<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Scurvy and explain in detail? [/INST] Scurvy is a disease resulting from a lack of vitamin C (ascorbic acid). Early symptoms of deficiency include weakness, feeling tired and sore arms and legs. Without treatment, decreased red blood cells, gum disease, changes to hair, and bleeding from the skin may occur. As scurvy worsens there can be poor wound healing, personality changes, and finally death from infection or bleeding.It takes at least a month of little to no vitamin C in the diet before symptoms occur. In modern times, scurvy occurs most commonly in people with mental disorders, unusual eating habits, alcoholism, and older people who live alone. Other risk factors include intestinal malabsorption and dialysis. While many animals produce their own vitamin C, humans and a few others do not. Vitamin C is required to make the building blocks for collagen. Diagnosis is typically based on physical signs, X-rays, and improvement after treatment.Treatment is with vitamin C supplements taken by mouth. Improvement often begins in a few days with complete recovery in a few weeks. Sources of vitamin C in the diet include citrus fruit and a number of vegetables, including red peppers, broccoli, and tomatoes. Cooking often decreases the residual amount of vitamin C in foods.Scurvy is rare compared to other nutritional deficiencies. It occurs more often in the developing world in association with malnutrition. Rates among refugees are reported at 5 to 45 percent. Scurvy was described as early as the time of ancient Egypt. It was a limiting factor in long-distance sea travel, often killing large numbers of people. During the Age of Sail, it was assumed that 50 percent of the sailors would die of scurvy on a major trip. A Scottish surgeon in the Royal Navy, James Lind, is generally credited with proving that scurvy can be successfully treated with citrus fruit in 1753. Nevertheless, it was not until 1795 that health reformers such as Gilbert Blane persuaded the Royal Navy to routinely give lemon juice to its sailors.

Signs and symptoms
Early symptoms are malaise and lethargy. After one to three months, patients develop shortness of breath and bone pain. Myalgias may occur because of reduced carnitine production. Other symptoms include skin changes with roughness, easy bruising and petechiae, gum disease, loosening of teeth, poor wound healing, and emotional changes (which may appear before any physical changes). Dry mouth and dry eyes similar to Sjögrens syndrome may occur. In the late stages, jaundice, generalised edema, oliguria, neuropathy, fever, convulsions, and eventual death are frequently seen.

Cause
Scurvy, including subclinical scurvy, is caused by a deficiency of dietary vitamin C since humans are unable to metabolically synthesize vitamin C. Provided the diet contains sufficient vitamin C, the lack of working L-gulonolactone oxidase (GULO) enzyme has no significance, and in modern Western societies, scurvy is rarely present in adults, although infants and elderly people are affected. Virtually all commercially available baby formulas contain added vitamin C, preventing infantile scurvy. Human breast milk contains sufficient vitamin C, if the mother has an adequate intake. Commercial milk is pasteurized, a heating process that destroys the natural vitamin C content of the milk.Scurvy is one of the accompanying diseases of malnutrition (other such micronutrient deficiencies are beriberi and pellagra) and thus is still widespread in areas of the world depending on external food aid.
Although rare, there are also documented cases of scurvy due to poor dietary choices by people living in industrialized nations.

Pathogenesis
Vitamins are essential to the production and use of enzymes that are involved in ongoing processes throughout the human body. Ascorbic acid is needed for a variety of biosynthetic pathways, by accelerating hydroxylation and amidation reactions. In the synthesis of collagen, ascorbic acid is required as a cofactor for prolyl hydroxylase and lysyl hydroxylase. These two enzymes are responsible for the hydroxylation of the proline and lysine amino acids in collagen. Hydroxyproline and hydroxylysine are important for stabilizing collagen by cross-linking the propeptides in collagen.
Collagen is a primary structural protein in the human body, necessary for healthy blood vessels, muscle, skin, bone, cartilage, and other connective tissues.
Defective connective tissue leads to fragile capillaries, resulting in abnormal bleeding, bruising, and internal hemorrhaging.
Collagen is an important part of bone, so bone formation is also affected. Teeth loosen, bones break more easily, and once-healed breaks may recur.
Defective collagen fibrillogenesis impairs wound healing.
Untreated scurvy is invariably fatal.

Diagnosis
Diagnosis is typically based on physical signs, X-rays, and improvement after treatment.

Differential diagnosis
Various childhood onset disorders can mimic the clinical and X-ray picture of scurvy such as:

Rickets
Osteochondrodysplasias especially osteogenesis imperfecta
Blounts disease
Osteomyelitis

Prevention
Scurvy can be prevented by a diet that includes uncooked vitamin C-rich foods such as amla, bell peppers (sweet peppers), blackcurrants, broccoli, chili peppers, guava, kiwifruit, and parsley. Other sources rich in vitamin C are fruits such as lemons, limes, oranges, papaya, and strawberries. It is also found in vegetables, such as brussels sprouts, cabbage, potatoes, and spinach. Some fruits and vegetables not high in vitamin C may be pickled in lemon juice, which is high in vitamin C. Nutritional supplements which provide ascorbic acid well in excess of what is required to prevent scurvy may cause adverse health effects.Some animal products, including liver, muktuk (whale skin), oysters, and parts of the central nervous system, including the adrenal medulla, brain, and spinal cord, contain large amounts of vitamin C, and can even be used to treat scurvy. Fresh meat from animals, notable internal organs, contains enough vitamin C to prevent scurvy, and even partly treat it. .Scotts 1902 Antarctic expedition used lightly fried seal meat and liver, whereby complete recovery from incipient scurvy was reported to have taken less than two weeks.

Treatment
Scurvy will improve with doses of vitamin C as low as 10 mg per day though doses of around 100 mg per day are typically recommended. Most people make a full recovery within 2 weeks.

History
Symptoms of scurvy have been recorded in Ancient Egypt as early as 1550 BCE. In Ancient Greece, the physician Hippocrates (460-370 BCE) described symptoms of scurvy, specifically a "swelling and obstruction of the spleen."
In 406 CE, the Chinese monk Faxian wrote that ginger was carried on Chinese ships to prevent scurvy.The knowledge that consuming foods containing vitamin C is a cure for scurvy has been repeatedly forgotten and rediscovered into the early 20th century.

Early modern era
In the 13th century, the Crusaders frequently developed scurvy. In the 1497 expedition of Vasco da Gama, the curative effects of citrus fruit were already known and confirmed by Pedro Álvares Cabral and his crew in 1507.The Portuguese planted fruit trees and vegetables in Saint Helena, a stopping point for homebound voyages from Asia, and left their sick, who had scurvy and other ailments, to be taken home by the next ship if they recovered.In 1500, one of the pilots of Cabrals fleet bound for India noted that in Malindi, its king offered the expedition fresh supplies such as lambs, chickens, and ducks, along with lemons and oranges, due to which "some of our ill were cured of scurvy".Unfortunately, these travel accounts did not stop further maritime tragedies caused by scurvy, first because of the lack of communication between travelers and those responsible for their health, and because fruits and vegetables could not be kept for long on ships.In 1536, the French explorer Jacques Cartier, exploring the St. Lawrence River, used the local natives knowledge to save his men who were dying of scurvy. He boiled the needles of the arbor vitae tree (eastern white cedar) to make a tea that was later shown to contain 50 mg of vitamin C per 100 grams. Such treatments were not available aboard ship, where the disease was most common.
In February 1601, Captain James Lancaster, while sailing to Sumatra, landed on the northern coast of Madagascar specifically to obtain lemons and oranges for his crew to stop scurvy. Captain Lancaster conducted an experiment using four ships under his command. One ships crew received routine doses of lemon juice while the other three ships did not receive any such treatment. As a result, members of the non-treated ships started to contract scurvy, with many dying as a result.During the Age of Exploration (between 1500 and 1800), it has been estimated that scurvy killed at least two million sailors. Jonathan Lamb wrote: "In 1499, Vasco da Gama lost 116 of his crew of 170; In 1520, Magellan lost 208 out of 230;...all mainly to scurvy."In 1579, the Spanish friar and physician Agustin Farfán published a book in which he recommended oranges and lemons for scurvy, a remedy that was already known in the Spanish Navy.In 1593, Admiral Sir Richard Hawkins advocated drinking orange and lemon juice as a means of preventing scurvy.In 1614, John Woodall, Surgeon General of the East India Company, published The Surgions Mate as a handbook for apprentice surgeons aboard the companys ships. He repeated the experience of mariners that the cure for scurvy was fresh food or, if not available, oranges, lemons, limes, and tamarinds. He was, however, unable to explain the reason why, and his assertion had no impact on the prevailing opinion of the influential physicians of the age, that scurvy was a digestive complaint.
Apart from ocean travel, even in Europe, until the late Middle Ages, scurvy was common in late winter, when few green vegetables, fruits and root vegetables were available. This gradually improved with the introduction from the Americas of potatoes; by 1800, scurvy was virtually unheard of in Scotland, where it had previously been endemic.: 11

