<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 Amniotic fluid embolism and explain in detail? [/INST] An amniotic fluid embolism (AFE) is a very uncommon childbirth (obstetric) emergency in which amniotic fluid enters the blood stream of the mother, triggering a serious reaction, which results in cardiorespiratory (heart and lung) collapse and massive bleeding (coagulopathy). The rate at which it occurs is 1 instance per 20,000 births and it comprises 10% of all maternal deaths. This condition is unpredictable and no risk factors have been verified.

Signs and symptoms
Amniotic fluid embolism is suspected when a woman giving birth experiences very sudden insufficient oxygen to body tissues, low blood pressure, and profuse bleeding due to defects in blood coagulation. Though symptoms and signs can be profound, they also can be entirely absent. There is much variation in how each instance progresses.

Causes
AFE is very rare and complex. The disorder occurs during the last stages of labor when amniotic fluid enters the circulatory system of the mother via tears in the placental membrane or uterine vein rupture. Upon later analysis, fetal cells are found in the maternal circulation. When the fetal cells and amniotic fluid enter the bloodstream, reactions occur that cause severe changes in the mechanisms that affect blood clotting. Disseminated intravascular coagulation occurs and results in serious bleeding. The condition can also develop after elective abortion, amniocentesis, cesarean delivery, or trauma </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 Bells palsy and explain in detail? [/INST] Bells palsy is a type of facial paralysis that results in a temporary inability to control the facial muscles on the affected side of the face. In most cases, the weakness is temporary and significantly improves over weeks. Symptoms can vary from mild to severe. They may include muscle twitching, weakness, or total loss of the ability to move one or, in rare cases, both sides of the face. Other symptoms include drooping of the eyelid, a change in taste, and pain around the ear. Typically symptoms come on over 48 hours. Bells palsy can trigger an increased sensitivity to sound known as hyperacusis.The cause of Bells palsy is unknown and it can occur in any age. Risk factors include diabetes, a recent upper respiratory tract infection, and pregnancy. It results from a dysfunction of cranial nerve VII (the facial nerve). Many believe that this is due to a viral infection that results in swelling. Diagnosis is based on a persons appearance and ruling out other possible causes. Other conditions that can cause facial weakness include brain tumor, stroke, Ramsay Hunt syndrome type 2, myasthenia gravis, and Lyme disease.The condition normally gets better by itself, with most achieving normal or near-normal function. Corticosteroids have been found to improve outcomes, while antiviral medications may be of a small additional benefit. The eye should be protected from drying up with the use of eye drops or an eyepatch. Surgery is generally not recommended. Often signs of improvement begin within 14 days, with complete recovery within six months. A few may not recover completely or have a recurrence of symptoms.Bells palsy is the most common cause of one-sided facial nerve paralysis (70%). It occurs in 1 to 4 per 10,000 people per year. About 1.5% of people are affected at some point in their lives. It most commonly occurs in people between ages 15 and 60. Males and females are affected equally. It is named after Scottish surgeon Charles Bell (1774–1842), who first described the connection of the facial nerve to the condition.

Signs and symptoms
Bells palsy is characterized by a one-sided facial droop that comes on within 72 hours. In rare cases (<1%), it can occur on both sides resulting in total facial paralysis.The facial nerve controls a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, salivation, flaring nostrils and raising eyebrows. It also carries taste sensations from the anterior two-thirds of the tongue, through the chorda tympani nerve (a branch of the facial nerve). Because of this, people with Bells palsy may present with loss of taste sensation in the anterior 2⁄3 of the tongue on the affected side.Although the facial nerve innervates the stapedius muscle of the middle ear (through the tympanic branch), sound sensitivity, causing normal sounds to be perceived as very loud (hyperacusis), and dysacusis are possible but hardly ever clinically evident.Although defined as a mononeuritis (involving only one nerve), people diagnosed with Bells palsy may have "myriad neurological symptoms" including "facial tingling, moderate or severe headache/neck pain, memory problems, balance problems, ipsilateral limb paresthesias, ipsilateral limb weakness, and a sense of clumsiness" that are "unexplained by facial nerve dysfunction".

Cause
The cause of Bells palsy is unknown. Risk factors include diabetes, a recent upper respiratory tract infection, and pregnancy.Some viruses are thought to establish a persistent (or latent) infection without symptoms, e.g., the varicella zoster virus and the Epstein–Barr virus, both of the herpes family. Reactivation of an existing (dormant) viral infection has been suggested as a cause of acute Bells palsy. As the facial nerve swells and becomes inflamed in reaction to the infection, it causes pressure within the Fallopian canal, resulting in the restriction of blood and oxygen to the nerve cells. Other viruses and bacteria that have been linked to the development of Bells palsy include HIV, sarcoidosis and Lyme Disease. This new activation could be triggered by trauma, environmental factors, and metabolic or emotional disorders.Familial inheritance has been found in 4–14% of cases. There may also be an association with migraines.In December 2020, the U.S. FDA recommended that recipients of the Pfizer and Moderna COVID-19 vaccines should be monitored for symptoms of Bells palsy after several cases were reported among clinical trial participants, though the data were not sufficient to determine a causal link.

Genetics
A meta-analysis of genome-wide association study (GWAS) identified the first unequivocal association with Bells palsy.

Pathophysiology
Bells palsy is the result of a malfunction of the facial nerve (cranial nerve VII), which controls the muscles of the face. Facial palsy is typified by inability to move the muscles of facial expression. The paralysis is of the infranuclear/lower motor neuron type.
It is thought that as a result of inflammation of the facial nerve, pressure is produced on the nerve where it exits the skull within its bony canal (the stylomastoid foramen), blocking the transmission of neural signals or damaging the nerve. Patients with facial palsy for which an underlying cause can be found are not considered to have Bells palsy per se. Possible causes of facial paralysis include tumor, meningitis, stroke, diabetes mellitus, head trauma and inflammatory diseases of the cranial nerves (sarcoidosis, brucellosis, etc.). In these conditions, the neurologic findings are rarely restricted to the facial nerve. Babies can be born with facial palsy. In a few cases, bilateral facial palsy has been associated with acute HIV infection.
In some research, the herpes simplex virus type 1 (HSV-1) has been identified in a majority of cases diagnosed as Bells palsy through endoneurial fluid sampling. Other research, however, identified, out of a total of 176 cases diagnosed as Bells palsy, HSV-1 in 31 cases (18%) and herpes zoster in 45 cases (26%).In addition, HSV-1 infection is associated with demyelination of nerves. This nerve damage mechanism is different from the above-mentioned—that edema, swelling and compression of the nerve in the narrow bone canal is responsible for nerve damage. Demyelination may not even be directly caused by the virus, but by an unknown immune response.

Diagnosis
Bells palsy is a diagnosis of exclusion, meaning it is diagnosed by elimination of other reasonable possibilities. By definition, no specific cause can be determined. There are no routine lab or imaging tests required to make the diagnosis. The degree of nerve damage can be assessed using the House-Brackmann score.
One study found that 45% of patients are not referred to a specialist, which suggests that Bells palsy is considered by physicians to be a straightforward diagnosis that is easy to manage.Other conditions that can cause similar symptoms include herpes zoster, Lyme disease, sarcoidosis, stroke, and brain tumors.

Differential diagnosis
Once the facial paralysis sets in, many people may mistake it as a symptom of a stroke; however, there are a few subtle differences. A stroke will usually cause a few additional symptoms, such as numbness or weakness in the arms and legs. And unlike Bells palsy, a stroke will usually let patients control the upper part of their faces. A person with a stroke will usually have some wrinkling of their forehead.In areas where Lyme disease is common, it accounts for about 25% of cases of facial palsy. In the U.S., Lyme is most common in the New England and Mid-Atlantic states and parts of Wisconsin and Minnesota. The first sign of about 80% of Lyme infections, typically one or two weeks after a tick bite, is usually an expanding rash that may be accompanied by headaches, body aches, fatigue, or fever. In up to 10–15% of Lyme infections, facial palsy appears several weeks later, and may be the first sign of infection that is noticed as the Lyme rash typically does not itch and is not painful. The likelihood that the facial palsy is caused by Lyme disease should be estimated, based on recent history of outdoor activities in likely tick habitats during warmer months, recent history of rash or symptoms such as headache and fever, and whether the palsy affects both sides of the face (much more common in Lyme than in Bells palsy). If that likelihood is more than negligible, a serological test for Lyme disease should be performed, and if it exceeds 10%, empiric therapy with antibiotics should be initiated, without corticosteroids, and reevaluated upon completion of laboratory tests for Lyme disease. Corticosteroids have been found to harm outcomes for facial palsy caused by Lyme disease.One disease that may be difficult to exclude in the differential diagnosis is involvement of the facial nerve in infections with the herpes zoster virus. The major differences in this condition are the presence of small blisters, or vesicles, on the external ear, significant pain in the jaw, ear face, and/or neck and hearing disturbances, but these findings may occasionally be lacking (zoster sine herpete). Reactivation of existing herpes zoster infection leading to facial paralysis in a Bells palsy type pattern is known as Ramsay Hunt syndrome type 2. The prognosis for Bells palsy patients is generally much better than for Ramsay Hunt syndrome type 2 patients.

Treatment
Steroids have been shown to be effective at improving recovery in Bells palsy while antivirals have not. In those who are unable to close their eyes, eye protective measures are required. Management during pregnancy is similar to management in the non-pregnant.

Steroids
Corticosteroids such as prednisone improve recovery at 6 months and are thus recommended. Early treatment (within 3 days after the onset) is necessary for benefit with a 14% greater probability of recovery.

