<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 Lupus and explain in detail? [/INST] Lupus, technically known as systemic lupus erythematosus (SLE), is an autoimmune disease in which the bodys immune system mistakenly attacks healthy tissue in many parts of the body. Symptoms vary among people and may be mild to severe. Common symptoms include painful and swollen joints, fever, chest pain, hair loss, mouth ulcers, swollen lymph nodes, feeling tired, and a red rash which is most commonly on the face. Often there are periods of illness, called flares, and periods of remission during which there are few symptoms.The cause of SLE is not clear. It is thought to involve a mixture of genetics combined with environmental factors. Among identical twins, if one is affected there is a 24% chance the other one will also develop the disease. Female sex hormones, sunlight, smoking, vitamin D deficiency, and certain infections are also believed to increase a persons risk. The mechanism involves an immune response by autoantibodies against a persons own tissues. These are most commonly anti-nuclear antibodies and they result in inflammation. Diagnosis can be difficult and is based on a combination of symptoms and laboratory tests. There are a number of other kinds of lupus erythematosus including discoid lupus erythematosus, neonatal lupus, and subacute cutaneous lupus erythematosus.There is no cure for SLE, but there are experimental and symptomatic treatments. Treatments may include NSAIDs, corticosteroids, immunosuppressants, hydroxychloroquine, and methotrexate. Although corticosteroids are rapidly effective, long-term use results in side effects. Alternative medicine has not been shown to affect the disease. Life expectancy is lower among people with SLE, but with modern treatment, 80-90% of patients can have a normal life span. SLE significantly increases the risk of cardiovascular disease with this being the most common cause of death. While women with lupus have higher risk pregnancies, most are successful.Rate of SLE varies between countries from 20 to 70 per 100,000. Women of childbearing age are affected about nine times more often than men. While it most commonly begins between the ages of 15 and 45, a wide range of ages can be affected. Those of African, Caribbean, and Chinese descent are at higher risk than those of European descent. Rates of disease in the developing world are unclear. Lupus is Latin for "wolf": the disease was so-named in the 13th century as the rash was thought to appear like a wolfs bite.

Signs and symptoms
SLE is one of several diseases known as "the great imitator" because it often mimics or is mistaken for other illnesses. SLE is a classical item in differential diagnosis, because SLE symptoms vary widely and come and go unpredictably. Diagnosis can thus be elusive, with some people having unexplained symptoms of SLE for years.Common initial and chronic complaints include fever, malaise, joint pains, muscle pains, and fatigue. Because these symptoms are so often seen in association with other diseases, these signs and symptoms are not part of the diagnostic criteria for SLE. When occurring in conjunction with other signs and symptoms, however, they are considered suggestive.While SLE can occur in both males and females, it is found far more often in women, and the symptoms associated with each sex are different. Females tend to have a greater number of relapses, a low white blood cell count, more arthritis, Raynauds phenomenon, and psychiatric symptoms. Males tend to have more seizures, kidney disease, serositis (inflammation of tissues lining the lungs and heart), skin problems, and peripheral neuropathy.

Skin
As many as 70% of people with lupus have some skin symptoms. The three main categories of lesions are chronic cutaneous (discoid) lupus, subacute cutaneous lupus, and acute cutaneous lupus. People with discoid lupus may exhibit thick, red scaly patches on the skin. Similarly, subacute cutaneous lupus manifests as red, scaly patches of skin but with distinct edges. Acute cutaneous lupus manifests as a rash. Some have the classic malar rash (commonly known as the butterfly rash) associated with the disease. This rash occurs in 30 to 60% of people with SLE.Hair loss, mouth and nasal ulcers, and lesions on the skin are other possible manifestations.

Muscles and bones
The most commonly sought medical attention is for joint pain, with the small joints of the hand and wrist usually affected, although all joints are at risk. More than 90 percent of those affected will experience joint or muscle pain at some time during the course of their illness. Unlike rheumatoid arthritis, lupus arthritis is less disabling and usually does not cause severe destruction of the joints. Fewer than ten percent of people with lupus arthritis will develop deformities of the hands and feet. People with SLE are at particular risk of developing osteoarticular tuberculosis.A possible association between rheumatoid arthritis and SLE has been suggested, and SLE may be associated with an increased risk of bone fractures in relatively young women.

Blood
Anemia is common in children with SLE and develops in about 50% of cases. Low platelet count and white blood cell count may be due to the disease or a side effect of pharmacological treatment. People with SLE may have an association with antiphospholipid antibody syndrome (a thrombotic disorder), wherein autoantibodies to phospholipids are present in their serum. Abnormalities associated with antiphospholipid antibody syndrome include a paradoxical prolonged partial thromboplastin time (which usually occurs in hemorrhagic disorders) and a positive test for antiphospholipid antibodies; the combination of such findings have earned the term "lupus anticoagulant-positive". Another autoantibody finding in SLE is the anti-cardiolipin antibody, which can cause a false positive test for syphilis.

Heart
SLE may cause pericarditis—inflammation of the outer lining surrounding the heart, myocarditis—inflammation of the heart muscle, or endocarditis—inflammation of the inner lining of the heart. The endocarditis of SLE is non-infectious, and is also called Libman–Sacks endocarditis. It involves either the mitral valve or the tricuspid valve. Atherosclerosis also occurs more often and advances more rapidly than in the general population.Steroids are sometimes prescribed as an anti-inflammatory treatment for lupus; however, they can increase ones risk for heart disease, high cholesterol, and atherosclerosis.

Lungs
SLE can cause pleuritic pain as well as inflammation of the pleurae known as pleurisy, which can rarely give rise to shrinking lung syndrome involving a reduced lung volume. Other associated lung conditions include pneumonitis, chronic diffuse interstitial lung disease, pulmonary hypertension, pulmonary emboli, and pulmonary hemorrhage.

Kidneys
Painless passage of blood or protein in the urine may often be the only presenting sign of kidney involvement. Acute or chronic renal impairment may develop with lupus nephritis, leading to acute or end-stage kidney failure. Because of early recognition and management of SLE with immunosuppressive drugs or corticosteroids, end-stage renal failure occurs in less than 5% of cases; except in the black population, where the risk is many times higher.
The histological hallmark of SLE is membranous glomerulonephritis with "wire loop" abnormalities. This finding is due to immune complex deposition along the glomerular basement membrane, leading to a typical granular appearance in immunofluorescence testing.

Neuropsychiatric
Neuropsychiatric syndromes can result when SLE affects the central or peripheral nervous system. The American College of Rheumatology defines 19 neuropsychiatric syndromes in systemic lupus erythematosus. The diagnosis of neuropsychiatric syndromes concurrent with SLE (now termed as NPSLE), is one of the most difficult challenges in medicine, because it can involve so many different patterns of symptoms, some of which may be mistaken for signs of infectious disease or stroke.A common neurological disorder people with SLE have is headache, although the existence of a specific lupus headache and the optimal approach to headache in SLE cases remains controversial.
Other common neuropsychiatric manifestations of SLE include cognitive dysfunction, mood disorder, cerebrovascular disease, seizures, polyneuropathy, anxiety disorder, psychosis, depression, and in some extreme cases, personality disorders. Steroid psychosis can also occur as a result of treating the disease. It can rarely present with intracranial hypertension syndrome, characterized by an elevated intracranial pressure, papilledema, and headache with occasional abducens nerve paresis, absence of a space-occupying lesion or ventricular enlargement, and normal cerebrospinal fluid chemical and hematological constituents.More rare manifestations are acute confusional state, Guillain–Barré syndrome, aseptic meningitis, autonomic disorder, demyelinating syndrome, mononeuropathy (which might manifest as mononeuritis multiplex), movement disorder (more specifically, chorea), myasthenia gravis, myelopathy, cranial neuropathy and plexopathy.Neurological disorders contribute to a significant percentage of morbidity and mortality in people with lupus. As a result, the neural side of lupus is being studied in hopes of reducing morbidity and mortality rates. One aspect of this disease is severe damage to the epithelial cells of the blood–brain barrier. In certain regions, depression affects up to 60% of women with SLE.

Eyes
Eye involvement is seen in up to one-third of people. The most common diseases are dry eye syndrome and secondary Sjögrens syndrome, but episcleritis, scleritis, retinopathy (more often affecting both eyes than one), ischemic optic neuropathy, retinal detachment, and secondary angle-closure glaucoma may occur. In addition, the medications used to treat SLE can cause eye disease: long-term glucocorticoid use can cause cataracts and secondary open-angle glaucoma, and long-term hydroxychloroquine treatment can cause vortex keratopathy and maculopathy.

Reproductive
While most pregnancies have positive outcomes, there is a greater risk of adverse events occurring during pregnancy. SLE causes an increased rate of fetal death in utero and spontaneous abortion (miscarriage). The overall live-birth rate in people with SLE has been estimated to be 72%. Pregnancy outcome appears to be worse in people with SLE whose disease flares up during pregnancy.Neonatal lupus is the occurrence of SLE symptoms in an infant born from a mother with SLE, most commonly presenting with a rash resembling discoid lupus erythematosus, and sometimes with systemic abnormalities such as heart block or enlargement of the liver and spleen. Neonatal lupus is usually benign and self-limited.Medications for treatment of SLE can carry severe risks for female and male reproduction. Cyclophosphamide (also known as Cytoxan), can lead to infertility by causing premature ovarian insufficiency (POI), the loss of normal function of ones ovaries prior to age forty. Methotrexate can cause termination or deformity in fetuses and is a common abortifacient, and for men taking a high dose and planning to father, a discontinuation period of 6 months is recommended before insemination.