18th century
In 2009, a handwritten household book authored by a Cornishwoman in 1707 was discovered in a house in Hasfield, Gloucestershire, containing a "Recp.t for the Scurvy" amongst other largely medicinal and herbal recipes. The recipe consisted of extracts from various plants mixed with a plentiful supply of orange juice, white wine or beer.In 1734, Leiden-based physician Johann Bachstrom published a book on scurvy in which he stated, "scurvy is solely owing to a total abstinence from fresh vegetable food, and greens; which is alone the primary cause of the disease", and urged the use of fresh fruit and vegetables as a cure.It was not until 1747 that James Lind formally demonstrated that scurvy could be treated by supplementing the diet with citrus fruit, in one of the first controlled clinical experiments reported in the history of medicine. As a naval surgeon on HMS Salisbury, Lind had compared several suggested scurvy cures: hard cider, vitriol, vinegar, seawater, oranges, lemons, and a mixture of balsam of Peru, garlic, myrrh, mustard seed and radish root. In A Treatise on the Scurvy (1753)
Lind explained the details of his clinical trial and concluded "the results of all my experiments was, that oranges and lemons were the most effectual remedies for this distemper at sea." However, the experiment and its results occupied only a few paragraphs in a work that was long and complex and had little impact. Lind himself never actively promoted lemon juice as a single cure. He shared medical opinion at the time that scurvy had multiple causes – notably hard work, bad water, and the consumption of salt meat in a damp atmosphere which inhibited healthful perspiration and normal excretion – and therefore required multiple solutions. Lind was also sidetracked by the possibilities of producing a concentrated rob of lemon juice by boiling it. This process destroyed the vitamin C and was therefore unsuccessful.During the 18th century, scurvy killed more British sailors than wartime enemy action. It was mainly by scurvy that George Anson, in his celebrated voyage of 1740–1744, lost nearly two-thirds of his crew (1,300 out of 2,000) within the first 10 months of the voyage. The Royal Navy enlisted 184,899 sailors during the Seven Years War; 133,708 of these were "missing" or died from disease, and scurvy was the leading cause.Although throughout this period sailors and naval surgeons were increasingly convinced that citrus fruits could cure scurvy, the classically trained physicians who determined medical policy dismissed this evidence as merely anecdotal, as it did not conform to their theories of disease. Literature championing the cause of citrus juice, therefore, had no practical impact. The medical theory was based on the assumption that scurvy was a disease of internal putrefaction brought on by faulty digestion caused by the hardships of life at sea and the naval diet. Although this basic idea was given different emphases by successive theorists, the remedies they advocated (and which the navy accepted) amounted to little more than the consumption of fizzy drinks to activate the digestive system, the most extreme of which was the regular consumption of elixir of vitriol – sulphuric acid taken with spirits and barley water, and laced with spices.
In 1764, a new and similarly inaccurate theory on scurvy appeared. Advocated by Dr David MacBride and Sir John Pringle, Surgeon General of the Army and later President of the Royal Society, this idea was that scurvy was the result of a lack of fixed air in the tissues which could be prevented by drinking infusions of malt and wort whose fermentation within the body would stimulate digestion and restore the missing gases. These ideas received wide and influential backing, when James Cook set off to circumnavigate the world (1768–1771) in HM Bark Endeavour, malt and wort were top of the list of the remedies he was ordered to investigate. The others were beer, Sauerkraut (a good source of vitamin C) and Linds rob. The list did not include lemons.Cook did not lose a single man to scurvy, and his report came down in favour of malt and wort, although it is now clear that the reason for the health of his crews on this and other voyages was Cooks regime of shipboard cleanliness, enforced by strict discipline, as well as frequent replenishment of fresh food and greenstuffs. Another beneficial rule implemented by Cook was his prohibition of the consumption of salt fat skimmed from the ships copper boiling pans, then a common practice elsewhere in the Navy. In contact with air, the copper formed compounds that prevented the absorption of vitamins by the intestines.The first major long distance expedition that experienced virtually no scurvy was that of the Spanish naval officer Alessandro Malaspina, 1789–1794. Malaspinas medical officer, Pedro González, was convinced that fresh oranges and lemons were essential for preventing scurvy. Only one outbreak occurred, during a 56-day trip across the open sea. Five sailors came down with symptoms, one seriously. After three days at Guam all five were healthy again. Spains large empire and many ports of call made it easier to acquire fresh fruit.Although towards the end of the century MacBrides theories were being challenged, the medical authorities in Britain remained committed to the notion that scurvy was a disease of internal putrefaction and the Sick and Hurt Board, run by administrators, felt obliged to follow its advice. Within the Royal Navy, however, opinion – strengthened by first-hand experience of the use of lemon juice at the siege of Gibraltar and during Admiral Rodneys expedition to the Caribbean – had become increasingly convinced of its efficacy. This was reinforced by the writings of experts like Gilbert Blane and Thomas Trotter and by the reports of up-and-coming naval commanders.
With the coming of war in 1793, the need to eliminate scurvy acquired a new urgency. But the first initiative came not from the medical establishment but from the admirals. Ordered to lead an expedition against Mauritius, Rear Admiral Gardner was uninterested in the wort, malt and elixir of vitriol which were still being issued to ships of the Royal Navy, and demanded that he be supplied with lemons, to counteract scurvy on the voyage. Members of the Sick and Hurt Board, recently augmented by two practical naval surgeons, supported the request, and the Admiralty ordered that it be done. There was, however, a last minute change of plan, and the expedition against Mauritius was cancelled. On 2 May 1794, only HMS Suffolk and two sloops under Commodore Peter Rainier sailed for the east with an outward bound convoy, but the warships were fully supplied with lemon juice and the sugar with which it had to be mixed.
In March 1795, it was reported that the Suffolk had arrived in India after a four-month voyage without a trace of scurvy and with a crew that was healthier than when it set out. The effect was immediate. Fleet commanders clamoured also to be supplied with lemon juice, and by June the Admiralty acknowledged the groundswell of demand in the navy and agreed to a proposal from the Sick and Hurt Board that lemon juice and sugar should in future be issued as a daily ration to the crews of all warships.It took a few years before the method of distribution to all ships in the fleet had been perfected and the supply of the huge quantities of lemon juice required to be secured, but by 1800, the system was in place and functioning. This led to a remarkable health improvement among the sailors and consequently played a critical role in gaining the advantage in naval battles against enemies who had yet to introduce the measures.
Scurvy was not only a disease of seafarers. The only colonists of Australia suffered greatly because of the lack of fresh fruit and vegetables in the winter. There the disease was called Spring fever or  Spring disease and described an often fatal condition associated with skin lesions, bleeding gums and lethargy. It was eventually identified as scurvy and the remedies already in use at sea implemented.

