<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Anorexia (symptom) and explain in detail? [/INST] Anorexia is a medical term for a loss of appetite. While the term in non-scientific publications is often used interchangeably with anorexia nervosa, many possible causes exist for a loss of appetite, some of which may be harmless, while others indicate a serious clinical condition or pose a significant risk.
Anorexia is a symptom, not a diagnosis. Anorexia is not to be confused with the mental health disorder anorexia nervosa. Because the term anorexia is often used as a short-form of anorexia nervosa, to avoid confusion a provider must clarify to a patient whether they are simply referring to a decreased appetite or the  mental health disorder. Anyone can manifest anorexia as a loss of appetite, regardless of their gender, age, or weight.
The symptom also occurs in other animals, such as cats, dogs, cattle, goats, and sheep. In these species, anorexia may be referred to as inappetence. As in humans, loss of appetite can be due to a range of diseases and conditions, as well as environmental and psychological factors.

Etymology
The term is from Ancient Greek: ανορεξία (ἀν-, without + όρεξις, spelled órexis, meaning appetite).

Common manifestations
Anorexia simply manifests as a decreased or loss of appetite. This can present as not feeling hungry or lacking the desire to eat. Sometimes people do not even notice they lack an appetite until they begin to lose weight from eating less. In other cases, it can be more noticeable, such as when a person becomes nauseated from just the thought of eating. Any form of decreased appetite that leads to changes in the body (such as weight loss or muscle loss) that is not done intentionally as part of dieting is clinically significant.

Physiology of anorexia
Appetite stimulation and suppression is a complex process involving many different parts of the brain and body by the use of various hormones and signals. Appetite is thought to be stimulated by interplay between peripheral signals to the brain (taste, smell, sight, gut hormones) as well as the balance of neurotransmitters and neuropeptides  in the hypothalamus. Examples of these signals or hormones include neuropeptide Y, leptin, ghrelin, insulin, serotonin, and orexins (also called hypocretins). Anything that causes an imbalance of these signals or hormones can lead to the symptom of anorexia. While it is known that these signals and hormones help control appetite, the complicated mechanisms regarding a pathological increase or decrease in appetite are still being explored.

Common causes
Acute radiation syndrome
Addisons disease
Alcoholism
Alcohol withdrawal
Anemia
Anorexia nervosa
Anxiety
Appendicitis
Babesiosis
Benzodiazepine withdrawal
Bipolar disorder
Cancer
Cannabinoid hyperemesis syndrome
Cannabis withdrawal
Celiac disease
Chronic kidney disease
Chronic pain
Common cold
Constipation
COPD
COVID-19
Crohns disease
Dehydration
Dementia
Depression
Ebola
Fatty liver disease
Fever
Food poisoning
Gastroparesis
Hepatitis
HIV/AIDS
Hypercalcemia
Hyperglycemia
Hypervitaminosis D
Hypothyroidism and sometimes hyperthyroidism
Irritable bowel syndrome
Ketoacidosis
Kidney failure
Low blood pressure
Mania
Metabolic disorders, particularly urea cycle disorders
MELAS syndrome
Nausea
Opioid use disorder
Pancreatitis
Pernicious anemia
Psychosis
Schizophrenia
Side effect of drugs
Stimulant use disorder
Stomach flu
Stress
Sickness behavior
Superior mesenteric artery syndrome
Syndrome of inappropriate antidiuretic hormone secretion
Tuberculosis
Thalassemia
Ulcerative colitis
Uremia
Vitamin B12 deficiency
Zinc deficiency
Infection: Anorexia of infection is part of the acute phase response (APR) to infection. The APR can be triggered by lipopolysaccharides and peptidoglycans from bacterial cell walls, bacterial DNA, and double-stranded viral RNA, and viral glycoproteins, which can trigger production of a variety of proinflammatory cytokines. These can have an indirect effect on appetite by a number of means, including peripheral afferents from their sites of production in the body, by enhancing production of leptin from fat stores. Inflammatory cytokines can also signal to the central nervous system more directly by specialized transport mechanisms through the blood–brain barrier, via circumventricular organs (which are outside the barrier), or by triggering production of eicosanoids in the endothelial cells of the brain vasculature. Ultimately, the control of appetite by this mechanism is thought to be mediated by the same factors normally controlling appetite, such as neurotransmitters (serotonin, dopamine, histamine, norepinephrine, corticotropin releasing factor, neuropeptide Y, and α-melanocyte-stimulating hormone).

Drugs
Stimulants, such as ephedrine, amphetamine, methamphetamine, MDMA, cathinone, methylphenidate, nicotine, cocaine, caffeine, etc.
Narcotics, such as heroin, morphine, codeine, hydrocodone, oxycodone, etc.
Antidepressants can have anorexia as a side effect, primarily selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine.
Byetta, a type II diabetes drug, will cause moderate nausea and loss of appetite.
Abruptly stopping appetite-increasing drugs, such as cannabis and corticosteroids.
Chemicals that are members of the phenethylamine group. (Individuals with anorexia nervosa may seek them to suppress appetite.)
Topiramate may cause anorexia as a side effect.
Other drugs may be used to intentionally cause anorexia in order to help a patient preoperative fasting prior to general anesthesia. It is important to avoid food before surgery to mitigate the risk of pulmonary aspiration, which can be fatal.

Other
During the post-operative recovery period for a tonsillectomy or adenoidectomy, it is common for adult patients to experience a lack of appetite until their throat significantly heals (usually 10–14 days).
Altitude sickness
Significant emotional pain caused by an event (rather than a mental disorder) can cause an individual to temporarily lose all interest in food.
Several Twelve-step programs including Overeaters Anonymous tackle psychological issues members believe lead to forms of deprivation
Psychological stress
Experiencing grotesque or unappealing thoughts or conversations, or viewing similar images
Being in the presence of unappealing things such as waste matter, dead organisms, or bad smells

Complications
Complications of anorexia may result due to poor food intake </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Adhesion (medicine) and explain in detail? [/INST] Adhesions are fibrous bands that form between tissues and organs, often as a result of injury during surgery. They may be thought of as internal scar tissue that connects tissues not normally connected.

Pathophysiology
Adhesions form as a natural part of the bodys healing process after surgery in a similar way that a scar forms. The term "adhesion" is applied when the scar extends from within one tissue across to another, usually across a virtual space such as the peritoneal cavity. Adhesion formation post-surgery typically occurs when two injured surfaces are close to one another. According to the "classical paradigm" of adhesion formation, the pathogenesis starts with inflammation and activation of the coagulation system which causes fibrin deposits onto the damaged tissues. The fibrin then connects the two adjacent structures where damage of the tissues occurred. The fibrin acts like a glue to seal the injury and builds the fledgling adhesion, said at this point to be "fibrinous." In body cavities such as the peritoneal, pericardial, and synovial cavities, a family of fibrinolytic enzymes may act to limit the extent of the initial fibrinous adhesion, and may even dissolve it. In many cases, the production or activity of these enzymes are compromised because of inflammation following injury or infection, however, and the fibrinous adhesion persists. A more recent study suggested that the formation of "fibrinous" adhesions is preceded by the aggregation of cavity macrophages, that can act like extravascular platelets in the abdominal cavity.If this is allowed to happen, tissue repair cells such as macrophages, fibroblasts, and blood vessel cells penetrate into the fibrinous adhesion and lay down collagen and other matrix substances to form a permanent fibrous adhesion. In 2002, Giuseppe Martucciellos research group showed a possible role could be played by microscopic foreign bodies (FB) inadvertently contaminating the operative field during surgery. These data suggested that two different stimuli are necessary for adhesion formation: a direct lesion of the mesothelial layers and a solid substrate foreign body (FB).
While some adhesions do not cause problems, others may prevent muscle and other tissues and organs from moving freely, sometimes causing organs to become twisted or pulled from their normal positions.

Regions affected
Adhesive capsulitis
In the case of adhesive capsulitis of the shoulder (also known as frozen shoulder), adhesions grow between the shoulder joint surfaces, restricting motion.

Abdominal adhesions
Abdominal adhesions (or intra-abdominal adhesions) are most commonly caused by abdominal surgical procedures. The adhesions start to form within hours of surgery and may cause internal organs to attach to the surgical site or to other organs in the abdominal cavity. Adhesion-related twisting and pulling of internal organs may result in complications such as  abdominal pain or intestinal obstruction.
Small bowel obstruction (SBO) is a significant consequence of post-surgical adhesions. A SBO may be caused when an adhesion pulls or kinks the small intestine and prevents the flow of content through the digestive tract. Obstruction may occur 20 years or more after the initial surgical procedure, if a previously benign adhesion allows the small bowel to twist spontaneously around itself and obstruct. Without immediate medical attention, SBO is an emergent, possibly fatal, condition.
According to statistics provided by the National Hospital Discharge Survey approximately 2,000 people die every year in the US from obstruction due to adhesions. Depending on the severity of the obstruction, a partial obstruction may relieve itself with conservative medical intervention. Many obstructive events require surgery, however, to loosen or dissolve the offending adhesion(s) or to resect the affected small intestine.

