<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Myiasis and can you explain it in depth? [/INST] Myiasis is the parasitic infestation of the body of a live animal by fly larvae (maggots) which grow inside the host while feeding on its tissue. Although flies are most commonly attracted to open wounds and urine- or feces-soaked fur, some species (including the most common myiatic flies—the botfly, blowfly, and screwfly) can create an infestation even on unbroken skin and have been known to use moist soil and non-myiatic flies (such as the common housefly) as vector agents for their parasitic larvae.
Because some animals (particularly non-native domestic animals) cannot react as effectively as humans to the causes and effects of myiasis, such infestations present a severe and continuing problem for livestock industries worldwide, causing severe economic losses where they are not mitigated by human action. Although typically a far greater issue for animals, myiasis is also a relatively frequent disease for humans in rural tropical regions where myiatic flies thrive, and often may require medical attention to surgically remove the parasites.Myiasis varies widely in the forms it takes and its effects on those affected. Such variations depend largely on the fly species and where the larvae are located. Some flies lay eggs in open wounds, other larvae may invade unbroken skin or enter the body through the nose or ears, and still others may be swallowed if the eggs are deposited on the lips or on food. There can also be accidental myiasis which E. tenax can cause in humans via water containing the larvae or in contaminated uncooked food. The name of the condition derives from ancient Greek μυῖα (myia), meaning "fly".

Signs and symptoms
How myiasis affects the human body depends on where the larvae are located. Larvae may infect dead, necrotic (prematurely dying) or living tissue in various sites: the skin, eyes, ears, stomach and intestinal tract, or in genitourinary sites. They may invade open wounds and lesions or unbroken skin. Some enter the body through the nose or ears. Larvae or eggs can reach the stomach or intestines if they are swallowed with food and cause gastric or intestinal myiasis.Several different presentations of myiasis and their symptoms:

Wound
Wound myiasis occurs when fly larvae infest open wounds. It has been a serious complication of war wounds in tropical areas, and is sometimes seen in neglected wounds in most parts of the world. Predisposing factors include poor socioeconomic conditions, extremes of age, neglect, mental disability, psychiatric illness, alcoholism, diabetes, and vascular occlusive disease.

Eye
Myiasis of the human eye or ophthalmomyiasis can be caused by Hypoderma tarandi, a parasitic botfly of caribou. It is known to lead to uveitis, glaucoma, and retinal detachment. Human ophthalmomyiasis, both external and internal, has been caused by the larvae of the botfly.

Cause
Life cycle
The life cycle in sheep is typical of the disease. The female flies lay their eggs on the sheep in damp, protected areas of the body that are soaked with urine and feces, mainly the sheeps breech (buttocks). It takes approximately eight hours to a day for the eggs to hatch, depending on the conditions. Once hatched, the larvae then lacerate the skin with their mouthparts, causing open sores. Once the skin has been breached, the larvae then tunnel through the sores into the hosts subcutaneous tissue, causing deep and irritating lesions highly subject to infection. After about the second day, bacterial infection is likely and, if left untreated, causes bacterial bloodstream infections or sepsis. This leads to anorexia and weakness and is generally fatal if untreated.

Human vectors
There are three main fly families causing economically important myiasis in livestock and also, occasionally, in humans:
Calliphoridae (blowflies)
Some examples include Calliphora vomitoria and Calliphora vicina
Oestridae (botflies)
Sarcophagidae (fleshflies) Sarcophaga barbata are usually found in dead and rotting meat and animal excrement, which are prime environments for them. This is because their larvae are facultative parasites, as they feed on organic tissue and use the hosts oxygen reserve.Other families occasionally involved are:
Anisopodidae
Piophilidae
Stratiomyidae
Syrphidae

Specific myiasis
Caused by flies that need a host for larval development
Dermatobia hominis (human botfly)
Cordylobia anthropophaga (tumbu fly)
Oestrus ovis (sheep botfly)
Hypoderma spp. (cattle botflies or ox warbles)
Gasterophilus spp. (horse botfly)
Cochliomyia hominivorax (new world screwworm fly)
Chrysomya bezziana (old world screwworm fly)
Auchmeromyia senegalensis (Congo floor maggot)
Cuterebra spp. (rodent and rabbit botfly)

Semispecific myiasis
Caused by flies that usually lay their eggs in decaying animal or vegetable matter, but that can develop in a host if open wounds or sores are present
Lucilia spp. (green-bottle fly)
Cochliomyia spp. (screw-worm fly)
Phormia spp. (black-bottle fly)
Calliphora spp. (blue-bottle fly)
Sarcophaga spp. (flesh fly or sarcophagids)Flesh flies, or sarcophagids, members of the family Sarcophagidae, can cause intestinal myiasis in humans if the females lay their eggs on meat or fruit.

Accidental myiasis
Also called pseudomyiasis. Caused by flies that have no preference or need to develop in a host but that will do so on rare occasions. Transmission occurs through accidental deposit of eggs on oral or genitourinary openings, or by swallowing eggs or larvae that are on food. The cheese fly (Piophila casei) sometimes causes myiasis through intentional consumption of its maggots (which are contained in the traditional Sardinian delicacy casu marzu). Other flies that can accidentally cause myiasis are:
Musca domestica (housefly)
Fannia spp. (latrine flies)
Eristalis tenax (rat-tailed maggots)
Muscina spp.The adult flies are not parasitic, but when they lay their eggs in open wounds and these hatch into their larval stage (also known as maggots or grubs), the larvae feed on live or necrotic tissue, causing myiasis to develop. They may also be ingested or enter through other body apertures.

Diagnosis
Myiasis is often misdiagnosed in the United States because it is rare and its symptoms are not specific. Intestinal myiasis and urinary myiasis are especially difficult to diagnose.Clues that myiasis may be present include recent travel to an endemic area, one or more non-healing lesions on the skin, itchiness, movement under the skin or pain, discharge from a central punctum (tiny hole), or a small, white structure protruding from the lesion. Serologic testing has also been used to diagnose the presence of botfly larvae in human ophthalmomyiasis.

Classifications
German entomologist Fritz Zumpt describes myiasis as "the infestation of live human and vertebrate animals with dipterous larvae, which at least for a period, feed on the hosts dead or living tissue, liquid body substances, or ingested food". For modern purposes however, this is too vague. For example, feeding on dead or necrotic tissue is not generally a problem except when larvae such as those of flies in the family Piophilidae attack stored food such as cheese or preserved meats; such activity suggests saprophagy rather than parasitism; it even may be medically beneficial in maggot debridement therapy (MDT).Currently myiasis commonly is classified according to aspects relevant to the case in question:

The classical description of myiasis is according to the part of the host that is infected. This is the classification used by ICD-10. For example:dermal
sub-dermal
cutaneous (B87.0)
creeping, where larvae burrow through or under the skin
furuncular, where a larva remains in one spot, causing a boil-like lesion
nasopharyngeal, in the nose, sinuses or pharynx (B87.3)
ophthalmic or ocular, in or about the eye (B87.2)
auricular, in or about the ear
gastric, rectal, or intestinal/enteric for the appropriate part of the digestive system (B87.8)
urogenital (B87.8)
Another aspect is the relationship between the host and the parasite and provides insight into the biology of the fly species causing the myiasis and its likely effect. Thus the myiasis is described as either:obligatory, where the parasite cannot complete its life cycle without its parasitic phase, which may be specific, semispecific, or opportunistic
facultative, incidental, or accidental, where it is not essential to the life cycle of the parasite; perhaps a normally free-living larva accidentally gained entrance to the hostAccidental myiasis commonly is enteric, resulting from swallowing eggs or larvae with ones food.  The effect is called pseudomyiasis. One traditional cause of pseudomyiasis was the eating of maggots of cheese flies in cheeses such as Stilton. Depending on the species present in the gut, pseudomyiasis may cause significant medical symptoms, but it is likely that most cases pass unnoticed.

Prevention
The first control method is preventive and aims to eradicate the adult flies before they can cause any damage and is called vector control. The second control method is the  treatment once the infestation is present, and concerns the infected animals (including humans).The principal control method of adult populations of myiasis inducing flies involves insecticide applications in the environment where the target livestock is kept. Organophosphorus or organochlorine compounds may be used, usually in a spraying formulation. One alternative prevention method is the sterile insect technique (SIT) where a significant number of artificially reared sterilized (usually through irradiation) male flies  are introduced. The male flies compete with wild breed males for females in order to copulate and thus cause females to lay batches of unfertilized eggs which cannot develop into the larval stage.One prevention method involves removing the environment most favourable to the flies, such as by removal of the tail. Another example is the crutching of sheep, which involves the removal of wool from around the tail and between the rear legs, which is a favourable environment for the larvae. Another, more permanent, practice which is used in some countries is mulesing, where skin is removed from young animals to tighten remaining skin – leaving it less prone to fly attack.To prevent myiasis in humans, there is a need for general improvement of sanitation, personal hygiene, and extermination of the flies by insecticides. Clothes should be washed thoroughly, preferably in hot water, dried away from flies, and ironed thoroughly. The heat of the iron kills the eggs of myiasis-causing flies.

