<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Neuromyotonia and can you explain it in depth? [/INST] Neuromyotonia (NMT) is a form of peripheral nerve hyperexcitability that causes spontaneous muscular activity resulting from repetitive motor unit action potentials of peripheral origin. NMT along with Morvans syndrome are the most severe types in the Peripheral Nerve Hyperexciteability spectrum. Example of two more common and less severe syndromes in the spectrum are Cramp Fasciculation Syndrome and Benign Fasciculation Syndrome.  NMT can have both hereditary and acquired (non- inherited) forms. The prevalence of NMT is unknown.

Signs and symptoms
NMT is a diverse disorder. As a result of muscular hyperactivity, patients may present with muscle cramps, stiffness, myotonia-like symptoms (slow relaxation), associated walking difficulties, hyperhidrosis (excessive sweating), myokymia (quivering of a muscle), fasciculations (muscle twitching), fatigue, exercise intolerance, myoclonic jerks and other related symptoms. The symptoms (especially the stiffness and fasciculations) are most prominent in the calves, legs, trunk, and sometimes the face and neck, but can also affect other body parts. NMT symptoms may fluctuate in severity and frequency. Symptoms range from mere inconvenience to debilitating. At least a third of people also experience sensory symptoms.

Causes
The three causes of NMT are:
Acquired
Paraneoplastic
HereditaryThe acquired form is the most common, accounting for up to 80 percent of all cases and is suspected to be autoimmune-mediated, which is usually caused by antibodies against the neuromuscular junction.
The exact cause is unknown. However, autoreactive antibodies can be detected in a variety of peripheral (e.g. myasthenia gravis, Lambert-Eaton myasthenic syndrome) and central nervous system (e.g. paraneoplastic cerebellar degeneration, paraneoplastic limbic encephalitis) disorders. Their causative role has been established in some of these diseases but not all. Neuromyotonia is considered to be one of these with accumulating evidence for autoimmune origin over the last few years. Autoimmune neuromyotonia is typically caused by antibodies that bind to potassium channels on the motor nerve resulting in continuous/hyper-excitability.  Onset is typically seen between the ages of 15–60, with most experiencing symptoms before the age of 40. Some neuromyotonia cases do not only improve after plasma exchange but they may also have antibodies in their serum samples against voltage-gated potassium channels. Moreover, these antibodies have been demonstrated to reduce potassium channel function in neuronal cell lines.

Diagnosis
Diagnosis is clinical and initially consists of ruling out more common conditions, disorders, and diseases, and usually begins at the general practitioner level. A doctor may conduct a basic neurological exam, including coordination, strength, reflexes, sensation, etc. A doctor may also run a series of tests that include blood work and MRIs.
From there, a patient is likely to be referred to a neurologist or a neuromuscular specialist. The neurologist or specialist may run a series of more specialized tests, including needle electromyography EMG/ and nerve conduction studies (NCS) (these are the most important tests), chest CT (to rule out paraneoplastic) and specific blood work looking for voltage-gated potassium channel antibodies, acetylcholine receptor antibody, and serum immunofixation, TSH, ANA ESR, EEG etc. Neuromyotonia is characterized electromyographically by doublet, triplet or multiplet single unit discharges that have a high, irregular intraburst frequency.  Fibrillation potentials and fasciculations are often also present with electromyography.Because the condition is so rare, it can often be years before a correct diagnosis is made.
NMT is not fatal and many of the symptoms can be controlled. However, because NMT mimics some symptoms of motor neuron disease (ALS) and other more severe diseases, which may be fatal, there can often be significant anxiety until a diagnosis is made. In some rare cases, acquired neuromyotonia has been misdiagnosed as amyotrophic lateral sclerosis (ALS) particularly if fasciculations may be evident in the absence of other clinical features of ALS. However, fasciculations are rarely the first sign of ALS as the hallmark sign is weakness. Similarly, multiple sclerosis has been the initial misdiagnosis in some NMT patients. In order to get an accurate diagnosis see a trained neuromuscular specialist.
People diagnosed with Benign Fasciculation Syndrome or Enhanced Physiological Tremor may experience similar symptoms as NMT, although it is unclear today whether BFS or EPT are weak forms of NMT.

Types
There are three main types of NMT:
Chronic
Monophasic (symptoms that resolve within several years of onset; postinfection, postallergic)
Relapsing Remitting

Peripheral nerve hyperexcitability
Neuromyotonia is a type of peripheral nerve hyperexcitability. Peripheral nerve hyperexcitability is an umbrella diagnosis that includes (in order of severity of symptoms from least severe to most severe) benign fasciculation syndrome, cramp fasciculation syndrome, neuromyotonia and morvans syndrome. Some doctors will only give the diagnosis of peripheral nerve hyperexcitability as the differences between the three are largely a matter of the severity of the symptoms and can be subjective. However, some objective EMG criteria have been established to help distinguish between the three.
Moreover, the generic use of the term peripheral nerve hyperexcitability syndromes to describe the aforementioned conditions is recommended and endorsed by several prominent researchers and practitioners in the field.

Treatments
There is no known cure for neuromyotonia, but the condition is treatable. Anticonvulsants, including phenytoin and carbamazepine, usually provide significant relief from the stiffness, muscle spasms, and pain associated with neuromyotonia. Plasma exchange and IVIg treatment may provide short-term relief for patients with some forms of the acquired disorder. It is speculated that the plasma exchange causes an interference with the function of the voltage-dependent potassium channels, one of the underlying issues of hyper-excitability in autoimmune neuromyotonia. Botox injections also provide short-term relief </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Developmental verbal dyspraxia and can you explain it in depth? [/INST] Developmental verbal dyspraxia (DVD), also known as childhood apraxia of speech (CAS) and developmental apraxia of speech (DAS), is a condition in which children have problems saying sounds, syllables and words. This is not because of muscle weakness or paralysis. The brain has problems planning to move the body parts (e.g., lips, jaw, tongue) needed for speech. The child knows what they want to say, but their brain has difficulty coordinating the muscle movements necessary to say those words.The exact cause of this disorder is usually unknown. Many observations suggest a genetic cause of DVD, as many with the disorder have a family history of communication disorders. The gene FOXP2 has been implicated in many studies of the condition, and when this is the cause, the condition is inherited in an autosomal dominant manner, however roughly 75% of these cases are de novo.There is no cure for DVD, but with appropriate, intensive intervention, people with this motor speech disorder can improve significantly.

Presentation
"Childhood apraxia of speech (CAS) is a neurological childhood (pediatric) speech sound disorder in which the precision and consistency of movements underlying speech are impaired in the absence of neuromuscular deficits (e.g., abnormal reflexes, abnormal tone). CAS may occur as a result of known neurological impairment, in association with complex neurobehavioral disorders of known or unknown origin, or as an idiopathic neurogenic speech sound disorder. The core impairment in planning and/or programming spatiotemporal parameters of movement sequences results in errors in speech sound production and prosody." American Speech-Language-Hearing Association (ASHA) Ad Hoc Committee on Apraxia of Speech in Children (2007)
There are three significant features that differentiate DVD/CAS from other childhood speech sound disorders. These features are:

"Inconsistent errors on consonants and vowels in repeated productions of syllables and words
Lengthened coarticulatory transitions between sounds and syllables
Inappropriate prosody, especially in the realization of lexical or phrasal stress"Even though DVD/CAS is a developmental disorder, it will not simply disappear when children grow older. Children with this disorder do not follow typical patterns of language acquisition and will need treatment in order to make progress.

Causes
DVD/CAS is a motor disorder, which means that the problem is located in the brain and its signals, and not in the mouth. In most cases, the cause is unknown. Possible causes include genetic syndromes and disorders.Recent research has focused on the significance of the FOXP2 gene in both species and individual development. Research regarding the KE family, where half the members of the extended family, over three generations, exhibited heritable developmental verbal dyspraxia, were found to have a defective copy of the FOXP2 gene. and further studies suggest that the FOXP2 gene as well as other genetic issues could explain DVD/CAS. including 16p11.2 microdeletion syndrome.New research suggests a role for the sodium channel SCN3A in the development of the perisylvian areas, which maintain key language circuits- Broca and Wernicke Area. Patients with mutations in SCN3A had oral-motor speech disorders.Birth/prenatal injuries, as well as stroke, can also be causes of DVD/CAS. Furthermore, DVD/CAS can occur as a secondary characteristic to a variety of other conditions. These include autism, some forms of epilepsy, fragile X syndrome, galactosemia and chromosome translocations involving duplications or deletions.