Pelvic adhesions
Pelvic adhesions are a form of abdominal adhesions in the pelvis. In women they typically affect reproductive organs and thus are of concern in reproduction or as a cause of chronic pelvic pain. Other than surgery, endometriosis and pelvic inflammatory disease are typical causes.
Surgery inside the uterine cavity (e.g., suction dilation and curettage, myomectomy, endometrial ablation) may result in Ashermans syndrome (also known as intrauterine adhesions, intra uterine synechiae), a cause of infertility.
The impairment of reproductive performance from adhesions may happen through many mechanisms, all of which usually stem from the distortion of the normal tubo-ovarian relationship. This distortion may prevent an ovum from traveling to the fimbriated end of the Fallopian tube.A meta-analysis in 2012 came to the conclusion that there is only little evidence for the surgical principle that using less invasive techniques, introducing fewer foreign bodies, or causing less ischemia reduces the extent and severity of adhesions in pelvic surgery.

Pericardial adhesions
Adhesions forming between the heart and the sternum after cardiac surgery place the heart at risk of catastrophic injury during re-entry for a subsequent procedure.

Peridural adhesions
Adhesions and scarring as epidural fibrosis may occur after spinal surgery that restricts the free movement of nerve roots, causing tethering and leading to pain.

Peritendinous adhesions
Adhesions and scarring occurring around tendons after hand surgery restrict the gliding of tendons in their sheaths and compromise digital mobility.

Association with surgical procedures
Applying adhesion barriers during surgery may help to prevent the formation of adhesions. There are two methods that are approved by the U.S. Food and Drug Administration (FDA) for adhesion prevention: Intercede and Seprafilm. One study found that Seprafilm is twice as effective at preventing adhesion formation when compared to just surgical technique alone. Surgical humidification therapy may also minimise the incidence of adhesion formation. Laparoscopic surgery has a reduced risk for creating adhesions. Steps may be taken during surgery to help prevent adhesions such as handling tissues and organs gently, using starch-free and latex-free gloves, not allowing tissues to dry out, and shortening surgery time.An unfortunate fact is, that adhesions are unavoidable in surgery and the main treatment for adhesions is more surgery. Besides intestinal obstructions caused by adhesions that may be seen in an X-ray, there are no diagnostic tests available to accurately diagnose an adhesion.

Abdominal surgery
A study showed that more than 90% of people develop adhesions following open abdominal surgery and that 55–100% of women develop adhesions following pelvic surgery. Adhesions from prior abdominal or pelvic surgery may obscure visibility and access at subsequent abdominal or pelvic surgery. In a very large study (29,790 participants) published in British medical journal The Lancet, 35% of patients who underwent open abdominal or pelvic surgery were readmitted to the hospital an average of two times after their surgery, due to adhesion-related or adhesion-suspected complications. Over 22% of all readmissions occurred in the first year after the initial surgery </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Renal osteodystrophy and explain in detail? [/INST] Renal osteodystrophy/adynamic bone disease is currently defined as an alteration of bone morphology in patients with chronic kidney disease (CKD).  It is one measure of the skeletal component of the systemic disorder of chronic kidney disease-mineral and bone disorder (CKD-MBD). The term "renal osteodystrophy" was coined in 1943, 60 years after an association was identified between bone disease and kidney failure.The traditional types of renal osteodystrophy have been defined on the basis of turnover and mineralization as follows: 1) mild, slight increase in turnover and normal mineralization; 2) osteitis fibrosa, increased turnover and abnormal mineralization; 3) osteomalacia, decreased turnover and abnormal mineralization; 4) adynamic, decreased turnover and acellularity; and, 5) mixed, increased turnover with abnormal mineralization. A Kidney Disease: Improving Global Outcomes report has suggested that bone biopsies in patients with CKD should be characterized by determining bone turnover, mineralization, and volume (TMV system).On the other hand, CKD-MBD is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following: 1) abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism; 2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (renal osteodystrophy); and 3) vascular or other soft-tissue calcification.

Signs and symptoms
Renal osteodystrophy may exhibit no symptoms; if it does show symptoms, they include:

Bone pain
Joint pain
Bone deformation
Bone fracture
The broader concept of chronic kidney disease-mineral and bone disorder (CKD-MBD) is not only associated with fractures but also with cardiovascular calcification, poor quality of life and increased morbidity and mortality in CKD patients (the so-called bone-vascular axis). These clinical consequences are acquiring such an importance that scientific working groups (such as the ERA-EDTA CKD-MBD Working Group) or international initiatives are trying to promote research in the field including basic, translational and clinical research.

Pathogenesis
Renal osteodystrophy has been classically described to be the result of hyperparathyroidism secondary to hyperphosphatemia combined with hypocalcemia, both of which are due to decreased excretion of phosphate by the damaged kidney.Low activated vitamin D3 levels are a result of the damaged kidneys inability to convert vitamin D3 into its active form, calcitriol, and result in further hypocalcemia </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Adrenal insufficiency and explain in detail? [/INST] Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of steroid hormones, primarily cortisol; but may also include impaired production of aldosterone (a mineralocorticoid), which regulates sodium conservation, potassium secretion, and water retention. Craving for salt or salty foods due to the urinary losses of sodium is common.Addisons disease and congenital adrenal hyperplasia can manifest as adrenal insufficiency. If not treated, adrenal insufficiency may result in abdominal pains, vomiting, muscle weakness and fatigue, depression, low blood pressure, weight loss, kidney failure, changes in mood and personality, and shock (adrenal crisis). An adrenal crisis may occur if the body is subjected to stress, such as an accident, injury, surgery, or severe infection; death may quickly follow.Adrenal insufficiency can also occur when the hypothalamus or the pituitary gland does not make adequate amounts of the hormones that assist in regulating adrenal function. This is called secondary or tertiary adrenal insufficiency and is caused by lack of production of ACTH in the pituitary or lack of CRH in the hypothalamus, respectively.

Types
There are three major types of adrenal insufficiency.

Primary adrenal insufficiency is due to impairment of the adrenal glands.
80% are due to an autoimmune disease called Addisons disease or autoimmune adrenalitis.
One subtype is called idiopathic, meaning of unknown cause.
It can also be due to congenital adrenal hyperplasia or an adenoma (tumor) of the adrenal gland.
Other causes include; Infections (TB, CMV, histoplasmosis, paracoccidioidomycosis), vascular (hemorrhage from sepsis, adrenal vein thrombosis, HIT), deposition disease (hemochromatosis, amyloidosis, sarcoidosis), drugs (azole anti-fungals, etomidate (even one dose), rifampin, anticonvulsants)
Secondary adrenal insufficiency is caused by impairment of the pituitary gland or hypothalamus. Its principal causes include pituitary adenoma (which can suppress production of adrenocorticotropic hormone (ACTH) and lead to adrenal deficiency unless the endogenous hormones are replaced; secondary adrenal insufficiency can be caused by steroids, inhaled steroids such as Flovent; and Sheehans syndrome, which is associated with impairment of only the pituitary gland.
Tertiary adrenal insufficiency is due to hypothalamic disease and a decrease in the release of corticotropin releasing hormone (CRH). Causes can include brain tumors and sudden withdrawal from long-term exogenous steroid use (which is the most common cause overall).

Signs and symptoms
Signs and symptoms include: hypoglycemia, hyperpigmentation, dehydration, weight loss, and disorientation. Additional signs and symptoms include weakness, tiredness, dizziness, low blood pressure that falls further when standing (orthostatic hypotension), cardiovascular collapse, muscle aches, nausea, vomiting, and diarrhea. These problems may develop gradually and insidiously. Addisons disease can present with tanning of the skin that may be patchy or even all over the body. Characteristic sites of tanning are skin creases (e.g. of the hands) and the inside of the cheek (buccal mucosa). Goitre and vitiligo may also be present. Eosinophilia may also occur. Hyponatremia is a sign of secondary insufficiency.