Antivirals
One review found that antivirals (such as aciclovir) are ineffective in improving recovery from Bells palsy beyond steroids alone in mild to moderate disease. Another review found a benefit when combined with corticosteroids but stated the evidence was not very good to support this conclusion.In severe disease it is also unclear. One 2015 review found no effect regardless of severity. Another review found a small benefit when added to steroids.They are commonly prescribed due to a theoretical link between Bells palsy and the herpes simplex and varicella zoster virus. There is still the possibility that they might result in a benefit less than 7% as this has not been ruled out.

Eye protection
When Bells palsy affects the blink reflex and stops the eye from closing completely, frequent use of tear-like eye drops or eye ointments is recommended during the day and protecting the eyes with patches or taping them shut is recommended for sleep and rest periods.

Physiotherapy
Physiotherapy can be beneficial to some individuals with Bells palsy as it helps to maintain muscle tone of the affected facial muscles and stimulate the facial nerve. It is important that muscle re-education exercises and soft tissue techniques be implemented prior to recovery in order to help prevent permanent contractures of the paralyzed facial muscles. To reduce pain, heat can be applied to the affected side of the face. There is no high quality evidence to support the role of electrical stimulation for Bells palsy.

Surgery
Surgery may be able to improve outcomes in facial nerve palsy that has not recovered. A number of different techniques exist. Smile surgery or smile reconstruction is a surgical procedure that may restore the smile for people with facial nerve paralysis. Adverse effects include hearing loss which occurs in 3–15% of people. A Cochrane review (updated in 2021), after reviewing applicable randomized and quasi-randomized controlled trials was unable to determine if early surgery is beneficial or harmful. As of 2007 the American Academy of Neurology did not recommend surgical decompression.

Alternative medicine
The efficacy of acupuncture remains unknown because the available studies are of low quality (poor primary study design or inadequate reporting practices). There is very tentative evidence for hyperbaric oxygen therapy in severe disease.

Prognosis
Most people with Bells palsy start to regain normal facial function within 3 weeks—even those who do not receive treatment. In a 1982 study, when no treatment was available, of 1,011 patients, 85% showed first signs of recovery within 3 weeks after onset. For the other 15%, recovery occurred 3–6 months later.
After a follow-up of at least one year or until restoration, complete recovery had occurred in more than two-thirds (71%) of all patients. Recovery was judged moderate in 12% and poor in only 4% of patients. Another study found that incomplete palsies disappear entirely, nearly always in the course of one month. The patients who regain movement within the first two weeks nearly always remit entirely. When remission does not occur until the third week or later, a significantly greater part of the patients develop sequelae. A third study found a better prognosis for young patients, aged below 10 years old, while the patients over 61 years old presented a worse prognosis.Major possible complications of the condition are chronic loss of taste (ageusia), chronic facial spasm, facial pain and corneal infections. Another complication can occur in case of incomplete or erroneous regeneration of the damaged facial nerve. The nerve can be thought of as a bundle of smaller individual nerve connections that branch out to their proper destinations. During regrowth, nerves are generally able to track the original path to the right destination—but some nerves may sidetrack leading to a condition known as synkinesis. For instance, regrowth of nerves controlling muscles attached to the eye may sidetrack and also regrow connections reaching the muscles of the mouth. In this way, movement of one also affects the other. For example, when the person closes the eye, the corner of the mouth lifts involuntarily.
Around 9% of people have some sort of ongoing problems after Bells palsy, typically the synkinesis already discussed, or spasm, contracture, tinnitus or hearing loss during facial movement or crocodile-tear syndrome. This is also called gustatolacrimal reflex or Bogorads syndrome and results in shedding tears while eating. This is thought to be due to faulty regeneration of the facial nerve, a branch of which controls the lacrimal and salivary glands. Gustatorial sweating can also occur.

Epidemiology
The number of new cases of Bells palsy ranges from about one to four cases per 10,000 population per year. The rate increases with age </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 Toxic leukoencephalopathy and explain in detail? [/INST] Toxic leukoencephalopathy is a rare condition that is characterized by progressive damage (-pathy) to white matter (-leuko-) in the brain (-encephalo-), particularly myelin, due to causes such as exposure to substance use, environmental toxins, or chemotherapeutic drugs. The prevalence of this disease is infrequent and often goes unreported, especially in cases resulting from substance use. Magnetic resonance imaging (MRI) is a popular method to study and diagnose the disease. However, even with technological advances, the exact mechanism and underlying pathophysiology of toxic leukoencephalopathy remains unknown and is thought to vary between sources of toxicity. The clinical severity of toxic leukoencephalopathy also varies among patients, exposure time, concentration, and purity of the toxic agent. Some reversibility of the condition has been seen in many cases when the toxic agent is removed.

Signs and symptoms
Symptoms vary widely between sources of toxicity, dosage, length of time patient was exposed to the toxic substance, patient history, and patient genetics. Especially in the case of leukoencephalopathy developing due to substance use or environmental toxins, symptoms typically do not develop until several days to months after exposure to the pharmacological agent. Clinical features range from inattention, forgetfulness, and changes in personality to dementia, coma, and even death. Obvious signs of the condition are difficulty with cognitive function and equilibrioception. Common initial symptoms include confusion, somnolence, generalized seizures, headaches, and vision impairment.Young acute lymphoblastic leukemia patients with methotrexate-induced leukoencephalopathy appear asymptomatic. However, toxic leukoencephalopathy induced by substance use or environmental toxins have had more damaging side effects. Heroin-induced leukoencephalopathy has had three stages described. The first stage features soft (pseudobulbar) speech, cerebellar ataxia, motor restlessness, and apathy/bradyphrenia. The intermediate stage includes pyramidal tract and pseudobulbar signs, spastic paresis, myoclonic jerks, and choreoathetoid movements. The final or terminal stage is characterized by stretching spasms, akinetic mutism, hypotonic paresis, central pyrexia, and death. Similarly, leukoencephalopathy induced by orally administered methotrexate for arthritis patients presents similar symptoms including ataxia, dysarthria, and seizures; however, long-term cognitive effects remain unknown. Symptoms of leukoencephalopathy caused by overdose of metronidazole medication include dysarthria, gait disturbance, weakness of extremities, and mental confusion.  Despite the pharmacological agent or source of toxicity, some patients completely recover from toxic leukoencephalopathy.

Related disorders
Posterior reversible encephalopathy syndrome (PRES) can also result from medication toxicity. Symptoms similar to those of leukoencephalopathy patients have been seen in PRES patients. However, the prognosis of toxic leukoencephalopathy is typically slightly worse than that of PRES because toxic leukoencephalopathy is more likely to lead to ataxia, dementia, or coma.Hypoglycemic encephalopathy is often seen in diabetics as a result to accidental overdose with the long-acting sulfonylurea drug group. Brain regions affected by toxic leukoencephalopathy have been seen to be affected by this disease as well; however, hypoglycaemic encephalopathy has been known to involve both white and grey matter abnormalities.

Causes
Various pharmacological agents have been known to cause toxic leukoencephalopathy. The most common causes are substance use and chemotherapy; however, the disease has also occurred on the rare occasion as a side effect of certain medications and environmental toxins.

Substance use
Leukoencephalopathy may result from the inhalation, intravenous injection, or ingestion of addictive substances. However, such occurrences are rare, sporadic, and often go undocumented. Leukoencephalopathy caused by inhalation of heroin, also known as "chasing the dragon" syndrome, is one of the most studied of these rare occurrences and has even been recognized for over twenty five years.It is believed by some researchers that heroin-induced leukoencephalopathy may be caused by a contaminant, or “cutting agent,” in the heroin. However, no such agent has been identified; and indeed, toxic leukoencephalopathy has been observed as a result of intoxication with contaminant-free opiates. Cases include a 65-year-old woman who had mistakenly been taking three times the dose of methadone that had been prescribed for pain management, and a young girl intoxicated with pure morphine sulfate tablets.Other drugs that have been associated with toxic leukoencephalopathy in much more rare occurrences include psychoactive drug 2C-E ("Europa"),  oxycodone, cocaine, and methadone.  The dose–response relationship for these substances remains unclear.

Chemotherapy
Various chemotherapy drugs have shown increased risk of cancer patients developing leukoencephalopathy. High doses of intravenous methotrexate, or intrathecal (injection into the spinal fluid) methotrexate are both necessary components of chemotherapy for acute lymphoblastic leukemia. However, these are known to cause asymptomatic leukoencephalopathy in children and young adults. Methotrexate-related leukoencephalopathy prevalence has been reported to decline with time and dosage. Other chemotherapeutic agents that have induced neurotoxicity include 5-fluorouracil and fludarabine.

Medication neurotoxicity
Besides its role in chemotherapy, methotrexate is also used as an orally administered treatment for rheumatoid arthritis. Leukoencephalopathy can develop from long-term treatment of methotrexate even at low doses. In contrast to intravenous methotrexate for cancer patients, leukoencephalopathy induced by orally taken methotrexate may be associated with cognitive dysfunction and even death.Oxycodone is the main active ingredient in various oral pain relief medications. High doses of opiates such as oxycodone can lead to leukoencephalopathy. The activity of various opioid and nociceptive receptors appear to play a role in the disease; however, the exact mechanism remains unknown.Metronidazole, an antibiotic used to treat anaerobic and protozoal infections, has been known at high doses to produce neurologic symptoms associated with toxic leukoencephalopathy.