Diagnosis
Developmental verbal dyspraxia can be diagnosed by a speech language pathologist (SLP) through specific exams that measure oral mechanisms of speech. The oral mechanisms exam involves tasks such as pursing lips, blowing, licking lips, elevating the tongue, and also involves an examination of the mouth. A complete exam also involves observation of the patient eating and talking. Tests such as the Kaufman Speech Praxis test, a more formal examination, are also used in diagnosis.
A differential diagnosis of DVD/CAS is often not possible for children under the age of two years old. Even when children are between 2–3 years, a clear diagnosis cannot always occur, because at this age, they may still be unable to focus on, or cooperate with, diagnostic testing.

Management
There is no cure for DVD/CAS, but with appropriate, intensive intervention, people with the disorder can improve significantly.DVD/CAS requires various forms of therapy which varies with the individual needs of the patient. Typically, treatment involves one-on-one therapy with a speech language pathologist (SLP). In children with DVD/CAS, consistency is a key element in treatment. Consistency in the form of communication, as well as the development and use of oral communication are extremely important in aiding a childs speech learning process.Many therapy approaches are not supported by thorough evidence; however, the aspects of treatment that do seem to be agreed upon are the following:

Treatment needs to be intense and highly individualized, with about 3–5 therapy sessions each week
A maximum of 30 minutes per session is best for young children
Principles of motor learning theory and intense speech-motor practice seem to be the most effective
Non-speech oral motor therapy is not necessary or sufficient
A multi-sensory approach to therapy may be beneficial: using sign language, pictures, tactile cues, visual prompts, and augmentative and alternative communication (AAC) can be helpful.Although these aspects of treatment are supported by much clinical documentation, they lack evidence from systematic research studies. In ASHAs position statement on DVD/CAS, ASHA states there is a critical need for collaborative, interdisciplinary, and programmatic research on the neural substrates, behavioral correlates, and treatment options for DVD/CAS.

Integral stimulation
One technique that is frequently used to treat DVD/CAS is integral stimulation. Integral stimulation is based on cognitive motor learning, focusing on the cognitive motor planning needed for the complex motor task of speech </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Gastroenteritis and can you explain it in depth? [/INST] Gastroenteritis, also known as infectious diarrhea and gastro, is inflammation of the gastrointestinal tract including the stomach and intestine. Symptoms may include diarrhea, vomiting, and abdominal pain. Fever, lack of energy, and dehydration may also occur. This typically lasts less than two weeks. It is not related to influenza, even though in the U.S. it is sometimes called the "stomach flu".Gastroenteritis is usually caused by viruses, gut bacteria, parasites, and fungi can also cause gastroenteritis. In children, rotavirus is the most common cause of severe disease. In adults, norovirus and Campylobacter are common causes. Eating improperly prepared food, drinking contaminated water or close contact with a person who is infected can spread the disease. Treatment is generally the same with or without a definitive diagnosis, so testing to confirm is usually not needed.For young children in impoverished countries, prevention includes hand washing with soap, drinking clean water, breastfeeding babies instead of using formula, and proper disposal of human waste. The rotavirus vaccine is recommended as a prevention for children. Treatment involves getting enough fluids. For mild or moderate cases, this can typically be achieved by drinking oral rehydration solution (a combination of water, salts and sugar). In those who are breastfed, continued breastfeeding is recommended. For more severe cases, intravenous fluids may be needed. Fluids may also be given by a nasogastric tube. Zinc supplementation is recommended in children. Antibiotics are generally not needed. However, antibiotics are recommended for young children with a fever and bloody diarrhea.In 2015, there were two billion cases of gastroenteritis, resulting in 1.3 million deaths globally. Children and those in the developing world are affected the most. In 2011, there were about 1.7 billion cases, resulting in about 700,000 deaths of children under the age of five. In the developing world, children less than two years of age frequently get six or more infections a year. It is less common in adults, partly due to the development of immunity.

Signs and symptoms
Gastroenteritis usually involves both diarrhea and vomiting. Sometimes, only one or the other is present. This may be accompanied by abdominal cramps. Signs and symptoms usually begin 12–72 hours after contracting the infectious agent. If due to a virus, the condition usually resolves within one week. Some viral infections also involve fever, fatigue, headache and muscle pain. If the stool is bloody, the cause is less likely to be viral and more likely to be bacterial. Some bacterial infections cause severe abdominal pain and may persist for several weeks.Children infected with rotavirus usually make a full recovery within three to eight days. However, in poor countries treatment for severe infections is often out of reach and persistent diarrhea is common.  Dehydration is a common complication of diarrhea. Severe dehydration in children may be recognized if the skin color and position returns slowly when pressed. This is called "prolonged capillary refill" and "poor skin turgor". Abnormal breathing is another sign of severe dehydration. Repeat infections are typically seen in areas with poor sanitation, and malnutrition. Stunted growth and long-term cognitive delays can result.Reactive arthritis occurs in 1% of people following infections with Campylobacter species. Guillain–Barré syndrome occurs in 0.1%. Hemolytic uremic syndrome (HUS) may occur due to infection with Shiga toxin-producing Escherichia coli or Shigella species. HUS causes low platelet counts, poor kidney function, and low red blood cell count (due to their breakdown). Children are more predisposed to getting HUS than adults. Some viral infections may produce benign infantile seizures.

Cause
Viruses (particularly rotavirus (in children) and norovirus (in adults)) and the bacteria Escherichia coli and Campylobacter species are the primary causes of gastroenteritis. There are, however, many other infectious agents that can cause this syndrome including parasites and fungus. Non-infectious causes are seen on occasion, but they are less likely than a viral or bacterial cause. Risk of infection is higher in children due to their lack of immunity. Children are also at higher risk because they are less likely to practice good hygiene habits. Children living in areas without easy access to water and soap are especially vulnerable.

Viral
Rotaviruses, noroviruses, adenoviruses, and astroviruses are known to cause viral gastroenteritis. Rotavirus is the most common cause of gastroenteritis in children, and produces similar rates in both the developed and developing world. Viruses cause about 70% of episodes of infectious diarrhea in the pediatric age group. Rotavirus is a less common cause in adults due to acquired immunity. Norovirus is the cause in about 18% of all cases. Generally speaking, viral gastroenteritis accounts for 21–40% of the cases of infectious diarrhea in developed countries.Norovirus is the leading cause of gastroenteritis among adults in America accounting for about 90% of viral gastroenteritis outbreaks. These localized epidemics typically occur when groups of people spend time proximate to each other, such as on cruise ships, in hospitals, or in restaurants. People may remain infectious even after their diarrhea has ended. Norovirus is the cause of about 10% of cases in children.

Bacterial
In some countries, Campylobacter jejuni is the primary cause of bacterial gastroenteritis, with half of these cases associated with exposure to poultry. In children, bacteria are the cause in about 15% of cases, with the most common types being Escherichia coli, Salmonella, Shigella, and Campylobacter species. If food becomes contaminated with bacteria and remains at room temperature for a period of several hours, the bacteria multiply and increase the risk of infection in those who consume the food. Some foods commonly associated with illness include raw or undercooked meat, poultry, seafood, and eggs; raw sprouts; unpasteurized milk and soft cheeses; and fruit and vegetable juices. In the developing world, especially sub-Saharan Africa and Asia, cholera is a common cause of gastroenteritis. This infection is usually transmitted by contaminated water or food.Toxigenic Clostridium difficile is an important cause of diarrhea that occurs more often in the elderly. Infants can carry these bacteria without developing symptoms. It is a common cause of diarrhea in those who are hospitalized and is frequently associated with antibiotic use. Staphylococcus aureus infectious diarrhea may also occur in those who have used antibiotics. Acute "travelers diarrhea" is usually a type of bacterial gastroenteritis, while the persistent form is usually parasitic. Acid-suppressing medication appears to increase the risk of significant infection after exposure to a number of organisms, including Clostridium difficile, Salmonella, and Campylobacter species. The risk is greater in those taking proton pump inhibitors than with H2 antagonists.