Causes
Causes of acute adrenal insufficiency are mainly sudden withdrawal of long-term corticosteroid therapy, Waterhouse–Friderichsen syndrome, and stress in people with underlying chronic adrenal insufficiency. The latter is termed critical illness–related corticosteroid insufficiency.For chronic adrenal insufficiency, the major contributors are autoimmune adrenalitis (Addisons Disease), tuberculosis, AIDS, and metastatic disease. Minor causes of chronic adrenal insufficiency are systemic amyloidosis, fungal infections, hemochromatosis, and sarcoidosis.Autoimmune adrenalitis may be part of Type 2 autoimmune polyglandular syndrome, which can include type 1 diabetes, hyperthyroidism, and autoimmune thyroid disease (also known as autoimmune thyroiditis, Hashimotos thyroiditis, and Hashimotos disease). Hypogonadism may also present with this syndrome. Other diseases that are more common in people with autoimmune adrenalitis include premature ovarian failure, celiac disease, and autoimmune gastritis with pernicious anemia.X-Linked Recessive Adrenoleukodystrophy can also cause adrenal insufficiency.Adrenal insufficiency can also result when a patient has a craniopharyngioma, which is a histologically benign tumor that can damage the pituitary gland and so cause the adrenal glands not to function. This would be an example of secondary adrenal insufficiency syndrome.Causes of adrenal insufficiency can be categorized by the mechanism through which they cause the adrenal glands to produce insufficient cortisol. These are adrenal dysgenesis (the gland has not formed adequately during development), impaired steroidogenesis (the gland is present but is biochemically unable to produce cortisol) or adrenal destruction (disease processes leading to glandular damage).

Corticosteroid withdrawal
Use of high-dose steroids for more than a week begins to produce suppression of the persons adrenal glands because the exogenous glucocorticoids suppress release of hypothalamic corticotropin-releasing hormone (CRH) and pituitary adrenocorticotropic hormone (ACTH). With prolonged suppression, the adrenal glands atrophy (physically shrink), and can take months to recover full function after discontinuation of the exogenous glucocorticoid. During this recovery time, the person is vulnerable to adrenal insufficiency during times of stress, such as illness, due to both adrenal atrophy and suppression of CRH and ACTH release. Use of steroids joint injections may also result in adrenal suppression after discontinuation.

Adrenal dysgenesis
All causes in this category are genetic, and generally very rare. These include mutations to the SF1 transcription factor, congenital adrenal hypoplasia due to DAX-1 gene mutations and mutations to the ACTH receptor gene (or related genes, such as in the Triple A or Allgrove syndrome). DAX-1 mutations may cluster in a syndrome with glycerol kinase deficiency with a number of other symptoms when DAX-1 is deleted together with a number of other genes.

Impaired steroidogenesis
To form cortisol, the adrenal gland requires cholesterol, which is then converted biochemically into steroid hormones. Interruptions in the delivery of cholesterol include Smith–Lemli–Opitz syndrome and abetalipoproteinemia.Of the synthesis problems, congenital adrenal hyperplasia is the most common (in various forms: 21-hydroxylase, 17α-hydroxylase, 11β-hydroxylase and 3β-hydroxysteroid dehydrogenase), lipoid CAH due to deficiency of StAR and mitochondrial DNA mutations. Some medications interfere with steroid synthesis enzymes (e.g. ketoconazole), while others accelerate the normal breakdown of hormones by the liver (e.g. rifampicin, phenytoin).

Adrenal destruction
Autoimmune adrenalitis is the most common cause of Addisons disease in the industrialised world. Autoimmune destruction of the adrenal cortex is caused by an immune reaction against the enzyme 21-hydroxylase (a phenomenon first described in 1992). This may be isolated or in the context of autoimmune polyendocrine syndrome (APS type 1 or 2), in which other hormone-producing organs, such as the thyroid and pancreas, may also be affected.Adrenal destruction is also a feature of adrenoleukodystrophy (ALD), and when the adrenal glands are involved in metastasis (seeding of cancer cells from elsewhere in the body, especially lung), hemorrhage (e.g. in Waterhouse–Friderichsen syndrome or antiphospholipid syndrome), particular infections (tuberculosis, histoplasmosis, coccidioidomycosis), or the deposition of abnormal protein in amyloidosis.

Pathophysiology
Hyponatremia can be caused by glucocorticoid deficiency. Low levels of glucocorticoids leads to systemic hypotension (one of the effects of cortisol is to increase peripheral resistance), which results in a decrease in stretch of the arterial baroreceptors of the carotid sinus and the aortic arch. This removes the tonic vagal and glossopharyngeal inhibition on the central release of ADH: high levels of ADH will ensue, which will subsequently lead to increase in water retention and hyponatremia.Differently from mineralocorticoid deficiency, glucocorticoid deficiency does not cause a negative sodium balance (in fact a positive sodium balance may occur).

Diagnosis
The best diagnostic tool to confirm adrenal insufficiency is the ACTH stimulation test; however, if a patient is suspected to be experiencing an acute adrenal crisis, immediate treatment with IV corticosteroids is imperative and should not be delayed for any testing, as the patients health can deteriorate rapidly and result in death without replacing the corticosteroids.Dexamethasone should be used as the corticosteroid if the plan is to do the ACTH stimulation test at a later time as it is the only corticosteroid that will not affect the test results.If not performed during crisis, then labs to be run should include: random cortisol, serum ACTH, aldosterone, renin, potassium and sodium. A CT of the adrenal glands can be used to check for structural abnormalities of the adrenal glands. An MRI of the pituitary can be used to check for structural abnormalities of the pituitary </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hypertrophic cardiomyopathy and explain in detail? [/INST] Hypertrophic cardiomyopathy (HCM, or HOCM when obstructive) is a condition in which the heart becomes thickened without an obvious cause. The parts of the heart most commonly affected are the interventricular septum and the ventricles.  This results in the heart being less able to pump blood effectively and also may cause electrical conduction problems.People who have HCM may have a range of symptoms.  People may be asymptomatic, or may have fatigue, leg swelling, and shortness of breath. It may also result in chest pain or fainting. Symptoms may be worse when the person is dehydrated.  Complications may include heart failure, an irregular heartbeat, and sudden cardiac death.HCM is most commonly inherited from a persons parents in an autosomal dominant pattern. It is often due to mutations in certain genes involved with making heart muscle proteins. Other inherited causes of left ventricular hypertrophy may include Fabry disease, Friedreichs ataxia, and certain medications such as tacrolimus. Other considerations for causes of enlarged heart are athletes heart and hypertension (high blood pressure). Making the diagnosis of HCM often involves a family history or pedigree, an electrocardiogram, echocardiogram, and stress testing. Genetic testing may also be done.  HCM can be distinguished from other inherited causes of cardiomyopathy by its autosomal dominant pattern, whereas Fabry disease is X-linked and Friedreichs Ataxia is inherited in an autosomal recessive pattern.Treatment may depend on symptoms and other risk factors.  Medications may include the use of beta blockers or disopyramide. An implantable cardiac defibrillator may be recommended in those with certain types of irregular heartbeat. Surgery, in the form of a septal myectomy or heart transplant, may be done in those who do not improve with other measures. With treatment, the risk of death from the disease is less than one percent per year.HCM affects about one in 500 people. Rates in men and women are about equal. People of all ages may be affected. The first modern description of the disease was by Donald Teare in 1958.

Signs and symptoms
The cause of HCM is variable. Many people are asymptomatic or mildly symptomatic, and many of those carrying disease genes for HCM do not have clinically detectable disease. The symptoms of HCM include shortness of breath due to stiffening and decreased blood filling of the ventricles, exertional chest pain (sometimes known as angina) due to reduced blood flow to the coronary arteries, uncomfortable awareness of the heart beat (palpitations), as well as disruption of the electrical system running through the abnormal heart muscle, lightheadedness, weakness, fainting and sudden cardiac death.Shortness of breath is largely due to increased stiffness of the left ventricle (LV), which impairs filling of the ventricles, but also leads to elevated pressure in the left ventricle and left atrium, causing back pressure and interstitial congestion in the lungs. Symptoms are not closely related to the presence or severity of an outflow tract gradient. Often, symptoms mimic those of congestive heart failure (esp. activity intolerance and dyspnea), but treatment of each is different. Beta blockers are used in both cases, but treatment with diuretics, a mainstay of CHF treatment, will exacerbate symptoms in hypertrophic obstructive cardiomyopathy by decreasing ventricular preload volume and thereby increasing outflow resistance (less blood to push aside the thickened obstructing tissue).Major risk factors for sudden death in individuals with HCM include prior history of cardiac arrest or ventricular fibrillation, spontaneous sustained ventricular tachycardia, abnormal exercise blood pressure and non-sustained ventricular tachycardia, unexplained syncope, family history of premature sudden death, and LVW thickness greater than 15 mm to 30 mm, on echocardiogram.
"Spike and dome" pulse and "triple ripple apical impulse" are two other signs that can be discovered in physical examination.

