<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 Myoglobinuria and can you explain it in depth? [/INST] Myoglobinuria is the presence of myoglobin in the urine, which usually results from rhabdomyolysis or muscle injury. Myoglobin is present in muscle cells as a reserve of oxygen.

Signs and symptoms
Signs and symptoms of myoglobinuria are usually nonspecific and needs some clinical prudence. Therefore, among the possible signs and symptoms to look for would be:
Swollen and painful muscles
Fever, nausea
Delirium (elderly individuals)
Myalgia
Dark urine
Calcium ion loss

Causes
Trauma, vascular problems, malignant hyperthermia, certain drugs and other situations can destroy or damage the muscle, releasing myoglobin to the circulation and thus to the kidneys. Under ideal situations myoglobin will be filtered and excreted with the urine, but if too much myoglobin is released into the circulation or in case of kidney problems, it can occlude the kidneys filtration system leading to acute tubular necrosis and acute kidney injury.
Other causes of myoglobinuria include:

McArdles disease
Phosphofructokinase deficiency
Carnitine palmitoyltransferase II deficiency
Malignant hyperthermia
Polymyositis
Lactate dehydrogenase deficiency
Adenosine monophosphate deaminase deficiency type 1
Thermal or electrical burn

Pathophysiology
Myoglobinuria pathophysiology consists of a series of metabolic actions in which damage to muscle cells affect calcium mechanisms, thereby increasing free ionized calcium in the cytoplasm of the myocytes (concurrently decreasing free ionized calcium in the bloodstream). This, in turn, affects several intracellular enzymes that are calcium-dependent, thereby compromising the cell membrane, which in turn causes the release of myoglobin.

Diagnosis
After centrifuging, the urine of myoglobinuria is red, where the urine of hemoglobinuria after centrifuge is pink to clear.

Treatment
Hospitalization and IV hydration should be the first step in any patient suspected of having myoglobinuria or rhabdomyolysis. The goal is to induce a brisk diuresis to prevent myoglobin precipitation and deposition, which can cause acute kidney injury. Mannitol can be added to assist with diuresis. Adding sodium bicarbonate to the IV fluids will cause alkalinization of the urine, believed to reduce the breakdown of myoglobin into its nephrotoxic metabolites, thus preventing renal damage. Often, IV normal saline is all that is needed to induce diuresis and alkalinize the urine.

Epidemiology
See also
Pigmenturia

References
Further reading
Pedley, edited by Lewis P. Rowland, Timothy A. (2010). Merritts neurology (12th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. p. 885. ISBN 978-0781791861. Retrieved 10 September 2015 </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 Shock 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 Neck pain and can you explain it in depth? [/INST] Neck pain, also known as cervicalgia, is a common problem, with two-thirds of the population having neck pain at some point in their lives.Neck pain, although felt in the neck, can be caused by numerous other spinal problems. Neck pain may arise due to muscular tightness in both the neck and upper back, or pinching of the nerves emanating from the cervical vertebrae. Joint disruption in the neck creates pain, as does joint disruption in the upper back.
The head is supported by the lower neck and upper back, and it is these areas that commonly cause neck pain. The top three joints in the neck allow for most movement of the neck and head. The lower joints in the neck and those of the upper back create a supportive structure for the head to sit on. If this support system is affected adversely, then the muscles in the area will tighten, leading to neck pain.
Neck pain affects about 5% of the global population as of 2010.

Differential diagnosis
Neck pain may come from any of the structures in the neck including: vascular, nerve, airway, digestive, and musculature / skeletal, or be referred from other areas of the body.Major and severe causes of neck pain (roughly in order of severity) include:

Carotid artery dissection
Referred pain from acute coronary syndrome
Head and neck cancer
Infections, including:
Meningitis of several types including sudden onset of severe neck or back pain particularly in teens and young adults which may be fatal if not treated quickly
Retropharyngeal abscess
Epiglottitis
Spinal disc herniation – protruding or bulging discs, or if severe prolapse.
Spondylosis - degenerative arthritis and osteophytes
Spinal stenosis – a narrowing of the spinal canalMore common and lesser neck pain causes include:

Stress – physical and emotional stresses
Prolonged postures – many people fall asleep on sofas and chairs and wake up with sore necks.
Minor injuries and falls – car accidents, sporting events, and day to day injuries that are really minor.
Referred pain – mostly from upper back problems
Over-use – muscular strain is one of the most common causes
Whiplash
Pinched nerveAlthough the causes are numerous, most are easily rectified by either professional help or using self help advice and techniques.
More causes can include: poor sleeping posture, torticollis, head injury, rheumatoid arthritis,
Carotidynia, congenital cervical rib, mononucleosis, rubella, certain cancers, ankylosing spondylitis,
cervical spine fracture, esophageal trauma, subarachnoid hemorrhage, lymphadenitis, thyroid trauma, and tracheal trauma.

Treatment
Treatment of neck pain depends on the cause.  For the vast majority of people, neck pain can be treated conservatively.  Recommendations in which it helps alleviate symptoms include applying heat or cold.   Other common treatments could include medication, body mechanics training, ergonomic reform, and physical therapy. Treatments may also include patient education, but existing evidence shows a lack of effectiveness.

Medication
Analgesics such as acetaminophen or NSAIDs are generally recommended for pain. A 2017 review, however found that paracetamol was not efficacious and that NSAIDs are minimally effective.Muscle relaxants may also be recommended. However, one study showed that one muscle relaxant called cyclobenzaprine was not effective for treatment of acute cervical strain (as opposed to neck pain from other etiologies or chronic neck pain).

Surgery
Surgery is usually not indicated for mechanical causes of neck pain. If neck pain is the result of instability, cancer, or other disease process surgery may be necessary. Surgery is usually not indicated for "pinched nerves" or herniated discs unless there is spinal cord compression or pain and disability have been protracted for many months and refractory to conservative treatment such as physical therapy.

Alternative medicine
Exercise plus joint manipulation has been found to be beneficial in both acute and chronic mechanical neck disorders. In particular, specific strengthening exercise may improve function and pain. Motor control using cranio-cervical flexion exercises has been shown to be effective for non-specific chronic neck pain.  Both cervical manipulation and cervical mobilization produce similar immediate-, and short-term changes. Multiple cervical manipulation sessions may provide better pain relief and functional improvement than certain medications at immediate to long-term follow-up. Thoracic manipulation may also improve pain and function. Low-level laser therapy has been shown to reduce pain immediately after treatment in acute neck pain and up to 22 weeks after completion of treatment in patients that experience chronic neck pain </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 Suicide attempt and can you explain it in depth? [/INST] A suicide attempt is an attempt to die by suicide that results in survival. It may be referred to as a "failed" or "unsuccessful" suicide attempt, though these terms are discouraged by mental health professionals for implying that a suicide resulting in death is a successful and positive outcome.

Epidemiology
In the United States, the National Institute of Mental Health reports there are 11 nonfatal suicide attempts for every suicide death. The American Association of Suicidology reports higher numbers, stating that there are 25 suicide attempts for every suicide completion. The ratio of suicide attempts to suicide death is about 25:1 in youths, compared to about 4:1 in elderly. A 2008 review found that nonfatal self-injury is more common in women, and a separate study from 2008/2009 found suicidal thoughts higher among females, as well as significant differences between genders for suicide planning and suicide attempts.Suicide attempts are more common among adolescents in developing countries than developed ones. A 12-month prevalence of suicide attempt in developing countries between 2003 and 2015 was reported as 17%.

Parasuicide and self-injury
Without commonly agreed-upon operational definitions, some suicidology researchers regard many suicide attempts as parasuicide (para=near) or self harm behavior, rather than "true" suicide attempts, as in lacking suicidal intent.

Methods
Some suicide methods have higher rates of lethality than others. The use of firearms results in death 90% of the time. Wrist-slashing has a much lower lethality rate, comparatively. 75% of all suicide attempts are by drug overdose, a method that is often thwarted because the drug is nonlethal, or is used at a nonlethal dosage. These people survive 97% of the time.

Repetition
A nonfatal suicide attempt is the strongest known clinical predictor of eventual suicide. Suicide risk among self-harm patients is hundreds of times higher than in the general population. It is often estimated that about 10–15% of people who attempt suicide eventually die by suicide. The mortality risk is highest during the first months and years after the attempt: almost 1% of individuals who attempt suicide will die by suicide if the attempt is repeated within one year. Recent meta-analytic evidence suggests that the association between suicide attempt and suicidal death may not be as strong as it was thought before.