Other
Toxic leukoencephalopathy may also result from carbon monoxide poisoning, ingestion of methanol, ingestion of ethylene, toluene toxicity, ethanol poisoning, ingestion of methylenedioxymethamphetamine (MDMA or "ecstasy"), or ingestion of paradichlorobenzene, which is a toxic agent in mothballs.

Diagnosis
Due to advances in MRI, this neurological disorder has been characterized more successfully in more recent years. MRI can aid in the detection of injured brain tissue; however, the severity and extent of the damage demonstrated by imaging does not always reflect patient clinical status. Toxic leukoencephalopathy encompasses the degeneration of white matter tracts devoted to higher cerebral function; however, white matter can appear normal until the disease has progressed more intensely. Toxic leukoencephalopathy-related damage to central nervous system (CNS) white matter, typically of the periventricular nucleus, and other structures in the brain is often bilateral and symmetric. Heroin-induced leukoencephalopathy often involves damage to cerebellar white matter, posterior cerebral white matter, posterior limb of internal capsule, and cerebellar peduncles </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 Colitis and explain in detail? [/INST] Colitis is an inflammation of the colon. Colitis may be acute and self-limited or long-term. It broadly fits into the category of digestive diseases.
In a medical context, the label colitis (without qualification) is used if:

The cause of the inflammation in the colon is undetermined; for example, colitis may be applied to Crohns disease at a time when the diagnosis is unknown, or
The context is clear; for example, an individual with ulcerative colitis is talking about their disease with a physician who knows the diagnosis.

Signs and symptoms
The signs and symptoms of colitis are quite variable and dependent on the cause of the given colitis and factors that modify its course and severity.Common symptoms of colitis may include: mild to severe abdominal pains and tenderness (depending on the stage of the disease), persistent hemorrhagic diarrhea with pus either present or absent in the stools, fecal incontinence, flatulence, fatigue, loss of appetite and unexplained weight loss.More severe symptoms may include: shortness of breath, a fast or irregular heartbeat and fever.Other less common or rare non-specific symptoms that may accompany colitis include: arthritis, mouth ulcers, painful, red and swollen skin and irritated, bloodshot eyes.Signs seen on colonoscopy include: colonic mucosal erythema (redness of the colons inner surface), ulcerations and hemorrhage.

Diagnosis
Symptoms suggestive of colitis are worked-up by obtaining the medical history, a physical examination and laboratory tests (CBC, electrolytes, stool culture and sensitivity, stool ova and parasites et cetera).  Additional tests may include medical imaging (e.g. abdominal computed tomography, abdominal X-rays) and an examination with a camera inserted into the rectum (sigmoidoscopy, colonoscopy).An important investigation in the assessment of colitis is biopsy. A very small piece of tissue (usually about 2mm) is removed from the bowel mucosa during endoscopy and examined under the microscope by a histopathologist. It can provide important information regarding the cause of the disease and the extent of bowel damage.

Types
There are many types of colitis. They are usually classified by the cause.
Types of colitis include:

Autoimmune
Inflammatory bowel disease (IBD) – a group of chronic colitides.
Ulcerative colitis (UC) – a chronic colitis that affects the large intestine.
Crohns disease (CD) – another type of IBD that often leads to colitis.

Unknown
Microscopic colitis – a colitis diagnosed by microscopic examination of colonic tissue; macroscopically ("to the eye") it appears normal.
Lymphocytic colitis
Collagenous colitis

Treatment-caused
Diversion colitis
Chemical colitis
Chemotherapy-induced colitis
Radiation colitis
Checkpoint inhibitor induced colitis

Vascular disease
Ischemic colitis

Infectious
Infectious colitisA subtype of infectious colitis is Clostridioides difficile colitis, which is informally abbreviated as "C-diff colitis". It classically forms pseudomembranes and is often referred to as pseudomembranous colitis, which is its (nonspecific) histomorphologic description.
Enterohemorrhagic colitis may be caused by Shiga toxin in Shigella dysenteriae or Shigatoxigenic group of Escherichia coli (STEC), which includes serotype O157:H7 and other enterohemorrhagic E. coli.Parasitic infections, like those caused by Entamoeba histolytica, can also cause colitis.

Unclassifiable colitides
Indeterminate colitis is the classification for colitis that has features of both Crohns disease and ulcerative colitis.  Indeterminate colitis behaviour is usually closer to ulcerative colitis than Crohns disease.Atypical colitis is a phrase that is occasionally used by physicians for a colitis that does not conform to criteria for accepted types of colitis.  It is not an accepted diagnosis per se and, as such, a colitis that cannot be definitively classified.

Treatment
Some people may be admitted into the hospital following the colonoscopy depending on results.  It is sometimes necessary to get the patient started on a steroid to speed up the healing of the colon. It may also be necessary to get the patient hydrated from the fluid loss and iron replaced from the loss of blood.  After a hospital stay, the patient may be put on a daily medication to manage their  chronic colitis </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 Ascending cholangitis and explain in detail? [/INST] Ascending cholangitis, also known as acute cholangitis or simply cholangitis, is inflammation of the bile duct, usually caused by bacteria ascending from its junction with the duodenum (first part of the small intestine). It tends to occur if the bile duct is already partially obstructed by gallstones.Cholangitis can be life-threatening, and is regarded as a medical emergency. Characteristic symptoms include yellow discoloration of the skin or whites of the eyes, fever, abdominal pain, and in severe cases, low blood pressure and confusion. Initial treatment is with intravenous fluids and antibiotics, but there is often an underlying problem (such as gallstones or narrowing in the bile duct) for which further tests and treatments may be necessary, usually in the form of endoscopy to relieve obstruction of the bile duct. The word is from Greek chol-, bile + ang-, vessel + -itis, inflammation.

Signs and symptoms
A person with cholangitis may complain of abdominal pain (particularly in the right upper quadrant of the abdomen), fever, rigors (uncontrollable shaking) and a feeling of uneasiness (malaise). Some may report jaundice (yellow discoloration of the skin and the whites of the eyes).Physical examination findings typically include jaundice and right upper quadrant tenderness. Charcots triad is a set of three common findings in cholangitis: abdominal pain, jaundice, and fever. This was assumed in the past to be present in 50–70% of cases, although more recently the frequency has been reported as 15–20%. Reynolds pentad includes the findings of Charcots triad with the presence of septic shock and mental confusion. This combination of symptoms indicates worsening of the condition and the development of sepsis, and is seen less commonly still.In the elderly, the presentation may be atypical; they may directly collapse due to sepsis without first showing typical features. Those with an indwelling stent in the bile duct (see below) may not develop jaundice.

Causes
Bile duct obstruction, which is usually present in acute cholangitis, is generally due to gallstones. 10–30% of cases, however, are due to other causes such as benign stricturing (narrowing of the bile duct without an underlying tumor), postoperative damage or an altered structure of the bile ducts such as narrowing at the site of an anastomosis (surgical connection), various tumors (cancer of the bile duct, gallbladder cancer, cancer of the ampulla of Vater, pancreatic cancer, cancer of the duodenum), anaerobic organisms such as Clostridium and Bacteroides (especially in the elderly and those who have undergone previous surgery of the biliary system).Parasites which may infect the liver and bile ducts may cause cholangitis; these include  the roundworm Ascaris lumbricoides and the liver flukes Clonorchis sinensis, Opisthorchis viverrini and Opisthorchis felineus. In people with AIDS, a large number of opportunistic organisms has been known to cause AIDS cholangiopathy, but the risk has rapidly diminished since the introduction of effective AIDS treatment. Cholangitis may also complicate medical procedures involving the bile duct, especially ERCP. To prevent this, it is recommended that those undergoing ERCP for any indication receive prophylactic (preventative) antibiotics.The presence of a permanent biliary stent (e.g. in pancreatic cancer) slightly increases the risk of cholangitis, but stents of this type are often needed to keep the bile duct patent under outside pressure.

Pathogenesis
Bile is produced by the liver, and serves to eliminate cholesterol and bilirubin from the body, as well as emulsifying of fats to make them more soluble in water and aid in their digestion. Bile is formed in the liver by hepatocytes (liver cells) and excreted into the common hepatic duct. Part of the bile is stored in the gall bladder because of back pressure (exerted by the sphincter of Oddi), and may be released at the time of digestion. The gallbladder also concentrates the bile by absorbing water and dissolved salts from it. All bile reaches the duodenum (first part of the small intestine) through the common bile duct and the ampulla of Vater. The sphincter of Oddi, located at the junction of the ampulla of Vater and the duodenum, is a circular muscle that controls the release of both bile and pancreatic secretions into the digestive tract.The biliary tree is normally relatively free of bacteria because of certain protective mechanisms. The sphincter of Oddi acts as a mechanical barrier. The biliary system normally has low pressure (8 to 12 cmH2O) and allows bile to flow freely through. The continuous forward flow of the bile in the duct flushes bacteria, if present, into the duodenum, and does not allow the establishment of an infection. The constitution of bile—bile salts and immunoglobulin secreted by the epithelium of the bile duct also has a protective role.
Bacterial contamination alone in absence of obstruction does not usually result in cholangitis. However increased pressure within the biliary system (above 20 cmH2O) resulting from obstruction in the bile duct widens spaces between the cells lining the duct, bringing bacterially contaminated bile in contact with the blood stream. It also adversely affects the function of Kupffer cells, which are specialized macrophage cells that assist in preventing bacteria from entering the biliary system. Finally, increased biliary pressure decreases production of IgA immunoglobulins in the bile. This results in bacteremia (bacteria in the blood stream) and gives rise to the systemic inflammatory response syndrome (SIRS) comprising fever (often with rigors), tachycardia, increased respiratory rate and increased white blood cell count; SIRS in the presence of suspected or confirmed infection is called sepsis. Biliary obstruction itself disadvantages the immune system and impairs its capability to fight infection, by impairing the function of certain immune system cells (neutrophil granulocytes) and modifying the levels of immune hormones (cytokines).In ascending cholangitis, it is assumed that organisms migrate backwards up the bile duct as a result of partial obstruction and decreased function of the sphincter of Oddi. Other theories about the origin of the bacteria, such as through the portal vein or transmigration from the colon, are considered less likely.