Genetics
Familial hypertrophic cardiomyopathy is inherited as an autosomal dominant trait and is attributed to mutations in one of a number of genes that encode for the sarcomere proteins.
Currently, about 50–60% of people with a high index of clinical suspicion for HCM will have a mutation identified in at least one of nine sarcomeric genes. Approximately 40% of these mutations occur in the β-myosin heavy chain gene on chromosome 14 q11.2-3, and approximately 40% involve the cardiac myosin-binding protein C gene. Since HCM is typically an autosomal dominant trait, children of a single HCM parent have 50% chance of inheriting the disease-causing mutation. Whenever such a mutation is identified, family-specific genetic testing can be used to identify relatives at-risk for the disease, although clinical severity and age of onset cannot be predicted.An insertion/deletion polymorphism in the gene encoding for angiotensin converting enzyme (ACE) alters the clinical phenotype of the disease. The D/D (deletion/deletion) genotype of ACE is associated with more marked hypertrophy of the left ventricle and may be associated with higher risk of adverse outcomes.Some mutations could have more harmful potential compared to others (β-myosin heavy chain). For example, troponin T mutations were originally associated with a 50% mortality before the age of 40. However, a more recent and larger study found a similar risk to other sarcomeric protein mutations. The age at disease onset of HCM with MYH7 is earlier and leads to more severe symptoms. Moreover, mutations on troponin C can alter Ca+2 sensibility on force development in cardiac muscle, these mutations are named after the amino acid that was changed after the location in which it happened, such as A8V, A31S, C84Y and D145E.

Diagnosis
A diagnosis of hypertrophic cardiomyopathy is based upon a number of features of the disease process. While there is use of echocardiography, cardiac catheterization, or cardiac MRI in the diagnosis of the disease, other important considerations include ECG, genetic testing (although not primarily used for diagnosis), and any family history of HCM or unexplained sudden death in otherwise healthy individuals.
In about 60 to 70% of the cases, cardiac MRI shows thickening of more than 15 mm of the lower part of the ventricular septum. T1-weighted imaging may identify scarring of cardiac tissues while T2-weighted imaging may identify oedema and inflammation of cardiac tissue which is associated with acute clinical signs of chest pain and fainting episodes.Pulsus bisferiens may occasional be found during examination.

Variants
Depending on whether the distortion of normal heart anatomy causes an obstruction of the outflow of blood from the left ventricle of the heart, HCM can be classified as obstructive or non-obstructive. The obstructive variant of HCM is hypertrophic obstructive cardiomyopathy (HOCM), also historically known as idiopathic hypertrophic subaortic stenosis(IHSS) or asymmetric septal hypertrophy (ASH). The diagnosis of left ventricular outflow tract obstruction is usually made by echocardiographic assessment and is defined as a peak left ventricular outflow tract gradient of ≥ 30 mmHg.Another, non-obstructive variant of HCM is apical hypertrophic cardiomyopathy (AHC), also called Yamaguchi syndrome. It was first described in individuals of Japanese descent.

Cardiac catheterization
Upon cardiac catheterization, catheters can be placed in the left ventricle and the ascending aorta, to measure the pressure difference between these structures. In normal individuals, during ventricular systole, the pressure in the ascending aorta and the left ventricle will equalize, and the aortic valve is open. In individuals with aortic stenosis or with HCM with an outflow tract gradient, there will be a pressure gradient (difference) between the left ventricle and the aorta, with the left ventricular pressure higher than the aortic pressure. This gradient represents the degree of obstruction that has to be overcome in order to eject blood from the left ventricle.The Brockenbrough–Braunwald–Morrow sign is observed in individuals with HCM with outflow tract gradient. This sign can be used to differentiate HCM from aortic stenosis. In individuals with aortic stenosis, after a premature ventricular contraction (PVC), the following ventricular contraction will be more forceful, and the pressure generated in the left ventricle will be higher. Because of the fixed obstruction that the stenotic aortic valve represents, the post-PVC ascending aortic pressure will increase as well. In individuals with HCM, however, the degree of obstruction will increase more than the force of contraction will increase in the post-PVC beat. The result of this is that the left ventricular pressure increases and the ascending aortic pressure decreases, with an increase in the LVOT gradient.While the Brockenbrough–Braunwald–Morrow sign is most dramatically demonstrated using simultaneous intra-cardiac and intra-aortic catheters, it can be seen on routine physical examination as a decrease in the pulse pressure in the post-PVC beat in individuals with HCM.

Screening
Although HCM may be asymptomatic, affected individuals may present with symptoms ranging from mild to critical heart failure and sudden cardiac death at any point from early childhood to seniority. HCM is the leading cause of sudden cardiac death in young athletes in the United States, and the most common genetic cardiovascular disorder. One study found that the incidence of sudden cardiac death in young competitive athletes declined in the Veneto region of Italy by 89% since the 1982 introduction of routine cardiac screening for athletes, from an unusually high starting rate. As of 2010, however, studies have shown that the incidence of sudden cardiac death, among all people with HCM, has declined to one percent or less. Screen-positive individuals who are diagnosed with cardiac disease are usually told to avoid competitive athletics.HCM can be detected with an echocardiogram (ECHO) with 80%+ accuracy, which can be preceded by screening with an electrocardiogram (ECG) to test for heart abnormalities. Cardiac magnetic resonance imaging (CMR), considered the gold standard for determining the physical properties of the left ventricular wall, can serve as an alternative screening tool when an echocardiogram provides inconclusive results. For example, the identification of segmental lateral ventricular hypertrophy cannot be accomplished with echocardiography alone. Also, left ventricular hypertrophy may be absent in children under thirteen years of age. This undermines the results of pre-adolescents echocardiograms.  Researchers, however, have studied asymptomatic carriers of an HCM-causing mutation through the use of CMR and have been able to identify crypts in the interventricular septal tissue in these people. It has been proposed that the formation of these crypts is an indication of myocyte disarray and altered vessel walls that may later result in the clinical expression of HCM. A possible explanation for this is that the typical gathering of family history only focuses on whether sudden death occurred or not. It fails to acknowledge the age at which relatives had had sudden cardiac death, as well as the frequency of the cardiac events. Furthermore, given the several factors necessary to be considered at risk for sudden cardiac death, while most of the factors do not have strong predictive value individually, there exists ambiguity regarding when to implement special treatment.

United States
There are several potential challenges associated with routine screening for HCM in the United States. First, the U.S. athlete population of 15 million is almost twice as large as Italys estimated athlete population. Second, these events are rare, with fewer than 100 deaths in the U.S. due to HCM in competitive athletes per year, or about 1 death per 220,000 athletes. Lastly, genetic testing would provide a definitive diagnosis; however, due to the numerous HCM-causing mutations, this method of screening is complex and is not cost-effective. Therefore, genetic testing in the United States is limited to individuals who exhibit clear symptoms of HCM, and their family members. This ensures that the test is not wasted on detecting other causes of ventricular hypertrophy (due to its low sensitivity), and that family members of the individual are educated on the potential risk of being carriers of the mutant gene(s).

Canada
Canadian genetic testing guidelines and recommendations for individuals diagnosed with HCM are as follows:
The main purpose of genetic testing is for screening family members.
According to the results, at-risk relatives may be encouraged to undergo extensive testing.
Genetic testing is not meant for confirming a diagnosis.
If the diagnosed individual has no relatives that are at risk, then genetic testing is not required.
Genetic testing is not intended for risk assessment or treatment decisions.
Evidence only supports clinical testing in predicting the progression and risk of developing complications of HCM.For individuals suspected of having HCM:

Genetic testing is not recommended for determining other causes of left ventricular hypertrophy (such as "athletes heart", hypertension, and cardiac amyloidosis).
HCM may be differentiated from other hypertrophy-causing conditions using clinical history and clinical testing.

Treatment
Asymptomatic people
A significant number of people with hypertrophic cardiomyopathy do not have any symptoms and will have a normal life expectancy, although they should avoid particularly strenuous activities or competitive athletics.  Asymptomatic people should be screened for risk factors for sudden cardiac death.  In people with resting or inducible outflow obstructions, situations that will cause dehydration or vasodilation (such as the use of vasodilatory or diuretic blood pressure medications) should be avoided.  Septal reduction therapy is not recommended in asymptomatic people.

Medications
The primary goal of medications is to relieve symptoms such as chest pain, shortness of breath, and palpitations. Beta blockers are considered first-line agents, as they can slow down the heart rate and decrease the likelihood of ectopic beats.  For people who cannot tolerate beta blockers, nondihydropyridine calcium channel blockers such as verapamil can be used, but are potentially harmful in people who also have low blood pressure or severe shortness of breath at rest. These medications also decrease the heart rate, though their use in people with severe outflow obstruction, elevated pulmonary artery wedge pressure, and low blood pressures should be done with caution.  Dihydropyridine calcium channel blockers should be avoided in people with evidence of obstruction. For people whose symptoms are not relieved by the above treatments, disopyramide can be considered for further symptom relief.  Diuretics can be considered for people with evidence of fluid overload, though cautiously used in those with evidence of obstruction. People who continue to have symptoms despite drug therapy can consider more invasive therapies. Intravenous phenylephrine (or another pure vasoconstricting agent) can be used in the acute setting of low blood pressure in those with obstructive hypertrophic cardiomyopathy who do not respond to fluid administration.Mavacamten was approved for medical use in the United States in April 2022.