Parasitic
A number of parasites can cause gastroenteritis. Giardia lamblia is most common, but Entamoeba histolytica, Cryptosporidium spp., and other species have also been implicated. As a group, these agents comprise about 10% of cases in children. Giardia occurs more commonly in the developing world, but this type of illness can occur nearly everywhere. It occurs more commonly in persons who have traveled to areas with high prevalence, children who attend day care, men who have sex with men, and following disasters.

Transmission
Transmission may occur from drinking contaminated water or when people share personal objects. Water quality typically worsens during the rainy season and outbreaks are more common at this time. In areas with four seasons, infections are more common in the winter. Worldwide, bottle-feeding of babies with improperly sanitized bottles is a significant cause. Transmission rates are also related to poor hygiene, (especially among children), in crowded households, and in those with poor nutritional status. Adults who have developed immunities might still carry certain organisms without exhibiting symptoms. Thus, adults can become natural reservoirs of certain diseases. While some agents (such as Shigella) only occur in primates, others (such as Giardia) may occur in a wide variety of animals.

Non-infectious
There are a number of non-infectious causes of inflammation of the gastrointestinal tract. Some of the more common include medications (like NSAIDs), certain foods such as lactose (in those who are intolerant), and gluten (in those with celiac disease). Crohns disease is also a non-infectious source of (often severe) gastroenteritis. Disease secondary to toxins may also occur. Some food-related conditions associated with nausea, vomiting, and diarrhea include: ciguatera poisoning due to consumption of contaminated predatory fish, scombroid associated with the consumption of certain types of spoiled fish, tetrodotoxin poisoning from the consumption of puffer fish among others, and botulism typically due to improperly preserved food.In the United States, rates of emergency department use for noninfectious gastroenteritis dropped 30% from 2006 until 2011. Of the twenty most common conditions seen in the emergency department, rates of noninfectious gastroenteritis had the largest decrease in visits in that time period.

Pathophysiology
Gastroenteritis is defined as vomiting or diarrhea due to inflammation of the small or large bowel, often due to infection. The changes in the small bowel are typically noninflammatory, while the ones in the large bowel are inflammatory. The number of pathogens required to cause an infection varies from as few as one (for Cryptosporidium) to as many as 108 (for Vibrio cholerae).

Diagnosis
Gastroenteritis is typically diagnosed clinically, based on a persons signs and symptoms. Determining the exact cause is usually not needed as it does not alter the management of the condition.However, stool cultures should be performed in those with blood in the stool, those who might have been exposed to food poisoning, and those who have recently traveled to the developing world. It may also be appropriate in children younger than 5, old people, and those with poor immune function. Diagnostic testing may also be done for surveillance. As hypoglycemia occurs in approximately 10% of infants and young children, measuring serum glucose in this population is recommended. Electrolytes and kidney function should also be checked when there is a concern about severe dehydration.

Dehydration
A determination of whether or not the person has dehydration is an important part of the assessment, with dehydration typically divided into mild (3–5%), moderate (6–9%), and severe (≥10%) cases. In children, the most accurate signs of moderate or severe dehydration are a prolonged capillary refill, poor skin turgor, and abnormal breathing. Other useful findings (when used in combination) include sunken eyes, decreased activity, a lack of tears, and a dry mouth. A normal urinary output and oral fluid intake is reassuring. Laboratory testing is of little clinical benefit in determining the degree of dehydration. Thus the use of urine testing or ultrasounds is generally not needed.

Differential diagnosis
Other potential causes of signs and symptoms that mimic those seen in gastroenteritis that need to be ruled out include appendicitis, volvulus, inflammatory bowel disease, urinary tract infections, and diabetes mellitus. Pancreatic insufficiency, short bowel syndrome, Whipples disease, coeliac disease, and laxative abuse should also be considered. The differential diagnosis can be complicated somewhat if the person exhibits only vomiting or diarrhea (rather than both).Appendicitis may present with vomiting, abdominal pain, and a small amount of diarrhea in up to 33% of cases. This is in contrast to the large amount of diarrhea that is typical of gastroenteritis. Infections of the lungs or urinary tract in children may also cause vomiting or diarrhea. Classical diabetic ketoacidosis (DKA) presents with abdominal pain, nausea, and vomiting, but without diarrhea. One study found that 17% of children with DKA were initially diagnosed as having gastroenteritis.

Prevention
Water, sanitation, hygiene
A supply of easily accessible uncontaminated water and good sanitation practices are important for reducing rates of infection and clinically significant gastroenteritis. Personal hygiene measures (such as hand washing with soap) have been found to decrease rates of gastroenteritis in both the developing and developed world by as much as 30%. Alcohol-based gels may also be effective. Food or drink that is thought to be contaminated should be avoided.Breastfeeding is important, especially in places with poor hygiene, as is improvement of hygiene generally. Breast milk reduces both the frequency of infections and their duration.

Vaccination
Due to both its effectiveness and safety, in 2009 the World Health Organization recommended that the rotavirus vaccine be offered to all children globally. Two commercial rotavirus vaccines exist and several more are in development. In Africa and Asia these vaccines reduced severe disease among infants and countries that have put in place national immunization programs have seen a decline in the rates and severity of disease. This vaccine may also prevent illness in non-vaccinated children by reducing the number of circulating infections. Since 2000, the implementation of a rotavirus vaccination program in the United States has substantially decreased the number of cases of diarrhea by as much as 80 percent. The first dose of vaccine should be given to infants between 6 and 15 weeks of age. The oral cholera vaccine has been found to be 50–60% effective over two years.There are a number of vaccines against gastroenteritis in development. For example, vaccines against Shigella and enterotoxigenic Escherichia coli (ETEC), which are two of the leading bacterial causes of gastroenteritis worldwide.

Management
Gastroenteritis is usually an acute and self-limiting disease that does not require medication. The preferred treatment in those with mild to moderate dehydration is oral rehydration therapy (ORT). For children at risk of dehydration from vomiting, taking a single dose of the anti vomiting medication metoclopramide or ondansetron, may be helpful, and butylscopolamine is useful in treating abdominal pain.

Rehydration
The primary treatment of gastroenteritis in both children and adults is rehydration. This is preferably achieved by drinking rehydration solution, although intravenous delivery may be required if there is a decreased level of consciousness or if dehydration is severe. Drinking replacement therapy products made with complex carbohydrates (i.e. those made from wheat or rice) may be superior to those based on simple sugars. Drinks especially high in simple sugars, such as soft drinks and fruit juices, are not recommended in children under five years of age as they may increase diarrhea. Plain water may be used if more specific ORT preparations are unavailable or the person is not willing to drink them. A nasogastric tube can be used in young children to administer fluids if warranted. In those who require intravenous fluids, one to four hours worth is often sufficient.

Dietary
It is recommended that breast-fed infants continue to be nursed in the usual fashion,  and that formula-fed infants continue their formula immediately after rehydration with ORT. Lactose-free or lactose-reduced formulas usually are not necessary. Children should continue their usual diet during episodes of diarrhea with the exception that foods high in simple sugars should be avoided. The BRAT diet (bananas, rice, applesauce, toast and tea) is no longer recommended, as it contains insufficient nutrients and has no benefit over normal feeding.A Cochrane Review from 2020 concludes that probiotics make little or no difference to people who have diarrhea lasting 2 days or longer and that there is no proof that they reduce its duration. They may be useful in preventing and treating antibiotic associated diarrhea. Fermented milk products (such as yogurt) are similarly beneficial. Zinc supplementation appears to be effective in both treating and preventing diarrhea among children in the developing world.

Antiemetics
Antiemetic medications may be helpful for treating vomiting in children. Ondansetron has some utility, with a single dose being associated with less need for intravenous fluids, fewer hospitalizations, and decreased vomiting. Metoclopramide might also be helpful. However, the use of ondansetron might possibly be linked to an increased rate of return to hospital in children. The intravenous preparation of ondansetron may be given orally if clinical judgment warrants. Dimenhydrinate, while reducing vomiting, does not appear to have a significant clinical benefit.

