<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 Lactic acidosis and can you explain it in depth? [/INST] Lactic acidosis is a medical condition characterized by a build-up of lactate (especially L-lactate) in the body, with formation of an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the bodys oxidative metabolism.
Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, Kussmaul breathing (laboured and deep), and generalised weakness.
The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death.

Classification
The Cohen–Woods classification categorizes causes of lactic acidosis as:
Type A: Decreased tissue oxygenation (e.g., from decreased blood flow)
Type B
B1: Underlying diseases (sometimes causing type A)
B2: Medication or intoxication
B3: Inborn error of metabolism

Signs and symptoms
Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids. Symptoms in humans include all those of typical metabolic acidosis (nausea, vomiting, generalized muscle weakness, and laboured and deep breathing).

Causes
The several different causes of lactic acidosis include:
Genetic conditions
Biotinidase deficiency, multiple carboxylase deficiency, or nongenetic deficiencies of biotin
Diabetes mellitus and deafness
Fructose 1,6-bisphosphatase deficiency
Glucose-6-phosphatase deficiency
GRACILE syndrome
Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes
Pyruvate dehydrogenase deficiency
Pyruvate carboxylase deficiency
Leigh syndrome
Drugs
Linezolid
Paracetamol/acetaminophen poisoning
Metformin: this risk is low (less than 10 cases for 100,000 patient years), but the risk of metformin-induced lactic acidosis (MALA) increases in certain situations where both the plasma levels of metformin are increased and lactate clearance is impaired. The older related and now withdrawn drug phenformin carried a much higher risk of lactic acidosis.
Isoniazid toxicity
Propofol
Epinephrine
Propylene glycol (D-lactic acidosis)
Nucleoside reverse-transcriptase inhibitors
Abacavir/dolutegravir/lamivudine
Emtricitabine/tenofovir
Potassium cyanide (cyanide poisoning)
Fialuridine
Other
Thiamine deficiency (especially during TPN)
Impaired delivery of oxygen to cells in the tissues (e.g., from impaired blood flow (hypoperfusion))
Bleeding
Polymyositis
Ethanol toxicity
Sepsis
Shock
Advanced liver disease
Diabetic ketoacidosis
Excessive exercise (overtraining)
Regional hypoperfusion (e.g., bowel ischemia or marked cellulitis)
Cancers such as Non-Hodgkins and Burkitt lymphomas
Pheochromocytoma
Tumor lysis syndrome
D-lactic acidosis due to intestinal bacterial flora production in short gut syndrome

Pathophysiology
Glucose metabolism begins with glycolysis, in which the molecule is broken down into pyruvate in ten enzymatic steps. A significant proportion of pyruvate is converted into lactate (usually 10:1). The human metabolism produces about 20 mmol/kg of lactic acid every 24 hours. This happens predominantly in tissues (especially muscle) that have high levels of the "A" isoform of the enzyme lactate dehydrogenase (LDHA), which predominantly converts pyruvate into lactate. The lactate is carried by the bloodstream to other tissues where it is converted at the expense of ATP back to pyruvate by the "B" isoform of LDH (LDHB). Firstly there is gluconeogenesis in the liver (as well as the kidney and some other tissues), where pyruvate is converted into glucose; this is known as the Cori cycle. In addition, lactate moved to other tissues enters the citric acid cycle and eventually oxidative phosphorylation, a process that yields ATP.Elevations in lactate are either a consequence of increased production or of decreased metabolism. With regards to metabolism, this predominantly takes place in the liver (70%), which explains that lactate levels may be elevated in the setting of liver disease.In "type A" lactic acidosis, the production of lactate is attributable to insufficient oxygen for aerobic metabolism. If there is no oxygen available for the parts of the glucose metabolism that require oxygen (citric acid cycle and oxidative phosphorylation), excess pyruvate will be converted in excess lactate. In "type B" lactic acidosis the lactate accumulates because there is a mismatch between glycolysis activity and the remainder of glucose metabolism. Examples are situations where the sympathetic nervous system is highly active (e.g. severe asthma). There is controversy as to whether elevated lactate in acute illness can be attributed to tissue hypoxia; there is limited empirical support for this theoretical notion.

Diagnosis
Acid-base disturbances such as lactic acidosis are typically first assessed using arterial blood gas tests. Testing of venous blood is also available as an alternative as they are effectively interchangeable. Normally resulting lactate concentrations are in the range indicated below:
Lactic acidosis is classically defined as an elevated lactate together with pH < 7.35 and bicarbonate below 20 mmol/L, but this is not required as lactic acidosis may exist together with other acid-base abnormalities that may affect these two parameters.

Treatment
If elevated lactate is present in acute illness, supporting the oxygen supply and blood flow are key initial steps. Some vasopressors (drugs that augment the blood pressure) are less effective when lactate levels are high, and some agents that stimulate the beta-2 adrenergic receptor can elevate the lactate further.Direct removal of lactate from the body (e.g. with hemofiltration or dialysis) is difficult, with limited evidence for benefit; it may not be possible to keep up with the lactate production.Limited evidence supports the use of sodium bicarbonate solutions to improve the pH (which is associated with increased carbon dioxide generation and may reduce the calcium levels).Lactic acidosis caused by inherited mitochondrial disorders (type B3) may be treated with a ketogenic diet and possibly with dichloroacetate (DCA), although this may be complicated by peripheral neuropathy and has a weak evidence base.

Prognosis
Mild and transient elevations in lactate have limited impact on mortality, whereas sustained and severe lactate elevations are associated with a high mortality.The mortality of lactic acidosis in people taking metformin was previously reported to be 50%, but in more recent reports this was closer to 25%.

Other animals
Reptiles
Reptiles, which rely primarily on anaerobic energy metabolism (glycolysis) for intense movements, can be particularly susceptible to lactic acidosis.  In particular, during the capture of large crocodiles, the animals use of their glycolytic muscles often alter the bloods pH to a point where they are unable to respond to stimuli or move.  Cases are recorded in which particularly large crocodiles which put up extreme resistance to capture later died of the resulting pH imbalance.Certain turtle species have been found to be capable of tolerating high levels of lactic acid without experiencing the effects of lactic acidosis. Painted turtles hibernate buried in mud or underwater and do not resurface for the entire winter. As a result, they rely on anaerobic respiration to provide the majority of their energy needs. Adaptations in particular in the turtles blood composition and shell allow it to tolerate high levels of lactic acid accumulation. In the anoxic conditions where anaerobic respiration is dominant, calcium levels in the blood plasma increase. This calcium serves as a buffer, reacting with the excess lactate to form the precipitate calcium lactate. This precipitate is suggested to be reabsorbed by the shell and skeleton, thereby removing it from the bloodstream; studies examining turtles that have been subjected to prolonged anoxic conditions have up to 45% of their lactate stored within their skeletal structure.

Ruminants
In ruminant livestock, the cause of clinically serious lactic acidosis is different from the causes described above.
In domesticated ruminants, lactic acidosis may occur as a consequence of ingesting large amounts of grain, especially when the rumen population is poorly adapted to deal with grain.  Activity of various rumen organisms results in accumulation of various volatile fatty acids (normally, mostly acetic, propionic, and butyric acids), which are partially dissociated.  Although some lactate is normally produced in the rumen, it is normally metabolized by such organisms as Megasphaera elsdenii and, to a lesser extent, Selenomonas ruminantium and some other organisms.  With high grain consumption, the concentration of dissociated organic acids can become quite high, resulting in rumen pH dropping below 6 </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 Pulmonary hemorrhage and can you explain it in depth? [/INST] Pulmonary hemorrhage (or pulmonary haemorrhage) is an acute bleeding from the lung, from the upper respiratory tract and the trachea, and the pulmonary alveoli. When evident clinically, the condition is usually massive. The onset of pulmonary hemorrhage is characterized by a cough productive of blood (hemoptysis) and worsening of oxygenation leading to cyanosis </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 Circulatory collapse and can you explain it in depth? [/INST] A circulatory collapse is defined as a general or specific failure of the circulation, either cardiac or peripheral in nature.  Although the mechanisms, causes and clinical syndromes are different, the pathogenesis is the same—the circulatory system fails to maintain the supply of oxygen and other nutrients to the tissues and to remove the carbon dioxide and other metabolites from them. The failure may be hypovolemic or distributive.
A common cause of this could be shock or trauma from injury or surgery.