Surgical septal myectomy
Surgical septal myectomy is an open-heart operation done to relieve symptoms in people who remain severely symptomatic despite medical therapy. It has been performed successfully since the early 1960s. Surgical septal myectomy uniformly decreases left ventricular outflow tract obstruction and improves symptoms, and in experienced centers has a surgical mortality of less than 1%, as well as 85% success rate.  It involves a median sternotomy (general anesthesia, opening the chest, and cardiopulmonary bypass) and removing a portion of the interventricular septum. Surgical myectomy resection that focuses just on the subaortic septum, to increase the size of the outflow tract to reduce Venturi forces, may be inadequate to abolish systolic anterior motion (SAM) of the anterior leaflet of the mitral valve. With this limited resection, the residual mid-septal bulge still redirects flow posteriorly; SAM persists because flow still gets behind the mitral valve. It is only when the deeper portion of the septal bulge is resected that flow is redirected anteriorly away from the mitral valve, abolishing SAM. With this in mind, a modification of the Morrow myectomy termed extended myectomy, mobilization and partial excision of the papillary muscles has become the excision of choice. In people with particularly large redundant mitral valves, anterior leaflet plication may be added to complete separation of the mitral valve and outflow. Complications of septal myectomy surgery include possible death, arrhythmias, infection, incessant bleeding, septal perforation/defect, and stroke.

Alcohol septal ablation
Alcohol septal ablation, introduced by Ulrich Sigwart in 1994, is a percutaneous technique that involves injection of alcohol into one or more septal branches of the left anterior descending artery. This is a catheter technique with results similar to the surgical septal myectomy procedure but is less invasive, since it does not involve general anaesthesia and opening of the chest wall and pericardium (which are done in a septal myectomy). In a select population with symptoms secondary to a high outflow tract gradient, alcohol septal ablation can reduce the symptoms of HCM.  In addition, older individuals and those with other medical problems, for whom surgical myectomy would pose increased procedural risk, would likely benefit from the less-invasive septal ablation procedure.When performed properly, an alcohol septal ablation induces a controlled heart attack, in which the portion of the interventricular septum that involves the left ventricular outflow tract is infarcted and will contract into a scar.  There is debate over which people are best served by surgical myectomy, alcohol septal ablation, or medical therapy.

Mitral clip
Since 2013, mitral clips have been implanted via catheter as a new strategy to correct the motion of the mitral valve in people with severe obstructive HCM. The device fastens together the mitral valve leaflets to improve the hearts blood outflow. The mitral clip has not yet established the long-term reliability of septal myectomy or alcohol septal ablation, but HCM specialists are increasingly offering the clip as a less-invasive treatment option.

Implantable pacemaker or defibrillator
The use of a pacemaker has been advocated in a subset of individuals, in order to cause asynchronous contraction of the left ventricle. Since the pacemaker activates the interventricular septum before the left ventricular free wall, the gradient across the left ventricular outflow tract may decrease. This form of treatment has been shown to provide less relief of symptoms and less of a reduction in the left ventricular outflow tract gradient when compared to surgical myectomy. Technological advancements have also led to the development of a dual-chamber pacemaker, which is only turned on when needed (in contrast to a regular pacemaker which provides a constant stimulus). Although the dual-chamber pacemaker has shown to decrease ventricular outflow tract obstruction, experimental trials have found only a few individuals with improved symptoms. Researchers suspect that these reports of improved symptoms are due to a placebo effect.The procedure includes an incision on the anterolateral area below the clavicle. Two leads are then inserted; one into the right atrium and the other into the right ventricular apex via the subclavian veins. Once in place, they are secured and attached to the generator which will remain inside the fascia, anterior to the pectoral muscle. Complications of this procedure include infection, electrical lead and generator malfunction which will require replacement.For people with HCM who exhibit one or more of the major risk factors for sudden cardiac death, an implantable cardioverter-defibrillator (ICD) or a combination pacemaker/ICD all-in-one unit may be recommended as an appropriate precaution. In 2014, European Society of Cardiology suggested a practical risk score to calculate that risk.

Cardiac transplantation
In cases that are unresponsive to all other forms of treatment, cardiac transplantation is one option. It is also the only treatment available for end-stage heart failure. However, transplantation must occur before the onset of symptoms such as pulmonary vessel hypertension, kidney malfunction, and thromboembolism in order for it to be successful. Studies have indicated a seven-year survival rate of 94% in people with HCM after transplantation.

Prognosis
A systematic review from 2002 concluded that: "Overall, HCM confers an annual mortality rate of about 1%... HCM may be associated with important symptoms and premature death but more frequently with no or relatively mild disability and normal life expectancy."

Children
Even though hypertrophic cardiomyopathy (HCM) may be present early in life and is most likely congenital, it is one of the most-uncommon cardiac malformations encountered in pediatric cardiology, largely because the presentation of symptoms is usually absent, incomplete, or delayed into adulthood. Most of the current information pertaining to HCM arises from studies in adult populations, and the implication of these observations for pediatric population is often uncertain. Nonetheless, recent studies in pediatric cardiology have revealed that HCM accounts for 42% of childhood cardiomyopathies, with an annual incidence rate of 0.47/100,000 in children. Further, in asymptomatic cases, sudden death is considered one of the most-feared complications associated with the disease in select pediatric populations. Consequently, the recommended practice is to screen children of affected individuals throughout childhood to detect cardiac abnormalities at an early stage, in the hope of preventing further complications of the disease.Generally, the diagnosis of HCM in a pediatric population is made during assessment for murmur, congestive heart failure, physical exhaustion, and genetic testing of children of affected individuals. Specifically, echocardiogram (ECHO) has been used as a definitive noninvasive diagnostic tool in nearly all children.  ECHO assesses cardiac ventricular size, wall thickness, systolic and diastolic function, and outflow obstruction. Thus, ECHO has been chosen as an ideal means to detect excessive wall thickening of cardiac muscle in HCM.For children with HCM, treatment strategies aim to reduce disease symptoms and lower the risk of sudden death. Due to the heterogeneity of the disease, treatment is usually modified according to individuals needs. β-blockers improve left ventricular filling and relaxation and thereby improve symptoms. In some children, β–blockers (e.g., propranolol) were shown effective to reduce the risk of sudden death. Further, calcium channel blockers (verapamil) and antiarrhythmic drugs may be used as an adjunct therapy to β-blockers in symptomatic children. Nonetheless, further testing is needed to determine their definitive benefits.

Other animals
Cats
Feline hypertrophic cardiomyopathy (HCM) is the most common heart disease in domestic cats; the disease process and genetics are believed to be similar to the disease in humans. In Maine Coon cats, HCM has been confirmed as an autosomal dominant inherited trait. Numerous cat breeds have HCM as a problem in the breed. The first genetic mutation (in cardiac myosin binding protein C) responsible for feline HCM was discovered in 2005 in Maine Coon cats. A test for this mutation (A31P) is available. About one-third of Maine Coon cats tested for the mutation are either heterozygous or homozygous for the mutation, although many of the cats that are heterozygous have no overt evidence of the disease on an echocardiogram (low penetrance). Some Maine Coon cats with clinical evidence of hypertrophic cardiomyopathy test negative for this mutation, strongly suggesting that another cause exists in the breed. The cardiac myosin binding protein C mutation identified in Maine Coon cats has not been found in any other breed of cat with HCM, but more recently another myosin binding protein C mutation has been identified in Ragdoll cats with HCM. As in humans, feline HCM is not present at birth but develops over time. It has been identified for the first time in cats as young as 6 months of age and at least as old as 7 years of age.Clinically, cats with hypertrophic cardiomyopathy commonly have a systolic anterior motion (SAM) of the mitral valve (see graphic). Cats with severe HCM often develop left heart failure (pulmonary edema; pleural effusion) because of severe diastolic dysfunction of the left ventricle. They may also develop a left atrial thrombus that embolizes, most commonly, to the terminal aorta creating acute pain and rear limb paralysis (see below). Sudden death can also occur but appears to be uncommon.Ultrasound of the heart (echocardiography) is necessary to diagnose HCM in cats. Measurement of circulating cardiac biomarkers, like N‐terminal‐proBNP (NT‐proBNP) and troponin I (TnI) may be used in cats to strengthen the suspicion of cardiac disease. There is a Point-of-care test for feline NT-proBNP available which can be used at the veterinary clinic when echocardiography is not possible to perform.There is no cure for feline HCM. Many but not all cats have a heart murmur. Many cats that have a heart murmur do not have HCM. Frequently the first signs that a cat has HCM are tachypnea/dyspnea due to heart failure or acute pain and paralysis due to systemic thromboembolism. While medication is commonly given to cats with HCM that have no clinical signs, no medication has been shown to be helpful at this stage and it has been shown that an ACE inhibitor is not beneficial until heart failure is present (at which time a diuretic is most beneficial). Diltiazem generally produces no demonstrable benefit. Atenolol is commonly administered when a severe systolic anterior motion of the mitral valve is present.Feline arterial thromboembolism (FATE) is a relatively common and devastating complication of feline HCM and other feline cardiomyopathies. The thrombus generally forms in the left atrium, most commonly the left auricle. The formation is thought to be primarily due to blood flow stasis. Classically, the thromboembolism lodges at the iliac trifurcation of the aorta, occluding either one or both of the common iliac arteries </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Burping and explain in detail? [/INST] Burping (also called belching and eructation) is the release of gas from the upper digestive tract (esophagus and stomach) of animals through the mouth. It is usually audible.
In humans, burping can be caused by normal eating processes, or as a side effect of other medical conditions. There is a range of levels of social acceptance for burping: within certain context and cultures, burping is acceptable, while in others it is offensive or unacceptable. Failure to burp can cause pain or other negative effects.
Humans are not the only animals that burp: it is very common among other mammals. In particular, burping by domesticated ruminants, such as cows or sheep, is a major contributor of methane emissions which cause climate change and negatively impacts animal agriculture on the environment. Significant research is being done to find mitigation strategies for ruminant burping, i.e. modifying the animals diets with Asparagopsis taxiformis (red seaweed).

