<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Laryngitis and can you explain it in depth? [/INST] Laryngitis is inflammation of the larynx (voice box). Symptoms often include a hoarse voice and may include fever, cough, pain in the front of the neck, and trouble swallowing. Typically, these last under two weeks.Laryngitis is categorised as acute if it lasts less than three weeks and chronic if symptoms last more than three weeks. Acute cases usually occur as part of a viral upper respiratory tract infection, other infections and trauma such as from coughing are other causes. Chronic cases may occur due to smoking, tuberculosis, allergies, acid reflux, rheumatoid arthritis, or sarcoidosis. The underlying mechanism involves irritation of the vocal cords.Concerning signs that may require further investigation include stridor, history of radiation therapy to the neck, trouble swallowing, duration of more than three weeks, and a history of smoking. If concerning signs are present the vocal cords should be examined via laryngoscopy. Other conditions that can produce similar symptoms include epiglottitis, croup, inhaling a foreign body, and laryngeal cancer.The acute form generally resolves without specific treatment. Resting the voice and sufficient fluids may help. Antibiotics generally do not appear to be useful in the acute form. The acute form is common while the chronic form is not. The chronic form occurs most often in middle age and is more common in men than women.

Signs and symptoms
The primary symptom of laryngitis is a hoarse voice.: 108  Because laryngitis can have various causes, other signs and symptoms may vary. They can include

Dry or sore throat
Coughing (both a causal factor and a symptom of laryngitis)
Frequent throat clearing
Increased saliva production
Dysphagia (difficulty swallowing)
Sensation of swelling in the area of the larynx (discomfort in the front of the neck)
Globus pharyngeus (feeling like there is a lump in the throat)
Cold or flu-like symptoms (which, like a cough, may also be a causal factor for laryngitis)
Swollen lymph nodes in the throat, chest, or face
Fever
General muscle pain (myalgia)
Shortness of breath, predominantly in children

Voice quality
Aside from a hoarse-sounding voice, changes to pitch and volume may occur with laryngitis. Speakers may experience a lower or higher pitch than normal, depending on whether their vocal folds are swollen or stiff. They may also have breathier voices, as more air flows through the space between the vocal folds (the glottis), quieter volume and a reduced range.

Causes
Laryngitis can be infectious as well as noninfectious in origin. The resulting inflammation of the vocal folds results in a distortion of the sound produced there. It normally develops in response to either an infection, trauma to the vocal folds, or allergies. Chronic laryngitis may also be caused by more severe problems, such as nerve damage, sores, polyps, or hard and thick lumps (nodules) on the vocal cords.[4]

Acute
Viral
Most acute cases of laryngitis are caused by viral infections, the most common of which tend to be rhinovirus, influenza virus, parainfluenza virus, adenovirus, coronavirus, and RSV. In patients who have a compromised immune system, other viruses such as herpes, HIV may also be potential causes.

Bacterial
This is another major cause of acute laryngitis, and may develop in conjunction with or due to a viral infection. Common bacterial strains are group A streptococcus, Streptococcus pneumoniae, C. diphtheriae, M. catarrhalis, Haemophilus influenzae, Bordetella pertussis, Bacillus anthracis, and M. tuberculosis. In developing countries, more unusual bacterial causes may occur, such as mycobacterial and syphilitic, though these may occur in developed nations as well.

Fungal
Laryngitis caused by fungal infection is common but not frequently diagnosed according to a review by BMJ and can account for up to 10% of acute laryngitis cases. Patients with both functioning and impaired immune systems can develop fungal laryngitis, which may develop as a result of recent antibiotic or inhaled corticosteroids use. Certain strains of fungi that may cause laryngitis include; Histoplasma, Blastomyces, Candida (especially in immunocompromised persons), and Cryptococcus and Coccidioides.

Trauma
Often due to excessive use of the vocal folds such as excessive yelling, screaming, or singing. Though this often results in damage to the outer layers of the vocal folds, the subsequent healing may lead to changes in the physiology of the folds. Another potential cause of inflammation may be overuse of the vocal cords.[5] [6] [7] [8] [9] Laryngeal trauma, including iatrogenic (caused by endotracheal intubation), can also result in inflammation of the vocal cords.

Chronic
Allergies
Findings are unclear as to whether asthma may cause symptoms commonly associated with laryngitis. Some researchers have posited that allergic causes of laryngitis are often misdiagnosed as being the result of acid reflux.

Reflux
One possible explanation of chronic laryngitis is that inflammation is caused by gastro-oesophageal reflux, which causes subsequent irritation of the vocal folds.

Autoimmune disorders
Approximately between 30 and 75% of persons with rheumatoid arthritis report symptoms of laryngitis.
Symptoms of laryngitis are present in only 0.5–5% of people that have sarcoidosis. According to a meta-analysis by Silva et al. (2007), this disease is often an uncommon cause of laryngeal symptoms and is frequently misdiagnosed as another voice disorder.

Diagnosis
Diagnosis of different forms of acute laryngitis

Laryngitis following trauma: This form of laryngitis is usually identified by obtaining a case history providing information on previous phono traumatic experiences, internal trauma caused by recent procedures as well as any previous neck injuries.
Acute viral laryngitis: This form of laryngitis is characterized by lower vocal pitch as well as hoarseness. The symptoms in this form of laryngitis are usually present for less than one week, however they can persist for 3–4 weeks. This form of laryngitis might also be accompanied by upper respiratory tract symptoms such as: sore throat, odynophagia, rhinorrhea, dyspnea, postnasal discharge, and congestion.
Fungal laryngitis: A biopsy and culture of abnormal lesion may help confirm fungal laryngitis.

Visual diagnosis
The larynx itself will often show erythema (reddening) and edema (swelling). This can be seen with laryngoscopy or stroboscopy (method depends on the type of laryngitis).: 108  Stroboscopy may be relatively normal or may reveal asymmetry, aperiodicity, and reduced mucosal wave patterns.Other features of the laryngeal tissues may include
Redness of the laryngeal tissues (acute)
Dilated blood vessels (acute)
Thick, yet dry laryngal tissue (chronic)
Stiff vocal folds
Sticky secretions between the vocal folds and nearby structures (the interarytenoid region)

Referral
Some signs and symptoms indicate the need for early referral. These include

Difficulty swallowing
Vocal stridor
Ear pain
Recent weight loss
History of smoking
Current or recent radiotherapy treatment (in the neck region)
Recent neck surgery or surgery involving endotracheal tubing
Person is a professional voice user (teacher, singer, actor, call center worker, and so on)

Differential diagnosis
Acute epiglottitis: This is more likely in those with stridor, drooling, and painful or trouble swallowing.
Spasmodic dysphonia
Reflux laryngitis
Chronic allergic laryngitis
Neoplasm
Croup: This presents with a barking cough, hoarseness of voice, and inspiratory stridor.

Treatment
Treatment is often supportive in nature, and depends on the severity and type of laryngitis (acute or chronic). General measures to relieve symptoms of laryngitis include behaviour modification, hydration and humidification.Vocal hygiene (care of the voice) is very important to relieve symptoms of laryngitis. Vocal hygiene involves measures such as: resting the voice, drinking sufficient water, reducing caffeine and alcohol intake, stopping smoking and limiting throat clearing.

Acute laryngitis
In general, acute laryngitis treatment involves vocal hygiene, painkillers (analgesics), humidification, and antibiotics.

Viral
The suggested treatment for viral laryngitis involves vocal rest, pain medication, and mucolytics for frequent coughing. Home remedies such as tea and honey may also be helpful. Antibiotics are not used for treatment of viral laryngitis.

Bacterial
Antibiotics may be prescribed for bacterial laryngitis, especially when symptoms of upper respiratory infection are present. However, the use of antibiotics is highly debated for acute laryngitis.  This relates to issues of effectiveness, side effects, cost, and possibility of antibiotic resistance patterns. Overall, antibiotics do not appear to be very effective in the treatment of acute laryngitis.In severe cases of bacterial laryngitis, such as supraglottitis or epiglottitis, there is a higher risk of the airway becoming blocked. An urgent referral should be made to manage the airway. Treatment may involve humidification, corticosteroids, intravenous antibiotics, and nebulised adrenaline.

Fungal
Fungal laryngitis can be treated with oral antifungal tablets and antifungal solutions. These are typically used for up to three weeks and treatment may need to be repeated if the fungal infection returns.

Trauma
Laryngitis caused by excessive use or misuse of the voice can be managed though vocal hygiene measures.

Chronic laryngitis
Reflux
Laryngopharyngeal reflux treatment primarily involves behavioural management and medication. Behavioural management involves aspects such as

Wearing loose clothing
Eating smaller, more frequent meals
Avoiding certain foods (e.g. caffeine, alcohol, spicy foods)Anti-reflux medications may be prescribed for patients with signs of chronic laryngitis and hoarse voice. If anti-reflux treatment does not result in a decrease of symptoms, other possible causes should be examined. Over-the-counter medications for neutralizing acids (antacids) and acid suppressants (H-2 blockers) may be used. Antacids are often short-acting and may not be sufficient for treatment. Proton pump inhibitors are an effective type of medication. These should only be prescribed for a set period of time, after which the symptoms should be reviewed. Proton pump inhibitors do not work for everyone </s>


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hemicrania continua and can you explain it in depth? [/INST] Hemicrania continua (HC) is a persistent unilateral headache that responds to indomethacin. It is usually unremitting, but rare cases of remission have been documented. Hemicrania continua is considered a primary headache disorder, meaning that it is not caused by another condition.