Diagnosis
Blood tests
Routine blood tests show features of acute inflammation (raised white blood cell count and elevated C-reactive protein level), and usually abnormal liver function tests (LFTs). In most cases the LFTs will be consistent with obstruction: raised bilirubin, alkaline phosphatase and γ-glutamyl transpeptidase. In the early stages, however, pressure on the liver cells may be the main feature and the tests will resemble those in hepatitis, with elevations in alanine transaminase and aspartate transaminase.Blood cultures are often performed in people with fever and evidence of acute infection. These yield the bacteria causing the infection in 36% of cases, usually after 24–48 hours of incubation. Bile, too, may be sent for culture during ERCP (see below). The most common bacteria linked to ascending cholangitis are gram-negative bacilli: Escherichia coli (25–50%), Klebsiella (15–20%) and Enterobacter (5–10%). Of the gram-positive cocci, Enterococcus causes 10–20%.

Medical imaging
Given that ascending cholangitis usually occurs in the setting of bile duct obstruction, various forms of medical imaging may be employed to identify the site and nature of this obstruction. The first investigation is usually ultrasound, as this is the most easily available. Ultrasound may show dilation of the bile duct and identifies 38% of bile duct stones; it is relatively poor at identifying stones farther down the bile duct. Ultrasound can help distinguish between cholangitis and cholecystitis (inflammation of the gallbladder), which has similar symptoms to cholangitis but appears differently on ultrasound. A better test is magnetic resonance cholangiopancreatography (MRCP), which uses magnetic resonance imaging (MRI); this has a comparable sensitivity to ERCP. Smaller stones, however, can still be missed on MRCP depending on the quality of the hospitals facilities.The gold standard test for biliary obstruction is still endoscopic retrograde cholangiopancreatography (ERCP). This involves the use of endoscopy (passing a tube through the mouth into the esophagus, stomach and thence to the duodenum) to pass a small cannula into the bile duct. At that point, radiocontrast is injected to opacify the duct, and X-rays are taken to get a visual impression of the biliary system. On the endoscopic image of the ampulla, one can sometimes see a protuberant ampulla from an impacted gallstone in the common bile duct or the frank extrusion of pus from the common bile duct orifice. On the X-ray images (known as cholangiograms), gallstones are visible as non-opacified areas in the contour of the duct. For diagnostic purposes, ERCP has now generally been replaced by MRCP. ERCP is only used first-line in critically ill patients in whom delay for diagnostic tests is not acceptable; however, if the index of suspicion for cholangitis is high, an ERCP is typically done to achieve drainage of the obstructed common bile duct.If other causes rather than gallstones are suspected (such as a tumor), computed tomography and endoscopic ultrasound (EUS) may be performed to identify the nature of the obstruction. EUS may be used to obtain biopsy (tissue sample) of suspicious masses. EUS may also replace diagnostic ERCP for stone disease, although this depends on local availability.

Treatment
Fluids and antibiotics
Cholangitis requires admission to hospital. Intravenous fluids are administered, especially if the blood pressure is low, and antibiotics are commenced. Empirical treatment with broad-spectrum antibiotics is usually necessary until it is known for certain which pathogen is causing the infection, and to which antibiotics it is sensitive. Combinations of penicillins and aminoglycosides are widely used, although ciprofloxacin has been shown to be effective in most cases, and may be preferred to aminoglycosides because of fewer side effects. Metronidazole is often added to specifically treat the anaerobic pathogens, especially in those who are very ill or at risk of anaerobic infections. Antibiotics are continued for 7–10 days. Drugs that increase the blood pressure (vasopressors) may also be required to counter the low blood pressure.

Endoscopy
The definitive treatment for cholangitis is relief of the underlying biliary obstruction. This is usually deferred until 24–48 hours after admission, when the patient is stable and has shown some improvement with antibiotics, but may need to happen as an emergency in case of ongoing deterioration despite adequate treatment, or if antibiotics are not effective in reducing the signs of infection (which happens in 15% of cases).Endoscopic retrograde cholangiopancreatography (ERCP) is the most common approach in unblocking the bile duct. This involves endoscopy (passing a fiberoptic tube through the stomach into the duodenum), identification of the ampulla of Vater and insertion of a small tube into the bile duct. A sphincterotomy (making a cut in the sphincter of Oddi) is typically done to ease the flow of bile from the duct and to allow insertion of instruments to extract gallstones that are obstructing the common bile duct; alternatively or additionally, the common bile duct orifice can be dilated with a balloon. Stones may be removed either by direct suction or by using various instruments, including balloons and baskets to trawl the bile duct in order to pull stones into the duodenum. Obstructions that are caused by larger stones may require the use of an instrument known as a mechanical lithotriptor in order to crush the stone prior to removal. Obstructing stones that are too large to be removed or broken mechanically by ERCP may be managed by extracorporeal shock wave lithotripsy. This technique uses acoustic shock waves administered outside the body to break down the stones.  An alternative technique to remove very large obstructing stones is electrohydraulic lithotripsy, where a small endoscope known as a cholangioscope is inserted by ERCP to directly visualize the stone. A probe uses electricity to generate shock waves that break down the obstructing stone.  Rarely, surgical exploration of the common bile duct (termed choledochotomy), which can be performed with laparoscopy, is required to remove the stone.Narrowed areas may be bridged by a stent, a hollow tube that keeps the duct open. Removable plastic stents are used in uncomplicated gallstone disease, while permanent self-expanding metal stents with a longer lifespan are used if the obstruction is due to pressure from a tumor such as pancreatic cancer. A nasobiliary drain may be left behind; this is a plastic tube that passes from the bile duct through the stomach and the nose and allows continuous drainage of bile into a receptible. It is similar to a nasogastric tube, but passes into the common bile duct directly, and allows for serial x-ray cholangiograms to be done to identify the improvement of the obstruction. The decision on which of the aforementioned treatments to apply is generally based on the severity of the obstruction, findings on other imaging studies, and whether the patient has improved with antibiotic treatment. Certain treatments may be unsafe if blood clotting is impaired, as the risk of bleeding (especially from sphincterotomy) is increased in the use of medication such as clopidogrel (which inhibits platelet aggregation) or if the prothrombin time is significantly prolonged. For a prolonged prothrombin time, vitamin K or fresh frozen plasma may be administered to reduce bleeding risk.

Percutaneous biliary drainage
In cases where a person is too ill to tolerate endoscopy or when a retrograde endoscopic approach fails to access the obstruction, a percutaneous transhepatic cholangiogram (PTC) may be performed to evaluate the biliary system for placement of a percutaneous biliary drain (PBD). This is often necessary in the case of a proximal stricture or a bilioenteric anastomosis (a surgical connection between the bile duct and small bowel, such as the duodenum or jejunum).  Once access across the stricture is obtained, balloon dilation can be performed and stones can be swept forward into the duodenum. Due to potential complications of percutaneous biliary drain placement and the necessity of regular drain maintenance, a retrograde approach via ERCP remains first-line therapy.

Cholecystectomy
Not all gallstones implicated in ascending cholangitis actually originate from the gallbladder, but cholecystectomy (surgical removal of the gallbladder) is generally recommended in people who have been treated for cholangitis due to gallstone disease. This is typically delayed until all symptoms have resolved and ERCP or MRCP have confirmed that the bile duct is clear of gallstones. Those who do not undergo cholecystectomy have an increased risk of recurrent biliary pain, jaundice, further episodes of cholangitis, and need for further ERCP or cholecystostomy; the risk of death is also significantly increased.

Prognosis
Acute cholangitis carries a significant risk of death, the leading cause being irreversible shock with multiple organ failure (a possible complication of severe infections). Improvements in diagnosis and treatment have led to a reduction in mortality: before 1980, the mortality rate was greater than 50%, but after 1980 it was 10–30%. Patients with signs of multiple organ failure are likely to die unless they undergo early biliary drainage and treatment with systemic antibiotics. Other causes of death following severe cholangitis include heart failure and pneumonia.Risk factors indicating an increased risk of death include older age, female gender, a history of liver cirrhosis, biliary narrowing due to cancer, acute kidney injury and the presence of liver abscesses. Complications following severe cholangitis include kidney failure, respiratory failure (inability of the respiratory system to oxygenate blood and/or eliminate carbon dioxide), abnormal heart rhythms, wound infection, pneumonia, gastrointestinal bleeding and myocardial ischemia (lack of blood flow to the heart, leading to heart attacks).

Epidemiology
In the Western world, about 15% of all people have gallstones in their gallbladder but the majority are unaware of this and have no symptoms. Over ten years, 15–26% will have one or more episodes of biliary colic (abdominal pain due to the passage of gallstones through the bile duct into the digestive tract), and 2–3% will develop complications of obstruction: acute pancreatitis, cholecystitis or acute cholangitis. Prevalence of gallstone disease increases with age and body mass index (a marker of obesity) </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 Cutaneous small-vessel vasculitis and explain in detail? [/INST] Cutaneous small-vessel vasculitis (CSVV), also known as hypersensitivity vasculitis, cutaneous leukocytoclastic vasculitis, hypersensitivity angiitis, cutaneous leukocytoclastic angiitis, cutaneous necrotizing vasculitis and cutaneous necrotizing venulitis, is inflammation of small blood vessels (usually post-capillary venules in the dermis), characterized by palpable purpura.: 831  It is the most common vasculitis  seen in clinical practice.
"Leukocytoclastic" refers to the damage caused by nuclear debris from infiltrating neutrophils in and around the vessels.