Antibiotics
Antibiotics are not usually used for gastroenteritis, although they are sometimes recommended if symptoms are particularly severe or if a susceptible bacterial cause is isolated or suspected. If antibiotics are to be employed, a macrolide (such as azithromycin) is preferred over a fluoroquinolone due to higher rates of resistance to the latter. Pseudomembranous colitis, usually caused by antibiotic use, is managed by discontinuing the causative agent and treating it with either metronidazole or vancomycin. Bacteria and protozoans that are amenable to treatment include Shigella Salmonella typhi, and Giardia species. In those with Giardia species or Entamoeba histolytica, tinidazole treatment is recommended and superior to metronidazole. The World Health Organization (WHO) recommends the use of antibiotics in young children who have both bloody diarrhea and fever.

Antimotility agents
Antimotility medication has a theoretical risk of causing complications, and although clinical experience has shown this to be unlikely, these drugs are discouraged in people with bloody diarrhea or diarrhea that is complicated by fever. Loperamide, an opioid analogue, is commonly used for the symptomatic treatment of diarrhea. Loperamide is not recommended in children, however, as it may cross the immature blood–brain barrier and cause toxicity. Bismuth subsalicylate, an insoluble complex of trivalent bismuth and salicylate, can be used in mild to moderate cases, but salicylate toxicity is theoretically possible.

Epidemiology
It is estimated that there were two billion cases of gastroenteritis that resulted in 1.3 million deaths globally in 2015. Children and those in the developing world are most commonly affected. As of 2011, in those younger than five, there were about 1.7 billion cases resulting in 0.7 million deaths, with most of these occurring in the worlds poorest nations. More than 450,000 of these fatalities are due to rotavirus in children under five years of age. Cholera causes about three to five million cases of disease and kills approximately 100,000 people yearly. In the developing world, children less than two years of age frequently get six or more infections a year that result in significant gastroenteritis. It is less common in adults, partly due to the development of acquired immunity.In 1980, gastroenteritis from all causes caused 4.6 million deaths in children, with the majority occurring in the developing world. Death rates were reduced significantly (to approximately 1.5 million deaths annually) by 2000, largely due to the introduction and widespread use of oral rehydration therapy. In the US, infections causing gastroenteritis are the second most common infection (after the common cold), and they result in between 200 and 375 million cases of acute diarrhea and approximately ten thousand deaths annually, with 150 to 300 of these deaths in children less than five years of age.

Society and culture
Gastroenteritis is associated with many colloquial names, including "Montezumas revenge", "Delhi belly", "la turista", and "back door sprint", among others. It has played a role in many military campaigns and is believed to be the origin of the term "no guts no glory".Gastroenteritis is the main reason for 3.7 million visits to physicians a year in the United States and 3 million visits in France. In the United States gastroenteritis as a whole is believed to result in costs of US$23 billion per year with that due to rotavirus alone resulting in estimated costs of US$1 billion a year.

Terminology
The first usage of "gastroenteritis" was in 1825. Before this time it was commonly known as typhoid fever or "cholera morbus", among others, or less specifically as "griping of the guts", "surfeit", "flux", "colic", "bowel complaint", or any one of a number of other archaic names for acute diarrhea. Cholera morbus is a historical term that was used to refer to gastroenteritis rather than specifically cholera.

Other animals
Many of the same agents cause gastroenteritis in cats and dogs as in humans. The most common organisms are Campylobacter, Clostridium difficile, Clostridium perfringens, and Salmonella. A large number of toxic plants may also cause symptoms.Some agents are more specific to a certain species. Transmissible gastroenteritis coronavirus (TGEV) occurs in pigs resulting in vomiting, diarrhea, and dehydration </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sialolithiasis and can you explain it in depth? [/INST] Sialolithiasis (also termed salivary calculi, or salivary stones) is a crystallopathy where a calcified mass or sialolith forms within a salivary gland, usually in the duct of the submandibular gland (also termed "Whartons duct"). Less commonly the parotid gland or rarely the sublingual gland or a minor salivary gland may develop salivary stones.
The usual symptoms are pain and swelling of the affected salivary gland, both of which get worse when salivary flow is stimulated, e.g. with the sight, thought, smell or taste of food, or with hunger or chewing. This is often termed "mealtime syndrome". Inflammation or infection of the gland may develop as a result. Sialolithiasis may also develop because of the presence of existing chronic infection of the glands, dehydration (e.g. use of phenothiazines), Sjögrens syndrome and/or increased local levels of calcium, but in many instances the cause is idiopathic (unknown).
The condition is usually managed by removing the stone, and several different techniques are available. Rarely, removal of the submandibular gland may become necessary in cases of recurrent stone formation. Sialolithiasis is common, accounting for about 50% of all disease occurring in the major salivary glands and causing symptoms in about 0.45% of the general population. Persons aged 30–60 and males are more likely to develop sialolithiasis.

Classification
The term is derived from the Greek words sialon (saliva) and lithos (stone), and the Greek -iasis meaning "process" or "morbid condition". A calculus (plural calculi) is a hard, stone-like concretion that forms within an organ or duct inside the body. They are usually made from mineral salts, and other types of calculi include tonsiloliths (tonsil stones) and renal calculi (kidney stones). Sialolithiasis refers to the formation of calculi within a salivary gland. If a calculus forms in the duct that drains the saliva from a salivary gland into the mouth, then saliva will be trapped in the gland. This may cause painful swelling and inflammation of the gland. Inflammation of a salivary gland is termed sialadenitis. Inflammation associated with blockage of the duct is sometimes termed "obstructive sialadenitis". Because saliva is stimulated to flow more with the thought, sight or smell of food, or with chewing, pain and swelling will often get suddenly worse just before and during a meal ("peri-prandial"), and then slowly decrease after eating, this is termed meal time syndrome. However, calculi are not the only reasons that a salivary gland may become blocked and give rise to the meal time syndrome. Obstructive salivary gland disease, or obstructive sialadenitis, may also occur due to fibromucinous plugs, duct stenosis, foreign bodies, anatomic variations, or malformations of the duct system leading to a mechanical obstruction associated with stasis of saliva in the duct.Salivary stones may be divided according to which gland they form in. About 85% of stones occur in the submandibular gland, and 5–10% occur in the parotid gland. In about 0–5% of cases, the sublingual gland or a minor salivary gland is affected. When minor glands are rarely involved, caliculi are more likely in the minor glands of the buccal mucosa and the maxillary labial mucosa. Submandibular stones are further classified as anterior or posterior in relation to an imaginary transverse line drawn between the mandibular first molar teeth. Stones may be radiopaque, i.e. they will show up on conventional radiographs, or radiolucent, where they not be visible on radiographs (although some of their effects on the gland may still be visible). They may also symptomatic or asymptomatic, according to whether they cause any problems or not.

Signs and symptoms
Signs and symptoms are variable and depend largely upon whether the obstruction of the duct is complete or partial, and how much resultant pressure is created within the gland. The development of infection in the gland also influences the signs and symptoms.

Pain, which is intermittent, and may suddenly get worse before mealtimes, and then slowly get better (partial obstruction).
Swelling of the gland, also usually intermittent, often suddenly appearing or increasing before mealtimes, and then slowly going down (partial obstruction).
Tenderness of the involved gland.
Palpable hard lump, if the stone is located near the end of the duct. If the stone is near the submandibular duct orifice, the lump may be felt under the tongue.
Lack of saliva coming from the duct (total obstruction).
Erythema (redness) of the floor of the mouth (infection).
Pus discharging from the duct (infection).
Cervical lymphadenitis (infection).
Bad breath.Rarely, when stones form in the minor salivary glands, there is usually only slight local swelling in the form of a small nodule and tenderness.