Causes
Burping is usually caused by swallowing air when eating or drinking and subsequently expelling it, in which case the expelled gas is mainly a mixture of nitrogen and oxygen.
Burps can be caused by drinking beverages containing carbon dioxide, such as beer and soft drinks, in which case the expelled gas is mainly carbon dioxide.
Diabetes drugs such as metformin and exenatide can cause burping, especially at higher doses. This often resolves in a few weeks.
Burping combined with other symptoms such as dyspepsia, nausea and heartburn may be a sign of an ulcer or hiatal hernia, and should be reviewed by a physician.
Other causes of burping include food allergies, gallbladder diseases, H. pylori, acid reflux disease and gastritis.

Complications
In microgravity environments, burping is frequently associated with regurgitation. With reduced gravity, the stomach contents are more likely to rise up into the esophagus when the gastroesophageal sphincter is relaxed, along with the expelled air.

Disorders
Inability to burp is uncommon.
Chest pain associated with burping can occur, but is rare.
Retrograde cricopharyngeus dysfunction (R-CPD) involves the cricopharyngeus muscle not being able to relax. R-CPD was first discovered in 2015 when a user inquired with symptoms on Reddit.  Several other users found the post online, mentioning they had a similar condition. Common symptoms include gurgling noises, bloating, flatulence, lesser but common symptoms can be potentially painful hiccups, nausea, constipation, hypersalivation, or shortness of breath.   80% of patients were successfully treated with Botox after a single injection. An alternative if the injection is unsuccessful is to undergo partial cricopharyngeal myotomy.

Society and culture
Acceptance
Some South Asian cultures view burping as acceptable in particular situations. For example, a burping guest can be a sign to the host that the meal satisfied them and they are full.In Japan, burping during a meal is considered bad manners. Burping during a meal is also considered unacceptable in Western cultures, such as North America and Europe. In Middle Eastern countries, it is not acceptable to burp out loud in public, and one should silence ones burp, or at least attempt to do so.Despite virtually no scientific research on the subject, small online communities exist for burping as a sexual fetish. Online, both men and women of any sexual orientation anecdotally report some attraction to burping, with what appears to be psychological and/or behavioural overlaps with other sexual fetishes including body inflation, feederism, vorarephilia, and farting fetishes. Anecdotally, the loudness aspect appears to be an important element to burp fetishists. Despite being a rather uncommon fetish, it continues to follow a general well-known pattern of sexual behaviour where hearing influences sexual arousal and response, noting that "it is the noise made rather than the action itself that appears to be what is sexualized and/or interpreted by the fetishist as sexually pleasurable and arousing".

Infants
Babies are likely to accumulate gas in the stomach while feeding and experience considerable discomfort (and agitation) until assisted. Burping an infant involves placing the child in a position conducive to gas expulsion (for example against the adults shoulder, with the infants stomach resting on the adults chest) and then lightly patting the lower back.  Because burping can cause vomiting, a "burp cloth" or "burp pad" is sometimes employed on the shoulder to protect clothing.

Contest
The Guinness World Record for the loudest burp is 109.9 dB, set by Paul Hunn at Butlins Bognor Regis, United Kingdom, on 23 August 2009. This is louder than a jackhammer at a distance of 1 m (3 ft 3 in).

Burped speech
It is possible to voluntarily induce burping through swallowing air and then expelling it, and by manipulation of the vocal tract produce burped speech.
While this is often employed as a means of entertainment or competition, it can also act as an alternative means of vocalisation for people who have undergone a laryngectomy, with the burp replacing laryngeal phonation. This is known as esophageal speech.

Other animals
Many other mammals, such as cows, dogs and sheep, also burp.

Ruminants
Much of the gas expelled is produced as a byproduct of the ruminants digestive process </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Cardiac fibrosis and explain in detail? [/INST] Cardiac fibrosis commonly refers to the excess deposition of extracellular matrix in the cardiac muscle, but the term may also refer to an abnormal thickening of the heart valves due to inappropriate proliferation of cardiac fibroblasts. Fibrotic cardiac muscle is stiffer and less compliant and is seen in the progression to heart failure. The description below focuses on a specific mechanism of valvular pathology but there are other causes of valve pathology and fibrosis of the cardiac muscle.
Fibrocyte cells normally secrete collagen, and function to provide structural support for the heart. When over-activated this process causes thickening and fibrosis of the valve, with white tissue building up primarily on the tricuspid valve, but also occurring on the pulmonary valve. The thickening and loss of flexibility eventually may lead to valvular dysfunction and right-sided heart failure.

Types
Following are types of myocardial fibrosis:

Interstitial fibrosis, which is unspecific, and has been described in congestive heart failure, hypertension, and normal aging.
Subepicardial fibrosis, also unspecific, and is associated with non-infarction diagnoses such as myocarditis and non-ischemic cardiomyopathy.
Replacement fibrosis, which indicates an older infarction.

Connection with excess blood serotonin (5-HT)
Certain diseases such as neuroendocrine tumor of the small intestine (also known by the obsolete term carcinoid), which sometimes release large amounts of 5-hydroxytryptamine, commonly known as 5-HT or serotonin into the blood, may produce a characteristic pattern of mostly right-sided cardiac fibrosis which can be identified with echocardiography. Cardiac fibrosis is a significant source of morbidity and mortality in patients with functional neuroendocrine tumors. This pathology has also been seen in certain East-African tribes who eat foods (Matoke —a green banana) containing excess amounts of serotonin.

Connection with direct serotonergic agonist drugs
Elevated prevalence of cardiac fibrosis and related valvopathies was found to be associated with use of a number of unrelated drugs following long-term statistical analysis once the drugs had been on the market for some time. The cause of this was unknown at the time, but eventually it was realised that all the implicated drugs acted as agonists at 5-HT2B receptors in the heart in addition to their intended sites of action elsewhere in the body.The precise mechanisms involved remain elusive however, as while the cardiotoxicity shows some dose–response relationship, it does not always develop, and consistent daily use over an extended period tends to be most strongly predictive of development of valvopathy.The drugs most classically associated with the condition are weight loss drugs such as fenfluramine and chlorphentermine, and antiparkinson drugs such as pergolide and cabergoline, which are prescribed for chronic use.The heart valve changes seen with moderate and intermittent use can result in permanent damage and life-threatening heart problems if use of the causative drug is increased or continued, however longitudinal studies of former patients suggest that the damage will heal over time to some extent at least.

Anorectics
Some appetite suppressant drugs such as fenfluramine (which in combination with phentermine was marketed as Pondimin and commonly referred to as fen-phen), chlorphentermine, and aminorex (along with its analogue 4-Methylaminorex which has seen sporadic use as a recreational drug) induce a similar pattern of cardiac fibrosis (and pulmonary hypertension), apparently by overstimulating 5HT2B receptors on the cardiac fibroblast cells.These drugs consequently tend to cause increased risk of heart valve damage and subsequent heart failure, which eventually led to them being withdrawn from the market.

Antimigraine drugs
Certain antimigraine drugs which are targeted at serotonin receptors as vasoconstrictive agents, have long been known to be associated with pulmonary hypertension and Raynauds phenomenon (both vasoconstrictive effects), as well as retroperitoneal fibrosis (a fibrotic cell/fibrocyte proliferation effect, thought to be similar to cardiac valve fibrosis).These drugs include ergotamine and methysergide and both drugs can also cause cardiac fibrosis.