Symptoms
In hemicrania continua, basal pain is a dull aching pressure similar to that of TTHs that occurs nearly always on the same side of the head and face. Pain ranges from mild to severe and is characterized by fluctuations where it increases in intensity up to three to five times per 24-hour cycle. The range of duration of exacerbations has no boundaries and varies from a few seconds to up to two weeks. While attacks tend to be more frequent at night, no circadian periodicity such as in cluster headache can be observed.
The nature of pain changes during the exacerbation phase, becoming more piercing, throbbing, and intense, generally paired with other highly debilitating symptoms such as nausea, vomiting, dizziness, and sensitivity to light and sounds. During these exacerbation phases, hemicrania continua may mimic other primary and secondary headache disorders, with up to 70% of patients fulfilling the diagnostic criteria for migraine. Physical exertion,changes in sleep patterns, stress, or alcohol consumption can make the headache pain more severe in some patients.In addition to persistent daily headache of HC, which is usually mild to moderate (and frequently severe), HC can present other symptoms. These additional symptoms of HC can be divided into three main categories:

Autonomic symptoms:
conjunctival injection
tearing
rhinorrhea
nasal stuffiness
eyelid edema
forehead sweating
Stabbing headaches:
Short, "jabbing" headaches superimposed over the persistent daily headache.
Usually lasting less than one minute.
Migrainous features:
throbbing pain
nausea and/or vomiting
phonophobia
photophobia

Cause
The cause of hemicrania continua is unknown.

Diagnosis
The following diagnostic criteria are given for hemicrania continua:
Headache for more than 3 months fulfilling other 3 criteria:
All of the following characteristics:
Unilateral pain without side-shift
Daily and continuous, without pain-free periods
Moderate intensity, but with exacerbations of severe pain
At least one of the following autonomic features occurs during exacerbations and ipsilateral to the side of pain:
Conjunctival injection and/or lacrimation
Nasal congestion and/or rhinorrhea
Ptosis and/or miosis
Complete response to therapeutic doses of indomethacin, although cases of hemicrania continua that do not resolve with indomethacin treatment have been documented.A variant on hemicrania continua has also been described, in which the attacks may shift sides, although meeting the above criteria in all other respects.There is no definitive diagnostic test for hemicrania continua. Diagnostic tests such as imaging studies may be ordered to rule out other causes for the headache. When the symptoms of hemicrania continua are present, its considered "diagnostic" if they respond completely to indomethacin </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Lipodystrophy and can you explain it in depth? [/INST] Lipodystrophy syndromes are a group of genetic or acquired disorders in which the body is unable to produce and maintain healthy fat tissue. The medical condition is characterized by abnormal or degenerative conditions of the bodys adipose tissue. A more specific term, lipoatrophy ("lipo" is Greek for "fat", and "dystrophy" is Greek for "abnormal or degenerative condition"), is used when describing the loss of fat from one area (usually the face). This condition is also characterized by a lack of circulating leptin which may lead to osteosclerosis. The absence of fat tissue is associated with insulin resistance, hypertriglyceridemia, non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome.

Types
Lipodystrophy can be divided into the following types:: 495–7
Congenital lipodystrophy syndromes
Congenital generalized lipodystrophy (Berardinelli-Seip syndrome)
Familial partial lipodystrophy
Marfanoid–progeroid–lipodystrophy syndrome
Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature syndrome
Acquired lipodystrophy syndromes
Acquired partial lipodystrophy (Barraquer-Simons syndrome)
Acquired generalized lipodystrophy
Centrifugal abdominal lipodystrophy (Lipodystrophia centrifugalis abdominalis infantilis)
Lipoatrophia annularis (Ferreira-Marques lipoatrophia)
Localized lipodystrophy
HIV-associated lipodystrophy

Epidemiology
Congenital lipodystrophy (due to inherited genetic defect) is estimated to be extremely rare, possibly affecting only one per million persons. Acquired lipodystrophy is much more common, especially affecting persons with HIV infection.

Pathogenesis
Due to an insufficient capacity of subcutaneous adipose tissue to store fat, fat is deposited in non-adipose tissue (lipotoxicity), leading to insulin resistance. Patients display hypertriglyceridemia, severe fatty liver disease and little or no adipose tissue. Average patient lifespan is approximately 30 years before death, with liver failure being the usual cause of death. In contrast to the high levels seen in non-alcoholic fatty liver disease associated with obesity, leptin levels are very low in lipodystropy.

Insulin injections
A lipodystrophy can be a lump or small dent in the skin that forms when a person performs injections repeatedly in the same spot. These types of lipodystrophies are harmless and can be avoided by changing (rotating) the locations of injections. For those with diabetes, using purified insulins may also help.
One of the side-effects of lipodystrophy is the rejection of the injected medication, the slowing down of the absorption of the medication, or trauma that can cause bleeding that, in turn, will reject the medication </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Superficial vein thrombosis and can you explain it in depth? [/INST] Superficial vein thrombosis (SVT) is a blood clot formed in a superficial vein, a vein near the surface of the body. Usually there is thrombophlebitis, which is an inflammatory reaction around a thrombosed vein, presenting as a painful induration (thickening of the skin) with redness. SVT itself has limited significance (in terms of direct morbidity and mortality) when compared to a deep vein thrombosis (DVT), which occurs deeper in the body at the deep venous system level. However, SVT can lead to serious complications (as well as signal other serious problems, such as genetic mutations that increase ones risk for clotting), and is therefore no longer regarded as a benign condition. If the blood clot is too near the saphenofemoral junction there is a higher risk of pulmonary embolism, a potentially life-threatening complication.
SVT has risk factors similar to those for other thrombotic conditions and can arise from a variety of causes. Diagnosis is often based on symptoms. There are multiple possible treatments, with the goal of providing symptomatic relief and preventing complications.

Signs and symptoms
SVT is recognized by the presence of pain, warmth, redness, and tenderness over a superficial vein. The SVT may present as a "cord-like" structure upon palpation. The affected vein may be hard along its entire length. SVTs tend to involve the legs, though they can affect any superficial vein (e.g. those in the arms).

Complications
SVT in the lower extremities can lead to a dangerous complication in which the clot travels to the lungs, called pulmonary embolism (PE). This is because lower limb SVTs can migrate from superficial veins into deeper veins. In a French population, the percent of people with SVTs that also suffered from PEs was 4.7%. In the same population, deep vein thrombosis (DVT) was found in 24.6% of people with SVTs. However, because superficial veins lack muscular support, any clots that form are far less likely to be squeezed by muscle contraction, dislodged, and induce a PE.SVTs can recur after they resolve, which is termed "migratory thrombophlebitis." Migratory thrombophlebitis is a complication that may be due to more serious disorders, such as cancer and other hypercoagulable states.

Causes
SVTs of the legs are often due to varicose veins, though most people with varicose veins do not develop SVTs. SVTs of the arms are often due to the placement of intravenous catheters.Many of the risk factors that are associated with SVT are also associated with other thrombotic conditions (e.g. DVT). These risk factors include age, cancer, history of thromboembolism, pregnancy, use of oral contraceptive medications (containing estrogen), hormone replacement therapy, recent surgery, and certain autoimmune diseases (especially Behçets and Buergers diseases). Other risk factors include immobilization (stasis) and laparoscopy.Hypercoagulable states due to genetic conditions that increase the risk of clotting may contribute to the development of SVT, such as factor V Leiden, prothrombin 20210A mutation, and protein C, S, and antithrombin III and factor XII deficiency.

Mechanism
The mechanism for the development of an SVT depends upon the specific etiology of the SVT. For example, varicose veins and prolonged bed rest both may induce SVTs due to slowing the flow of blood through superficial veins.

Diagnosis
SVTs may be diagnosed based upon clinical criteria by a healthcare professional. A more specific evaluation can be made by ultrasound. An ultrasound can be useful in situations in which an SVT occurs above the knee and is not associated with a varicose vein, because ultrasounds can detect more serious clots like DVTs. The diagnostic utility of D-dimer testing in the setting of SVTs has yet to be fully established.

Classification
SVTs can be classified as either varicose vein (VV) or non-varicose (NV) associated. NV-SVTs are more likely to be associated with genetic procoagulable states compared to VV-SVTs. SVTs can also be classified by pathophysiology. That is, primary SVTs are characterized by inflammation that is localized to the veins. Secondary SVTs are characterized by systemic inflammatory processes.A subclass of SVTs are septic thrombophlebitis, which are SVTs that occur in the setting of an infection.

Treatment
The goal of treatment in SVT is to reduce local inflammation and prevent the SVT from extending from its point of origin. Treatment may entail the use of compression, physical activity, medications, or surgical interventions. The optimal treatment for many SVT sites (i.e. upper limbs, neck, abdominal and thoracic walls, and the penis) has not been determined.

Compression
Multiple compression bandages exist. Fixed compression bandages, adhesive short stretch bandages, and graduated elastic compression stockings have all be used in the treatment of SVTs. The benefit of compression stockings is unclear, though they are frequently used.

Physical activity
Inactivity is contraindicated in the aftermath of an SVT. Uninterrupted periods of sitting or standing may cause the SVT to elongate from its point of origin, increasing the risk for complications and clinical worsening.

Medications
Medications used for the treatment of SVT include anticoagulants, NSAIDs (except aspirin), antibiotics, and corticosteroids.

Anticoagulants
SVTs that occur within the great saphenous vein within 3 cm of the saphenofemoral junction are considered to be equivalent in risk to DVTs.  These high risk SVTs are treated identically with therapeutic anticoagulation. Anticoagulation is also used for intermediate risk SVTs that are greater than 3 cm from the saphenofemoral junction or are greater than 4–5 cm in length.Anticoagulation for high risk SVTs includes the use of vitamin K antagonists or novel oral anticoagulants (NOACs) for 3 months. Anticoagulation for intermediate risk SVTs includes fondaparinux 2.5 mg daily for 45 days or the use of intermediate to therapeutic dose low molecular weight heparin for 4–6 weeks.