Outcomes
Suicide attempts can result in serious and permanent injuries and/or disabilities. 700,000 (or more) Americans survive a suicide attempt each year. People who attempt either hanging or carbon monoxide poisoning and survive can face permanent brain damage due to cerebral anoxia </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 Craft and can you explain it in depth? [/INST] A craft or trade is a pastime or an occupation that requires particular skills and knowledge of skilled work. In a historical sense, particularly the Middle Ages and earlier, the term is usually applied to people occupied in small scale production of goods, or their maintenance, for example by tinkers. The traditional term craftsman is nowadays often replaced by artisan and by craftsperson (craftspeople).
Historically, the more specialized crafts with high-value products tended to concentrate in urban centers and formed guilds. The skill required by their professions and the need to be permanently involved in the exchange of goods often demanded a generally higher level of education, and craftsmen were usually in a more privileged position than the peasantry in societal hierarchy. The households of craftsmen were not as self-sufficient as those of people engaged in agricultural work, and therefore had to rely on the exchange of goods.  Some crafts, especially in areas such as pottery, woodworking, and various stages of textile production, could be practiced on a part-time basis by those also working in agriculture, and often formed part of village life.
When an apprentice finished his apprenticeship, he became a journeyman searching for a place to set up his own shop and make a living. After he set up his own shop, he could then call himself a master of his craft.
This stepwise approach to mastery of a craft, which includes the attainment of some education and skill, has survived in some countries until today. But crafts have undergone deep structural changes since and during the era of the Industrial Revolution. The mass production of goods by large-scale industry has limited crafts to market segments in which industrys modes of functioning or its mass-produced goods do not satisfy the preferences of potential buyers. As an outcome of these changes, craftspeople today increasingly make use of semi-finished components or materials and adapt these to their customers requirements or demands. Thus, they participate in a certain division of labour between industry and craft.

Classification
There are three aspects to human creativity - art, crafts, and science. Roughly determined, art relies upon intuitive sensing, vision and expression, crafts upon sophisticated technique and science upon knowledge.

Handicraft
Handicraft is the "traditional" main sector of the crafts, it is a type of work where useful and decorative devices are made completely by hand or by using only simple tools. The term is usually applied to traditional means of making goods. The individual artisanship of the items is a paramount criterion, such items often have cultural and/or religious significance </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 Hepatorenal syndrome and can you explain it in depth? [/INST] Hepatorenal syndrome (often abbreviated HRS) is a life-threatening medical condition that consists of rapid deterioration in kidney function in individuals with cirrhosis or fulminant liver failure. HRS is usually fatal unless a liver transplant is performed, although various treatments, such as dialysis, can prevent advancement of the condition.
HRS can affect individuals with cirrhosis, severe alcoholic hepatitis, or liver failure, and usually occurs when liver function deteriorates rapidly because of a sudden insult such as an infection, bleeding in the gastrointestinal tract, or overuse of diuretic medications.  HRS is a relatively common complication of cirrhosis, occurring in 18% of people within one year of their diagnosis, and in 39% within five years of their diagnosis. Deteriorating liver function is believed to cause changes in the circulation that supplies the intestines, altering blood flow and blood vessel tone in the kidneys. The kidney failure of HRS is a consequence of these changes in blood flow, rather than direct damage to the kidney. The diagnosis of hepatorenal syndrome is based on laboratory tests of individuals susceptible to the condition.  Two forms of hepatorenal syndrome have been defined: Type 1 HRS entails a rapidly progressive decline in kidney function, while type 2 HRS is associated with ascites (fluid accumulation in the abdomen) that does not improve with standard diuretic medications.
The risk of death in hepatorenal syndrome is very high; the mortality of individuals with type 1 HRS is over 50% over the short term, as determined by historical case series. The only long-term treatment option for the condition is liver transplantation.  While awaiting transplantation, people with HRS often receive other treatments that improve the abnormalities in blood vessel tone, including supportive care with medications, or the insertion of a transjugular intrahepatic portosystemic shunt (TIPS), which is a small shunt placed to reduce blood pressure in the portal vein.  Some patients may require hemodialysis to support kidney function, or a newer technique called liver dialysis which uses a dialysis circuit with albumin-bound membranes to bind and remove toxins normally cleared by the liver, providing a means of extracorporeal liver support until transplantation can be performed.

Classification
Hepatorenal syndrome is a particular and common type of kidney failure that affects individuals with liver cirrhosis or, less commonly, with fulminant liver failure. The syndrome involves constriction of the blood vessels of the kidneys and dilation of blood vessels in the splanchnic circulation, which supplies the intestines. The classification of hepatorenal syndrome identifies two categories of kidney failure, termed type 1 and type 2 HRS, which both occur in individuals with either cirrhosis or fulminant liver failure.  In both categories, the deterioration in kidney function is quantified either by an elevation in creatinine level in the blood, or by decreased clearance of creatinine in the urine.

Type 1 hepatorenal syndrome
Type 1 HRS is characterized by rapidly progressive kidney failure, with a doubling of serum creatinine to a level greater than 221 μmol/L (2.5 mg/dL) or a halving of the creatinine clearance to less than 20 mL/min over a period of less than two weeks. The prognosis of individuals with type 1 HRS is particularly grim, with a mortality rate exceeding 50% after one month. Patients with type 1 HRS are usually ill, may have low blood pressure, and may require therapy with drugs to improve the strength of heart muscle contraction (inotropes) or other drugs to maintain blood pressure (vasopressors). Unlike type II, in type I hepatorenal syndrome the kidney failure improves with treatment and stabilizes. Vasoconstrictors and volume expanders are the mainstay of treatment.

Type 2 hepatorenal syndrome
In contrast, type 2 HRS is slower in onset and progression, and is not associated with an inciting event.  It is defined by an increase in serum creatinine level to >133 μmol/L (1.5 mg/dL) or a creatinine clearance of less than 40 mL/min, and a urine sodium < 10 μmol/L. It also carries a poor outlook, with a median survival of approximately six months unless the affected individual undergoes liver transplantation.  Type 2 HRS is thought to be part of a spectrum of illness associated with increased pressures in the portal vein circulation, which begins with the development of fluid in the abdomen (ascites). The spectrum continues with diuretic-resistant ascites, where the kidneys are unable to excrete sufficient sodium to clear the fluid even with the use of diuretic medications.  Most individuals with type 2 HRS have diuretic-resistant ascites before they develop deterioration in kidney function.

Signs and symptoms
Both types of hepatorenal syndrome share three major components: altered liver function, abnormalities in circulation, and kidney failure.  As these phenomena may not necessarily produce symptoms until late in their course, individuals with hepatorenal syndrome are typically diagnosed with the condition on the basis of altered laboratory tests.  Most people who develop HRS have cirrhosis, and may have signs and symptoms of the same, which can include jaundice, altered mental status, evidence of decreased nutrition, and the presence of ascites.  Specifically, the production of ascites that is resistant to the use of diuretic medications is characteristic of type 2 HRS.  Oliguria, which is a decrease in urine volume, may occur as a consequence of kidney failure; however, some individuals with HRS continue to produce a normal amount of urine.  As these signs and symptoms may not necessarily occur in HRS, they are not included in the major and minor criteria for making a diagnosis of this condition; instead HRS is diagnosed in an individual at risk for the condition on the basis of the results of laboratory tests, and the exclusion of other causes.

Causes
Hepatorenal syndrome usually affects individuals with cirrhosis and elevated pressures in the portal vein system (termed portal hypertension).  While HRS may develop in any type of cirrhosis, it is most common in individuals with alcoholic cirrhosis, particularly if there is concomitant alcoholic hepatitis identifiable on liver biopsies.  HRS can also occur in individuals without cirrhosis, but with acute onset of liver failure, termed fulminant liver failure.Certain precipitants of HRS have been identified in vulnerable individuals with cirrhosis or fulminant liver failure. These include bacterial infection, acute alcoholic hepatitis, or bleeding in the upper gastrointestinal tract.  Spontaneous bacterial peritonitis, which is the infection of ascites fluid, is the most common precipitant of HRS in cirrhotic individuals.  HRS can sometimes be triggered by treatments for complications of liver disease: iatrogenic precipitants of HRS include the aggressive use of diuretic medications or the removal of large volumes of ascitic fluid by paracentesis from the abdominal cavity without compensating for fluid losses by intravenous replacement.