Types
A general failure is one that occurs across a wide range of locations in the body, such as systemic shock after the loss of a large amount of blood collapsing all the circulatory systems in the legs. A specific failure can be traced to a particular point, such as a clot.
Cardiac circulatory collapse affects the vessels of the heart such as the aorta and is almost always fatal </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 Dysthymia and can you explain it in depth? [/INST] Dysthymia ( dihs-THIY-mee-uh), also known as persistent depressive disorder (PDD), is a mental and behavioral disorder, specifically a disorder primarily of mood, consisting of similar cognitive and physical problems as major depressive disorder, but with longer-lasting symptoms. The concept was used by Robert Spitzer as a replacement for the term "depressive personality" in the late 1970s.In the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), dysthymia is a serious state of chronic depression, which persists for at least two years (one year for children and adolescents). Dysthymia is not a minor form of major depressive disorder, and for some may be more disabling.As dysthymia is a chronic disorder, those with the condition may experience symptoms for many years before it is diagnosed, if diagnosis occurs at all. As a result, they may believe that depression is a part of their character, so they may not even discuss their symptoms with doctors, family members or friends. In the DSM-5, dysthymia is replaced by persistent depressive disorder. This new condition includes both chronic major depressive disorder and the previous dysthymic disorder. The reason for this change is that there was no evidence for meaningful differences between these two conditions.

Signs and symptoms
Dysthymia characteristics include an extended period of depressed mood combined with at least two other symptoms which may include insomnia or hypersomnia, fatigue or low energy, eating changes (more or less), low self-esteem, or feelings of hopelessness. Poor concentration or difficulty making decisions are treated as another possible symptom. Irritability is one of the more common symptoms in children and adolescents.Mild degrees of dysthymia may result in people withdrawing from stress and avoiding opportunities for failure. In more severe cases of dysthymia, people may withdraw from daily activities. They will usually find little pleasure in usual activities and pastimes.
Diagnosis of dysthymia can be difficult because of the subtle nature of the symptoms and patients can often hide them in social situations, making it challenging for others to detect symptoms. Additionally, dysthymia often occurs at the same time as other psychological disorders, which adds a level of complexity in determining the presence of dysthymia, particularly because there is often an overlap in the symptoms of disorders.There is a high incidence of comorbid illness in those with dysthymia. Suicidal behavior is also a particular problem with those with dysthymia. It is vital to look for signs of major depression, panic disorder, generalised anxiety disorder, alcohol and substance use disorders, and personality disorder.

Causes
There are no known biological causes that apply consistently to all cases of dysthymia, which suggests diverse origin of the disorder. However, there are some indications that there is a genetic predisposition to dysthymia: "The rate of depression in the families of people with dysthymia is as high as fifty percent for the early-onset form of the disorder". Other factors linked with dysthymia include stress, social isolation, and lack of social support.In a study using identical and fraternal twins, results indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is in part caused by heredity means.

Co-occurring conditions
Dysthymia often co-occurs with other mental disorders. A "double depression" is the occurrence of episodes of major depression in addition to dysthymia. Switching between periods of dysthymic moods and periods of hypomanic moods is indicative of cyclothymia, which is a mild variant of bipolar disorder.
"At least three-quarters of patients with dysthymia also have a chronic physical illness or another psychiatric disorder such as one of the anxiety disorders, cyclothymia, drug addiction, or alcoholism". Common co-occurring conditions include major depression (up to 75%), anxiety disorders (up to 50%), personality disorders (up to 40%), somatoform disorders (up to 45%) and substance use disorders (up to 50%). People with dysthymia have a higher-than-average chance of developing major depression. A 10-year follow-up study found that 95% of dysthymia patients had an episode of major depression. When an intense episode of depression occurs on top of dysthymia, the state is called "double depression."

Double depression
Double depression occurs when a person experiences a major depressive episode on top of the already-existing condition of dysthymia. It is difficult to treat, as patients accept these major depressive symptoms as a natural part of their personality or as a part of their life that is outside of their control. The fact that people with dysthymia may accept these worsening symptoms as inevitable can delay treatment. When and if such people seek out treatment, the treatment may not be very effective if only the symptoms of the major depression are addressed, but not the dysthymic symptoms. Patients with double depression tend to report significantly higher levels of hopelessness than is normal. This can be a useful symptom for mental health services providers to focus on when working with patients to treat the condition. Additionally, cognitive therapies can be effective for working with people with double depression in order to help change negative thinking patterns and give individuals a new way of seeing themselves and their environment.It has been suggested that the best way to prevent double depression is by treating the dysthymia. A combination of antidepressants and cognitive therapies can be helpful in preventing major depressive symptoms from occurring. Additionally, exercise and good sleep hygiene (e.g., improving sleep patterns) are thought to have an additive effect on treating dysthymic symptoms and preventing them from worsening.

Pathophysiology
There is evidence that there may be neurological indicators of early onset dysthymia. There are several brain structures (corpus callosum and frontal lobe) that are different in women with dysthymia than in those without dysthymia. This may indicate that there is a developmental difference between these two groups.Another study, which used fMRI techniques to assess the differences between individuals with dysthymia and other people, found additional support for neurological indicators of the disorder. This study found several areas of the brain that function differently. The amygdala (associated with processing emotions such as fear) was more activated in dysthymia patients. The study also observed increased activity in the insula (which is associated with sad emotions). Finally, there was increased activity in the cingulate gyrus (which serves as the bridge between attention and emotion).A study comparing healthy individuals to people with dysthymia indicates there are other biological indicators of the disorder. An anticipated result appeared as healthy individuals expected fewer negative adjectives to apply to them, whereas people with dysthymia expected fewer positive adjectives to apply to them in the future. Biologically these groups are also differentiated in that healthy individuals showed greater neurological anticipation for all types of events (positive, neutral, or negative) than those with dysthymia. This provides neurological evidence of the dulling of emotion that individuals with dysthymia have learned to use to protect themselves from overly strong negative feelings, compared to healthy people.There is some evidence of a genetic basis for all types of depression, including dysthymia. A study using identical and fraternal twins indicated that there is a stronger likelihood of identical twins both having depression than fraternal twins. This provides support for the idea that dysthymia is caused in part by heredity.A new model has recently surfaced in the literature regarding the HPA axis (structures in the brain that get activated in response to stress) and its involvement with dysthymia (e.g. phenotypic variations of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP), and down-regulation of adrenal functioning) as well as forebrain serotonergic mechanisms. Since this model is highly provisional, further research is still needed.

Diagnosis
The Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV), published by the American Psychiatric Association, characterizes dysthymic disorder. The essential symptom involves the individual feeling depressed for the majority of days, and parts of the day, for at least two years. Low energy, disturbances in sleep or in appetite, and low self-esteem typically contribute to the clinical picture as well. Those with the condition have often experienced dysthymia for many years before it is diagnosed. People around them often describe them in words similar to "just a moody person". The following are the diagnostic criteria:
During a majority of days for two years or more, the adult patient reports depressed mood, or appears depressed to others for most of the day.
When depressed, the patient has two or more of:
decreased or increased appetite;
decreased or increased sleep (insomnia or hypersomnia);
fatigue or low energy;
reduced self-esteem;
decreased concentration or problems making decisions;
feelings of hopelessness or pessimism.
During this two-year period, the above symptoms are never absent longer than two consecutive months.
During the duration of the two-year period, the patient may have had a perpetual major depressive episode.
The patient has not had any manic, hypomanic, or mixed episodes.
The patient has never fulfilled criteria for cyclothymic disorder.
The depression does not exist only as part of a chronic psychosis (such as schizophrenia or delusional disorder).
The symptoms are often not directly caused by a medical illness or by substances, including substance use or other medications.
The symptoms may cause significant problems or distress in social, work, academic, or other major areas of life functioning.In children and adolescents, mood can be irritable, and duration must be at least one year, in contrast to two years needed for diagnosis in adults.
Early onset (diagnosis before age 21) is associated with more frequent relapses, psychiatric hospitalizations, and more co-occurring conditions. For younger adults with dysthymia, there is a higher co-occurrence in personality abnormalities and the symptoms are likely chronic. However, in older adults with dysthymia, the psychological symptoms are associated with medical conditions and/or stressful life events and losses.Dysthymia can be contrasted with major depressive disorder by assessing the acute nature of the symptoms. Dysthymia is far more chronic (long lasting) than major depressive disorder, in which symptoms may be present for as little as two weeks. Also dysthymia often presents itself at an earlier age than major depressive disorder.

Prevention
Though there is no clear-cut way to prevent dysthymia from occurring, some suggestions have been made. Since dysthymia will often first occur in childhood, it is important to identify children who may be at risk. It may be beneficial to work with children in helping to control their stress, increase resilience, boost self-esteem, and provide strong networks of social support. These tactics may be helpful in warding off or delaying dysthymic symptoms.