NSAIDs
NSAIDs (non-steroidal anti-inflammatory drugs) can be used in both oral or topical formulations for the relief of SVT symptoms </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Coalworkers pneumoconiosis and can you explain it in depth? [/INST] Coal workers pneumoconiosis (CWP), also known as black lung disease or black lung, is an occupational type of pneumoconiosis caused by long-term exposure to coal dust. It is common in coal miners and others who work with coal. It is similar to both silicosis from inhaling silica dust and asbestosis from inhaling asbestos dust. Inhaled coal dust progressively builds up in the lungs and leads to inflammation, fibrosis, and in worse cases, necrosis.
Coal workers pneumoconiosis, severe state, develops after the initial, milder form of the disease known as anthracosis (from the Greek άνθρακας, or anthracas —coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers due to air pollution. Prolonged exposure to large amounts of coal dust can result in more serious forms of the disease, simple coal workers pneumoconiosis and complicated coal workers pneumoconiosis (or progressive massive fibrosis, or PMF). More commonly, workers exposed to coal dust develop industrial bronchitis, clinically defined as chronic bronchitis (i.e. productive cough for 3 months per year for at least 2 years) associated with workplace dust exposure. The incidence of industrial bronchitis varies with age, job, exposure, and smoking. In nonsmokers (who are less prone to develop bronchitis than smokers), studies of coal miners have shown a 16% to 17% incidence of industrial bronchitis.
In 2013 CWP resulted in 25,000 deaths globally—down from 29,000 deaths in 1990. However, a later 2018 study by the National Institute of Occupational Safety and Health shows a resurgence, recording the highest rate of CWP in roughly two decades.

Pathogenesis
Coal dust is not as fibrogenic as silica dust. Coal dust that enters the lungs can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar or interstitial macrophages and remain in the lungs, residing in the connective tissue or pulmonary lymph nodes. Coal dust provides a sufficient stimulus for the macrophage to release various products, including enzymes, cytokines, oxygen radicals, and fibroblast growth factors, which are important in the inflammation and fibrosis of CWP. Aggregations of carbon-laden macrophages can be visualized under a microscope as granular, black areas. In serious cases, the lung may grossly appear black. These aggregations can cause inflammation and fibrosis, as well as the formation of nodular lesions within the lungs. The centers of dense lesions may become necrotic due to ischemia, leading to large cavities within the lung.

Appearance
Simple CWP is marked by the presence of 1–2 mm nodular aggregations of anthracotic macrophages, supported by a fine collagen network, within the lungs. Those 1–2 mm in diameter are known as coal macules, with larger aggregations known as coal nodules. These structures occur most frequently around the initial site of coal dust accumulation—the upper regions of the lungs around respiratory bronchioles. The coal macule is the basic pathological feature of CWP and has a surrounding area of enlargement of the airspace, known as focal emphysema. Focal emphysema extends into progressive centrilobular emphysema. Less commonly a variant of panacinar emphysema develops.Continued exposure to coal dust following the development of simple CWP may progress to complicated CWP with progressive massive fibrosis (PMF), wherein large masses of dense fibrosis develop, usually in the upper lung zones, measuring greater than 1 cm in diameter, with accompanying decreased lung function. These cases generally require a number of years to develop. Grossly, the lung itself appears blackened. Pathologically, these consist of fibrosis with haphazardly-arranged collagen and many pigment-laden macrophages and abundant free pigment. Radiographically, CWP can appear strikingly similar to silicosis. In simple CWP, small rounded nodules (see ILO Classification) predominate, tending to first appear in the upper lung zones. The nodules may coalesce and form large opacities (>1 cm), characterizing complicated CWP, or PMF.

Diagnosis
There are three basic criteria for the diagnosis of CWP:

Chest radiography consistent with CWP
An exposure history to coal dust (typically underground coal mining) of sufficient amount and latency
Exclusion of alternative diagnoses (mimics of CWP)Symptoms and pulmonary function testing relate to the degree of respiratory impairment but are not part of the diagnostic criteria. As noted above, the chest X-ray appearance for CWP can be virtually indistinguishable from silicosis. Chest CT, particularly high-resolution scanning (HRCT), are more sensitive than plain X-ray for detecting the small round opacities.

Treatment
There is no cure or discovered treatments for pneumoconiosis. Some patients are given oxygen to help with their breathing and are advised to stop smoking to prevent further decline in lung function. In the most extreme cases a lung transplant could be done to help prolong the patients life expectancy.

Prevention of pneumoconiosis
The main way to avoid contracting coal workers pneumoconiosis is to avoid the inhalation of coal dust. Some of the ways to prevent this disease include: not smoking, wearing ventilated masks when coming in contact with potentially dangerous airborne particles, regular pulmonary exams, and becoming educated about the risks of lung diseases in your work environment.

Epidemiology
In 2013 CWP resulted in 25,000 deaths down from 29,000 deaths in 1990. Between 1970 and 1974, prevalence of CWP among US coal miners who had worked over 25 years was 32%; the same group saw a prevalence of 9% in 2005–2006.
In Australia, CWP was considered to be eliminated in the 1970s due to strict hazard control measures. However, there has been a resurgence of CWP in Australia, with the first new cases being detected in May 2015. From 1999 to 2016, the average years of life lost due to CWP increased from 8.1 to 12.6 years, most likely due to the increased severity and progression of CWP.

History
Black lung is actually a set of conditions and until the 1950s its dangers were not well understood.  The prevailing view was that silicosis was very serious but it was solely caused by silica and not coal dust.  The miners union, the United Mine Workers of America, realized that rapid mechanization meant drills that produced much more dust, but under John L. Lewis they decided not to raise the black lung issue because it might impede the mechanization that was producing higher productivity and higher wages.  Union priorities were to maintain the viability of the long-fought-for welfare and retirement fund, which would be sustained by higher outputs of coal.  After the death of Lewis, the union dropped its opposition to calling black lung a disease and realized the financial advantages of a fund for its disabled members.
In the Federal Coal Mine Health and Safety Act of 1969, the US Congress set up standards to reduce dust and created the Black Lung Disability Trust.  The mining companies agreed to a clause, by which a ten-year history of mine work, coupled with X-ray or autopsy evidence of severe lung damage, guaranteed compensation. Equally important was a "rate retention" clause that allowed workers with progressive lung disease to transfer to jobs with lower exposure without loss of pay, seniority, or benefits.  Financed by a federal tax on coal, the Trust by 2009 had distributed over $44 billion in benefits to miners disabled by the disease and their widows. A miner who has spent 25 years in underground coal mines has a 5–10% risk of contracting the disease.

21st century
After the Federal Coal Mine Health and Safety Act of 1969 became law in the United States, the percentage of American miners with black lung disease decreased by about 90 percent. More recently, however, rates of the disease have been on the rise. The National Institute for Occupational Safety and Health (NIOSH) reported that close to 9 percent of miners with 25 years or more experience tested positive for black lung in 2005–2006, compared with 4 percent in the late 1990s.New findings have shown that CWP can be a risk for surface coal miners, who are 48% of the workforce. Data from the Coal Workers Health Surveillance Program of NIOSH, which examined chest X-rays from more than 2,000 miners in 16 US states from 2010 to 2011, showed that 2% of miners with greater than one year of surface mining experience developed CWP. 0.5% of these miners had PMF </s>


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Variably protease-sensitive prionopathy and can you explain it in depth? [/INST] Variably protease-sensitive prionopathy (VPSPr) (formerly known as Protease Sensitive Prionopathy) is a sporadic prion protein disease first described in an abstract for a conference on prions in 2006, and this study was published in a 2008 report on 11 cases. The study was conducted by Gambetti P., Zou W.Q., and coworkers from the United States National Prion Disease Pathology Surveillance Center. It was first identified as a distinct disease in 2010 by Zou W.Q. and coworkers from the United States National Prion Disease Pathology Surveillance Center.VPSPr is very rare, occurring in just 2 or 3 out of every 100 million people. As of 2018, fourteen cases have been reported in the UK. It has similarities to Creutzfeldt–Jakob disease, but clinical manifestations differ somewhat, and the abnormal prion protein (PrP) is less resistant to digestion by proteases; some variants are more sensitive to proteases than others, hence the name: variably protease-sensitive.
Patients present with behavioral and psychiatric symptoms, speech deficits (aphasia and/or dysarthria) and progressive cognitive and motor decline (dementia, ataxia, parkinsonism, psychosis, aphasia and mood disorder). Average age at onset is 70 years, and duration of survival is 24 months. About 40% of patients have a family history of dementia. Like CJD, it can be mistaken for Alzheimers dementia.
Diagnosis is difficult, as pathognomonic signs on MRI such as cortical ribboning or hockey stick sign, periodic sharp wave complexes on EEG, and tests for 14-3-3 protein and tau protein are usually not helpful, and no mutations have been observed in the coding region of the PrP gene, unlike CJD and Variant CJD. The diagnosis can be made on pathological examination. There are unique microscopic and immunohistochemical features, and the prions cannot be digested using proteases. Because 8 out of 10 patients had a positive family history of dementia in the original study, a genetic cause was suspected.
Some have suggested the disease may be a sporadic form of Gerstmann–Sträussler–Scheinker syndrome (GSS).In 2013, Zou W.Q. and coworkers revealed that the peculiar protease-resistant PrP (PrPres) originally found in VPSPr is also detectable in the brain of patients with a genetic CJD linked to PrP Valine (V) to isoleucine (I) mutation at residue 180 (PrPV180I); moreover, they found that the pathological PrP from both VPSPr and gCJDPrPV180I shares a similar glycoform-selective prion formation mechanism.[8,9] Interestingly, the authors further demonstrated that the protease-resistant PrPres from both VPSPr and gCJDV180I lacks the PrP species glycosylated at the first N-linked glycosylation site at residue 181 and they proposed that the deficiency in PrP glycosylation may be involved in the pathogenesis of the two conditions. In 2014, Gambetti P., Zou W.Q., and coworkers found that approximately 54% of mice inoculated with VPSPr brain homogenates exhibited histopathologic lesions and 34% harbored abnormal PrP similar to that of VPSPr on the first passage but no prion disease was detected on the second passage,[10] suggesting that the infectivity of the pathological PrP from VPSPr is lower compared to that from the most common sporadic CJD.