19th century
The surgeon-in-chief of Napoleons army at the Siege of Alexandria (1801), Baron Dominique-Jean Larrey, wrote in his memoirs that the consumption of horse meat helped the French to curb an epidemic of scurvy. The meat was cooked but was freshly obtained from young horses bought from Arabs, and was nevertheless effective. This helped to start the 19th-century tradition of horse meat consumption in France.Lauchlin Rose patented a method used to preserve citrus juice without alcohol in 1867, creating a concentrated drink known as Roses lime juice. The Merchant Shipping Act of 1867 required all ships of the Royal Navy and Merchant Navy to provide a daily lime ration of one pound to sailors to prevent scurvy. The product became nearly ubiquitous, hence the term "limey", first for British sailors, then for English immigrants within the former British colonies (particularly America, New Zealand and South Africa), and finally, in old American slang, all British people.The plant Cochlearia officinalis, also known as "common scurvygrass", acquired its common name from the observation that it cured scurvy, and it was taken on board ships in dried bundles or distilled extracts. Its very bitter taste was usually disguised with herbs and spices; however, this did not prevent scurvygrass drinks and sandwiches from becoming a popular fad in the UK until the middle of the nineteenth century, when citrus fruits became more readily available.West Indian limes began to supplement lemons, when Spains alliance with France against Britain in the Napoleonic Wars made the supply of Mediterranean lemons problematic, and because they were more easily obtained from Britains Caribbean colonies and were believed to be more effective because they were more acidic. It was the acid, not the (then-unknown) Vitamin C that was believed to cure scurvy. In fact, the West Indian limes were significantly lower in Vitamin C than the previous lemons and further were not served fresh but rather as lime juice, which had been exposed to light and air, and piped through copper tubing, all of which significantly reduced the Vitamin C. Indeed, a 1918 animal experiment using representative samples of the Navy and Merchant Marines lime juice showed that it had virtually no antiscorbutic power at all.The belief that scurvy was fundamentally a nutritional deficiency, best treated by consumption of fresh food, particularly fresh citrus or fresh meat, was not universal in the 19th and early 20th centuries, and thus sailors and explorers continued to have scurvy into the 20th century. For example, the Belgian Antarctic Expedition of 1897–1899 became seriously affected by scurvy when its leader, Adrien de Gerlache, initially discouraged his men from eating penguin and seal meat.
In the Royal Navys Arctic expeditions in the 19th century it was widely believed that scurvy was prevented by good hygiene on board ship, regular exercise, and maintaining the morale of the crew, rather than by a diet of fresh food. Navy expeditions continued to be plagued by scurvy even while fresh (not jerked or tinned) meat was well known as a practical antiscorbutic among civilian whalers and explorers in the Arctic. Even cooking fresh meat did not entirely destroy its antiscorbutic properties, especially as many cooking methods failed to bring all the meat to high temperature.
The confusion is attributed to a number of factors:
while fresh citrus (particularly lemons) cured scurvy, lime juice that had been exposed to light, air and copper tubing did not – thus undermining the theory that citrus cured scurvy;
fresh meat (especially organ meat and raw meat, consumed in arctic exploration) also cured scurvy, undermining the theory that fresh vegetable matter was essential to preventing and curing scurvy;
increased marine speed via steam shipping, and improved nutrition on land, reduced the incidence of scurvy – and thus the ineffectiveness of copper-piped lime juice compared to fresh lemons was not immediately revealed.In the resulting confusion, a new hypothesis was proposed, following the new germ theory of disease – that scurvy was caused by ptomaine, a waste product of bacteria, particularly in tainted tinned meat.
Infantile scurvy emerged in the late 19th century because children were being fed pasteurized cows milk, particularly in the urban upper class. While pasteurization killed bacteria, it also destroyed vitamin C. This was eventually resolved by supplementing with onion juice or cooked potatoes. Native Americans helped save some newcomers from scurvy by directing them to eat wild onions.

20th century
By the early 20th century, when Robert Falcon Scott made his first expedition to the Antarctic (1901–1904), the prevailing theory was that scurvy was caused by "ptomaine poisoning", particularly in tinned meat. However, Scott discovered that a diet of fresh meat from Antarctic seals cured scurvy before any fatalities occurred.In 1907, an animal model which would eventually help to isolate and identify the "antiscorbutic factor" was discovered. Axel Holst and Theodor Frølich, two Norwegian physicians studying shipboard beriberi contracted by ships crews in the Norwegian Fishing Fleet, wanted a small test mammal to substitute for the pigeons then used in beriberi research. They fed guinea pigs their test diet of grains and flour, which had earlier produced beriberi in their pigeons, and were surprised when classic scurvy resulted instead. This was a serendipitous choice of animal. Until that time, scurvy had not been observed in any organism apart from humans and had been considered an exclusively human disease. Certain birds, mammals, and fish are susceptible to scurvy, but pigeons are unaffected, since they can synthesize ascorbic acid internally. Holst and Frølich found they could cure scurvy in guinea pigs with the addition of various fresh foods and extracts. This discovery of an animal experimental model for scurvy, which was made even before the essential idea of "vitamins" in foods had been put forward, has been called the single most important piece of vitamin C research.In 1915, New Zealand troops in the Gallipoli Campaign had a lack of vitamin C in their diet which caused many of the soldiers to contract scurvy. It is thought that scurvy is one of many reasons that the Allied attack on Gallipoli failed.Vilhjalmur Stefansson, an arctic explorer who had lived among the Inuit, proved that the all-meat diet they consumed did not lead to vitamin deficiencies. He participated in a study in New Yorks Bellevue Hospital in February 1928, where he and a companion ate only meat for a year while under close medical observation, yet remained in good health.In 1927, Hungarian biochemist Albert Szent-Györgyi isolated a compound he called "hexuronic acid". Szent-Györgyi suspected hexuronic acid, which he had isolated from adrenal glands, to be the antiscorbutic agent, but he could not prove it without an animal-deficiency model. In 1932, the connection between hexuronic acid and scurvy was finally proven by American researcher Charles Glen King of the University of Pittsburgh. Kings laboratory was given some hexuronic acid by Szent-Györgyi and soon established that it was the sought-after anti-scorbutic agent. Because of this, hexuronic acid was subsequently renamed ascorbic acid.

21st century
Rates of scurvy in most of the world are low. Those most commonly affected are malnourished people in the developing world and the homeless. There have been outbreaks of the condition in refugee camps. Case reports in the developing world of those with poorly healing wounds have occurred.

Human trials
Notable human dietary studies of experimentally induced scurvy were conducted on conscientious objectors during World War II in Britain and in the United States on Iowa state prisoner volunteers in the late 1960s. These studies both found that all obvious symptoms of scurvy previously induced by an experimental scorbutic diet with extremely low vitamin C content could be completely reversed by additional vitamin C supplementation of only 10 mg per day. In these experiments, no clinical difference was noted between men given 70 mg vitamin C per day (which produced blood levels of vitamin C of about 0.55 mg/dl, about 1⁄3 of tissue saturation levels), and those given 10 mg per day (which produced lower blood levels) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Seasonal affective disorder and explain in detail? [/INST] Seasonal affective disorder (SAD) is a mood disorder subset, in which people who have normal mental health throughout most of the year exhibit depressive symptoms at the same time each year, most commonly in winter. Common symptoms include sleeping too much, having little to no energy, and overeating. The condition in the summer can include heightened anxiety.In the Diagnostic and Statistical Manual of Mental Disorders DSM-IV and DSM-5, its status was changed. It is no longer classified as a unique mood disorder, but is now a specifier, called "with seasonal pattern", for recurrent major depressive disorder that occurs at a specific time of the year, and fully remits otherwise. Although experts were initially skeptical, this condition is now recognized as a common disorder. However, the validity of SAD has been questioned by a 2016 analysis by the Center for Disease Control, in which no links were detected between depression and seasonality or sunlight exposure.

In the United States, the percentage of the population affected by SAD ranges from 1.4% of the population in Florida, to 9.9% in Alaska. SAD was formally described and named in 1984, by Norman E. Rosenthal and colleagues at the National Institute of Mental Health.

History
SAD was first systematically reported and named in the early 1980s, by Norman E. Rosenthal, M.D., and his associates at the National Institute of Mental Health (NIMH). Rosenthal was initially motivated by his desire to discover the cause of his own experience of depression during the dark days of the northern US winter, called polar night. He theorized that the reduction in available natural light during winter was the cause. Rosenthal and his colleagues then documented the phenomenon of SAD in a placebo-controlled study utilizing light therapy. A paper based on this research was published in 1984. Although Rosenthals ideas were initially greeted with skepticism, SAD has become well recognized, and his 1993 book, Winter Blues has become the standard introduction to the subject.Research on SAD in the United States began in 1979, when Herb Kern, a research engineer, had also noticed that he felt depressed during the winter months. Kern suspected that scarcer light in winter was the cause, and discussed the idea with scientists at the NIMH who were working on bodily rhythms. They were intrigued, and responded by devising a lightbox to treat Kerns depression. Kern felt much better within a few days of treatments, as did other patients treated in the same way.