Treatments
Persistent depressive disorder can be treated with psychotherapy and pharmacotherapy. The overall rate and degree of treatment success is somewhat lower than for non-chronic depression, and a combination of psychotherapy and pharmacotherapy shows best results.

Therapy
Psychotherapy can be effective in treating dysthymia.
In a meta-analytic study from 2010, psychotherapy had a small but significant effect when compared to control groups. However, psychotherapy is significantly less effective than pharmacotherapy in direct comparisons.There are many different types of therapy, and some are more effective than others.

The empirically most studied type of treatment is cognitive-behavioral therapy. This type of therapy is very effective for non-chronic depression, and it appears to be also effective for chronic depression.
Cognitive behavioral analysis system of psychotherapy (CBASP) has been designed specifically to treat PDD. Empirical results on this form of therapy are inconclusive: While one study showed remarkably high treatment success rates, a later, even larger study showed no significant benefit of adding CBASP to treatment with antidepressants.
Schema therapy and psychodynamic psychotherapy have been used for PDD, though good empirical results are lacking.
Interpersonal psychotherapy has also been said to be effective in treating the disorder, though it only shows marginal benefit when added to treatment with antidepressants.

Medications
In a 2010 meta-analysis, the benefit of pharmacotherapy was limited to selective serotonin reuptake inhibitors (SSRIs) rather than tricyclic antidepressants (TCA).
According to a 2014 meta-analysis, antidepressants are at least as effective for persistent depressive disorder as for major depressive disorder.
The first line of pharmacotherapy is usually SSRIs due to their purported more tolerable nature and reduced side effects compared to the irreversible monoamine oxidase inhibitors or tricyclic antidepressants. Studies have found that the mean response to antidepressant medications for people with dysthymia is 55%, compared with a 31% response rate to a placebo. The most commonly prescribed antidepressants/SSRIs for dysthymia are escitalopram, citalopram, sertraline, fluoxetine, paroxetine, and fluvoxamine. It often takes an average of 6–8 weeks before the patient begins to feel these medications therapeutic effects. Additionally, STAR*D, a multi-clinic governmental study, found that people with overall depression will generally need to try different brands of medication before finding one that works specifically for them. Research shows that 1 in 4 of those who switch medications get better results regardless of whether the second medication is an SSRI or some other type of antidepressant.In a meta-analytic study from 2005, it was found that SSRIs and TCAs are equally effective in treating dysthymia. They also found that MAOIs have a slight advantage over the use of other medication in treating this disorder. However, the author of this study cautions that MAOIs should not necessarily be the first line of defense in the treatment of dysthymia, as they are often less tolerable than their counterparts, such as SSRIs.Tentative evidence supports the use of amisulpride to treat dysthymia but with increased side effects.

Combination treatment
When pharmacotherapy alone is compared with combined treatment with pharmacotherapy plus psychotherapy, there is a strong trend in favour of combined treatment. Working with a psychotherapist to address the causes and effects of the disorder, in addition to taking antidepressants to help eliminate the symptoms, can be extremely beneficial </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 Gastric outlet obstruction and can you explain it in depth? [/INST] Gastric outlet obstruction (GOO) is a medical condition where there is an obstruction at the level of the pylorus, which is the outlet of the stomach.  Individuals with gastric outlet obstruction will often have recurrent vomiting of food that has accumulated in the stomach, but which cannot pass into the small intestine due to the obstruction.  The stomach often dilates to accommodate food intake and secretions.  Causes of gastric outlet obstruction include both benign causes (such as peptic ulcer disease affecting the area around the pylorus), as well as malignant causes, such as gastric cancer.
Causation related to ulcers may involve severe pain which the patient may interpret as a heart condition/attack.Treatment of the condition depends upon the underlying cause; it can involve antibiotic treatment when Helicobacter pylori is related to an ulcer,  endoscopic therapies (such as dilation of the obstruction with balloons or the placement of self expandable metallic stents), other medical therapies, or surgery to resolve the obstruction.

Signs and symptoms
The main symptom is vomiting, which typically occurs after meals, of undigested food devoid of any bile </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 Anal fissure and can you explain it in depth? [/INST] An anal fissure is a break or tear in the skin of the anal canal. Anal fissures may be noticed by bright red anal bleeding on toilet paper and undergarments, or sometimes in the toilet. If acute they are painful after defecation, but with chronic fissures, pain intensity often reduces. Anal fissures usually extend from the anal opening and are usually located posteriorly in the midline, probably because of the relatively unsupported nature and poor perfusion of the anal wall in that location. Fissure depth may be superficial or sometimes down to the underlying sphincter muscle. Untreated fissures develop a hood-like skin tag (sentinel piles) which cover the fissure and cause discomfort and pain.

Causes
Most anal fissures are caused by stretching of the anal mucous membrane beyond its capability.Superficial or shallow anal fissures look much like a paper cut, and may be hard to detect upon visual inspection; they will generally self-heal within a couple of weeks. However, some anal fissures become chronic and deep and will not heal. The most common cause of non-healing is spasming of the internal anal sphincter muscle which results in impaired blood supply to the anal mucosa. The result is a non-healing ulcer, which may become infected by fecal bacteria.
In adults, fissures may be caused by constipation, the passing of large, hard stools, or by prolonged diarrhea. In older adults, anal fissures may be caused by decreased blood flow to the area. When fissures are found laterally, tuberculosis, occult abscesses, leukemic infiltrates, carcinoma, acquired immunodeficiency syndrome (AIDS) or inflammatory bowel disease should be considered as causes. Some sexually transmitted infections can promote the breakdown of tissue resulting in a fissure. Examples of sexually transmitted infections that may affect the anorectal area are syphilis, herpes, chlamydia and human papilloma virus.Other common causes of anal fissures include:

childbirth trauma in women
anal sex
Crohns disease
ulcerative colitis
poor toileting in young children.

Diagnosing
External anal fissures on the anal verge can be diagnosed by visual inspection.Internal anal fissures in adults on anterior side, posterior side or within any part of the inner circumference of the anal sphincter muscle can be diagnosed with beak proctoscope 23mm diameter, Chelsea Eaton anal speculum 23mm diameter, Park anal retractor or by digital rectal examination with a finger inside the anal sphincter muscle. Narrow anal fissures might not be felt by finger during rectal examination due to the glove.Note that colonoscopy, sigmoidoscopy, or normal proctoscopy is for diagnosing internal hemorrhoids and other internal rectal diseases and not for diagnosing anal fissures.

Prevention
For adults, the following may help prevent anal fissures:

Avoiding straining when defecating. This includes treating and preventing constipation by eating food rich in dietary fiber, drinking enough water, occasional use of a stool softener, and avoiding constipating agents. Similarly, prompt treatment of diarrhea may reduce anal strain.
Careful anal hygiene after defecation, including using soft toilet paper and cleaning with water, plus the use of sanitary wipes.
In cases of pre-existing or suspected fissure, use of a lubricating ointment (It is important to note that hemorrhoid ointment is contraindicated because it constricts small blood vessels, thus causes a decrease in blood flow, which prevents healing).In infants, frequent diaper change can prevent anal fissure. As constipation can be a cause, making sure the infant is drinking enough fluids (i.e. breastmilk, proper ratios when mixing formulas) is beneficial. In infants, once an anal fissure has occurred, addressing underlying causes is usually enough to ensure healing occurs.

Treatment
Non-surgical treatments are recommended initially for acute and chronic anal fissures. These include topical nitroglycerin or calcium channel blockers (e.g. diltiazem), or injection of botulinum toxin into the anal sphincter.Other measures include warm sitz baths, topical anesthetics, high-fiber diet and stool softeners.

Medication
Local application of medication to relax the sphincter muscle, thus allowing the healing to proceed, was first proposed in 1994 with nitroglycerine ointment,
and then calcium channel blockers in 1999 with nifedipine ointment,
and the following year with topical diltiazem.
Branded preparations are now available of topical nitroglycerine ointment (Rectogesic (Rectiv) as 0.2% in Australia and 0.4% in UK and US), topical nifedipine 0.3% with lidocaine 1.5% ointment (Antrolin in Italy since April 2004) and diltiazem 2% (Anoheal in UK, although still in Phase III development). A common side effect drawback of nitroglycerine ointment is headache, caused by systemic absorption of the drug, which limits patient acceptability.
A combined surgical and pharmacological treatment, administered by colorectal surgeons, is the direct injection of botulinum toxin (Botox) into the anal sphincter to relax it. This treatment was first investigated in 1993. However, in many cases involving Botox injections, the patients eventually had to choose another cure as the injections proved less and less potent, spending thousands of dollars in the meantime for a partial cure. Lateral sphincterotomy is the Gold Standard for curing this condition.
Combination of medical therapies may offer up to 98% cure rates.