Antiparkinson drugs
Certain antiparkinson drugs, although targeted at dopaminergic receptors, cross-react with serotoninergic 5-HT2B receptors as well, and have been reported to cause cardiac fibrosis.
These drugs include pergolide and cabergoline.

Antihypertensive drugs
Guanfacine may be a 5-HT2B agonist, based on the results of theoretical modeling and high-throughput screening.

Pergolide
Pergolide was an antiparkinson medications that was in decreasing use since reported in 2003 to be associated with cardiac fibrosis. In March 2007, pergolide was withdrawn from the U.S. market due to serious valvular damage that was shown in two independent studies.

Cabergoline
Like pergolide, cabergoline has been linked to cardiac damage </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Fasciculation and explain in detail? [/INST] A fasciculation, or muscle twitch, is a spontaneous, involuntary muscle contraction and relaxation, involving fine muscle fibers. They are common, with as many as 70% of people experiencing them. They can be benign, or associated with more serious conditions.  When no cause or pathology is identified, they are diagnosed as benign fasciculation syndrome.

Diagnosis
The most effective way to detect fasciculations may be surface electromyography (EMG). Surface EMG is more sensitive than needle electromyography and clinical observation in the detection of fasciculation in people with amyotrophic lateral sclerosis.Deeper areas of contraction can be detected by electromyography (EMG) testing, though they can happen in any skeletal muscle in the body. Fasciculations arise as a result of spontaneous depolarization of a lower motor neuron leading to the synchronous contraction of all the skeletal muscle fibers within a single motor unit. An example of normal spontaneous depolarization is the constant contractions of cardiac muscle, causing the heart to beat. Usually, intentional movement of the involved muscle causes fasciculations to cease immediately, but they may return once the muscle is at rest again.
Tics must also be distinguished from fasciculations. Small twitches of the upper or lower eyelid, for example, are not tics, because they do not involve a whole muscle, rather are twitches of a few muscle fibre bundles, that are not suppressible.

Causes
Fasciculations have a variety of causes, the majority of which are benign, but can also be due to disease of the motor neurons. They are encountered by up to 70% of all healthy people, though for most, it is quite infrequent. In some cases, the presence of fasciculations can be annoying and interfere with quality of life. If a neurological examination is otherwise normal and EMG testing does not indicate any additional pathology, a diagnosis of  benign fasciculation syndrome is usually made.

Risk factors
Risk factors for benign fasciculations are age, stress, fatigue, and strenuous exercise. Fasciculations can be caused by anxiety, caffeine or alcohol and thyroid disease </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Goodpasture syndrome and explain in detail? [/INST] Goodpasture syndrome (GPS), also known as anti–glomerular basement membrane disease,  is a rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs, glomerulonephritis, and kidney failure. It is thought to attack the alpha-3 subunit of type IV collagen, which has therefore been referred to as Goodpastures antigen. Goodpasture syndrome may quickly result in permanent lung and kidney damage, often leading to death. It is treated with medications that suppress the immune system such as corticosteroids and cyclophosphamide, and with plasmapheresis, in which the antibodies are removed from the blood.
The disease was first described by an American pathologist Ernest Goodpasture of Vanderbilt University in 1919 and was later named in his honor.

Signs and symptoms
The anti–glomerular basement membrane (GBM) antibodies primarily attack the kidneys and lungs, although, generalized symptoms like malaise, weight loss, fatigue, fever, and chills are also common, as are joint aches and pains. 60 to 80% of those with the condition experience both lung and kidney involvement; 20-40% have kidney involvement alone, and less than 10% have lung involvement alone. Lung symptoms usually antedate kidney symptoms and usually include: coughing up blood, chest pain (in less than 50% of cases overall), cough, and shortness of breath. Kidney symptoms usually include blood in the urine, protein in the urine, unexplained swelling of limbs or face, high amounts of urea in the blood, and high blood pressure.

Cause
While the exact cause is unknown, the genetic predisposition to GPS involves the human leukocyte antigen (HLA) system, specifically HLA-DR15. In addition to genetic susceptibility, an initial environmental insult to the pulmonary vasculature is needed to allow the anti-glomerular basement membrane (anti-GBM) antibodies to reach the alveolar capillaries. Examples of such an insult include: exposure to organic solvents (e.g. chloroform) or hydrocarbons, exposure to tobacco smoke, infection (such as influenza A), cocaine inhalation, metal dust inhalation, bacteremia, sepsis, high-oxygen environments, and antilymphocyte therapies (especially with monoclonal antibodies). Exposure to dry cleaning chemicals and Paraquat brand weed killer have also been implicated as potential insults.  In GPS, anti-GBM antibodies are produced and circulated throughout the bloodstream, damaging the membranes lining the lungs and kidneys as well as targeting their capillaries.

Pathophysiology
GPS is caused by abnormal plasma cell production of anti-GBM antibodies. The major target of these abnormal antibodies is the non-collagen domain of the alpha-3 chain of type 4 collagen, which is mostly found in the basal membranes of glomerular and alveolar capillaries, explaining the obscurely specific symptoms of this condition. This preferred targeting of these alpha-3 collagen chains specifically in the basal membranes of glomerular and alveolar capillaries can be explained by the higher accessible exposure of epitopes, a larger expansion of the alpha-3 collagen units, and because these alpha-3 collagen chains structurally provide higher accessibility for the targeting antibodies.  These antibodies bind their reactive epitopes to the basement membranes and activate the complement cascade, leading to the death of tagged cells. A specific antibody and epitope binding that shows the highest affinity and is pathogenic occurs between GPA antibodies and the anti-GBM epitope region, designated EA, which is residues 17-31 of the alpha 3 subunit of non-collagenous domain of type IV collagen. T cells are also implicated, though it is generally considered a type II hypersensitivity reaction.

Diagnosis
The diagnosis of GPS is often difficult, as numerous other diseases can cause the various manifestations of the condition and the condition itself is rare. The most accurate means of achieving the diagnosis is testing the affected tissues by means of a biopsy, especially the kidney, as it is the best-studied organ for obtaining a sample for the presence of anti-GBM antibodies </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Water intoxication and explain in detail? [/INST] Water intoxication, also known as water poisoning, hyperhydration, overhydration, or water toxemia, is a potentially fatal disturbance in brain functions that results when the normal balance of electrolytes in the body is pushed outside safe limits by excessive water intake.
Under normal circumstances, accidentally consuming too much water is exceptionally rare. Nearly all deaths related to water intoxication in normal individuals have resulted either from water-drinking contests, in which individuals attempt to consume large amounts of water, or from long bouts of exercise during which excessive amounts of fluid were consumed. In addition, water cure, a method of torture in which the victim is forced to consume excessive amounts of water, can cause water intoxication.Water, just like any other substance, can be considered a poison when over-consumed in a brief period of time. Water intoxication mostly occurs when water is being consumed in a high quantity without adequate electrolyte intake.Excess of body water may also be a result of a medical condition or improper treatment; see "hyponatremia" for some examples. Water is considered one of the least toxic chemical compounds, with an LD50 of over 150 ml/kg in rats.

Risk factors
Low body mass (infants)
It can be very easy for children under one year old (especially those under nine months) to absorb too much water. Because of their small body mass, it is easy for them to take in a large amount of water relative to body mass and total body sodium stores.

Endurance sports
Marathon runners are susceptible to water intoxication if they drink too much while running. This is caused when sodium levels drop below 135 mmol/L when athletes consume large amounts of fluid. This has been noted to be the result of the encouragement of excessive fluid replacement by various guidelines. This has largely been identified in marathon runners as a dilutional hyponatremia. A study conducted on runners completing the 2002 Boston Marathon found that thirteen percent finished the race with hyponatremia. The study concluded that the strongest predictor of hyponatremia was weight gain while racing (over-hydration), and hyponatremia was just as likely to occur in runners who chose sports drinks as those who chose water.

Military training
Hyponatremia and other physical conditions associated with water intoxication are more often seen in those participating in military training. One US Army study found 17 trainees were admitted to hospital over a years period for water intoxication while another found that three soldiers had died, leading to a recommendation that no more than 1-1.5L of water should be consumed per hour of heavy sweating.

Overexertion and heat stress
Any activity or situation that promotes heavy sweating can lead to water intoxication when water is consumed to replace lost fluids. Persons working in extreme heat and/or humidity for long periods must take care to drink and eat in ways that help to maintain electrolyte balance. People using drugs such as MDMA (often referred to colloquially as "Ecstasy") may overexert themselves, perspire heavily, feel increased thirst, and then drink large amounts of water to rehydrate, leading to electrolyte imbalance and water intoxication – this is compounded by MDMA use increasing the levels of antidiuretic hormone (ADH), decreasing the amount of water lost through urination. Even people who are resting quietly in extreme heat or humidity may run the risk of water intoxication if they drink large amounts of water over short periods for rehydration.