Signs and symptoms
Skin lesions
Initially red to pink, flat spots (formally, "macules") and raised bumps (formally, "papules") may be seen on the skin.Once fully developed, the classic appearance is "non-blanching, palpable purpura". This appears as deep red to purple spots that feel raised to the touch. Purpura refers to the red-purple discolored spots, while palpable implies that these spots can be felt as raised from the surrounding skin. Additionally, when gently pressed, the color does not fade to a lighter color ("non-blanching"). The red-purple color of the lesions is due to the inflammation in the blood vessels causing red blood cells to escape into the dermis skin layer.Small fluid-filled blisters (or "vesicles"), pus-filled bumps resembling a pimple (or "pustules"), or shallow ulcers may also develop but are less common.The location of skin lesions varies but are most commonly found symmetrically below the waist, primarily on the buttocks and legs. Other distributions include localized areas on the upper body or over several areas of the body.With treatment, the lesions typically resolve in weeks to months and leave behind flat spots that are darker than the surrounding skin (see "Postinflammatory hyperpigmentation" on "Hyperpigmentation").
A portion of cases may be persistent or recurrent. This tends to occur when the vasculitis is associated with chronic conditions such as connective tissue diseases.

Associated symptoms
In most cases skin lesions do not cause symptoms, however itching, burning, or pain may occur.Frequently reported symptoms include mild fever, muscle pain, joint pain, or an overall feeling of discomfort. Additional symptoms depend on the cause of the vasculitis and if other organ systems are involved. For example, if the vasculitis is a manifestation of Henoch–Schönlein purpura, individuals may also experience abdominal pain or blood in the urine.

Cause
Cutaneous vasculitis can have various causes including but not limited to medications, bacterial and viral infections or allergens. It is estimated that 45–55% of cases are idiopathic, meaning the cause is unknown. In cases where a cause can be determined, medications and infectious pathogens are most common in adults, while IgA vasculitis (Henoch–Schönlein purpura) frequently affects children. Other etiologies include autoimmune conditions and malignancies, usually hematologic (related to the blood).
The small vessels in the skin affected are located in the superficial dermis and include arterioles (small arteries carrying blood to capillaries), capillaries, and venules (small veins receiving blood from capillaries). In general, immune complexes deposit in vessel walls leading to activation of the complement system. C3a and C5a, proteins produced from the complement system, attract neutrophils to the vessels. Once activated, neutrophils then release preformed substances, including enzymes causing damage to vessel tissue. Evidence of this process can be seen with a sample of removed skin tissue, or biopsy, viewed under a microscope. Neutrophils are seen surrounding blood vessels and their debris within vessel walls, causing fibrinoid necrosis. This finding on histological examination is termed "leukocytoclastic vasculitis".Considering the wide range of potential causes leading to cutaneous small vessel vasculitis, there are subtle variations in the underlying pathophysiology for each cause. For example, medications are metabolized to smaller molecules that can attach to proteins in the blood or vessel walls. The immune system senses these altered proteins as foreign and produces antibodies in efforts to eliminate them from the body. A similar process occurs with infectious agents, such as bacteria, in which antibodies target microbial components.

Diagnosis
The diagnostic testing for vasculitis should be guided by the patients history and physical exam. The clinician should ask about the duration, onset, and presence any associated symptoms such as weight loss or fatigue (that would indicate a systemic cause). It is important to distinguish between IgA and non-IgA vasculitis. IgA vasculitis is more likely to present with abdominal pain, bloody urine, and joint pain </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 Fissure and explain in detail? [/INST] A fissure is a long, narrow crack opening along the surface of Earth. The term is derived from the Latin word fissura, which means cleft or crack. Fissures emerge in Earths crust, on ice sheets and glaciers, and on volcanoes.

Ground fissure
A ground fissure, also called an earth fissure, is a long, narrow crack or linear opening in the Earths crust. Ground fissures can form naturally, such as from tectonic faulting and earthquakes, or as a consequence of human activity, such as oil mining and groundwater pumping. Once formed, ground fissures can be extended and eroded by torrential rain. They can be hazardous to people and livestock living on the affected surfaces and damaging to property and infrastructure, such as roads, underground pipes, canals, and dams.In circumstances where there is the extensive withdrawal of groundwater, the earth above the water table can subside causing fissures to form at the surface. This typically occurs at the floor of arid valleys having rock formations and compacted soils with a high percentage of fine-grained material.

Crevasse
A crevasse, also called an ice fissure, is a deep linear crack in an ice sheet or glacier resulting from  the opposing force produced by their movement at different rates of speed. The force builds until their associated shear stress is sufficient to break the ice along the faces. The breakage often forms vertical or near-vertical walls, which can melt and create seracs, arches, and other ice formations. A crevasse may be as deep as 45 metres (148 ft) and as wide as 20 metres (66 ft). A crevasse may be covered, but not necessarily filled, by a snow bridge made of the previous years accumulation and snow drifts </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 Refeeding syndrome and explain in detail? [/INST] Refeeding syndrome is a metabolic disturbance that occurs as a result of reinstitution of nutrition in people and animals who are starved, severely malnourished, or metabolically stressed because of severe illness. When too much food or liquid nutrition supplement is eaten during the initial four to seven days following a malnutrition event, the production of glycogen, fat and protein in cells may cause low serum concentrations of potassium, magnesium and phosphate. Cardiac, pulmonary and neurological symptoms can be signs of refeeding syndrome. The low serum minerals, if severe enough, can be fatal.

Cause
Any individual who has had a negligible nutrient intake for many consecutive days and/or is metabolically stressed from a critical illness or major surgery is at risk of refeeding syndrome. Refeeding syndrome usually occurs within four days of starting to re-feed. Patients can develop fluid and electrolyte imbalance, especially hypophosphatemia, along with neurologic, pulmonary, cardiac, neuromuscular, and hematologic complications.During fasting, the body switches its main fuel source from carbohydrates to fat tissue fatty acids and amino acids as the main energy sources. The spleen decreases its rate of red blood cell breakdown thus conserving red blood cells. Many intracellular minerals become severely depleted during this period, although serum levels remain normal. Importantly, insulin secretion is suppressed in this fasting state, and glucagon secretion is increased.During refeeding, insulin secretion resumes in response to increased blood sugar, resulting in increased glycogen, fat, and protein synthesis. Refeeding increases the basal metabolic rate. The process requires phosphates, magnesium and potassium which are already depleted, and the stores rapidly become used up. Formation of phosphorylated carbohydrate compounds in the liver and skeletal muscle depletes intracellular ATP and 2,3-diphosphoglycerate in red blood cells, leading to cellular dysfunction and inadequate oxygen delivery to the bodys organs. Intracellular movement of electrolytes occurs along with a fall in the serum electrolytes, including phosphate and magnesium. Levels of serum glucose may rise, and B1 vitamin thiamine may fall. Abnormal heart rhythms are the most common cause of death from refeeding syndrome, with other significant risks including confusion, coma and convulsions and cardiac failure.

Clinical situations
The syndrome can occur at the beginning of treatment for anorexia nervosa when patients have an increase in calorie intake and can be fatal. It can also occur after the onset of a severe illness or major surgery. The shifting of electrolytes and fluid balance increases cardiac workload and heart rate. This can lead to acute heart failure. Oxygen consumption is increased which strains the respiratory system and can make weaning from ventilation more difficult.

Diagnosis
Refeeding syndrome can be fatal if not recognized and treated properly. An awareness of the condition and a high index of suspicion are required in order to make the diagnosis. The electrolyte disturbances of the refeeding syndrome can occur within the first few days of refeeding.  Close monitoring of blood biochemistry is therefore necessary in the early refeeding period.

Treatment
In critically ill patients admitted to an intensive care unit, if phosphate drops to below 0.65 mmol/L (2.0 mg/dL) from a previously normal level within three days of starting enteral or parenteral nutrition, caloric intake should be reduced to 480 kcals per day for at least two days while electrolytes are replaced. Daily doses of thiamine, vitamin B complex (strong) and a multivitamin and mineral preparation are strongly recommended. Blood biochemistry should be monitored regularly until it is stable. Although clinical trials are lacking in patients other than those admitted to intensive care, it is commonly recommended that energy intake should remain lower than that normally required for the first 3–5 days of treatment of refeeding syndrome for all patients.

History
In his 5th century BC work On Fleshes (De Carnibus), Hippocrates writes, "if a person goes
seven days without eating or drinking anything, in this period most die; but there are some who survive that time but still die, and others are persuaded not to starve themselves to death but to eat and drink: however, the cavity no longer admits anything because the jejunum (nêstis) has grown together in that many days, and these people too die." Though Hippocrates misidentifies the cause of death, this passage likely represents an early description of refeeding syndrome. The Roman Historian Flavius Josephus writing in the first century described classic symptoms of the syndrome among survivors of the siege of Jerusalem. He described the death of those who overindulged in food after the famine, whereas those who ate at a more restrained pace survived.There were numerous cases of refeeding syndrome in the Siege of Leningrad during World War II, with Soviet civilians trapped in the city having becoming malnourished due to the German blockade. (Machado).A common error, repeated in multiple papers, is that "The syndrome was first described after World War II in Americans who, held by the Japanese as prisoners of war, had become malnourished during captivity and who were then released to the care of United States personnel in the Philippines."
However, closer inspection of the 1951 paper by Schnitker reveals the prisoners under study were not American POWs but Japanese soldiers who, already malnourished, surrendered in the Philippines during 1945, after the war was over.It is difficult to ascertain when the syndrome was first discovered and named, but it is likely the associated electrolyte disturbances were identified perhaps in Holland, the Netherlands during the closing months of World War II.