Diagnosis
There can be many causes of kidney failure in individuals with cirrhosis or fulminant liver failure.  Consequently, it is a challenge to distinguish hepatorenal syndrome from other entities that cause kidney failure in the setting of advanced liver disease.  As a result, additional major and minor criteria have been developed to assist in the diagnosis of hepatorenal syndrome.The major criteria include liver disease with portal hypertension; kidney failure; the absence of shock, infection, recent treatment with medications that affect the function of the kidney (nephrotoxins), and fluid losses; the absence of sustained improvement in kidney function despite treatment with 1.5 litres of intravenous normal saline; the absence of proteinuria (protein in the urine); and, the absence of kidney disease or obstruction of kidney outflow as seen on ultrasound.The minor criteria are the following: a low urine volume (less than 500 mL (18 imp fl oz; 17 US fl oz) per day), low sodium concentration in the urine, a urine osmolality that is greater than that in the blood, the absence of red blood cells in the urine, and a serum sodium concentration of less than 130 mmol/L.Many other diseases of the kidney are associated with liver disease and must be excluded before making a diagnosis of hepatorenal syndrome.  Individuals with pre-renal kidney failure do not have damage to the kidneys, but as in individuals with HRS, have kidney dysfunction due to decreased blood flow to the kidneys. Also, similarly to HRS, pre-renal kidney failure causes the formation of urine that has a very low sodium concentration. In contrast to HRS, however, pre-renal kidney failure usually responds to treatment with intravenous fluids, resulting in reduction in serum creatinine and increased excretion of sodium.  Acute tubular necrosis (ATN) involves damage to the tubules of the kidney, and can be a complication in individuals with cirrhosis, because of exposure to toxic medications or the development of decreased blood pressure.  Because of the damage to the tubules, ATN affected kidneys usually are unable to maximally resorb sodium from the urine.  As a result, ATN can be distinguished from HRS on the basis of laboratory testing, as individuals with ATN will have urine sodium measurements that are much higher than in HRS; however, this may not always be the case in cirrhotics.  Individuals with ATN also may have evidence of hyaline casts or muddy-brown casts in the urine on microscopy, whereas the urine of individuals with HRS is typically devoid of cellular material, as the kidneys have not been directly injured.  Some viral infections of the liver, including hepatitis B and hepatitis C can also lead to inflammation of the glomerulus of the kidney.  Other causes of kidney failure in individuals with liver disease include drug toxicity (notably, the antibiotic gentamicin) or contrast nephropathy, caused by intravenous administration of contrast agents used for medical imaging tests.

Pathophysiology
The kidney failure in hepatorenal syndrome is believed to arise from abnormalities in blood vessel tone in the kidneys. The predominant theory (termed the underfill theory) is that blood vessels in the kidney circulation are constricted because of the dilation of blood vessels in the splanchnic circulation (which supplies the intestines), which is mediated by factors released by liver disease. Nitric oxide, prostaglandins, and other vasoactive substances have been hypothesized as powerful mediators of splanchnic vasodilation in cirrhosis. The consequence of this phenomenon is a decrease in the "effective" volume of blood sensed by the juxtaglomerular apparatus, leading to the secretion of renin and the activation of the renin–angiotensin system, which results in the vasoconstriction of vessels systemically and in the kidney specifically. However, the effect of this is insufficient to counteract the mediators of vasodilation in the splanchnic circulation, leading to persistent "underfilling" of the kidney circulation and worsening kidney vasoconstriction, leading to kidney failure.Studies to quantify this theory have shown that there is an overall decreased systemic vascular resistance in hepatorenal syndrome, but that the measured femoral and kidney fractions of cardiac output are respectively increased and reduced, suggesting that splanchnic vasodilation is implicated in the kidney failure. Many vasoactive chemicals have been hypothesized as being involved in mediating the systemic hemodynamic changes, including atrial natriuretic factor, prostacyclin, thromboxane A2, and endotoxin. In addition to this, it has been observed that the administration of medications to counteract splanchnic vasodilation (such as ornipressin, terlipressin, and octreotide) leads to improvement in glomerular filtration rate (which is a quantitative measure of kidney function) in patients with hepatorenal syndrome, providing further evidence that splanchnic vasodilation is a key feature of its pathogenesis.
The underfill theory involves activation of the renin–angiotensin–aldosterone system, which leads to an increase in absorption of sodium from the kidney tubule (termed renal sodium avidity) mediated by aldosterone, which acts on mineralocorticoid receptors in the distal convoluted tubule.  This is believed to be a key step in the pathogenesis of ascites in cirrhotics as well. It has been hypothesized that the progression from ascites to hepatorenal syndrome is a spectrum where splanchnic vasodilation defines both resistance to diuretic medications in ascites (which is commonly seen in type 2 HRS) and the onset of kidney vasoconstriction (as described above) leading to hepatorenal syndrome.

Prevention
The risk of death in hepatorenal syndrome is very high; consequently, there is a significant emphasis on the identification of patients who are at risk for HRS, and prevention of triggers for onset of HRS.  As infection (specifically spontaneous bacterial peritonitis) and gastrointestinal hemorrhage are both complications in individuals with cirrhosis, and are common triggers for HRS, specific care is made in early identification and treatment of cirrhotics with these complications  to prevent HRS.  Some of the triggers for HRS are induced by treatment of ascites and can be preventable.  The aggressive use of diuretic medications should be avoided.  In addition, many medications that are either used to treat cirrhotic complications (such as some antibiotics) or other conditions may cause sufficient impairment in kidney function in the cirrhotic to lead to HRS.  Also, large volume paracentesis—which is the removal of ascites fluid from the abdomen using a needle or catheter in order to relieve discomfort—may cause enough alteration in hemodynamics to precipitate HRS, and should be avoided in individuals at risk.  The concomitant infusion of albumin can avert the circulatory dysfunction that occurs after large-volume paracentesis and may prevent HRS.  Conversely, in individuals with very tense ascites, it has been hypothesized that removal of ascitic fluid may improve kidney function if it decreases the pressure on the renal veins.Individuals with ascites that have become infected spontaneously (termed spontaneous bacterial peritonitis or SBP) are at an especially high risk for the development of HRS.  In individuals with SBP, one randomized controlled trial found that the administration of intravenous albumin on the day of admission and on the third day in hospital reduced both the rate of kidney insufficiency and the mortality rate.

Treatment
Transplantation
The definitive treatment for hepatorenal syndrome is liver transplantation, and all other therapies can best be described as bridges to transplantation.  While liver transplantation is by far the best available management option for HRS, the mortality of individuals with HRS has been shown to be as high as 25% within the first month after transplantation.  Individuals with HRS and evidence of greater hepatic dysfunction (quantified as MELD scores above 36) have been found to be at greatest risk of early mortality after liver transplantation.  A further deterioration of kidney function even after liver transplantation in individuals with HRS has been demonstrated in several studies; however, this is transient and thought to be due to the use of medications with toxicity to the kidneys, and specifically the introduction of immunosuppressants such as tacrolimus and cyclosporine that are known to worsen kidney function.  Over the long-term, however, individuals with HRS who are the recipients of liver transplants almost universally recover kidney function, and studies show that their survival rates at three years are similar to those who have received liver transplants for reasons other than HRS.In anticipation of liver transplantation (which may be associated with considerable in-hospital delay), several other strategies have been found to be beneficial in preserving kidney function.  These include the use of intravenous albumin infusion, medications (for which the best evidence is for analogues of vasopressin, which causes splanchnic vasoconstriction), radiological shunts to decrease pressure in the portal vein, dialysis, and a specialized albumin-bound membrane dialysis system termed molecular adsorbents recirculation system (MARS) or liver dialysis.

Medical therapy
Many major studies showing improvement in kidney function in patients with hepatorenal syndrome have involved expansion of the volume of the plasma with albumin given intravenously. The quantity of albumin administered intravenously varies: one cited regimen is 1 gram of albumin per kilogram of body weight intravenously on the first day, followed by 20 to 40 grams daily.  Notably, studies have shown that treatment with albumin alone is inferior to treatment with other medications in conjunction with albumin; most studies evaluating pre-transplant therapies for HRS involve the use of albumin in conjunction with other medical or procedural treatment.Midodrine is an alpha-agonist and octreotide is an analogue of somatostatin, a hormone involved in regulation of blood vessel tone in the gastrointestinal tract.  The medications are respectively systemic vasoconstrictors and inhibitors of splanchnic vasodilation, and were not found to be useful when used individually in treatment of hepatorenal syndrome.  However, one study of 13 patients with hepatorenal syndrome showed significant improvement in kidney function when the two were used together (with midodrine given orally, octreotide given subcutaneously and both dosed according to blood pressure), with three patients surviving to discharge. Another nonrandomized, observational study of individuals with HRS treated with subcutaneous octreotide and oral midodrine showed that there was increased survival at 30 days.The vasopressin analogue ornipressin was found in a number of studies to be useful in improvement of kidney function in patients with hepatorenal syndrome, but has been limited in its use, as it can cause severe ischemia to major organs.  Terlipressin is a vasopressin analogue that has been found in one large study to be useful for improving kidney function in patients with hepatorenal syndrome with a lesser incidence of ischemia but is not available in the United States. A randomized control trial led by Florence Wong demonstrated improved renal function in individuals with Type 1 HRS treated with terlipressin and albumin over placebo. A key criticism of all of these medical therapies has been heterogeneity in the populations investigated and the use of kidney function, instead of mortality, as an outcome measure.Other agents that have been investigated for use in treatment of HRS include pentoxifylline, acetylcysteine, and misoprostol.  The evidence for all of these therapies is based on either case series, or in the case of pentoxifylline, extrapolated from a subset of patients treated for alcoholic hepatitis.