See also
Creutzfeldt–Jakob disease

References
8. Xiao X, Yuan J, Haïk S, Cali I, Zhan YA, Moudjou M, Li B, Laplanche JL, Laude H, Langeveld J, Gambetti P, Kitamoto T, Kong Q, Brandel JP, Cobb BA, Petersen RB & Zou WQ. Glycoform-selective prion formation in sporadic and familial forms of prion disease </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Freeman–Sheldon syndrome and can you explain it in depth? [/INST] Freeman–Sheldon syndrome (FSS) is a very rare form of multiple congenital contracture (MCC) syndromes (arthrogryposes) and is the most severe form of distal arthrogryposis (DA). It was originally described by Ernest Arthur Freeman and Joseph Harold Sheldon in 1938.: 577 As of 2007, only about 100 cases had been reported in medical literature.

Signs and symptoms
The symptoms of Freeman–Sheldon syndrome include drooping of the upper eyelids, strabismus, low-set ears, a long philtrum, gradual hearing loss, scoliosis and walking difficulties. Gastroesophageal reflux has been noted during infancy, but usually improves with age. The tongue may be small, and the limited movement of the soft palate may cause nasal speech. Often there is an H- or Y-shaped dimpling of the skin over the chin.

Cause
FSS is caused by genetic changes. Krakowiak et al. (1998) mapped the distal arthrogryposis multiplex congenita (DA2B; MIM #601680) gene, a syndrome very similar in phenotypic expression to classic FSS, to 11p15.5-pter. Other mutations have been found as well. In FSS, inheritance may be either autosomal dominant, most often demonstrated. or autosomal recessive (MIM 277720). Alves and Azevedo (1977) note most reported cases of DA2A have been identified as new allelic variation. Toydemir et al. (2006) showed that mutations in embryonic myosin heavy chain 3 (MYH3; MIM *160270), at 17p-13.1-pter, caused classic FSS phenotype, in their screening of 28 (21 sporadic and 7 familial) probands with distal arthrogryposis type 2A. In 20 patients (12 and 8 probands, respectively), missense mutations (R672H; MIM *160270.0001 and R672C; MIM *160270.0002) caused substitution of arg672, an embryonic myosin residue retained post-embryonically. Of the remaining 6 patients in whom they found mutations, 3 had missense private de novo (E498G; MIM *160270.0006 and Y583S) or familial mutations (V825D; MIM *160270.0004); 3 other patients with sporadic expression had de novo mutations (T178I; MIM *160270.0003), which was also found in DA2B; 2 patients had no recognized mutations.

Diagnosis
Freeman–Sheldon syndrome is a type of distal arthrogryposis, related to distal arthrogryposis type 1 (DA1). In 1996, more strict criteria for the diagnosis of Freeman–Sheldon syndrome were drawn up, assigning Freeman–Sheldon syndrome as distal arthrogryposis type 2A (DA2A).On the whole, DA1 is the least severe; DA2B is more severe with additional features that respond less favourably to therapy. DA2A (Freeman–Sheldon syndrome) is the most severe of the three, with more abnormalities and greater resistance to therapy.Freeman–Sheldon syndrome has been described as a type of congenital myopathy.In March 2006, Stevenson et al. published strict diagnostic criteria for distal arthrogryposis type 2A (DA2A) or Freeman–Sheldon syndrome. These included two or more features of distal arthrogryposis: microstomia, whistling-face, nasolabial creases, and H-shaped chin dimple.

Management
Surgical and anesthetic considerations
Patients must have early consultation with craniofacial and orthopaedic surgeons, when craniofacial, clubfoot, or hand correction is indicated to improve function or aesthetics. Operative measures should be pursued cautiously, with avoidance of radical measures and careful consideration of the abnormal muscle physiology in Freeman–Sheldon syndrome. Unfortunately, many surgical procedures have suboptimal outcomes, secondary to the myopathy of the syndrome.When operative measures are to be undertaken, they should be planned for as early in life as is feasible, in consideration of the tendency for fragile health. Early interventions hold the possibility to minimise developmental delays and negate the necessity of relearning basic functions.Due to the abnormal muscle physiology in Freeman–Sheldon syndrome, therapeutic measures may have unfavourable outcomes. Difficult endotracheal intubations and vein access complicate operative decisions in many DA2A patients, and malignant hyperthermia (MH) may affect individuals with FSS, as well. Cruickshanks et al. (1999) reports uneventful use of non-MH-triggering agents. Reports have been published about spina bifida occulta in anaesthesia management and cervical kyphoscoliosis in intubations.

Medical emphasis
General health maintenance should be the therapeutic emphasis in Freeman–Sheldon syndrome </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Emberger syndrome and can you explain it in depth? [/INST] The Emberger syndrome is a rare, autosomal dominant, genetic disorder caused by familial or sporadic inactivating mutations in one of the two parental GATA2 genes. The mutation results in a haploinsufficiency (i.e. reduction) in the levels of the genes product, the GATA2 transcription factor. This transcription factor is critical for the embryonic development, maintenance, and functionality of blood-forming, lympathic-forming, and other tissues. The syndrome includes as its primary symptoms: serious abnormalities of the blood such as the myelodysplastic syndrome and acute myeloid leukemia; lymphedema (i.e. fluid retention and tissue swelling caused by a compromised lymphatic system) of the lower limbs, and sensorineural hearing loss. However, the anomalies caused by GATA2 mutations are highly variable with some individuals showing little or no such symptoms even in old age while others exhibit non-malignant types of hematological anomalies; lymphedema in areas besides the lower limbs, little or no hearing loss; or anomalies in other tissues. The syndrome may present with relatively benign signs and/or symptoms and then progress rapidly or slowly (i.e. over years or decades) to the myelodysplastic syndrome and/or acute myeloid leukemia. Alternatively, it may present with one of the latter two life-threatening disorders.The Emberger syndrome is only one of the manifestations of inactivating GATA2 mutations. Other manifestations include: 1 Monocytopenia and Mycobacterium Avium Complex/Dendritic Cell, Monocyte, B and NK Lymphocyte deficiency (i.e. MonoMAC or MonoMAC/DCML); 2) familial myelodysplastic syndrome/acute myeloid leukemia (i.e. familial MDS/AML); 3) chronic myelomonocytic leukemia; 4) pediatric myelodysplastic syndrome; and 5) various other hematological abnormalities such as aplastic anemia, anemia, chronic neutropenia; and/or various immunological defects. Individuals with the Emberger syndrome may exhibit signs or symptoms that are more characteristic of the latter manifestations. Since most individuals with inactivating GATA2 mutations progress to a leukemic disorder, the Emberger syndrome is a Precancerous condition.The age of onset and types of symptoms that occur in individuals afflicted with the Emberger syndrome are highly variable even in family members presumed to have identical GATA2 gene mutations. This variability as well as the variability in the different manifestations of GATA2-inactivating mutations are not fully understood. They likely relate, at least in part, to: individual differences in the: 1) levels of the GATA2 transcription factor which are expressed; 2) genetic backgrounds; 3) occurrence of illnesses or other events that stress the bone marrow; and, possibly, 4) development of other "secondary" genetic abnormalities that often develop during the course of these disorders. Because of these many complexities, recent reports have grouped together all of the different manifestations of GATA2 inactivating mutations into a single pleotropic genetic disorder termed GATA2 deficiency, GATA2 haploinsufficiency, or the GATA2 deficiency syndrome. Even currently, however, the Emberger syndrome (e.g. its MIM entry is #614038) and MonoMac/DCML (e.g. its MIM entry is #614172) are often classified as distinct clinical disorders. The Emberger syndrome is here considered as a distinct disorder.

Signs and symptoms
The age of onset of the Emberger syndrome is variable with rare individuals showing first symptoms such as lymphedema occurring in early infancy while others are symptomless or develop first symptoms in their middle and latter years. This variability can occur between members of the same family who are documented to have the same GATA2 mutation. The syndromes most common times of onset are infancy and early childhood. The syndrome may present with unexplained lymphedema, hearing loss, and/or hematological defects like  neutropenia, anemia, thrombocytopenia, and/or the circulation of abnormal blood cells. Other defects less commonly associated with and the syndrome include hypotelorism, epicanthic folds, hydrocele, webbed neck, and warts caused be human papillomavirus infection. In these case of relatively benign symptoms and signs, the syndrome commonly progresses rapidly or slowly to myelodysplastic syndrome followed by acute myeloid leukemia. Less commonly, Emberger syndrome presents with the myelodysplastic syndrome and/or acute myeloid leukemia.