Systemic
Fatigue in SLE is probably multifactorial and has been related to not only disease activity or complications such as anemia or hypothyroidism, but also to pain, depression, poor sleep quality, poor physical fitness and lack of social support.

Causes
SLE is presumably caused by a genetic susceptibility coupled with an environmental trigger which results in defects in the immune system. One of the factors associated with SLE is vitamin D deficiency.

Genetics
SLE does run in families, but no single causal gene has been identified. Instead, multiple genes appear to influence a persons chance of developing lupus when triggered by environmental factors. HLA class I, class II, and class III genes are associated with SLE, but only classes I and II contribute independently to increased risk of SLE. Other genes which contain risk variants for SLE are IRF5, PTPN22, STAT4, CDKN1A, ITGAM, BLK, TNFSF4 and BANK1.Some of the susceptibility genes may be population specific. Genetic studies of the rates of disease in families supports the genetic basis of this disease with a heritability of >66%. Identical (monozygotic) twins were found to share susceptibility to the disease at >35% rate compared to fraternal (dizygotic) twins and other full siblings who only showed a 2–5% concordance in shared inheritance.Since SLE is associated with many genetic regions, it is likely an oligogenic trait, meaning that there are several genes that control susceptibility to the disease.SLE is regarded as a prototype disease due to the significant overlap in its symptoms with other autoimmune diseases.

Drug reactions
Drug-induced lupus erythematosus is a (generally) reversible condition that usually occurs in people being treated for a long-term illness. Drug-induced lupus mimics SLE. However, symptoms of drug-induced lupus generally disappear once the medication that triggered the episode is stopped. More than 38 medications can cause this condition, the most common of which are procainamide, isoniazid, hydralazine, quinidine, and phenytoin.

Non-systemic forms of lupus
Discoid (cutaneous) lupus is limited to skin symptoms and is diagnosed by biopsy of rash on the face, neck, scalp or arms. Approximately 5% of people with DLE progress to SLE.

Pathophysiology
SLE is triggered by environmental factors that are unknown. In SLE, the bodys immune system produces antibodies against self-protein, particularly against proteins in the cell nucleus. These antibody attacks are the immediate cause of SLE.SLE is a chronic inflammatory disease believed to be a type III hypersensitivity response with potential type II involvement. Reticulate and stellate acral pigmentation should be considered a possible manifestation of SLE and high titers of anti-cardiolipin antibodies, or a consequence of therapy.People with SLE have intense polyclonal B-cell activation, with a population shift towards immature B cells. Memory B cells with increased CD27+/IgD—are less susceptible to immunosuppression. CD27-/IgD- memory B cells are associated with increased disease activity and renal lupus. T cells, which regulate B-cell responses and infiltrate target tissues, have defects in signaling, adhesion, co-stimulation, gene transcription, and alternative splicing. The cytokines B-lymphocyte stimulator (BLyS), also known as B-cell activating factor (BAFF), interleukin 6, interleukin 17, interleukin 18, type I interferons, and tumor necrosis factor α (TNFα) are involved in the inflammatory process and are potential therapeutic targets.SLE is associated with low C3 levels in the complement system.

Cell death signaling
Apoptosis is increased in monocytes and keratinocytes
Expression of Fas by B cells and T cells is increased
There are correlations between the apoptotic rates of lymphocytes and disease activity.
Necrosis is increased in T lymphocytes.Tingible body macrophages (TBMs) – large phagocytic cells in the germinal centers of secondary lymph nodes – express CD68 protein. These cells normally engulf B cells that have undergone apoptosis after somatic hypermutation. In some people with SLE, significantly fewer TBMs can be found, and these cells rarely contain material from apoptotic B cells. Also, uningested apoptotic nuclei can be found outside of TBMs. This material may present a threat to the tolerization of B cells and T cells. Dendritic cells in the germinal center may endocytose such antigenic material and present it to T cells, activating them. Also, apoptotic chromatin and nuclei may attach to the surfaces of follicular dendritic cells and make this material available for activating other B cells that may have randomly acquired self-protein specificity through somatic hypermutation. Necrosis, a pro-inflammatory form of cell death, is increased in T lymphocytes, due to mitochondrial dysfunction, oxidative stress, and depletion of ATP.

Clearance deficiency
Impaired clearance of dying cells is a potential pathway for the development of this systemic autoimmune disease. This includes deficient phagocytic activity, impaired lysosomal degradation, and scant serum components in addition to increased apoptosis.
SLE is associated with defects in apoptotic clearance, and the damaging effects caused by apoptotic debris. Early apoptotic cells express “eat-me” signals, of cell-surface proteins such as phosphatidylserine, that prompt immune cells to engulf them. Apoptotic cells also express find-me signals to attract macrophages and dendritic cells. When apoptotic material is not removed correctly by phagocytes, they are captured instead by antigen-presenting cells, which leads to the development of antinuclear antibodies.Monocytes isolated from whole blood of people with SLE show reduced expression of CD44 surface molecules involved in the uptake of apoptotic cells. Most of the monocytes and tingible body macrophages (TBMs), which are found in the germinal centres of lymph nodes, even show a definitely different morphology; they are smaller or scarce and die earlier. Serum components like complement factors, CRP, and some glycoproteins are, furthermore, decisively important for an efficiently operating phagocytosis. With SLE, these components are often missing, diminished, or inefficient.
Macrophages during SLE fail to mature their lysosomes and as a result have impaired degradation of internalized apoptotic debris, which results in chronic activation of Toll-like receptors and permeabilization of the phagolysosomal membrane, allowing activation of cytosolic sensors. In addition, intact apoptotic debris recycles back to the cell membrane and accumulate on the surface of the cell.Recent research has found an association between certain people with lupus (especially those with lupus nephritis) and an impairment in degrading neutrophil extracellular traps (NETs). These were due to DNAse1 inhibiting factors, or NET protecting factors in peoples serum, rather than abnormalities in the DNAse1 itself. DNAse1 mutations in lupus have so far only been found in some Japanese cohorts.The clearance of early apoptotic cells is an important function in multicellular organisms. It leads to a progression of the apoptosis process and finally to secondary necrosis of the cells if this ability is disturbed. Necrotic cells release nuclear fragments as potential autoantigens, as well as internal danger signals, inducing maturation of dendritic cells (DCs) since they have lost their membranes integrity. Increased appearance of apoptotic cells also stimulates inefficient clearance. That leads to the maturation of DCs and also to the presentation of intracellular antigens of late apoptotic or secondary necrotic cells, via MHC molecules.Autoimmunity possibly results from the extended exposure to nuclear and intracellular autoantigens derived from late apoptotic and secondary necrotic cells. B and T cell tolerance for apoptotic cells is abrogated, and the lymphocytes get activated by these autoantigens; inflammation and the production of autoantibodies by plasma cells is initiated. A clearance deficiency in the skin for apoptotic cells has also been observed in people with cutaneous lupus erythematosus (CLE).

Germinal centers
In healthy conditions, apoptotic lymphocytes are removed in germinal centers (GC) by specialized phagocytes, the tingible body macrophages (TBM), which is why no free apoptotic and potential autoantigenic material can be seen. In some people with SLE, a buildup of apoptotic debris can be observed in GC because of an ineffective clearance of apoptotic cells. Close to TBM, follicular dendritic cells (FDC) are localised in GC, which attach antigen material to their surface and, in contrast to bone marrow-derived DC, neither take it up nor present it via MHC molecules.
Autoreactive B cells can accidentally emerge during somatic hypermutation and migrate into the germinal center light zone. Autoreactive B cells, maturated coincidentally, normally do not receive survival signals by antigen planted on follicular dendritic cells and perish by apoptosis. In the case of clearance deficiency, apoptotic nuclear debris accumulates in the light zone of GC and gets attached to FDC.
This serves as a germinal centre survival signal for autoreactive B-cells. After migration into the mantle zone, autoreactive B cells require further survival signals from autoreactive helper T cells, which promote the maturation of autoantibody-producing plasma cells and B memory cells. In the presence of autoreactive T cells, a chronic autoimmune disease may be the consequence.

Anti-nRNP autoimmunity
Anti-nRNP autoantibodies to nRNP A and nRNP C initially targeted restricted, proline-rich motifs. Antibody binding subsequently spread to other epitopes. The similarity and cross-reactivity between the initial targets of nRNP and Sm autoantibodies identifies a likely commonality in cause and a focal point for intermolecular epitope spreading.

Others
Elevated expression of HMGB1 was found in the sera of people and mice with systemic lupus erythematosus, high mobility group box 1 (HMGB1) is a nuclear protein participating in chromatin architecture and transcriptional regulation. Recently, there is increasing evidence HMGB1 contributes to the pathogenesis of chronic inflammatory and autoimmune diseases due to its inflammatory and immune stimulating properties.