Procedural treatments
A transjugular intrahepatic portosystemic shunt (TIPS) involves the decompression of the high pressures in the portal circulation by placing a small stent between a portal and hepatic vein. This is done through radiologically guided catheters which are passed into the hepatic vein either through the internal jugular vein or the femoral vein.  Theoretically, a decrease in portal pressures is thought to reverse the hemodynamic phenomena that ultimately lead to the development of hepatorenal syndrome.  TIPS has been shown to improve kidney function in patients with hepatorenal syndrome.  Complications of TIPS for treatment of HRS include the worsening of hepatic encephalopathy (as the procedure involves the forced creation of a porto-systemic shunt, effectively bypassing the ability of the liver to clear toxins), inability to achieve adequate reduction in portal pressure, and bleeding.Liver dialysis involves extracorporeal dialysis to remove toxins from the circulation, usually through the addition of a second dialysis circuit that contains an albumin-bound membrane.  The molecular adsorbents recirculation system (MARS) has shown some utility as a bridge to transplantation in patients with hepatorenal syndrome, yet the technique is still nascent.Renal replacement therapy may be required to bridge individuals with hepatorenal syndrome to liver transplantation, although the condition of the patient may dictate the modality used. The use of dialysis, however, does not lead to recuperation or preservation of kidney function in patients with HRS, and is essentially only used to avoid complications of kidney failure until transplantation can take place. In patients who undergo hemodialysis, there may even be an increased risk of mortality due to low blood pressure in patients with HRS, although appropriate studies have yet to be performed. As a result, the role of renal replacement therapy in patients with HRS remains unclear.

Epidemiology
As the majority of individuals with hepatorenal syndrome have cirrhosis, much of the epidemiological data on HRS comes from the cirrhotic population.  The condition is quite common: approximately 10% of individuals admitted to hospital with ascites have HRS. A retrospective case series of cirrhotic patients treated with terlipressin suggested that 20.0% of acute kidney failure in cirrhotics was due to type 1 HRS, and 6.6% was due to type 2 HRS. It is estimated that 18% of individuals with cirrhosis and ascites will develop HRS within one year of their diagnosis with cirrhosis, and 39% of these individuals will develop HRS within five years of diagnosis </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 Tetany and can you explain it in depth? [/INST] Tetany or tetanic seizure is a medical sign consisting of the involuntary contraction of muscles, which may be caused by disorders that increase the action potential frequency of muscle cells or the nerves that innervate them.
Muscle cramps caused by the disease tetanus are not classified as tetany; rather, they are due to a lack of inhibition to the neurons that supply muscles. Tetanic contractions (physiologic tetanus) are a broad range of muscle contraction types, of which tetany is only one.

Signs and symptoms
Tetany is characterized by contraction of distal muscles of the hands (carpal spasm with extension of interphalangeal joints and adduction and flexion of the metacarpophalangeal joints) and feet (pedal spasm) and is associated with tingling around the mouth and distally in the limbs.

Causes
The usual cause of tetany is a deficiency of calcium </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 Haverhill fever and can you explain it in depth? [/INST] Haverhill fever (or epidemic arthritic erythema) is a systemic illness caused by the bacterium Streptobacillus moniliformis, an organism common in rats and mice. If untreated, the illness can have a mortality rate of up to 13%. Among the two types of rat-bite fever, Haverhill fever caused by Streptobacillus moniliformis is most common in North America. The other type of infection caused by Spirillum minus is more common in Asia and is also known as Sodoku.The initial non-specific presentation of the disease and hurdles in culturing the causative microorganism are at times responsible for a delay or failure in the diagnosis of the disease. Although non-specific in nature, initial symptoms like relapsing fever, rash and migratory polyarthralgia are the most common symptoms of epidemic arthritic erythema.Bites and scratches from rodents carrying the bacteria are generally responsible for the affliction. However, the disease can be spread even without physical lacerations by rodents. In fact, the disease was first recognized from a milk-associated outbreak which occurred in Haverhill, Massachusetts in January, 1926. The organism S. moniliformis was isolated from the patients and epidemiologically, consumption of milk from one particular dairy was implicated in association with the infection. Hence, ingestion of food and drink contaminated with the bacteria can also result in the development of the disease.

Symptoms and signs
The illness resembles a severe influenza, with a moderate fever (38-40 °C, or 101-104 °F), sore throat, chills, myalgia, headache, vomiting, and a diffuse red rash (maculopapular, petechial, or purpuric), located mostly on the hands and feet. The incubation period for the bacteria generally lasts from three-ten days. As the disease progresses. almost half the patients experience migratory polyarthralgias.

Mechanism
Although the specific form of pathogenesis is still a subject of ongoing research, the bacteria has been observed to result in morphological symptoms that are atypical of bacterial infection. Autopsy of the victims vividly exhibit erythrophagocytosis, hepatosplenomegaly, interstitial pneumonia, and lymph node sinus hyperplasia. In addition, Myocarditis and Endocarditis have also been demonstrated in such patients. Synovial and serosal surfaces may be more suited for the growth of the bacteria within the body. Furthermore, leukocytoclastic vasculitis has been observed in the skin lesions.

Diagnosis
The microaerophilic conditions needed for the bacteria to grow, makes its detection incredibly difficult. Trypticase soy agar or broth enriched with 20% blood, serum, or ascitic fluid is necessary for the optimal growth of the bacteria under laboratory conditions. The organism may take up to seven days to grow and the colonies generally have a circular, grayish and shiny appearance on agar. Once the microbe has grown, primary identification can be carried out via biochemical and carbohydrate fermentation analysis. Biochemical tests such as oxidase, catalase, indole, and nitrate can be used to detect the bacteria. However, S. moniliformis can be biochemically differentiated from similar bacteria by their negative production of indole, catalase, and oxidase, while reduction of nitrate to nitrite.
PCR assay specific for Streptobacillus moniliformis can also be used to detect the bacteria in a patient sample with high accuracy.
The PCR assay utilizes primers based on the 16S rRNA gene base sequences of human and rodent strains of S. moniliformis (forward primer, 5′ GCT TAA CAC ATG CAA ATC TAT 3′ and reverse primer, 5′ AGT AAG GGC CGT ATC TCA 3′). These primers exhibit 100% complementarity to S. moniliformis ATCC 14674T and S. moniliformis ANL 370-1. The PCR assay generates a 296-bp product which upon treatment with BfaI restriction enzyme, leads to the generation of three distinct fragments (128, 92, and 76 bp), which are specific to S. moniliformis. Hence, this assay can be used to detect S </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 Osteomalacia and can you explain it in depth? [/INST] Osteomalacia is a disease characterized by the softening of the bones caused by impaired bone metabolism primarily due to inadequate levels of available phosphate, calcium, and vitamin D, or because of resorption of calcium. The impairment of bone metabolism causes inadequate bone mineralization. Osteomalacia in children is known as rickets, and because of this, use of the term "osteomalacia" is often restricted to the milder, adult form of the disease. Signs and symptoms can include diffuse body pains, muscle weakness, and fragility of the bones. In addition to low systemic levels of circulating mineral ions (for example, caused by vitamin D deficiency or renal phosphate wasting) that result in decreased bone and tooth mineralization, accumulation of mineralization-inhibiting proteins and peptides (such as osteopontin and ASARM peptides), and small inhibitory molecules (such as pyrophosphate), can occur in the extracellular matrix of bones and teeth, contributing locally to cause matrix hypomineralization (osteomalacia/odontomalacia).  A relationship describing local, physiologic double-negative (inhibiting inhibitors) regulation of mineralization has been termed the Stenciling Principle of mineralization, whereby enzyme-substrate pairs imprint mineralization patterns into the extracellular matrix (most notably described for bone) by degrading mineralization inhibitors (e.g. TNAP/TNSALP/ALPL enzyme degrading the pyrophosphate inhibition, and PHEX enzyme degrading the osteopontin inhibition). The Stenciling Principle for mineralization is particularly relevant to the osteomalacia and odontomalacia observed in hypophosphatasia (HPP) and X-linked hypophosphatemia (XLH).
The most common cause of osteomalacia is a deficiency of vitamin D, which is normally derived from sunlight exposure and, to a lesser extent, from the diet. The most specific screening test for vitamin D deficiency in otherwise healthy individuals is a serum 25(OH)D level. Less common causes of osteomalacia can include hereditary deficiencies of vitamin D or phosphate (which would typically be identified in childhood) or malignancy.
Vitamin D and calcium supplements are measures that can be used to prevent and treat osteomalacia. Vitamin D should always be administered in conjunction with calcium supplementation (as the pair work together in the body) since most of the consequences of vitamin D deficiency are a result of impaired mineral ion homeostasis.Nursing home residents and the homebound elderly population are at particular risk for vitamin D deficiency, as these populations typically receive little sun exposure. In addition, both the efficiency of vitamin D synthesis in the skin and the absorption of vitamin D from the intestine decline with age, thus further increasing the risk in these populations. Other groups at risk include individuals with malabsorption secondary to gastrointestinal bypass surgery or celiac disease, and individuals who immigrate from warm climates to cold climates, especially women who wear traditional veils or dresses that prevent sun exposure.