Genetics
GATA2 gene
GATA2 is a member of the evolutionarily conserved GATA transcription factor family of genes:: all tested vertebrates express six GATA genes. The human GATA2 gene is located on the long arm (or "q" arm) of chromosome 3 at position 21.3 (i.e. located at 3q21.3). In humans, it is expressed in hematologic cells at the stem cell and later progenitor cell stages of their development. Increases and/or decreases in the genes expression regulate the progression of these immature cells toward their final forms as blood cells such as erythrocytess, certain types of lymphocytes, monocytes, and platelets) as well as certain types of tissue cells such as macrophages and mast cells. The GATA2 gene is also expressed in human endothelium, certain types of non-hematological stem cells, and, to lesser extents, prostate, endometrium, and some cancerous tissues.Monosomy of chromosome 7 (i.e. lose of one of the two chromosomes 7) or deletion of the "q" (i.e. short) in one of these two chromosomes often occurs in the various GATA2 deficiency manifestations including the Emberger syndrome. These genetic abnormalities are known causes of acute myeloid leukemia and, while not essential for, may contribute to the development of acute myeloid leukemia in the syndrome  by, for example, lowering the age and/or increasing the chances of the disorder evolving into acute myeloid leukemia.

GATA2 transcription factor
The GATA2 transcription factor contains two zinc finger (i.e. ZnF) structural motifs. C-ZnF is located toward the proteins C-terminus and is responsible for binding to specific DNA sites. N-ZnF is located toward the proteins N-terminus and is responsible for interacting with various other nuclear proteins that regulate its activity. The transcription factor also contains two transactivation domains and one negative regulatory domain which interact with nuclear proteins to up-regulate and down-regulate, respectively, its activity.GATA2 binds to a specific nucleic acid sequence  viz., (T/A(GATA)A/G) on the promoter and enhancer sites of its target genes and in doing so either stimulates or suppresses these genes expression. However, there are thousands of sites in human DNA with this nucleotide sequence but, for unknown reasons, GATA2 binds to <1% of these. Furthermore, all members of the GATA transcription factor family bind to this same nucleotide sequence and in doing so may interfere with GATA2 binding or even displace GATA2 already bound to these sites. For example, the displacement of GATA2 bond to this sequence by GATA1 appears important for the normal development of certain hematological stem cells. This phenomenon is termed the "GATA switch". Given these many variables, the GATA2 transcription factors actions in promoting or inhibiting its target genes is exceedingly complex and not completely understood.

Pathophysiology
The GATA2 transcription factor is critical for the emergence of hematologic stem cells from the hemogenic endothelium during embryogenesis. Deletion of both Gata2 genes in mice is lethal by about day 10 of embryogenesis due to collapse in the formation of mature blood cells. Inactivation of one mouse Gata2 gene is neither lethal nor associated with most of the signs of human GATA2 deficiency except that these animals have ~50% reduction in their hematologic stem cells. The latter findings as well as clinical studies in vitro experiments on human tissues support the notion that both parental GATA2 genes are needed to produce levels of the GATA2 transcription factor sufficient for developing and maintaining normal levels of hematological stem and progenitor cells in humans. The transcription factors role in performing this function involves complex and incompletely understood interactions with a network of hematopoietic transcription factors including RUNX1, TAL1, MYB, GFI1, FLI1, LYL1, and PU.1. It is not exactly clear how reduced levels of GATA2 cause any of Emberger syndromes hematological disorders.The role of GATA2 in promoting the normal development of the lymphatic stem cells may be responsible for the other two key features of the Emberger syndrome. That is, failure to develop competent valves and/or vessels in the lymphatic system, it is proposed, is responsible for the lymphedema of Emberger syndrome while failure to generate the perilymphatic space around the inner ears semicircular canals, it is proposed, is responsible for the syndromes sensorineural hearing loss.

Diagnosis
Examination of circulating blood cells, bone marrow cells, and the GATA2 nucleotide sequence of individuals with Emberger syndrome typically evidences abnormalities which are not distinctively different from those of individuals with other manifestations of GATA2 deficiency. The specific diagnosis of Emberger syndrome depends on detecting mutations of the GATA2 gene in a setting of clinical findings of hematological disorders, lymphedema, and neurosensory hearing loss. It may be especially difficult to diagnose the syndrome in the absence of at least one of the latter two clinical signs or in individuals who exhibit anomalies strongly associated with one of the other manifestations of GATA2 deficiency. DNA sequencing of the full GATA2 gene coding region including the intron4 enhancer by Sanger sequencing or high-throughput methods along with DNA copy number analysis should establish the presence of GATA2 gene mutations; comparison of detected gene mutations to the list of inactivating GATA2 gene mutations plus the clinical presentation and family history are essentials in making the diagnosis of the syndrome and its type of presentation.

Treatment
Standard measures are use for the treatment of lymphedema, sensorineural hearing loss, and the other non-malignant anomalies associated with the Emberger syndrome. However, treatment of the disorders myelodysplastic syndrome and acute myeloid leukemia differs somewhat from standard measures. Like other GATA2 insufficiencies, Emberger syndrome is associated with a deficiency of hematological stem and early progenitor cells that is often due to a hereditary loss of one GATA2 gene. Consequently, the use of radical myeloablative conditioning regimens to remove native bone marrow stem/progenitor cells in preparation for hematopoietic stem cell transplantation may entail excessive morbidity and mortality. While no controlled studies on the treatment of the hematological disorders of the syndrome have been reported, current recommendations by multiple authorities suggest the use of hematopoietic stem cell transplantation using non-myeloablative conditioning methods be used when indicated. The use of this procedure should be anticipatory and occur before the development of an excess of progenitor cells populate the bone marrow in cases of myelodyspasia as well as before the development of acute myeloid leukemia </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hibernoma and can you explain it in depth? [/INST] A hibernoma is a benign neoplasm of vestigial brown fat. The term was originally used by the French anatomist Louis Gery in 1914.

Signs and symptoms
Patients present with a slow-growing, painless, solitary mass, usually of the subcutaneous tissues. It is much less frequently noted in the intramuscular tissue. It is not uncommon for symptoms to be present for years.
Benign neoplasm with brown fat is noted.

Diagnosis
Imaging findings
In general, imaging studies show a well-defined, heterogeneous mass, usually showing a mass which is hypointense to subcutaneous fat on magnetic resonance T1-weight images. Serpentine, thin, low signal bands (septations or vessels) are often seen throughout the tumor.

Pathology findings
From a macroscopic perspective, there is a well-defined, encapsulated or circumscribed mass, showing a soft, yellow tan to deep brown mass. The size ranges from 1 to 27 cm, although the mean is about 10 cm.
 The tumors histologically resemble brown fat. There are four histologic types recognized, but one is the most frequently seen (typical). There is a background of rich vascularity.
Lobular type: Variable degrees of differentiation of uniform, round to oval cells with granular eosinophilic cells with prominent borders, alternating with coarsely multivacuolated fat cells (pale cells). There are usually small centrally placed nuclei without pleomorphism. The cells have large cytoplasmic lipid droplets interspersed throughout.
Myxoid variant: Loose, basophilic matrix, with thick fibrous septa, and foamy histiocytes
Lipoma-like variant: Univacuolated lipocytes, with only isolated hibernoma cells
Spindle cell variant: Spindle cell lipoma combined with hibernoma

Histochemistry
Oil Red O-positive droplets of cytoplasmic lipid can be seen in most cases

Immunohistochemistry
The neoplastic cells are S100 protein positive (approximately 80%), and show membrane and vacuole CD31 immunoreactivity. Uncoupling protein 1 (UCP1), a unique brown fat mitochondrial protein, is also positive.

Cytogenetics
There are structural rearrangements of 11q13-21, which are considered most characteristic. This alteration can be detected by metaphase fluorescent in situ hybridization (FISH). MEN1 gene (11q13.1) is most frequently deleted, while GARP gene (11q13.5) may also be involved.

Cytology
The fine needle aspiration smears show small, round, brown fat-like cells, with uniform, small cytoplasmic vacuoles and regular, small, round nuclei. There is usually a rich vascular background of branching capillaries. It is not uncommon to also have mature fat cells.

Differential diagnoses
It is important to separate hiberoma from adult rhabdomyoma, a granular cell tumor and a true liposarcoma.

Classification
This lesion has been called a fetal lipoma, lipoma of embryonic fat or a lipoma of immature fat.

Management
Complete surgical excision is the treatment of choice, associated with an excellent long term clinical outcome.

Epidemiology
The tumor is rare, affecting adults in the 4th decade most commonly. Patients are usually younger than those who present with a lipoma. There is a slight male predominance </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Piriformis syndrome and can you explain it in depth? [/INST] Piriformis syndrome is a condition which is believed to result from compression of the sciatic nerve by the piriformis muscle. Symptoms may include pain and numbness in the buttocks and down the leg. Often symptoms are worsened with sitting or running.Causes may include trauma to the gluteal muscle, spasms of the piriformis muscle, anatomical variation, or an overuse injury. Few cases in athletics, however, have been described. Diagnosis is difficult as there is no definitive test. A number of physical exam maneuvers can be supportive. Medical imaging is typically normal. Other conditions that may present similarly include a herniated disc.Treatment may include avoiding activities that cause symptoms, stretching, physiotherapy, and medication such as NSAIDs. Steroid or botulinum toxin injections may be used in those who do not improve. Surgery is not typically recommended. The frequency of the condition is unknown, with different groups arguing it is more or less common.

Signs and symptoms
The signs and symptoms include gluteal pain that may radiate down buttock and the leg, and that is made worse in some sitting positions.

