent follow-ups using ultransonography to monitor fetal developmental and placental and umbilical cord structure and function.Research directions continue to investigate methods in which circumvallate placenta may be more commonly diagnosed during pregnancy before complications can transpire. Biomarkers such as Sflt/PlGF can be used to predict severe pregnancy complications in high-risk pregnancies. Circumvallate placenta appears to be correlated with reduced placental efficacy due to increased placental thickness and abnormal villi function, affecting the Sflt/PlGF ratio. It is thought that obtaining Sflt/PlGF ratios can be used to determine deficiencies in placental function in cases of placental abnormalities. Future research analyzing the contribution of biomarkers like Sflt/PlGF to predict placental abnormalities would be influential to our understanding of many placental deformities, including circumvallate placenta.Due to the rare occurrences of circumvallate placenta, more extensive research trials are unavailable, resulting in data limitations. Therefore, the clinical importance of circumvallate placenta remains uncertain. See also circummarginate placenta References == External links ==

Aarogya, could you share information about a health condition involving Brown-Séquard syndrome

Brown-Séquard syndrome

Brown-Séquard syndrome (also known as Brown-Séquards hemiplegia, Brown-Séquards paralysis, hemiparaplegic syndrome, hemiplegia et hemiparaplegia spinalis, or spinal hemiparaplegia) is caused by damage to one half of the spinal cord, i.e. hemisection of the spinal cord resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the lesion. It is named after physiologist Charles-Édouard Brown-Séquard, who first described the condition in 1850. Causes Brown-Séquard syndrome may be caused by injury to the spinal cord resulting from a spinal cord tumor, trauma [such as a fall or injury from gunshot or puncture to the cervical or thoracic spine], ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis. In its pure form, it is rarely seen. The most common cause is penetrating trauma such as a gunshot wound or stab wound to the spinal cord. Decompression sickness may also be a cause of Brown-Séquard syndrome.The presentation can be progressive and incomplete. It can advance from a typical Brown-Séquard syndrome to complete paralysis. It is not always permanent and progression or resolution depends on the severity of the original spinal cord injury and the underlying pathology that caused it in the first place. Pathophysiology The hemisection of the cord results in a lesion of each of the three main neural systems: the principal upper motor neuron pathway of the corticospinal tract one or both dorsal columns the spinothalamic tractAs a result of the injury to these three main brain pathways the patient will present with three lesions: The corticospinal lesion produces spastic paralysis on the same side of the body below the level of the lesion (due to loss of moderation by the UMN). At the level of the lesion, there will be flaccid paralysis of the muscles supplied by the nerve of that level (since lower motor neurons are affected at the level of the lesion). The lesion to fasciculus gracilis or fasciculus cuneatus (dorsal column) results in ipsilateral loss of vibration and proprioception (position sense) as well as loss of all sensation of fine touch. The loss of the spinothalamic tract leads to pain and temperature sensation being lost from the contralateral side beginning one or two segments below the lesion.In addition, if the lesion occurs above T1 of the spinal cord it will produce ipsilateral Horners syndrome with involvement of the oculosympathetic pathway. Diagnosis Magnetic resonance imaging (MRI) is the imaging of choice in spinal cord lesions.Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by findings on clinical examination which reflect hemisection of the spinal cord (cutting the spinal cord in half on one or the other side). It is diagnosed by finding motor (muscle) paralysis on the same (ipsilateral) side as the lesion and deficits in pain and temperature sensation on the opposite (contralateral) side. This is called ipsilateral hemiplegia and contralateral pain and temperature sensation deficits. The loss of sensation on the opposite side of the lesion is because the nerve fibers of the spinothalamic tract (which carry information about pain and temperature) crossover once they meet the spinal cord from the peripheries. Classification Any presentation of spinal injury that is an incomplete lesion (hemisection) can be called a partial Brown-Séquard or incomplete Brown-Séquard syndrome.Brown-Séquard syndrome is characterized by loss of motor function (i.e. hemiparaplegia), loss of vibration sense and fine touch, loss of proprioception (position sense), loss of two-point discrimination, and signs of weakness on the ipsilateral (same side) of the spinal injury. This is a result of a lesion affecting the dorsal column-medial lemniscus tract, well localized (deep) touch, conscious proprioception, vibration, pressure and 2-point discrimination, and the corticospinal tract, which carries motor fibers. On the contralateral (opposite side) of the lesion, there will be a loss of pain and temperature sensation and crude touch 1 or 2 segments below the level of the lesion via the Spinothalamic Tract of the Anterolateral System. Bilateral (both sides) ataxia may also occur if the ventral spinocerebellar tract and dorsal spinocerebellar tract are affected.Crude touch, pain and temperature fibers are carried in the spinothalamic tract. These fibers decussate at the level of the spinal cord. Therefore, a hemi-section lesion to the spinal cord will demonstrate loss of these modalities on the contralateral side of the lesion, while preserving them on the ipsilateral side. Upon touching this side, the patient will not be able to localize where they were touched, only that they were touched. This is because fine touch fibers are carried in the dorsal column-medial lemniscus pathway. The fibers in this pathway decussate at the level of the medulla. Therefore, a hemi-section lesion of the spinal cord will demonstrate loss of fine touch on ipsilateral side (preserved on the contralateral side) and crude touch (destruction of the decussated spinothalamic fibers from the contralateral side) on the contralateral side.Pure Brown-Séquard syndrome is associated with the following: Interruption of the lateral corticospinal tracts: Ipsilateral spastic paralysis below the level of the lesion Babinski sign ipsilateral to lesion Abnormal reflexes and Babinski sign may not be present in acute injury Interruption of posterior white column: Ipsilateral loss of tactile discrimination, vibratory, and position sensation below the level of the lesion Interruption of lateral spinothalamic tracts: Contralateral loss of pain and temperature sensation. This usually occurs 2–3 segments below the level of the lesion. Treatment Treatment is directed at the pathology causing the paralysis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant. Epidemiology Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord. History Charles-Édouard Brown-Séquard studied the anatomy and physiology of the spinal cord. He described this injury after observing spinal cord trauma which happened to farmers while cutting sugar cane in Mauritius. French physician, Paul Loye, attempted to confirm Brown-Séquards observations on the nervous system by experimentation with decapitation of dogs and other animals and recording the extent of each animals movement after decapitation. Notes Sources Egido Herrero JA, Saldanã C, Jiménez A, Vázquez A, Varela de Seijas E, Mata P (1992). "Spontaneous cervical epidural hematoma with Brown-Séquard syndrome and spontaneous resolution. Case report". J Neurosurg Sci. 36 (2): 117–19. PMID 1469473. Ellger T, Schul C, Heindel W, Evers S, Ringelstein EB (June 2006). "Idiopathic spinal cord herniation causing progressive Brown-Séquard syndrome". Clin Neurol Neurosurg. 108 (4): 388–91. doi:10.1016/j.clineuro.2004.07.005. PMID 16483712. S2CID 35644328. Finelli PF, Leopold N, Tarras S (May 1992). "Brown-Sequard syndrome and herniated cervical disc". Spine. 17 (5): 598–600. doi:10.1097/00007632-199205000-00022. PMID 1621163. S2CID 37493662. Hancock JB, Field EM, Gadam R (1997). "Spinal epidural hematoma progressing to Brown-Sequard syndrome: report of a case". J Emerg Med. 15 (3): 309–12. doi:10.1016/S0736-4679(97)00010-3. PMID 9258779. Harris P (November 2005). "Stab wound of the back causing an acute subdural haematoma and a Brown-Sequard neurological syndrome". Spinal Cord. 43 (11): 678–9. doi:10.1038/sj.sc.3101765. PMID 15852056. Henderson SO, Hoffner RJ (1998). "Brown-Sequard syndrome due to isolated blunt trauma". J Emerg Med. 16 (6): 847–50. doi:10.1016/S0736-4679(98)00096-1. PMID 9848698. Hwang W, Ralph J, Marco E, Hemphill JC (June 2003). "Incomplete Brown-Séquard syndrome after methamphetamine injection into the neck". Neurology. 60 (12): 2015–16. doi:10.1212/01.wnl.0000068014.89207.99. PMID 12821761. S2CID 13491137. Kraus JA, Stüper BK, Berlit P (1998). "Multiple sclerosis presenting with a Brown-Séquard syndrome". J. Neurol. Sci. 156 (1): 112–13. doi:10.1016/S0022-510X(98)00016-1. PMID 9559998. S2CID 44403915. Lim E, Wong YS, Lo YL, Lim SH (April 2003). "Traumatic atypical Brown-Sequard syndrome: case report and literature review". Clin Neurol Neurosurg. 105 (2): 143–45. doi:10.1016/S0303-8467(03)00009-X. PMID 12691810. S2CID 37419566. Lipper MH, Goldstein JH, Do HM (August 1998). "Brown-Séquard syndrome of the cervical spinal cord after chiropractic manipulation". AJNR Am J Neuroradiol. 19 (7): 1349–52. PMID 9726481. Mastronardi L, Ruggeri A (January 2004). "Cervical disc herniation producing Brown-Sequard syndrome: case report". Spine. 29 (2): E28–31. doi:10.1097/01.BRS.0000105984.62308.F6. PMID 14722422. S2CID 36231998. Miyake S, Tamaki N, Nagashima T, Kurata H, Eguchi T, Kimura H (February 1998). "Idiopathic spinal cord herniation. Report of two cases and review of the literature". J. Neurosurg. 88 (2): 331–35. doi:10.3171/jns.1998.88.2.0331. PMID 9452246. Rumana CS, Baskin DS (April 1996). "Brown-Sequard syndrome produced by cervical disc herniation: case report and literature review". Surg Neurol. 45 (4): 359–61. doi:10.1016/0090-3019(95)00412-2. PMID 8607086. Stephen AB, Stevens K, Craigen MA, Kerslake RW (October 1997). "Brown-Séquard syndrome due to traumatic brachial plexus root avulsion". Injury. 28 (8): 557–58. doi:10.1016/S0020-1383(97)83474-2. PMID 9616398. External links Case studies of Brown-Séquard syndrome