Diagnosis
Laboratory tests
Antinuclear antibody (ANA) testing and anti-extractable nuclear antigen (anti-ENA) form the mainstay of serologic testing for SLE. If ANA is negative the disease can be ruled out.Several techniques are used to detect ANAs. The most widely used is indirect immunofluorescence (IF). The pattern of fluorescence suggests the type of antibody present in the peoples serum. Direct immunofluorescence can detect deposits of immunoglobulins and complement proteins in peoples skin. When skin not exposed to the sun is tested, a positive direct IF (the so-called lupus band test) is evidence of systemic lupus erythematosus.ANA screening yields positive results in many connective tissue disorders and other autoimmune diseases, and may occur in normal individuals. Subtypes of antinuclear antibodies include anti-Smith and anti-double stranded DNA (dsDNA) antibodies (which are linked to SLE) and anti-histone antibodies (which are linked to drug-induced lupus). Anti-dsDNA antibodies are highly specific for SLE; they are present in 70% of cases, whereas they appear in only 0.5% of people without SLE.Laboratory tests can also help distinguish between closely related connective tissue diseases. A multianalyte panel (MAP) of autoantibodies, including ANA, anti-dsDNA, and anti-Smith in combination with the measurement of cell-bound complement activation products (CB-CAPs) with an integrated algorithm has demonstrated 80% diagnostic sensitivity and 86% specificity in differentiating diagnosed SLE from other autoimmune connective tissue diseases. The MAP approach has been further studied in over 40,000 patients tested with either the MAP or traditional ANA testing strategy (tANA), demonstrating patients who test MAP positive are at up to 6-fold increased odds of receiving a new SLE diagnosis and up to 3-fold increased odds of starting a new SLE medication regimen as compared to patients testing positive with the tANA approach.The anti-dsDNA antibody titers also tend to reflect disease activity, although not in all cases. Other ANA that may occur in people with SLE are anti-U1 RNP (which also appears in systemic sclerosis and mixed connective tissue disease), SS-A (or anti-Ro) and SS-B (or anti-La; both of which are more common in Sjögrens syndrome). SS-A and SS-B confer a specific risk for heart conduction block in neonatal lupus.Other tests routinely performed in suspected SLE are complement system levels (low levels suggest consumption by the immune system), electrolytes and kidney function (disturbed if the kidney is involved), liver enzymes, and complete blood count.
The lupus erythematosus (LE) cell test was commonly used for diagnosis, but it is no longer used because the LE cells are only found in 50–75% of SLE cases and they are also found in some people with rheumatoid arthritis, scleroderma, and drug sensitivities. Because of this, the LE cell test is now performed only rarely and is mostly of historical significance.

Diagnostic criteria
Some physicians make a diagnosis based on the American College of Rheumatology (ACR) classification criteria. However, these criteria were primarily established for use in scientific research, including selection for randomized controlled trials, which require higher confidence levels. As a result, many people with SLE may not meet the full ACR criteria.

Criteria
The American College of Rheumatology (ACR) established eleven criteria in 1982, which were revised in 1997 as a classificatory instrument to operationalise the definition of SLE in clinical trials. They were not intended to be used to diagnose individuals and do not do well in that capacity. For the purpose of identifying people for clinical studies, a person has SLE if any 4 out of 11 symptoms are present simultaneously or serially on two separate occasions.

Malar rash (rash on cheeks); sensitivity = 57%; specificity = 96%.
Discoid rash (red, scaly patches on skin that cause scarring); sensitivity = 18%; specificity = 99%.
Serositis: Pleurisy (inflammation of the membrane around the lungs) or pericarditis (inflammation of the membrane around the heart); sensitivity = 56%; specificity = 86% (pleural is more sensitive; cardiac is more specific).
Oral ulcers (includes oral or nasopharyngeal ulcers); sensitivity = 27%; specificity = 96%.
Arthritis: nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion; sensitivity = 86%; specificity = 37%.
Photosensitivity (exposure to ultraviolet light causes rash, or other symptoms of SLE flareups); sensitivity = 43%; specificity = 96%.
Blood—hematologic disorder—hemolytic anemia (low red blood cell count), leukopenia (white blood cell count<4000/µl), lymphopenia (<1500/µl), or low platelet count (<100000/µl) in the absence of offending drug; sensitivity = 59%; specificity = 89%. Hypocomplementemia is also seen, due to either consumption of C3 and C4 by immune complex-induced inflammation or to congenitally complement deficiency, which may predispose to SLE.
Renal disorder: More than 0.5 g per day protein in urine or cellular casts seen in urine under a microscope; sensitivity = 51%; specificity = 94%.
Antinuclear antibody test positive; sensitivity = 99%; specificity = 49%.
Immunologic disorder: Positive anti-Smith, anti-ds DNA, antiphospholipid antibody, or false positive serological test for syphilis; sensitivity = 85%; specificity = 93%. Presence of anti-ss DNA in 70% of cases (though also positive with rheumatic disease and healthy persons).
Neurologic disorder: Seizures or psychosis; sensitivity = 20%; specificity = 98%.Other than the ACR criteria, people with lupus may also have:
Fever (over 100 °F/ 37.7 °C)
Extreme fatigue
Hair loss
Fingers turning white or blue when cold (Raynauds phenomenon)

Criteria for individual diagnosis
Some people, especially those with antiphospholipid syndrome, may have SLE without four of the above criteria, and also SLE may present with features other than those listed in the criteria.Recursive partitioning has been used to identify more parsimonious criteria. This analysis presented two diagnostic classification trees:

Simplest classification tree: SLE is diagnosed if a person has an immunologic disorder (anti-DNA antibody, anti-Smith antibody, false positive syphilis test, or LE cells) or malar rash. It has sensitivity = 92% and specificity = 92%.
Full classification tree: Uses 6 criteria. It has sensitivity = 97% and specificity = 95%.Other alternative criteria have been suggested, e.g. the St. Thomas Hospital "alternative" criteria in 1998.

Treatment
The treatment of SLE involves preventing flares and reducing their severity and duration when they occur.
Treatment can include corticosteroids and anti-malarial drugs. Certain types of lupus nephritis such as diffuse proliferative glomerulonephritis require intermittent cytotoxic drugs. These drugs include cyclophosphamide and mycophenolate. Cyclophosphamide increases the risk of developing infections, pancreas problems, high blood sugar, and high blood pressure.Hydroxychloroquine was approved by the FDA for lupus in 1955. Some drugs approved for other diseases are used for SLE off-label. In November 2010, an FDA advisory panel recommended approving belimumab (Benlysta) as a treatment for the pain and flare-ups common in lupus. The drug was approved by the FDA in March 2011.In terms of healthcare utilization and costs, one study found that "patients from the US with SLE, especially individuals with moderate or severe disease, utilize significant healthcare resources and incur high medical costs."

Medications
Due to the variety of symptoms and organ system involvement with SLE, its severity in an individual must be assessed to successfully treat SLE. Mild or remittent disease may, sometimes, be safely left untreated. If required, nonsteroidal anti-inflammatory drugs and antimalarials may be used. Medications such as prednisone, mycophenolic acid and tacrolimus have been used in the past.

Disease-modifying antirheumatic drugs
Disease-modifying antirheumatic drugs (DMARDs) are used preventively to reduce the incidence of flares, the progress of the disease, and the need for steroid use; when flares occur, they are treated with corticosteroids. DMARDs commonly in use are antimalarials such as hydroxychloroquine and immunosuppressants (e.g. methotrexate and azathioprine). Hydroxychloroquine is an FDA-approved antimalarial used for constitutional, cutaneous, and articular manifestations. Hydroxychloroquine has relatively few side effects, and there is evidence that it improves survival among people who have SLE.Cyclophosphamide is used for severe glomerulonephritis or other organ-damaging complications. Mycophenolic acid is also used for the treatment of lupus nephritis, but it is not FDA-approved for this indication, and FDA is investigating reports that it may be associated with birth defects when used by pregnant women.

Immunosuppressive drugs
In more severe cases, medications that modulate the immune system (primarily corticosteroids and immunosuppressants) are used to control the disease and prevent recurrence of symptoms (known as flares). Depending on the dosage, people who require steroids may develop Cushings syndrome, symptoms of which may include obesity, puffy round face, diabetes mellitus, increased appetite, difficulty sleeping, and osteoporosis. These may subside if and when the large initial dosage is reduced, but long-term use of even low doses can cause elevated blood pressure and cataracts.
Numerous new immunosuppressive drugs are being actively tested for SLE. Rather than broadly suppressing the immune system, as corticosteroids do, they target the responses of specific types of immune cells. Some of these drugs are already FDA-approved for treatment of rheumatoid arthritis, however due to high-toxicity, their use remains limited.

Analgesia
Since a large percentage of people with SLE have varying amounts of chronic pain, stronger prescription analgesics (painkillers) may be used if over-the-counter drugs (mainly nonsteroidal anti-inflammatory drugs) do not provide effective relief. Potent NSAIDs such as indomethacin and diclofenac are relatively contraindicated for people with SLE because they increase the risk of kidney failure and heart failure.Pain is typically treated with opioids, varying in potency based on the severity of symptoms. When opioids are used for prolonged periods, drug tolerance, chemical dependency, and addiction may occur. Opiate addiction is not typically a concern since the condition is not likely to ever completely disappear. Thus, lifelong treatment with opioids is fairly common for chronic pain symptoms, accompanied by periodic titration that is typical of any long-term opioid regimen.

Intravenous immunoglobulins (IVIGs)
Intravenous immunoglobulins may be used to control SLE with organ involvement, or vasculitis. It is believed that they reduce antibody production or promote the clearance of immune complexes from the body, even though their mechanism of action is not well understood. Unlike immunosuppressives and corticosteroids, IVIGs do not suppress the immune system, so there is less risk of serious infections with these drugs.

Lifestyle changes
Avoiding sunlight in SLE is critical since sunlight is known to exacerbate skin manifestations of the disease. Avoiding activities that induce fatigue is also important since those with SLE fatigue easily and it can be debilitating. These two problems can lead to people becoming housebound for long periods of time. Drugs unrelated to SLE should be prescribed only when known not to exacerbate the disease. Occupational exposure to silica, pesticides, and mercury can also worsen the disease.

Kidney transplantation
Kidney transplants are the treatment of choice for end-stage kidney disease, which is one of the complications of lupus nephritis, but the recurrence of the full disease is common in up to 30% of people.