Etiology
Causes of piriformis syndrome include the following

Anatomic anomalies, present since birth:Bipartite piriformis muscleSciatic nerve course/branching variations with respect to the piriformis muscle: In over 80% of the population, the sciatic nerve courses deep to and exits inferiorly to the piriformis muscle belly/tendon. Early (proximal) divisions of the sciatic nerve into its tibial and common peroneal components can predispose patients to piriformis syndrome, with these branches passing through and below the piriformis muscle or above and below the muscle.AcquiredSitting for prolonged periods (office workers, taxi drivers, bicycle riders)Overuse syndromes: Piriformis muscle hypertrophy (viz., in athletes)Trauma to the hip or buttock area

Pathophysiology
When the piriformis muscle shortens or spasms due to trauma or overuse, it can compress or strangle the sciatic nerve beneath the muscle. Generally, conditions of this type are referred to as nerve entrapment or as entrapment neuropathies; the particular condition known as piriformis syndrome refers to sciatica symptoms not originating from spinal roots and/or spinal disc compression, but involving the overlying piriformis muscle.In 17% of an assumed normal population the sciatic nerve passes through the piriformis muscle, rather than underneath it; however, in patients undergoing surgery for suspected piriformis syndrome such an anomaly was found only 16.2% of the time leading to doubt about the importance of the anomaly as a factor in piriformis syndrome. Some researchers discount the importance of this relationship in the etiology of the syndrome.MRI findings have shown that both hypertrophy (unusual largeness) and atrophy (unusual smallness) of the piriformis muscle correlate with the supposed condition.Piriformis syndrome may also be associated with direct trauma to the piriformis muscle, such as in a fall or from a knife wound.

Diagnosis
Piriformis syndrome occurs when the sciatic nerve is compressed or pinched by the piriformis muscle of the hip. It usually only affects one hip at a given time, though both hips may produce piriformis syndrome at some point in the patients lifetime, and having had it once greatly increases the chance that it will recur in one hip or the other at some future point unless action is taken to prevent it. Indications include sciatica (radiating pain in the buttock, posterior thigh, and lower leg) and the physical exam finding of tenderness in the area of the sciatic notch. If the piriformis muscle can be located beneath the other gluteal muscles, it will feel noticeably cord-like and will be painful to compress or massage. The pain is exacerbated with any activity that causes flexion of the hip including lifting, prolonged sitting, or walking.
The diagnosis is largely clinical and is one of exclusion. During a physical examination, attempts may be made to stretch the irritated piriformis and provoke sciatic nerve compression, such as the Freiberg test, the Pace test, the FABER test (flexion, abduction, external rotation), and the FAIR test (flexion, adduction, internal rotation). Sciatica secondary to conditions to be ruled out include herniated nucleus pulposus (HNP), facet arthropathy, spinal stenosis, and lumbar muscle strain. Pathology in the sacroiliac joint region, Sacroiliac joint dysfunction and Sacroiliitis are other conditions that present with pain in the low back and hip regions, which may radiate down along the back of the thigh, rarely going down below knee.
Wallet neuritis is an extra-spinal tunnel neuropathy of sciatic nerve, occurring mostly in men. Sitting down on a thick Wallet in the back pocket produces uneven pressure in the hip region that impinges on the Piriformis muscle and / or sciatic nerve. Wallet induced chronic sciatic nerve constriction produces gluteal and ipsilateral lower extremity pain, tingling, and burning sensation.Diagnostic modalities such as ultrasound Imaging, MRI, CT scan, and EMG are mostly useful in excluding other conditions. Increased thickness [iTh] and increased cross‐sectional area [iCSA] for piriformis muscle may be demonstrated on ultrasound imaging and MRI.Magnetic resonance neurography is a medical imaging technique that can show the presence of irritation of the sciatic nerve at the level of the sciatic notch where the nerve passes under the piriformis muscle. However, Magnetic resonance neurography is considered "investigational/not medically necessary" by some insurance companies. Neurography can determine whether or not a patient has a split sciatic nerve or a split piriformis muscle – this may be important in getting a good result from injections or surgery. Image guided injections carried out in an open MRI scanner, or other 3D image guidance can accurately relax the piriformis muscle to test the diagnosis. Other injection methods such as blind injection, fluoroscopic guided injection, ultrasound, or EMG guidance can work but are not as reliable and have other drawbacks.

Prevention
The most common etiology of piriformis syndrome is that resulting from a specific previous injury due to trauma. Large injuries include trauma to the buttocks while "micro traumas" result from small repeated bouts of stress on the piriformis muscle itself. To the extent that piriformis syndrome is the result of some type of trauma and not neuropathy, such secondary causes are considered preventable, especially those occurring in daily activities: according to this theory, periods of prolonged sitting, especially on hard surfaces, produce minor stress that can be relieved with bouts of standing. An individuals environment, including lifestyle factors and physical activity, determine susceptibility to trauma of any given type. Although empirical research findings on the subject have never been published, many believe that taking sensible precautions during high-impact sports and when working in physically demanding conditions may decrease the risk of experiencing piriformis syndrome, either by forestalling injury to the muscle itself or injury to the nerve root that causes it to spasm. In this vein, proper safety and padded equipment should be worn for protection during any type of regular, firm contact (i.e., American football, etc.). In the workplace, individuals are encouraged to make regular assessments of their surroundings and attempt to recognize those things in ones routine that might produce micro or macro traumas. No research has substantiated the effectiveness of any such routine, however, and participation in one may do nothing but heighten an individuals sense of worry over physical minutiae while have no effect in reducing the likeliness of experiencing or re-experiencing piriformis syndrome.Other suggestions from some researchers and physical therapists have included prevention strategies include warming up before physical activity, practicing correct exercise form, stretching, and doing strength training, though these are often suggested for helping treat or prevent any physical injury and are not piriformis-specific in their approach As with any type of exercise, it is thought that warmups will decrease the risk of injury during flexion or rotation of the hip. Stretching increases range of motion, while strengthening hip adductors and abductors theoretically allows the piriformis to tolerate trauma more readily.

Treatment
Immediate though temporary relief of piriformis syndrome can usually be brought about by injection of a local anaesthetic into the piriformis muscle. Symptomatic relief of muscle and nerve pain can also sometimes be obtained by nonsteroidal anti-inflammatory drugs and/or muscle relaxants, though the use of such medication or even more powerful prescription medication for relief of sciatica is often assessed by patients to be largely ineffective at relieving pain. Conservative treatment usually begins with stretching exercises, myofascial release, massage, and avoidance of contributory activities such as running, bicycling, rowing, heavy lifting, etc. Some clinicians recommend formal physical therapy, including soft tissue mobilization, hip joint mobilization, teaching stretching techniques, and strengthening of the gluteus maximus, gluteus medius, and biceps femoris to reduce strain on the piriformis. More advanced physical therapy treatment can include pelvic-trochanter isometric stretching, hip abductor, external rotator and extensor strengthening exercises, transcutaneous electrical nerve stimulation (TENS), and massage physiotherapy of the piriformis muscle region. One study of 14 people with what appeared to be piriformis syndrome indicated that rehabilitation programs that included physical therapy, low doses of muscle relaxants and pain relief medication were effective at alleviating most muscle and nerve pain caused by what the research subjects had been told was piriformis syndrome. However, as this study included very few individuals and did not have a control group not receiving treatment (both serious methodological flaws), it provides no insight as to whether the pain in the piriformis would have simply dissipated on its own without any treatment at all, and is therefore not only uninformative, it may actually be misleading. The injury is considered largely self-limiting and spontaneous recovery is usually on the order of a few days or a week to six weeks or longer if left untreated.

Stretching
Most practitioners agree that spasm, strain, or pain in any muscle can often be treated by regular stretching exercise of that muscle, no matter the cause of the pain. Stretching is recommended every two to three waking hours. Anterior and posterior movement of the hip joint capsule may help optimize the patients stretching capacity. The muscle can be manually stretched by applying pressure perpendicular to the long axis of the muscle and parallel to the surface of the buttocks until the muscle is relaxed. Another stretching exercise is to lie on the side opposite of the pain with the hip and knee of the upper leg flexed and adducted towards the ground while the torso is rotated so that the back of the upper shoulder touches the ground. Physical Therapists may suggest stretching exercises that will target the piriformis, but may also include the hamstrings and hip muscles in order to adequately reduce pain and increase range of motion. Patients with piriformis syndrome may also find relief from applications of ice which will help reduce inflammation and so may help limit pressure on the sciatic nerve. This treatment can be helpful when pain starts or immediately after an activity that is likely to cause pain. As the length of time progresses, heat may provide temporary relief from many types of muscle pain and will temporarily increase muscle flexibility.

Local injections
Failure of conservative treatments such as stretching and strengthening of the piriformis muscle or a high level of immediate pain intensity may bring into consideration various therapeutic injections such as local anesthetics (e.g., lidocaine), anti-inflammatory drugs and/or corticosteroids, botulinum toxin (BTX, Botox), or a combination of the three, all of which have a well-documented effectiveness at relieving muscle-related pain. Injection technique is a significant issue since the piriformis is a very deep-seated muscle. A radiologist may assist in this clinical setting by injecting a small dose of medication containing a paralysing agent such as botulinum toxin under high-frequency ultrasound or CT control. This inactivates the piriformis muscle for 3 to 6 months, without resulting in leg weakness or impaired activity. Though the piriformis muscle becomes inactivated, the surrounding muscles quickly take over its role without any noticeable change in strength or gait. Such treatments may be more or less curative (with no return to pain), or may have limited timespans of effectiveness.

Surgery
For rare cases with unrelenting chronic pain, surgery may be recommended. Surgical release of the piriformis muscle is often effective. Minimal access surgery using newly reported techniques has also proven successful in a large-scale formal outcome published in 2005. As with injections, the deactivated/ excised muscles role in leg movement is completely compensated for by surrounding hip muscles.
Failure of piriformis syndrome treatment may be secondary to an underlying internal obturator muscle injury.