Hi Aarogya, could you help me understand about Thrombotic microangiopathy

Thrombotic microangiopathy

Thrombotic microangiopathy (TMA) is a pathology that results in thrombosis in capillaries and arterioles, due to an endothelial injury. It may be seen in association with thrombocytopenia, anemia, purpura and kidney failure. The classic TMAs are hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. Other conditions with TMA include atypical hemolytic uremic syndrome, disseminated intravascular coagulation, scleroderma renal crisis, malignant hypertension, antiphospholipid antibody syndrome, and drug toxicities, e.g. calcineurin inhibitor toxicity. Signs and symptoms The clinical presentation of TMA, although dependent on the type, typically includes: fever, microangiopathic hemolytic anemia (see schistocytes in a blood smear), kidney failure, thrombocytopenia and neurological manifestations. Generally, renal complications are particularly predominant with Shiga-toxin-associated hemolytic uremic syndrome (STx-HUS) and atypical HUS, whereas neurologic complications are more likely with TTP. Individuals with milder forms of TTP may have recurrent symptomatic episodes, including seizures and vision loss. With more threatening cases of TMA, and also as the condition progresses without treatment, multi-organ failure or injury is also possible, as the hyaline thrombi can spread to and affect the brain, kidneys, heart, liver, and other major organs. Cause The specific cause is dependent of the type of TMA that is presented, but the two main pathways that lead to TMA are external triggers of vascular injury, such as viruses, bacterial Shiga toxins or endotoxins, antibodies, and drugs; and congenital predisposing conditions, including decreased levels of tissue factors necessary for the coagulation cascade. Either of these pathways will result in decreased endothelial thromboresistance, leukocyte adhesion to damaged endothelium, complement consumption, enhanced vascular shear stress, and abnormal vWF fragmentation. The central and primary event in this progression is injury to the endothelial cells, which reduces the production of prostaglandin and prostacyclin, ultimately resulting in the loss of physiological thromboresistance, or high thrombus formation rate in blood vessels. Leukocyte adhesion to the damaged endothelial wall and abnormal von Willebrand factor (or vWF) release can also contribute to the increase in thrombus formation. More recently, researchers have attributed both TTP and HUS to targeted agents, such as targeted cancer therapies, immunotoxins, and anti-VEGF therapy.Bacterial toxins are the primary cause of one category of thrombotic microangiopathy known as HUS or hemolytic uremic syndrome. HUS can be divided into two main categories: Shiga-toxin-associated HUS (STx-HUS), which normally presents with diarrhea, and atypical HUS. The Shiga-toxin inhibits the binding of eEF-1-dependent binding of aminoacyl tRNA to the 60S subunit of the ribosome, thus inhibiting protein synthesis. The cytotoxicity from the lack of protein damages glomerular endothelial cells by creating voids in the endothelial wall and detaching the basement membrane of the endothelial layer, activating the coagulation cascade. Atypical HUS may be caused by an infection or diarrheal illness or it may be genetically transmitted. This category of TMA encompasses all forms that do not have obvious etiologies. Mutations in three of the proteins in the complement cascade have been identified in patients with atypical HUS. Several chemotherapeutic drugs have also been shown to cause damage to the epithelial layer by reducing the ability for the cells to produce prostacyclin, ultimately resulting in chemotherapy-associated HUS, or C-HUS.The second category of TMAs is TTP thrombotic thrombocytopenic purpura, which can be divided into 3 categories: congenital, idiopathic, and non-idiopathic. Congenital and idiopathic TTP are generally associated with deficiencies in ADAMTS13, a zinc metalloprotease responsible for cleaving Very Large vWF Multimers in order to prevent inappropriate platelet aggregation and thrombosis in the microvasculature. Natural genetic mutations resulting in the deficiency of ADAMTS13 have been found in homozygous and heterozygous pedigrees in Europe. Researchers have identified common pathways and links between TTP and HUS, while other sources express skepticism about their common pathophysiology.The repression of the vascular endothelial growth factor (VEGF) can also cause glomerular TMA (damage to the glomerular microvasculature). It is likely that the absence of VEGF results in the collapse of fenestrations in the glomerular endothelium, thus causing microvascular injury and blockages associated with TMA.Manifestations resembling thrombotic microangiopathy have been reported in clinical trials evaluating high doses of valacyclovir (8000 mg/day) administered for prolonged periods (months to years) for prophylaxis of cytomegalovirus (CMV) infection and disease, particularly in persons with HIV infection. A number of factors may have contributed to the incidence of thrombotic microangiopathy in those trials including profound immunosuppression, underlying diseases (advanced HIV disease, graft-versus-host disease), and other classes of drug, particularly antifungal agents. There were no reports of thrombotic microangiopathy among the 3050 subjects in the four trials evaluating Valacyclovir for suppression of recurrent genital herpes. Although one of the trials was in HIV-infected subjects, the patients did not have advanced HIV disease. The implication is that the occurrence of thrombotic microangiopathy is restricted to severely immunosuppressed persons receiving higher Valacyclovir dosages than are required to control HSV infection. Diagnosis CBC and blood film: decreased platelets and schistocytes PT, aPTT, fibrinogen: normal markers of hemolysis: increased unconjugated bilirubin, increased LDH, decreased haptoglobin negative Coombs test. Creatinine, urea, to follow renal function ADAMSTS-13 gene, activity or inhibitor testing (TTP). Treatment The course of treatment and the success rate is dependent on the type of TMA. Some patients with atypical HUS and TTP have responded to plasma infusions or exchanges, a procedure which replaces proteins necessary for the complement cascade that the patient does not have; however, this is not a permanent solution or treatment, especially for patients with congenital predispositions. Monoclonal antibodies like eculizumab and caplacizumab can assist with atypical hemolytic uremic syndrome and acquired thrombotic thrombocytopenic purpura respectively whilst dexamethasone can help with immune thrombotic thrombocytopenic purpura and low molecular weight heparin can help with disseminated intravascular coagulation. See also Microangiopathy Microangiopathic hemolytic anemia References == External links ==

Aarogya, could you share information about a health condition involving Joint

Joint

A joint or articulation (or articular surface) is the connection made between bones, ossicles, or other hard structures in the body which link an animals skeletal system into a functional whole. They are constructed to allow for different degrees and types of movement. Some joints, such as the knee, elbow, and shoulder, are self-lubricating, almost frictionless, and are able to withstand compression and maintain heavy loads while still executing smooth and precise movements. Other joints such as sutures between the bones of the skull permit very little movement (only during birth) in order to protect the brain and the sense organs. The connection between a tooth and the jawbone is also called a joint, and is described as a fibrous joint known as a gomphosis. Joints are classified both structurally and functionally. Classification The number of joints depends on if sesamoids are included, age of the human and the definition of joints. However, the number of sesamoids is the same in most people with variations being rare.Joints are mainly classified structurally and functionally. Structural classification is determined by how the bones connect to each other, while functional classification is determined by the degree of movement between the articulating bones. In practice, there is significant overlap between the two types of classifications. Clinical, numerical classification monoarticular – concerning one joint oligoarticular or pauciarticular – concerning 2–4 joints polyarticular – concerning 5 or more joints Structural classification (binding tissue) Structural classification names and divides joints according to the type of binding tissue that connects the bones to each other. There are four structural classifications of joints: fibrous joint – joined by dense regular connective tissue that is rich in collagen fibers cartilaginous joint – joined by cartilage. There are two types: primary cartilaginous joints composed of hyaline cartilage, and secondary cartilaginous joints composed of hyaline cartilage covering the articular surfaces of the involved bones with fibrocartilage connecting them. synovial joint – not directly joined – the bones have a synovial cavity and are united by the dense irregular connective tissue that forms the articular capsule that is normally associated with accessory ligaments. facet joint – joint between two articular processes between two vertebrae. Functional classification (movement) Joints can also be classified functionally according to the type and degree of movement they allow: Joint movements are described with reference to the basic anatomical planes. synarthrosis – permits little or no mobility. Most synarthrosis joints are fibrous joints (e.g., skull sutures). amphiarthrosis – permits slight mobility. Most amphiarthrosis joints are cartilaginous joints (e.g., intervertebral discs). synovial joint (also known as a diarthrosis) – freely movable. Synovial joints can in turn be classified into six groups according to the type of movement they allow: plane joint, ball and socket joint, hinge joint, pivot joint, condyloid joint and saddle joint.Joints can also be classified, according to the number of axes of movement they allow, into nonaxial (gliding, as between the proximal ends of the ulna and radius), monoaxial (uniaxial), biaxial and multiaxial. Another classification is according to the degrees of freedom allowed, and distinguished between joints with one, two or three degrees of freedom. A further classification is according to the number and shapes of the articular surfaces: flat, concave and convex surfaces. Types of articular surfaces include trochlear surfaces. Biomechanical classification Joints can also be classified based on their anatomy or on their biomechanical properties. According to the anatomic classification, joints are subdivided into simple and compound, depending on the number of bones involved, and into complex and combination joints: Simple joint: two articulation surfaces (e.g. shoulder joint, hip joint) Compound joint: three or more articulation surfaces (e.g. radiocarpal joint) Complex joint: two or more articulation surfaces and an articular disc or meniscus (e.g. knee joint) Anatomical The joints may be classified anatomically into the following groups: Joints of hand Elbow joints Wrist joints Axillary joints Sternoclavicular joints Vertebral articulations Temporomandibular joints Sacroiliac joints Hip joints Knee joints Articulations of footUnmyelinated nerve fibers are abundant in joint capsules and ligaments as well as in the outer part of intraarticular menisci. These nerve fibers are responsible for pain perception when a joint is strained. Clinical significance Damaging the cartilage of joints (articular cartilage) or the bones and muscles that stabilize the joints can lead to joint dislocations and osteoarthritis. Swimming is a great way to exercise the joints with minimal damage.A joint disorder is termed arthropathy, and when involving inflammation of one or more joints the disorder is called arthritis. Most joint disorders involve arthritis, but joint damage by external physical trauma is typically not termed arthritis. Arthropathies are called polyarticular (multiarticular) when involving many joints and monoarticular when involving only a single joint. Arthritis is the leading cause of disability in people over the age of 55. There are many different forms of arthritis, each of which has a different cause. The most common form of arthritis, osteoarthritis (also known as degenerative joint disease), occurs following trauma to the joint, following an infection of the joint or simply as a result of aging and the deterioration of articular cartilage. Furthermore, there is emerging evidence that abnormal anatomy may contribute to early development of osteoarthritis. Other forms of arthritis are rheumatoid arthritis and psoriatic arthritis, which are autoimmune diseases in which the body is attacking itself. Septic arthritis is caused by joint infection. Gouty arthritis is caused by deposition of uric acid crystals in the joint that results in subsequent inflammation. Additionally, there is a less common form of gout that is caused by the formation of rhomboidal-shaped crystals of calcium pyrophosphate. This form of gout is known as pseudogout. Temporomandibular joint syndrome (TMJ) involves the jaw joints and can cause facial pain, clicking sounds in the jaw, or limitation of jaw movement, to name a few symptoms. It is caused by psychological tension and misalignment of the jaw (malocclusion), and may be affecting as many as 75 million Americans. History Etymology The English word joint is a past participle of the verb join, and can be read as joined. Joint is derived from Latin iunctus, past participle of the Latin verb iungere, join, unite, connect, attach.The English term articulation is derived from Latin articulatio.Humans have also developed lighter, more fragile joint bones over time due to the decrease in physical activity compared to thousands of years ago. See also Arthrology Cracking joints Kinesiology Ligament Replacement joint References External links Synovial joints Illustrations and Classification