Causes
There are thought to be a series of stages that lead to the formation of a calculus (lithogenesis). Initially, factors such as abnormalities in calcium metabolism, dehydration, reduced salivary flow rate, altered acidity (pH) of saliva caused by oropharyngeal infections, and altered solubility of crystalloids, leading to precipitation of mineral salts, are involved. Other sources state that no systemic abnormality of calcium or phosphate metabolism is responsible.The next stage involves the formation of a nidus which is successively layered with organic and inorganic material, eventually forming a calcified mass. In about 15-20% of cases the sialolith will not be sufficiently calcified to appear radiopaque on a radiograph, and will therefore be difficult to detect.
Other sources suggest a retrograde theory of lithogenesis, where food debris, bacteria or foreign bodies from the mouth enter the ducts of a salivary gland and are trapped by abnormalities in the sphincter mechanism of the duct opening (the papilla), which are reported in 90% of cases. Fragments of bacteria from salivary calculi were reported to be Streptococci species which are part of the normal oral microbiota and are present in dental plaque.Stone formation occurs most commonly in the submandibular gland for several reasons. The concentration of calcium in saliva produced by the submandibular gland is twice that of the saliva produced by the parotid gland. The submandibular gland saliva is also relatively alkaline and mucous. The submandibular duct (Whartons duct) is long, meaning that saliva secretions must travel further before being discharged into the mouth. The duct possesses two bends, the first at the posterior border of the mylohyoid muscle and the second near the duct orifice. The flow of saliva from the submandibular gland is often against gravity due to variations in the location of the duct orifice </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Epilepsia partialis continua and can you explain it in depth? [/INST] Epilepsia partialis continua is a rare type of brain disorder in which a patient experiences recurrent motor epileptic seizures that are focal (hands and face), and recur every few seconds or minutes for extended periods (days to years). It is sometimes called Kozhevnikovs epilepsia named after Russian psychiatrist Aleksei Yakovlevich Kozhevnikov who first described this type of epilepsy.

Signs and symptoms
During these seizures, there is repetitive focal myoclonus or Jacksonian march.
After a seizure has subsided, Todds phenomenon may be observed, which includes transient unilateral weakness.

Causes
There are numerous causes for this kind of seizure and they differ depending somewhat on the age at which the seizures begin. Epilepsy most often occurs at the extremes of life – in childhood or in very old age – but can develop at any time throughout ones life.
Although these seizures are usually due to large, acute brain lesions resulting from strokes in adults and focal cortical inflammatory processes in children (Rasmussens encephalitis), possibly caused by chronic viral infections, edema, or autoimmune processes.
They are very medication and therapy-resistant, and the primary therapeutic goal is to stop secondary generalization. There are also many other reasons why these seizures occur. For example, they could be due to genetics, infections, or problems with brain development. Commonly the cause is unknown.
Genetic background determines such features as height, eye color, and potential to develop certain diseases like diabetes, but it also determines all the chemicals and structures that make up the brain, therefore playing a role in epilepsia partialis continua. The chemicals and structures that make up the brain have similarities across different people, but they vary in certain enzymes and receptors. These variations are not usually enough to cause a problem, but occasionally they do. For example, if a person has a mutation in a gene that creates the sodium channel (a part of the neuron required for firing) it makes it easier for neuronal firing to get out of control.
An infection of the brain (encephalitis) can also be a contributing factor. Although this sort of infection is uncommon it can be due to a virus, bacterium, or (very rarely) fungus. If a seizure happens during the infection itself, the person most likely doesnt have epilepsy but has "symptomatic seizures" or seizures occurring because of a known injury to the brain. Once the infection is stopped the seizures will stop. Another more common infection is "meningitis", infection of the membranes surrounding the brain </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Greig cephalopolysyndactyly syndrome and can you explain it in depth? [/INST] Greig cephalopolysyndactyly syndrome is a disorder that affects development of the limbs, head, and face. The features of this syndrome are highly variable, ranging from very mild to severe. People with this condition typically have one or more extra fingers or toes (polydactyly) or an abnormally wide thumb or big toe (hallux).

Presentation
The skin between the fingers and toes may be fused (cutaneous syndactyly). This disorder is also characterized by widely spaced eyes (ocular hypertelorism), an abnormally large head size (macrocephaly), and a high, prominent forehead. Rarely, affected individuals may have more serious medical problems including seizures and developmental delay.

Pathophysiology
Greig cephalopolysyndactyly syndrome is a chromosomal condition related to chromosome 7. Mutations in the GLI3 gene cause Greig cephalopolysyndactyly syndrome. The GLI3 gene provides instructions for making a protein that controls gene expression, which is a process that regulates whether genes are turned on or off in particular cells. By interacting with certain genes at specific times during development, the GLI3 protein plays a role in the normal shaping (patterning) of many organs and tissues before birth.Different genetic changes involving the Gli3 gene can cause Greig cephalopolysyndactyly syndrome. In some cases, the condition results from a chromosomal abnormality, such as a large deletion or translocation of genetic material, in the region of chromosome 7 that contains the GLI3 gene. In other cases, a mutation in the GLI3 gene itself is responsible for the disorder. Each of these genetic changes prevents one copy of the gene in each cell from producing any functional protein. It remains unclear how a reduced amount of this protein disrupts early development and causes the characteristic features of Greig cephalopolysyndactyly syndrome.This condition is inherited in an autosomal dominant pattern, which means the defective gene is located on an autosome, and only one copy of the defective GLI3 gene is sufficient to cause the disorder. In cases of dominant inheritance, an affected person inherits the genetic mutation or chromosomal abnormality from one affected parent.Rare instances of this disorder are sporadic, and occur in people with no history of the condition in their family.

Diagnosis
The disease is not easily definable. The main form of diagnosis is presumptive, if the person has the usual triad of preaxial polydactyly with cutaneous syndactyly of at least one limb, macrocephaly, and  hypertelorism. However, a definitive diagnosis can be made if there is a phenotype that is caused by a Gcps and a Gli3 gene mutation. It can also be made if the person has a family member or relative with the disease </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Iridodialysis and can you explain it in depth? [/INST] Iridodialysis is a localized separation or tearing away of the iris from its attachment to the ciliary body.

Symptoms and signs
Those with small iridodialyses may be asymptomatic and require no treatment, but those with larger dialyses may have corectopia or polycoria and experience monocular diplopia, glare, or photophobia. Iridodialyses often accompany angle recession and may cause glaucoma or hyphema. Hypotony may also occur.

Complications
Those with traumatic iridodialyses (particularly by blunt trauma) are at high risk for angle recession, which may cause glaucoma. This is typically seen about 100 days after the injury, and as such is sometimes  called "100-day glaucoma" </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Fibromatosis colli and can you explain it in depth? [/INST] Fibromatosis colli (FMC), also termed sternocleidomastoid tumor of infancy, pseudotumor of infancy, and infancy sternocleidomastoid pseudotumor, is an uncommon (incidence: 0.4%-1.3% of live births), congenital tumor in one of the two sternocleidomastoid neck muscles although rare cases have presented with a FMC tumor in both sternocleidomastoid muscles. A tumor is here defined as a growth of tissue that is not coordinated with the normal surrounding tissue and persists in growing even if the original trigger for its growth is removed. FMC tumors are benign growths that may cause disfigurements but are not cancers and do not metastasize (i.e. spread) to distant tissues.As judged by microscopic cytology analyses, fibromatosis colli tumors consist of spindle-shaped fibroblasts (i.e. the most common cell type in connective tissue) located in a background of collagen fibers, decomposing skeletal muscle fibers, and, in some cases, regenerating skeletal muscle fibers. The fibroblasts have a completely normal appearance with no evidence suggesting that they are malignant. The World Health Organization, 2020, classified fibromatosis colli as in the category of benign fibroblastic and myofibroblastic tumors.In the majority of cases, FMC tumors decrease in size and completely resolve by the newborns second year. If left untreated, however, a significant percentage of cases progress to, and are the most frequent cause of, congenital muscular torticollis, i.e. an abnormal, asymmetrical head or neck position commonly called wry neck. Untreated FMC tumors may also progress to facial asymmetry, plagiocephaly (i.e. flattened head), permanent loss of neck mobility, scoliosis (i.e. sidewise curvature of the spine), or other structural disfigurements that result from compensatory mechanisms.

Presentation
FMC tumors most commonly present as slow-growing, firm, mobile, nontender, spindle-shaped masses in the lower two-thirds of the sternocleidomastoid muscle of infants within 8 weeks (average: 24 days) of delivery. At diagnosis, these infants heads may tilt toward the side with the mass while their chins tilt to the opposite, uninvolved side. This tilting is due to sternocleidomastoid muscle contracture. FMC tumors are more common in males and the right sternocleidomastoid muscle  although very rare cases present with bilateral tumors. Untreated, the masses may continue to grow for weeks after birth but then stabilize, start regressing after 4–8 months of life, and over the ensuing 1–2 years typically fully resolve. In three studies, >25%, >50% and >80% of these infants have had difficult deliveries such as a breech birth, delivery requiring forceps, primigravida birth (i.e. mothers first child), prolonged, difficult labor, or delivery by Caesarean section. From 6-20% of newborns with fibromatosis colli also present with other congenital lesions such as hip dysplasia or, less commonly, facial asymmetry.