Signs and symptoms
SAD is a type of major depressive disorder, and those with the condition may exhibit any of the associated symptoms, such as feelings of hopelessness and worthlessness, thoughts of suicide, loss of interest in activities, withdrawal from social interaction, sleep and appetite problems, difficulty with concentrating and making decisions, decreased libido, a lack of energy, or agitation. Symptoms of winter SAD often include falling asleep earlier or in less than 5 minutes in the evening, oversleeping or difficulty waking up in the morning, nausea, and a tendency to overeat, often with a craving for carbohydrates, which leads to weight gain. SAD is typically associated with winter depression, but springtime lethargy or other seasonal mood patterns are not uncommon. Although each individual case is different, in contrast to winter SAD, people who experience spring and summer depression may be more likely to show symptoms such as insomnia, decreased appetite and weight loss, and agitation or anxiety.

Bipolar disorder
With seasonal pattern is a specifier for bipolar and related disorders, including bipolar I disorder and bipolar II disorder.
Most people with SAD experience major depressive disorder, but as many as 20% may have a bipolar disorder. It is important to distinguish between diagnoses because there are important treatment differences. In these cases, people who have the With seasonal pattern specifier may experience a depressive episode either due to major depressive disorder or as part of bipolar disorder during the winter and remit in the summer. Around 25% of patients with bipolar disorder may present with a depressive seasonal pattern, which is associated with bipolar II disorder, rapid cycling, eating disorders, and more depressive episodes. Differences in biological sex display distinct clinical characteristics associated to seasonal pattern: males present with more Bipolar II disorder and a higher number of depressive episodes, and females with rapid cycling and eating disorders.

Cause
In many species, activity is diminished during the winter months, in response to the reduction in available food, the reduction of sunlight (especially for diurnal animals), and the difficulties of surviving in cold weather. Hibernation is an extreme example, but even species that do not hibernate often exhibit changes in behavior during the winter. The preponderance of women with SAD suggests that the response may also somehow regulate reproduction.Various proximate causes have been proposed. One possibility is that SAD is related to a lack of serotonin, and serotonin polymorphisms could play a role in SAD, although this has been disputed. Mice incapable of turning serotonin into N-acetylserotonin (by serotonin N-acetyltransferase) appear to express "depression-like" behavior, and antidepressants such as fluoxetine increase the amount of the enzyme serotonin N-acetyltransferase, resulting in an antidepressant-like effect. Another theory is that the cause may be related to melatonin, which is produced in dim light and darkness by the pineal gland, since there are direct connections, via the retinohypothalamic tract and the suprachiasmatic nucleus, between the retina and the pineal gland. Melatonin secretion is controlled by the endogenous circadian clock, but can also be suppressed by bright light.One study looked at whether some people could be predisposed to SAD based on personality traits. Correlations between certain personality traits, higher levels of neuroticism, agreeableness, openness, and an avoidance-oriented coping style, appeared to be common in those with SAD.

Pathophysiology
Seasonal mood variations are believed to be related to light. An argument for this view is the effectiveness of bright-light therapy. SAD is measurably present at latitudes in the Arctic region, such as northern Finland (64°00′N), where the rate of SAD is 9.5%. Cloud cover may contribute to the negative effects of SAD. There is evidence that many patients with SAD have a delay in their circadian rhythm, and that bright light treatment corrects these delays which may be responsible for the improvement in patients.The symptoms of it mimic those of dysthymia or even major depressive disorder. There is also potential risk of suicide in some patients experiencing SAD. One study reports 6–35% of people with the condition required hospitalization during one period of illness. At times, patients may not feel depressed, but rather lack energy to perform everyday activities.Subsyndromal Seasonal Affective Disorder is a milder form of SAD experienced by an estimated 14.3% (vs. 6.1% SAD) of the U.S. population. The blue feeling experienced by both those with SAD and with SSAD can usually be dampened or extinguished by exercise and increased outdoor activity, particularly on sunny days, resulting in increased solar exposure. Connections between human mood, as well as energy levels, and the seasons are well documented, even in healthy individuals.

Diagnosis
According to the American Psychiatric Association DSM-IV criteria, Seasonal Affective Disorder is not regarded as a separate disorder. It is called a "course specifier" and may be applied as an added description to the pattern of major depressive episodes in patients with major depressive disorder or patients with bipolar disorder.
The "Seasonal Pattern Specifier" must meet four criteria: depressive episodes at a particular time of the year; remissions or mania/hypomania at a characteristic time of year; these patterns must have lasted two years with no nonseasonal major depressive episodes during that same period; and these seasonal depressive episodes outnumber other depressive episodes throughout the patients lifetime. The Mayo Clinic describes three types of SAD, each with its own set of symptoms.

Management
Treatments for classic (winter-based) seasonal affective disorder include light therapy, medication, ionized-air administration, cognitive-behavioral therapy, and carefully timed supplementation of the hormone melatonin.

Light therapy
Photoperiod-related alterations of the duration of melatonin secretion may affect the seasonal mood cycles of SAD. This suggests that light therapy may be an effective treatment for SAD. Light therapy uses a lightbox, which emits far more lumens than a customary incandescent lamp. Bright white "full spectrum" light at 10,000 lux, blue light at a wavelength of 480 nm at 2,500 lux or green (actually cyan or blue-green) light at a wavelength of 500 nm at 350 lux are used, with the first-mentioned historically preferred.Bright light therapy is effective with the patient sitting a prescribed distance, commonly 30–60 cm, in front of the box with her/his eyes open, but not staring at the light source, for 30–60 minutes. A study published in May 2010 suggests that the blue light often used for SAD treatment should perhaps be replaced by green or white illumination. Discovering the best schedule is essential. One study has shown that up to 69% of patients find lightbox treatment inconvenient, and as many as 19% stop use because of this.Dawn simulation has also proven to be effective; in some studies, there is an 83% better response when compared to other bright light therapy. When compared in a study to negative air ionization, bright light was shown to be 57% effective vs. dawn simulation 50%. Patients using light therapy can experience improvement during the first week, but increased results are evident when continued throughout several weeks. Certain symptoms like hypersomnia, early insomnia, social withdrawal, and anxiety resolve more rapidly with light therapy than with cognitive behavioral therapy. Most studies have found it effective without use year round, but rather as a seasonal treatment lasting for several weeks, until frequent light exposure is naturally obtained.Light therapy can also consist of exposure to sunlight, either by spending more time outside or using a computer-controlled heliostat to reflect sunlight into the windows of a home or office. Although light therapy is the leading treatment for seasonal affective disorder, prolonged direct sunlight or artificial lights that dont block the ultraviolet range should be avoided, due to the threat of skin cancer.The evidence base for light therapy as a preventive treatment for seasonal affective disorder is limited. The decision to use light therapy to treat people with a history of winter depression before depressive symptoms begin should be based on a persons preference of treatment.

Medication
SSRI (selective serotonin reuptake inhibitor) antidepressants have proven effective in treating SAD. Effective antidepressants are fluoxetine, sertraline, or paroxetine. Both fluoxetine and light therapy are 67% effective in treating SAD, according to direct head-to-head trials conducted during the 2006 Can-SAD study. Subjects using the light therapy protocol showed earlier clinical improvement, generally within one week of beginning the clinical treatment. Bupropion extended-release has been shown to prevent SAD for one in four people, but has not been compared directly to other preventive options in trials. In a 2021 updated Cochrane review of second-generation antidepressant medications for the treatment of SAD, a definitive conclusion could not be drawn, due to lack of evidence, and the need for larger randomized controlled trials.Modafinil may be an effective and well-tolerated treatment in patients with seasonal affective disorder/winter depression.Another explanation is that vitamin D levels are too low when people do not get enough Ultraviolet-B on their skin. An alternative to using bright lights is to take vitamin D supplements. However, studies did not show a link between vitamin D levels and depressive symptoms in elderly Chinese, nor among elderly British women given only 800IU when 6,000IU is needed. 5-HTP (an amino acid that helps to produce serotonin, and is often used to help those with depression) has also been suggested as a supplement that may help treat the symptoms of SAD, by lifting mood, and regulating sleep schedule for those with the condition. However, those who take antidepressants are not advised to take 5-HTP, as antidepressant medications may combine with the supplement to create dangerously high levels of serotonin – potentially resulting in serotonin syndrome.