Signs and symptoms
Osteomalacia is a generalized bone condition in which there is inadequate mineralization of the bone. Many of the effects of the disease overlap with the more common osteoporosis, but the two diseases are significantly different. There are two main causes of osteomalacia:

insufficient calcium absorption from the intestine because of lack of dietary calcium or a deficiency of, or resistance to, the action of vitamin D, or due to undiagnosed celiac disease.
phosphate deficiency caused by increased renal losses.Symptoms:

Osteomalacia in adults starts insidiously as aches and pains in the lumbar (lower back) region and thighs before spreading to the arms and ribs. The pain is symmetrical, non-radiating and accompanied by sensitivity in the involved bones. Proximal muscles are weak, and there is difficulty in climbing upstairs and getting up from a squatting position.
As a result of demineralization, the bones become less rigid. Physical signs include deformities like triradiate pelvis and lordosis. The patient has a typical "waddling" gait </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 Herpesviral encephalitis and can you explain it in depth? [/INST] Herpesviral encephalitis, or herpes simplex encephalitis (HSE), is encephalitis due to herpes simplex virus. It is estimated to affect at least 1 in 500,000 individuals per year, and some studies suggest an incidence rate of 5.9 cases per 100,000 live births.About 90% of cases of herpes encephalitis are caused by herpes simplex virus-1 (HSV-1), the same virus that causes cold sores. According to a 2006 estimate, 57% of American adults were infected with HSV-1, which is spread through droplets, casual contact and sometimes sexual contact, though most infected people never have cold sores. The rest of cases are due to HSV-2, which is typically spread through sexual contact and is the cause of genital herpes.
Two-thirds of HSE cases occur in individuals already seropositive for HSV-1, few of whom (only 10%) have history of recurrent orofacial herpes, while about one third of cases results from an initial infection by HSV-1, predominantly occurring in individuals under the age of 18. Approximately half of individuals who develop HSE are over 50 years of age.

Signs and symptoms
Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as confusion, and changes in personality. Increased numbers of white blood cells can be found in patients cerebrospinal fluid, without the presence of pathogenic bacteria and fungi. Patients typically have a fever and may have seizures. The electrical activity of the brain changes as the disease progresses, first showing abnormalities in one temporal lobe of the brain, which spread to the other temporal lobe 7–10 days later. Imaging by CT or MRI shows characteristic changes in the temporal lobes (see Figure).
Definite diagnosis requires testing of the cerebrospinal fluid (CSF) by a lumbar puncture (spinal tap) for presence of the virus. The testing takes several days to perform, and patients with suspected Herpes encephalitis should be treated with acyclovir immediately while waiting for test results. Atypical stroke-like presentation of HSV encephalitis has been described as well and the clinicians should be aware that HSV encephalitis can mimic a stroke.

Associated conditions
Herpesviral encephalitis can serve as a trigger of anti-NMDA receptor encephalitis. About 30% of HSE patients develop this secondary immunologic reaction, which is associated with impaired neurocognitive recovery.

Epidemiology
The annual incidence of herpesvial encephalitis is from 2 to 4 cases per 1 million population.

Pathophysiology
HSE is thought to be caused by the transmission of virus from a peripheral site on the face following HSV-1 reactivation, along a nerve axon, to the brain. The virus lies dormant in the ganglion of the trigeminal cranial nerve, but the reason for reactivation, and its pathway to gain access to the brain, remains unclear, though changes in the immune system caused by stress clearly play a role in animal models of the disease. The olfactory nerve may also be involved in HSE, which may explain its predilection for the temporal lobes of the brain, as the olfactory nerve sends branches there. In horses, a single-nucleotide polymorphism is sufficient to allow the virus to cause neurological disease; but no similar mechanism has been found in humans.

Diagnosis
Brain CT scan (with/without contrast) </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 Admission 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 Bullous impetigo and can you explain it in depth? [/INST] Bullous impetigo is a bacterial skin infection caused by Staphylococcus aureus that results in the formation of large blisters called bullae, usually in areas with skin folds like the armpit, groin, between the fingers or toes, beneath the breast, and between the buttocks. It accounts for 30% of cases of impetigo, the other 70% being non-bullous impetigo.The bullae are caused by exfoliative toxins produced by Staphylococcus aureus that cause the connections between cells in the uppermost layer of the skin to fall apart. Bullous impetigo in newborns, children, or adults who are immunocompromised and/or are experiencing kidney failure, can develop into a more severe and generalized form called staphylococcal scalded skin syndrome (SSSS). The mortality rate is less than 3% for infected children, but up to 60% in adults.

Signs and symptoms
Bullous impetigo can appear around the diaper region, axilla, or neck. The bacteria causes a toxin to be produced that reduces cell-to-cell stickiness (adhesion), causing for the top layer of skin (epidermis), and lower layer of skin (dermis) to separate. Vesicles rapidly enlarge and form the bullae which is a blister more than 5mm across. Bullae is also known as staphylococcal scalded skin syndrome. Other associated symptoms are itching, swelling of nearby glands, fever and diarrhea. Pain is very rare.Long-term effects: once the scabs on the bullous have fallen off, scarring is minimal.  Possible long-term  effects are kidney disease.

Cause
Exposure is most commonly seen in hospital wards and nurseries, and can be passed from person to person in other settings, such as close contact sports. Therefore, the patient is advised to try to limit human contact as much as possible to minimize the risk of spreading the infection.

Infectious period
After 48 hours the disease is considered no longer contagious assuming the proper antibiotic treatments have been administered.

Pathogenesis
Exfoliating toxins are serine proteases that specifically bind to and cleave desmoglein 1 (Dsg1). Previous studies suggested that exfoliating toxins bind to gangliosides, causing a release of protease by keratinocytes acting as superantigens in stimulating the skins immune system. A more recent proposal states there are three known exfoliating toxins; ETA, ETB, and ETD which act as a glutamic acid-specific serine protease with concentrated specificity. Which results in the cleavage of human Dsg1 at a unique site after glutamic acid residues causing deactivation. Proteolysis of the peptide bond leading up to the dysfunction of Dsg1 and the desmosome allows for an understanding as to why the bullous forms, making the peptide bond crucial for proper function if Dsg1.

S. aureus
A phyogenic non-motile Gram-positive cocci which forms into grape like clusters. Just like other forms of staph, S. aureus has a variety of virulence factors which include surface proteins involved in adherence, secretion of enzymes that degrade proteins, and secrete toxins which damage the hosts cells.S. aureus expresses surface receptors for fibrinogen, fibronectin, and vitronectin. These surface receptors allow a bridge to be formed which binds to host endothelial cells. Lipases allow for the degradation of lipids on the skin surface and its expression can be directly correlated with its ability of the bacteria to produce abscesses.

Diagnosis
Observing the skins physical appearance, or swabbing a culture of the lesion for S. aureus. Nasal swabs from the patients immediate family members are necessary to identify them as being asymptomatic nasal carriers of S. aureus.

Histology
The epidermis is composed of four layers, stratum basale, stratum spinosum, stratum granulosum, and stratum corneum.

The cleavage plane can be found either subcorneally or within the upper stratum granulosum. The roof of the pustule is parakeratotic stratum corneum, and the floor is formed of keratinocytes, which may or may not be acantholytic </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 Compartment syndrome and can you explain it in depth? [/INST] Compartment syndrome is a condition in which increased pressure within one of the bodys anatomical compartments results in insufficient blood supply to tissue within that space. There are two main types: acute and chronic. Compartments of the leg or arm are most commonly involved.Symptoms of acute compartment syndrome (ACS) can include severe pain, poor pulses, decreased ability to move, numbness, or a pale color of the affected limb. It is most commonly due to physical trauma such as a bone fracture (up to 75% of cases) or crush injury, but it can also be caused by acute exertion during sport. It can also occur after blood flow returns following a period of poor blood flow. Diagnosis is generally based upon a persons symptoms and may be supported by measurement of intracompartmental pressure before, during, and after activity. Normal compartment pressure should be within 12-18 mmHg; anything greater than that is considered abnormal and would need treatment. Treatment is by surgery to open the compartment, completed in a timely manner. If not treated within six hours, permanent muscle or nerve damage can result.In chronic compartment syndrome (aka chronic exertional compartment syndrome), there is generally pain with exercise but the pain dissipates once activity ceases. Other symptoms may include numbness. Symptoms typically resolve with rest. Common activities that trigger chronic compartment syndrome include running and biking. Generally, this condition does not result in permanent damage. Other conditions that may present similarly include stress fractures and tendinitis. Treatment may include physical therapy or—if that is not effective—surgery.Acute compartment syndrome occurs in about 3% of those who have a midshaft fracture of the forearm. Rates in other areas of the body and for chronic cases are unknown. The condition occurs more often in males and people under the age of 35, in line with the occurrence of trauma. Compartment syndrome was first described in 1881 by German surgeon Richard von Volkmann. Untreated, acute compartment syndrome can result in Volkmanns contracture.

Signs and symptoms
Compartment syndrome usually presents within a few hours of an inciting event, but may present anytime up to 48 hours after. The limb affected by compartment syndrome is often associated with a firm, wooden feeling or a deep palpation, and is usually described as feeling tight. There may also be decrease pulses in the limb along with associated paresthesia. Usually, the pain cannot be relieved by NSAIDs. Range of motion may be limited while the compartment pressure is high. In acute compartment syndrome, the pain will not be relieved with rest. In chronic exertional compartment syndrome the pain will dissipate with rest.