Surgery
Surgical procedures are generally reserved for people with anal fissure who have tried medical therapy for at least one to three months and have not healed. It is not the first option in treatment.
The main concern with surgery is the development of anal incontinence. Anal incontinence can include the inability to control gas, mild fecal soiling, or loss of solid stool. Some degree of incontinence can occur in up to 45 percent of patients in the immediate surgical recovery period. However, incontinence is rarely permanent and is usually mild. The risk should be discussed with ones surgeon.
Surgical treatment, under general anaesthesia, was either anal stretch (Lords operation) or lateral sphincterotomy where the internal anal sphincter muscle is incised. Both operations aim to decrease sphincter spasming and thereby restore normal blood supply to the anal mucosa. Surgical operations involve a general or regional anaesthetia. Anal stretch is also associated with anal incontinence in a small proportion of cases and thus sphincterotomy is the operation of choice.

Lateral internal sphincterotomy
Lateral internal sphincterotomy (LIS) is the surgical procedure of choice for anal fissures due to its simplicity and its high success rate (~95%). In this procedure the internal anal sphincter is partially divided in order to reduce spasming and thus improve the blood supply to the perianal area. This improvement in the blood supply helps to heal the fissure, and the weakening of the sphincter is also believed to reduce the potential for recurrence. The procedure is generally performed as a day surgery after the patient is given general anesthesia. The pain from the sphincterotomy is usually mild and is often less than the pain of the fissure itself </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 Hypertrichosis and can you explain it in depth? [/INST] Hypertrichosis is an abnormal amount of hair growth over the body. The two distinct types of hypertrichosis are generalized hypertrichosis, which occurs over the entire body, and localized hypertrichosis, which is restricted to a certain area. Hypertrichosis can be either congenital (present at birth) or acquired later in life.  The excess growth of hair occurs in areas of the skin with the exception of androgen-dependent hair of the pubic area, face, and axillary regions.Several circus sideshow performers in the 19th and early 20th centuries, such as Julia Pastrana, had hypertrichosis. Many of them worked as freaks and were promoted as having distinct human and animal traits.

Classification
Two methods of classification are used for hypertrichosis.  One divides them into either generalized versus localized hypertrichosis, while the other divides them into congenital versus acquired.

Congenital
Congenital forms of hypertrichosis are caused by genetic mutations, and are extremely rare, unlike acquired forms. Congenital hypertrichosis is always present at birth.
Hypertrichosis lanuginosa
Congenital hypertrichosis lanuginosa can be noticed at birth, with the infant completely covered in thin lanugo hair. In normal circumstances, lanugo hair is shed before birth and replaced by vellus hair; however, in a person with congenital hypertrichosis lanuginosa, the lanugo hair remains after birth. The palms of the hands, soles of the feet, and mucous membranes are not affected. As the person ages, the lanugo hair may thin, leaving only limited areas of hypertrichosis.
Generalized hypertrichosis
Congenital generalized hypertrichosis causes males to exhibit excessive facial and upper body hair, whereas women exhibit less severe asymmetrical hair distribution. The palms, soles, and mucous membranes are not affected.
Terminal hypertrichosis
Congenital terminal hypertrichosis is characterized by the presence of fully pigmented terminal hair that covers the entire body. This condition is usually accompanied by gingival hyperplasia. This form is most responsible for the term "werewolf syndrome" because of the thick, dark hair that appears. People with this condition are sometimes performers at circuses because of their unusual appearance.
Circumscribed hypertrichosis
Congenital circumscribed hypertrichosis is associated with the presence of thick vellus hair on the upper extremities. Circumscribed signifies this type of hypertrichosis is restricted to certain parts of the body, in this case, the extensor surfaces of the upper extremities. Hairy elbow syndrome, a type of congenital circumscribed hypertrichosis, shows excessive growth on and around the elbows.  This type of hypertrichosis is present at birth, becomes more prominent during aging, and regresses at puberty.
Localized hypertrichosis
Congenital localized hypertrichosis is a localized increase in hair density and length.
Nevoid hypertrichosis
Nevoid hypertrichosis may be present at birth or appear later in life. It features an isolated area of excessive terminal hair and is usually not related to any other diseases.

Acquired
Acquired hypertrichosis appears after birth. The multiple causes include the side effects of drugs, associations with cancer, and possible links with eating disorders. Acquired forms can usually be reduced with various treatments.

Hypertrichosis lanuginosa
Acquired hypertrichosis lanuginosa is characterized by rapid growth of lanugo hair, particularly on the face. Hair also appears on the trunk and armpits, while palms and soles are unaffected. The excess hair is commonly referred to as malignant down. This hair is very fine and unpigmented.
Generalized hypertrichosis
Acquired generalized hypertrichosis commonly affects the cheeks, upper lip, and chin.  This form also affects the forearms and legs, but is less common in these areas. Another deformity associated with acquired generalized hypertrichosis is multiple hairs occupying the same follicle. It may also include abnormal hair growth patterns as what happens to the eyelashes in a condition known as trichiasis. Oral minoxidil treatments for hypertension are known to cause this condition. Topical minoxidil used for alopecia causes hair growth in the areas where it is applied; however, this hair disappears shortly after discontinuing the use of topical minoxidil.
Patterned hypertrichosis
Acquired patterned hypertrichosis is an increase in hair growth in a pattern formation. It is similar to acquired generalized hypertrichosis and is a sign of internal malignancy.
Localized hypertrichosis
Acquired localized hypertrichosis is an increase in hair density and length often secondary to irritation or trauma. This form is restricted to certain areas of the body.

Hirsutism
Hypertrichosis is often mistakenly classified as hirsutism. Hirsutism is a type of hypertrichosis exclusive to women and children, resulting from an excess of androgen-sensitive hair growth. Patients with hirsutism exhibit patterns of adult male hair growth. Chest and back hair are often present on women with hirsutism.Hirsutism is both congenital and acquired. It is linked to excessive male hormones in women, thus symptoms may include acne, deepening of the voice, irregular menstrual periods, and the formation of a more masculine body shape. Increases in androgen (male hormone) levels are the primary cause of most hirsutism cases. If caused by increased levels of androgens, it can be treated with medications that reduce androgen levels. Some birth control pills and spironolactone reduce androgen levels.

Signs and symptoms
The primary characteristic of all forms of hypertrichosis is excessive hair. Hair in hypertrichosis is usually longer than expected and may consist of any hair type (lanugo, vellus, or terminal). Patterned forms of hypertrichosis cause hair growth in patterns. Generalized forms of hypertrichosis result in hair growth over the entire body. Circumscribed and localized forms lead to hair growth restricted to a certain area.

Cause
Genetic
Hypertrichosis lanuginosa
Congenital hypertrichosis lanuginosa may be caused by a paracentric inversion mutation of the q22 band of chromosome 8; however, it could also possibly be the result of a spontaneous genetic mutation rather than inheritance. This form is an autosomal (not located on the sex chromosomes) dominant cutaneous disorder, that affects the skin.
Generalized hypertrichosis
Congenital generalized hypertrichosis has a dominant pattern of inheritance and has been linked to chromosome Xq24-27.1. An affected female (carrying the hypertrichosis gene) has a 50% chance of passing it to her offspring. An affected male will pass this form of hypertrichosis to his daughters, but never the sons.
Generalized hypertrichosis terminalis
Congenital generalized hypertrichosis terminalis is thought to be caused by genetic changes on chromosome 17 resulting in the addition or removal of millions of nucleotides. The gene MAP2K6 may be a factor contributing to this condition. This condition may also be due to the change in the chromosome affecting the transcription of genes.
Other hypertrichosis patterns
Porphyria cutanea tarda may manifest in some patients as hypertrichosis on the face (mainly on top of the cheeks).

Medical conditions
Acquired hypertrichosis lanuginosa is commonly present with cancer. This condition is also linked to metabolic disorders, such as anorexia, hormone imbalances, such as hyperthyroidism, or as a side effect of certain drugs.Acquired generalized hypertrichosis may be caused by cancer. The resulting hair growth is known as malignant down. The mechanism behind cancer induced hypertrichosis is unknown. Oral and topical minoxidil treatments are also known to cause acquired generalized hypertrichosis.

Medications
Several medications can cause generalized or localized acquired hypertrichosis including:

Anticonvulsants: phenytoin
Immunosuppressants: cyclosporine
Vasodilators: diazoxide and minoxidil
Antibiotics: streptomycin
Diuretics: acetazolamide
Photosensitizers: PsoralenThe acquired hypertrichosis is usually reversible once these medications are discontinued.