Antiphospholipid syndrome
Approximately 20% of people with SLE have clinically significant levels of antiphospholipid antibodies, which are associated with antiphospholipid syndrome. Antiphospholipid syndrome is also related to the onset of neural lupus symptoms in the brain. In this form of the disease, the cause is very different from lupus: thromboses (blood clots or "sticky blood") form in blood vessels, which prove to be fatal if they move within the bloodstream. If the thromboses migrate to the brain, they can potentially cause a stroke by blocking the blood supply to the brain.
If this disorder is suspected in people, brain scans are usually required for early detection. These scans can show localized areas of the brain where blood supply has not been adequate. The treatment plan for these people requires anticoagulation. Often, low-dose aspirin is prescribed for this purpose, although for cases involving thrombosis anticoagulants such as warfarin are used.

Management of pregnancy
While most infants born to mothers who have SLE are healthy, pregnant mothers with SLE should remain under medical care until delivery. Neonatal lupus is rare, but identification of mothers at the highest risk for complications allows for prompt treatment before or after birth. In addition, SLE can flare up during pregnancy, and proper treatment can maintain the health of the mother longer. Women pregnant and known to have anti-Ro (SSA) or anti-La antibodies (SSB) often have echocardiograms during the 16th and 30th weeks of pregnancy to monitor the health of the heart and surrounding vasculature.Contraception and other reliable forms of pregnancy prevention are routinely advised for women with SLE since getting pregnant during active disease was found to be harmful. Lupus nephritis was the most common manifestation.

Prognosis
No cure is available for SLE but there are many treatments for the disease.In the 1950s, most people diagnosed with SLE lived fewer than five years. Today, over 90% now survive for more than ten years, and many live relatively symptom-free. 80–90% can expect to live a normal lifespan. Mortality rates are however elevated compared to people without SLE.Prognosis is typically worse for men and children than for women; however, if symptoms are present after age 60, the disease tends to run a more benign course. Early mortality, within 5 years, is due to organ failure or overwhelming infections, both of which can be altered by early diagnosis and treatment. The mortality risk is fivefold when compared to the normal population in the late stages, which can be attributed to cardiovascular disease from accelerated atherosclerosis, the leading cause of death for people with SLE. To reduce the potential for cardiovascular issues, high blood pressure and high cholesterol should be prevented or treated aggressively. Steroids should be used at the lowest dose for the shortest possible period, and other drugs that can reduce symptoms should be used whenever possible.

Epidemiology
The global rates of SLE are approximately 20–70 per 100,000 people. In females, the rate is highest between 45 and 64 years of age. The lowest overall rate exists in Iceland and Japan. The highest rates exist in the US and France. However, there is not sufficient evidence to conclude why SLE is less common in some countries compared to others; it could be the environmental variability in these countries. For example, different countries receive different levels of sunlight, and exposure to UV rays affects dermatological symptoms of SLE.Certain studies hypothesize that a genetic connection exists between race and lupus which affects disease prevalence. If this is true, the racial composition of countries affects disease and will cause the incidence in a country to change as the racial makeup changes. To understand if this is true, countries with largely homogenous and racially stable populations should be studied to better understand incidence. Rates of disease in the developing world are unclear.The rate of SLE varies between countries, ethnicity, and sex, and changes over time. In the United States, one estimate of the rate of SLE is 53 per 100,000; another estimate places the total affected population at 322,000 to over 1 million (98 to over 305 per 100,000). In Northern Europe the rate is about 40 per 100,000 people. SLE occurs more frequently and with greater severity among those of non-European descent. That rate has been found to be as high as 159 per 100,000 among those of Afro-Caribbean descent. Childhood-onset systemic lupus erythematosus generally presents between the ages of 3 and 15 and is four times more common in girls.While the onset and persistence of SLE can show disparities between genders, socioeconomic status also plays a major role. Women with SLE and of lower socioeconomic status have been shown to have higher depression scores, higher body mass index, and more restricted access to medical care than women of higher socioeconomic statuses with the illness. People with SLE had more self-reported anxiety and depression scores if they were from a lower socioeconomic status.

Ethnicity
There are assertions that race affects the rate of SLE. However, a 2010 review of studies that correlate race and SLE identified several sources of systematic and methodological error, indicating that the connection between race and SLE may be spurious. For example, studies show that social support is a modulating factor which buffers against SLE-related damage and maintains physiological functionality. Studies have not been conducted to determine whether people of different racial backgrounds receive differing levels of social support.If there is a difference, this could act as a confounding variable in studies correlating race and SLE. Another caveat to note when examining studies about SLE is that symptoms are often self-reported. This process introduces additional sources of methodological error. Studies have shown that self-reported data is affected by more than just the patients experience with the disease- social support, the level of helplessness, and abnormal illness-related behaviors also factor into a self-assessment. Additionally, other factors like the degree of social support that a person receives, socioeconomic status, health insurance, and access to care can contribute to an individuals disease progression.Racial differences in lupus progression have not been found in studies that control for the socioeconomic status [SES] of participants. Studies that control for the SES of its participants have found that non-white people have more abrupt disease onset compared to white people and that their disease progresses more quickly. Non-white patients often report more hematological, serosal, neurological, and renal symptoms. However, the severity of symptoms and mortality are both similar in white and non-white patients. Studies that report different rates of disease progression in late-stage SLE are most likely reflecting differences in socioeconomic status and the corresponding access to care. The people who receive medical care have often accrued less disease-related damage and are less likely to be below the poverty line. Additional studies have found that education, marital status, occupation, and income create a social context that affects disease progression.

Sex
SLE, like many autoimmune diseases, affects females more frequently than males, at a rate of about 9 to 1. The X chromosome carries immunological related genes, which can mutate and contribute to the onset of SLE. The Y chromosome has no identified mutations associated with autoimmune disease.Hormonal mechanisms could explain the increased incidence of SLE in females. The onset of SLE could be attributed to the elevated hydroxylation of estrogen and the abnormally decreased levels of androgens in females. In addition, differences in GnRH signalling have also been shown to contribute to the onset of SLE. While females are more likely to relapse than males, the intensity of these relapses is the same for both sexes.In addition to hormonal mechanisms, specific genetic influences found on the X chromosome may also contribute to the development of SLE. Studies indicate that the X chromosome can determine the levels of sex hormones. A study has shown an association between Klinefelter syndrome and SLE. XXY males with SLE have an abnormal X–Y translocation resulting in the partial triplication of the PAR1 gene region.

Changing rate of disease
The rate of SLE in the United States increased from 1.0 in 1955 to 7.6 in 1974. Whether the increase is due to better diagnosis or an increased frequency of the disease is unknown.

History
The history of SLE can be divided into three periods: classical, neoclassical, and modern. In each period, research and documentation advanced the understanding and diagnosis of SLE, leading to its classification as an autoimmune disease in 1851, and to the various diagnostic options and treatments now available to people with SLE. The advances made by medical science in the diagnosis and treatment of SLE have dramatically improved the life expectancy of a person diagnosed with SLE.

Etymology
There are several explanations ventured for the term lupus erythematosus. Lupus is Latin for "wolf", and "erythro" is derived from ερυθρός, Greek for "red". All explanations originate with the reddish, butterfly-shaped malar rash that the disease classically exhibits across the nose and cheeks. The reason the term lupus was used to describe this disease comes from the mid-19th century. Many diseases that caused ulceration or necrosis were given the term "lupus" due to the wound being reminiscent of a wolfs bite. This is similar to the naming of lupus vulgaris or chronic facial tuberculosis, where the lesions are ragged and punched out and are said to resemble the bite of a wolf.

Classical period
The classical period began when the disease was first recognized in the Middle Ages. The term lupus is attributed to 12th-century Italian physician Rogerius Frugard, who used it to describe ulcerating sores on the legs of people. No formal treatment for the disease existed and the resources available to physicians to help people were limited.

Neoclassical period
The neoclassical period began in 1851 when the skin disease which is now known as discoid lupus was documented by the French physician, Pierre Cazenave. Cazenave termed the illness lupus and added the word erythematosus to distinguish this disease from other illnesses that affected the skin except they were infectious. Cazenave observed the disease in several people and made very detailed notes to assist others in its diagnosis. He was one of the first to document that lupus affected adults from adolescence into the early thirties and that facial rash is its most distinguishing feature.Research and documentation of the disease continued in the neoclassical period with the work of Ferdinand von Hebra and his son-in-law, Moritz Kaposi. They documented the physical effects of lupus as well as some insights into the possibility that the disease caused internal trauma. Von Hebra observed that lupus symptoms could last many years and that the disease could go "dormant" after years of aggressive activity and then re-appear with symptoms following the same general pattern. These observations led Hebra to term lupus a chronic disease in 1872.Kaposi observed that lupus assumed two forms: the skin lesions (now known as discoid lupus) and a more aggravated form that affected not only the skin but also caused fever, arthritis, and other systemic disorders in people. The latter also presented a rash confined to the face, appearing on the cheeks and across the bridge of the nose; he called this the "butterfly rash". Kaposi also observed those patients who developed the butterfly rash were often afflicted with another disease such as tuberculosis, anemia, or chlorisis which often caused death. Kaposi was one of the first people to recognize what is now termed systemic lupus erythematosus in his documentation of the remitting and relapsing nature of the disease and the relationship of skin and systemic manifestations during disease activity.The 19th centurys research into lupus continued with the work of Sir William Osler who, in 1895, published the first of his three papers about the internal complications of erythema exudativum multiforme. Not all the patient cases in his paper had SLE but Oslers work expanded the knowledge of systemic diseases and documented extensive and critical visceral complications for several diseases including lupus. Noting that many people with lupus had a disease that not only affected the skin but many other organs in the body as well, Osler added the word "systemic" to the term lupus erythematosus to distinguish this type of disease from discoid lupus erythematosus.Oslers second paper noted that reoccurrence is a special feature of the disease and that attacks can be sustained for months or even years. Further study of the disease led to a third paper, published in 1903, documenting afflictions such as arthritis, pneumonia, the inability to form coherent ideas, delirium, and central nervous system damage as all affecting patients diagnosed with SLE.