Epidemiology
Piriformis syndrome (PS) data is often confused with other conditions due to differences in definitions, survey methods and whether or not occupational groups or general population are surveyed. This causes a lack of group harmony about the diagnosis and treatment of PS, affecting its epidemiology. In a study, 0.33% of 1293 patients with low back pain cited an incident for PS. A separate study showed 6% of 750 patients with the same incidence. About 6–8% of low back pain occurrences were attributed to PS, though other reports concluded about 5–36%. In a survey conducted on the general population, 12.2–27% included a lifetime occurrence of PS, while 2.2–19.5% showed an annual occurrence. However further studies show that the proportion of the sciatica, in terms of PS, is about 0.1% in orthopaedic practice. This is more common in women with a ratio of 3 to 1 and most likely due to the wider quadriceps femoris muscle angle in the os coxae. Between the years of 1991–1994, PS was found to be 75% prevalent in New York, Connecticut, New Jersey, Pennsylvania; 20% in other American urban centers; and 5% in North and South America, Europe, Asia, Africa and Australia. The common ages of occurrence happen between thirty and forty, and are scarcely found in patients younger than twenty; this has been known to affect all lifestyles.Piriformis syndrome is often left undiagnosed and mistaken with other pains due to similar symptoms with back pain, quadriceps pain, lower leg pain, and buttock pain. These symptoms include tenderness, tingling and numbness initiating in low back and buttock area and then radiating down to the thigh and to the leg.
A precise test for piriformis syndrome has not yet been developed and thus hard to diagnose this pain.
The pain is often initiated by sitting and walking for a longer period.
In 2012, 17.2% of low back pain patients developed piriformis syndrome.
Piriformis syndrome does not occur in children, and is mostly seen in women of age between thirty and forty. This is due to hormone changes throughout their life, especially during pregnancy, where muscles around the pelvis, including piriformis muscles, tense up to stabilize the area for birth.
In 2011, out of 263 patients between the ages of 45 to 84 treated for piriformis syndrome, 53.3% were female </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Parkinsonism and can you explain it in depth? [/INST] Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia (slowed movements), rigidity, and postural instability </s>


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


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Freys syndrome and can you explain it in depth? [/INST] Freys syndrome (also known as Baillargers syndrome, Dupuys syndrome, auriculotemporal syndrome, or Frey-Baillarger syndrome) is a rare neurological disorder resulting from damage to or near the parotid glands responsible for making saliva, and from damage to the auriculotemporal nerve often from surgery.The symptoms of Freys syndrome are redness and sweating on the cheek area adjacent to the ear (see focal hyperhidrosis). They can appear when the affected person eats, sees, dreams, thinks about or talks about certain kinds of food which produce strong salivation. Observing sweating in the region after eating a lemon wedge may be diagnostic.

Signs and symptoms
Signs and symptoms include erythema (redness or flushing) and sweating in the cutaneous distribution of the auriculotemporal nerve, usually in response to gustatory stimuli. There is sometimes pain in the same area, often burning in nature. Between attacks of pain there may be numbness or other altered sensations (anesthesia or paresthesia). This is sometimes termed "gustatory neuralgia".

Causes
Freys syndrome often results as a complication of surgeries of or near the parotid gland or due to injury to the auriculotemporal nerve, which passes through the parotid gland in the early part of its course. The auriculotemporal branch of the mandibular branch (V3) of the trigeminal nerve carries parasympathetic fibers to the parotid salivary gland and sympathetic fibers to the sweat glands of the scalp. As a result of severance and inappropriate regeneration, the parasympathetic nerve fibers may switch course to a sympathetic response, resulting in "gustatory sweating" or sweating in the anticipation of eating, instead of the normal salivary response.
It is often seen with patients who have undergone endoscopic thoracic sympathectomy, a surgical procedure wherein part of the sympathetic trunk is cut or clamped to treat sweating of the hands or blushing </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Koenens tumor and can you explain it in depth? [/INST] Koenens tumor (KT), also commonly termed periungual angiofibroma,: 668  is a subtype of the angiofibromas. Angiofibromas are benign papule, nodule, and/or tumor lesions that are separated into various subtypes based primarily on the characteristic locations of their lesions. KTs are angiofibromas that develop in and under the toenails and/or fingernails. KTs were once considered as the same as another subtype of the angiofibromas viz., acral angiofibromas. While the literature may still sometimes regard KTs as acral angiofibromas, acral angiofibromas are characteristically located in areas close to but not in the toenails and fingernails as well as in the soles of the feet and palms of the hands. KTs are here regarded as distinct from acral angiofibromas.
KTs most commonly develop in individuals who have the rare genetic disease, tuberous sclerosis (a heritable neurocutaneous disorder) and uncommonly in individuals that do not have this genetic disease. One individual with another rare genetic disease that has similarities to tuberous sclerosis, the Birt-Hogg-Dube syndrome, has also been reported to have typical KT findings.KTs are strictly benign (i.e. do not metastasize) but may be painful, disfiguring, and sometimes large and/or incapacitating lesions. They have often been treated by strictly local surgical resections. However, they do have a high rate of recurrence at the site of resection and therefore have been treated with various other non-invasive local measures in efforts to avoid recurrences; these other methods have also been preferred to treat numerous tumors in individuals, for cosmetic reasons, and/or to relieve tumor-induce incapacitations.

Presentation
In individuals with tuberous sclerosis, KTs commonly present with multiple firm red-colored to skin-colored nodules or tumors that emanate from the proximal nail fold or, less often, proximal skin beneath the nail. They often develop after puberty; increase in number over time; more frequently occur in the toenails than fingernails (the most common sites are on the big toe and thumb); are generally 5 to 10 mm in length but occasionally grow to far larger sizes; and may be or become disfiguring, painful, and/or incapacitating. Nearly 50% of post-puberty individuals with tuberous sclerosis have KTs. (Tuberous sclerosis is also associated with a second type of angiofibroma, adenoma sebaceum, also termed facial angiofibroma, in ~75% of cases.) Individuals presenting with KTs that do not have tuberous sclerosis commonly present with a single lesion in a nail bed. KT may also present as a recurrence of a lesion at the site where it was surgically removed. Rare cases of KTs have had a history of crushing trauma at the sites where the KTs later developed.

Pathology
Microscopic histopathological analyses of KTs commonly reveal a lesion with epidermal acanthosis (i.e. thickening of the skin), hyperkeratosis (i.e. thickening of the outermost layer of the epidermis), and skin features typical of angiofibroma viz., spindle-shaped or star-shaped fibroblasts and ectatic blood vessels in a dense collagen fiber connective tissue background.

Etiology
In cases associated with tuberous sclerosis, KTs appear to be a result of this diseases associated genetic abnormalies, i.e. loss-of-function mutations in one of the two normally paired TSC1 or one of the two normally paired TSC2 tumor suppressor genes </s>


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


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Occupational lung disease and can you explain it in depth? [/INST] Occupational lung diseases are work-related, lung conditions that have been caused or made worse by the materials a person is exposed to within the workplace. It includes a broad group of diseases, including occupational asthma, industrial bronchitis, chronic obstructive pulmonary disease (COPD), bronchiolitis obliterans, inhalation injury, interstitial lung diseases (such as pneumoconiosis, hypersensitivity pneumonitis, lung fibrosis), infections, lung cancer and mesothelioma. These diseases can be caused directly or due to immunological response to an exposure to a variety of dusts, chemicals, proteins or organisms.
Occupational cases of interstitial lung disease may be misdiagnosed as COPD, idiopathic pulmonary fibrosis, or a myriad of other diseases; leading to a delay in identification of the causative agent.

Types of occupational lung diseases
Asthma
Asthma is a respiratory disease that can begin or worsen due to exposure at work and is characterized by episodic narrowing of the respiratory tract. Occupational asthma has a variety of causes, including sensitization to a specific substance, causing an allergic response; or a reaction to an irritant that is inhaled in the workplace. Exposure to various substances can also worsen pre-existing asthma. People who work in isocyanate manufacturing, who use latex gloves, or who work in an indoor office environment are at higher risk for occupational asthma than the average US worker. Approximately 2 million people in the US have occupational asthma.

Bronchiolitis obliterans
Bronchiolitis obliterans, also known as constrictive bronchiolitis or obliterative bronchiolitis is a respiratory disease caused by injury to the smallest airways, called bronchioles. It has been reported to occur from exposure to inhaled toxins and gases including sulfur mustard gas, nitrogen oxides, diacetyl (used in many food and beverage flavorings), 2,3-pentanedione, fly ash and fiberglass.

COPD
Chronic obstructive pulmonary disease is a respiratory disease that can encompass chronic bronchitis and/or emphysema. 15% of the cases of COPD in the United States can be attributed to occupational exposure, including exposure to silica and coal dust. People who work in mining, construction, manufacturing (specifically textiles, rubber, plastic, and leather), building, and utilities are at higher risk for COPD than the average US worker.

Hypersensitivity pneumonitis
Hypersensitivity pneumonitis (HP; also called allergic alveolitis, bagpipe lung, or extrinsic allergic alveolitis, EAA) is an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled organic dusts.

Lung cancer
Numerous categories of ionizing radiation, chemicals and mixtures, occupational exposures, metals, dust and fibers have been linked to occurrence of lung cancer.

Mesothelioma
Mesothelioma is a cancer of the mesothelium, part of which is the pleura, the lining of the lungs. Mesothelioma is caused by exposure to asbestos.

Pneumoconiosis
Pneumoconiosis are occupational lung diseases that are caused due to accumulation of dust in the lungs and bodys reaction to its presence. Most common pneumoconiosis are silicosis, coal workers’ pneumoconiosis (CWP), and asbestosis. Other examples include minerals (such kaolin, talc, mica), beryllium lung disease, hard metal disease and silicon carbide pneumoconiosis.