Pathology
Microscopic histopathological analyses of biopsied FMC tumor tissues typically find benign-appearing, spindle-shaped fibroblasts, decomposing skeletal muscle fibers, and, in some cases, regenerating skeletal muscle fibers in a collagen fiber-containing background. If necessary, these tumors are typically diagnosed by microscopic examination of fine-needle aspiration samples rather than the more invasive approach of tumor biopsy sampling. The asperates show scant to moderately cellular, scattered, oval-shaped to spindle-shaped fibroblasts, naked nuclei (i.e. cell nuclei virtually devoid of other cell elements such as the cytoplasm), wisps of collagen, atrophic, degenerating muscle fibers, regenerating muscle fibers, and intact skeletal muscle cells containing multiple nuclei. There is no evidence of inflammation, hemorrhage, cell necrosis, or rapidly dividing and/or proliferating cells.

Etiology
It has been postulated that the FMC tumor mass itself is a remnant of a hematoma caused by tissue injury occurring during delivery. However, there are no features of hematomas (e.g. hemosiderin released by dying red blood cells) in theses lesions at diagnosis and no evidence of trauma (e.g. overlying skin changes or discolorations) at birth in infants who later present with FMC tumors. It has also been suggested that venous outflow obstruction occurring in the fetus while in the uterus or during delivery leads to degeneration of sternocleidomastoid muscle fibers and subsequent fibrosis of the damaged areas. Finally, it has been suggested that an injury due to poor fetal head positioning in the uterus produces a compartment syndrome-like pressure-induced injury to the sternocleidomastoid muscle that results in muscle cell death followed by tissue fibrosis and the usual pathology of FMC tumors.

Diagnosis
The recommended first step after clinically detecting a sternocleidomastoid mass in a newborn infant is Doppler ultrasonography combined with duplex ultrasonography. This method commonly reveals diagnostic (up to 100% sensitivity rates) findings of diffuse or focal enlargement of sternocleidomastoid muscle that has no cysts or other ultrasonography-detected abnormalities </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Open fracture and can you explain it in depth? [/INST] An open fracture, also  called a compound fracture, is a type of bone fracture in orthopedics that is frequently caused by high energy trauma. It is a bone fracture associated with a break in the skin continuity which can cause complications such as infection, malunion, and nonunion. Gustilo open fracture classification is the most commonly used method to classify open fractures, to guide treatment and to predict clinical outcomes. Advanced trauma life support is the first line of action in dealing with open fractures and to rule out other life-threatening condition in cases of trauma. Cephalosporins are generally the first line of antibiotics. The antibiotics are continued for 24 hours to minimize the risk of infections. Therapeutic irrigation, wound debridement, early wound closure and bone fixation are the main management of open fractures. All these actions aimed to reduce the risk of infections.

Causes
Open fractures can occur due to direct impacts such as high-energy physical forces (trauma), motor vehicular accidents, firearms, and falls from height.  Indirect mechanisms include twisting (torsional injuries) and falling from a standing position. These mechanisms are usually associated with substantial degloving of the soft-tissues, but can also have a subtler appearance with a small poke hole and accumulation of clotted blood in the tissues. Depending on the nature of the trauma, it can cause different types of fractures:

Common fractures
Result from significant trauma to the bone. This trauma can come from a variety of forces – a direct blow, axial loading, angular forces, torque, or a mixture of these.

Pathological fractures
Result from minor trauma to diseased bone. These preexisting processes include metastatic lesions, bone cysts, advanced osteoporosis, etc.

Fracture-dislocations
Severe injury in which both fracture and dislocation take place simultaneously.

Gunshot wounds
Caused by high-speed projectiles, they cause damage as they go through the tissue, through secondary shock wave and cavitation.

Diagnosis
The initial evaluation for open fractures is to rule out any other life-threatening injuries. Advanced Trauma Life Support (ATLS) is the initial protocol to rule out such injuries. Once the patient is stabilised, orthopedic injuries can be evaluated. Mechanism of injury is important to know the amount energy that is transferred to the patient and the level of contamination. Every limb should be exposed to evaluate any other hidden injuries. Characteristics of the wound should be noted in detail. Neurology and the vascular status of the affected limb are important to rule out any nerve or blood vessels injuries. High index of suspicion of compartment syndrome should be maintained for leg and forearm fractures.There are a number of classification systems attempting to categorise open fractures such as Gustilo open fracture classification, Tscherne classification, and Müller AO Classification of fractures. However, Gustilo open fracture classification is the most commonly used classification system. Gustilo system grades the fracture according to energy of injury, soft tissue damage, level of contamination, and comminution of fractures. The higher the grade, the worse the outcome of the fracture.
However, Gustilo system is not without its limitations. The system has limited interobserver reliability at 50% to 60%. The size of injury on the skin surface does not necessarily reflect the extent of deep underlying soft tissue injury. Therefore, the true grading of Gustilo can only be done in operating theatre.

Management
Acute management
Urgent interventions, including therapeutic irrigation and wound debridement, are often necessary to clean the area of injury and minimize the risk of infection. Other risks of delayed intervention include long-term complications, such as deep infection, vascular compromise and complete limb loss. After wound irrigation, dry or wet gauze should be applied to the wound to prevent bacterial contamination. Taking photographs of the wound can help to reduce the need of multiple examinations by different doctors, which could be painful. Limb should be reduced and placed in a well-padded splint for immobilization of fractures. Pulses should be documented before and after reduction.Wound cultures are positive in 22% of pre-debridement cultures and 60% of post-debridement cultures of infected cases. Therefore, pre-operative cultures no longer recommended. The value of post-operative cultures is unknown. Tetanus prophylaxis is routinely given to enhance immune response against Clostridium tetani. Anti-tetanus immunoglobulin is only indicated for those with highly contaminated wounds with uncertain vaccination history. Single intramuscular dose of 3000 to 5000 units of tetanus immunoglobulin is given to provide immediate immunity.Another important clinical decision during acute management of open fractures involves the effort to avoid preventable amputations, where functional salvage of the limb is clearly desirable. Care must be taken to ensure this decision is not solely based on an injury severity tool score, but rather a decision made following a full discussion of options between doctors and the person, along with their family and care team.

Antibiotics
Administration of antibiotics as soon as possible is necessary to reduce the risk of infection. However, antibiotics may not provide necessary benefits in open finger fractures and low velocity firearms injury. First generation cephalosporin (cefazolin) is recommended as first line antibiotics for the treatment of open fractures. The antibiotic is useful against gram positive cocci and gram negative rods such as Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae. To extend the coverage of antibiotics against more bacteria in Type III Gustilo fractures, combination of first generation cephalosporin and aminoglycoside (gentamicin or tobramycin) or a third generation cephalosporin is recommended to cover against nosocomial gram negative bacilli such as Pseudomonas aeruginosa. Adding penicillin to cover for gas gangrene caused by anaerobic bacteria Clostridium perfringens is a controversial practice. Studies has shown that such practice may not be necessary as the standard antibiotic regimen is enough to cover for Clostridial infections. Antibiotic impregnated devices such as tobramycin impregnated Poly(methyl methacrylate) (PMMA) beads and antibiotic bone cement are helpful in reducing rates of infection. The use of absorbable carriers with implant coatings at the time of surgical fixation is also an effective means of delivering local antibiotics.There has been no agreement on the optimal duration of antibiotics. Studies has shown that there is no additional benefits of risk of infection when giving antibiotics for one day, when compared to giving antibiotics for three days or five days. However, at present, there is only low to moderate evidence for this and more research is needed. Some authors recommended that antibiotics to be given for three doses for Gustilo Grade I fractures, for one day after wound closure in Grade II fractures, three days in Grade IIIA fractures, and three days after wound closure for Grade IIIB and IIIC.