Other treatments
Depending upon the patient, one treatment (e.g., lightbox) may be used in conjunction with another (e.g., medication).Negative air ionization, which involves releasing charged particles into the sleep environment, has been found effective, with a 47.9% improvement if the negative ions are in sufficient density (quantity).Physical exercise has shown to be an effective form of depression therapy, particularly when in addition to another form of treatment for SAD. One particular study noted marked effectiveness for treatment of depressive symptoms, when combining regular exercise with bright light therapy. Patients exposed to exercise which had been added to their treatments in 20 minutes intervals on the aerobic bike during the day, along with the same amount of time underneath the UV light were seen to make a quick recovery.Of all the psychological therapies aimed at the prevention of SAD, cognitive-behaviour therapy, typically involving thought records, activity schedules and a positive data log, has been the subject of the most empirical work. However, evidence for CBT or any of the psychological therapies aimed at preventing SAD remains inconclusive.

Epidemiology
Nordic countries
Winter depression is a common slump in the mood of some inhabitants of most of the Nordic countries. Iceland, however, seems to be an exception. A study of more than 2000 people there found the prevalence of seasonal affective disorder and seasonal changes in anxiety and depression to be unexpectedly low in both sexes. The studys authors suggested that propensity for SAD may differ due to some genetic factor within the Icelandic population. A study of Canadians of wholly Icelandic descent also showed low levels of SAD. It has more recently been suggested that this may be attributed to the large amount of fish traditionally eaten by Icelandic people </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Seborrhoeic dermatitis and explain in detail? [/INST] Seborrhoeic dermatitis, sometimes inaccurately referred to as seborrhoea, is a long-term skin disorder. Symptoms include red, scaly, greasy, itchy, and inflamed skin. Areas of the skin rich in oil-producing glands are often affected including the scalp, face, and chest. It can result in social or self-esteem problems. In babies, when the scalp is primarily involved, it is called cradle cap. Dandruff is a milder form of the condition without inflammation.The cause is unclear but believed to involve a number of genetic and environmental factors. Risk factors include poor immune function, Parkinsons disease, and alcoholic pancreatitis. The condition may worsen with stress or during the winter. The Malassezia yeast is believed to play a role. It is not a result of poor hygiene. Diagnosis is typically based on the symptoms. The condition is not contagious.The typical treatment is antifungal cream and anti-inflammatory agents. Specifically, ketoconazole or ciclopirox are effective. It is unclear if other antifungals, such as miconazole, are equally effective as they have been poorly studied. Other options may include salicylic acid, coal tar, benzoyl peroxide, and phototherapy.The condition is most common in infants within the first 3 months or in adults aged 30 to 70 years. In adults between 1% and 10% of people are affected. Males are more often affected than females. Up to 70% of babies may be affected at some point in time.

Signs and symptoms
Seborrhoeic dermatitis symptoms appear gradually, and usually the first signs are flaky skin and scalp. Symptoms occur most commonly anywhere on the skin of the scalp, behind the ears, on the face, and in areas where the skin folds. Flakes may be yellow, white or grayish. Redness and flaking may also occur on the skin near the eyelashes, on the forehead, around the sides of the nose, on the chest, and on the upper back.
In more severe cases, yellowish to reddish scaly pimples appear along the hairline, behind the ears, in the ear canal, on the eyebrows, on the bridge of the nose, around the nose, on the chest, and on the upper back.Commonly, patients experience mild redness, scaly skin lesions and in some cases hair loss. Other symptoms include patchy scaling or thick crusts on the scalp, red, greasy skin covered with flaky white or yellow scales, itching, soreness and yellow or white scales that may attach to the hair shaft.Seborrhoeic dermatitis can occur in infants younger than three months and it causes a thick, oily, yellowish crust around the hairline and on the scalp. Itching is not common among infants. Frequently, a stubborn diaper rash accompanies the scalp rash.

Causes
The cause of seborrhoeic dermatitis has not been fully clarified.In addition to the presence of Malassezia, genetic, environmental, hormonal, and immune-system factors are necessary for and/or modulate the expression of seborrhoeic dermatitis. The condition may be aggravated by illness, psychological stress, fatigue, sleep deprivation, change of season, and reduced general health. In children and babies, excessive vitamin A intake or issues with Δ6-desaturase enzymes have been correlated with increased risk. Seborrhoeic dermatitis-like eruptions are also associated with vitamin B6 deficiency. Those with immunodeficiency (especially infection with HIV) and with neurological disorders such as Parkinsons disease (for which the condition is an autonomic sign) and stroke are particularly prone to it.

Climate
Low humidity and low temperature are responsible for high frequency of seborrheic dermatitis.

Fungi
The condition is thought to be due to a local inflammatory response to over-colonization by Malassezia fungi species in sebum-producing skin areas including the scalp, face, chest, back, underarms, and groin. This is based on observations of high counts of Malassezia species in skin affected by seborrhoeic dermatitis and on the effectiveness of antifungals in treating the condition. Such species of Malassezia include M. furfur (formerly Pityrosporum ovale), M. globosa, M. restricta, M. sympodialis, and M. slooffiae. Although Malassezia appears to be the central predisposing factor in seborrhoeic dermatitis, it is thought that other factors are necessary for the presence of Malassezia to result in the pathology characteristic of the condition. This is based on the fact that summer growth of Malassezia in the skin alone does not result in seborrhoeic dermatitis. Besides antifungals, the effectiveness of anti-inflammatory drugs, which reduce inflammation, and antiandrogens, which reduce sebum production, provide further insights into the pathophysiology of seborrhoeic dermatitis. Eunuchs, owing to their low androgen levels and small sebaceous glands, do not develop seborrheic dermatitis.

Management
Humidity
A humidifier can be used to prevent low indoor humidity during winter (especially with indoor heating), and dry season. And a dehumidifier can be used during seasons with excessive humidity.

Medications
A variety of different types of medications are able to reduce symptoms of seborrhoeic dermatitis. These include certain antifungals, anti-inflammatory agents like corticosteroids and nonsteroidal anti-inflammatory drugs, antiandrogens, and antihistamines, among others.

Antifungals
Regular use of an over-the-counter or prescription antifungal shampoo or cream may help those with recurrent episodes. The topical antifungal medications ketoconazole and ciclopirox have the best evidence. It is unclear if other antifungals are equally effective as this has not been sufficiently studied. Antifungals that have been studied and found to be effective in the treatment of seborrhoeic dermatitis include ketoconazole, fluconazole, miconazole, bifonazole, sertaconazole, clotrimazole, flutrimazole, ciclopirox, terbinafine, butenafine, selenium sulfide, and lithium salts such as lithium gluconate and lithium succinate. Topical climbazole appears to have little effectiveness in the treatment of seborrhoeic dermatitis. Systemic therapy with oral antifungals including itraconazole, fluconazole, ketoconazole, and terbinafine is effective.

Anti-inflammatory treatments
Topical corticosteroids have been shown to be effective in short-term treatment of seborrhoeic dermatitis and are as effective or more effective than antifungal treatment with azoles. There is also evidence for the effectiveness of calcineurin inhibitors like tacrolimus and pimecrolimus as well as lithium salt therapy.Oral immunosuppressive treatment, such as with prednisone, has been used in short courses as a last resort in seborrhoeic dermatitis due to its potential side effects.

Antiandrogens
Seborrhoea, which is sometimes associated with seborrhoeic dermatitis, is recognized as an androgen-sensitive condition – that is, it is caused or aggravated by androgen sex hormones such as testosterone and dihydrotestosterone – and is a common symptom of hyperandrogenism (e.g., that seen in polycystic ovary syndrome). In addition, seborrhoea, as well as acne, are commonly associated with puberty due to the steep increase of androgen levels at that time.In accordance with the involvement of androgens in seborrhoea, antiandrogens, such as cyproterone acetate, spironolactone, flutamide, and nilutamide, are highly effective in alleviating the condition. As such, they are used in the treatment of seborrhoea, particularly severe cases. While beneficial in seborrhoea, effectiveness may vary with different antiandrogens; for instance, spironolactone (which is regarded as a relatively weak antiandrogen) has been found to produce a 50% improvement after three months of treatment, whereas flutamide has been found to result in an 80% improvement within three months. Cyproterone acetate, similarly more potent and effective than spironolactone, results in considerable improvement or disappearance of acne and seborrhoea in 90% of patients within three months.Systemic antiandrogen therapy is generally used to treat seborrhoea only in women, not in men, as these medications can result in feminization (e.g., gynecomastia), sexual dysfunction, and infertility in males. In addition, antiandrogens theoretically have the potential to feminize male fetuses in pregnant women and, for this reason, are usually combined with effective birth control in sexually active women who can or may become pregnant.