See also
Minnesota Starvation Experiment

References
Bibliography
Shils, M.E., Shike, M., Ross, A.C., Caballero, B. & Cousins, R.J.  (2006). Modern nutrition in health and disease, 10th ed. Lippincott, Williams & Wilkins. Baltimore, MD.
Mahan, L.K. & Escott-Stump, S.E. (2004) Krauses Food, Nutrition, & Diet Therapy, 11th ed. Saunders, Philadelphia, PA.
Hearing S (2004). "Refeeding syndrome: Is underdiagnosed and undertreated, but treatable". BMJ. 328 (7445): 908–9. doi:10.1136/bmj.328.7445.908. PMC 390152. PMID 15087326.
Crook M, Hally V, Panteli J (2001). "The importance of the refeeding syndrome". Nutrition. 17 (7–8): 632–7. doi:10.1016/S0899-9007(01)00542-1. PMID 11448586.
Lauts N (2005). "Management of the patient with refeeding syndrome". J Infus Nurs. 28 (5): 337–42. doi:10.1097/00129804-200509000-00007 </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 Paraplegia and explain in detail? [/INST] Paraplegia, or paraparesis, is an impairment in motor or sensory function of the lower extremities. The word comes from Ionic Greek (παραπληγίη)
"half-stricken". It is usually caused by spinal cord injury or a congenital condition that affects the neural (brain) elements of the spinal canal. The area of the spinal canal that is affected in paraplegia is either the thoracic, lumbar, or sacral regions. If four limbs are affected by paralysis, tetraplegia or quadriplegia is the correct term. If only one limb is affected, the correct term is monoplegia. Spastic paraplegia is a form of paraplegia defined by spasticity of the affected muscles, rather than flaccid paralysis.
The American Spinal Injury Association classifies spinal cord injury severity in the following manner. ASIA A is the complete loss of sensory function and motor skills below the injury. ASIA B is having some sensory function below the injury, but no motor function. In ASIA C, there is some motor function below the level of injury, but half of the muscles cannot move against gravity. In ASIA D, more than half of the muscles below the level of injury can move against gravity. ASIA E is the restoration of all neurologic function.

Treatment
Individuals with paraplegia can range in their level of disability, requiring treatments to vary from case to case. Rehabilitation aims to help the patient regain as much functionality and independence as possible. Physiotherapy may help to improve strength, range of motion, stretching and transfer skills. Most paraplegics will be reliant on a wheelchair as a mode of transportation </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 Congenital afibrinogenemia and explain in detail? [/INST] Congenital afibrinogenemia is a rare, genetically inherited blood fibrinogen disorder in which the blood does not clot normally due to the lack of fibrinogen, a blood protein necessary for coagulation. This disorder is autosomal recessive, meaning that two unaffected parents can have a child with the disorder. The lack of fibrinogen expresses itself with excessive and, at times, uncontrollable bleeding.

Signs and symptoms
As this is a disorder that is present in an individual from birth, there are no warning signs to look for. The first symptom usually seen is hemorrhage from the umbilical cord that is difficult to stop.Other symptoms include:
Nasal and oral mucosa bleeds
Gastrointestinal bleeding
Excessive/spontaneous bleeding or bruising from minor injury
Prolonged menstruation in women
Spontaneous abortion during pregnancy
CNS hemorrhagingSpontaneous bleeding of the mouth, nose, and gastrointestinal tract are common. Since blood clots can not be formed, minor injuries tend to lead to excessive bleeding or bruising. The biggest concern for individuals with afibrinogenemia is CNS hemorrhage, bleeding in the brain, which can be fatal.
Many of these symptoms are chronic, and will continue to occur for the entirety of the affected individuals life.

Causes
A missense or nonsense mutation to the genes that code for the fibrinogen protein are affected. Usually the mutation leads to an early stop in the production of the protein. Due to the problem being genetically based, there is no way to prevent the disease. Individuals can get genetic testing done to see if they are a carrier of the trait, and if so may choose to complete genetic counseling to better understand the disorder and help manage family planning. Parents can choose to do prenatal genetic testing for the disorder to determine if their child will have the disease. The only risk factor is if both parents of a child carry the recessive allele linked to the disorder.

Mechanism
Individuals with the disorder have a mutation to their fibrinogen gene that prevents the formation of the protein. In normal conditions, fibrinogen is converted to fibrin when it is cleaved by the enzyme thrombin in the blood. The newly formed fibrin forms a fiber-rich network that helps trap red blood cells to start the coagulation process and form a clot. Since there is no fibrinogen present during afibrinogenemia, fibrin can not be formed to aid in this process.

Diagnosis
Diagnostic tests
When a problem of fibrinogen is suspected, the following tests can be ordered:

PT
PTT
Fibrinogen level in blood (total and clottable)
Reptilase time
Thrombin timeBlood fibrinogen levels of less than 0.1 g/L and prolonged bleeding test times are indicators of an individual having afibrinogenemia.A suspicion of congenital afibrinogenemia may appear on a platelet aggregation function test.

Treatment
The most common treatment is fibrinogen replacement therapy, including cryoprecipitate, blood plasma, and fibrinogen concentration transfusions to help with bleeding episodes or prior to surgery. Although some thrombotic complications have been reported following replacement theory, transfusions of fibrinogen concentrate are widely considered to be the most beneficial </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 Breast cyst and explain in detail? [/INST] A breast cyst is a fluid-filled sac within the breast. One breast can have one or more breast cysts. They are often described as round or oval lumps with distinct edges. In texture, a breast cyst usually feels like a soft grape or a water-filled balloon, but sometimes a breast cyst feels firm.Breast cysts can be painful and may be worrisome but are generally benign. They are most common in pre-menopausal women in their 30s or 40s. They usually disappear after menopause, but may persist or reappear when using hormone therapy. They are also common in adolescents.
Breast cysts can be part of fibrocystic disease. The pain and swelling is usually worse in the second half of the menstrual cycle or during pregnancy.
Treating breast cysts is usually not necessary unless they are painful or cause discomfort. In most cases, the discomfort they cause may be alleviated by draining the fluid from the cyst. The cysts form as a result of the growth of the milk glands and their size may range from smaller than a pea to larger than a ping pong ball. While some large cysts feel like lumps, most cysts cannot be identified during physical examinations.
Breast cysts are not to be confused with "milk cysts" (galactoceles), which usually appear during weaning.

Signs and symptoms
Signs and symptoms of breast cysts include:

A smooth, easily movable round or oval breast lump with distinct edges
Breast pain or tenderness in the area of the lump
Increased lump size and tenderness just before menstruation
Decreased lump size and resolution of other signs and symptoms after menstruation
Having one or many simple breast cysts does not increase a persons risk of breast cancer.Lumps in the breast are often not found during self-examinations or physical exams. However, in some cases they can be felt at touch, especially if they are larger.
Breasts are usually lumpy or nodular as a result of the hormonal changes that women go through during their menstrual cycle. However, new breast lumps should always be referred to a specialist.
Cysts can also be confused with infections that form on the nipple or the areola. A common cyst look-alike is a localised infection of a duct in the nipple. These can happen whether youre breast feeding or not, (if you are breast feeding it could also be a bleb) this becomes a bump that may then start to look yellow and white (pus filled). Check with your doctor if you are unsure or have other symptoms that are worrying you.

Fluid leaking from a cyst, as may happen due to puncture or vigorous compression during mammography, or due to seat belt injury in the course of an automobile accident, may trigger an aseptic inflammation in the surrounding breast tissue.

Diagnosis
The cystic nature of a breast lump can be confirmed by ultrasound examination, aspiration (removal of contents with needle), or mammogram. Ultrasound can also show if the cyst contains solid nodules, a sign that the lesion may be pre-cancerous or cancerous. Examination by a cytopathologist of the fluid aspirated from the cyst may also help with this diagnosis. In particular, it should be sent to a laboratory for testing if it is blood-stained.
Commonly, cysts are detected with the help of mammograms. However, the medical history and physical examination also play an important role in establishing an accurate diagnosis. During these tests, the doctor will try to find out as much information as possible regarding the symptoms the patient has experienced, their intensity and duration and the physical examination is performed regularly to check for other abnormalities that may exist within the breast.
As mentioned above, cysts are often undetectable at touch. Therefore, a mammogram can provide valuable and clear images of the breast tissue. Generally, if there is any abnormality within the breast tissue, it will be shown on the mammogram. There are two types of mammograms available. One of them is primarily used in screening, and are ordered for patients who do not show any symptoms and these are called screening mammograms. Diagnostic mammograms are used on patients who developed certain symptoms of a breast condition or in patients whose screening mammograms showed abnormalities.
Patients suspected of breast cysts will normally be given a diagnosing mammogram, although they are not suspected of cancer. This type of mammogram provides the doctor with the possibility of performing a breast ultrasound at the same time and this is the reason why they are often preferred over the screening mammograms. Breast ultrasound is considered the best option when diagnosing breast cysts because it is 95 to 100% accurate, it provides a clear image on the cysts appearance (simple or complex) and it may also distinguish between solid lumps and fluid-filled cysts, which a mammogram cannot do. Breast ultrasounds are performed with the help of a handheld medical instrument which is placed on the skin, after a special type of fluid has been applied on it. The instruments picks up the echo resulted from the sound waves it sends to the breast. These echoes are transmitted to a computer which translates it into a picture.
Breast cysts may remain stable for many years or may resolve spontaneously. Most simple cysts are benign and do not require any treatment or further diagnostic workup. Some complex cysts may require further diagnostic measures such as fine needle aspiration or biopsy to exclude breast cancer however the overwhelming majority is of benign nature. Aspiration both diagnoses and removes cysts at the same time. That is, cysts will usually resolve on their own after the fluid is drained. Otherwise, if the lump is not a cyst, the fluid aspirated may contain blood or there may not be fluid at all. Whereas in the first case, the fluid is sent to the laboratory for further examination, the latter circumstance is a sign that the breast lump is solid. This type of tumor needs to be biopsied in order to determine whether it is malignant or benign.