Wound irrigation
There has been no agreement for the optimal solution for wound irrigation. Studies found out that there is no difference in infection rates by using normal saline or other various forms of water (distilled, boiled, or tap). There is also no difference in infection rates when using normal saline with castile soap compared with normal saline together with bacitracin in irrigating wounds. Studies also have shown that there is no difference in infection rates using low pressure pulse lavage (LPPL) when compared to high pressure pulse lavage (HPPL) in irrigating wounds. Optimal amount of fluid for irrigation also has not been established. It is recommended that the amount of irrigation solution to be determined by the severity of the fracture, with 3 litres for type I fractures, 6 litres for type II fractures, and 9 litres for type III fractures.

Wound debridement
The purpose of wound debridement is to remove all contaminated and non-viable tissues including skin, subcutaneous fat, muscles and bones. Viability of bones and soft tissues are determined by their capacity to bleed. Meanwhile, the viability of muscles is determined by colour, contractility, consistency, and their capacity to bleed. The optimal timing of performing wound debridement and closure is debated and dependent on the severity of the injury, resources and antibiotics available, and individual needs. Debridement time can vary from 6 to 72 hours, and closure time can be immediate (less than 72 hours) or delayed (72 hours to up to 3 months). There is no difference in infection rates for performing surgery within 6 hours of injury when compared to until 72 hours after injury.

Surgical management
Early fracture immobilisation and fixation helps to prevent further soft tissue injury and promotes wound and bone healing. This is especially important in the treatment of intraarticular fractures where early fixation allows early joint motion to prevent joint stiffness. Fracture management depends on the persons overall well-being, fracture pattern and location, and the extent of soft tissue injury. Both reamed and unreamed intramedullary nailing are accepted surgical treatments for open tibial fracture. Both techniques have similar rates of postoperative healing, postoperative infection, implant failure and compartment syndrome. Unreamed intramedullary nailing is advantageous because it has a lower incidence of superficial infection and malunion compared to external fixation.  However, unreamed intramedullary nailing can result in high rates of hardware failure if a persons weight bearing after surgery is not closely controlled.  Compared to external fixation, unreamed intramedullary nailing has similar rates of deep infection, delayed union and nonunion following surgery </s>


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


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


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Inguinal lymphadenopathy and can you explain it in depth? [/INST] Inguinal lymphadenopathy causes swollen lymph nodes in the groin area. It can be a symptom of infective or neoplastic processes.
Infective aetiologies include Tuberculosis, HIV, non-specific or reactive lymphadenopathy to recent lower limb infection or groin infections </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hypoparathyroidism and can you explain it in depth? [/INST] Hypoparathyroidism is decreased function of the parathyroid glands with underproduction of parathyroid hormone (PTH). This can lead to low levels of calcium in the blood, often causing cramping and twitching of muscles or tetany (involuntary muscle contraction), and several other symptoms. It is a very rare disease. The condition can be inherited, but it is also encountered after thyroid or parathyroid gland surgery, and it can be caused by immune system-related damage as well as a number of rarer causes. The diagnosis is made with blood tests, and other investigations such as genetic testing depending on the results. The primary treatment of hypoparathyroidism is calcium and vitamin D supplementation. Calcium replacement or vitamin D can ameliorate the symptoms but can increase the risk of kidney stones and chronic kidney disease. Additionally, injectable medications such as recombinant human parathyroid hormone or teriparatide may be given by injection to replace the missing hormone.

Signs and symptoms
The main symptoms of hypoparathyroidism are the result of the low blood calcium level, which interferes with normal muscle contraction and nerve conduction. As a result, people with hypoparathyroidism can experience paresthesia, an unpleasant tingling sensation around the mouth and in the hands and feet, as well as muscle cramps and severe spasms known as "tetany" that affect the hands and feet. Many also report a number of subjective symptoms such as fatigue, headaches, bone pain and insomnia. Crampy abdominal pain may occur. Physical examination of someone with hypocalcemia may show tetany, but it is also possible to provoke tetany of the facial muscles by tapping on the facial nerve (a phenomenon known as Chvosteks sign) or by using the cuff of a sphygmomanometer to temporarily obstruct the blood flow to the arm (a phenomenon known as Trousseaus sign of latent tetany).A number of medical emergencies can arise in people with low calcium levels. These are seizures, severe irregularities in the normal heart beat, as well as spasm of the upper part of the airways or the smaller airways known as the bronchi (both potentially causing respiratory failure).

Related conditions
Causes
Hypoparathyroidism can have the following causes:
Removal of, or trauma to, the parathyroid glands due to thyroid surgery (thyroidectomy), parathyroid surgery (parathyroidectomy) or other surgical interventions in the central part of the neck (such as operations on the larynx and/or pharynx) is a recognized cause. It is the most common cause of hypoparathyroidism. Although surgeons generally make attempts to spare normal parathyroid glands at surgery, inadvertent injury to the glands or their blood supply is still common. When this happens, the parathyroids may cease functioning. This is usually temporary but occasionally long term (permanent).
Kenny-Caffey Syndrome
Autoimmune invasion and destruction is the most common non-surgical cause. It can occur as part of autoimmune polyendocrine syndromes.
Hemochromatosis can lead to iron accumulation and consequent dysfunction of a number of endocrine organs, including the parathyroids.
Absence or dysfunction of the parathyroid glands is one of the components of chromosome 22q11 microdeletion syndrome (other names: DiGeorge syndrome, Schprintzen syndrome, velocardiofacial syndrome).
Magnesium deficiency
A defect in the calcium receptor leads to a rare congenital form of the disease
Idiopathic (of unknown cause)
Occasionally due to other hereditary causes (e.g. Barakat syndrome (HDR syndrome) a genetic development disorder resulting in hypoparathyroidism, sensorineural deafness, and kidney disease)

Mechanism
The parathyroid glands are so named because they are usually located behind the thyroid gland in the neck. They arise during fetal development from structures known as the third and fourth pharyngeal pouch. The glands, usually four in number, contain the parathyroid chief cells that sense the level of calcium in the blood through the calcium-sensing receptor and secrete parathyroid hormone. Magnesium is required for PTH secretion. Under normal circumstances, the parathyroids secrete PTH to maintain a calcium level within normal limits, as calcium is required for adequate muscle and nerve function (including the autonomic nervous system). PTH acts on several organs to increase calcium levels. It increases calcium absorption in the bowel, while in the kidney it prevents calcium excretion and increases phosphate release and in bone it increases calcium through bone resorption.

Diagnosis
Diagnosis is by measurement of calcium, serum albumin (for correction) and PTH in blood </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is White sponge nevus and can you explain it in depth? [/INST] White sponge nevus (WSN) is an autosomal dominant condition of the oral mucosa (the mucous membrane lining of the mouth). It is caused by a mutations in certain genes coding for keratin, which causes a defect in the normal process of keratinization of the mucosa. This results in lesions which are thick, white and velvety on the inside of the cheeks within the mouth. Usually, these lesions are present from birth or develop during childhood </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Brain herniation and can you explain it in depth? [/INST] Brain herniation is a potentially deadly side effect of very high pressure within the skull that occurs when a part of the brain is squeezed across structures within the skull. The brain can shift across such structures as the falx cerebri, the tentorium cerebelli, and even through the foramen magnum (the hole in the base of the skull through which the spinal cord connects with the brain).  Herniation can be caused by a number of factors that cause a mass effect and increase intracranial pressure (ICP): these include traumatic brain injury, intracranial hemorrhage, or brain tumor.Herniation can also occur in the absence of high ICP when mass lesions such as hematomas occur at the borders of brain compartments. In such cases local pressure is increased at the place where the herniation occurs, but this pressure is not transmitted to the rest of the brain, and therefore does not register as an increase in ICP.Because herniation puts extreme pressure on parts of the brain and thereby cuts off the blood supply to various parts of the brain, it is often fatal. Therefore, extreme measures are taken in hospital settings to prevent the condition by reducing intracranial pressure, or decompressing (draining) a hematoma which is putting local pressure on a part of the brain.

Signs and symptoms
Brain herniation frequently presents with abnormal posturing, a characteristic positioning of the limbs indicative of severe brain damage. These patients have a lowered level of consciousness, with Glasgow Coma Scores of three to five. One or both pupils may be dilated and fail to constrict in response to light. Vomiting can also occur due to compression of the vomiting center in the medulla oblongata. Severe headaches and seizures as a result of increased intracranial pressure are not uncommon. Cardiovascular and pulmonary symptoms may also be present as the brain loses function, but might also be associated with bleeding. They can include: hypertension, respiratory depression, arrhythmia and in severe cases cardiac arrest.