Do you know what is Nipple discharge, Aarogya

Nipple discharge

Nipple discharge is fluid from the nipple, with or without squeezing the breast. The discharge can be milky, clear, green, purulent, bloody, or faintly yellow. The consistency can be thick, thin, sticky, or watery.Nipple discharge may be normal, such as milk in late pregnancy or after childbirth, and in newborns during the first weeks of life. It may also be normal following squeezing, in women during the reproductive years. It is likely abnormal if it occurs in men, contains blood, is from only one breast, or is associated with a breast lump, swelling, redness or overlying skin changes. Reasons for abnormal discharge include an intraductal papilloma, duct ectasia, blocked milk duct, infected breast (mastitis or breast abscess), breast cancer, certain medications, and conditions that raise prolactin.Milky discharge in a non-pregnant, non-breast feeding women is evaluated differently to other abnormal nipple discharge. Often, the cause can be determined based on symptoms and examination. Blood tests may be done to rule out low thyroid or high prolactin. Other tests may include mammography, breast ultrasound, breast biopsy, or skin biopsy.Treatment depends on the underlying cause. Duct ectasia may be treated with surgical removal of the ducts involved. Infectious causes may require antibiotics or incision and drainage. Nipple discharge is the third most common breast complaint by women, after breast pain and a breast lump. About 3% of breast cancer cases are associated with discharge. Signs and symptoms Nipple discharge is fluid from the nipple, with or without squeezing the breast. The discharge can be milky, clear, green, purulent, bloody, or faintly yellow. The consistency can be thick, thin, sticky, or watery. Causes Nipple discharge can arise from any one or more of the 15 to 20 milk ducts that each breast contains, and its causes can be divided into normal (physiological) and abnormal (pathological). Normal Milky liquid from nipples is normal during the last few weeks of pregnancy, after childbirth and during breastfeeding. Some newborn babies may leak a milky liquid which is usually normal and lasts a couple of weeks.Stimulation of breasts by massage, using a breast pump or after mammography, may induce yellow, milky, or green nipple discharge in many healthy women of reproductive age. Abnormal Spontaneous nipple discharge unrelated to pregnancy or lactation is considered abnormal, but mostly have a non-serious cause. Nipple discharge in men is not normal. Discharge from nipples is also more likely to be abnormal (pathological) if it is crystal clear or blood-stained, is from only one breast, or is associated with a breast lump, swelling, redness or overlying skin changes.A blocked or enlarged milk duct can result in nipple discharge.Intraductal papillomas are non-cancerous lesions and commonest in women age 30 to 50. Divided into central and peripheral papillomas, nipple discharge is more frequently observed when they are central. Up to half of women with intraductal papillomas may present with bloody nipple discharge, but it can also be straw-coloured. They are usually too small to feel and have a rare association with breast cancer.15-20% of people with nipple discharge are found to have duct ectasia. This is usually in perimenopausal and menopausal women, who may have associated pain and retraction of the nipple. A lump may also be present.Ductal carcinoma in situ (DCIS) usually presents with abnormal findings on mammography, but can less frequently present with a lump or nipple discharge in women, whereas in men with DCIS, nipple discharge is the common presentation.Infection in a breast, either mastitis or breast abscess may cause a discharge. Eczema of the nipple may result in a discharge with crusting of the nipple skin.Nipple discharge may be due to breast cancer, particularly if there is an accompanying breast lump. A blood-stained discharge may appear in Pagets disease. Milky Some condition that cause a raised prolactin can result in a milky liquid appearing from nipples. These include endocrine causes such as pituitary and thyroid disease, and some medications. Such medications include: Medication for hypertension: Methyldopa, reserpine, verapamil Gastrointestinal agents: Cimetidine, metoclopramide Hormones: Estrogen, birth control pill Opiates: Codeine, heroin, methadone, morphine Psychotropic drugs: Antipsychotics, monoamine oxidase inhibitors, neuroleptics, selective serotonin reuptake inhibitors, tricyclic antidepressantsSome herbs including anise and fennel have also been implicated as causing leaking of fluid from nipples. Diagnosis The evaluation of milky nipple discharge in a non-pregnant, not breast feeding women is different to the assessment of other abnormal nipple discharge. Often, the cause can be ascertained without performing tests.When blood tests are requested, they usually include thyroid tests and prolactin to rule out hypothyroidism and hyperprolactinemia. Other tests that may be considered include mammography, breast ultrasound, CT scan of the head to rule out a pituitary tumour, breast biopsy, x-ray imaging of breast ducts or skin biopsy.The absence of cancerous cells in samples of nipple discharge does not exclude cancer, hence cytology of the nipple discharge is not usually performed. However, guidance on investigations varies and tests are more likely performed if the discharge is bloody, from one breast, and the woman is age over 50. If the test is performed and malignant cells are found, an underlying cancer is highly likely. Treatment Initially, an evaluation for cancer is indicated. Treatment will depend on the cause found, and may involve changing medication, having a lump removed, applying a cream to treat a skin condition or being given medication to treat the condition causing the discharge. Duct ectasia may be treated with surgical removal of the ducts involved. Infectious causes may require antibiotics and/or incision and drainage. Sometimes, no treatment is required.If no abnormality is found, a surgical duct excision may resolve the symptoms. Treatment also depends on whether single-duct or multiple-duct discharge is present, and whether the symptoms of nipple discharge are distressing to the person. In some cases, there may be no need for any further intervention; in others, microdochectomy or a total duct excision may be appropriate. If the person wishes to conserve the ability to breastfeed and only single-duct discharge is present, then ductoscopy or galactography should be considered in view of performing a localised duct excision. Epidemiology Nipple discharge is the third most common breast complaint by women, after breast pain and a breast lump. 10% of women can notice a nipple discharge when squeezing their breast and more than 50% of women can experience this using a breast pump.Most abnormal nipple discharge is not associated with breast cancer, but 1-5% of breast cancers present with nipple discharge. References == External links ==

Aarogya, explain a scenario commonly referred as Crushed

Crushed

Crushed may refer to: "Crushed" (Ms. Marvel), a 2022 episode of the American television series Ms. Marvel "Crushed" (Roland Lee Gift song) a 2009 single by Roland Lee Gift "Crushed" (The Suite Life of Zack & Cody episode), an episode of the television show The Suite Life of Zack & Cody "Crushed", a song by Limp Bizkit from the 1999 soundtrack album End of Days "Crushed", a song by Eighteen Visions from the 2004 album Obsession "Crushed", a song by Dala from the 2009 album Everyone Is Someone "Crushed", a song by Parkway Drive from the 2015 album Ire "Crushed", a song by Rosette Sharma See also Crush (disambiguation) Crusher (disambiguation) All pages with titles beginning with Crushed All pages with titles containing Crushed

Could you describe Therapy, to me Aarogya

Therapy

A therapy or medical treatment (often abbreviated tx, Tx, or Tx) is the attempted remediation of a health problem, usually following a medical diagnosis. As a rule, each therapy has indications and contraindications. There are many different types of therapy. Not all therapies are effective. Many therapies can produce unwanted adverse effects. Medical treatment and therapy are generally considered synonyms. However, in the context of mental health, the term therapy may refer specifically to psychotherapy. History Before the creating of therapy as a formal procedure, people told stories to one another to inform and assist about the world. The term "healing through words" was used over 3,500 years ago in Greek and Egyptian writing. The term psychotherapy was invented in the 19th century, and psychoanalysis was founded by Sigmund Freud under a decade later. Semantic field The words care, therapy, treatment, and intervention overlap in a semantic field, and thus they can be synonymous depending on context. Moving rightward through that order, the connotative level of holism decreases and the level of specificity (to concrete instances) increases. Thus, in health care contexts (where its senses are always noncount), the word care tends to imply a broad idea of everything done to protect or improve someones health (for example, as in the terms preventive care and primary care, which connote ongoing action), although it sometimes implies a narrower idea (for example, in the simplest cases of wound care or postanesthesia care, a few particular steps are sufficient, and the patients interaction with that provider is soon finished). In contrast, the word intervention tends to be specific and concrete, and thus the word is often countable; for example, one instance of cardiac catheterization is one intervention performed, and coronary care (noncount) can require a series of interventions (count). At the extreme, the piling on of such countable interventions amounts to interventionism, a flawed model of care lacking holistic circumspection—merely treating discrete problems (in billable increments) rather than maintaining health. Therapy and treatment, in the middle of the semantic field, can connote either the holism of care or the discreteness of intervention, with context conveying the intent in each use. Accordingly, they can be used in both noncount and count senses (for example, therapy for chronic kidney disease can involve several dialysis treatments per week). The words aceology and iamatology are obscure and obsolete synonyms referring to the study of therapies. The English word therapy comes via Latin therapīa from Greek: θεραπεία and literally means "curing" or "healing". Types of therapies Therapy comes in different forms. These include, cognitive behavioral therapy, dialectical behavior therapy, mindful based cognitive therapy, physical therapy, etc. Therapists are here for use and used daily by many people. Therapist are