Smoke Inhalation
Inhaling smoke and other byproducts of combustion can cause pulmonary injury. A third of all burn victims admitted to a hospital are affected by pulmonary injury from inhaling smoke and fatality from inhalation injuries is higher than burn injuries - mortality exceeds 50% for burn victims with severe burn and inhalation injury. Tissue oxygenation is significantly affected and thermal injury to the upper airways, lower airways, and lung parenchyma occurs.
Poor tissue oxygenation is a life-threatening conditions and results from inhaling carbon monoxide, cyanide, a gas mixtures devoid of  oxygen, or from an imbalance between alveolar ventilation and blood supply.
Carbon monoxide is a colorless and odorless gas, which can interfere with and impede respiration. Oxygens tendency to bind with hemoglobin is 250 times less than carbon monoxide, severely reducing the quantity of circulating oxygen and limiting tissue oxygenation in carbon monoxide poisoning. Exposure can be deliberate (suicidal) or accidental and can come from automobile exhaust pipes, inhaling smoke during a fire accident, and poorly vented gas heaters, generators, and other appliances.Cyanide is inhaled into the lungs in gaseous form – as hydrogen cyanide. Cyanide can also be diffused through the skin or ingested. Rapid infusion of high-dose cyanide cause cyanide poisoning. It is produced when nitroprusside is broken down into its constituents. It inhibits cells from properly utilizing oxygen by disrupting cytochrome oxidase, and can be more damaging to the brain and heart.Cyanide is a highly toxic chemical often used in industries and in laboratories. Finger nail glue remover products contain acetonitrile and its metabolic break down produces cyanide. In some plants such as in pits of apricots, cyanide can be found as glycosides can synthesize cyanide. Smoking cigarettes is a major avenue of exposure.

Pulmonary Aspiration Syndromes
Deglutition is the main cause for minute food and fluid to get aspirated into the lungs. Impaired consciousness and esophageal disorders can cause deglutition.
Acute Aspiration of Gastric Content (Mendelson Syndrome): pulmonary response to aspirated content depend on the quantity and constituent of aspirated gastric content. Chemical pneumonitis is severe if aspirated content is acidic and aspirated gastric acid – pH less than 2.5 – can inflame bronchial epithelium and cause bronchiolitis, hemorrhagen, and pulmonary edema.Chronic Aspiration of Gastric Contents: disorders of the larynx and the esophagus are major causes of chronic aspiration of gastric content – achalasia, esophageal stricture, systemic sclerosis (scleroderma), esophageal carcinoma, esophagitis, and gastro-esophageal reflux. Pulmonary aspiration can result when the lower intestinal sphincter relax and spill out gastric content into the esophagus.Smoking, consuming alcohol or caffeine, and the drug theophylline used in asthma patients are known to cause lower intestinal sphincter relaxation. Gastro-esophageal reflux and chronic aspiration are associated with few pulmonary disorders: asthma, chronic cough, bronchiectasis, and pulmonary fibrosis.Difficulty swallowing, ageing, dental problems impeding proper chewing, consuming alcohol, and taking sedatives cause café coronary, obstruction of the upper airways by food particles.Retaining an Aspirated Foreign Body: poor clearance of aspirated material out of the tracheobronchial tree can result in acute and chronic conditions including atelectasis, post obstructive hyperinflation, acute and recurrent pneumonia, bronchiectasis, and lung abscesses. Retained aspirated foreign body can sometimes get misdiagnosed as asthma, chronic obstructive pulmonary disease (COPD), or lung cancerAspirating an Inert Material: aspirating large inert material coupled with an impaired cough can cause asphyxiaHydrocarbon Pneumonitis: secondary aspiration following vomiting ingested petroleum products – gasoline, kerosene, furniture polish, and other petroleum products used around home environment – can injure lungs and result in hydrocarbon pneumonitisLipoid Pneumonia: is a chronic disorder common among older people who have difficulty swallowing, with aspiration of oily material - mineral oil, cod liver oil, and oily nose drops - as its mains cause

Occupational environmental exposure
Arsenic
Arsenic is classified as an IARC Group 1 carcinogen and is a cause of lung cancer. Workers can be exposed to arsenic through work with some pesticides or in copper smelting.

Asbestos
Asbestos is a mineral which was extensively used in the United States to fireproof buildings and textiles, among other items, in the 1950s-1980s. Workers are frequently exposed to asbestos during demolition and renovation work, which can cause asbestosis and/or mesothelioma. Asbestos exposure can also cause pleural effusion, diffuse pleural fibrosis, pleural plaques, and non-mesothelioma lung cancer. Smoking greatly increases the lung cancer risk of asbestos exposure.Residents and workers of asbestos mining centers such as the town of Asbest, Russia experience dangerous exposure to asbestos and asbestos dust.

BCME
BCME (Bis(chloromethyl) ether) is associated with small cell lung cancer in workers who have been exposed. Exposure can occur via direct manufacture of BCME or its presence as a byproduct.

Beryllium
Beryllium is classified as an IARC Group 1 carcinogen and can also cause interstitial lung disease. Manufacturing workers, dental technicians, machinists, jewelers, plumbers, electricians, precious metal reclamation workers, and welders are at risk for beryllium exposure.

Cadmium
Cadmium is classified as an IARC Group 1 carcinogen and it is a cause of several cancers, including lung cancer. Workers can be exposed to cadmium through welding, zinc smelting, copper smelting, lead smelting, electroplating, battery manufacture, plastics manufacture, and in alloying.

Chromium
Chromium is classified as an IARC Group 1 carcinogen and is linked to lung cancer. Workers can be exposed to chromium via welding, steel manufacturing, pigment/dye manufacturing, and electroplating.

Coal dust
Exposure to coal dust is the cause of coalworkers pneumoconiosis, also called "black lung disease", is an interstitial lung disease caused by long-term exposure (over 10 years) to coal dust. Symptoms include shortness of breath and lowered pulmonary function. It can be fatal when advanced. Between 1970 and 1974, prevalence of CWP among US coal miners who had worked over 25 years was 32%; the same group saw a prevalence of 9% in 2005–2006. It can also exacerbate or cause COPD.

Diesel exhaust
Diesel exhaust contains a variety of gaseous and particulate chemicals, including soot, polycyclic aromatic hydrocarbons, and other known carcinogens.

Flock
Flocking is the technique of adding small pieces of nylon or other material to a backing, usually a textile, to create a contrasting texture. Inhalation of flock can cause flock workers lung.

Indium lung
Indium lung is an interstitial lung disease caused by occupational exposure to indium tin oxide.

Nanoparticles
The high surface area to volume ratio of nanoparticles may make them an inhalation hazard for workers exposed to them. This is a topic of ongoing research as of 2015.

Nickel
Nickel is classified by the IARC as a Group 1 carcinogen; nickel compound exposure is associated with nasal cancer as well as lung cancer. Workers may be exposed to nickel in machining/grinding industry, nickel extraction/production, welding, and electroplating.

Polycyclic aromatic hydrocarbons
Polycyclic aromatic hydrocarbons (PAHs), fused-ring chemicals formed during the combustion of fossil fuels, are metabolized by the cytochrome P450 complex to highly reactive carbocations, which can mutate DNA and cause cancer. Workers may be exposed to PAHs while working in a foundry, in the roofing industry, or due to environmental tobacco smoke.

Silica
Exposure to silica can cause Silicosis, which is a fibrosing interstitial lung disease caused by inhaling fine particles of silica, most commonly in the form of quartz or cristobalite </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Gingival recession and can you explain it in depth? [/INST] Gingival recession, also known as receding gums, is the exposure in the roots of the teeth caused by a loss of gum tissue and/or retraction of the gingival margin from the crown of the teeth. Gum recession is a common problem in adults over the age of 40, but it may also occur starting in adolescence, or around the age of 10. It may exist with or without concomitant decrease in crown-to-root ratio (recession of alveolar bone).

Classification
Various classifications have been proposed to classify gingival recession, Miller’s classification system being the one that is most widely followed. Many cases which are encountered in daily clinical practice cannot be classified according to the criteria of the present classification systems. Kumar & Masamattis classification system gives a comprehensive depiction of recession defect that can be used to include cases that cannot be classified according to present classifications. A separate classification system for palatal recessions (PR) has been given. A new comprehensive classification system classifies recession on the basis of the position of interdental papilla and buccal/lingual/palatal recessions. Kumar & Masamattis classification system tries to overcome the limitations of Millers classification.

Causes
There are many possible causes for gingival recession:

By far the most common cause is gum disease (periodontal disease).
Overaggressive brushing also causes gum recession. One systemic review of the literature concluded that "The data to support or refute the association between tooth brushing and gingival recession are inconclusive," although aggressive or forceful brushing was not specifically addressed. A subsequent study found horizontal tooth brushing technique (versus Bass technique or circular methods), medium-hardness toothbrush use and brushing only once daily were associated with gingival recession.
Improper flossing (i.e., flossing too roughly or aggressively) which may cut into the gums.
Hereditary thin, fragile or insufficient gingival tissue predisposes to gingival recession.
Dipping tobacco, which affects the mucous membrane lining in the mouth and will cause receding gums over time
Self-inflicted trauma, such as habits like digging a fingernail or pencil into the gum. This type of recession more commonly associated with children and persons with psychiatric disorders.
Scurvy (lack of dietary vitamin C)
Acute necrotizing ulcerative gingivitis
Abnormal tooth position, such as tooth crowding, giving inadequate cover of one or more teeth by the jaw bone.
Piercings in the lip or tongue that wear away the gum by rubbing against it.
Intentional gingival retraction. For example, the adult tooth may not grow out of the gum, and to remedy this, a procedure called an exposure is done. It involves the gum tissue being cut open to allow the adult tooth to grow out. This is a less common cause of gum recession.

Symptoms
Gum recession is generally not an acute condition. In most cases, receding of gums is a progressive condition that occurs gradually over the years. This is one reason that it is common over the age of 40 </s>