Acute
There are five characteristic signs and symptoms related to acute compartment syndrome: pain, paraesthesia (reduced sensation), paralysis, pallor, and pulselessness. Pain and paresthesia are the early symptoms of compartment syndrome.
CommonPain – A person may experience pain disproportionate to the findings of the physical examination. This pain may not be relieved by strong analgesic medications. The pain is aggravated by passively stretching the muscle group within the compartment. However, such pain may disappear in the late stages of the compartment syndrome. The role of local anesthesia in delaying the diagnosis of compartment syndrome is still being debated.
Paresthesia (altered sensation)  – A person may complain of "pins & needles", numbness, and a tingling sensation. This may progress to loss of sensation (anesthesia) if no intervention is made.UncommonParalysis –  Paralysis of the limb is a rare, late finding. It may indicate both a nerve or muscular lesion.
Pallor and pulselessness – A lack of pulse rarely occurs in patients, as pressures that cause compartment syndrome are often well below arterial pressures. Absent pulses only occur when there is arterial injury or during the late stages of the compartment syndrome, when compartment pressures are very high. Pallor can also result from arterial occlusion.

Chronic
The symptoms of chronic exertional compartment syndrome, CECS, may involve pain, tightness, cramps, weakness, and diminished sensation. This pain can occur for months, and in some cases over a period of years, and may be relieved by rest.  Moderate weakness in the affected region can also be observed. These symptoms are brought on by exercise and consist of a sensation of extreme tightness in the affected muscles followed by a painful burning sensation if exercise is continued. After exercise is ceased, the pressure in the compartment will decrease within a few minutes, relieving painful symptoms. Symptoms will occur at a certain threshold of exercise which varies from person to person but is rather consistent for a given individual.  This threshold can range anywhere from 30 seconds of running to 2–3 miles of running. CECS most commonly occurs in the lower leg, with the anterior compartment being the most frequently affected compartment.  Foot drop is a common symptom of CECS.

Complications
Failure to relieve the pressure can result in the death of tissues (necrosis) in the affected anatomical compartment, since the ability of blood to enter the smallest vessels in the compartment (capillary perfusion pressure) will fall.  This, in turn, leads to progressively increasing oxygen deprivation of the tissues dependent on this blood supply. Without sufficient oxygen, the tissue will die.  On a large scale, this can cause Volkmanns contracture in affected limbs, a permanent and irreversible process.  Other reported complications include neurological deficits of the affected limb, gangrene, and chronic regional pain syndrome.    Rhabdomyolysis and subsequent kidney failure are also possible complications.  In some case series, rhabdomyolysis is reported in 23% of patients with ACS.

Causes
Acute
Acute compartment syndrome (ACS) is a medical emergency that can develop after traumatic injuries, such as in automobile accidents or dynamic sporting activities – for example, a severe crush injury or an open or closed fracture of an extremity. Rarely, ACS can develop after a relatively minor injury, or due to another medical issue.  The lower legs and the forearms are the most frequent sites affected by compartment syndrome. Other areas of the body such as thigh, buttock, hand, abdomen, and foot can also be affected. The most common cause of acute compartment syndrome is fracture of a bone, most commonly the tibia. There is no difference between acute compartment syndrome originating from an open or closed fracture. Leg compartment syndrome is found in 2% to 9% of tibial fractures. It is strongly related to fractures involving the tibial diaphysis as well as other sections of the tibia. Direct injury to blood vessels can lead to compartment syndrome by reducing the downstream blood supply to soft tissues. This reduction in blood supply can cause a series of inflammatory reactions that promote the swelling of the soft tissues. Such inflammation can be further worsened by reperfusion therapy. Because the fascia layer that defines the compartment of the limbs does not stretch, a small amount of bleeding into the compartment, or swelling of the muscles within the compartment, can cause the pressure to rise greatly. Intravenous drug injection, casts, prolonged limb compression, crush injuries, anabolic steroid use, vigorous exercise, and eschar from burns can also cause compartment syndrome. Patients on anticoagulant therapy have an increased risk of bleeding into a closed compartment.Abdominal compartment syndrome occurs when the intra-abdominal pressure exceeds 20 mmHg and abdominal perfusion pressure is less than 60 mmHg.  This disease process is associated with organ dysfunction and multiple organ failures. There are many causes, which can be broadly grouped into three mechanisms: primary (internal bleeding and swelling); secondary (vigorous fluid replacement as an unintended complication of resuscitative medical treatment, leading to the acute formation of ascites and a rise in intra-abdominal pressure); and recurrent (compartment syndrome that has returned after the initial treatment of secondary compartment syndrome).Compartment syndrome after snake bite is rare. Its incidence varies from 0.2 to 1.36% as recorded in case reports. Compartment syndrome is more common in children possibly due to inadequate volume of the bodily fluid to dilute the snake venom. Increased white blood cell count of more than 1,650/μL and aspartate transaminase (AST) level of more than 33.5 U/L could increase the risk of developing compartment syndrome. Otherwise, those bitten by venomous snake should be observed for 48 hours to exclude the possibility of compartment syndrome.Acute compartment syndrome due to severe/uncontrolled hypothyroidism is rare.

Chronic
When compartment syndrome is caused by repetitive use of the muscles, it is known as chronic compartment syndrome (CCS). This is usually not an emergency, but the loss of circulation can cause temporary or permanent damage to nearby nerves and muscles.
A subset of chronic compartment syndrome is chronic exertional compartment syndrome (CECS), often called exercise-induced compartment syndrome (EICS). Oftentimes, CECS is a diagnosis of exclusion. CECS of the leg is a condition caused by exercise which results in increased tissue pressure within an anatomical compartment due to an acute increase in muscle volume – as much as 20% is possible during exercise. When this happens, pressure builds up in the tissues and muscles causing tissue ischemia. An increase in muscle weight will reduce the compartment volume of the surrounding fascial borders and result in an increased compartment pressure. An increase in the pressure of the tissue can force fluid to leak into the interstitial space (extracellular fluid), leading to a disruption of the micro-circulation of the leg. This condition occurs commonly in the lower leg and various other locations within the body, such as the foot or forearm. CECS can be seen in athletes who train rigorously in activities that involve constant repetitive actions or motions.

Pathophysiology
In a normal human body, blood flow from the arterial system (higher pressure) to venous system (lower pressure) requires a pressure gradient. When this pressure gradient is diminished, blood flow from the artery to the vein is reduced. This causes a backup of blood and excessive fluid to leak from the capillary wall into spaces between the soft tissues cells, causing swelling of the extracellular space and a rise in intracompartmental pressure. This swelling of the soft tissues surrounding the blood vessels compresses the blood and lymphatic vessels further, causing more fluid to enter the extracellular spaces, leading to additional compression. The pressure continues to increase due to the non-compliant nature of the fascia containing the compartment.  This worsening cycle can eventually lead to a lack of sufficient oxygen in the soft tissues (tissue ischemia) and tissue death (necrosis). Tingling and abnormal sensation (paraesthesia) can begin as early as 30 minutes from the start of tissue ischemia and permanent damage can occur as early as 12 hours from the onset of the inciting injury.

Diagnosis
Compartment syndrome is a clinical diagnosis, meaning that a medical providers examination and the patients history usually give the diagnosis. Apart from the typical signs and symptoms, measurement of intracompartmental pressure can also be important for diagnosis. Using a combination of clinical diagnosis and serial intracompartmental pressure measurements increases both the sensitivity and specificity of diagnosing compartment syndrome. A transducer connected to a catheter is inserted 5 cm into the zone of injury. A compartment pressure no less than 30 mmHg of the diastolic pressure in a conscious or unconscious person is associated with compartment syndrome. Fasciotomy is indicated in that case. For those patients with low blood pressure (hypotension), a pressure of 20 mmHg higher than the intracompartmental pressure is associated with compartmental syndrome. Noninvasive methods of diagnosis such as near-infraredspectroscopy (NIRS) which uses sensors on the skin, shows promise in controlled settings. However, with limited data in uncontrolled settings, clinical presentation and intracompartmental pressure remain the gold standard for diagnosis.Chronic exertional compartment syndrome is usually a diagnosis of exclusion, with the hallmark finding being absence of symptoms at rest.  Measurement of intracompartmental pressures during symptom reproduction (usually immediately following running) is the most useful test. Imaging studies (X-ray, CT, MRI) can be useful in ruling out other more common diagnoses instead of confirming the diagnosis of compartment syndrome. Additionally, MRI has been shown to be effective in diagnosing chronic exertional compartment syndrome. The average duration of symptoms prior to diagnosis is 28 months.