trained to provide treatment to an individual or group. Therapy was invented in the 1800s and the founder was Franz Mesmer, the "Father of Western Psychotherapy". Sigmund Freud then comes into play and shows us the understanding depth of all the different types included in therapy. Therapy is used in many ways to shape and help reform a person. This type of treatment allows individuals to regain gain goals lost or wanting to accomplish. Many individuals come into therapy looking for ways to cope with issues and to receive an emotional release. For example, healing from trauma, in need of support, emotional issues, and many more. . Allowing yourself to express your thoughts and feelings go a long way in therapy recovery, this is called the therapeutic process. By chronology, priority, or intensity Levels of care Levels of care classify health care into categories of chronology, priority, or intensity, as follows: Emergency care handles medical emergencies and is a first point of contact or intake for less serious problems, which can be referred to other levels of care as appropriate. Intensive care, also called critical care, is care for extremely ill or injured patients. It thus requires high resource intensity, knowledge, and skill, as well as quick decision making. Ambulatory care is care provided on an outpatient basis. Typically patients can walk into and out of the clinic under their own power (hence "ambulatory"), usually on the same day. Home care is care at home, including care from providers (such as physicians, nurses, and home health aides) making house calls, care from caregivers such as family members, and patient self-care. Primary care is meant to be the main kind of care in general, and ideally a medical home that unifies care across referred providers. Secondary care is care provided by medical specialists and other health professionals who generally do not have first contact with patients, for example, cardiologists, urologists and dermatologists. A patient reaches secondary care as a next step from primary care, typically by provider referral although sometimes by patient self-initiative. Tertiary care is specialized consultative care, usually for inpatients and on referral from a primary or secondary health professional, in a facility that has personnel and facilities for advanced medical investigation and treatment, such as a tertiary referral hospital. Follow-up care is additional care during or after convalescence. Aftercare is generally synonymous with follow-up care. End-of-life care is care near the end of ones life. It often includes the following: Palliative care is supportive care, most especially (but not necessarily) near the end of life. Hospice care is palliative care very near the end of life when cure is very unlikely. Its main goal is comfort, both physical and mental. Lines of therapy Treatment decisions often follow formal or informal algorithmic guidelines. Treatment options can often be ranked or prioritized into lines of therapy: first-line therapy, second-line therapy, third-line therapy, and so on. First-line therapy (sometimes referred to as induction therapy, primary therapy, or front-line therapy) is the first therapy that will be tried. Its priority over other options is usually either: (1) formally recommended on the basis of clinical trial evidence for its best-available combination of efficacy, safety, and tolerability or (2) chosen based on the clinical experience of the physician. If a first-line therapy either fails to resolve the issue or produces intolerable side effects, additional (second-line) therapies may be substituted or added to the treatment regimen, followed by third-line therapies, and so on. An example of a context in which the formalization of treatment algorithms and the ranking of lines of therapy is very extensive is chemotherapy regimens. Because of the great difficulty in successfully treating some forms of cancer, one line after another may be tried. In oncology the count of therapy lines may reach 10 or even 20. Often multiple therapies may be tried simultaneously (combination therapy or polytherapy). Thus combination chemotherapy is also called polychemotherapy, whereas chemotherapy with one agent at a time is called single-agent therapy or monotherapy. Adjuvant therapy is therapy given in addition to the primary, main, or initial treatment, but simultaneously (as opposed to second-line therapy). Neoadjuvant therapy is therapy that is begun before the main therapy. Thus one can consider surgical excision of a tumor as the first-line therapy for a certain type and stage of cancer even though radiotherapy is used before it; the radiotherapy is neoadjuvant (chronologically first but not primary in the sense of the main event). Premedication is conceptually not far from this, but the words are not interchangeable; cytotoxic drugs to put a tumor "on the ropes" before surgery delivers the "knockout punch" are called neoadjuvant chemotherapy, not premedication, whereas things like anesthetics or prophylactic antibiotics before dental surgery are called premedication. Step therapy or stepladder therapy is a specific type of prioritization by lines of therapy. It is controversial in American health care because unlike conventional decision-making about what constitutes first-line, second-line, and third-line therapy, which in the U.S. reflects safety and efficacy first and cost only according to the patients wishes, step therapy attempts to mix cost containment by someone other than the patient (third-party payers) into the algorithm. Therapy freedom and the negotiation between individual and group rights are involved. By intent By therapy composition Treatments can be classified according to the method of treatment: By matter by drugs: pharmacotherapy, chemotherapy (also, medical therapy often means specifically pharmacotherapy) by medical devices: implantation cardiac resynchronization therapy by specific molecules: molecular therapy (although most drugs are specific molecules, molecular medicine refers in particular to medicine relying on molecular biology) by specific biomolecular targets: targeted therapy molecular chaperone therapy by chelation: chelation therapy by specific chemical elements: by metals: by heavy metals: by gold: chrysotherapy (aurotherapy) by platinum-containing drugs: platin therapy by biometals by lithium: lithium therapy by potassium: potassium supplementation by magnesium: magnesium supplementation by chromium: chromium supplementation; phonemic neurological hypochromium therapy by copper: copper supplementation by nonmetals: by diatomic oxygen: oxygen therapy, hyperbaric oxygen therapy (hyperbaric medicine) transdermal continuous oxygen therapy by triatomic oxygen (ozone): ozone therapy by fluoride: fluoride therapy by other gases: medical gas therapy by water: hydrotherapy aquatic therapy rehydration therapy oral rehydration therapy water cure (therapy) by biological materials (biogenic substances, biomolecules, biotic materials, natural products), including their synthetic equivalents: biotherapy by whole organisms by viruses: virotherapy by bacteriophages: phage therapy by animal interaction: see animal interaction section by constituents or products of organisms by plant parts or extracts (but many drugs are derived from plants, even when the term phytotherapy is not used) scientific type: phytotherapy traditional (prescientific) type: herbalism by animal parts: quackery involving shark fins, tiger parts, and so on, often driving threat or endangerment of species by genes: gene therapy gene therapy for epilepsy gene therapy for osteoarthritis gene therapy for color blindness gene therapy of the human retina gene therapy in Parkinsons disease by epigenetics: epigenetic therapy by proteins: protein therapy (but many drugs are proteins despite not being called protein therapy) by enzymes: enzyme replacement therapy by hormones: hormone therapy hormonal therapy (oncology) hormone replacement therapy estrogen replacement therapy androgen replacement therapy hormone replacement therapy (menopause) transgender hormone therapy feminizing hormone therapy masculinizing hormone therapy antihormone therapy androgen deprivation therapy by whole cells: cell therapy (cytotherapy) by stem cells: stem cell therapy by immune cells: see immune system products below by immune system products: immunotherapy, host modulatory therapy by immune cells: T-cell vaccination cell transfer therapy autologous immune enhancement therapy TK cell therapy by humoral immune factors: antibody therapy by whole serum: serotherapy, including antiserum therapy by immunoglobulins: immunoglobulin therapy by monoclonal antibodies: monoclonal antibody therapy by urine: urine therapy (some scientific forms; many prescientific or pseudoscientific forms) by food and dietary choices: medical nutrition therapy grape therapy (quackery) by salts (but many drugs are the salts of organic acids, even when drug therapy is not called by names reflecting that) by salts in the air by natural dry salt air: "taking the cure" in desert locales (especially common in prescientific medicine; for example, one 19th-century way to treat tuberculosis) by artificial dry salt air: low-humidity forms of speleotherapy negative air ionization therapy by moist salt air: by natural moist salt air: seaside cure (especially common in prescientific medicine) by artificial moist salt air: water vapor forms of speleotherapy by salts in the water by mineral water: spa cure ("taking the waters") (especially common in prescientific medicine) by seawater: seaside cure (especially common 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animal bath By meditation by mindfulness: mindfulness-based cognitive therapy By reading by bibliotherapy By creativity by expression: expressive therapy by writing: writing therapy journal therapy by play: play therapy by art: art therapy sensory art therapy comic book therapy by gardening: horticultural therapy by dance: dance therapy by drama: drama therapy by recreation: recreational therapy by music: music therapy By sleeping and waking by deep sleep: deep sleep therapy by sleep deprivation: wake therapy See also Biophilia hypothesis Classification of Pharmaco-Therapeutic Referrals Cure Interventionism (medicine) Inverse benefit law List of therapies Greyhound therapy Mature minor doctrine Medicine Medication Nutraceutical Prevention Psychotherapy Treatment as prevention Therapeutic inertia Therapeutic nihilism, the idea that treatment is useless References External links Media related to Therapies at Wikimedia Commons The dictionary definition of therapy at Wiktionary "Chapter Nine of the Book of Medicine Dedicated to Mansur, with the Commentary of Sillanus de Nigris" is a Latin book by Rhazes, from 1483, that is known for its ninth chapter, which is about therapeutics