Other
Unknown causes
The exact genetic mutation that causes congenital circumscribed, localized, and nevoid hypertrichosis is unknown.

Pathophysiology
A number of mechanisms can lead to hypertrichosis.  One cause involves areas of the skin that are transforming from the small vellus type to the larger terminal type. This change normally occurs during adolescence, when vellus hair follicles in the underarms and groin grow into terminal hair follicles. Hypertrichosis involves this same type of switching, but in areas that do not normally produce terminal hair. The mechanisms for this switch are poorly understood.Another mechanism involves a change in the hair cycle. There are three stages of the hair cycle: the anagen phase (hair growth), the catagen phase (hair follicle death), and the telogen phase (hair shedding). If the anagen phase increases beyond what is normal, that region of the body will experience excessive hair growth.

Diagnosis
Hypertrichosis is diagnosed clinically by the occurrence of hair in excess of what is expected for age, sex, and ethnicity in areas that are not androgen-sensitive.  The excess can be in the form of excessive length or density and may consist of any hair type (lanugo, vellus, or terminal).

Management
There is no cure for any congenital forms of hypertrichosis. The treatment for acquired hypertrichosis is based on attempting to address the underlying cause. Acquired forms of hypertrichosis have a variety of sources, and are usually treated by removing the factor causing hypertrichosis, e.g. a medication with undesired side-effects. All hypertrichosis, congenital or acquired, can be reduced through hair removal. Hair removal treatments are categorized into two principal subdivisions: temporary removal and permanent removal. Treatment may have adverse effects by causing scarring, dermatitis, or hypersensitivity.Temporary hair removal may last from several hours to several weeks, depending on the method used. These procedures are purely cosmetic. Depilation methods, such as trimming, shaving, and depilatories, remove hair to the level of the skin and produce results that last several hours to several days. Epilation methods, such as plucking, electrology, waxing, sugaring, threading remove the entire hair from the root, the results lasting several days to several weeks.Permanent hair removal uses chemicals, energy of various types, or a combination to target the cells that cause hair growth. Laser hair removal is an effective method of hair removal on hairs that have color. Laser cannot treat white hair.  The laser targets the melanin color in the lower third of the hair follicle, which is the target zone. Electrolysis (electrology) uses electrical current, and/or localized heating. The U.S. Food and Drug Administration (FDA) allows only electrology to use the term "permanent hair removal" because it has been shown to be able to treat all colors of hair.Medication to reduce production of hair is currently under testing. One medicinal option suppresses testosterone by increasing the sex hormone-binding globulin. Another controls the overproduction of hair through the regulation of a luteinizing hormone.

Epidemiology
Congenital forms of hypertrichosis are rare. Only 50 cases of congenital hypertrichosis lanuginosa have been recorded since the Middle Ages, and fewer than 100 cases of congenital generalized hypertrichosis have been documented in scientific publications and by the media. Congenital generalized hypertrichosis is isolated to one family in Mexico. Acquired hypertrichosis and hirsutism are more common. For example, hirsutism occurs in about 10% of women between ages 18 and 45.

Society and culture
People with hair often found jobs as circus performers, making the best of their unusual appearance. Fedor Jeftichew ("Jo-Jo the Dog-faced Man"), Stephan Bibrowski ("Lionel the Lion-faced Man"), Jesús "Chuy" Aceves ("Wolfman"), Annie Jones ("the bearded woman") and Alice Elizabeth Doherty ("The Minnesota Woolly Girl") all had hypertrichosis. Extensive hypertrichosis carries an emotional burden and can cause cosmetic embarrassment; however, some people attempt no treatments because they say it defines who they are.

The Gonsalvus family
Petrus Gonsalvus (1537–1618) was referred to by Italian naturalist Ulisse Aldrovandi as "the man of the woods". Four of his seven children were also afflicted with hypertrichosis and painted.

Barbara van Beck
Barbara van Beck (1629–1668?) is one of the first people to be depicted with Ambras syndrome. She was the only member of her family with the condition. She travelled around Europe, living in court and appearing before the nobility in cities such as London and Paris.

The hairy family of Burma
One record in history concerning congenital hypertrichosis lanuginosa is the hairy family of Burma, a four-generational pedigree of the disease. In 1826, John Crawford was leading a mission for the Governor-General of India through Burma. He tells of meeting a hairy man, Shwe-Maong. Shwe-Maong lived in the court of King Ava and acted as an entertainer. Shwe-Maong had four children: three unaffected children, and one child with congenital hypertrichosis, named Maphoon. On a second mission to Ava, Maphoon was described as a thirty-year-old woman with two sons, one of which had hypertrichosis. The affected son was named Maong-Phoset. He had an affected daughter named Mah-Me. Whereas all affected members of the family had dental problems, the unaffected members had perfect teeth.

Julia Pastrana
Julia Pastrana (1834–1860) travelled throughout the United States in a freak show as the bearded lady, capturing the attention of many artists. She is portrayed as having dark extensive hairs distributed equally throughout the surface of her body, even on the palms of her hands. Originally, she was believed to have congenital hypertrichosis lanuginosa; however, the generalized form of the syndrome coupled with her gingival hyperplasia indicated that her condition was congenital terminal hypertrichosis. This was not confirmed until after her death, when it became clear that her X-linked syndrome resulted in terminal hairs.

Supattra Sasupan
In 2011, Supattra Sasupan (Thai: สุพัตรา สะสุพันธ์; born August 5, 2000), an 11-year-old girl from Thailand with hypertrichosis was named the worlds hairiest girl by the Guinness Book of World Records (as Supatra Sasuphan).

Etymology
Origin of the word hypertrichosis is in Greek roots (hyper-, ʽexcessʼ; trikhos, hair and -osis, ʽformationʼ) and means a disorder that causes excessive hair growth over the body. Medieval sources do not use this term, however prefer hairy men and women instead. These men and women are often mistaken for savages, who similarly have excessive hair, but hairy and savage individuals belong to different categories, since savagery is associated with social or religious isolation. Having exceptional strength, they are deemed closer to the animal than to the human plane. On the contrary, hairy men and women with hypertrichosis are not necessarily isolated and they often live in courts as entertainers, together with other monster-like subjects.

History
The first recorded case of hypertrichosis was Petrus Gonsalvus of the Canary Islands. This was documented by Ulisse Aldrovandi and published in his posthumous Monstrorum Historia cum Paralipomenis historiae omnium animalium in 1642. He noted that two daughters, a son, and a grandchild in Gonsalvus family all had hypertrichosis </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 Paraplegia and can you explain it in depth? [/INST] Paraplegia, or paraparesis, is an impairment in motor or sensory function of the lower extremities. The word comes from Ionic Greek (παραπληγίη)
"half-stricken". It is usually caused by spinal cord injury or a congenital condition that affects the neural (brain) elements of the spinal canal. The area of the spinal canal that is affected in paraplegia is either the thoracic, lumbar, or sacral regions. If four limbs are affected by paralysis, tetraplegia or quadriplegia is the correct term. If only one limb is affected, the correct term is monoplegia. Spastic paraplegia is a form of paraplegia defined by spasticity of the affected muscles, rather than flaccid paralysis.
The American Spinal Injury Association classifies spinal cord injury severity in the following manner. ASIA A is the complete loss of sensory function and motor skills below the injury. ASIA B is having some sensory function below the injury, but no motor function. In ASIA C, there is some motor function below the level of injury, but half of the muscles cannot move against gravity. In ASIA D, more than half of the muscles below the level of injury can move against gravity. ASIA E is the restoration of all neurologic function.

Treatment
Individuals with paraplegia can range in their level of disability, requiring treatments to vary from case to case. Rehabilitation aims to help the patient regain as much functionality and independence as possible. Physiotherapy may help to improve strength, range of motion, stretching and transfer skills. Most paraplegics will be reliant on a wheelchair as a mode of transportation </s>


<s> [INST] <<SYS>> You are a 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 Seborrhoeic dermatitis and can you explain it in depth? [/INST] Seborrhoeic dermatitis, sometimes inaccurately referred to as seborrhoea, is a long-term skin disorder. Symptoms include red, scaly, greasy, itchy, and inflamed skin. Areas of the skin rich in oil-producing glands are often affected including the scalp, face, and chest. It can result in social or self-esteem problems. In babies, when the scalp is primarily involved, it is called cradle cap. Dandruff is a milder form of the condition without inflammation.The cause is unclear but believed to involve a number of genetic and environmental factors. Risk factors include poor immune function, Parkinsons disease, and alcoholic pancreatitis. The condition may worsen with stress or during the winter. The Malassezia yeast is believed to play a role. It is not a result of poor hygiene. Diagnosis is typically based on the symptoms. The condition is not contagious.The typical treatment is antifungal cream and anti-inflammatory agents. Specifically, ketoconazole or ciclopirox are effective. It is unclear if other antifungals, such as miconazole, are equally effective as they have been poorly studied. Other options may include salicylic acid, coal tar, benzoyl peroxide, and phototherapy.The condition is most common in infants within the first 3 months or in adults aged 30 to 70 years. In adults between 1% and 10% of people are affected. Males are more often affected than females. Up to 70% of babies may be affected at some point in time.