Modern period
The modern period, beginning in 1920, saw major developments in research into the cause and treatment of discoid and systemic lupus. Research conducted in the 1920s and 1930s led to the first detailed pathologic descriptions of lupus and demonstrated how the disease affected the kidney, heart, and lung tissue. A breakthrough was made in 1948 with the discovery of the LE cell (the lupus erythematosus cell—a misnomer, as it occurs with other diseases as well). Discovered by a team of researchers at the Mayo Clinic, they discovered that the white blood cells contained the nucleus of another cell that was pushing against the whites cell proper nucleus.Noting that the invading nucleus was coated with antibody that allowed it to be ingested by a phagocytic or scavenger cell, they named the antibody that causes one cell to ingest another the LE factor and the two nuclei cell result in the LE cell. The LE cell, it was determined, was a part of an anti-nuclear antibody (ANA) reaction; the body produces antibodies against its own tissue. This discovery led to one of the first definitive tests for lupus since LE cells are found in approximately 60% of all people diagnosed with lupus. The LE cell test is rarely performed as a definitive lupus test today as LE cells do not always occur in people with SLE and can occur in individuals with other autoimmune diseases. Their presence can help establish a diagnosis but no longer indicates a definitive SLE diagnosis.
The discovery of the LE cell led to further research and this resulted in more definitive tests for lupus. Building on the knowledge that those with SLE had auto-antibodies that would attach themselves to the nuclei of normal cells, causing the immune system to send white blood cells to fight off these "invaders", a test was developed to look for the anti-nuclear antibody (ANA) rather than the LE cell specifically. This ANA test was easier to perform and led not only to a definitive diagnosis of lupus but also many other related diseases. This discovery led to the understanding of what is now known as autoimmune diseases.To ensure that the person has lupus and not another autoimmune disease, the American College of Rheumatology (ACR) established a list of clinical and immunologic criteria that, in any combination, point to SLE </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 Types of volcanic eruptions and explain in detail? [/INST] Several types of volcanic eruptions—during which lava, tephra (ash, lapilli, volcanic bombs and volcanic blocks), and assorted gases are expelled from a volcanic vent or fissure—have been distinguished by volcanologists. These are often named after famous volcanoes where that type of behavior has been observed. Some volcanoes may exhibit only one characteristic type of eruption during a period of activity, while others may display an entire sequence of types all in one eruptive series.
There are three different types of eruptions:

Magmatic eruptions are the most well-observed type of eruption. They involve the decompression of gas within magma that propels it forward.
Phreatic eruptions are driven by the superheating of steam due to the close proximity of magma. This type exhibits no magmatic release, instead causing the granulation of existing rock.
Phreatomagmatic eruptions are driven by the direct interaction of magma and water, as opposed to phreatic eruptions, where no fresh magma reaches the surface.Within these wide-defining eruptive types are several subtypes. The weakest are Hawaiian and submarine, then Strombolian, followed by Vulcanian and Surtseyan. The stronger eruptive types are Pelean eruptions, followed by Plinian eruptions; the strongest eruptions are called Ultra-Plinian. Subglacial and phreatic eruptions are defined by their eruptive mechanism, and vary in strength. An important measure of eruptive strength is the Volcanic Explosivity Index an order-of-magnitude scale, ranging from 0 to 8, that often correlates to eruptive types

Eruption mechanisms
Volcanic eruptions arise through three main mechanisms:
Gas release under decompression, causing magmatic eruptions
Ejection of entrained particles during steam eruptions, causing phreatic eruptions
Thermal contraction from chilling on contact with water, causing phreatomagmatic eruptionsThere are two types of eruptions in terms of activity, explosive eruptions and effusive eruptions. Explosive eruptions are characterized by gas-driven explosions that propels magma and tephra. Effusive eruptions, meanwhile, are characterized by the outpouring of lava without significant explosive eruption.Volcanic eruptions vary widely in strength. On the one extreme there are effusive Hawaiian eruptions, which are characterized by lava fountains and fluid lava flows, which are typically not very dangerous. On the other extreme, Plinian eruptions are large, violent, and highly dangerous explosive events. Volcanoes are not bound to one eruptive style, and frequently display many different types, both passive and explosive, even in the span of a single eruptive cycle. Volcanoes do not always erupt vertically from a single crater near their peak, either. Some volcanoes exhibit lateral and Fissure eruptions. Notably, many Hawaiian eruptions start from rift zones. Scientists believed that pulses of magma mixed together in the magma chamber before climbing upward—a process estimated to take several thousands of years. However, Columbia University volcanologists found that the eruption of Costa Ricas Irazú Volcano in 1963 was likely triggered by magma that took a nonstop route from the mantle over just a few months.

Volcanic explosivity index
The volcanic explosivity index (commonly shortened to VEI) is a scale, from 0 to 8, for measuring the strength of eruptions. It is used by the Smithsonian Institutions Global Volcanism Program in assessing the impact of historic and prehistoric lava flows. It operates in a way similar to the Richter scale for earthquakes, in that each interval in value represents a tenfold increasing in magnitude (it is logarithmic). The vast majority of volcanic eruptions are of VEIs between 0 and 2.

Magmatic eruptions
Magmatic eruptions produce juvenile clasts during explosive decompression from gas release. They range in intensity from the relatively small lava fountains on Hawaii to catastrophic Ultra-Plinian eruption columns more than 30 km (19 mi) high, bigger than the eruption of Mount Vesuvius in 79 that buried Pompeii.

Hawaiian
Hawaiian eruptions are a type of volcanic eruption named after the Hawaiian volcanoes with which this eruptive type is hallmark. Hawaiian eruptions are the calmest types of volcanic events, characterized by the effusive eruption of very fluid basalt-type lavas with low gaseous content. The volume of ejected material from Hawaiian eruptions is less than half of that found in other eruptive types. Steady production of small amounts of lava builds up the large, broad form of a shield volcano. Eruptions are not centralized at the main summit as with other volcanic types, and often occur at vents around the summit and from fissure vents radiating out of the center.Hawaiian eruptions often begin as a line of vent eruptions along a fissure vent, a so-called "curtain of fire." These die down as the lava begins to concentrate at a few of the vents. Central-vent eruptions, meanwhile, often take the form of large lava fountains (both continuous and sporadic), which can reach heights of hundreds of meters or more. The particles from lava fountains usually cool in the air before hitting the ground, resulting in the accumulation of cindery scoria fragments; however, when the air is especially thick with clasts, they cannot cool off fast enough due to the surrounding heat, and hit the ground still hot, the accumulation of which forms spatter cones. If eruptive rates are high enough, they may even form splatter-fed lava flows. Hawaiian eruptions are often extremely long lived; Puʻu ʻŌʻō, a volcanic cone on Kilauea, erupted continuously for over 35 years. Another Hawaiian volcanic feature is the formation of active lava lakes, self-maintaining pools of raw lava with a thin crust of semi-cooled rock.

Flows from Hawaiian eruptions are basaltic, and can be divided into two types by their structural characteristics. Pahoehoe lava is a relatively smooth lava flow that can be billowy or ropey. They can move as one sheet, by the advancement of "toes," or as a snaking lava column. Aa lava flows are denser and more viscous than pahoehoe, and tend to move slower. Flows can measure 2 to 20 m (7 to 66 ft) thick. Aa flows are so thick that the outside layers cools into a rubble-like mass, insulating the still-hot interior and preventing it from cooling. Aa lava moves in a peculiar way—the front of the flow steepens due to pressure from behind until it breaks off, after which the general mass behind it moves forward. Pahoehoe lava can sometimes become Aa lava due to increasing viscosity or increasing rate of shear, but Aa lava never turns into pahoehoe flow.Hawaiian eruptions are responsible for several unique volcanological objects. Small volcanic particles are carried and formed by the wind, chilling quickly into teardrop-shaped glassy fragments known as Peles tears (after Pele, the Hawaiian volcano deity). During especially high winds these chunks may even take the form of long drawn-out strands, known as Peles hair. Sometimes basalt aerates into reticulite, the lowest density rock type on earth.Although Hawaiian eruptions are named after the volcanoes of Hawaii, they are not necessarily restricted to them; the highest lava fountain recorded was during the 23 November 2013 eruption of Mount Etna in Italy, which reached a stable height of around 2,500 m (8,200 ft) for 18 minutes, briefly peaking at a height of 3,400 m (11,000 ft).Volcanoes known to have Hawaiian activity include:

Puʻu ʻŌʻō, a parasitic cinder cone located on Kilauea on the island of Hawaiʻi which erupted continuously from 1983 to 2018. The eruptions began with a 6 km (4 mi)-long fissure-based "curtain of fire" on 3 January 1983. These gave way to centralized eruptions on the site of Kilaueas east rift, eventually building up the cone.
For a list of all of the volcanoes of Hawaii, see List of volcanoes in the Hawaiian – Emperor seamount chain.
Mount Etna, Italy.
Mount Mihara in 1986 (see above paragraph)

Strombolian
Strombolian eruptions are a type of volcanic eruption named after the volcano Stromboli, which has been erupting nearly continuously for centuries. Strombolian eruptions are driven by the bursting of gas bubbles within the magma. These gas bubbles within the magma accumulate and coalesce into large bubbles, called gas slugs. These grow large enough to rise through the lava column. Upon reaching the surface, the difference in air pressure causes the bubble to burst with a loud pop, throwing magma in the air in a way similar to a soap bubble. Because of the high gas pressures associated with the lavas, continued activity is generally in the form of episodic explosive eruptions accompanied by the distinctive loud blasts. During eruptions, these blasts occur as often as every few minutes.The term "Strombolian" has been used indiscriminately to describe a wide variety of volcanic eruptions, varying from small volcanic blasts to large eruptive columns. In reality, true Strombolian eruptions are characterized by short-lived and explosive eruptions of lavas with intermediate viscosity, often ejected high into the air. Columns can measure hundreds of meters in height. The lavas formed by Strombolian eruptions are a form of relatively viscous basaltic lava, and its end product is mostly scoria. The relative passivity of Strombolian eruptions, and its non-damaging nature to its source vent allow Strombolian eruptions to continue unabated for thousands of years, and also makes it one of the least dangerous eruptive types.