Treatment
This applies once an infestation is established. In many circles the first response to cutaneous myiasis once the breathing hole has formed, is to cover the air hole thickly with petroleum jelly. Lack of oxygen then forces the larva to the surface, where it can more easily be dealt with. In a clinical or veterinary setting there may not be time for such tentative approaches, and the treatment of choice might be more direct, with or without an incision. First the larva must be eliminated through pressure around the lesion and the use of forceps. Secondly the wound must be cleaned and disinfected. Further control is necessary to avoid further reinfestation.Livestock may be treated prophylactically with slow-release boluses containing ivermectin, which can provide long-term protection against the development of the larvae. Sheep also may be dipped, a process which involves drenching the animals in persistent insecticide to poison the larvae before they develop into a problem.

Epidemiology
The most common infected animal worldwide is the domestic sheep, for more information see fly strike in sheep. This condition is caused by the blowfly (particularly Lucilia sericata and its sister species L. cuprina), especially where the weather is often hot and wet. Blowfly strike accounts for over A$170 million a year in losses in the Australian sheep industry, the largest such losses in the world. Given the seriousness of the risk, Australian sheep farmers commonly perform preventive measures such as mulesing designed to remove the most common targets for the flies. The docking of lambs tails (another frequently-soiled area that flies target) is also commonly practiced by sheep farmers worldwide. Maggots also occasionally infest the vulvar area, causing the condition called vulvar myiasis.
Such problems are not peculiar to Australia and New Zealand; they occur worldwide, especially in countries where livestock, particularly sheep, are kept under hot, wet, conditions, including most of Africa and the Americas, ranging from the cold temperate regions in the north, to corresponding latitudes in the south. Myiasis is also not restricted to sheep; screwworm flies (Cochliomyia hominivorax in particular) regularly cause upwards of US$100 million in annual damages to domestic cows and goats, though the impact has been heavily mitigated in recent years by the sterile insect technique.

History
Frederick William Hope coined the term myiasis in 1840 to refer to diseases resulting from dipterous larvae as opposed to those caused by other insect larvae (the term for this was scholechiasis). Hope described several cases of myiasis from Jamaica caused by unknown larvae, one of which resulted in death.Even though the term myiasis was first used in 1840, such conditions have been known since ancient times. Ambroise Paré, the chief surgeon to King Charles IX and King Henry III, observed that maggots often infested open wounds.

Maggot therapy
Throughout recorded history, maggots have been used therapeutically to clean out necrotic wounds, an application known as maggot therapy.Fly larvae that feed on dead tissue can clean wounds and may reduce bacterial activity and the chance of a secondary infection. They dissolve dead tissue by secreting digestive enzymes onto the wound as well as actively eating the dead tissue with mouth hooks, two hard, probing appendages protruding on either side of the "mouth". Maggot therapy – also known as maggot debridement therapy (MDT), larval therapy, larva therapy, or larvae therapy – is the intentional introduction by a health care practitioner of live, disinfected green bottle fly maggots into the non-healing skin and soft tissue wounds of a human or other animal for the purpose of selectively cleaning out only the necrotic tissue within a wound in order to promote healing.Although maggot therapy has been used in the US for the past 80 years, it was approved by the FDA as a medical device only in 2004 (along with leeches). Maggots were the first live organism to be marketed in the US according to FDA regulations, and are approved for treating neuropathic (diabetic) foot ulcers, pressure ulcers, venous stasis ulcers, and traumatic and post-surgical wounds that are unresponsive to conventional therapies. Maggots were used in medicine before this time, but were not federally regulated. In 1990, California internist Ronald Sherman began treating patients with maggots produced at his lab at the UC Irvine School of Medicine. Sherman went on to co-found Monarch Labs in 2005, which UC Irvine contracted to produce maggots for Shermans own continuing clinical research on myiasis at the university. Monarch Labs also sells maggots to hospitals and other medical practices, the first US commercial supplier to do so since the last one closed in 1935.In the US, demand for these fly larvae doubled after the FDA ruling. Maggot therapy is now used in more than 300 sites across the country. The American Medical Association and Centers for Medicare and Medicaid Services recently clarified the reimbursement guidelines to the wound care community for medicinal maggots, and this therapy may soon be covered by insurance. The larvae of the green bottle fly (a type of blow-fly) are now used exclusively for this purpose, since they preferentially devour only necrotic tissue, leaving healthy tissue intact. This is an important distinction, as most other major varieties of myiasitic fly larvae attack both live and dead wound tissue indiscriminately, effectively negating their benefit in non-harmful wound debridement. Medicinal maggots are placed on the wound and covered with a sterile dressing of gauze and nylon mesh </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Psychogenic pruritus and can you explain it in depth? [/INST] Psychogenic pruritus, also known as psychogenic itch or functional itch disorder is pruritus not associated with a dermatologic or systemic cause. More often than not, it is attributed to a psychiatric cause. Psychogenic pruritus is not the same as neuropathic itch though both are conditions which require more research. This condition is not explained well in DSM-V and is typically considered a diagnosis of exclusion. This condition is not well-studied and it is difficult to ascertain as it is seen by both dermatologists and psychiatrists. In order to provide some consensus to this condition, The French Psychodermatology Group have created diagnostic criteria for this condition.

Symptoms
Psychogenic pruritus typically appears as itching on the face and on the extensor surfaces of the body. This includes the back side of the arms, the abdomen, the side of the legs and the upper back and shoulders. These areas are more frequent because they are within hands reach.

Diagnosis
When considering the diagnosis of psychogenic pruritus, it is important to rule out medical, dermatologic and neuropathic causes. A strong history should be obtained and appropriate labwork should be drawn. One should consider drawing for a CBC (Complete Blood Count), ESR (Erythrocyte Sedimentation Rate), liver, renal and thyroid panel as abnormalities with any can contribute to pruritus. Pruritus can be seen with hepatic and renal disease such as cholestasis, alcoholic liver disease, primary biliary cholangitis, hepatitis B and C, and chronic kidney disease. Drug and alcohol use can contribute to pruritus as well so it is worthwhile to gather a social history. Those who use cocaine and amphetamines may experience pruritus due to feelings of abnormal cutaneous sensations called delusions of parasitosis, also known as "meth mites" </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hypertension and can you explain it in depth? [/INST] Hypertension (HTN or HT), also known as high blood pressure (HBP), is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. High blood pressure usually  does not cause symptoms. Long-term high blood pressure, however, is a major risk factor for stroke, coronary artery disease,  heart failure, atrial fibrillation, peripheral arterial disease, vision loss, chronic kidney disease, and dementia. Hypertension is a major cause of premature death worldwide.High blood pressure is classified as primary (essential) hypertension or secondary hypertension. About 90–95% of cases are primary, defined as high blood pressure due to nonspecific lifestyle and genetic factors. Lifestyle factors that increase the risk include excess salt in the diet, excess body weight, smoking, and alcohol use. The remaining 5–10% of cases are categorized as secondary high blood pressure, defined as high blood pressure due to an identifiable cause, such as chronic kidney disease, narrowing of the kidney arteries, an endocrine disorder, or the use of birth control pills.Blood pressure is classified by two measurements, the systolic and diastolic pressures, which are the maximum and minimum pressures, respectively. For most adults, normal blood pressure at rest is within the range of 100–130 millimeters mercury (mmHg) systolic and 60–80 mmHg diastolic. For most adults, high blood pressure is present if the resting blood pressure is persistently at or above 130/80 or 140/90 mmHg. Different numbers apply to children. Ambulatory blood pressure monitoring over a 24-hour period appears more accurate than office-based blood pressure measurement.Lifestyle changes and medications can lower blood pressure and decrease the risk of health complications. Lifestyle changes include weight loss, physical exercise, decreased salt intake, reducing alcohol intake, and a healthy diet. If lifestyle changes are not sufficient, then blood pressure medications are used. Up to three medications taken concurrently can control blood pressure in 90% of people. The treatment of moderately high arterial blood pressure (defined as >160/100 mmHg) with medications is associated with an improved life expectancy. The effect of treatment of blood pressure between 130/80 mmHg and 160/100 mmHg is less clear, with some reviews finding benefit and others finding unclear benefit. High blood pressure affects between 16 and 37% of the population globally. In 2010 hypertension was believed to have been a factor in 18% of all deaths (9.4 million globally).

Signs and symptoms
Hypertension is rarely accompanied by symptoms, and its identification is usually through screening, or when seeking healthcare for an unrelated problem. Some people with high blood pressure report headaches (particularly at the back of the head and in the morning), as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes. These symptoms, however, might be related to associated anxiety rather than the high blood pressure itself.On physical examination, hypertension may be associated with the presence of changes in the optic fundus seen by  ophthalmoscopy. The severity of the changes typical of hypertensive retinopathy is graded from I to IV; grades I and II may be difficult to differentiate. The severity of the retinopathy correlates roughly with the duration or the severity of the hypertension.

Secondary hypertension
Secondary hypertension is hypertension due to an identifiable cause, and may result in certain specific additional signs and symptoms. For example, as well as causing high blood pressure, Cushings syndrome frequently causes truncal obesity, glucose intolerance, moon face, a hump of fat behind the neck and shoulders (referred to as a buffalo hump), and purple abdominal stretch marks. Hyperthyroidism frequently causes weight loss with increased appetite, fast heart rate, bulging eyes, and tremor. Renal artery stenosis (RAS) may be associated with a localized abdominal bruit to the left or right of the midline (unilateral RAS), or in both locations (bilateral RAS). Coarctation of the aorta frequently causes a decreased blood pressure in the lower extremities relative to the arms, or delayed or absent femoral arterial pulses. Pheochromocytoma may cause abrupt episodes of hypertension accompanied by headache, palpitations, pale appearance, and excessive sweating.