Psychiatric conditions
Psychogenic polydipsia is the psychiatric condition in which patients feel compelled to drink large quantities of water, thus putting them at risk of water intoxication. This condition can be especially dangerous if the patient also exhibits other psychiatric indications (as is often the case), as the care-takers might misinterpret the hyponatremic symptoms.

Iatrogenic
When an unconscious person is being fed intravenously (for example, total parenteral nutrition) or via a nasogastric tube, the fluids given must be carefully balanced in composition to match fluids and electrolytes lost. These fluids are typically hypertonic, and so water is often co-administered. If the electrolytes are not monitored (even in an ambulatory patient), either hypernatremia or hyponatremia may result.Some neurological/psychiatric medications (oxcarbazepine, among others) have been found to cause hyponatremia in some patients. Patients with diabetes insipidus are particularly vulnerable due to rapid fluid processing.

Pathophysiology
At the onset of this condition, fluid outside the cells has an excessively low amount of solutes, such as sodium and other electrolytes, in comparison to fluid inside the cells, causing the fluid to move into the cells to balance its osmotic concentration. This causes the cells to swell. The swelling increases intracranial pressure in the brain, which leads to the first observable symptoms of water intoxication: headache, personality changes, changes in behavior, confusion, irritability, and drowsiness. These are sometimes followed by difficulty breathing during exertion, muscle weakness & pain, twitching, or cramping, nausea, vomiting, thirst, and a dulled ability to perceive and interpret sensory information. As the condition persists, papillary and vital signs may result including bradycardia and widened pulse pressure. The cells in the brain may swell to the point where blood flow is interrupted resulting in cerebral edema. Swollen brain cells may also apply pressure to the brain stem causing central nervous system dysfunction. Both cerebral edema and interference with the central nervous system are dangerous and could result in seizures, brain damage, coma or death.

Prevention
Water intoxication can be prevented if a persons intake of water does not grossly exceed their losses </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pulmonary fibrosis and explain in detail? [/INST] Pulmonary fibrosis is a condition in which the lungs become scarred over time. Symptoms include shortness of breath, a dry cough, feeling tired, weight loss, and nail clubbing. Complications may include pulmonary hypertension, respiratory failure, pneumothorax, and lung cancer.Causes include environmental pollution, certain medications, connective tissue diseases, infections, and interstitial lung diseases. Idiopathic pulmonary fibrosis (IPF), an interstitial lung disease of unknown cause, is most common. Diagnosis may be based on symptoms, medical imaging, lung biopsy, and lung function tests.There is no cure and there are limited treatment options available. Treatment is directed towards efforts to improve symptoms and may include oxygen therapy and pulmonary rehabilitation. Certain medications may be used to try to slow the worsening of scarring. Lung transplantation may occasionally be an option. At least 5 million people are affected globally. Life expectancy is generally less than five years.

Signs and symptoms
Symptoms of pulmonary fibrosis are mainly:
Shortness of breath, particularly with exertion
Chronic dry, hacking coughing
Fatigue and weakness
Chest discomfort including chest pain
Loss of appetite and rapid weight lossPulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. Sometimes fine inspiratory crackles can be heard at the lung bases on auscultation. A chest X-ray may or may not be abnormal, but high-resolution CT will frequently demonstrate abnormalities.

Cause
Pulmonary fibrosis may be a secondary effect of other diseases.  Most of these are classified as interstitial lung diseases. Examples include autoimmune disorders, viral infections and bacterial infection like tuberculosis which may cause fibrotic changes in both lungs upper or lower  lobes and other microscopic injuries to the lung. However, pulmonary fibrosis can also appear without any known cause.  In this case,  it is termed "idiopathic". Most idiopathic cases are diagnosed as idiopathic pulmonary fibrosis.  This is a diagnosis of exclusion of a characteristic set of histologic/pathologic features known as usual interstitial pneumonia (UIP). In either case, there is a growing body of evidence which points to a genetic predisposition in a subset of patients. For example, a mutation in surfactant protein C (SP-C) has been found to exist in some families with a history of pulmonary fibrosis. Autosomal dominant mutations in the TERC or TERT genes, which encode telomerase, have been identified in about 15 percent of pulmonary fibrosis patients.Diseases and conditions that may cause pulmonary fibrosis as a secondary effect include:
Inhalation of environmental and occupational pollutants, such as metals in asbestosis, silicosis and exposure to certain gases. Coal miners, ship workers and sand blasters among others are at higher risk.
Hypersensitivity pneumonitis, most often resulting from inhaling dust contaminated with bacterial, fungal, or animal products
Cigarette smoking can increase the risk or make the illness worse
Some typical connective tissue diseases such as rheumatoid arthritis, ankylosing spondylitis, SLE and scleroderma
Other diseases that involve connective tissue, such as sarcoidosis and granulomatosis with polyangiitis
Infections, including COVID-19
Certain medications, e.g. amiodarone, bleomycin (pingyangmycin), busulfan, methotrexate, apomorphine, and nitrofurantoin
Radiation therapy to the chest

Pathogenesis
Pulmonary fibrosis involves gradual exchange of normal lung parenchyma with fibrotic tissue. The replacement of normal lung with scar tissue causes irreversible decrease in oxygen diffusion capacity, and the resulting stiffness or decreased compliance makes pulmonary fibrosis a restrictive lung disease.
Pulmonary fibrosis is perpetuated by aberrant wound healing, rather than chronic inflammation.
It is the main cause of restrictive lung disease that is intrinsic to the lung parenchyma. In contrast, quadriplegia and kyphosis are examples of causes of restrictive lung disease that do not necessarily involve pulmonary fibrosis.

Diagnosis
The diagnosis can be confirmed by lung biopsy. A videoscopic assisted thoracoscopic wedge biopsy (VATS) under general anesthesia may be necessary to obtain enough tissue to make an accurate diagnosis. This kind of biopsy involves placement of several tubes through the chest wall, one of which is used to cut off a piece of lung to send for evaluation. The removed tissue is examined histopathologically by microscopy to confirm the presence and pattern of fibrosis as well as presence of other features that may indicate a specific cause e.g. specific types of mineral dust or possible response to therapy e.g. a pattern of so-called non-specific interstitial fibrosis.
Misdiagnosis is common because, while overall pulmonary fibrosis is not rare, each individual type of pulmonary fibrosis is uncommon and the evaluation of patients with these diseases is complex and requires a multidisciplinary approach. Terminology has been standardized but difficulties still exist in their application. Even experts may disagree with the classification of some cases.On spirometry, as a restrictive lung disease, both the FEV1 (forced expiratory volume in 1 second) and FVC (forced vital capacity) are reduced so the FEV1/FVC ratio is normal or even increased in contrast to obstructive lung disease where this ratio is reduced. The values for residual volume and total lung capacity are generally decreased in restrictive lung disease.

Treatment
Pulmonary fibrosis creates scar tissue. The scarring is permanent once it has developed. Slowing the progression and prevention depends on the underlying cause:

Treatment options for idiopathic pulmonary fibrosis are very limited. Though research trials are ongoing, there is no evidence that any medications can significantly help this condition. Lung transplantation is the only therapeutic option available in severe cases. Since some types of lung fibrosis can respond to corticosteroids (such as prednisone) and/or other medications that suppress the bodys immune system, these types of drugs are sometimes prescribed in an attempt to slow the processes that lead to fibrosis.The immune system is felt to play a central role in the development of many forms of pulmonary fibrosis. The goal of treatment with immune suppressive agents such as corticosteroids is to decrease lung inflammation and subsequent scarring. Responses to treatment are variable. Those whose conditions improve with immune suppressive treatment probably do not have idiopathic pulmonary fibrosis, for idiopathic pulmonary fibrosis has no significant treatment or cure.Two pharmacological agents intended to prevent scarring in mild idiopathic fibrosis are pirfenidone, which reduced reductions in the 1-year rate of decline in FVC. Pirfenidone also reduced the decline in distances on the 6-minute walk test, but had no effect on respiratory symptoms. The second agent is nintedanib, which acts as antifibrotic, mediated through the inhibition of a variety of tyrosine kinase receptors (including platelet-derived growth factor, fibroblast growth factor, and vascular endothelial growth factor). A randomized clinical trial showed it reduced lung-function decline and acute exacerbations.
Anti-inflammatory agents have only limited success in reducing the fibrotic process. Some of the other types of fibrosis, such as non-specific interstitial pneumonia, may respond to immunosuppressive therapy such as corticosteroids. However, only a minority of patients respond to corticosteroids alone, so additional immunosuppressants, such as cyclophosphamide, azathioprine, methotrexate, penicillamine, and cyclosporine may be used </s>