Prevention
The development of breast cysts may be prevented to some degree, according to the majority of the specialists. The recommended measures one is able to take in order to avoid the formation of the cysts include practicing good health and avoiding certain medications, eating a balanced diet, taking necessary vitamins and supplements, getting exercise, and avoiding stress.Although caffeine consumption does not have a scientifically proved connection with the process of cyst development, many women claim that their symptoms are relieved if avoiding it. Some doctors recommend reducing the amount of caffeine in ones diet in terms of both beverages and foods (such as chocolate). Also reducing salt intake may help in alleviating the symptoms of breast cysts, although, again, there is no scientific linkage between these two. Excessive sugar consumption as well as undetected food allergies, such as to gluten or lactose, may also contribute to cyst development.

Treatment
Breast cysts do not require treatment unless a cyst is large and painful or otherwise uncomfortable. In that case, draining the fluid from a breast cyst can ease symptoms.Nipple cysts (commonly duct infections) may benefit from a hot compress to draw out the pus and antibacterial cream. These infected ducts typically clear up within a few days.
Typical treatment involves a Needle aspiration biopsy which is typically done with a 10 cc syringe attached to a fine needle aspiration needle.  Fine needle aspiration allows retrieval of cytological samples that can be sent for pathological review to determine if the cyst is benign or malignant.  Aspirated cysts often recur (come back); definitive treatment may require surgery. During an excisional biopsy an incision is made around the mass creating a superior and inferior flap </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 Uterine contraction and explain in detail? [/INST] Uterine contractions are muscle contractions of the uterine smooth muscle that occur during the menstrual cycle and labour. Uterine contractions occur throughout the menstrual cycle in the non-pregnant state and throughout gestation.

Throughout menstrual cycle
Uterine contractions that occur throughout the menstrual cycle, also termed endometrial waves or contractile waves, appear to involve only the sub-endometrial layer of the myometrium.

Follicular and luteal phase
In the early follicular phase, uterine contractions in the non-pregnant woman occur 1—2 times per minute and last 10–15 seconds with a low intensity of usually 30 mmHg or less. This sub-endometrial layer is rich in estrogen and progesterone receptors. The frequency of contractions increases to 3–4 per minute towards ovulation. During the luteal phase, the frequency and intensity decrease, possibly to facilitate any implantation.

Menstruation
If implantation does not occur, the frequency of contractions remains low; but at menstruation the intensity increases dramatically to between 50 and 200 mmHg producing labor-like contractions. These contractions are sometimes termed menstrual cramps, although that term is also used for menstrual pain in general. These contractions may be uncomfortable or even painful, but they are generally significantly less painful than contractions during labour. Painful contractions are called dysmenorrhea.

Directionality of contractions
A shift in the myosin expression of the uterine smooth muscle has been hypothesized as arising for changes in the directions of uterine contractions during the menstrual cycle.

Labour
Uterine contractions are part of the process of natural childbirth (i.e., not by Caesarean section). During labor, uterine contractions changes from episodic and uncoordinated to highly-coordinated. This change typically occurs at night, suggesting neural control, and significantly increases intrauterine pressure. Some women may experience contractions before labour is due. These are Braxton Hicks contractions, which are sometimes referred to as "false labour." There are several endogenous compounds involved in coordinating uterine contractility in labour, including oxytocin and prostaglandins.

Oxytocin
The hormone oxytocin has been identified as inducing uterine contractions, and labour in general. Oxytocin is produced by the body naturally and since the 1950s has also been available in synthetic pharmaceutical form.  In either form, oxytocin stimulates uterine contractions to accelerate the process of childbirth. Production and secretion of oxytocin is controlled by a positive feedback mechanism, where its initial release, either naturally or in pharmaceutical form, stimulates production and release of further oxytocin. For example, when oxytocin is released during a contraction of the uterus at the start of childbirth, this stimulates production and release of more oxytocin and an increase in the duration, intensity and frequency of contractions. This process compounds in intensity and frequency and continues until the triggering activity ceases.

Prostaglandins
The concentration of prostaglandins in the blood plasma and amniotic fluid increases during labor. These inflammatory mediators encourage myometrial contractions to induce labor. Prostaglandins are also related to the changes in gap junction formation and connexin-43 expression during labor.

In orgasm
Uterine and vaginal contractions usually take place during female sexual stimulation, including sexual arousal, and orgasm.

Monitors
Uterine contractions can be monitored by cardiotocography, in which a device is affixed to the skin of the mother or directly to the fetal scalp </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 Ovarian torsion and explain in detail? [/INST] Ovarian torsion (OT) or adnexal torsion is an abnormal condition where an ovary twists on its attachment to other structures, such that blood flow is decreased. Symptoms typically include pelvic pain on one side. While classically the pain is sudden in onset, this is not always the case. Other symptoms may include nausea. Complications may include infection, bleeding, or infertility.Risk factors include ovarian cysts, ovarian enlargement, ovarian tumors, pregnancy, fertility treatment, and prior tubal ligation. The diagnosis may be supported by an ultrasound done via the vagina or CT scan, but these do not completely rule out the diagnosis. Surgery is the most accurate method of diagnosis.Treatment is by surgery to either untwist and fix the ovary in place or to remove it. The ovary will often recover, even if the condition has been present for some time. In those who have had a prior ovarian torsion, there is a 10% chance the other will also be affected. The diagnosis is relatively rare, affecting about 6 per 100,000 women per year. While it most commonly occurs in those of reproductive age, it can occur at any age.

Signs and symptoms
Patients with ovarian torsion often present with sudden onset of sharp and usually unilateral lower abdominal pain, in 70% of cases accompanied by nausea and vomiting.

Pathophysiology
The development of an ovarian mass is related to the development of torsion. In the reproductive years, regular growth of large corpus luteal cysts are a risk factor for rotation. The mass effect of ovarian tumors is also a common cause of torsion. Torsion of the ovary usually occurs with torsion of the fallopian tube as well on their shared vascular pedicle around the broad ligament, although in rare cases the ovary rotates around the mesovarium or the fallopian tube rotates around the mesosalpinx. In 80%, torsion happens unilaterally, with slight predominance on the right. In ovarian torsion, the ovary rotates around both the infundibulopelvic ligament (ie, suspensory ligament) and the utero-ovarian ligament (i.e. ovarian ligament), disrupting blood flow to the ovary.

Diagnosis
Ovarian torsion is difficult to diagnose accurately, and operation is often performed before certain diagnosis is made. A study at an  obstetrics and gynaecology department found that preoperative diagnosis of ovarian torsion was confirmed in only 46% of people.

Ultrasound
Gynecologic ultrasonography is the imaging modality of choice. Use of doppler ultrasound  in the diagnosis has been suggested. However, doppler flow is not always absent in torsion – the definitive diagnosis is often made in the operating room.Lack of ovarian blood flow on doppler sonography seems to be a good predictor of ovarian torsion. Women with pathologically low flow are more likely to have torsion. The sensitivity and specificity of abnormal ovarian flow are 44% and 92%, respectively, with a positive and negative predictive value of 78% and 71%, respectively. Specific flow features on Doppler sonography include:
Little or no intra-ovarian venous flow </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 Uterine perforation 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 Pediculosis and explain in detail? [/INST] Pediculosis is an infestation of lice from the sub-order Anoplura, family Pediculidae. Accordingly, the infestation with head lice is named pediculosis capitis, while this with body lice, pediculosis corporis.  Although pediculosis in humans may properly refer to lice infestation of any part of the body, the term is sometimes used loosely to refer to pediculosis capitis, the infestation of the human head with the specific head louse.

Classification
Pediculosis may be divided into the following types:: 446–8
Pediculosis capitis (Head lice infestation)
Pediculosis corporis (Body louse infestation, also known as Pediculosis vestimenti, Vagabonds disease)
Pediculosis pubis (Pubic louse infestation, also known as phthiriasis)

Head lice
Presentation
Head-lice infestation is most frequent on children aged 3–10 and their families.  Approximately 3% of school children in the United States contract head lice. Females aged 3–12 years are most commonly infested. Those of African descent rarely experience infestation due to differences in hair texture.Head lice are spread through direct head-to-head contact with an infested person. From each egg or "nit" may hatch one nymph that will grow and develop to the adult louse. Lice feed on blood once or more often each day by piercing the skin with their tiny needle-like mouthparts. While feeding they excrete saliva, which irritates the skin and causes itching. Lice cannot burrow into the skin.