Hypertensive crisis
Severely elevated blood pressure (equal to or greater than a systolic 180 or diastolic of 110) is referred to as a hypertensive crisis. Hypertensive crisis is categorized as either hypertensive urgency or hypertensive emergency, according to the absence or presence of end organ damage, respectively.In hypertensive urgency, there is no evidence of end organ damage resulting from the elevated blood pressure. In these cases, oral medications are used to lower the BP gradually over 24 to 48 hours.In hypertensive emergency, there is evidence of direct damage to one or more organs. The most affected organs include the brain, kidney, heart and lungs, producing symptoms which may include confusion, drowsiness, chest pain and breathlessness. In hypertensive emergency, the blood pressure must be reduced more rapidly to stop ongoing organ damage, however, there is a lack of randomized controlled trial evidence for this approach.

Pregnancy
Hypertension occurs in approximately 8–10% of pregnancies. Two blood pressure measurements six hours apart of greater than 140/90 mm Hg are diagnostic of hypertension in pregnancy. High blood pressure in pregnancy can be classified as pre-existing hypertension, gestational hypertension, or pre-eclampsia.Pre-eclampsia is a serious condition of the second half of pregnancy and following delivery characterised by increased blood pressure and the presence of protein in the urine. It occurs in about 5% of pregnancies and is responsible for approximately 16% of all maternal deaths globally. Pre-eclampsia also doubles the risk of death of the baby around the time of birth. Usually there are no symptoms in pre-eclampsia and it is detected by routine screening. When symptoms of pre-eclampsia occur the most common are headache, visual disturbance (often "flashing lights"), vomiting, pain over the stomach, and swelling. Pre-eclampsia can occasionally progress to a life-threatening condition called eclampsia, which is a hypertensive emergency and has several serious complications including vision loss, brain swelling, seizures, kidney failure, pulmonary edema, and disseminated intravascular coagulation (a blood clotting disorder).In contrast, gestational hypertension is defined as new-onset hypertension during pregnancy without protein in the urine.

Children
Failure to thrive, seizures, irritability, lack of energy, and difficulty in breathing can be associated with hypertension in newborns and young infants. In older infants and children, hypertension can cause headache, unexplained irritability, fatigue, failure to thrive, blurred vision, nosebleeds, and facial paralysis.

Causes
Primary hypertension
Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified as well as some rare genetic variants with large effects on blood pressure. Also, genome-wide association studies (GWAS) have identified 35 genetic loci related to blood pressure; 12 of these genetic loci influencing blood pressure were newly found. Sentinel SNP for each new genetic locus identified has shown an association with DNA methylation at multiple nearby CpG sites. These sentinel SNP are located within genes related to vascular smooth muscle and renal function. DNA methylation might affect in some way linking common genetic variation to multiple phenotypes even though mechanisms underlying these associations are not understood. Single variant test performed in this study for the 35 sentinel SNP (known and new) showed that genetic variants singly or in aggregate contribute to risk of clinical phenotypes related to high blood pressure.Blood pressure rises with aging when associated with a western diet and lifestyle and the risk of becoming hypertensive in later life is significant. Several environmental factors influence blood pressure. High salt intake raises the blood pressure in salt sensitive individuals; lack of exercise, central obesity can play a role in individual cases. The possible roles of other factors such as caffeine consumption, and vitamin D deficiency are less clear. Insulin resistance, which is common in obesity and is a component of syndrome X (or the metabolic syndrome), also contributes to hypertension.Events in early life, such as low birth weight, maternal smoking, and lack of breastfeeding may be risk factors for adult essential hypertension, although the mechanisms linking these exposures to adult hypertension remain unclear. An increased rate of high blood uric acid has been found in untreated people with hypertension in comparison with people with normal blood pressure, although it is uncertain whether the former plays a causal role or is subsidiary to poor kidney function. Average blood pressure may be higher in the winter than in the summer. Periodontal disease is also associated with high blood pressure.

Secondary hypertension
Secondary hypertension results from an identifiable cause. Kidney disease is the most common secondary cause of hypertension. Hypertension can also be caused by endocrine conditions, such as Cushings syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conns syndrome or hyperaldosteronism, renal artery stenosis (from atherosclerosis or fibromuscular dysplasia), hyperparathyroidism, and pheochromocytoma. Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta, excessive eating of liquorice, excessive drinking of alcohol, certain prescription medicines, herbal remedies, and stimulants such as coffee, cocaine and methamphetamine. Arsenic exposure through drinking water has been shown to correlate with elevated blood pressure. Depression was also linked to hypertension. Loneliness is also a risk factor.A 2018 review found that any alcohol increased blood pressure in males while over one or two drinks increased the risk in females.

Pathophysiology
In most people with established essential hypertension, increased resistance to blood flow (total peripheral resistance) accounts for the high pressure while cardiac output remains normal. There is evidence that some younger people with prehypertension or borderline hypertension have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension. These individuals develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age. Whether this pattern is typical of all people who ultimately develop hypertension is disputed. The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles, although a reduction in the number or density of capillaries may also contribute.It is not clear whether or not vasoconstriction of arteriolar blood vessels plays a role in hypertension. Hypertension is also associated with decreased peripheral venous compliance which may increase venous return, increase cardiac preload and, ultimately, cause diastolic dysfunction.
Pulse pressure (the difference between systolic and diastolic blood pressure) is frequently increased in older people with hypertension. This can mean that systolic pressure is abnormally high, but diastolic pressure may be normal or low, a condition termed isolated systolic hypertension. The high pulse pressure in elderly people with hypertension or isolated systolic hypertension is explained by increased arterial stiffness, which typically accompanies aging and may be exacerbated by high blood pressure.Many mechanisms have been proposed to account for the rise in peripheral resistance in hypertension. Most evidence implicates either disturbances in the kidneys salt and water handling (particularly abnormalities in the intrarenal renin–angiotensin system) or abnormalities of the sympathetic nervous system. These mechanisms are not mutually exclusive and it is likely that both contribute to some extent in most cases of essential hypertension. It has also been suggested that endothelial dysfunction and vascular inflammation may also contribute to increased peripheral resistance and vascular damage in hypertension. Interleukin 17 has garnered interest for its role in increasing the production of several other immune system chemical signals thought to be involved in hypertension such as tumor necrosis factor alpha, interleukin 1, interleukin 6, and interleukin 8.Excessive sodium or insufficient potassium in the diet leads to excessive intracellular sodium, which contracts vascular smooth muscle, restricting blood flow and so increases blood pressure.

Diagnosis
Hypertension is diagnosed on the basis of a persistently high resting blood pressure. The American Heart Association (AHA) recommends at least three resting measurements on at least two separate health care visits. The UK National Institute for Health and Care Excellence recommends ambulatory blood pressure monitoring to confirm the diagnosis of hypertension if a clinic blood pressure is 140/90 mmHg or higher.

Measurement technique
For an accurate diagnosis of hypertension to be made, it is essential for proper blood pressure measurement technique to be used. Improper measurement of blood pressure is common and can change the blood pressure reading by up to 10 mmHg, which can lead to misdiagnosis and misclassification of hypertension. Correct blood pressure measurement technique involves several steps. Proper blood pressure measurement requires the person whose blood pressure is being measured to sit quietly for at least five minutes which is then followed by application of a properly fitted blood pressure cuff to a bare upper arm. The person should be seated with their back supported, feet flat on the floor, and with their legs uncrossed. The person whose blood pressure is being measured should avoid talking or moving during this process. The arm being measured should be supported on a flat surface at the level of the heart. Blood pressure measurement should be done in a quiet room so the medical professional checking the blood pressure can hear the Korotkoff sounds while listening to the brachial artery with a stethoscope for accurate blood pressure measurements. The blood pressure cuff should be deflated slowly (2–3 mmHg per second) while listening for the Korotkoff sounds. The bladder should be emptied before a persons blood pressure is measured since this can increase blood pressure by up to 15/10 mmHg. Multiple blood pressure readings (at least two) spaced 1–2 minutes apart should be obtained to ensure accuracy. Ambulatory blood pressure monitoring over 12 to 24 hours is the most accurate method to confirm the diagnosis. An exception to this is those with very high blood pressure readings especially when there is poor organ function.With the availability of 24-hour ambulatory blood pressure monitors and home blood pressure machines, the importance of not wrongly diagnosing those who have white coat hypertension has led to a change in protocols. In the United Kingdom, current best practice is to follow up a single raised clinic reading with ambulatory measurement, or less ideally with home blood pressure monitoring over the course of 7 days. The United States Preventive Services Task Force also recommends getting measurements outside of the healthcare environment. Pseudohypertension in the elderly or noncompressibility artery syndrome may also require consideration. This condition is believed to be due to calcification of the arteries resulting in abnormally high blood pressure readings with a blood pressure cuff while intra arterial measurements of blood pressure are normal. Orthostatic hypertension is when blood pressure increases upon standing.