Antihistamines
Antihistamines are used primarily to reduce itching, if present </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Seborrheic keratosis and explain in detail? [/INST] A seborrheic keratosis is a non-cancerous (benign) skin tumour that originates from cells in the outer layer of the skin. Like liver spots, seborrheic keratoses are seen more often as people age.The tumours (also called lesions) appear in various colours, from light tan to black. They are round or oval, feel flat or slightly elevated, like the scab from a healing wound, and range in size from very small to more than 2.5 centimetres (1 in) across. They can often come in association with other skin conditions, including basal cell carcinoma. Rarely seborrheic keratosis and basal cell carcinoma occur at the same location. At clinical examination the differential diagnosis includes warts and melanoma. Because only the top layers of the epidermis are involved, seborrheic keratoses are often described as having a "pasted on" appearance. Some dermatologists refer to seborrheic keratoses as "seborrheic warts", because they resemble warts, but strictly speaking the term "warts" refers to lesions that are caused by human papillomavirus.

Cause
The cause of seborrheic keratosis is not known. The only definitive association is that its prevalence increases with age.

Diagnosis
Visual diagnosis is made by the "stuck on" appearance, horny pearls or cysts embedded in the structure. Darkly pigmented lesions can be challenging to distinguish from nodular melanomas. Furthermore, thin seborrheic keratoses on facial skin can be very difficult to differentiate from lentigo maligna even with dermatoscopy. Clinically, epidermal nevi are similar to seborrheic keratoses in appearance.  Epidermal nevi are usually present at or near birth </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sézary disease and explain in detail? [/INST] Sézary disease, or Sézary syndrome, is a type of cutaneous T-cell lymphoma that was first described by Albert Sézary. The affected T cells, known as Sézarys cells or Lutzner cells, have pathological quantities of mucopolysaccharides. Sézary disease is sometimes considered a late stage of mycosis fungoides with lymphadenopathy.

Signs and symptoms
Sézary disease and mycosis fungoides are cutaneous T-cell lymphomas having a primary manifestation in the skin. The diseases origin is a peripheral CD4+ T-lymphocyte, although rarer CD8+/CD4- cases have been observed </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Shigellosis and explain in detail? [/INST] Shigellosis is an infection of the intestines caused by Shigella bacteria. Symptoms generally start one to two days after exposure and include diarrhea, fever, abdominal pain, and feeling the need to pass stools even when the bowels are empty. The diarrhea may be bloody. Symptoms typically last five to seven days and it may take several months before bowel habits return entirely to normal. Complications can include reactive arthritis, sepsis, seizures, and hemolytic uremic syndrome.Shigellosis is caused by four specific types of Shigella. These are typically spread by exposure to infected feces. This can occur via contaminated food, water, or hands or sexual contact. Contamination may be spread by flies or when changing diapers (nappies). Diagnosis is by stool culture.The risk of infection can be reduced by properly washing the hands. There is no vaccine. Shigellosis usually resolves without specific treatment. Rest, and sufficient fluids by mouth, are recommended. Bismuth subsalicylate may help with the symptoms; however, medications that slow the bowels such as loperamide are not recommended. In severe cases antibiotics may be used but resistance is common. Commonly used antibiotics include ciprofloxacin and azithromycin.A 2005 report by the World Health Organization estimated that shigellosis occurs in at least 80 million people and results in about 700,000 deaths a year globally. Most cases occur in the developing world. Young children are most commonly affected. Outbreaks of disease may occur in childcare settings and schools. It is also relatively common among travelers. In the United States about half a million cases occur a year.

Signs and symptoms
Signs and symptoms may range from mild abdominal discomfort to full-blown dysentery characterized by cramps, diarrhea, with slimy-consistent stools, fever, blood, pus, or mucus in stools or tenesmus. Onset time is 12 to 96 hours, and recovery takes 5 to 7 days.
Infections are associated with mucosal ulceration, rectal bleeding, and drastic dehydration. Reactive arthritis and hemolytic uremic syndrome are possible sequelae that have been reported in the aftermath of shigellosis.The most common neurological symptom includes seizures.

Cause
Bacteria
Shigellosis is caused by a bacterial infection with Shigella, a bacterium that is genetically similar to and was once classified as E. coli. There are three serogroups and one serotype of Shigella:

Shigella flexneri
Shigella boydii
Shigella dysenteriae and
Shigella sonnei (serotype)The probability of being infected by any given strain of Shigella varies around the world. For instance, S. sonnei is the most common in the United States, while S. dysenteriae and S. boydii are rare in the U.S.

Transmission
Shigella is transmitted through the fecal-oral route of individuals infected with the disease, whether or not they are exhibiting symptoms. Long-term carriers of the bacteria are rare. The bacteria can infect not just humans but other primates as well.

Mechanism
Upon ingestion, the bacteria pass through the gastrointestinal tract until they reach the small intestine. There they begin to multiply until they reach the large intestine. In the large intestine, the bacteria cause cell injury and the beginning stages of Shigellosis via two main mechanisms: direct invasion of epithelial cells in the large intestine and production of enterotoxin 1 and enterotoxin 2.Unlike other bacteria, Shigella is not destroyed by the gastric acid in the stomach. As a result, it takes only 10 to 200 cells to cause an infection. This infectious dose is several order of magnitudes smaller than that of other species of bacteria (e.g. cholera, caused by the bacterium Vibrio cholerae, has an infectious dose between 108 and 1011 cells).

Diagnosis
The diagnosis of shigellosis is made by isolating the organism from diarrheal fecal sample cultures. Shigella species are negative for motility and are generally not lactose fermenters, but S. sonnei can ferment lactose. They typically do not produce gas from carbohydrates (with the exception of certain strains of S. flexneri) and tend to be overall biochemically inert. Shigella should also be urea hydrolysis negative. When inoculated to a triple sugar iron slant, they react as follows: K/A, gas -, and H2S -. Indole reactions are mixed, positive and negative, with the exception of S. sonnei, which is always indole negative. Growth on Hektoen enteric agar produces bluish-green colonies for Shigella and bluish-green colonies with black centers for Salmonella.

Prevention
Simple precautions can be taken to prevent getting shigellosis: wash hands before handling food and thoroughly cook all food before eating. The primary prevention methods are improved sanitation and personal and food hygiene, but a low-cost and efficacious vaccine would complement these methods.Since shigellosis is spread very quickly among children, keeping infected children out of daycare for 24 hours after their symptoms have disappeared, will decrease the occurrence of shigellosis in daycares.

Vaccine
Currently, no licensed vaccine targeting Shigella exists. Several vaccine candidates for Shigella are in various stages of development including live attenuated, conjugate, ribosomal, and proteosome vaccines. Shigella has been a longstanding World Health Organization target for vaccine development, and sharp declines in age-specific diarrhea/dysentery attack rates for this pathogen indicate that natural immunity does develop following exposure; thus, vaccination to prevent the disease should be feasible. Shigellosis is resistant to many antibiotics used to treat the disease, so vaccination is an important part of the strategy to reduce morbidity and mortality.

Treatment
Treatment consists mainly of replacing fluids and salts lost because of diarrhea. Replacement by mouth is satisfactory for most people, but some may need to receive fluids intravenously. Antidiarrheal drugs (such as diphenoxylate or loperamide) may prolong the infection and should not be used.