Diagnosis
To diagnose infestation, the entire scalp should be combed thoroughly with a louse comb and the teeth of the comb should be examined for the presence of living lice after each time the comb passes through the hair. The use of a louse comb is the most effective way to detect living lice.The most characteristic symptom of infestation is pruritus (itching) on the head which normally intensifies 3 to 4 weeks after the initial infestation. The bite reaction is very mild and it can be rarely seen between the hairs. Excessive scratching of the infested areas can cause sores, which may become infected.

Treatment
The number of diagnosed cases of human louse infestations (or pediculosis) has increased worldwide since the mid-1960s, reaching hundreds of millions annually.  There is no product or method which assures 100% destruction of the eggs and hatched lice after a single treatment.  However, there are a number of treatment methods that can be employed with varying degrees of success. These methods include chemical treatments, natural products, combs, shaving, hot air, silicone-based lotions, and ethanol (ethyl alcohol).Pediculosis is commonly treated with permethrin lotion.

Epidemiology
About 14 million people, mainly children, are treated annually for head lice in the United States alone. Only a small proportion of those treated, however, may have objective evidence of an extant infestation. High levels of louse infestations have also been reported from all over the world including Denmark, Sweden, U.K., France and Australia.
Normally head lice infest a new host only by close contact between individuals, making social contacts among children and parent child interactions more likely routes of infestation than shared combs, brushes, towels, clothing, beds or closets. Head-to-head contact is by far the most common route of lice transmission.The United Kingdoms National Health Service, and many American health agencies, report that lice "prefer" clean hair, because its easier to attach eggs and to cling to the strands.Head lice (Pediculus humanus capitis) are not known to be vectors of diseases, unlike body lice (Pediculus humanus humanus), which are known vectors of epidemic or louse-borne typhus (Rickettsia prowazekii), trench fever (Rochalimaea quintana) and louse-borne relapsing fever (Borrelia recurrentis).

Body lice
This condition is caused by body louse (Pediculus humanus humanus, sometimes called Pediculus humanus corporis), a louse which infests humans and is adapted to lay eggs in clothing, rather than at the base of hairs, and is thus of recent evolutionary origin. Pediculosis is a more serious threat due to possible contagion of diseases such as typhus. Epidemiology and treatment of human body lice is described in the article on body lice.

Pubic lice
The pubic or crab louse (Pthirus pubis) is a parasitic insect which spends its entire life on human hair and feeds exclusively on blood. Humans are the only known host of this parasite, although it is more closely related to the louse parasites in other primate species, than are human head or body lice which probably evolved from it as the "original" louse infestation of humans. Epidemiology and treatment of pubic lice is discussed in the article on pubic lice.

Other animals
Pediculosis is more common in cattle than any other type of domesticated animal. This is a significant problem, as it can cause weight loss of 55 to 75 pounds per animal. Some species of lice infesting cattle include the cattle biting louse (Bovicola bovis), the shortnosed cattle louse (Haematopinus eurysternus), the longnosed cattle louse (Linognathus vituli), and the little blue cattle louse (Solenopotes capillatus).

Treatment
Cattle infested with bovine pediculosis are generally treated chemically, by drugs like ivermectin and cypermethrin.

History
In the 15th century, topical mercury treatment was used to treat pediculosis.

See also
Nitpicking

References
External links

Head louse infestations: Biology, prevention and control  by Prof. Kosta Y. Mumcuoglu
Head lice: Biology and Management at IdentifyUS LLC
National Pediculosis Association
Frankowski BL, Weiner LB (September 2002). "Head lice". Pediatrics. 110 (3): 638–643 </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 Laxative and explain in detail? [/INST] Laxatives, purgatives, or aperients are substances that loosen stools and increase bowel movements. They are used to treat and prevent constipation.
Laxatives vary as to how they work and the side effects they may have. Certain stimulant, lubricant and saline laxatives are used to evacuate the colon for rectal and bowel examinations, and may be supplemented by enemas under certain circumstances. Sufficiently high doses of laxatives may cause diarrhea.
Some laxatives combine more than one active ingredient.
Laxatives may be administered orally or rectally.

Types
Bulk-forming agents
Bulk-forming laxatives, also known as roughage, are substances, such as fiber in food and hydrophilic agents in over-the-counter drugs, that add bulk and water to stools so that they can pass more easily through the intestines (lower part of the digestive tract).Properties

Site of action: small and large intestines
Onset of action: 12–72 hours
Examples: dietary fiber, Metamucil, Citrucel, FiberConBulk-forming agents generally have the gentlest of effects among laxatives, making them ideal for long-term maintenance of regular bowel movements.

Dietary fiber
Foods that help with laxation include fiber-rich foods. Dietary fiber includes insoluble fiber and soluble fiber, such as:
Fruits, such as bananas, though this depends on their ripeness, kiwifruits, prunes, apples (with skin), pears (with skin), and raspberries
Vegetables, such as broccoli, string beans, kale, spinach, cooked winter squash, cooked taro and poi, cooked peas, and baked potatoes (with skin)
Whole grains
Bran products
Nuts
Legumes, such as beans, peas, and lentils

Emollient agents (stool softeners)
Emollient laxatives, also known as stool softeners, are anionic surfactants that enable additional water and fats to be incorporated in the stool, making it easier for them to move through the gastrointestinal tract.
Properties

Site of action: small and large intestines
Onset of action: 12–72 hours
Examples: Docusate (Colace, Diocto), Gibs-EzeEmollient agents prevent constipation rather than treating long-term constipation.

Lubricant agents
Lubricant laxatives are substances that coat the stool with slippery lipids and decrease colonic absorption of water so that the stool slides through the colon more easily. Lubricant laxatives also increase the weight of stool and decrease intestinal transit time.Properties

Site of action: colon
Onset of action: 6–8 hours
Example: mineral oilMineral oil is the only nonprescription lubricant. Mineral oil may decrease the absorption of fat-soluble vitamins and some minerals.One example is Liquid paraffin.

Hyperosmotic agents
Hyperosmotic laxatives are substances that cause the intestines to hold more water within and create an osmotic effect that stimulates a bowel movement.Properties

Site of action: colon
Onset of action: 12–72 hours (oral), 0.25–1 hour (rectal)
Examples: glycerin suppositories (Hallens), sorbitol, lactulose, and PEG (Colyte, MiraLax)Lactulose works by the osmotic effect, which retains water in the colon; lowering the pH through bacterial fermentation to lactic, formic and acetic acid; and increasing colonic peristalsis. Lactulose is also indicated in portal-systemic encephalopathy. Glycerin suppositories work mostly by hyperosmotic action, but the sodium stearate in the preparation also causes local irritation to the colon.
Solutions of polyethylene glycol and electrolytes (sodium chloride, sodium bicarbonate, potassium chloride, and sometimes sodium sulfate) are used for whole bowel irrigation, a process designed to prepare the bowel for surgery or colonoscopy and to treat certain types of poisoning. Brand names for these solutions include GoLytely, GlycoLax, Cosmocol, CoLyte, Miralax, Movicol, NuLytely, Suprep, and Fortrans. Solutions of sorbitol (SoftLax) have similar effects.

Saline laxative agents
Saline laxatives are non-absorbable osmotically active substances that attract and retain water in the intestinal lumen, increasing intraluminal pressure that mechanically stimulates evacuation of the bowel. Magnesium-containing agents also cause the release of cholecystokinin, which increases intestinal motility and fluid secretion. Saline laxatives may alter a patients fluid and electrolyte balance.
Properties

Site of action: small and large intestines
Onset of action: 0.5–3 hours (oral), 2–15 minutes (rectal)
Examples: sodium phosphate (and variants), magnesium citrate, magnesium hydroxide (milk of magnesia), and magnesium sulfate (Epsom salt)

Stimulant agents
Stimulant laxatives are substances that act on the intestinal mucosa or nerve plexus, altering water and electrolyte secretion. They also stimulate peristaltic action and can be dangerous under certain circumstances.Properties

Site of action: colon
Onset of action: 6–10 hours
Examples: senna, bisacodylProlonged use of stimulant laxatives can create drug dependence by damaging the colons haustral folds, making a user less able to move feces through the colon on their own. A study of patients with chronic constipation found that 28% of chronic stimulant laxative users lost haustral folds over the course of one year, while none of the control group did.

Miscellaneous
Castor oil is a glyceride that is hydrolyzed by pancreatic lipase to ricinoleic acid, which produces laxative action by an unknown mechanism.
Properties

Site of action: colon,small intestine (see below)
Onset of action: 2–6 hours
Examples: castor oilLong-term use of castor oil may result in loss of fluid, electrolytes, and nutrients.

Serotonin agonist
These are motility stimulants that work through activation of 5-HT4 receptors of the enteric nervous system in the gastrointestinal tract. However, some have been discontinued or restricted due to potentially harmful cardiovascular side-effects.
Tegaserod (brand name Zelnorm) was removed from the general U.S. and Canadian markets in 2007, due to reports of increased risks of heart attack or stroke. It is still available to physicians for patients in emergency situations that are life-threatening or require hospitalization.Prucalopride (brand name Resolor) is a current
drug approved for use in the EU since October 15, 2009, in Canada (brand name Resotran) since December 7, 2011, and in the United States since December 2018.

Chloride channel activators
Lubiprostone is used in the management of chronic idiopathic constipation and irritable bowel syndrome. It causes the intestines to produce a chloride-rich fluid secretion that softens the stool, increases motility, and promotes spontaneous bowel movements (SBM).

Comparison of available agents
Effectiveness
For adults, a randomized controlled trial found PEG (MiraLax or GlycoLax) 17 grams once per day to be superior to tegaserod at 6 mg twice per day </s>