Other investigations
Once the diagnosis of hypertension has been made, healthcare providers should attempt to identify the underlying cause based on risk factors and other symptoms, if present. Secondary hypertension is more common in preadolescent children, with most cases caused by kidney disease. Primary or essential hypertension is more common in adolescents and adults and has multiple risk factors, including obesity and a family history of hypertension. Laboratory tests can also be performed to identify possible causes of secondary hypertension, and to determine whether hypertension has caused damage to the heart, eyes, and kidneys. Additional tests for diabetes and high cholesterol levels are usually performed because these conditions are additional risk factors for the development of heart disease and may require treatment.Initial assessment of the hypertensive people should include a complete history and physical examination. Serum creatinine is measured to assess for the presence of kidney disease, which can be either the cause or the result of hypertension. Serum creatinine alone may overestimate glomerular filtration rate and recent guidelines advocate the use of predictive equations such as the Modification of Diet in Renal Disease (MDRD) formula to estimate glomerular filtration rate (eGFR). eGFR can also provide a baseline measurement of kidney function that can be used to monitor for side effects of certain anti-hypertensive drugs on kidney function. Additionally, testing of urine samples for protein is used as a secondary indicator of kidney disease. Electrocardiogram (EKG/ECG) testing is done to check for evidence that the heart is under strain from high blood pressure. It may also show whether there is thickening of the heart muscle (left ventricular hypertrophy) or whether the heart has experienced a prior minor disturbance such as a silent heart attack. A chest X-ray or an echocardiogram may also be performed to look for signs of heart enlargement or damage to the heart.

Classification in adults
In people aged 18 years or older hypertension is defined as either a systolic or a diastolic blood pressure measurement consistently higher than an accepted normal value (this is above 129 or 139 mmHg systolic, 89 mmHg diastolic depending on the guideline). Other thresholds are used (135 mmHg systolic or 85 mmHg diastolic) if measurements are derived from 24-hour ambulatory or home monitoring. Recent international hypertension guidelines have also created categories below the hypertensive range to indicate a continuum of risk with higher blood pressures in the normal range. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC7) published in 2003 uses the term prehypertension for blood pressure in the range 120–139 mmHg systolic or 80–89 mmHg diastolic, while European Society of Hypertension Guidelines (2007) and British Hypertension Society (BHS) IV (2004) use optimal, normal and high normal categories to subdivide pressures below 140 mmHg systolic and 90 mmHg diastolic. Hypertension is also sub-classified: JNC7 distinguishes hypertension stage I, hypertension stage II, and isolated systolic hypertension. Isolated systolic hypertension refers to elevated systolic pressure with normal diastolic pressure and is common in the elderly. The ESH-ESC Guidelines (2007) and BHS IV (2004) additionally define a third stage (stage III hypertension) for people with systolic blood pressure exceeding 179 mmHg or a diastolic pressure over 109 mmHg. Hypertension is classified as "resistant" if medications do not reduce blood pressure to normal levels. In November 2017, the American Heart Association and American College of Cardiology published a joint guideline which updates the recommendations of the JNC7 report. The 2020 International Society of Hypertension guidelines define hypertension based on office blood pressure ≥140/90 mmHg or home monitoring blood pressure ≥135/85 mmHg, or 24-hour ambulatory blood pressure average ≥130/80 mmHg (daytime average ≥135/85 mmHg or nighttime average BP ≥120/70 mmHg).

Children
Hypertension occurs in around 0.2 to 3% of newborns; however, blood pressure is not measured routinely in healthy newborns. Hypertension is more common in high risk newborns. A variety of factors, such as gestational age, postconceptional age and birth weight needs to be taken into account when deciding if a blood pressure is normal in a newborn.Hypertension defined as elevated blood pressure over several visits affects 1% to 5% of children and adolescents and is associated with long-term risks of ill-health. Blood pressure rises with age in childhood and, in children, hypertension is defined as an average systolic or diastolic blood pressure on three or more occasions equal or higher than the 95th percentile appropriate for the sex, age and height of the child. High blood pressure must be confirmed on repeated visits however before characterizing a child as having hypertension. Prehypertension in children has been defined as average systolic or diastolic blood pressure that is greater than or equal to the 90th percentile, but less than the 95th percentile. In adolescents, it has been proposed that hypertension and pre-hypertension are diagnosed and classified using the same criteria as in adults.The value of routine screening for hypertension in children over the age of 3 years is debated. In 2004 the National High Blood Pressure Education Program recommended that children aged 3 years and older have blood pressure measurement at
least once at every health care visit and the National Heart, Lung, and Blood Institute and American Academy of Pediatrics made a similar recommendation. However, the American Academy of Family Physicians supports the view of the U.S. Preventive Services Task Force that the available evidence is insufficient to determine the balance of benefits and harms of screening for hypertension in children and adolescents who do not have symptoms.

Prevention
Much of the disease burden of high blood pressure is experienced by people who are not labeled as hypertensive. Consequently, population strategies are required to reduce the consequences of high blood pressure and reduce the need for antihypertensive medications. Lifestyle changes are recommended to lower blood pressure, before starting medications. The 2004 British Hypertension Society guidelines proposed lifestyle changes consistent with those outlined by the US National High BP Education Program in 2002 for the primary prevention of hypertension:

maintain normal body weight for adults (e.g. body mass index 20–25 kg/m2)
reduce dietary sodium intake to <100 mmol/ day (<6 g of sodium chloride or <2.4 g of sodium per day)
engage in regular aerobic physical activity such as brisk walking (≥30 min per day, most days of the week)
limit alcohol consumption to no more than 3 units/day in men and no more than 2 units/day in women
consume a diet rich in fruit and vegetables (e.g. at least five portions per day);
Stress reductionAvoiding or learning to manage stress can help a person control blood pressure.
A few relaxation techniques that can help relieve stress are:

meditation
warm baths
yoga
going on long walksEffective lifestyle modification may lower blood pressure as much as an individual antihypertensive medication. Combinations of two or more lifestyle modifications can achieve even better results. There is considerable evidence that reducing dietary salt intake lowers blood pressure, but whether this translates into a reduction in mortality and cardiovascular disease remains uncertain. Estimated sodium intake ≥6g/day and <3g/day are both associated with high risk of death or major cardiovascular disease, but the association between high sodium intake and adverse outcomes is only observed in people with hypertension. Consequently, in the absence of results from randomized controlled trials, the wisdom of reducing levels of dietary salt intake below 3g/day has been questioned. ESC guidelines mention periodontitis is associated with poor cardiovascular health status.

Management
According to one review published in 2003, reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34%, of ischemic heart disease by 21%, and reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease.

Target blood pressure
Various expert groups have produced guidelines regarding how low the blood pressure target should be when a person is treated for hypertension. These groups recommend a target below the range 140–160 / 90–100 mmHg for the general population. Cochrane reviews recommend similar targets for subgroups such as people with diabetes and people with prior cardiovascular disease.  Additionally, Cochrane reviews have found that for older individuals with moderate to high cardiovascular risk, the benefits of trying to achieve a lower than standard blood pressure target (at or below 140/90 mmHg) are outweighed by the risk associated with the intervention.  These findings may not be applicable to other populations.Many expert groups recommend a slightly higher target of 150/90 mmHg for those over somewhere between 60 and 80 years of age. The JNC-8 and American College of Physicians recommend the target of 150/90 mmHg for those over 60 years of age, but some experts within these groups disagree with this recommendation. Some expert groups have also recommended slightly lower targets in those with diabetes or chronic kidney disease with protein loss in the urine, but others recommend the same target as for the general population. The issue of what is the best target and whether targets should differ for high risk individuals is unresolved, although some experts propose more intensive blood pressure lowering than advocated in some guidelines.For people who have never experienced cardiovascular disease who are at a 10-year risk of cardiovascular disease of less than 10%, the 2017 American Heart Association guidelines recommend medications if the systolic blood pressure is >140 mmHg or if the diastolic BP is >90 mmHg. For people who have experienced cardiovascular disease or those who are at a 10-year risk of cardiovascular disease of greater than 10%, it recommends medications if the systolic blood pressure is >130 mmHg or if the diastolic BP is >80 mmHg.

Lifestyle modifications
The first line of treatment for hypertension is lifestyle changes, including dietary changes, physical exercise, and weight loss. Though these have all been recommended in scientific advisories, a  Cochrane systematic review found no evidence for effects of weight loss diets on death, long-term complications or adverse events in persons with hypertension. The review did find a decrease in body weight and blood pressure. Their potential effectiveness is similar to and at times exceeds a single medication. If hypertension is high enough to justify immediate use of medications, lifestyle changes are still recommended in conjunction with medication.
Dietary changes shown to reduce blood pressure include diets with low sodium, the DASH diet (Dietary Approaches to Stop Hypertension), and plant-based diets. There is some evidence green tea consumption may help lower blood pressure, but this is insufficient for it to be recommended as a treatment. There is evidence from randomized, double-blind, placebo-controlled clinical trials that Hibiscus tea consumption significantly reduces systolic blood pressure (-4.71 mmHg, 95% CI [-7.87, -1.55]) and diastolic blood pressure (-4.08 mmHg, 95% CI [-6.48, -1.67]). Beetroot juice consumption also significantly lowers the blood pressure of people with high blood pressure.Increasing dietary potassium has a potential benefit for lowering the risk of hypertension. The 2015 Dietary Guidelines Advisory Committee (DGAC) stated that potassium is one of the shortfall nutrients which is under-consumed in the United States. However, people who take certain antihypertensive medications (such as ACE-inhibitors or ARBs) should not take potassium supplements or potassium-enriched salts due to the risk of high levels of potassium.Physical exercise regimens which are shown to reduce blood pressure include isometric resistance exercise, aerobic exercise, resistance exercise, and device-guided breathing.Stress reduction techniques such as biofeedback or transcendental meditation may be considered as an add-on to other treatments to reduce hypertension, but do not have evidence for preventing cardiovascular disease on their own. Self-monitoring and appointment reminders might support the use of other strategies to improve blood pressure control, but need further evaluation.