Antibiotics
Antibiotics should only be used in severe cases or for certain populations with mild symptoms (elderly, immunocompromised, food service industry workers, child care workers). For Shigella-associated diarrhea, antibiotics shorten the length of infection, but they are usually avoided in mild cases because many Shigella strains are becoming resistant to common antibiotics. Furthermore, effective medications are often in short supply in developing countries, which carry the majority of the disease burden from Shigella. Antidiarrheal agents may worsen the sickness, and should be avoided.In most cases, the disease resolves within four to eight days without antibiotics </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Short bowel syndrome and explain in detail? [/INST] Short bowel syndrome (SBS, or simply short gut) is a rare malabsorption disorder caused by a lack of functional small intestine. The primary symptom is diarrhea, which can result in dehydration, malnutrition, and weight loss. Other symptoms may include bloating, heartburn, feeling tired, lactose intolerance, and foul-smelling stool. Complications can include anemia and kidney stones.Most cases are due to the surgical removal of a large portion of the small intestine. This is most often required due to Crohns disease in adults and necrotising enterocolitis in young children. Other causes include damage to the small intestine from other means and being born with an abnormally short intestine. It usually does not develop until less than 2 m (6.6 ft) of the normally 6.1 m (20 ft) small intestine remains.Treatment may include a specific diet, medications, or surgery. The diet may include slightly salty and slightly sweet liquids, vitamin and mineral supplements, small frequent meals, and the avoidance of high fat food. Occasionally nutrients need to be given through an intravenous line, known as parenteral nutrition. Medications used may include antibiotics, antacids, loperamide, teduglutide, and growth hormone. Different types of surgery, including an intestinal transplant, may help some people.Short bowel syndrome newly occurs in about three per million people each year. There are estimated to be about 15,000 people with the condition in the United States. The prevalence in the United States is approximately 30 cases per million and in Europe it is approximately 1.4 cases per million (but the rate varies widely between countries). The prevalence of short bowel syndrome has increased by more than 2 fold in the last 40 years. It is classified as a rare disease by the European Medicines Agency. Outcomes depend on the amount of bowel remaining and whether or not the small bowel remains connected with the large bowel.

Signs and symptoms
The symptoms of short bowel syndrome can include:
Abdominal pain
Diarrhea and steatorrhea (oily, bulky stool, which can be malodorous)
Fluid depletion
Weight loss and malnutrition
FatiguePersons with short bowel syndrome may have complications caused by malabsorption of vitamins and minerals, such as deficiencies in vitamins A, D, E, K, B9 (folic acid), and B12, calcium, magnesium, iron, and zinc.  These may appear as anemia, hyperkeratosis (scaling of the skin), easy bruising, muscle spasms, poor blood clotting, and bone pain.

Causes
Short bowel syndrome in adults and children is most commonly caused by surgery (intestinal resection). In those who undergo intestinal resection, approximately 15% eventually develop small bowel syndrome (75% of those due to 1 large resection and 25% due to multiple separate intestinal resections). This surgery may be done for:

Crohns disease, an inflammatory disorder of the digestive tract
Mesenteric ischemia, embolic or thrombotic events that may occur in the arteries or veins that supply or drain the intestines respectively, leading to disruption of blood supply to the intestines and ischemia.
Volvulus, a twisting of the small intestine often caused by intestinal malrotation that quickly cuts off blood supply and leads to tissue death
Tumors of the small intestine
Radiation enteropathy, radiation injury to the small intestine, due to radiation therapy for cancer
Injury or trauma to the small intestine
Necrotizing enterocolitis (premature newborn)
Bypass surgery to treat obesity
Surgery to remove diseases or damaged portion of the small intestineSome children are also born with an abnormally short small intestine, known as congenital short bowel.Surgical complications, requiring re-surgery, are a common cause of small bowel syndrome, contributing up to 50% of cases based on some estimates. These surgical complications include internal hernias, volvuli, ischemia or profound hypotension.

Pathophysiology
The length of the small intestine can vary greatly, from as short as 2.75 m (9.0 ft) to as long as 10.49 m (34.4 ft). On average it is about 6.1 m (20 ft). Due to this variation it is recommended that following surgery the amount of bowel remaining be specified rather than the amount removed.Short bowel syndrome usually develops when there is less than 2 meters (6.6 feet) of the small intestine left to absorb sufficient nutrients.The resection of specific areas of the small bowel can lead to distinct symptoms in short bowel syndrome. The resection of the ileum leads to a malabsorption of vitamin B12, bile acids and the fat soluble vitamins A, D, E and K. Loss of the distal ileum also leads to loss of inhibitory hormones; leading to gastric hypersecretion, intestinal hypermotility (decreases in the intestinal transit time) leading to secretory diarrhea and macronutrient, micronutrient, vitamin and mineral deficiencies. Loss of the ileocecal valve leads to small intestinal bacterial overgrowth(SIBO) as bacterial flora normally found in the large intestines migrate proximally and colonize the small intestines leading to further malabsorption. SIBO leads to malabsorption as the bacteria colonizing the small intestine metabolize nutrients, directly competing with the intestinal absorption of nutrients. The bacteria colonizing the small intestines in SIBO may also cause bile acid deconjugation leading to malabsorption of lipids.In a process called intestinal adaptation, physiological changes to the remaining portion of the small intestine occur to increase its absorptive capacity. These changes usually take place over 1-2 years.  These changes include:

Enlargement (increased diameter) and lengthening of the villi found in the lining
Increase in the diameter of the small intestine
Slow down in peristalsis or movement of food through the small intestine (an increase in the transit time) to increase the time available for nutrient absorptionOsteoporosis is a very common comorbidity in people with short bowel syndrome who are on parenteral nutrition, with an estimated prevalence of 57-67%. The contributing factors to the osteoporosis include malnutrition, vitamin D deficiency due to malabsorption and vitamin D deficiency due to scarce sunlight exposure due to chronic disability.

Diagnosis
Definition
Intestinal failure is decreased intestinal function such that nutrients, water, and electrolytes are not sufficiently absorbed. Short bowel syndrome is when there is less than 2 m (6.6 ft) of working bowel and is the most common cause of intestinal failure.

Treatments
Symptoms of short bowel syndrome are usually addressed with medication.  These include:
Anti-diarrheal medicine (e.g. loperamide, codeine)
Vitamin, mineral supplements and L-glutamine powder mixed with water
H2 blocker and proton pump inhibitors to reduce stomach acid
Lactase supplement (to improve the bloating and diarrhea associated with lactose intolerance)In 2004, the USFDA approved a therapy that reduces the frequency and volume of total parenteral nutrition (TPN), comprising:  NutreStore (oral solution of glutamine) and Zorbtive (growth hormone, of recombinant DNA origin, for injection) together with a specialized oral diet. After 24 weeks of successful Phase III patient treatment trials, Teduglutide was shown to be relatively safe and effective with varying degrees of benefits and adverse effects per patient. Adequate safety evaluations prove to be difficult due to a limited sample size available for study, however. In 2012, an advisory panel to the USFDA voted unanimously to approve for treatment of SBS the agent teduglutide, a glucagon-like peptide-2 analog developed by NPS Pharmaceuticals, who intend to market the agent in the United States under the brandname Gattex </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hypersalivation and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Night terror and explain in detail? [/INST] Night terror, also called sleep terror, is a sleep disorder causing feelings of panic or dread and typically occurring during the first hours of stage 3–4 non-rapid eye movement (NREM) sleep and lasting for 1 to 10 minutes. It can last longer, especially in children. Sleep terror is classified in the category of NREM-related parasomnias in the International Classification of Sleep Disorders. There are two other categories: REM-related parasomnias and other parasomnias. Parasomnias are qualified as undesirable physical events or experiences that occur during entry into sleep, during sleep, or during arousal from sleep.Sleep terrors usually begin in childhood and usually decrease as age increases. Factors that may lead to sleep terrors are young age, sleep deprivation, medications, stress, fever, and intrinsic sleep disorders. The frequency and severity differ among individuals; the interval between episodes can be as long as weeks and as short as minutes or hours. This has created a situation in which any type of nocturnal attack or nightmare may be confused with and reported as a night terror.Night terrors tend to happen during periods of arousal from delta sleep, or slow-wave sleep. Delta sleep occurs most often during the first half of a sleep cycle, which indicates that people with more delta-sleep activity are more prone to night terrors. However, they can also occur during daytime naps. Night terrors can often be mistaken for confusional arousal.While nightmares (bad dreams during REM sleep that cause feelings of horror or fear) are relatively common during childhood, night terrors occur less frequently. The prevalence of sleep terrors in general is unknown. The number of small children who experience sleep terror episodes (distinct from sleep terror disorder, which is recurrent and causes distress or impairment) are estimated at 36.9% at 18 months of age and at 19.7% at 30 months. In adults, the prevalence is lower, at only 2.2%. Night terrors have been known since ancient times, although it was impossible to differentiate them from nightmares until rapid eye movement was studied.