Hello Aarogya, what is Follicular lymphoma

Follicular lymphoma

Follicular lymphoma (FL) is a cancer that involves certain types of white blood cells known as lymphocytes. The cancer originates from the uncontrolled division of specific types of B-cells known as centrocytes and centroblasts. These cells normally occupy the follicles (nodular swirls of various types of lymphocytes) in the germinal centers of lymphoid tissues such as lymph nodes. The cancerous cells in FL typically form follicular or follicle-like structures (see adjacent Figure) in the tissues they invade. These structures are usually the dominant histological feature of this cancer.There are several synonymous and obsolete terms for FL such as CB/CC lymphoma (centroblastic and centrocytic lymphoma), nodular lymphoma, Brill-Symmers Disease, and the subtype designation, follicular large-cell lymphoma. In the US and Europe, this disease is the second most common form of non-Hodgkins lymphomas, exceeded only by diffuse large B-cell lymphoma. FL accounts for 10-20% of non-Hodgkins lymphomas with ~15,000 new cases of it being newly diagnosed each year in the US and Europe. Recent studies indicate that FL is similarly prevalent in Japan.FL is a broad and extremely complex clinical entity with a wide range of manifestations which have not yet been fully systematized. It is commonly preceded by a benign precancerous disorder in which abnormal centrocytes and/or centroblasts accumulate in lymphoid tissue. They may then circulate in the blood to cause an asymptomatic condition termed in situ lymphoid neoplasia of the follicular lymphoma type (i.e. ISFL). A small percentage of these cases progress to FL. Most commonly, however, FL presents as a swelling of lymph nodes in the neck, armpits, and/or groin. Less often, it presents as a gastrointestinal tract cancer, a cancer in children involving lymphoid tissues of the head and neck area (e.g. tonsils), or one or more masses in non-lymphoid tissues such as the testes.FL typically has a slow disease course which persists essentially unchanged for years. However, each year 2-3% of FL cases progress to a highly aggressive form often termed stage 3B FL, to an aggressive diffuse large B-cell lymphoma, or to another type of aggressive B-cell cancer. These transformed follicular lymphomas (t-FL) are essentially incurable. However, recent advancements in the treatment of t-FL (e.g. the addition to standard chemotherapy of agents such as rituximab) have improved overall survival times. These newer regimens may also delay the transformation of FL to t-FL. Additional advances in understanding FL may lead to further improvements in treating the disease. Pathophysiology Genomic alterations The serial progressions of in situ FL to FL and FL to t-FL appear to involve the accumulation of increasing numbers of genomic alterations (i.e. chromosome abnormalities and gene mutations) in the formative B-cell precursors to these disorders. At least some of these alterations appear to cause the over-expression or under-expression of the products of genes that regulate these cells susceptibility to develop further genomic alterations, to survive, to proliferate, and/or to spread to other tissues. In consequence, multiple B-cell clones that exhibit increasing genomic alterations and malignant behaviors populate the disorder. No single genomic alteration seems responsible for the development of each of the spectrum of FL disorders. Rather, interactions between multiple genomic alterations appear to underlie this serial progression. In situ follicular lymphoma In situ follicular lymphoma is an accumulation of monoclonal B cells (i.e. cells descendent from a single ancestral cell) in the germinal centers of lymphoid tissue. These cells commonly bear a pathological genomic abnormality, i.e. a translocation between position 32 on the long (i.e. "q") arm of chromosome 14 and position 21 on chromosome 18s q arm. This translocation juxtaposes the B-cell lymphoma 2 (BCL2) gene on chromosome 18 at position q21.33 near to the immunoglobulin heavy chain locus (IGH@) on chromosome 14 at position q21. In consequence, BCL2 overexpresses its product, BCL2 apoptosis regulator (i.e. Bcl2). Bcl2 functions to inhibit programmed cell death thereby prolonging cell survival. The overexpression of Bcl2 in the B-cells of ISFL is thought to be a critical factor in their pathological accumulation and subsequent malignant progression. Small numbers (e.g. 1 in 100,000) of circulating nucleated blood cells bearing this t(14:18)q32:q21) translocation are found in 50-67% of otherwise healthy individuals. The prevalence of this finding increases with age and years of tobacco smoking. Since most individuals with this translocation in their blood cells do not develop ISFL, the t(14:18)(q32:q21) translocation, while prolonging cell survival, must be just one step in the development of ISFN. This translocation is proposed to occur during the early development of immature bone marrow B-cells (i.e. pre-B-cells/pro-B-cells) after which these cells circulate freely and in rare cases accumulate and mature to centrocytes and/or centroblasts in the germinal centers of lymphoid follicles to form ISFL. The mechanism favoring this localization and further accumulation is unclear.Individuals with ISFL progress to FL at a rate of 2-3%/year for at least the first 10 years following diagnosis. This progression likely involves the acquisition of genomic aberrations besides the t(14:18)q32:q21) translocation in the ISFL B-cells. Suspect mutations include those in the following genes: 1) EZH2 (encodes polycomb repressive complex 2 family protein which is involved in maintaining the transcriptional repressive state of various genes and is found in up to 27% of FL cases); 2) CREBBP (encodes CREB-binding protein which contributes to the activation of various genes); 3) TNFSF14 (encodes tumor necrosis factor superfamily member 14, a member of the tumor necrosis factor superfamily which may function as a co-stimulatory factor for the activation of lymphoid cells); and 4) KMT2D (encodes histone-lysine N-methyltransferase 2D, a histone methyltransferase which regulates the expression of various genes). ISFL may also acquire numerous copy-number variations (i.e. duplications and deletions of a portion of a chromosome along with any of the genes contained therein) that may contribute to FL. In all cases, the number of genetic abnormalities acquired in the B-cells of ISFL are much less than those in FL. Follicular lymphoma The genomic alterations found in FL include 1) the t(14:18)(q32:q21.3) translocation (85-90% of cases); 2) 1p36 deletions (i.e. deletions in the q arm of chromosome 1 at position 36, [60-70% of cases]) that lead to lose of TNFAIP3 (encodes tumor necrosis factor, alpha-induced protein 3 which inhibits the activation of NF-κB, blocks cell death due to apoptosis, and regulates lymphocyte-based immune responses through its ubiquitin ligase activity); 3) mutations in PRDM1 (encodes the PR domain zinc finger protein which promotes the maturation and proliferation of B-cells); and 4) the same mutations seen in ISFL including KMT2D (85-90% of cases), CREEBP (40-65% of cases), BCL2 (40-65% of cases), and EZH2 (20-30% of cases) as well as other mutations such as those in the histone-modifying gene HIST1H1E (20-30% of cases), the RRAGC gene (~17% of cases) which regulates cell growth, survival, death, and proliferation, and, in ≤15% of cases several other genes including MEF2B, STAT6, EP300, ARID1A, SLC22A2, CARD11, FOXO1, GNA12, B2M (i.e. the gene for beta-2 microglobulin), and SGK1. Except for the t(14:18)(q32:q21.3) translocation and EZH2 mutations which lead to gains in the expression and function, respectively, of their products, the genetic alterations generally lead to a loss in the production or function of the cited genes products. However, the exact roles, if any, of these genomic abnormalities in promoting the progression of ISFL to FL are unclear. Transformed follicular lymphoma The transformation of FL to a more aggressive state or other type of aggressive lymphoma is associated with: 1) primarily gene-activating mutations in CREEBP, KMT2D, STAT6, CARD11 (encoding a guanylate kinase which interacts with BCL10 and activates NF-κB to regulate cell survival); 2) changes in the expression of diverse genes; 3) the overproduction of various cell-activating cytokines and CD79B (encoding the Ig-beta protein component of the B-cell receptor); 4) gene-inactivating mutations in TNFAIP3, CD58 (encoding the cell adhesion molecule, lymphocyte function-associated antigen 3, that is involved in activating T-cells), CDKN2A (encoding p16INK4a and p14arf tumor suppressor proteins) or CDKN2B (encoding cyclin dependent kinase inhibitor 2B multiple tumor suppressor 2) (inactivation of either CDKN2 gene causes genome instability, i.e. increased frequency of other gene mutations), and TNFRSF4 (encoding one type of tumor necrosis factor receptor); and 5) gene-activating or -inactivating mutations in, or other causes for the under- or over-expression of, c-MYC ((encoding the c-Myc proto-oncogene transcription factor that regulates the expression of diverse genes many of which promote cell proliferation). Tumor environment The non-neoplastic immune and stromal cells as well as the extracellular matrix in tissues may enable neoplastic follicular cells to survive, proliferate, and avoid surveillance by the immune system. For example, laboratory studies show that: 1) follicular dendritic cells, fibroblastic reticular cells, and T helper cells provide growth and survival signals to neoplastic follicular B-cells; 2) neoplastic follicular B-cells recruit regulatory T cells that act to suppress immune responses to them; 3) the cytotoxic T-cells which normally kill neoplastic cells become dysfunctional in the presence of neoplastic follicular cells that are embedded in this multicellular environment; and 4) bone marrow stromal cells directly support the growth of neoplastic follicular cells. Reduced levels of immune-infiltration has been shown to be strongly associated with early progression of disease. Presentation and course In situ follicular lymphoma FL is commonly preceded by but uncommonly progresses to ISFL, an asymptomatic disorder that usually is discovered in tissues which are biopsied for other reasons. FL lymphoma may be diagnosed in the uncommon cases in which individuals with ISFL are found to have FL on follow-up examinations. Similarly, individuals with >1 in 10,000 circulating lymphocytes containing the t(14:18)q32:q21) translocation are at increased but still small risk of developing FL and being diagnosed as having FL on follow up examinations. Follicular lymphoma FL commonly presents as an otherwise asymptomatic enlargement of lymph nodes in the neck, armpit, groin, femoral canal, or other sites in individuals (median age 65) without a known history of ISFL or abnormal numbers of circulating t(14:18)q32:q21-conatianing lymphocytes. These enlargements may have been present for months to years and during this time waxed and waned in size. Less commonly, FL presents as extra-nodal masses in the skin, thyroid gland, salivary gland, breast, testicles. spleen, liver, and/or lung. Regardless of the type of presentation, FL is usually (~80% of cases) at an advanced stage at diagnosis as indicated by involvement of the bone marrow (50% to 70% of cases), multiple lymph nodes in different parts of the body, and/or other tissues. A minority (<33%) of FL patients present with B symptoms, i.e. recurrent unexplained fevers, recurrent night sweats, and/or weight loss ≥10% in the past 6 months. Generally, the disease has an indolent and prolonged course with a median life expectancy of 15–20 years: a large percentage of patients die from other causes than their FL disease. However, each year, including the early years after diagnosis, some 2-3% of FL cases transform to t-FL; Median survival has been ~4.5 years after the onset of this transformation.There are less common subtypes of FL that differ not only in their presentation but also in their histopathology, genetic abnormalities, and course. These subtypes, which are now (i.e. primary gastrointestinal tract FL) or may in the future (pediatric-type FL) be considered distinctive diseases, are: Duodenal-type follicular lymphoma Duodenal-type follicular lymphoma (DFL) was initially considered to be a type of Primary gastrointestinal tract (GI tract) follicular lymphoma (PGTFL), i.e. a follicular lymphoma in which GI tract lesions were prominent parts of the disease. However, a subset of PGTFL cases had lesions that were localized to the duodenum and other parts of the small intestine usually without involving other parts of the GI tract or tissues outside of the GI tract. This contrasts with the other cases of PGTFL which were systemic diseases involving a wide range of GI tract and non-GI tract tissues. Consequently, the World Health Organization (2017) removed the localized disease from the primary gastrointestinal tract follicular lymphoma category, reclassified it as a distinct disease entity, and termed it duodenal-type follicular lymphoma. DFL is most often an asymptomatic disease that is diagnosed on endoscopic examination of the GI tract conducted for other reasons. Less commonly, it presents with vague abdominal symptoms. In one review of former studies, the lesions in 85% of primary duodenal follicular lymphoma were located not only in the duodenum but also other sites in the intestine (i.e. jejunum and/or ileum), with rare cases having lesions in the rectum or cecum PDF is an indolent disease that may spontaneously remit and relapse but only