Medications
Several classes of medications, collectively referred to as antihypertensive medications, are available for treating hypertension.
First-line medications for hypertension include thiazide-diuretics, calcium channel blockers, angiotensin converting enzyme inhibitors (ACE inhibitors), and angiotensin receptor blockers (ARBs). These medications may be used alone or in combination (ACE inhibitors and ARBs are not recommended for use in combination); the latter option may serve to minimize counter-regulatory mechanisms that act to restore blood pressure values to pre-treatment levels. Most people require more than one medication to control their hypertension. Medications for blood pressure control should be implemented by a stepped care approach when target levels are not reached.Previously beta-blockers such as atenolol were thought to have similar beneficial effects when used as first-line therapy for hypertension. However, a Cochrane review that included 13 trials found that the effects of beta-blockers are inferior to that of other antihypertensive medications in preventing cardiovascular disease.

Resistant hypertension
Resistant hypertension is defined as high blood pressure that remains above a target level, in spite of being prescribed three or more antihypertensive drugs simultaneously with different mechanisms of action. Failing to take prescribed medications as directed is an important cause of resistant hypertension. Resistant hypertension may also result from chronically high activity of the autonomic nervous system, an effect known as neurogenic hypertension. Electrical therapies that stimulate the baroreflex are being studied as an option for lowering blood pressure in people in this situation.Some common secondary causes of resistant hypertension include obstructive sleep apnea, pheochromocytoma, renal artery stenosis, coarctation of the aorta, and primary aldosteronism.  As many as one in five people with resistant hypertension have primary aldosteronism, which is a treatable and sometimes curable condition.

Refractory hypertension
Refractory hypertension is characterized by uncontrolled elevated blood pressure unmitigated by five or more antihypertensive agents of different classes, including a long-acting thiazide-like diuretic, a calcium channel blocker, and a blocker of the renin-angiotensin system. People with refractory hypertension typically have increased sympathetic nervous system activity, and are at high risk for more severe cardiovascular diseases and all-cause mortality.

Non-modulating
Non-modulating essential hypertension is a form of salt-sensitive hypertension, where sodium intake does not modulate either adrenal or renal vascular responses to angiotensin II. Individuals with this subset have been termed non-modulators. They make up 25–30% of the hypertensive population.

Epidemiology
Adults
As of 2014, approximately one billion adults or ~22% of the population of the world have hypertension. It is slightly more frequent in men, in those of low socioeconomic status, and it becomes more common with age. It is common in high, medium, and low income countries. In 2004 rates of high blood pressure were highest in Africa, (30% for both sexes) and lowest in the Americas (18% for both sexes). Rates also vary markedly within regions with rates as low as 3.4% (men) and 6.8% (women) in rural India and as high as 68.9% (men) and 72.5% (women) in Poland. Rates in Africa were about 45% in 2016.In Europe hypertension occurs in about 30–45% of people as of 2013. In 1995 it was estimated that 43 million people (24% of the population) in the United States had hypertension or were taking antihypertensive medication. By 2004 this had increased to 29% and further to 32% (76 million US adults) by 2017. In 2017, with the change in definitions for hypertension, 46% of people in the United States are affected. African-American adults in the United States have among the highest rates of hypertension in the world at 44%. It is also more common in Filipino Americans and less common in US whites and Mexican Americans. Differences in hypertension rates are multifactorial and under study.

Children
Rates of high blood pressure in children and adolescents have increased in the last 20 years in the United States. Childhood hypertension, particularly in pre-adolescents, is more often secondary to an underlying disorder than in adults. Kidney disease is the most common secondary cause of hypertension in children and adolescents. Nevertheless, primary or essential hypertension accounts for most cases.

Prognosis
Hypertension is the most important preventable risk factor for premature death worldwide. It increases the risk of ischemic heart disease, strokes, peripheral vascular disease, and other cardiovascular diseases, including heart failure, aortic aneurysms, diffuse atherosclerosis, chronic kidney disease, atrial fibrillation, cancers, leukemia and pulmonary embolism. Hypertension is also a risk factor for cognitive impairment and dementia. Other complications include hypertensive retinopathy and hypertensive nephropathy.

History
Measurement
Modern understanding of the cardiovascular system began with the work of physician William Harvey (1578–1657), who described the circulation of blood in his book "De motu cordis". The English clergyman Stephen Hales made the first published measurement of blood pressure in 1733.  However, hypertension as a clinical entity came into its own with the invention of the cuff-based sphygmomanometer by Scipione Riva-Rocci in 1896. This allowed easy measurement of systolic pressure in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is ausculted with a stethoscope while the sphygmomanometer cuff is deflated. This permitted systolic and diastolic pressure to be measured.

Identification
The symptoms similar to symptoms of patients with hypertensive crisis are discussed in medieval Persian medical texts in the chapter of "fullness disease". The symptoms include headache, heaviness in the head, sluggish movements, general redness and warm to touch feel of the body, prominent, distended and tense vessels, fullness of the pulse, distension of the skin, coloured and dense urine, loss of appetite, weak eyesight, impairment of thinking, yawning, drowsiness, vascular rupture, and hemorrhagic stroke. Fullness disease was presumed to be due to an excessive amount of blood within the blood vessels.
Descriptions of hypertension as a disease came among others from Thomas Young in 1808 and especially Richard Bright in 1836. The first report of elevated blood pressure in a person without evidence of kidney disease was made by Frederick Akbar Mahomed (1849–1884).

Treatment
Historically the treatment for what was called the "hard pulse disease" consisted in reducing the quantity of blood by bloodletting or the application of leeches. This was advocated by The Yellow Emperor of China, Cornelius Celsus, Galen, and Hippocrates.  The therapeutic approach for the treatment of hard pulse disease included changes in lifestyle (staying away from anger and sexual intercourse) and dietary program for patients (avoiding the consumption of wine, meat, and pastries, reducing the volume of food in a meal, maintaining a low-energy diet and the dietary usage of spinach and vinegar).
In the 19th and 20th centuries, before effective pharmacological treatment for hypertension became possible, three treatment modalities were used, all with numerous side-effects: strict sodium restriction (for example the rice diet), sympathectomy (surgical ablation of parts of the sympathetic nervous system), and pyrogen therapy (injection of substances that caused a fever, indirectly reducing blood pressure).The first chemical for hypertension, sodium thiocyanate, was used in 1900 but had many side effects and was unpopular. Several other agents were developed after the Second World War, the most popular and reasonably effective of which were tetramethylammonium chloride, hexamethonium, hydralazine, and reserpine (derived from the medicinal plant Rauvolfia serpentina). None of these were well tolerated. A major breakthrough was achieved with the discovery of the first well-tolerated orally available agents. The first was chlorothiazide, the first thiazide diuretic and developed from the antibiotic sulfanilamide, which became available in 1958. Subsequently, beta blockers, calcium channel blockers, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and renin inhibitors were developed as antihypertensive agents.

Society and culture
Awareness
The World Health Organization has identified hypertension, or high blood pressure, as the leading cause of cardiovascular mortality. The World Hypertension League (WHL), an umbrella organization of 85 national hypertension societies and leagues, recognized that more than 50% of the hypertensive population worldwide are unaware of their condition. To address this problem, the WHL initiated a global awareness campaign on hypertension in 2005 and dedicated May 17 of each year as World Hypertension Day (WHD). Over the past three years, more national societies have been engaging in WHD and have been innovative in their activities to get the message to the public. In 2007, there was record participation from 47 member countries of the WHL. During the week of WHD, all these countries – in partnership with their local governments, professional societies, nongovernmental organizations and private industries – promoted hypertension awareness among the public through several media and public rallies. Using mass media such as Internet and television, the message reached more than 250 million people </s>


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<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Central centrifugal cicatricial alopecia and can you explain it in depth? [/INST] Central centrifugal cicatricial alopecia (CCCA), is a type of alopecia first noticed in African Americans in the 1950s and reported by LoPresti et al. in  1968 as a result of application of petrolatum followed by a stove-heated iron comb. The original theory was that the hot petrolatum would travel down to the hair root, burn the follicle, and after repetitive injury scarring would result. Later CCCA was realized to affect men and women without a history significant for use of such styling techniques. Consequently, the terms "follicular degeneration syndrome" per Sperling and Sau in 1992 and then CCCA per Olsent et al. in 2003 were evolved.  Plausible contributing factors may include other African-American styling techniques such as relaxers, tight braids, heavy extensions, certain oils, gels or pomades.

Presentation
CCCA usually begins at the central (sagittal) midline of the scalp. It is symmetric and exhibits scarring as the name suggests. It involves solely the top of the scalp or may progress to Hamilton–Norwood scale Type VI or VII. Early symptoms may include pruritus, dysesthesias and tenderness. On examination the skin is thin with few follicular ostia and later in the disease the scalp may appear shiny.