Strombolian eruptions eject volcanic bombs and lapilli fragments that travel in parabolic paths before landing around their source vent. The steady accumulation of small fragments builds cinder cones composed completely of basaltic pyroclasts. This form of accumulation tends to result in well-ordered rings of tephra.Strombolian eruptions are similar to Hawaiian eruptions, but there are differences. Strombolian eruptions are noisier, produce no sustained eruptive columns, do not produce some volcanic products associated with Hawaiian volcanism (specifically Peles tears and Peles hair), and produce fewer molten lava flows (although the eruptive material does tend to form small rivulets).Volcanoes known to have Strombolian activity include:

Parícutin, Mexico, which erupted from a fissure in a cornfield in 1943. Two years into its life, pyroclastic activity began to wane, and the outpouring of lava from its base became its primary mode of activity. Eruptions ceased in 1952, and the final height was 424 m (1,391 ft). This was the first time that scientists are able to observe the complete life cycle of a volcano.
Mount Etna, Italy, which has displayed Strombolian activity in recent eruptions, for example in 1981, 1999, 2002–2003, and 2009.
Mount Erebus in Antarctica, the southernmost active volcano in the world, having been observed erupting since 1972. Eruptive activity at Erebus consists of frequent Strombolian activity.
Mount Batutara, Indonesia, exhibited continuous Strombolian eruption since 2014.
Stromboli itself. The namesake of the mild explosive activity that it possesses has been active throughout historical time; essentially continuous Strombolian eruptions, occasionally accompanied by lava flows, have been recorded at Stromboli for more than a millennium.

Vulcanian
Vulcanian eruptions are a type of volcanic eruption named after the volcano Vulcano. It was named so following Giuseppe Mercallis observations of its 1888–1890 eruptions. In Vulcanian eruptions, intermediate viscous magma within the volcano make it difficult for vesiculate gases to escape. Similar to Strombolian eruptions, this leads to the buildup of high gas pressure, eventually popping the cap holding the magma down and resulting in an explosive eruption. However, unlike Strombolian eruptions, ejected lava fragments are not aerodynamic; this is due to the higher viscosity of Vulcanian magma and the greater incorporation of crystalline material broken off from the former cap. They are also more explosive than their Strombolian counterparts, with eruptive columns often reaching between 5 and 10 km (3 and 6 mi) high. Lastly, Vulcanian deposits are andesitic to dacitic rather than basaltic.Initial Vulcanian activity is characterized by a series of short-lived explosions, lasting a few minutes to a few hours and typified by the ejection of volcanic bombs and blocks. These eruptions wear down the lava dome holding the magma down, and it disintegrates, leading to much more quiet and continuous eruptions. Thus an early sign of future Vulcanian activity is lava dome growth, and its collapse generates an outpouring of pyroclastic material down the volcanos slope.

Deposits near the source vent consist of large volcanic blocks and bombs, with so-called "bread-crust bombs" being especially common. These deeply cracked volcanic chunks form when the exterior of ejected lava cools quickly into a glassy or fine-grained shell, but the inside continues to cool and vesiculate. The center of the fragment expands, cracking the exterior. However the bulk of Vulcanian deposits are fine grained ash. The ash is only moderately dispersed, and its abundance indicates a high degree of fragmentation, the result of high gas contents within the magma. In some cases these have been found to be the result of interaction with meteoric water, suggesting that Vulcanian eruptions are partially hydrovolcanic.Volcanoes that have exhibited Vulcanian activity include:

Sakurajima, Japan has been the site of Vulcanian activity near-continuously since 1955.
Tavurvur, Papua New Guinea, one of several volcanoes in the Rabaul Caldera.
Irazú Volcano in Costa Rica exhibited Vulcanian activity in its 1965 eruption.
Anak Krakatoa, Indonesia, repeated vulcanian activities since its rise in 1930 until the present time.Vulcanian eruptions are estimated to make up at least half of all known Holocene eruptions.

Peléan
Peléan eruptions (or nuée ardente) are a type of volcanic eruption named after the volcano Mount Pelée in Martinique, the site of a Peléan eruption in 1902 that is one of the worst natural disasters in history. In Peléan eruptions, a large amount of gas, dust, ash, and lava fragments are blown out the volcanos central crater, driven by the collapse of rhyolite, dacite, and andesite lava dome collapses that often create large eruptive columns. An early sign of a coming eruption is the growth of a so-called Peléan or lava spine, a bulge in the volcanos summit preempting its total collapse. The material collapses upon itself, forming a fast-moving pyroclastic flow (known as a block-and-ash flow) that moves down the side of the mountain at tremendous speeds, often over 150 km (93 mi) per hour. These landslides make Peléan eruptions one of the most dangerous in the world, capable of tearing through populated areas and causing serious loss of life. The 1902 eruption of Mount Pelée caused tremendous destruction, killing more than 30,000 people and completely destroying St. Pierre, the worst volcanic event in the 20th century.Peléan eruptions are characterized most prominently by the incandescent pyroclastic flows that they drive. The mechanics of a Peléan eruption are very similar to that of a Vulcanian eruption, except that in Peléan eruptions the volcanos structure is able to withstand more pressure, hence the eruption occurs as one large explosion rather than several smaller ones.Volcanoes known to have Peléan activity include:

Mount Pelée, Martinique. The 1902 eruption of Mount Pelée completely devastated the island, destroying St. Pierre and leaving only 3 survivors. The eruption was directly preceded by lava dome growth.
Mayon Volcano, the Philippines most active volcano. It has been the site of many different types of eruptions, Peléan included. Approximately 40 ravines radiate from the summit and provide pathways for frequent pyroclastic flows and mudflows to the lowlands below. Mayons most violent eruption occurred in 1814 and was responsible for over 1200 deaths.
The 1951 eruption of Mount Lamington. Prior to this eruption the peak had not even been recognized as a volcano. Over 3,000 people were killed, and it has become a benchmark for studying large Peléan eruptions.
Mount Sinabung, Indonesia. History of its eruptions since 2013 are showing the volcano emits pyroclastic flows with frequent collapses of its lava domes.

Plinian
Plinian eruptions (or Vesuvian eruptions) are a type of volcanic eruption named for the historical eruption of Mount Vesuvius in 79 AD that buried the Roman towns of Pompeii and Herculaneum and, specifically, for its chronicler Pliny the Younger. The process powering Plinian eruptions starts in the magma chamber, where dissolved volatile gases are stored in the magma. The gases vesiculate and accumulate as they rise through the magma conduit. These bubbles agglutinate and once they reach a certain size (about 75% of the total volume of the magma conduit) they explode. The narrow confines of the conduit force the gases and associated magma up, forming an eruptive column. Eruption velocity is controlled by the gas contents of the column, and low-strength surface rocks commonly crack under the pressure of the eruption, forming a flared outgoing structure that pushes the gases even faster.These massive eruptive columns are the distinctive feature of a Plinian eruption, and reach up 2 to 45 km (1 to 28 mi) into the atmosphere. The densest part of the plume, directly above the volcano, is driven internally by gas expansion. As it reaches higher into the air the plume expands and becomes less dense, convection and thermal expansion of volcanic ash drive it even further up into the stratosphere. At the top of the plume, powerful prevailing winds drive the plume away from the volcano.

These highly explosive eruptions are usually associated with volatile-rich dacitic to rhyolitic lavas, and occur most typically at stratovolcanoes. Eruptions can last anywhere from hours to days, with longer eruptions being associated with more felsic volcanoes. Although they are usually associated with felsic magma, Plinian eruptions can occur at basaltic volcanoes, if the magma chamber differentiates with upper portions rich in silicon dioxide, or if magma ascends rapidly.Plinian eruptions are similar to both Vulcanian and Strombolian eruptions, except that rather than creating discrete explosive events, Plinian eruptions form sustained eruptive columns. They are also similar to Hawaiian lava fountains in that both eruptive types produce sustained eruption columns maintained by the growth of bubbles that move up at about the same speed as the magma surrounding them.Regions affected by Plinian eruptions are subjected to heavy pumice airfall affecting an area 0.5 to 50 km3 (0 to 12 cu mi) in size. The material in the ash plume eventually finds its way back to the ground, covering the landscape in a thick layer of many cubic kilometers of ash.