rarely progresses to a more aggressive form. A watch-and-wait strategy has been a generally recommended method for the initial treatment of the disease. Primary gastrointestinal tract follicular lymphoma PGTFL is a follicular lymphoma (which as currently defined excludes cases of duodenal-type follicular lymphoma) that has a prominent component of GI tract involvement. The disease may present with signs and symptoms typical of the common type of follicular lymphoma. For example, enlargement of lymph nodes in the neck, armpit, groin, femoral canal, and/or other areas, and/or signs and symptoms of GI tract disease due to lesions in the stomach, small intestine, large intestine or rectum may be seen. These signs and symptoms may include abdominal pain, bowel obstruction, persistent nausea and vomiting, hematochezia (i.e. passage of fresh blood usually on feces through the rectum), or melena (i.e. passage of tarry feces containing blood that has been digested in the stomach or upper intestine). PGTFL is generally treated like cases of common follicular lymphoma: depending on the severity of the disease and its symptoms, patients are treated with watchful waiting, surgery, chemotherapy, radiation, immunotherapy plus radiotherapy, or combinations of these modalities. Predominantly diffuse follicular lymphoma with 1p36 deletion Predominantly diffuse follicular lymphoma with 1p36 deletion is a rare subtype of FL in which involved lymph nodes show infiltrations of centrocytes and centoblasts that generally do not form the nodular, swirling patterns characteristic of most types of FL. In addition, these cells lack the t(14:18)(q32:q21.3) translocation commonly found in other FL types but, similar to many FL cases, have a deletion in the terminal part of the short (i.e. "p") arm of chromosome 1 that encodes the TNFRSF14 gene (see pathophysiology section). Predominantly diffuse follicular lymphoma with 1p36 deletion usually presents with bulky enlargements of inguinal (i.e. groin) lymph nodes but may present with enlargements of the axillary (i.e. armpit) or cervical (i.e., neck) lymph nodes. In rare cases, there may be involvement of the bone marrow. In spite of the evidence of bulky and disseminated disease, predominantly diffuse follicular lymphoma with 1p36 deletion appears to be an indolent disorder that may require long-term observation rather than overtreatment. Pediatric-type follicular lymphoma Pediatric-type follicular lymphoma (PTFL) was initially reported to occur in children ages 1–17 years old (median age ~13-14) but more recently has been reported to occur in adults. The disorder was recently defined by the World Health Organization (2016) as a distinct entity that occurs mostly in males and involves swollen lymph nodes in the head (including tonsils and adenoids), neck, or, rarely, axillary, or inguinal areas, or non-lymphoid tissues. Currently, however, patients who had exhibited or are exhibiting involvement of areas or tissues outside of the head, neck, armpit, or groin areas are now regarded as far more likely to have a newly and provisionally defined disease, large B-cell lymphoma with IRF4 rearrangement.The lesions in PTFL consists of infiltrates containing rapidly proliferating centrocytes and centroblasts that lack the t(14:18)(q32:q21.3) translocation but nonetheless often overexpress the BCL2 gene. These cells may show a loss of heterozygosity at 1p36 (20-50% of cases) that results in decreased expression of the TNFRSF14 gene (see Pathophysiology section) as well as mutations in the IRF8 (10-50% of cases), which contributes to the development and function of B cells, and the MAP2K1 gene (10-40% of cases), which regulates activation of the ERK cell signaling pathway. More than 2 dozen other genes have been reported to be mutated in rare cases of PTFL but in general the genetic abnormalities found in this disorder are fewer and less complex than those in other types of FL. PTFL has an indolent, relapsing and remitting course with a 5-year survival rate of >95%. Patients diagnosed with PTFL have been treated with chemotherapy, surgery, and combinations of these treatments. In general, these patients did well (100% survival with <5% of cases relapsing regardless of treatment modality). More recently, 36 patients have been treated with surgical resection alone followed by observation; all these patients survived with only one having a relapse. Thus, PTFL appears to be a highly indolent type of FL in which multiple studies have reported overall and progression-free survival rates of 100% and >90%, respectively, for >2 years and an estimated probability of 5-year event-free survival rate of ~96%. The therapeutic regimens versus follow-up observations that best treat this disorder in children, adolescents, and adults (adults may require different treatments than children and adolescents) requires further study. Primary follicular lymphoma of the testis Primary follicular lymphoma of the testis (PFLT), also termed testicular follicular lymphoma, was classified as a distinct form of FL by the World Health Organization in 2016. It is an extremely rare disease that has been recognized as occurring primarily in children and adolescents but also has been reported in 5 adults. PFLT differs from cases of typical follicular lymphoma that involve the testis in that it more often occurs in children and adolescents; involves malignant B-cells that do have the t(14:18)q32:q21) translocation; and presents with disease that is strictly limited to the testis. While similar to pediatric-type follicular lymphoma in not involving cells that bear the t(14:18)q32:q21) translocation, PFLT differs from the former disease in that it is limited to the testis and involves malignant cells that do not express Bcl2. PFTL is an extremely indolent disease which is manifested by lesions that exhibit a typical FL histology or, more commonly, a mixed FL-diffuse large cell lymphoma histology. It usually involves a 2-4 centimeter lesion in a single testicle. Patients have been treated with removal of the involved testes followed by various standard anti-lymphoma chemotherapy regimens to attain excellent results, i.e. 100% completed remissions with no recurrence of disease in 15 child and adolescent patients observed for 4–96 months. No cases of primary follicular lymphoma of the testis have been reported to progress to t-FL. Surgery followed by less strenuous or even no chemotherapy may prove to be the optimal treatment for this disease. Transformed follicular lymphoma FL progresses at a rate of 2-3% per year for at least the first 10 years after diagnosis to a more aggressive form, principally diffuse large B-cell lymphoma (~93% of cases) or Burkitt-like lymphoma (~7% of cases) or in rare cases exhibit the histology resembling precursor B-cell lymphoblastic leukemia, plasmablastic lymphoma, the high grade subtype of B-cell lymphoma, Hodgkin lymphoma of the B-cell type, chronic lymphocytic leukemia/small cell lymphcytic lymphoma, or histiocytic sarcoma. t-FL is almost always diagnosed in patients being followed for FL. These FL patients present with the: fast growth of lymph nodes; formation of extra-nodal lesions in extra-nodal sites such as the central nervous system, liver or bone; the onset of B-symptoms (i.e. fever, night sweats, weight loss); development of hypercalcemia (i.e. high serum levels of calcium); and/or sudden rises in serum levels of the enzyme lactate dehydrogenase. A minority of t-FL patients present without a history of FL. These patients generally present with advanced, bulky disease that may be accompanied by extra-nodal lesions and B-symptoms. Typically, all the various forms of t-FL are aggressive, rapidly progressive diseases with overall media survival times in treated patients of ~4.5 years. The transformation of FL to DLBCL is in over 70% of cases associated with the gain of MYC activity by genetic or non-genetic mechanisms. Diagnosis The diagnosis of FL depends on examining involved tissues for histological, immunological, and chromosomal abnormalities that are indicative of the disease. FL usually involves enlarged lymph nodes populated by abnormal follicles (see adjacent picture) that when examined histologically contain a mixture of centrocytes or centroblast surrounded by non-malignant cells, mostly T-cells. The centrocytes, which typically outnumber centroblasts, are small to medium-sized B-cell lymphocytes that characteristically exhibit cleaved nuclei; the centropblasts are larger B-cell lymphocytes without cleaved nuclei. Rare cases of FL may show lesions that contain tissue infiltrations dominated by B-cells with features of precursor (i.e. "blast") cells, monocytes, or malignant mantle cells such as those found in mantle cell lymphoma. Immunochemical analyses reveal that these cells generally express B-cell surface markers including the CD10 (60% of cases), CD20, CD19, CD22, and CD79 but not CD5, CD11c, or CD23 cell surface proteins; genomic analyses reveal that these cells contain t(14:18)(q32:q21.3) translocation (85-90% of cases), 1p36 deletions (60-70% of cases), and with far less frequency the other genomic abnormalities listed in the above sections on Pathophysiology and Presentation and course. None of these protein markers or genomic abnormalities are diagnostic for FL, e.g. the t(14:18)(q32:q21.3) translocation is found in 30% of diffuse large B-cell lymphoma and in a small number of reactive benign lymph nodes. Rather, the diagnosis is made by a combination of histological, immunological, and genomic abnormalities. According to World Health Organization (WHO) criteria, differences in the microscopically determined morphology of these tissues can be used to diagnose and categorized FL into the following 3 Grades with grade 3 having A and B subtypes: Grade 1: follicles have <5 centroblasts per high-power field (hpf). Grade 2: follicles have 6 to 15 centroblasts per hpf. Grade 3: follicles have >15 centroblasts per hpf. Grade 3A: Grade 3 in which the follicles contain predominantly centrocytes. Grade 3B: Grade 3 in which the follicles consist almost entirely of centroblasts.Grades 1 and 2 are regarded as low grade FL; Grade 3A is usually also regarded as low grade FL although some studies have regarded it as high grade FL; and Grade 3B is regarded as a highly aggressive FL in the t-FL category.In addition to grade 3B disease, histologic examinations may reveal other evidence of t-FL such as histologic findings consistent with FL and diffuse large cell lymphoma in the same tissue (referred to as composite lymphomas) or in separate tissues (referred to as (discordant lymphomas) or histologic findings similar to those found in Burkitt lymphoma, precursor B-cell lymphoblastic leukemia, plasmablastic lymphoma, the high grade subtype of B-cell lymphoma, Hodgkin lymphoma of the B-cell type, chronic lymphocytic leukemia/small cell lymphocytic lymphoma, or histiocytic sarcoma. Other findings indicating the presence of this transformation include rapid growth in size of lymph nodes, recently acquired or new B symptoms, recent development of FL lesions in non-nodal tissue, rapid rises in serum lactate dehydrogenase levels, and the presence of high levels of serum calcium. Differential diagnosis FL may be confused with marginal zone B-cell lymphoma, mantle cell lymphoma, and the small lymphocytic lymphoma variant of chronic lymphocytic leukemia. The malignant cells in marginal zone B-cell lymphoma may form follicular structures but commonly proliferate in the marginal zone rather than germinal center of lymphoid tissues. These malignant cells often show features of monocytes or plasma cells. Mantle cell lymphomas show monotonous, medium-sized lymphocytes, monocytes, and atrophied germinal centers; unlike FL, the malignant lymphocytes in this disease are positive for Cyclin D1 by immunohistochemistry staining. Small lymphocytic lymphomas are composed of nodular structures with small- to medium-sized malignant cells surrounding immature lymphocytes and immunoblasts. The malignant cells in this disease, unlike FL, stain positive for CD5 and CD23. Treatment and prognosis FL is typically a slowly growing lymphoma with an overall median life expectancy for treated patients of 10–15 years with many cases of it waxing and waning in the size of their lesions and rare cases of it remitting spontaneously. These considerations favor the use of observation over intervention in patients whose particular form of FL has a favorable prognosis or who are intolerant to aggressive treatments. However, most cases of FL have a less favorable prognosis at some stage of their disease and will therefore require intervention. There is little consensus regarding the guidelines to be used to define the prognosis and treatment for FL at its presentation or during its course.. Currently used indicators for this include the diseases: 1) histology; 2) subtype; 3) predicted indolence and potential for transformation; and 4) extent of disease as measured by clinical examinations, bone marrow biopsy to determine bone marrow involvement, and PET/CT imaging of the chest, abdomen, pelvis, and any areas outside of these regions if physical examination suggests involvement. Some suggested guidelines using these parameters to indicate the prognosis and need for treatment in FL include: The WHO criteria using histological grade (see previous section): Patients with Grades 1, 2, and 3A disease are predicted to have the same low risk prognosis that is seen in cases of typical FL while patients with grade 3B disease are predicted to have the high risk prognosis typical of t-FL. The Follicular Lymphoma International Prognostic Index (FLIPI): FLIPI