Treatment
Acute
Any external compression (tourniquet, orthopedic casts or dressings applied on the affected limb) should be removed. Cutting of the cast will reduce the intracompartmental pressure by 65%, followed by 10 to 20% pressure reduction once padding is cut. After removal of the external compression the limb should be placed at the level of the heart. The vital signs of the patient should be closely monitored. If the clinical condition does not improve, then fasciotomy is indicated to decompress the compartments. An incision large enough to decompress all the compartments is necessary. This surgical procedure is performed inside an operating theater under general or local anesthesia. The timing of the fasciotomy wound closure is debated.  Some surgeons suggest wound closure should be done seven days after fasciotomy. Multiple techniques exist for closure of the surgical site including vacuum-assisted and shoelace. Both techniques are acceptable methods for closure, but the vacuum-assisted technique has led to longer hospitalization time. A skin graft may be required to close the wound, which would complicate the treatment with a much longer hospitalization stay.

Chronic
Treatment for chronic exertional compartment syndrome can include decreasing or subsiding exercise and/or exacerbating activities, massage, non-steroidal anti-inflammatory medication, and physiotherapy. Chronic compartment syndrome in the lower leg can be treated conservatively or surgically. Conservative treatment includes rest, anti-inflammatory medications, and manual decompression. Warming the affected area with a heating pad may help to loosen the fascia prior to exercise. Icing the area may result in further constriction of the fascia and is not recommended before exercise. The use of devices that apply external pressure to the area, such as splints, casts, and tight wound dressings, should be avoided. If symptoms persist after conservative treatment or if an individual does not wish to give up the physical activities which bring on symptoms, compartment syndrome can be treated by a surgery known as a fasciotomy.
A US military study conducted in 2012 found that teaching individuals with lower leg chronic exertional compartment syndrome to change their running style to a forefoot running technique abated symptoms in those with symptoms limited to the anterior compartment. Running with a forefoot strike limits use of the tibialis anterior muscle which may explain the relief in symptoms in those with anterior compartment syndrome.
Hyperbaric oxygen therapy has been suggested by case reports – though as of 2011 not proven in randomized control trials – to be an effective adjunctive therapy for crush injury, compartment syndrome, and other acute traumatic ischemias, by improving wound healing and reducing the need for repetitive surgery.

Prognosis
A mortality rate of 47% has been reported for acute compartment syndrome of the thigh. According to one study the rate of fasciotomy for acute compartment syndrome varied from 2% to 24%. This is due to uncertainty and differences in labeling a condition as acute compartment syndrome. The most significant prognostic factor in people with acute compartment syndrome is time to diagnosis and subsequent fasciotomy. In people with a missed or late diagnosis of acute compartment syndrome, limb amputation may be necessary for survival. Following a fasciotomy, some symptoms may be permanent depending on factors such as which compartment, time until fasciotomy, and muscle necrosis </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 Secondary hyperparathyroidism and can you explain it in depth? [/INST] Secondary hyperparathyroidism  is the medical condition of excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels), with resultant hyperplasia of these glands. This disorder is primarily seen in patients with chronic kidney failure. It is sometimes abbreviated "SHPT" in medical literature.

Signs and symptoms
Bone and joint pain are common, as are limb deformities. The elevated PTH has also pleiotropic effects on the blood, immune system, and neurological system.

Cause
Chronic kidney failure is the most common cause of secondary hyperparathyroidism. Failing kidneys do not convert enough vitamin D to its active form, and they do not adequately excrete phosphate. When this happens, insoluble calcium phosphate forms in the body and removes calcium from the circulation. Both processes lead to hypocalcemia and hence secondary hyperparathyroidism </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 Filariasis and can you explain it in depth? [/INST] Filariasis is a parasitic disease caused by an infection with roundworms of the Filarioidea type. These are spread by blood-feeding insects such as black flies and mosquitoes. They belong to the group of diseases called helminthiases.
These parasites exist in the wild in subtropical parts of southern Asia, Africa, the South Pacific, and parts of South America. One does not acquire them in temperate areas like Europe or the United States.Eight known filarial worms have humans as a definitive host. These are divided into three groups according to the part of the body they affect:

Lymphatic filariasis is caused by the worms Wuchereria bancrofti, Brugia malayi, and Brugia timori. These worms occupy the lymphatic system, including the lymph nodes; in chronic cases, these worms lead to the syndrome of elephantiasis.
Subcutaneous filariasis is caused by Loa loa (the eye worm), Mansonella streptocerca, and Onchocerca volvulus. These worms occupy the layer just under the skin. L. loa causes Loa loa filariasis, while O. volvulus causes river blindness.
Serous cavity filariasis is caused by the worms Mansonella perstans and Mansonella ozzardi, which occupy the serous cavity of the abdomen. Dirofilaria immitis, the dog heartworm, rarely infects humans.The adult worms, which usually stay in one tissue, release early larval forms known as microfilariae into the persons blood. These circulating microfilariae can be taken up during a blood meal by an insect vector; in the vector, they develop into infective larvae that can be spread to another person.
Individuals infected by filarial worms may be described as either "microfilaraemic" or "amicrofilaraemic", depending on whether microfilariae can be found in their peripheral blood. Filariasis is diagnosed in microfilaraemic cases primarily through direct observation of microfilariae in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic cases based on clinical observations and, in some cases, by finding a circulating antigen in the blood.

Signs and symptoms
The most spectacular symptom of lymphatic filariasis is elephantiasis – edema with thickening of the skin and underlying tissues—which was the first disease discovered to be transmitted by mosquito bites. Elephantiasis results when the parasites lodge in the lymphatic system.Elephantiasis affects mainly the lower extremities, while the ears, mucous membranes, and amputation stumps are affected less frequently. However, different species of filarial worms tend to affect different parts of the body; Wuchereria bancrofti can affect the legs, arms, vulva, breasts, and scrotum (causing hydrocele formation), while Brugia timori rarely affects the genitals. Those who develop the chronic stages of elephantiasis are usually free from microfilariae (amicrofilaraemic), and often have adverse immunological reactions to the microfilariae, as well as the adult worms.The subcutaneous worms present with rashes, urticarial papules, and arthritis, as well as hyper- and hypopigmentation macules. Onchocerca volvulus manifests itself in the eyes, causing "river blindness" (onchocerciasis), one of the leading causes of blindness in the world. Serous cavity filariasis presents with symptoms similar to subcutaneous filariasis, in addition to abdominal pain, because these worms are also deep-tissue dwellers.

Cause
Human filarial nematode worms have complicated life cycles, which primarily consists of five stages. After the male and female worms mate, the female gives birth to live microfilariae by the thousands. The microfilariae are taken up by the vector insect (intermediate host) during a blood meal. In the intermediate host, the microfilariae molt and develop into third-stage (infective) larvae. Upon taking another blood meal, the vector insect, such as Culex pipiens, injects the infectious larvae into the dermis layer of the skin. After about one year, the larvae molt through two more stages, maturing into the adult worms.

Diagnosis
Filariasis is usually diagnosed by identifying microfilariae on Giemsa stained, thin and thick blood film smears, using the "gold standard" known as the finger prick test. The finger prick test draws blood from the capillaries of the finger tip; larger veins can be used for blood extraction, but strict windows of the time of day must be observed. Blood must be drawn at appropriate times, which reflect the feeding activities of the vector insects. Examples are W. bancrofti, whose vector is a mosquito; night is the preferred time for blood collection. Loa loas vector is the deer fly; daytime collection is preferred. This method of diagnosis is only relevant to microfilariae that use the blood as transport from the lungs to the skin. Some filarial worms, such as M. streptocerca and O. volvulus, produce microfilariae that do not use the blood; they reside in the skin only. For these worms, diagnosis relies upon skin snips and can be carried out at any time.

Concentration methods
Various concentration methods are applied: membrane filter, Knotts concentration method, and sedimentation technique.Polymerase chain reaction (PCR) and antigenic assays, which detect circulating filarial antigens, are also available for making the diagnosis. The latter are particularly useful in amicrofilaraemic cases. Spot tests for antigen are far more sensitive, and allow the test to be done anytime, rather in the late hours.
Lymph node aspirate and chylous fluid may also yield microfilariae.  Medical imaging, such as CT or MRI, may reveal "filarial dance sign" in the chylous fluid; X-ray tests can show calcified adult worms in lymphatics. The DEC provocation test is performed to obtain satisfying numbers of parasites in daytime samples. Xenodiagnosis is now obsolete, and eosinophilia is a nonspecific primary sign.

Treatment
The recommended treatment for people outside the United States is albendazole combined with ivermectin. A combination of diethylcarbamazine and albendazole is also effective. Side effects of the drugs include nausea, vomiting, and headaches. All of these treatments are microfilaricides; they have no effect on the adult worms. While the drugs are critical for treatment of the individual, proper hygiene is also required. There is good evidence that albendazole alone; or addition of albendazole to diethylcarbamazine or ivermectin, makes minimal difference in clearing microfilaria or adult worms from blood circulation. Diethylcarbamazine-medicated salt is effective in controlling lymphatic filariasis while maintaining its coverage at 90% in the community for six months.Different trials were made to use the known drug at its maximum capacity in absence of new drugs. In a study from India, it was shown that a formulation of albendazole had better anti-filarial efficacy than albendazole itself.In 2003, the common antibiotic doxycycline was suggested for treating elephantiasis. Filarial parasites have symbiotic bacteria in the genus Wolbachia, which live inside the worm and seem to play a major role in both its reproduction and the development of the disease. This drug has shown signs of inhibiting the reproduction of the bacteria, further inducing sterility.
Clinical trials in June 2005 by the Liverpool School of Tropical Medicine reported an eight-week course almost eliminated microfilaraemia.