However the most dangerous eruptive feature are the pyroclastic flows generated by material collapse, which move down the side of the mountain at extreme speeds of up to 700 km (435 mi) per hour and with the ability to extend the reach of the eruption hundreds of kilometers. The ejection of hot material from the volcanos summit melts snowbanks and ice deposits on the volcano, which mixes with tephra to form lahars, fast moving mudflows with the consistency of wet concrete that move at the speed of a river rapid.Major Plinian eruptive events include:

The AD 79 eruption of Mount Vesuvius buried the Roman towns of Pompeii and Herculaneum under a layer of ash and tephra. It is the model Plinian eruption. Mount Vesuvius has erupted several times since then. Its last eruption was in 1944 and caused problems for the allied armies as they advanced through Italy. It was the contemporary report by Pliny the Younger that led scientists to refer to Vesuvian eruptions as "Plinian".
The 1980 eruption of Mount St. Helens in Washington, which ripped apart the volcanos summit, was a Plinian eruption of Volcanic Explosivity Index (VEI) 5.
The strongest types of eruptions, with a VEI of 8, are so-called "Ultra-Plinian" eruptions, such as the one at Lake Toba 74 thousand years ago, which put out 2800 times the material erupted by Mount St. Helens in 1980.
Hekla in Iceland, an example of basaltic Plinian volcanism being its 1947–48 eruption. The past 800 years have been a pattern of violent initial eruptions of pumice followed by prolonged extrusion of basaltic lava from the lower part of the volcano.
Pinatubo in the Philippines on 15 June 1991, which produced 5 km3 (1 cu mi) of dacitic magma, a 40 km (25 mi) high eruption column, and released 17 megatons of sulfur dioxide.
Kelud, Indonesia erupted in 2014 and ejected around 120,000,000 to 160,000,000 cubic metres (4.2×109 to 5.7×109 cu ft) volcanic ashes which caused economic disruptions across Java.

Phreatomagmatic eruptions
Phreatomagmatic eruptions are eruptions that arise from interactions between water and magma. They are driven by thermal contraction of magma when it comes in contact with water (as distinguished from magmatic eruptions, which are driven by thermal expansion). This temperature difference between the two causes violent water-lava interactions that make up the eruption. The products of phreatomagmatic eruptions are believed to be more regular in shape and finer grained than the products of magmatic eruptions because of the differences in eruptive mechanisms.There is debate about the exact nature of phreatomagmatic eruptions, and some scientists believe that fuel-coolant reactions may be more critical to the explosive nature than thermal contraction. Fuel coolant reactions may fragment the volcanic material by propagating stress waves, widening cracks and increasing surface area that ultimately leads to rapid cooling and explosive contraction-driven eruptions.

Surtseyan
A Surtseyan (or hydrovolcanic) eruption is a type of volcanic eruption characterized by shallow-water interactions between water and lava, named after its most famous example, the eruption and formation of the island of Surtsey off the coast of Iceland in 1963. Surtseyan eruptions are the "wet" equivalent of ground-based Strombolian eruptions, but because they take place in water they are much more explosive. As water is heated by lava, it flashes into steam and expands violently, fragmenting the magma it contacts into fine-grained ash. Surtseyan eruptions are typical of shallow-water volcanic oceanic islands, but they are not confined to seamounts. They can happen on land as well, where rising magma that comes into contact with an aquifer (water-bearing rock formation) at shallow levels under the volcano can cause them. The products of Surtseyan eruptions are generally oxidized palagonite basalts (though andesitic eruptions do occur, albeit rarely), and like Strombolian eruptions Surtseyan eruptions are generally continuous or otherwise rhythmic.A defining feature of a Surtseyan eruption is the formation of a pyroclastic surge (or base surge), a ground hugging radial cloud that develops along with the eruption column. Base surges are caused by the gravitational collapse of a vaporous eruptive column, one that is denser overall than a regular volcanic column. The densest part of the cloud is nearest to the vent, resulting in a wedge shape. Associated with these laterally moving rings are dune-shaped depositions of rock left behind by the lateral movement. These are occasionally disrupted by bomb sags, rock that was flung out by the explosive eruption and followed a ballistic path to the ground. Accumulations of wet, spherical ash known as accretionary lapilli are another common surge indicator.Over time Surtseyan eruptions tend to form maars, broad low-relief volcanic craters dug into the ground, and tuff rings, circular structures built of rapidly quenched lava. These structures are associated with single vent eruptions. However, if eruptions arise along fracture zones, rift zones may be dug out. Such eruptions tend to be more violent than those which form tuff rings or maars, an example being the 1886 eruption of Mount Tarawera. Littoral cones are another hydrovolcanic feature, generated by the explosive deposition of basaltic tephra (although they are not truly volcanic vents). They form when lava accumulates within cracks in lava, superheats and explodes in a steam explosion, breaking the rock apart and depositing it on the volcanos flank. Consecutive explosions of this type eventually generate the cone.Volcanoes known to have Surtseyan activity include:

Surtsey, Iceland. The volcano built itself up from depth and emerged above the Atlantic Ocean off the coast of Iceland in 1963. Initial hydrovolcanics were highly explosive, but as the volcano grew, rising lava interacted less with water and more with air, until finally Surtseyan activity waned and became more Strombolian.
Ukinrek Maars in Alaska, 1977, and Capelinhos in the Azores, 1957, both examples of above-water Surtseyan activity.
Mount Tarawera in New Zealand erupted along a rift zone in 1886, killing 150 people.
Ferdinandea, a seamount in the Mediterranean Sea, breached sea level in July 1831 and caused a sovereignty dispute between Italy, France, and Great Britain. The volcano did not build tuff cones strong enough to withstand erosion and soon disappeared back below the waves.
The underwater volcano Hunga Tonga in Tonga breached sea level in 2009. Both of its vents exhibited Surtseyan activity for much of the time. It was also the site of an earlier eruption in May 1988.

Submarine
Submarine eruptions occur underwater. An estimated 75% of volcanic eruptive volume is generated by submarine eruptions near mid ocean ridges alone, however problems detecting deep sea volcanics meant they remained virtually unknown until advances in the 1990s made it possible to observe them.Submarine eruptions may produce seamounts, which may break the surface and form volcanic islands.
Submarine volcanism is driven by various processes. Volcanoes near plate boundaries and mid-ocean ridges are built by the decompression melting of mantle rock that rises on an upwelling portion of a convection cell to the crustal surface. Eruptions associated with subducting zones, meanwhile, are driven by subducting plates that add volatiles to the rising plate, lowering its melting point. Each process generates different rock; mid-ocean ridge volcanics are primarily basaltic, whereas subduction flows are mostly calc-alkaline, and more explosive and viscous.Spreading rates along mid-ocean ridges vary widely, from 2 cm (0.8 in) per year at the Mid-Atlantic Ridge, to up to 16 cm (6 in) along the East Pacific Rise. Higher spreading rates are a probable cause for higher levels of volcanism. The technology for studying seamount eruptions did not exist until advancements in hydrophone technology made it possible to "listen" to acoustic waves, known as T-waves, released by submarine earthquakes associated with submarine volcanic eruptions. The reason for this is that land-based seismometers cannot detect sea-based earthquakes below a magnitude of 4, but acoustic waves travel well in water and over long periods of time. A system in the North Pacific, maintained by the United States Navy and originally intended for the detection of submarines, has detected an event on average every 2 to 3 years.The most common underwater flow is pillow lava, a rounded lava flow named for its unusual shape. Less common are glassy, marginal sheet flows, indicative of larger-scale flows. Volcaniclastic sedimentary rocks are common in shallow-water environments. As plate movement starts to carry the volcanoes away from their eruptive source, eruption rates start to die down, and water erosion grinds the volcano down. The final stages of eruption cap the seamount in alkalic flows. There are about 100,000 deepwater volcanoes in the world, although most are beyond the active stage of their life. Some exemplary seamounts are Kamaʻehuakanaloa (formerly Loihi), Bowie Seamount, Davidson Seamount, and Axial Seamount.

Subglacial
Subglacial eruptions are a type of volcanic eruption characterized by interactions between lava and ice, often under a glacier. The nature of glaciovolcanism dictates that it occurs at areas of high latitude and high altitude. It has been suggested that subglacial volcanoes that are not actively erupting often dump heat into the ice covering them, producing meltwater. This meltwater mix means that subglacial eruptions often generate dangerous jökulhlaups (floods) and lahars.The study of glaciovolcanism is still a relatively new field. Early accounts described the unusual flat-topped steep-sided volcanoes (called tuyas) in Iceland that were suggested to have formed from eruptions below ice. The first English-language paper on the subject was published in 1947 by William Henry Mathews, describing the Tuya Butte field in northwest British Columbia, Canada. The eruptive process that builds these structures, originally inferred in the paper, begins with volcanic growth below the glacier. At first the eruptions resemble those that occur in the deep sea, forming piles of pillow lava at the base of the volcanic structure. Some of the lava shatters when it comes in contact with the cold ice, forming a glassy breccia called hyaloclastite. After a while the ice finally melts into a lake, and the more explosive eruptions of Surtseyan activity begins, building up flanks made up of mostly hyaloclastite. Eventually the lake boils off from continued volcanism, and the lava flows become more effusive and thicken as the lava cools much more slowly, often forming columnar jointing. Well-preserved tuyas show all of these stages, for example Hjorleifshofdi in Iceland.Products of volcano-ice interactions stand as various structures, whose shape is dependent on complex eruptive and environmental interactions. Glacial volcanism is a good indicator of past ice distribution, making it an important climatic marker. Since they are embedded in ice, as glacial ice retreats worldwide there are concerns that tuyas and other structures may destabilize, resulting in mass landslides. Evidence of volcanic-glacial interactions are evident in Iceland and parts of British Columbia, and it is even possible that they play a role in deglaciation.