Signs and symptoms
The universal feature of night terrors is inconsolability, very similar to that of a panic attack. During night terror bouts, people are usually described as "bolting upright" with their eyes wide open and a look of fear and panic on their faces. They will often yell, scream, or attempt to speak, though such speech is often incomprehensible. Furthermore, they will usually sweat, exhibit rapid breathing, and have a rapid heart rate (autonomic signs). In some cases, individuals are likely to have even more elaborate motor activity, such as a thrashing of limbs—which may include punching, swinging, or fleeing motions. There is a sense that the individuals are trying to protect themselves and/or escape from a possible threat of bodily injury. Although people may seem to be awake during a night terror, they will appear confused, be inconsolable and/or unresponsive to attempts to communicate with them, and may not recognize others familiar to them. Occasionally, when a person with a night terror is awakened, they will lash out at the one awakening them, which can be dangerous to that individual. Most people who experience this do not remember the incident the next day, although brief dream images or hallucinations may occur and be recalled. Sleepwalking is also common during night-terror bouts, as sleepwalking and night terrors are different manifestations of the same parasomnia. Both children and adults may display behaviour indicative of attempting to escape; some may thrash about or get out of bed and begin walking or running around aimlessly while inconsolable, increasing the risk of accidental injury. The risk of injury to others may be exacerbated by inadvertent provocation by nearby people, whose efforts to calm the individual may result in a physically violent response from the individual as they attempt to escape.During lab tests, subjects are known to have very high voltages of electroencephalography (EEG) delta activity, an increase in muscle tone, and a doubled or faster heart rate. Brain activities during a typical episode show theta and alpha activity when monitored with an EEG. Episodes can include tachycardia. Night terrors are also associated with intense autonomic discharge of tachypnea, flushing, diaphoresis, and mydriasis—that is, unconscious or involuntary rapid breathing, reddening of the skin, profuse sweating, and dilation of the pupils. Abrupt but calmer arousal from NREM sleep, short of a full night-terror episode, is also common.
In children with night terrors, there is no increased occurrence of psychiatric diagnoses. However, in adults with night terrors there is a close association with psychopathology and mental disorders. There may be an increased occurrence of night terrors—particularly among those with post-traumatic stress disorder (PTSD) and generalized anxiety disorder (GAD). It is also likely that some personality disorders may occur in individuals with night terrors, such as dependent, schizoid, and borderline personality disorders. There have been some symptoms of depression and anxiety that have increased in individuals that have frequent night terrors. Low blood sugar is associated with both pediatric and adult night terrors. A study of adults with thalamic lesions of the brain and brainstem have been occasionally associated with night terrors. Night terrors are closely linked to sleepwalking and frontal lobe epilepsy.

Children
Night terrors typically occur in children between the ages of three and twelve years, with a peak onset in children aged three and a half years old.
An estimated 1–6% of children experience night terrors. Children of both sexes and all ethnic backgrounds are affected equally. In children younger than three and a half years old, peak frequency of night terrors is at least one episode per week. Among older children, peak frequency of night terrors is one or two episodes per month. The children will most likely have no recollection of the episode the next day. Pediatric evaluation may be sought to exclude the possibility that the night terrors are caused by seizure disorders or breathing problems. Most children will outgrow sleep terrors.

Adults
Night terrors in adults have been reported in all age ranges. Though the symptoms of night terrors in adolescents and adults are similar, the cause, prognosis and treatment are qualitatively different. These night terrors can occur each night if the individual does not eat a proper diet, get the appropriate amount or quality of sleep (e.g. sleep apnea), is enduring stressful events, or if he or she remains untreated. Adult night terrors are much less common, and often respond to treatments to rectify causes of poor quality or quantity of sleep. Night terrors are classified as a mental and behavioral disorder in the ICD. A study done about night terrors in adults showed that other psychiatric symptoms were prevalent in most patients experiencing night terrors hinting at the comorbidity of the two. There is some evidence of a link between night terrors and hypoglycemia.When a night terror happens, it is typical for a person to wake up yelling and kicking and to be able to recognize what he or she is saying. The person may even run out of the house (more common among adults) which can then lead to violent actions. It has been found that some adults who have been on a long-term intrathecal clonidine therapy show side effects of night terrors, such as feelings of terror early in the sleep cycle. This is due to the possible alteration of cervical/brain clonidine concentration. In adults, night terrors can be symptomatic of neurological disease and can be further investigated through an MRI procedure.

Causes
There is some evidence that a predisposition to night terrors and other parasomnias may be congenital. Individuals frequently report that past family members have had either episodes of sleep terrors or sleepwalking. In some studies, a ten-fold increase in the prevalence of night terrors in first-degree biological relatives has been observed—however, the exact link to inheritance is not known. Familial aggregation has been found suggesting that there is an autosomal mode of inheritance. In addition, some laboratory findings suggest that sleep deprivation and having a fever can increase the likelihood of a night terror episode occurring. Other contributing factors include nocturnal asthma, gastroesophageal reflux, central nervous system medications, and a constricted nasal passage. Special consideration must be used when the subject with narcolepsy, as there may be a link. There have been no findings that show a cultural difference between manifestations of night terrors, though it is thought that the significance and cause of night terrors differ within cultures.
Also, older children and adults provide highly detailed and descriptive images associated with their sleep terrors compared to younger children, who either cannot recall or only vaguely remember. Sleep terrors in children are also more likely to occur in males than females; in adults, the ratio between sexes is equal. A longitudinal study examined twins, both identical and fraternal, and found that a significantly higher concordance rate of night terror was found in identical twins than in fraternal.Though the symptoms of night terrors in adolescents and adults are similar, their causes, prognoses, and treatments are qualitatively different. There is some evidence that suggests that night terrors can occur if the individual does not eat a proper diet, does not get the appropriate amount or quality of sleep (e.g., because of sleep apnea), or is enduring stressful events. Adults who have experienced sexual abuse are more likely to receive a diagnosis of sleep disorders, including night terrors. Overall, though, adult night terrors are much less common and often respond best to treatments that rectify causes of poor quality or quantity of sleep.

Diagnosis
The DSM-5 diagnostic criteria for sleep terror disorder requires:
Recurrent periods where the individual abruptly but not completely wakes from sleep, usually occurring during the first third major period of sleep.
The individual experiences intense fear with a panicky scream at the beginning and symptoms of autonomic arousal, such as increased heart rate, heavy breathing, and increased perspiration. The individual cannot be soothed or comforted during the episode.
The individual is unable or almost unable to remember images of the dream (only a single visual scene for example).
The episode is completely forgotten.
The occurrence of the sleep terror episode causes clinically significant distress or impairment in the individuals functioning.
The disturbance is not due to the effects of a substance, general medical condition or medication.
Coexisting mental or medical disorders do not explain the episodes of sleep terrors.

Differential diagnosis
Night terrors are distinct from nightmares. In fact, in nightmares there are almost never vocalization or agitation, and if there are any, they are less strong in comparison to night terrors. In addition, nightmares appear ordinarily during REM sleep in contrast to night terrors, which occur in NREM sleep. Finally, individuals with nightmares can wake up completely and easily and have clear and detailed memories of their dreams.A distinction between night terrors and epileptic seizure is required. Indeed, an epileptic seizure could happen during the night but also during the day. To make the difference between both of them, an EEG can be done and if there are some anomalies on it, it would rather be an epileptic seizure.

Assessment
The assessment of sleep terrors is similar to the assessment of other parasomnias and must include:
When the episode occurs during the sleep period
Age of onset
How often these episodes occur (frequency) and how long they last for (duration)
Description of the episode, including behavior, emotions, and thoughts during and after the event
How responsive the patient is to external stimuli during the episode
How conscious or aware the patient is, when awakened from an episode
If the episode is remembered afterwards
The triggers or precipitating factors
Sleep–wake pattern and sleep environment
Daytime sleepiness
Other sleep disorders that might be present
Family history for NREM parasomnias and other sleep disorders
Medical, psychiatric, and neurological history
Medication and substance use historyAdditionally, a home video might be helpful for a proper diagnosis. A polysomnography in the sleep laboratory is recommended for ruling out other disorders, however, sleep terrors occur less frequently in the sleep laboratory than at home and a polysomnography can therefore be unsuccessful at recording the sleep terror episode.

Treatment
In most children, night terrors eventually subside and do not need to be treated. It may be helpful to reassure the child and their family that they will outgrow this disorder.The duration of one episode is mostly brief but it may last longer if parents try to wake up the child. Awakening the child may make their agitation stronger </s>