Society and culture
Research teams
In 2015 William C. Campbell and Satoshi Ōmura were co-awarded half of that years Nobel prize in Physiology or Medicine for the discovery of the drug avermectin, which, in the further developed form ivermectin, has decreased the occurrence of lymphatic filariasis.

Prospects for elimination
Filarial diseases in humans offer prospects for elimination by means of vermicidal treatment. If the human link in the chain of infection can be broken, then notionally the disease could be wiped out in a season </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 Papulosquamous disorder 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 Brain ischemia and can you explain it in depth? [/INST] Brain ischemia is a condition in which there is insufficient bloodflow to the brain to meet metabolic demand.  This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ischemic stroke.  It is a sub-type of stroke along with subarachnoid hemorrhage and  intracerebral hemorrhage.Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis.There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue.
The main symptoms of brain ischemia involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage.
An interruption of blood flow to the brain for more than 10 seconds causes unconsciousness, and an interruption in flow for more than a few minutes generally results in irreversible brain damage.  In 1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to an hour can be at least partially recovered. Accordingly, this discovery raised the possibility of intervening after brain ischemia before the damage becomes irreversible.

Symptoms and signs
The symptoms of brain ischemia reflect the anatomical region undergoing blood and oxygen deprivation. Ischemia within the arteries branching from the internal carotid artery may result in symptoms such as blindness in one eye, weakness in one arm or leg, or weakness in one entire side of the body. Ischemia within the arteries branching from the vertebral arteries in the back of the brain may result in symptoms such as dizziness, vertigo, double vision, or weakness on both sides of the body. Other symptoms include difficulty speaking, slurred speech, and the loss of coordination.  The symptoms of brain ischemia range from mild to severe.  Further, symptoms can last from a few seconds to a few minutes or extended periods of time.  If the brain becomes damaged irreversibly and infarction occurs, the symptoms may be permanent.Similar to cerebral hypoxia, severe or prolonged brain ischemia will result in unconsciousness, brain damage or death,  mediated by the ischemic cascade.Multiple cerebral ischemic events may lead to subcortical ischemic depression, also known as vascular depression. This condition is most commonly seen in elderly depressed patients. Late onset depression is increasingly seen as a distinct sub-type of depression, and can be detected with an MRI.

Causes
Brain ischemia has been linked to a variety of diseases or abnormalities.  Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison to the average population. Sickle cell anemia may cause brain ischemia associated with the irregularly shaped blood cells. Sickle shaped blood cells clot more easily than normal blood cells, impeding blood flow to the brain.Compression of blood vessels may also lead to brain ischemia, by blocking the arteries that carry oxygen to the brain. Tumors are one cause of blood vessel compression.Ventricular tachycardia represents a series of irregular heartbeats that may cause the heart to completely shut down resulting in cessation of oxygen flow. Further, irregular heartbeats may result in formation of blood clots, thus leading to oxygen deprivation to all organs.Blockage of arteries due to plaque buildup may also result in ischemia.  Even a small amount of plaque build up can result in the narrowing of passageways, causing that area to become more prone to blood clots. Large blood clots can also cause ischemia by blocking blood flow.A heart attack can also cause brain ischemia due to the correlation that exists between heart attack and low blood pressure. Extremely low blood pressure usually represents the inadequate oxygenation of tissues. Untreated heart attacks may slow blood flow enough that blood may start to clot and prevent the flow of blood to the brain or other major organs. Extremely low blood pressure can also result from drug overdose and reactions to drugs. Therefore, brain ischemia can result from events other than heart attacks.Congenital heart defects may also cause brain ischemia due to the lack of appropriate artery formation and connection. People with congenital heart defects may also be prone to blood clots.Other pathological events that may result in brain ischemia include cardiorespiratory arrest, stroke, and severe irreversible brain damage.Recently, Moyamoya disease has also been identified as a potential cause for brain ischemia.  Moyamoya disease is an extremely rare cerebrovascular condition that limits blood circulation to the brain, consequently leading to oxygen deprivation.

Pathophysiology
During brain ischemia, the brain cannot perform aerobic metabolism due to the loss of oxygen and substrate. The brain is not able to switch to anaerobic metabolism and, because it does not have any long term energy stored, the levels of adenosine triphosphate (ATP) drop rapidly, approaching zero within 4 minutes. In the absence of biochemical energy, cells begin to lose the ability to maintain electrochemical gradients. Consequently, there is a massive influx of calcium into the cytosol, a massive release of glutamate from synaptic vesicles, lipolysis, calpain activation, and the arrest of protein synthesis. Additionally, removal of metabolic wastes is slowed.  The interruption of blood flow to the brain for ten seconds results in the immediate loss of consciousness.  The interruption of blood flow for twenty seconds results in the stopping of electrical activity. An area called a penumbra may result, wherein neurons do not receive enough blood to communicate, however do receive sufficient oxygenation to avoid cell death for a short period of time.

Diagnosis
Classification
The broad term, "stroke" can be divided into three categories: brain ischemia, subarachnoid hemorrhage and  intracerebral hemorrhage.  Brain ischemia can be further subdivided, by cause, into thrombotic, embolic, and hypoperfusion.  Thrombotic and embolic are generally focal or multifocal in nature while hypoperfusion affects the brain globally.

Focal brain ischemia
Focal brain ischemia occurs when a blood clot has occluded a cerebral vessel.  Focal brain ischemia reduces blood flow to a specific brain region, increasing the risk of cell death to that particular area.  It can be either caused by thrombosis or embolism.

Global brain ischemia
Global brain ischemia occurs when blood flow to the brain is halted or drastically reduced. This is commonly caused by cardiac arrest. If sufficient circulation is restored within a short period of time, symptoms may be transient. However, if a significant amount of time passes before restoration, brain damage may be permanent.  While reperfusion may be essential to protecting as much brain tissue as possible, it may also lead to reperfusion injury. Reperfusion injury is classified as the damage that ensues after restoration of blood supply to ischemic tissue.Due to different susceptibility to ischemia of various brain regions, a global brain ischemia may cause focal brain infarction. The cerebral cortex and striatum are more susceptible than the thalamus, and the thalamus in turn is more sensitive than the brainstem. Partial cerebral cortex infarction from global brain ischemia typically manifests as watershed stroke.

Biomarker
Use of biomarker is one method that has been evaluated to predict the risk of stroke, diagnose stroke and its causes, predict stroke severity and outcome, and guide prevention therapy.
Blood Biomarkers: Many proteins and RNA biomarkers identified are connected to ischemic stroke pathophysiology includes
Central Nervous System Tissue Injury Biomarkers- S100B, Glial fibrillary acidic protein, enolase 2,Anti-NMDA receptor encephalitis.
Inflammatory Biomarkers - c-reactive protein, Interleukin 6, Tumor necrosis factor α,VCAM-1.
Coagulation / Thrombosis Biomarkers - Fibrinogen, D-dimer,Von Willebrand factor
Other Biomarkers- PARK7, B-type neurotrophic growth factor.

Treatment
Alteplase (t-PA) is an effective medication for acute ischemic stroke.  When given within 3 hours, treatment with tpa significantly improves the probability of a favourable outcome versus treatment with placebo.The outcome of brain ischemia is influenced by the quality of subsequent supportive care.  Systemic blood pressure (or slightly above) should be maintained so that cerebral blood flow is restored.  Also, hypoxaemia and hypercapnia should be avoided.  Seizures can induce more damage; accordingly, anticonvulsants should be prescribed and should a seizure occur, aggressive treatment should be undertaken.  Hyperglycaemia should also be avoided during brain ischemia.

Management
When someone presents with an ischemic event, treatment of the underlying cause is critical for prevention of further episodes.Anticoagulation with warfarin or heparin may be used if the patient has atrial fibrillation.Operative procedures such as carotid endarterectomy and carotid stenting may be performed if the patient has a significant amount of plaque in the carotid arteries associated with the local ischemic events.

Research
Therapeutic hypothermia has been attempted to improve results post brain ischemia.  This procedure was suggested to be beneficial based on its effects post cardiac arrest.  Evidence supporting the use of therapeutic hypothermia after brain ischemia, however, is limited.A closely related disease to brain ischemia is brain hypoxia.  Brain hypoxia is the condition in which there is a decrease in the oxygen supply to the brain even in the presence of adequate blood flow.  If hypoxia lasts for long periods of time, coma, seizures, and even brain death may occur.  Symptoms of brain hypoxia are similar to ischemia and include inattentiveness, poor judgment, memory loss, and a decrease in motor coordination </s>