uses the following criteria: age ≥60 years; Ann Arbor disease stage III (i.e. lesions located both above and below the thoracic diaphragm) or IV (i.e. disseminated lesions involving one or more non-lymphatic organs); blood hemoglobin <12 gram/deciliter; serum lactose dehydrogenase level above normal; and involvement of >4 lymph nodes. Patients positive for 0–1, 2, or ≥3 of these factors are classified as in low, intermediate, and high risk group, respectively, and after treatment with regimens that include rituximab have 2 year predicted progression free survivals of 84, 72, and 65%, respectively, and overall survivals of 98, 94, and 87%, respectively. The FLIP2 index. This modification of FLIP1 uses age ≥60; blood hemoglobin <12 gram/deciliter; serum lactose dehydrogenase level above normal; serum beta-2 microglobulin level above normal; ≥1 lymph node with a diameter >6 centimeters; and bone marrow involvement. The predicted percentage of therapy-treated patients with progression free survival at 5 years for individuals positive for 0, 1–2, and ≥3 of these factors are 80, 51, and 19%, respectively. CT/PET imaging: This method measures total body tumor volume as detected by tissue uptake of radioactive fludeoxyglucose (F18). Progression free and overall survival at 5 years for patients with estimated tumor volumes above versus below 510 cubic centimeters are reported to be 32.7 and 84.8% versus 65.1 and 94.7%, respectively. Lugano staging: this method classifies Stage I disease as involving a single lymphatic region or extra-lymphatic site; Stage II disease as involving ≥2 lymphatic sites or 1 lymphatic site plus 1 extralympatic site with all lesions being on the same side of the diaphragm; Stage III disease as involving ≥2 lymphatic regions that are on opposite sides of the diaphragm; and Stage IV disease as disseminated lesions that are found to be in ≥1 non-lymphatic organs. Response-based prognosis: FL patients whose disease progresses within 24 months of initiating treatment with chemotherapy and immunotherapy versus patients whose disease does not progress within 24 months are predicted to have 5 year survival rates of 50-74% versus ~90%, respectively.The prognosis and treatment for the specific presentations of typical FL cases (see above sections for the prognoses and treatment recommendations for primary gastrointestinal tract FL, predominantly diffuse FL with 1p36 deletion, pediatric-type FL, and primary FL of the testis) that are in common use are as follows: In situ follicular lymphoma ISFL is a benign condition that may be reevaluated periodically to detect the rare cases of it which progress to FL; otherwise ISFL is not treated. Localized follicular lymphoma In 10-20% of cases, FL appears limited to single radiation field, does not involve the bone marrow, and is therefore regarded as localized early-stage FL. In these cases, which are sometimes classified as Ann Arbor stage I (i.e. disease limited to a single restricted region) or stage II (i.e. disease restricted to two sites that are on the same side of the diaphragm), radiation therapy achieves 10 year overall survival rates of 60-80% and median overall survival times of 19 years. It seems likely that many of the relapses in these cases are due to undetected disease outside of the radiation field at the time of radiation treatment. The use of PET/CT imaging is strongly recommended to insure that the FL is localized. In any case, the excellent results achieved with radiation therapy strongly support its use in localized disease. The use of an immunotherapeutic agent such as Rituximab alone or in combination with a chemotherapeutic regimen such as CVP (i.e. cyclophosphamide, vincristine, prednisone and rituximab) in cases of localized, early-stage disease may be appropriate choices for some of these early-stage patients. However, the latter approach is recommended for cases of localized disease in which the disease extends beyond a single field: 56% of patients treated in this manner had progression-free survival at 10 years while patients treated with other regimens had progression free survivals of 41%. Nonetheless, overall survival did not differ between the two groups. Asymptomatic follicular lymphoma Patients with asymptomatic but not localized low grade FL, gastrointestinal tract FL, and pediatric-type follicular lymphoma have been served by careful follow-up without therapeutic intervention. Even high grade, aggressive, relapsed, or transformed FL may also be served with observation in patients who are asymptomatic. Findings in asymptomatic patients who have been recommended as triggers for starting treatment include one or more of the following: tumor size ≥7 cm in diameter; involvement of ≥3 nodes in 3 distinct areas, each of which is ≥3 cm in diameter; organ compression; presence of ascites or pleural effusion (i.e. build-up of fluid in the abdominal or pleural cavities); poor performance status due to the disease; elevated levels of serum lactose dehydrogenase or beta-2 microglobulin; presence of localized bone lesions; kidney involvement; reduced levels of circulating blood platelets or any of the various types of white blood cells; onset of significant pruritus (i.e. itching sensation) or other B symptoms; and enlargement (i.e. ≥50% increase in size over a period of at least 6 months) of lymph nodes, spleen, or other follicular lymphoma-infiltrated organs or tissues. Symptomatic follicular lymphoma Symptomatic FL requires treatments directed at relieving symptoms by reducing the load of tumor cells. Various chemotherapeutic regimens have been used for this including combinations of alkylating antineoplastic agents, nucleoside analogues, and/or anthracyclines. Two commonly used chemotherapeutic regimens are CVP (see Localized FL section) and CHOP (i.e. CVP plus the anthracycline adriamycin). Newer agents used to treat FL include monoclonal antibodies such as rituximab, obinutuzumab, galiximab, inotuzumab ozogamicin, or epratuzumab and immunomodulators such as lenalidomide and interferon. The latter medications have been used in combination or alone to treat symptomatic FL. Most such regimens add rituximab (a monoclonal antibody which binds and thereby kills the CD20 cell surface protein on B cells) with CVP or CHOP regimens (termed R-CVP and R-CHOP regimens). The R-CHOP regimen appears superior to the R-CVP regimen with, for example, one study finding 8-year progression-free survival rates of 57% versus 46% for the two respective regimens. More recently, FL patients have been treated with other regimens including: 1) rituximab combined with the chemotherapeutic alkylating agent bendamustine; 2) rituximab combined with the chemotherapeutic agent fludarabine and the inhibitor of Type II topoisomerase, mitoxantrone; and 3) rituximab combined with another immunotherapeutic agent such as galiximab, epratuzumab (monoclonal antibodies directed respectively against the CD80 or CD22 cell surface proteins on immune cells including B cells), or the immunomodulating medication, lenalidomide. While it is too soon to judge the long-term results of the latter regimens, the regimens have shown similar results when analyzed based on poor treatment responses (~10-20% poor responses). Bendamustine with rituximab may be preferable to R-CHOP or R-CVP for treating low-grade (i.e. Grades 1, 2, and possibly 3A) FL; R-CHOP may be preferred in FL that has high-risk characteristics (e.g. high levels of Beta-2 macroglobulin or bone marrow involvement). The combination of lenalidomide with rituximab has shown good potential in treating indolent cases of FL.Studies indicate that maintenance therapy with rituximab following successful induction therapy prolongs progression-free survival; for example one study found progression-free survival after 6 years of treatment was 59.2% in patients treated with rituximab maintenance and 42.7% without this maintenance; however, overall survival at 6 years was similar in the two groups, 87.4% and 88.7%, respectively. Another study found that prolonged maintenance with rituximab did not have any benefits over an eight-month maintenance period. Finally, surgery and radiation are additional therapies that can be used to relieve symptoms caused by bulky t-FL disease or to treat lesions in patients who cannot withstand other types of treatment. Transformed follicular lymphoma Early studies on treating t-FL with various purely chemotherapy regimens gave poor results with median overall survival times of 1–2 years. However, the addition of rituximab to the regimens such as CVP and CHOP as part of induction and maintenance therapies (i.e. R-CVP and R-CHOP) greatly improved overall 5 year survival to rates of 73%. The R-CHOP regimen is a good option for treating such cases. However, these regimens need not be started in people with FL who are asymptomatic and have low tumor burdens: the outcomes in such patients show no difference between early versus delayed treatment. Some recent studies found that the use of rituximab in combination with bendamustine (i.e. the RB regimen) provided better results than R-CHOP: progression-free survival times in one study were 69.5 months for RB and 31.2 months for R-CHOP. Similar results were obtained when RB was compared to R-CVP. These studies also found no overall survival time benefit between the RB and R-CHOP regimens. Other recently examined regimens include 1) the use of obinutuzumab instead of rituximab in the R-CHOP and R-CVP regiments to attain progression-free survival rates at 3 years of 80% for the obinutuzumab-chemotherapy regimen versus 73% for the rituximab-chemotherapy regimen and 2) the combination of rituximab with lenalidomide (no chemotherapy agent) versus various chemotherapy plus immunotherapy (principally rituximab) to achieve similar complete remission and 3 year progression-free survival rates but with rituximab plus lenalidomide causing less toxicity (i.e. severe neutropenia). Many of these studies did use rituximab maintenance therapy after induction therapy. Prevention Several studies, while not conclusive, suggest that the early treatment of low risk FL reduces the incidence of the disease progressing to t-FL. The treatments used in these studies include chemotherapy, radiation therapy, and immunotherapy combinations plus rituximab maintenance therapy. Relapsed follicular lymphoma Patients who relapse after initial therapy for FL may be followed closely without therapy if asymptomatic. When treatment is required, patients may be treated with the initial treatment regimen when such treatment led to a remission that lasted for at least one year; otherwise an alternative regimen is used. The regimens commonly used in relapsed lymphoma include R-CHOP, R-CVP, RFM (i.e. rituximab, fludarabine, and mitoxantrone), and RB (Bendamustine plus rituximab). Patients who have early treatment failure (e.g. within 1–2 years of initial treatment) or multiple relapses have also been treated with either autologous (i.e. stem cells taken from patient) or allogeneic (i.e. stem cells taken from a donor) stem cell bone marrow transplantation. While studies are inconclusive, autologous stem cell bone marrow transplantation appears to prolong survival in early treatment failure patients who are healthy enough to withstand this therapy. Unfit patients may benefit from initial treatment with obinutuzumab plus bendamustine followed by maintenance treatment with obinutuzumab (if they have not been treated previously with obinutuzumab).Other mostly experimental treatments currently under study in patients with multiple treatment failures include: 1) Phosphoinositide 3-kinase inhibitors such as copanlisib, duvelisib, and idelalisib which block the phosphoinositide 3-kinase signaling pathway that promotes the survival, proliferation, and other potentially malignant behaviors of cells; 2) infusion of tisagenlecleucel chimeric antigen receptor T cells (i.e. CAR T cells) (i.e. T cells that have been isolated from patients, engineered to express a receptor for the CD19 protein on, and thereby kill, T cells, and then infused back into the donor patient); 3) Bruons tyrosine kinase inhibitor, ibrutinib, to block the B-cell maturating actions of this kianase; 4) BCL inhibitor venetoclax to block Bcl2s action in promoting B-cell survival and proliferation; 5) histone deacetylase inhibitors abexinostat and tazemetostat to modify the expression of various genes; and 6) Checkpoint inhibitors nivolumab, pidilizumab, and pembrolizumab to promote the immune systems ability to suppress cancer cell growth. In preliminary studies on FL patients who were known or thought to be refractor to more conventional therapies these drugs, when combined with more conventional drugs, particularly rituximab, produced promising results. Phosphoionsitide 3-kinase inhibitors produced overall response rates of 10–12.5 months in 42-59%; tisagenlecleuce cells produced an overall progression-free response rate of 70% after a follow-up of 28 months; phosphoinositide 3-kinase inhibitors produced overall response rates of ~40% and complete response rates of 1-20%; Brutons tyrosine kinase inhibitor produced overall and complete response rates of 38% and 18%, respectively; the Bcl inhibitor produce overall and complete response rates of 33% and 14%, respectively; histone deacetylase inhibitors produce overall response rates of 35%-71%; and checkpoint inhibitors produce overall response rates of 40%-80% and complete response rates of 10-60%. See also List of hematologic conditions large-cell lymphoma In situ follicular lymphoma References External links Follicular large cell lymphoma entry in the public domain NCI Dictionary of Cancer Terms