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

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

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

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

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

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

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

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

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

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


<s> [INST] <<SYS>> You are a 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 Tachyphylaxis and can you explain it in depth? [/INST] Tachyphylaxis (Greek ταχύς, tachys, "rapid", and φύλαξις, phylaxis, "protection") is a medical term describing an acute, sudden decrease in response to a drug after its administration; i.e. a rapid and short-term onset of drug tolerance. It can occur after an initial dose or after a series of small doses. Increasing the dose of the drug may be able to restore the original response.

Characteristics
Tachyphylaxis is characterized by the rate sensitivity: the response of the system depends on the rate with which a stimulus is presented. To be specific, a high-intensity prolonged stimulus or often-repeated stimulus may bring about a diminished response also known as desensitization.

Molecular interaction
In biological sciences, molecular interactions are the physical bases of the operation of the system. The control of the operation, in general, involves interaction of a stimulus molecule with a receptor/enzyme subsystem by, typically, binding to the macromolecule A and causing an activation or an inhibition of the subsystem by forming an activated form of the macromolecule B. The following schematic represents the activity:

        A

            →

              p

        B

    {\displaystyle A{\xrightarrow {\ \ p\ \ }}B}

where p is the activation rate coefficient. It is customary that p is called a rate constant, but, since the p stands for measure of the intensity of the stimulus causing the activation, p may be variable (non-constant).
More complete is an open system, namely, in its simplest form,

        R

            →

        A

            →

              p
              (
              S
              )

        B

            →

              q

        ,

    {\displaystyle R{\xrightarrow {}}A{\xrightarrow {\ \ p(S)\ \ }}B{\xrightarrow {\ \ q\ \ }},}

where R stands for the rate of production of A, p(S) is the activation rate coefficient explicitly expressing its dependence on the stimulus intensity S and q represents the rate coefficient of removal from the state B. In this elementally open system the steady state of B always equal to R/q.
The above scheme is only the necessary condition for the rate sensitivity phenomenon, and other pathways of deactivation of B may be considered, with the subsequent return to the inactive form of the receptor/enzyme A. Examples offer particular use of such (mathematical) models in endocrinology, physiology and pharmacology.

Examples
Psychedelics
Psychedelics such as LSD-25 and psilocybin-containing mushrooms demonstrate very rapid tachyphylaxis.

Opioids
In a patient fully withdrawn from opioids, going back to an intermittent schedule or maintenance dosing protocol, a fraction of the old tolerance level will rapidly develop, usually starting two days after therapy is resumed and, in general, leveling off after day 7. Whether this is caused directly by opioid receptors modified in the past or affecting a change in some metabolic set-point is unclear </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 Nerve injury and can you explain it in depth? [/INST] Nerve injury is an injury to nervous tissue. There is no single classification system that can describe all the many variations of nerve injuries. In 1941, Seddon introduced a classification of nerve injuries based on three main types of nerve fiber injury and whether there is continuity of the nerve. Usually, however, peripheral nerve injuries are classified in five stages, based on the extent of damage to both the nerve and the surrounding connective tissue, since supporting glial cells may be involved.Unlike in the central nervous system, neuroregeneration in the peripheral nervous system is possible. The processes that occur in peripheral regeneration can be divided into the following major events: Wallerian degeneration, axon regeneration/growth, and reinnervation of nervous tissue. The events that occur in peripheral regeneration occur with respect to the axis of the nerve injury. The proximal stump refers to the end of the injured neuron that is still attached to the neuron cell body; it is the part that regenerates. The distal stump refers to the end of the injured neuron that is still attached to the end of the axon; it is the part of the neuron that will degenerate, but the stump remains capable of regenerating its axons.
The study of peripheral nerve injury began during the American Civil War and greatly expanded during modern medicine with such advances as use of growth-promoting molecules.

Types
To assess the location and severity of a peripheral nerve injury, clinical assessment is commonly combined with electrodiagnostic tests. Injuries to the myelin are usually the least severe (neuropraxia), while injuries to the axons and supporting structures are more severe (axonotmesis is moderate injury, while neurotmesis is severe injury). It may be difficult to differentiate the severity by clinical findings due to common neurological impairments, including motor and sensory impairments distal to the lesion.

Neurapraxia
Neurapraxia is the least severe form of nerve injury, with complete recovery. In this case, the axon remains intact, but there is myelin damage causing an interruption in conduction of the impulse down the nerve fiber. Most commonly, this involves compression of the nerve or disruption to the blood supply (ischemia). There is a temporary loss of function which is reversible within hours to months of the injury (the average is 6–8 weeks). Wallerian degeneration does not occur, so recovery does not involve actual regeneration. There is frequently greater involvement of motor than sensory function with autonomic function being retained. In electrodiagnostic testing with nerve conduction studies, there is a normal compound motor action potential amplitude distal to the lesion at day 10, and this indicates a diagnosis of mild neurapraxia instead of axonotmesis or neurotmesis.

Axonotmesis
This is a more severe nerve injury with disruption of the neuronal axon, but with maintenance of the epineurium. This type of nerve damage may cause paralysis of the motor, sensory, and autonomic, and is mainly seen in crush injury.If the force creating the nerve damage is removed in a timely fashion, the axon may regenerate, leading to recovery.  Electrically, the nerve shows rapid and complete degeneration, with loss of voluntary motor units. Regeneration of the motor end plates will occur, as long as the endoneural tubules are intact.Axonotmesis involves the interruption of the axon and its covering of myelin, but with preservation of the connective tissue framework of the nerve (the encapsulating tissue, the epineurium and perineurium, are preserved). Because axonal continuity is lost, Wallerian degeneration occurs. Electromyography (EMG) performed 2 to 4 weeks later shows fibrillations and denervation potentials in musculature distal to the injury site. Loss in both motor and sensory spines is more complete with axonotmesis than with neurapraxia, and recovery occurs only through regenerations of the axons, a process requiring time.
Axonotmesis is usually the result of a more severe crush or contusion than neurapraxia, but can also occur when the nerve is stretched (without damage to the epineurium). There is usually an element of retrograde proximal degeneration of the axon, and for regeneration to occur, this loss must first be overcome. The regeneration fibers must cross the injury site and regeneration through the proximal or retrograde area of degeneration may require several weeks. Then the neuritis tip progresses down the distal site, such as the wrist or hand. Proximal lesion may grow distally as fast as 2 to 3 mm per day and distal lesion as slowly as 1.5 mm per day. Regeneration occurs over weeks to years.

Neurotmesis
Neurotmesis is the most severe lesion with no potential of full recovery. It occurs on severe contusion, stretch, or laceration. The axon and encapsulating connective tissue lose their continuity. The last (extreme) degree of neurotmesis is transsection, but most neurotmetic injuries do not produce gross loss of continuity of the nerve but rather internal disruption of nerve structures sufficient to involve perineurium and endoneurium as well as axons and their covering. Denervation changes recorded by EMG are the same as those seen with axonotmetic injury. There is a complete loss of motor, sensory and autonomic function. If the nerve has been completely divided, axonal regeneration causes a neuroma to form in the proximal stump. For neurotmesis, it is better to use a new more complete classification called the Sunderland System.

Overview of peripheral regeneration
Wallerian degeneration is a process that occurs before nerve regeneration and can be described as a cleaning or clearing process that essentially prepares the distal stump for reinnervation. Schwann cells are glial cells in the peripheral nervous system that support neurons by forming myelin that encases nerves. During Wallerian degeneration Schwann cells and macrophages interact to remove debris, specifically myelin and the damaged axon, from the distal injury site. Calcium has a role in the degeneration of the damage axon. Bands of Büngner are formed when uninnervated Schwann cells proliferate and the remaining connective tissue basement membrane forms endoneurial tubes. Bands of Büngner are important for guiding the regrowing axon.At the neuronal cell body, a process called chromatolysis occurs in which the nucleus migrates to the periphery of the cell body and the endoplasmic reticulum breaks up and disperses. Nerve damage causes the metabolic function of the cell to change from that of producing molecules for synaptic transmission to that of producing molecules for growth and repair. These factors include GAP-43, tubulin and actin. Chromatolysis is reversed when the cell is prepared for axon regeneration.Axon regeneration is characterized by the formation of a growth cone, which has the ability to produce a protease that digests any material or debris that remains in its path of regeneration toward the distal site. The growth cone responds to molecules produced by Schwann cells such as laminin and fibronectin.