Glaciovolcanic products have been identified in Iceland, the Canadian province of British Columbia, the U.S. states of Hawaii and Alaska, the Cascade Range of western North America, South America and even on the planet Mars. Volcanoes known to have subglacial activity include:

Mauna Kea in tropical Hawaii. There is evidence of past subglacial eruptive activity on the volcano in the form of a subglacial deposit on its summit. The eruptions originated about 10,000 years ago, during the last ice age, when the summit of Mauna Kea was covered in ice.
In 2008, the British Antarctic Survey reported a volcanic eruption under the Antarctica ice sheet 2,200 years ago. It is believed to be that this was the biggest eruption in Antarctica in the last 10,000 years. Volcanic ash deposits from the volcano were identified through an airborne radar survey, buried under later snowfalls in the Hudson Mountains, close to Pine Island Glacier.
Iceland, well known for both glaciers and volcanoes, is often a site of subglacial eruptions </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 Patient and explain in detail? [/INST] A patient is any recipient of health care services that are performed by healthcare professionals. The patient is most often ill or injured and in need of treatment by a physician, nurse, optometrist, dentist, veterinarian, or other health care provider.

Etymology
The word patient originally meant one who suffers. This English noun comes from the Latin word patienscode: lat promoted to code: la , the present participle of the deponent verb, patiorcode: lat promoted to code: la , meaning I am suffering, and akin to the Greek verb πάσχεινcode: ell promoted to code: el  (paskhein, to suffer) and its cognate noun πάθοςcode: ell promoted to code: el  (pathos).
This language has been construed as meaning that the role of patients is to passively accept and tolerate the suffering and treatments prescribed by the healthcare providers, without engaging in shared decision-making about their care.

Outpatients and inpatients
An outpatient (or out-patient) is a patient who attends an outpatient clinic with no plan to stay beyond the duration of the visit.  Even if the patient will not be formally admitted with a note as an outpatient, their attendance is still registered, and the provider will usually give a note explaining the reason for the visit, tests, or procedure/surgery, which should include the names and titles of the participating personnel, the patients name and date of birth, signature of informed consent, estimated pre-and post-service time for history and exam (before and after), any anesthesia, medications or future treatment plans needed, and estimated time of discharge absent any (further) complications.  Treatment provided in this fashion is called ambulatory care.  Sometimes surgery is performed without the need for a formal hospital admission or an overnight stay, and this is called outpatient surgery or day surgery, which has many benefits including lowered healthcare cost, reducing the amount of medication prescribed, and using the physicians or surgeons time more efficiently.  Outpatient surgery is suited best for more healthy patients undergoing minor or intermediate procedures (limited urinary-tract, eye, or ear, nose, and throat procedures and procedures involving superficial skin and the extremities).  More procedures are being performed in a surgeons office, termed office-based surgery, rather than in a hospital-based operating room.

An inpatient (or in-patient), on the other hand, is "admitted" to stay in a hospital overnight or for an indeterminate time, usually, several days or weeks, though in some extreme cases, such as with coma or persistent vegetative state, patients can stay in hospitals for years, sometimes until death.  Treatment provided in this fashion is called inpatient care. The admission to the hospital involves the production of an admission note. The leaving of the hospital is officially termed discharge, and involves a corresponding discharge note, and sometimes an assessment process to consider ongoing needs.  In the English National Health Service this may take the form of "Discharge to Assess" - where the assessment takes place after the patient has gone home.Misdiagnosis is the leading cause of medical error in outpatient facilities. When the U.S. Institute of Medicine’s groundbreaking 1999 report, To Err Is Human, found up to 98,000 hospital patients die from preventable medical errors in the U.S. each year, early efforts focused on inpatient safety. While patient safety efforts have focused on inpatient hospital settings for more than a decade, medical errors are even more likely to happen in a doctor’s office or outpatient clinic or center.

Day patient
A day patient or (day-patient) is a patient who is using the full range of services of a hospital or clinic but is not expected to stay the night. The term was originally used by psychiatric hospital services using of this patient type to care for people needing support to make the transition from in-patient to out-patient care. However, the term is now also heavily used for people attending hospitals for day surgery.

Alternative terminology
Because of concerns such as dignity, human rights and political correctness, the term "patient" is not always used to refer to a person receiving health care. Other terms that are sometimes used include health consumer, healthcare consumer, customer or client.  However, such terminology may be offensive to those receiving public health care, as it implies a business relationship.
In veterinary medicine, the client is the owner or guardian of the patient. These may be used by governmental agencies, insurance companies, patient groups, or health care facilities. Individuals who use or have used psychiatric services may alternatively refer to themselves as consumers, users, or survivors.
In nursing homes and assisted living facilities, the term resident is generally used in lieu of patient. Similarly, those receiving home health care are called clients.

Patient-centered healthcare
The doctor–patient relationship has sometimes been characterized as silencing the voice of patients. It is now widely agreed that putting patients at the centre of healthcare by trying to provide a consistent, informative and respectful service to patients will improve both outcomes and patient satisfaction.When patients are not at the centre of healthcare, when institutional procedures and targets eclipse local concerns, then patient neglect is possible. Incidents, such as the Stafford Hospital scandal, Winterbourne View hospital abuse scandal and the Veterans Health Administration controversy of 2014 have shown the dangers of prioritizing cost control over the patient experience. Investigations into these and other scandals have recommended that healthcare systems put patient experience at the center, and especially that patients themselves are heard loud and clear within health services.There are many reasons for why health services should listen more to patients. Patients spend more time in healthcare services than regulators or quality controllers, and can recognize problems such as service delays, poor hygiene, and poor conduct. Patients are particularly good at identifying soft problems, such as attitudes, communication, and caring neglect, that are difficult to capture with institutional monitoring.One important way in which patients can be placed at the centre of healthcare is for health services to be more open about patient complaints. Each year many hundreds of thousands of patients complain about the care they have received, and these complaints contain valuable information for any health services which want to learn about and improve patient experience.

See also
References
External links

Jadad AR, Rizo CA, Enkin MW (June 2003). "I am a good patient, believe it or not". BMJ. 326 (7402): 1293–5 </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 Penile fracture and explain in detail? [/INST] Penile fracture is rupture of one or both of the tunica albuginea, the fibrous coverings that envelop the peniss corpora cavernosa. It is caused by rapid blunt force to an erect penis, usually during vaginal intercourse, or aggressive masturbation. It sometimes also involves partial or complete rupture of the urethra or injury to the dorsal nerves, veins and arteries.

Signs and symptoms
A popping or cracking sound, significant pain, swelling, immediate loss of erection leading to flaccidity, and skin hematoma of various sizes are commonly associated with the sexual event.

Causes
Penile fracture is a relatively uncommon clinical condition. Vaginal intercourse and aggressive masturbation are the most common causes. A 2014 study of accident and emergency records at three hospitals in Campinas, Brazil, showed that woman on top positions caused the greatest risk with the missionary position being the safest. The research conjectured that when the receptive partner is on top, they usually control the movement and are not able to interrupt movement when the penis suffers a misaligned penetration. Conversely, when the penetrative partner is controlling the movement, they have better chances of stopping in response to pain from misalignment, minimizing harm.The practice of taqaandan (also taghaandan) also puts men at risk of penile fracture. Taqaandan, which comes from a Kurdish word meaning "to click", involves bending the top part of the erect penis while holding the lower part of the shaft in place, until a click is heard and felt.  Taqaandan is said to be painless and has been compared to cracking ones knuckles, but the practice of taqaandan has led to an increase in the prevalence of penile fractures in western Iran. Taqaandan may be performed to achieve detumescence.

Diagnosis
Imaging studies
Ultrasound examination is able to depict the tunica albuginea tear in the majority of cases (as a hypoechoic discontinuity in the normally echogenic tunica). In a study on 25 patients, Zare Mehrjardi et al. concluded that ultrasound is unable to find the tear just when it is located at the penile base. In their study magnetic resonance imaging (MRI) accurately diagnosed all of the tears (as a discontinuity in the normally low signal tunica on both T1- and T2-weighted sequences). They concluded that ultrasound should be considered as the initial imaging method, and MRI can be helpful in cases that ultrasound does not depict any tear but clinical suspicions for fracture are still high. In the same study, authors investigated accuracy of ultrasound and MRI for determining the tear location (mapping of fracture) in order to perform a tailored surgical repair. MRI was more accurate than ultrasound for this purpose, but ultrasound mapping was well correlated with surgical results in cases where the tear was clearly visualized on ultrasound exam. The advantage of ultrasound in the diagnosis of penile fracture is unrivaled when its noninvasive, cost-effective, and nonionising nature are considered.Penile trauma can result from a blunt or penetrating injury, the latter being rarely investigated by imaging methods, almost always requiring immediate surgical exploration. In the erect penis, trauma results from stretching and narrowing of the tunica albuginea, which can undergo segmental rupture of one or both of the corpora cavernosa, constituting a penile fracture.In the ultrasound examination, a lesion of the tunica albuginea presents as an interruption in (loss of continuity of) the echoic line representing it (Figure 4). Small, moderate, or broad hematomas demonstrate the extent of that discontinuity. Intracavernous hematomas, sometimes without the presence of a tunica albuginea fracture, can be observed when there is a lesion of the smooth muscle of the trabeculae surrounding the sinusoid spaces or the subtunical venular plexus.

In 10-15% of penile traumas, there can be an accompanying urethral lesion. When blood is observed in the urethral meatus, contrast-enhanced evaluation of the urethra is necessary. In cases in which the ultrasound findings are inconclusive, the use of magnetic resonance imaging can facilitate the diagnosis and is recommended by various authors.

Treatment
Penile fracture is a medical emergency, and emergency surgical repair is the usual treatment. Delay in seeking treatment increases the complication rate. Non-surgical approaches result in 10–50% complication rates including erectile dysfunction, permanent penile curvature, damage to the urethra and pain during sexual intercourse, while operatively treated patients experience an 11% complication rate.In some cases, retrograde urethrogram may be performed to rule out concurrent urethral injury.

Legal issues
In the United States, the case of Doe v. Moe, 63 Mass. App </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 46 and explain in detail? [/INST]  </s>