Cause
The mechanism of pathology of CCCA remains unknown; thus, the cause has only been postulated and not proven.  CCCA is suspected to have a multi-factored cause. However, one theory involves pressure exerted on the internal root sheath leading to damage, which leads to the recruitment of inflammatory cells and the result of scarring. African Americans are found to be at increased risk. Historically, some have hypothesized that CCCA represents an end stage of traction alopecia. However, the veracity of this theory is low as many patients who have CCCA have not employed traction hairstyling.

Histopathologic features
Histopathologic features include a perifollicular lymphocytic infiltrate, concentric lamellar fibrosis (layers of fibroblasts in the papillary dermis), sebaceous gland loss and premature disintegration of the internal root sheath. Additionally, granulomatous inflammation secondary to follicular rupture has been noted. Perifollicular erythema and follicular keratosis is usually absent.

Treatment
Treatments for CCCA remain investigational. Altering hair care practices has not been proven to assist in hair rejuvenation. High-dose topical steroids, antibiotics, immunomodulators such as tacrolimus (Protopic) and pimecrolimus (Elidel), and anti-androgen/5alpha Reductase inhibitors have been used with unknown efficacy.: 648–9 : 760

Epidemiology
CCCA tends to present itself in the 20s and progresses over 20–30 years. One should consider this diagnosis in African Americans with what appears to be a female-pattern hair loss.

Terminology
The terminology of CCCA has been a source of regular confusion. Recent clarifications have been made, with the term "central centrifugal cicatritial alopecia" adopted as a diagnostic category by the North American Hair Research Society </s>


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<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Jugular foramen syndrome and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is High-altitude pulmonary edema and can you explain it in depth? [/INST] High-altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). However, cases have also been reported between 1,500–2,500 metres or 4,900–8,200 feet in more vulnerable subjects.
Classically, HAPE occurs in persons normally living at low altitude who travel to an altitude above 2,500 meters (8,200 feet). Re-entry HAPE is also an entity that has been described in persons who normally live at high altitude but who develop pulmonary edema after returning from a stay at low altitude. It is severe presentation of altitude sickness.
There are many factors that can make a person more susceptible to developing HAPE, including genetic factors, but detailed understanding is lacking and currently under investigation. HAPE remains the major cause of death related to high-altitude exposure, with a high mortality rate in the absence of adequate emergency treatment.

Signs and symptoms
Physiological and symptomatic changes often vary according to the altitude involved.The Lake Louise Consensus Definition for high-altitude pulmonary edema has set widely used criteria for defining HAPE symptoms.In the presence of a recent gain in altitude, the presence of the following:
Symptoms: at least two of:

Shortness of breath at rest
Cough
Weakness or decreased exercise performance
Chest tightness or congestionSigns: at least two of:

Crackles or wheezing (while breathing) in at least one lung field
Central blue skin color
Tachypnea (rapid breathing)
Tachycardia (rapid heart rate)Acute mountain sickness and high altitude cerebral edema may also be present in conjunction with HAPE, however these symptoms may be subtle or not present at all. The most reliable sign of HAPE is severe fatigue or exercise intolerance, especially in a climber that was previously not displaying this symptom.

Risk factors
There are multiple factors that can contribute to the development of HAPE, including sex (male), genetic factors, prior development of HAPE, ascent rate, cold exposure, peak altitude, intensity of physical exertion, and certain underlying medical conditions (e.g., pulmonary hypertension). Anatomic abnormalities that are predisposing include congenital absence of pulmonary artery, and left-to-right intracardiac shunts (e.g., atrial and ventricular septal defects), both of which increase pulmonary blood flow. HAPE-susceptible (HAPE-s) individuals were also found to be four times more likely to have a patent foramen ovale (PFO) than those who were HAPE-resistant. There is currently no indication or recommendation for people with PFO to pursue closure prior to extreme altitude exposure.In studies performed at sea level, HAPE-s people were found to have exaggerated circulatory response to both hypoxia at rest and during exercise. In these individuals, the pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) were shown to be abnormally high. Microneurographic recordings in these individuals developed a direct link between PAP rise and sympathetic nervous system over-activation, which could explain the exaggerated response to hypoxia in these persons.Endothelial tissue dysfunction has also been linked to development of HAPE, including reduced synthesis of NO (a potent vasodilator), increased levels of endothelin (a potent vasconstrictor), and an impaired ability to transport sodium and water across the epithelium and out of the alveoli.Data on the genetic basis for HAPE susceptibility is conflicting and interpretation is difficult. Genes implicated in the development of HAPE include those in the renin-angiotensin system (RAS), NO pathway, and hypoxia-inducible factor pathway (HIF). Future genomic testing could provide a clearer picture of the genetic factors that contribute to HAPE.

Pathophysiology
Though it remains a topic of intense investigation, multiple studies and reviews over the last several years have helped to elucidate the proposed mechanism of HAPE. The inciting factor of HAPE is the decrease in partial pressure of arterial oxygen caused by the lower air pressure at high altitudes (pulmonary gas pressures). The resultant hypoxemia is then thought to precipitate the development of:

Increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction.
Increased capillary pressure (hydrostatic pressure) with over-distention of the capillary beds and increased permeability of the vascular endothelium, also known as "stress failure." This leads to subsequent leakage of cells and proteins into the alveoli, aka pulmonary edema.Hypoxic pulmonary vasoconstriction (HPV) occurs diffusely, leading to arterial vasoconstriction in all areas of the lung. This is evidenced by the appearance of "diffuse," "fluffy," and "patchy" infiltrates described on imaging studies of climbers with known HAPE.Although higher pulmonary arterial pressures are associated with the development of HAPE, the presence of pulmonary hypertension may not in itself be sufficient to explain the development of edema; severe pulmonary hypertension can exist in the absence of clinical HAPE in subjects at high altitude.

Diagnosis
The diagnosis of HAPE is entirely based on symptoms and many of the symptoms overlap with other diagnoses. Before HAPE was understood it was commonly confused with pneumonia which resulted in inappropriate treatment.HAPE generally develops in the first 2 to 4 days of hiking at altitudes >2,500 meters (8,200 ft), and symptoms seem to worsen most commonly on the second night. Initial symptoms are vague and include shortness of breath, decreased exercise ability, increased recovery time, fatigue, and weakness, especially with walking uphill. People then develop a dry, persistent cough, and often cyanosis of the lips. Another cardinal feature of HAPE is the rapid progression to dyspnea at rest. The development of pink, frothy, or frankly bloody sputum are late features of HAPE. In some cases, people will develop concomitant neurological features such as poor coordination, altered consciousness, or cerebral edema (High-altitude cerebral edema).On physical exam, increased breathing rates, increased heart rates, and a low-grade fever 38.5o (101.3o F) are common. Listening to the lungs may reveal crackles in one or both lungs, often starting in the right middle lobe. Imaging studies such as X-ray and CT imaging of the chest may reveal thoracic infiltrates that can be seen as opaque patches. One distinct feature of HAPE is that pulse oximetry saturation levels (SpO2) are often decreased from what would be expected for the altitude. People typically do not appear as ill as SpO2 and chest X-ray films would suggest. Giving extra oxygen rapidly improves symptoms and SpO2 values; in the setting of infiltrative changes on chest X-ray, this is nearly pathognomonic for HAPE.

Severity
The severity of HAPE is graded. The grades of mild, moderate, or severe HAPE are assigned based upon symptoms, clinical signs, and chest x-ray results for individuals. The symptoms that are taken in to account while evaluation the severity of HAPE are difficulty breathing while exerting or while at rest, the presence of a cough and the quality of that cough, and the level of fatigue of the patient. On physical exam of a suspected HAPE patient the exam findings used to grade the severity are the heart rate, respiratory rate, signs of cyanosis, and severity of lung sounds. Both symptoms and signs on physical exam can be used to evaluate a patient in the field. Chest X-rays are also used to evaluate the severity of HAPE when they are available.

Differential diagnosis
Differential diagnosis:
Pneumonia
Bronchitis
Mucous plugging
Pulmonary embolism
Acute coronary syndrome
Acute decompensated heart failure
Asthma
Reactive airway disease
Exercise-associated hyponatremia
Pneumothorax

Prevention
The primary recommendation for the prevention of HAPE is gradual ascent. The suggested rate of ascent is the same that applies to the prevention of acute mountain sickness and high-altitude cerebral edema.
The Wilderness Medical Society (WMS) recommends that, above 3,000 metres (9,800 ft), climbers

not increase the sleeping elevation by more than 500 metres (1,600 ft) a day, and
include a rest day every 3–4 days (i.e., no additional ascent).In the event that adherence to these recommendations is limited by terrain or logistical factors, the WMS recommends rest days either before or after days with large gains. Overall, WMS recommends that the average ascent rate of the entire trip be less than 500 metres (1,600 ft) per day.The most studied and preferred medication for prevention of HAPE is nifedipine, a pulmonary vasodilator which prevents the altitude induced pulmonary hypertension. The recommendation for its use is strongest for individuals with a history of HAPE. According to published data, treatment is most effective if given one day prior to ascent and continued for four to five days, or until descent below 2,500 meters (8,200 ft).Additional medications that are being considered for prevention but require further research to determine efficacy and treatment guidelines include acetazolamide, salmeterol, tadalafil (and other PDE5 inhibitors), and dexamethasone. Acetazolamide has proven to be clinically effective, but formal studies are lacking. Salmeterol is considered an adjunctive therapy to nifedipine, though only in highly susceptible climbers with clearly demonstrated recurrence of HAPE. Tadalafil was found to be effective at preventing HAPE in HAPE-s individuals during rapid ascent, but optimal dosing and frequency has yet to be established. Use of dexamethasone is currently indicated for the treatment of moderate-to-severe acute mountain sickness, as well as high-altitude cerebral edema. It has also been found to prevent HAPE, but its routine use is not yet recommended.Notably, each of these medications acts to block hypoxic pulmonary hypertension, lending evidence to the proposed pathophysiology of HAPE outlined above.It is recommended that those who go to high altitude avoid alcohol or sleeping medications.