Neuron-intrinsic changes
Immediately following injury, neurons undergo a large number of transcriptional and proteomic changes which switch the cell from a mature, synaptically active neuron to a synaptically silent, growth state. This process is dependent on new transcription, as blocking the ability of cells to transcribe new mRNA severely impairs regeneration. A number of signaling pathways have been shown to be turned on by axon injury and help to enable long distance regeneration including BMP, TGFβ, and MAPKs. Similarly, a growing number of transcription factors also boost the regenerative capacity of peripheral neurons including ASCL1, ATF3, CREB1, HIF1α, JUN, KLF6, KLF7, MYC, SMAD1, SMAD2, SMAD3, SOX11, SRF, STAT3, TP53, and XBP1. Several of these can also boost the regenerative capacity of CNS neurons, making them potential therapeutic targets for treating spinal cord injury and stroke.

Role of Schwann cells
Schwann cells are active in Wallerian degeneration. They not only have a role in phagocytosis of myelin, but they also have a role in recruitment of macrophages to continue the phagocytosis of myelin. The phagocytic role of Schwann cells has been investigated by studying the expression of molecules in Schwann cells that are typically specific to inflammatory macrophages. Expression of one such molecule MAC-2, a galactose-specific lectin, is observed in not only degenerating nerves that are macrophage-rich but also degenerating nerves that are macrophage-scarce and Schwann cell-rich. Furthermore, the effects of MAC-2 in degenerating nerves are associated with myelin phagocytosis. There was a positive correlation between the amount of MAC-2 expression and the extent of myelin phagocytosis. A deficiency in MAC-2 expression can even cause inhibition of myelin removal from injury sites.Schwann cells are active in demyelination of injured nerves before macrophages are even present at the site of nerve injury.  Electron microscopy and immunohistochemical staining analysis of teased nerve fibers shows that before macrophages arrive at the injury site, myelin is fragmented and myelin debris and lipid droplets are found in the cytoplasm of Schwann cells, indicating phagocytic activity before macrophages arrive.Schwann cell activity includes recruitment of macrophages to the injury site. Monocyte chemoattractant protein (MCP-1) plays a role in recruiting monocytes/macrophages. In tellurium-induced demylenation with no axon degeneration, nerve crush with axon degeneration, and nerve transection with axon degeneration an increase in MCP-1 mRNA expression followed by an increase in macrophage recruitment occurred. In addition varying levels of MCP-1 mRNA expression also had an effect. Increased MCP-1 mRNA levels correlated positively with an increase in macrophage recruitment. Furthermore, in situ hybridation determined that the cellular source of MCP-1 was Schwann cells.Schwann cells play an important role in not only producing neurotrophic factors such as nerve growth factor (NGF) and ciliary neurotrophic factor (CNTF), which promote growth, of both the damaged nerve and supporting Schwann cells, but also producing neurite promoting factors, which guide the growing axon, both of which are discussed below.

Role of macrophages
The primary role of macrophages in peripheral regeneration is demylenation during Wallerian degeneration. Immunohistochemical analysis showed that in tellurium demylenated, crushed, and cut nerves, expression of lysozyme, which is a marker for myelin phagocytosis, and of ED1, which is a marker for macrophages, occurred in the same region. Lysozyme was also investigated with respect to the temporal progression of myelin phagocytosis by macrophages in nerve injury.  Northern blotting showed that peak lysozyme mRNA expression occurred at an appropriate time with respect to temporal models of myelin phagocytosis. Macrophages do not phagocytose all cellular debris at the nerve injury site; they are selective and will salvage certain factors. Macrophages produce apolipoprotein E which is involved in rescuing cholesterol in damaged nerves. In the same investigation, temporal levels of apolipoprotein E mRNA expression in the three models for demylenation and nerve damage were consistent with respect to models for cholesterol salvage in nerve injury. Macrophages play a role in salvaging cholesterol during nerve injury.Macrophages also play a role in inducing the proliferation of Schwann cells that occurs during Wallerian degeneration. Supernatant has been collected from medium in which macrophages are active in myelin phagocytosis where lysosomal processing of the myelin occurs within the macrophage. The supernatant contains a mitogenic factor, a mitosis promoting factor, that is characterized heat and trypsin sensitivity, both of which characterize it as a peptide. Treatment of Schwann cells with the collected supernatant shows that it is a mitogenic factor and thus plays an important role in the proliferation of Schwann cells.Macrophages are also involved in the secretion factors that promote nerve regeneration. Macrophages secrete not only interleukin-1, a cytokine that induces expression of nerve growth factor (NGF) in Schwann cells but also an interleukin-1 receptor antagonist (IL-1ra). Expression of IL-1ra in mice with transected sciatic nerves via implantation of a tube releasing IL-1ra showed the regrowth of fewer myelinated and unmyelinated axons. Macrophage secretion of interleukin-1 is involved in stimulation of nerve regeneration.

Role of neurotrophic factors
Neurotrophic factors are those that promote survival and growth of neurons. A trophic factor can be described as a factor that is associated with providing nourishment to allow for growth. In general they are protein ligands for tyrosine kinase receptors; binding to the specific receptor yields autophosphorylation and subsequent phosphorylation of tyrosine residues on proteins that participate in further downstream signaling to activate proteins and genes involved in growth and proliferation. Neurotrophic factors act through retrograde transport in neurons, in which they are taken up by the growth cone of the injured neuron and transported back to the cell body. These neurotrophic factors have both autocrine and paracrine effects, as they promote growth of the damaged neurons as well as the adjacent Schwann cells.
Nerve growth factor (NGF) typically has a low level of expression in nerves that are healthy and not growing or developing, but in response to nerve injury NGF expression increases in Schwann cells. This is a mechanism to increase growth and proliferation of Schwann cells at the distal stump in order to prepare for reception of the regenerating axon. NGF has not only a trophic role but also a tropic or guiding role. The Schwann cells that form the bands of Bungner at the distal injury site express NGF receptors as a guiding factor for the regenerating axon of the injured neuron. NGF bound to the receptors on Schwann cells provides the growing neurons that are contacted with a trophic factor to promote further growth and regenerationCiliary neurotrophic factor (CNTF) typically has a high level of expression in Schwann cells associated with nerves that are healthy, but in response to nerve injury CNTF expression decreases in Schwann cells distal to the injury site and remains relatively low unless the injured axon begins to regrow. CNTF has numerous trophic roles in motor neurons in the peripheral nervous system including the prevention of atrophy of dennervated tissue and the prevention of degeneration and death of motor neurons after nerve injury. (frostick)  In sciatic motor neurons both CNTF receptor mRNA expression and CNTF receptor is increased after injury for a prolonged time frame compared to the short time frame in the central nervous system suggesting a role for CNTF in nerve regeneration.Insulin-like growth factors (IGFs) have been shown to increase the rate of peripheral nervous system axon regeneration. IGF-I and IGF-II mRNA levels are significantly increased distal to the site of crush injury in rat sciatic nerves. At the site of nerve repair, locally delivered IGF-I can significantly increase the rate of axon regeneration within a nerve graft and help expedite functional recovery of a paralyzed muscle.

Role of neurite-promoting factors
Neurite promoting factors include many extracellular matrix proteins produced by Schwann cells at the distal stump including fibronectin and laminin. Fibronectin are components of the basal lamina and promote neurite growth and adhesion of the growth cone to the basal lamina. In regenerating neural cells, neurite promoting factors play a role in adhesion of the axon and include neural cell adhesion molecule (N-CAM) and N-cadherin.

Treatment
Unless otherwise demonstrated, nerve injuries are commonly irreversible, and therefore complete treatment is rather difficult, though still possible and hence lifelong management of disabilities arising due to nerve injuries is necessary.