Aarogya, What does Gastrointestinal stromal tumor mean

Gastrointestinal stromal tumor

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract. GISTs arise in the smooth muscle pacemaker interstitial cell of Cajal, or similar cells. They are defined as tumors whose behavior is driven by mutations in the KIT gene (85%), PDGFRA gene (10%), or BRAF kinase (rare). 95% of GISTs stain positively for KIT (CD117). Most (66%) occur in the stomach and gastric GISTs have a lower malignant potential than tumors found elsewhere in the GI tract. Classification GIST was introduced as a diagnostic term in 1983.: 1060  Until the late 1990s, many non-epithelial tumors of the gastrointestinal tract were called "gastrointestinal stromal tumors". Histopathologists were unable to specifically distinguish among types we now know to be dissimilar molecularly. Subsequently, CD34, and later CD117 were identified as markers that could distinguish the various types. Additionally, in the absence of specific therapy, the diagnostic categorization had only a limited influence on prognosis and therapy. The understanding of GIST biology changed significantly with identification of the molecular basis of GIST,: 1065  particularly c-KIT. Historically, literature reviews prior to the molecular definition of GIST, and for a short time thereafter, asserted that 70-80% of GISTs were benign. The identification of a molecular basis for GIST led to the exclusion of many tumors that had been considered as GIST previously, and also the incorporation of a much larger number of tumors that had been labeled as other types of sarcomas and undifferentiated carcinomas.: 1065  For example, some previous diagnoses of stomach and small bowel leiomyosarcomas (malignant tumor of smooth muscle) would be reclassified as GISTs on the basis of immunohistochemical staining. All GIST tumors are now considered to have malignant potential, and no GIST tumor can be definitively classified as "benign". Hence, all GISTs are eligible for cancer staging in the AJCC (7th edition) / UICC. Nonetheless, different GISTs have different risk assessments of their tendency to recur or to metastasize, dependent on their site of origin, size, and number of mitotic figures. Due to the change in definition, clinical pathways of care before the year 2000 are largely uninformative in the current era. Signs and symptoms GISTs may present with trouble swallowing, gastrointestinal bleeding, or metastases (mainly in the liver). Intestinal obstruction is rare, due to the tumors outward pattern of growth. Often, there is a history of vague abdominal pain or discomfort, and the tumor has become rather large by time the diagnosis is made. Pathophysiology GISTs are tumors of connective tissue, i.e. sarcomas; unlike most gastrointestinal tumors, they are nonepithelial. About 70% occur in the stomach, 20% in the small intestine and less than 10% in the esophagus. Small tumors are generally not aggressive, especially when cell division rate is slow. GIST tumors commonly metastasize to the liver (in 28% of cases) and/or to the greater omentum, lesser omentum, or mesentery (in 30% of cases). Less common areas of metastasis include the lungs, subcutaneous tissue, lymph nodes or bones.GISTs are thought to arise from interstitial cells of Cajal (ICC), that are normally part of the autonomic nervous system of the intestine. They serve a pacemaker function in controlling motility. Genetics Most GISTs are sporadic. Less than 5% occur as part of hereditary familial or idiopathic multitumor syndromes. These include, in descending order of frequency, neurofibromatosis Recklinghausen (NF-1), Carneys triad (gastric GIST, pulmonary chondroma and extra-adrenal paraganglioma), germline gain-of-function mutations in c-KIT/PDGFRA, and the Carney-Stratakis syndrome. The Carney-Stratakis syndrome is a dyad of hereditary GIST and paraganglioma, that is caused by germline mutations in the mitochondrial tumor suppressor gene pathway involving the succinate dehydrogenase (SDH) subunits SDHD, SDHC and SDHB. c-KIT mutations Approximately 85% GISTs are associated with an abnormal c-KIT pathway. c-KIT is a gene that encodes for a transmembrane receptor for a growth factor termed stem cell factor (scf). The abnormal c-KIT pathway most commonly (85%) arises from mutation of the gene itself; a smaller subset of c-KIT-associated GISTs are associated with constitutive activity of the KIT enzymatic pathway, found by immunoblotting.: 1062  The c-KIT product/CD117 is expressed on ICCs and a large number of other cells, mainly bone marrow cells, mast cells, melanocytes and several others. In the gut, however, a mass staining positive for CD117 is likely to be a GIST, arising from ICC cells. The c-KIT molecule comprises a long extracellular domain, a transmembrane segment, and an intracellular part. Mutations generally occur in the DNA encoding the intracellular part (exon 11), which acts as a tyrosine kinase to activate other enzymes. Mutations make c-KITfunction independent of activation by scf, leading to a high cell division rate and possibly genomic instability. Additional mutations are likely "required" for a cell with a c-KIT mutation to develop into a GIST, but the c-KIT mutation is probably the first step of this process. Mutations in the exons 11, 9 and rarely 13 and 17 of the c-KIT gene are known to occur in GIST. The tyrosine kinase function of c-KIT is important in the medical therapy for GISTs, as described below. KIT-D816V point mutations in c-KIT exon 17 are responsible for resistance to targeted therapy drugs like imatinib mesylate, a tyrosine kinase inhibitor. KIT-p.D419del (exon 8) — A subset of gastrointestinal stromal tumors previously regarded as wild-type tumors carries somatic activating mutations in KIT exon 8 (p.D419del). PDGFRA mutations Most GIST cells with wildtype (i.e. not mutated) c-KIT instead have a mutation in another gene, PDGFR-α (platelet-derived growth factor receptor alpha), which is a related tyrosine kinase. Mutations in c-KIT and PDGFrA are mutually exclusive [4][5]. Wild-type tumors Lesser numbers of GISTs appear to be associated with neither c-KIT nor PDGFR-α abnormalities.: 1062  About 10-15% of gastrointestinal stromal tumors (GISTs) carry wild-type sequences in all hot spots of KIT and platelet-derived growth factor receptor alpha (PDGFRA) (wt-GISTs). These tumors are currently defined by having no mutations in exons 9, 11, 13, and 17 of the KIT gene and exons 12, 14, and 18 of the PDGFRA gene. Diagnosis CT scanning is often undertaken (see the radiology section). The definitive diagnosis is made with a biopsy, which can be obtained endoscopically, percutaneously with CT or ultrasound guidance or at the time of surgery. A biopsy sample will be investigated under the microscope by a pathologist physician. The pathologist examines the histopathology to identify the characteristics of GISTs (spindle cells in 70-80%, epitheloid aspect in 20-30%). Smaller tumors can usually be confined to the muscularis propria layer of the intestinal wall. Large ones grow, mainly outward, from the bowel wall until the point where they outstrip their blood supply and necrose (die) on the inside, forming a cavity that may eventually come to communicate with the bowel lumen. When GIST is suspected—as opposed to other causes for similar tumors—the pathologist can use immunohistochemistry (specific antibodies that stain the molecule CD117 [also known as c-KIT] —see below). 95% of all GISTs are CD117-positive (other possible markers include CD34, DOG-1, desmin, and vimentin). Other cells that show CD117 positivity are mast cells. If the CD117 stain is negative and suspicion remains that the tumor is a GIST, the newer antibody DOG-1 (Discovered On GIST-1) can be used. Also, sequencing of KIT and PDGFRA can be used to prove the diagnosis. Imaging The purpose of radiologic imaging is to locate the lesion, evaluate for signs of invasion and detect metastasis. Features of GIST vary depending on tumor size and organ of origin. The diameter can range from a few millimeters to more than 30 cm. Larger tumors usually cause symptoms in contrast to those found incidentally which tend to be smaller and have better prognosis. Large tumors tend to exhibit malignant behavior but small GISTs may also demonstrate clinically aggressive behavior. Plain radiographs are not very helpful in the evaluation of GISTs. If an abnormality is seen, it will be an indirect sign due to the tumor mass effect on adjacent organs. On abdominal x-ray, stomach GISTs may appear as a radiopaque mass altering the shape of the gastric air shadow. Intestinal GISTs may displace loops of bowel and larger tumors may obstruct the bowel and films will show an obstructive pattern. If cavitations are present, plain radiographs will show collections of air within the tumor. Calcification is an unusual feature of GIST but if present can be visible on plain films. Barium fluoroscopic examinations and CT are commonly used to evaluate the patient with abdominal complaints. Barium swallow images show abnormalities in 80% of GIST cases. However, some GISTs may be located entirely outside the lumen of the bowel and will not be appreciated with a barium swallow. Even in cases when the barium swallow is abnormal, an MRI or CT scan must follow since it is impossible to evaluate abdominal cavities and other abdominal organs with a barium swallow alone. In a CT scan, abnormalities may be seen in 87% of patients and it should be made with both oral and intravenous contrast. Among imaging studies, MRI has the best tissue contrast, which aids in the identification of masses within the GI tract (intramural masses). Intravenous contrast material is needed to evaluate lesion vascularity. Preferred imaging modalities in the evaluation of GISTs are CT and MRI,: 20–21  and, in selected situations, endoscopic ultrasound. CT advantages include its ability to demonstrate evidence of nearby organ invasion, ascites, and metastases. The ability of an MRI to produce images in multiple planes is helpful in determining the bowel as the organ of origin (which is difficult when the tumor is very large), facilitating diagnosis. Small GISTs Since GISTs arise from the bowel layer called muscularis propria (which is deeper to the mucosa and submucosa from a luminal perspective), small GIST imaging usually suggest a submucosal process or a mass within the bowel wall. In barium swallow studies, these GISTs most commonly present with smooth borders forming right or obtuse angles with the nearby bowel wall, as seen with any other intramural mass. The mucosal surface is usually intact except for areas of ulceration, which are generally present in 50% of GISTs. Ulcerations fill with barium causing a bulls eye or target lesion appearance. In contrast-enhanced CT, small GISTs are seen as smooth, sharply defined intramural masses with homogeneous attenuation. Large GISTs As the tumor grows it may project outside the bowel (exophytic growth) and/or inside the bowel (intraluminal growth), but they most commonly grow exophytically such that the bulk of the tumor projects into the abdominal cavity. If the tumor outstrips its blood supply, it can necrose internally, creating a central fluid-filled cavity with bleeding and cavitations that can eventually ulcerate and communicate into the lumen of the bowel. In that case, barium swallow may show an air, air-fluid levels or oral contrast media accumulation within these areas. Mucosal ulcerations may also be present. In contrast-enhanced CT images, large GISTs appear as heterogeneous masses due to areas of living tumor cells surrounding bleeding, necrosis or cysts, which is radiographically seen as a peripheral enhancement pattern with a low attenuation center. In MRI studies, the degree of necrosis and bleeding affects the signal intensity pattern. Areas of bleeding within the tumor will vary its signal intensity depending on how long ago the bleeding occurred. The solid portions of the tumor are typically low signal intensity on T1-weighted images, are high signal intensity on T2-weighted images and enhanced after administration of gadolinium. Signal-intensity voids are present if there is gas within areas of necrotic tumor. Features of malignancy Malignancy is characterized by local invasion and metastases, usually to the liver, omentum and peritoneum. However, cases of metastases to bone, pleura, lungs and retroperitoneum have been seen. In distinction to gastric adenocarcinoma or gastric/small bowel lymphoma, malignant lymphadenopathy (swollen lymph nodes) is uncommon (<10%) and thus imaging usually shows absence of lymph node enlargement. If metastases are not present, other radiologic features suggesting malignancy include: size (>5 cm), heterogeneous enhancement after contrast administration, and ulcerations. Also, overtly malignant behavior (in distinction to malignant potential of lesser degree) is less commonly seen in gastric tumors, with a ratio of behaviorally benign to overtly malignant of 3-5:1. Even if radiographic malignant features are present, these findings may also represent other tumors and definitive diagnosis must be made immunochemically. Management For localized, resectable adult GISTs, if anatomically and physiologically feasible, surgery is the primary treatment of choice.: 69  Surgery can be potentially curative, but watchful waiting may be considered in small tumors in carefully selected situations. Post-surgical adjuvant treatment may be recommended. Lymph node metastases are rare, and routine removal of lymph nodes is typically not necessary. Laparoscopic surgery, a minimally invasive abdominal surgery using telescopes and specialized instruments, has been shown to be effective for removal of these tumors without needing large incisions. The clinical issues of exact surgical indications for tumor size are controversial. The decision of appropriate laparoscopic surgery is affected by tumor size, location, and growth pattern.Radiotherapy has not historically been effective for GISTs: 1122  and GISTs do not respond to most chemotherapy medications,: 1122  with responses in less than 5%.: 1065  However, four medications have been identified for clinical benefit in GIST: imatinib, sunitinib, regorafenib, and ripretinib. Imatinib (Glivec/Gleevec), an orally administered drug initially marketed for chronic myelogenous leukemia based on bcr-abl inhibition, also inhibits both c-KIT tyrosine kinase mutations and PDGFRA mutations other than D842V, and is useful in treating GISTs in several situations. Imatinib has been used in selected neoadjuvant settings.: 23  In the adjuvant treatment setting, the majority of GIST tumors are cured by surgery, and do not need adjuvant therapy. An exception to this is where the anatomical position of the tumour means that surgery is technically difficult or complex. For example, rectal GIST often requires radical surgery to achieve complete resection, involving abdominoperineal resection and permanent stoma. In these situations, the use of neoadjuvant imatinib can significantly decrease both tumour size and mitotic activity, and permit less radical sphincter-preserving surgery.A substantial proportion of GIST tumors have a high risk of recurrence as estimated by a number of validated risk stratification schemes, and can be considered for adjuvant therapy. The selection criteria underpinning the decision for possible use of imatinib in these settings, including a risk assessment based on pathological factors such as tumor size, mitotic rate and location, can be used to predict the risk of recurrence in GIST patients. Tumors <2 cm with a mitotic rate of <5/50 HPF have been shown to have lower risk of recurrence than larger or more aggressive tumors. Following surgical resection of GISTs, adjuvant treatment with imatinib reduces the risk of disease recurrence in higher risk groups. In selected higher risk adjuvant situations, imatinib is recommended for 3 years.Imatinib was approved for metastatic and unresectable GIST by the US FDA, February 1, 2002. The two-year survival of patients with advanced disease has risen to 75–80% following imatinib treatment.If resistance to imatinib is encountered, the multiple tyrosine kinase inhibitor sunitinib (marketed as Sutent) can be considered.: 26 and 31 The effectiveness of imatinib and sunitinib depend on the genotype. c-KIT- and PDGFRA-mutation negative GIST tumors are usually resistant to treatment with imatinib, as is neurofibromatosis-1-associated wild-type GIST. A specific subtype of PDGFRA mutation, D842V, is also insensitive to imatinib. Recently, in PDGFRA-mutated GIST, avapritinib has been approved by FDA. Now there are real-world data coming for avapritinib as well (Dr Sameer Rastogi, et al.)Regorafenib (Stivarga) was FDA-approved in 2013 for advanced GISTs that cannot be surgically removed and that no longer respond to imatinib (Gleevec) and sunitinib (Sutent). Epidemiology GISTs occur in 10-20 per one million people. The true incidence might be higher, as novel laboratory methods are much more sensitive in diagnosing GISTs. The estimated incidence of GIST in the United States is approximately 5000 cases annually.: 1063  This makes GIST the most common form of sarcoma, which constitutes more than 70 types of cancer. The majority of GISTs present at ages 50–70 years. Across most of the age spectrum, the incidence of GIST is similar in men and women.: 1122 Adult GISTs are rare before age 40. Pediatric GISTs are considered to be biologically distinct. Unlike GISTs at other ages, pediatric GISTs are more common in girls and young women. They appear to lack oncogenic activating tyrosine kinase mutations in both KIT and PDGFRA. Pediatric GISTs are treated differently from adult GISTs. Although the generally accepted definition of pediatric GIST is a tumor that is diagnosed at the age of 18 years or younger, "pediatric-type" GISTs can be seen in adults, which affects risk assessment, the role of lymph node resection, and choice of therapy. Citations General sources de Silva CM, Reid R (2003). "Gastrointestinal stromal tumors (GIST): c-KIT mutations, CD117 expression, differential diagnosis and targeted cancer therapy with Imatinib" (PDF). Pathol Oncol Res. 9 (1): 13–9. doi:10.1007/BF03033708. PMID 12704441. S2CID 3814815. Kitamura Y, Hirota S, Nishida T (Apr 2003). "Gastrointestinal stromal tumors (GIST): a model for molecule-based diagnosis and treatment of solid tumors". Cancer Sci. 94 (4): 315–20. doi:10.1111/j.1349-7006.2003.tb01439.x. PMID 12824897. S2CID 31070671. External links GIST Cancer UK Surgery Questions in GIST ESUN (August 15, 2006) SPAEN (Sarcoma Patients EuroNet) - European Network of Sarcoma, GIST and Desmoid Patient Advocacy Groups GIST Support International Life Raft Group International GIST Advocacy Organization American Cancer Society Patient Guide to GIST tumors. Cancer.Net: Gastrointestinal Stromal Tumor

Hey Aarogya, explain a situation where Accidental occurs

Accidental

Accidental may refer to: Accidental (music), a symbol which changes the pitch of a note Accidental (album), by Fred Frith Accidental (biology), a biological phenomenon more commonly known as vagrancy The Accidental, a 2005 novel by Ali Smith The Accidental (band), a UK folk band Accidental property, a philosophical term See also Accidence (or inflection), a modification of a word to express different grammatical categories Accident (disambiguation) Adventitious, which is closely related to "accidental" as used in philosophy and in biology Random, which often is used incorrectly where accidental or adventitious would be appropriate