Treatment
The recommended first line treatment is descent to a lower altitude as quickly as possible, with symptomatic improvement seen in as few as 500 to 1,000 meters (1,640 feet to 3,281 feet). However, descent is not mandatory in people with mild HAPE and treatment with warming techniques, rest, and supplemental oxygen can improve symptoms. Giving oxygen at flow rates high enough to maintain an SpO2 at or above 90% is a fair substitute for descent. In the hospital setting, oxygen is generally given by nasal cannula or face mask for several hours until the person is able to maintain oxygen saturations above 90% while breathing the surrounding air. In remote settings where resources are scarce and descent is not feasible, a reasonable substitute can be the use of a portable hyperbaric chamber, which simulates descent, combined with additional oxygen and medications.As with prevention, the standard medication once a climber has developed HAPE is nifedipine, although its use is best in combination with and does not substitute for descent, hyperbaric therapy, or oxygen therapy. Though they have not formally been studied for the treatment of HAPE, phosphodiesterase type 5 inhibitors such as sildenafil and tadalafil are also effective and can be considered as add-on treatment if first-line therapy is not possible; however, they may worsen the headache of mountain sickness. There is no established role for the inhaled beta-agonist salmeterol, though its use can be considered.Dexamethasone has a potential role in HAPE, though there are currently no studies to support its effectiveness as treatment. However, as outlined in the 2014 WMS Practice Guidelines, its use is recommended for the treatment of people with concomitant HAPE and HACE at the treatment doses recommended for HACE alone. Additionally, they support its use in HAPE with neurologic symptoms or hypoxic encephalopathy that cannot be distinguished from HACE.

Epidemiology
Rates of HAPE differs depending on altitude and speed of ascent. In general, there is about a 0.2 to 6 percent incidence at 4,500 metres (14,800 ft), and about 2 to 15 percent at 5,500 metres (18,000 ft). The higher incidence of 6% has been seen when climbers ascend at a rate > 600m/day. It has been reported that about 1 in 10,000 skiers who travel to moderate altitudes in Colorado develop HAPE; one study reported 150 cases over 39 months at a Colorado resort located at 2,928 metres (9,606 ft). About 1 in 50 climbers who ascended Denali [6,194 metres or 20,322 feet] developed pulmonary edema, and as high as 6% of climbers ascending rapidly in the Alps [4,559 metres or 14,957 feet] </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Arcus senilis and can you explain it in depth? [/INST] Arcus senilis (AS), also known as gerontoxon, arcus lipoides, arcus cornae, corneal arcus, arcus adiposus, or arcus cornealis, are rings in the peripheral cornea. It‘s usually caused by cholesterol deposits, so it may be a sign of high cholesterol. It is the most common peripheral corneal opacity, and is usually found in the elderly where it is considered a benign condition. When AS is found in patients less than 50 years old it is termed arcus juvenilis. The finding of arcus juvenilis in combination with hyperlipidemia in younger men represents an increased risk for cardiovascular disease.

Pathophysiology
AS is caused by leakage of lipoproteins from limbal capillaries into the corneal stroma </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Trichilemmal carcinoma and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Pilocytic astrocytoma and can you explain it in depth? [/INST] Pilocytic astrocytoma (and its variant pilomyxoid astrocytoma) is a brain tumor that occurs most commonly in children and young adults (in the first 20 years of life). They usually arise in the cerebellum, near the brainstem, in the hypothalamic region, or the optic chiasm, but they may occur in any area where astrocytes are present, including the cerebral hemispheres and the spinal cord. These tumors are usually slow growing and benign, corresponding to WHO malignancy grade 1.

Signs and symptoms
Children affected by pilocytic astrocytoma can present with different symptoms that might include failure to thrive (lack of appropriate weight gain/ weight loss), headache, nausea, vomiting, irritability, torticollis (tilt neck or wry neck), difficulty to coordinate movements, and visual complaints (including nystagmus). The complaints may vary depending on the location and size of the neoplasm. The most common symptoms are associated with increased intracranial pressure due to the size of the tumor mass.

Causes
Pilocytic astrocytoma can be associated with the genetic condition neurofibromatosis type 1  (NF1), and optic nerve gliomas are among the most frequently encountered tumors in patients with this disorder.  The majority of pilocytic astrocytomas, however, arise sporadically - with no evidence of a link to an underlying hereditary predisposition or lifestyle factor. They are associated with genetic alterations in the MAPK/ERK pathway, most frequently a characteristic KIAA1549-BRAF fusion gene.

Diagnosis
Usually – depending on the interview of the patient and after a clinical exam which includes a neurological exam and an ophthalmological exam – a CT scan and/or an MRI scan will be performed to confirm the presence of a tumor.  They are usually easily distinguishable from normal brain structures using these imaging techniques.  A special dye may be injected into a vein before these scans to provide contrast and make tumors easier to identify.  Pilocytic astrocytomas are typically clearly visible on such scans, but it is often difficult to say based on imaging alone what type of tumor is present.
If a tumor is found, it will be necessary for a neurosurgeon to perform a biopsy of it. This involves the removal of a small amount of tumorous tissue, which is then sent to a (neuro)pathologist for examination and staging. The biopsy may take place before surgical removal of the tumor, or the sample may be taken during surgery to remove the bulk of the tumor.

Microscopic appearance
Pilocytic astrocytomas are often cystic tumors, and, if solid, tend to be well-circumscribed.
Under the microscope, the tumor is seen to be composed of bipolar cells with long "hair-like" GFAP-positive processes, giving the designation "pilocytic" (that is, made up of cells that look like fibers when viewed under a microscope).  Some pilocytic astrocytomas may be more fibrillary and dense in composition.  The presence of Rosenthal fibers, eosinophilic granular bodies, and microcysts can often be seen.  Myxoid foci and oligodendroglioma-like cells may also be present, though these are not specific to pilocytic astrocytoma.  Long-standing lesions may show hemosiderin-laden macrophages and calcifications.

Treatment
The most common form of treatment is having the tumor surgically removed.  Complete removal of the tumor will generally allow functional survival for many years </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Salla disease and can you explain it in depth? [/INST] Salla disease (SD) is an autosomal recessive lysosomal storage disease characterized by early physical impairment and intellectual disability. It was first described in 1979, after Salla, a municipality in Finnish Lapland. Salla disease is one of 40 Finnish heritage diseases and affects approximately 130 individuals, mainly from Finland and Sweden.

Presentation
Individuals with Salla disease may present with nystagmus in the first months of life as well as hypotonia, reduced muscle tone and strength, and cognitive impairment </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Impulse-control disorder and can you explain it in depth? [/INST] Impulse-control disorder (ICD) is a class of psychiatric disorders characterized by impulsivity – failure to resist a temptation, an urge, or an impulse; or having the inability to not speak on a thought. Many psychiatric disorders feature impulsivity, including substance-related disorders, behavioral addictions, attention deficit hyperactivity disorder, fetal alcohol spectrum disorders, antisocial personality disorder, borderline personality disorder, conduct disorder and some mood disorders.
The fifth edition of the American Psychiatric Associations Diagnostic and statistical manual of mental disorders (DSM-5) that was published in 2013 includes a new chapter (not in DSM-IV-TR) on disruptive, impulse-control, and conduct disorders covering disorders "characterized by problems in emotional and behavioral self-control". Five behavioral stages characterize impulsivity: an impulse, growing tension, pleasure on acting, relief from the urge, and finally guilt (which may or may not arise).

Types
Disorders characterized by impulsivity that were not categorized elsewhere in the DSM-IV-TR were also included in the category "Impulse-control disorders not elsewhere classified". Trichotillomania (hair-pulling) and skin-picking were moved in DSM-5 to the obsessive-compulsive chapter. Additionally, other disorders not specifically listed in this category are often classed as impulsivity disorders. Terminology was changed in the DSM-V from "Not Otherwise Classified" to "Not Elsewhere Classified".

Sexual compulsion
Sexual compulsion includes an increased urge in sexual behavior and thoughts. This compulsion may also lead to several consequences in the individuals life, including risky partner selection, increased chance for STIs and depression, as well as unwanted pregnancy. There has not yet been a determined estimate of its prevalence due to the secretiveness of the disorder. However, research conducted in the early 1990s in the United States gave prevalence estimates between 5–6% in the U.S. population, with male cases being higher than female.