Nerve regeneration therapies
Electrical stimulation can promote nerve regeneration. The positive effect of electrical stimulation on nerve regeneration is due to its molecular influence on the damaged neuron and Schwann cells. Electrical stimulation can directly accelerate the expression of cyclic adenosine monophosphate (cAMP) both in neurons and Schwann cells. cAMP is a molecule that stimulates multiple signaling pathways that aid nerve regeneration by enhancing the expression of several neurotrophic factors. Electrical stimulation also results in the influx of calcium ions, which further triggers multiple regeneration pathways.The frequency of stimulation is an important factor in the success of both quality and quantity of axon regeneration as well as growth of the surrounding myelin and blood vessels that support the axon. Histological analysis and measurement of regeneration showed that low frequency stimulation had a more successful outcome than high frequency stimulation on regeneration of damaged sciatic nerves.Other studies have used both oscillating current (AC) and non-oscillating direct current (DC) stimulation to regenerate mammalian peripheral nerves. Mammalian neurons preferentially orient and grow towards the cathode in DC electric fields.Surgery can be done in case a nerve has become cut or otherwise divided. Recovery of a nerve after surgical repair depends mainly on the age of patients. Younger the patients, better the prognosis, because of better healing capacity of young tissues. Young children can recover almost normal nerve function </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 Rectal pain and can you explain it in depth? [/INST] Rectal pain is the symptom of pain in the area of the rectum </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 Intestinal ischemia and can you explain it in depth? [/INST] Intestinal ischemia is a medical condition in which injury to the large or small intestine occurs due to not enough blood supply. It can come on suddenly, known as acute intestinal ischemia, or gradually, known as chronic intestinal ischemia. The acute form of the disease often presents with sudden severe abdominal pain and is associated with a high risk of death. The chronic form typically presents more gradually with abdominal pain after eating, unintentional weight loss, vomiting, and fear of eating.Risk factors for acute intestinal ischemia include atrial fibrillation, heart failure, chronic kidney failure, being prone to forming blood clots, and previous myocardial infarction. There are four mechanisms by which poor blood flow occurs: a blood clot from elsewhere getting lodged in an artery, a new blood clot forming in an artery, a blood clot forming in the superior mesenteric vein, and insufficient blood flow due to low blood pressure or spasms of arteries. Chronic disease is a risk factor for acute disease. The best method of diagnosis is angiography, with computed tomography (CT) being used when that is not available.Treatment of acute ischemia may include stenting or medications to break down the clot provided at the site of obstruction by interventional radiology. Open surgery may also be used to remove or bypass the obstruction and may be required to remove any intestines that may have died. If not rapidly treated outcomes are often poor. Among those affected even with treatment the risk of death is 70% to 90%. In those with chronic disease bypass surgery is the treatment of choice. Those who have thrombosis of the vein may be treated with anticoagulation such as heparin and warfarin, with surgery used if they do not improve.Acute intestinal ischemia affects about five per hundred thousand people per year in the developed world. Chronic intestinal ischemia affects about one per hundred thousand people. Most people affected are over 60 years old. Rates are about equal in males and females of the same age. Intestinal ischemia was first described in 1895.

Signs and symptoms
While not always present and often overlapping, three progressive phases of intestinal ischemia have been described:
A hyper active stage occurs first, in which the primary symptoms are severe abdominal pain and the passage of bloody stools. Many patients get better and do not progress beyond this phase.
A paralytic phase can follow if ischemia continues; in this phase, the abdominal pain becomes more widespread, the belly becomes more tender to the touch, and bowel motility decreases, resulting in abdominal bloating, no further bloody stools, and absent bowel sounds on exam.
Finally, a shock phase can develop as fluids start to leak through the damaged colon lining. This can result in shock and metabolic acidosis with dehydration, low blood pressure, rapid heart rate, and confusion. Patients who progress to this phase are often critically ill and require intensive care.

Clinical findings
Symptoms of intestinal ischemia vary and can be acute (especially if embolic), subacute, or chronic.Case series report prevalence of clinical findings and provide the best available, yet biased, estimate of the sensitivity of clinical findings. In a series of 58 patients with intestinal ischemia due to mixed causes:
abdominal pain was present in 95% (median of 24 hours duration). The other three patients presented with shock and metabolic acidosis.
nausea in 44%
vomiting in 35%
diarrhea in 35%
heart rate > 100 in 33%
rectal bleeding in 16% (not stated if this number also included occult blood – presumably not)
constipation in 7%

Diagnostic heuristics
In the absence of adequate quantitative studies to guide diagnosis, various heuristics help guide diagnosis:

Intestinal ischemia" should be suspected when individuals, especially those at high risk for acute intestinal ischemia, develop severe and persisting abdominal pain that is disproportionate to their abdominal findings"., or simply, pain out of proportion to exam.
Regarding intestinal arterial thrombosis or embolism: "early symptoms are present and are relative mild in 50% of cases for three to four days before medical attention is sought".
Regarding intestinal arterial thrombosis or embolism: "Any patient with an arrhythmia such as atrial fibrillation who complains of abdominal pain is highly suspected of having embolization to the superior mesenteric artery until proved otherwise."
Regarding nonocclusive intestinal ischemia: "Any patient who takes digitalis and diuretics and who complains of abdominal pain must be considered to have nonocclusive ischemia until proved otherwise."

Diagnosis
It is difficult to diagnose intestinal ischemia early.

Blood tests
In a series of 58 patients with intestinal ischemia due to mixed causes:
White blood cell count >10.5 in 98% (probably an overestimate as only tested in 81% of patients)
Lactic acid elevated 91% (probably an overestimate as only tested in 57% of patients)In very early or very extensive acute intestinal ischemia, elevated lactate and white blood cell count may not yet be present. In extensive mesenteric ischemia, bowel may be ischemic but separated from the blood flow such that the byproducts of ischemia are not yet circulating.

During endoscopy
A number of devices have been used to assess the sufficiency of oxygen delivery to the colon. The earliest devices were based on tonometry, and required time to equilibrate and estimate the pHi, roughly an estimate of local CO2 levels. The first device approved by the U.S. FDA (in 2004) used visible light spectroscopy to analyze capillary oxygen levels. Use during aortic aneurysm repair detected when colon oxygen levels fell below sustainable levels, allowing real-time repair. In several studies, specificity has been 83% for chronic intestinal ischemia and 90% or higher for acute colonic ischemia, with a sensitivity of 71%-92%. This device must be placed using endoscopy, however.Findings on gastroscopy may include edematous gastric mucosa, and hyperperistalsis.Finding on colonoscopy may include: fragile mucosa, segmental erythema, longitudinal ulcer, and loss of haustrations

Plain X-ray
Plain X-rays are often normal or show non-specific findings.

Computed tomography
Computed tomography (CT scan) is often used. The accuracy of the CT scan depends on whether a small bowel obstruction (SBO) is present.SBO absent

prevalence of intestinal ischemia 23%
sensitivity 64%
specificity 92%
positive predictive value (at prevalence of 23%) 79%
negative predictive value (at prevalence of 23%) 95%SBO present

prevalence of intestinal ischemia 62%
sensitivity 83%
specificity 93%
positive predictive value (at prevalence of 62%) 93%
negative predictive value (at prevalence of 62%) 61%Early findings on CT scan include:

Intestinal mesenteric edema
Bowel dilatation
Bowel wall thickening
Intestinal mesenteric stranding
Evidence of adjacent solid organ infarctions to the kidney or spleen, consistent with a cardiac embolic shower phenomenonIn embolic acute intestinal ischemia, CT-Angiography can be of great value for diagnosis and treatment. It may reveal the emboli itself lodged in the superior mesenteric artery, as well as the presence or absence of distal mesenteric branches.Late findings, which indicate dead bowel, include:

Intramural bowel gas
Portal venous gas
Free abdominal air

Angiography
As the cause of the ischemia can be due to embolic or thrombotic occlusion of the mesenteric vessels or nonocclusive ischemia, the best way to differentiate between the etiologies is through the use of mesenteric angiography. Though it has serious risks, angiography provides the possibility of direct infusion of vasodilators in the setting of nonocclusive ischemia.

Treatment
The treatment of intestinal ischemia depends on the cause and can be medical or surgical. However, if bowel has become necrotic, the only treatment is surgical removal of the dead segments of bowel.In non-occlusive disease, where there is no blockage of the arteries supplying the bowel, the treatment is medical rather than surgical. People are admitted to the hospital for resuscitation with intravenous fluids, careful monitoring of laboratory tests, and optimization of their cardiovascular function. NG tube decompression and heparin anticoagulation may also be used to limit stress on the bowel and optimize perfusion, respectively.Surgical revascularisation remains the treatment of choice for intestinal  ischaemia related to an occlusion of the vessels supplying the bowel, but thrombolytic medical treatment and vascular interventional  radiological techniques have a growing role.If the ischemia has progressed to the point that the affected intestinal segments are gangrenous, a bowel resection of those segments is called for </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 Gastric distension and can you explain it in depth? [/INST]  </s>