Causes
Causes of brain herniation include:
Brain edema
Hematoma
Stroke
Tumour
Infection

Classification
The tentorium is an extension of the dura mater that separates the cerebellum from the cerebrum. There are two major classes of herniation: supratentorial and infratentorial. Supratentorial refers to herniation of structures normally found above the tentorial notch, and infratentorial refers to structures normally found below it.
Supratentorial herniation1) Uncal (transtentorial)
2) Central
3) Cingulate (subfalcine/transfalcine)
4) Transcalvarial
5) Tectal (posterior)

Infratentorial herniation6) Upward (upward cerebellar or upward transtentorial)
7) Tonsillar (downward cerebellar)

Uncal herniation
In uncal herniation, a common subtype of transtentorial herniation, the innermost part of the temporal lobe, the uncus, can be squeezed so much that it moves towards the tentorium and puts pressure on the brainstem, most notably the midbrain. The tentorium is a structure within the skull formed by the dura mater of the meninges.  Tissue may be stripped from the cerebral cortex in a process called decortication.The uncus can squeeze the oculomotor nerve (a.k.a. CN III), which may affect the parasympathetic input to the eye on the side of the affected nerve, causing the pupil of the affected eye to dilate and fail to constrict in response to light as it should. Pupillary dilation often precedes the somatic motor effects of CN III compression called oculomotor nerve palsy or third nerve palsy. This palsy presents as deviation of the eye to a "down and out" position due to loss of innervation to all ocular motility muscles except for the lateral rectus (innervated by abducens nerve (a.k.a. CN VI) and the superior oblique (innervated by trochlear nerve a.k.a. CN IV). The symptoms occur in this order because the parasympathetic fibers surround the motor fibers of CN III and are hence compressed first.Compression of the ipsilateral posterior cerebral artery will result in ischemia of the ipsilateral primary visual cortex and contralateral visual field deficits in both eyes (contralateral homonymous hemianopsia).
Another important finding is a false localizing sign, the so-called Kernohans notch, which results from compression of the contralateral cerebral crus containing descending corticospinal and some corticobulbar tract fibers. This leads to Ipsilateral hemiparesis in reference to the herniation and contralateral hemiparesis with reference to the cerebral crus.With increasing pressure and progression of the hernia there will be distortion of the brainstem leading to Duret hemorrhages (tearing of small vessels in the parenchyma) in the median and paramedian zones of the mesencephalon and pons. The rupture of these vessels leads to linear or flamed shaped hemorrhages. The disrupted brainstem can lead to decorticate posture, respiratory center depression and death. Other possibilities resulting from brain stem distortion include lethargy, slow heart rate, and pupil dilation.Uncal herniation may advance to central herniation. The sliding uncus syndrome represents uncal herniation without alteration in the level of consciousness and other sequelae mentioned above.

Central herniation
In central herniation, the diencephalon and parts of the temporal lobes of both of the cerebral hemispheres are squeezed through a notch in the tentorium cerebelli.  Transtentorial herniation can occur when the brain moves either up or down across the tentorium, called ascending and descending transtentorial herniation respectively; however descending herniation is much more common.  Downward herniation can stretch branches of the basilar artery (pontine arteries), causing them to tear and bleed, known as a Duret hemorrhage. The result is usually fatal. Other symptoms of this type of herniation include small, fixed pupils with paralysis of upward eye movement giving the characteristic appearance of "sunset eyes". Also found in these patients, often as a terminal complication is the development of diabetes insipidus due to the compression of the pituitary stalk.  Radiographically, downward herniation is characterized by obliteration of the suprasellar cistern from temporal lobe herniation into the tentorial hiatus with associated compression on the cerebral peduncles.  Upwards herniation, on the other hand, can be radiographically characterized by obliteration of the quadrigeminal cistern. Intracranial hypotension syndrome has been known to mimic downwards transtentorial herniation.

Cingulate herniation
In cingulate or subfalcine herniation, the most common type, the innermost part of the frontal lobe is scraped under part of the falx cerebri, the dura mater at the top of the head between the two hemispheres of the brain. Cingulate herniation can be caused when one hemisphere swells and pushes the cingulate gyrus by the falx cerebri. This does not put as much pressure on the brainstem as the other types of herniation, but it may interfere with blood vessels in the frontal lobes that are close to the site of injury (anterior cerebral artery), or it may progress to central herniation.  Interference with the blood supply can cause dangerous increases in ICP that can lead to more dangerous forms of herniation.  Symptoms for cingulate herniation are not well defined.  Usually occurring in addition to uncal herniation, cingulate herniation may present with abnormal posturing and coma.  Cingulate herniation is frequently believed to be a precursor to other types of herniation.

Transcalvarial herniation
In transcalvarial herniation, the brain squeezes through a fracture or a surgical site in the skull. Also called "external herniation", this type of herniation may occur during craniectomy, surgery in which a flap of skull is removed, the protruding brain region preventing the piece of skull from being replaced during the operation.

Upward herniation
Increased pressure in the posterior fossa can cause the cerebellum to move up through the tentorial opening in upward, or cerebellar herniation.  The midbrain is pushed through the tentorial notch upward. This is also known as ascending transtentorial herniation since it occurs across the tentorium cerebelli.

Tonsillar herniation
In tonsillar herniation, also called downward cerebellar herniation, transforaminal herniation, or "coning", the cerebellar tonsils move downward through the foramen magnum possibly causing compression of the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum. Increased pressure on the brainstem can result in dysfunction of the centers in the brain responsible for controlling respiratory and cardiac function. The most common signs are intractable headache, head tilt, and neck stiffness due to tonsillar impaction. The level of consciousness may decrease and also give rise to flaccid paralysis. Blood pressure instability is also evident in these patients.Congenital tonsillar herniation of the cerebellum is also known as a Chiari malformation (CM),  or previously an Arnold-Chiari malformation (ACM).  There are four types of Chiari malformation, and they represent very different disease processes with different symptoms and prognosis.  These conditions can be found in asymptomatic patients as an incidental finding, or can be so severe as to be life-threatening.  This condition is now being diagnosed more frequently by radiologists, as more patients undergo MRI scans of their heads, especially upright MRI, which is more than twice as sensitive for detecting this condition.  Cerebellar tonsillar ectopia (CTE) is a term used by radiologists to describe cerebellar tonsils that are "low lying" but that do not meet the radiographic criteria for definition as a Chiari malformation.  The currently accepted radiographic definition for a Chiari malformation is that cerebellar tonsils lie at least 5mm below the level of the foramen magnum.  Some clinicians have reported that some patients appear to experience symptoms consistent with a Chiari malformation without radiographic evidence of tonsillar herniation </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Thanatophoric dysplasia and can you explain it in depth? [/INST] Thanatophoric dysplasia is a severe skeletal disorder characterized by a disproportionately small ribcage, extremely short limbs and folds of extra skin on the arms and legs.

Symptoms and signs
Infants with this condition have disproportionately short arms and legs with extra folds of skin. Other signs of the disorder include a narrow chest, small ribs, underdeveloped lungs, and an enlarged head with a large forehead and prominent, wide-spaced eyes.
Thanatophoric dysplasia is a lethal skeletal dysplasia divided into two subtypes. Type I is characterized by extreme rhizomelia, bowed long bones, narrow thorax, a relatively large head, normal trunk length and absent cloverleaf skull. The spine shows platyspondyly, the cranium has a short base, and, frequently, the foramen magnum is decreased in size. The forehead is prominent, and hypertelorism and a saddle nose may be present. Hands and feet are normal, but fingers are short. Type II is characterized by short, straight long bones and cloverleaf skull.
It presents with typical telephone-handle shaped long bones and H-shaped vertebrae.

Causes
It can be associated with missense mutations in fibroblast growth factor receptor-3. It is inherited in an autosomal dominant manner.

Diagnosis
Classification
Infants with type 1 thanatophoric dysplasia also have curved thigh bones, flattened bones of the spine (platyspondyly) and shortened thoracic ribs. Note: Prenatal ultra-sound images of the ribs sometimes appear asymmetrical when in fact they are not </s>


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


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