Internet addiction
The disorder of Internet addiction has only recently been taken into consideration and has been added as a form of ICD. It is characterized by excessive and damaging usage of Internet with increased amount of time spent chatting, web surfing, gambling, shopping or consuming pornography. Excessive and problematic Internet use has been reported across all age, social, economic, and educational ranges. Although initially thought to occur mostly in males, increasing rates have been also observed in females. However, no epidemiological study has been conducted yet to understand its prevalence.

Compulsive shopping
Compulsive shopping or buying is characterized by a frequent irresistible urge to shop even if the purchases are not needed or cannot be afforded. The prevalence of compulsive buying in the U.S. has been estimated to be 2–8% of the general adult population, with 80–95% of these cases being females. The onset is believed to occur in late teens or early twenties and the disorder is considered to be generally chronic.

Pyromania
Pyromania is characterized by impulsive and repetitive urges to deliberately start fires.
Because of its nature, the number of studies performed for fire-setting are understandably limited. However, studies done on children and adolescents with pyromania have reported its prevalence to be between 2.4 and 3.5% in the United States. It has also been observed that the incidence of fire-setting is more common in juvenile and teenage boys than girls of the same age.

Intermittent explosive disorder
Intermittent explosive disorder or IED is a clinical condition of experiencing recurrent aggressive episodes that are out of proportion of any given stressor. Earlier studies reported a prevalence rate between 1–2% in a clinical setting, however a study done by Coccaro and colleagues in 2004 had reported about 11.1% lifetime prevalence and 3.2% one month prevalence in a sample of a moderate number of individuals (n=253). Based on the study, Coccaro and colleagues estimated the prevalence of IED in 1.4 million individuals in the US and 10 million with lifetime IED.

Kleptomania
Kleptomania is characterized by an impulsive urge to steal purely for the sake of gratification.
In the U.S. the presence of kleptomania is unknown but has been estimated at 6 per 1000 individuals. Kleptomania is also thought to be the cause of 5% of annual shoplifting in the U.S. If true, 100,000 arrests are made in the U.S. annually due to kleptomaniac behavior.

Signs and symptoms
The signs and symptoms of impulse-control disorders vary based on the age of the persons with them, the actual type of impulse-control that they are struggling with, the environment in which they are living, and whether they are male or female.

Co-morbidity
Complications of late Parkinsons disease may include a range of impulse-control disorders, including eating, buying, compulsive gambling, sexual behavior, and related behaviors (punding, hobbyism and walkabout). Prevalence studies suggest that ICDs occur in 13.6–36.0% of Parkinsons patients exhibited at least one form of ICD. There is a significant co-occurrence of pathological gambling and personality disorder, and is suggested to be caused partly by their common "genetic vulnerability". The degree of heritability to ICD is similar to other psychiatric disorders including substance use disorder. There has also been found a genetic factor to the development of ICD just as there is for substance use disorder. The risk for subclinical PG in a population is accounted for by the risk of alcohol dependence by about 12–20% genetic and 3–8% environmental factors. There is a high rate of co-morbidity between ADHD and other impulse-control disorders.

Mechanism
Dysfunction of the striatum may prove to be the link between OCD, ICD and SUD. According to research, the impulsiveness that occurs in the later stages of OCD is caused by progressive dysfunction of the ventral striatal circuit. Whereas in case of ICD and SUD, the increased dysfunction of dorsal striatal circuit increases the "ICD and SUD behaviours that are driven by the compulsive processes". OCD and ICD have traditionally been viewed as two very different disorders, the former one is generally driven by the desire to avoid harm whereas the latter one driven "by reward-seeking behaviour". Still, there are certain behaviors similar in both, for example the compulsive actions of ICD patients and the behavior of reward-seeking (for example hoarding) in OCD patients.

Treatment
Impulse-control disorders have two treatment options: psychosocial and pharmacological. Treatment methodology is informed by the presence of comorbid conditions.

Medication
In the case of pathological gambling, along with fluvoxamine, clomipramine has been shown effective in the treatment, with reducing the problems of pathological gambling in a subject by up to 90%. Whereas in trichotillomania, the use of clomipramine has again been found to be effective, fluoxetine has not produced consistent positive results. Fluoxetine, however, has produced positive results in the treatment of pathological skin picking disorder, although more research is needed to conclude this information. Fluoxetine has also been evaluated in treating IED and demonstrated significant improvement in reducing frequency and severity of impulsive aggression and irritability in a sample of 100 subjects who were randomized into a 14-week, double-blind study </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Iliopsoas bursitis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tracheomalacia and can you explain it in depth? [/INST] Tracheomalacia is a condition or incident where the cartilage that keeps the airway (trachea) open is soft such that the trachea partly collapses especially during increased airflow. This condition is most commonly seen in infants and young children. The usual symptom is stridor when a person breathes out. This is usually known as a collapsed windpipe.
The trachea normally opens slightly during breathing in and narrows slightly during breathing out. These processes are exaggerated in tracheomalacia, leading to airway collapse on breathing out.
If the condition extends further to the large airways (bronchi) (if there is also bronchomalacia), it is termed tracheobronchomalacia. The same condition can also affect the larynx, which is called laryngomalacia. The term is from trachea and the Greek μαλακία, softening

Signs and symptoms
Tracheomalacia occurs when the walls of the trachea collapse. This can happen because the walls of the windpipe are weak, or it can happen because something is pressing on it. This may include hypotonia of the trachealis muscle. The whole windpipe can be affected, or only a short piece of it. If the collapsed part of the windpipe goes past the area where the windpipe branches off into the two lungs, it is called bronchomalacia.This problem causes noisy or difficult breathing in the first 1 to 2 months after birth. This is called congenital tracheomalacia (it was present at birth). It is not very common. Babies born with tracheomalacia may have other health issues like a heart defect, reflux or developmental delay. Some children get tracheomalacia because of other health issues. Symptoms can be mild to severe.Symptoms inside the lung include noisy breathing that may get better when you change your babys position or while he or she is asleep. Breathing problems that get worse during coughing, crying, feeding or colds. High-pitched sound during breathing (stridor).
High-pitched cough. Rattling noise or wheezing with breathing.

Diagnosis
There is no standardized, defined set of diagnostic criteria for the diagnosis of tracheomalacia, mainly due to the nonspecific symptoms associated with it. Current diagnostic approaches include pulmonary function testing which shows a characteristic reduction in peak expiratory flow (PEF), physical examination, and imaging such as computed tomography (CT) or magnetic resonance imaging (MRI), fiberoptic bronchoscopy (FB) is considered the best diagnostic method because an inserted camera down the throat shows a direct view of the airways and lungs, detecting changes in the size or appearance of the tracheas lumen and mucosa and any signs of inflammation, fistulas, or external compressions to precisely determine the location and severity of the malacia </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Dyssomnia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Plastic bronchitis and can you explain it in depth? [/INST] Plastic bronchitis (PB) is a disorder in which branching casts of the airways are expectorated.  PB is not a single disease with a defined mechanism that explains the cast formation in all conditions.  Examples of diseases associated with expectoration of casts, and which sometimes are labeled PB include tuberculosis, atypical mycobacterial disease, allergic bronchopulmonary aspergillosis, and asthma.
When casts are very large with many branches, an abnormal communication or leakage of lymphatic fluid into the airway is often the cause.  This entity is termed lymphatic plastic bronchitis (LPB).  LPB is a lymphatic flow disorder characterized by the recurrent formation of branching, rubbery bronchial casts composed primarily of proteinaceous and sometimes chylous material and lymphocytes.  Lymphatic fluids deposited into the airspaces become gelatinous as they cool, forming large string cheese-like casts of the airways, which can obstruct airflow.  Attempts to expectorate casts can be quite frightening, leading to fears of asphyxiation.

Signs and symptoms
The clinical presentation of plastic bronchitis beyond expectoration of casts includes a productive cough, dyspnea, fever and wheezing.  Focal wheezing is a characteristic, if not specific, physical examination finding.  If the casts completely obstruct the airway, breath sounds will be decreased and dullness will be present with percussion.  With partial obstruction, a “fan sound” or “flag flapping” sound can be heard during auscultation.  Bronchial casts can sometimes fill the airways of almost an entire lung, and present as an acute, life-threatening emergency.

Pathology
The majority of PB cases are associated with an underlying disease.  Several systemic illnesses have been associated with plastic bronchitis:
Cardiac: constrictive pericarditis, congenital heart disease
Pulmonary: asthma, allergic bronchopulmonary aspergillosis, aspergillosis, bronchiectasis, cystic fibrosis, tuberculosis, pneumonia, and bronchocentric granulomatosis
Disorders of lymphatic drainage: lymphangiectasia, lymphangiomatosis
Miscellaneous: acute chest syndrome/sickle cell disease, amyloidosis, rheumatoid arthritis, membranous colitis, inhaled irritants, neoplastic (lymphoma)The most common form of plastic bronchitis follows cardiac surgery for congenital heart disease, especially the Fontan procedure.  Systemic blood flow is diverted to pulmonary flow, elevating pressures in the pulmonary venous system, and promoting leaks of proteinaceous and lipid-rich fluids from the lymphatics into the bronchial tree.

Diagnosis
The diagnosis of plastic bronchitis is confirmed by recovery of casts that have been coughed up or visualized during a bronchoscopy. There is no specific cytologic, pathologic or laboratory test that is diagnostic for casts due to lymphatic PB.

Imaging
Simple chest X-rays may reveal collapse due to airway obstruction.  The contralateral lung may be hyperinflated </s>