<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Irritant diaper dermatitis and explain in detail? [/INST] Irritant diaper dermatitis (IDD, also called a diaper/nappy rash) is a generic term applied to skin rash in the diaper nappy area that are caused by various skin disorders and/or irritants.
Generic irritant diaper/nappy  dermatitis is characterized by joined patches of erythema and scaling mainly seen on the convex surfaces, with the skin folds spared.
Diaper/nappy dermatitis with secondary bacterial or fungal involvement tends to spread to concave surfaces (i.e. skin folds), as well as convex surfaces, and often exhibits a central red, beefy erythema with satellite pustules around the border.
It is usually considered a form of irritant contact dermatitis. The word "diaper" is in the name not because the diaper/nappy itself causes the rash but rather because the rash is associated with diaper use, being caused by the materials trapped by the diaper (usually feces). Allergic contact dermatitis has also been suggested, but there is little evidence for this cause. In adults with incontinence (fecal, urinary, or both), the rash is sometimes called incontinence-associated dermatitis (IAD).The term diaper candidiasis is used when a fungal origin is identified. The distinction is critical because the treatment (antifungals) is completely different.

Causes
Irritant diaper dermatitis develops when skin is exposed to prolonged wetness, increased skin pH caused by the combination, and subsequent reactions, of urine and feces, and resulting breakdown of the stratum corneum, or outermost layer of the skin.  This may be due to diarrhea, frequent stools, tight diapers, overexposure to ammonia, or allergic reactions.  In adults, the stratum corneum is composed of 25 to 30 layers of flattened dead keratinocytes, which are continuously shed and replaced from below. These dead cells are interlaid with lipids secreted by the stratum granulosum just underneath, which help to make this layer of the skin a waterproof barrier. The stratum corneums function is to reduce water loss, repel water, protect deeper layers of the skin from injury, and to repel microbial invasion of the skin. In infants, this layer of the skin is much thinner and more easily disrupted.

Urine
Although wetness alone has the effect of macerating the skin, softening the stratum corneum, and greatly increasing susceptibility to friction injury, urine has an additional impact on skin integrity because of its effect on skin pH. While studies show that ammonia alone is only a mild skin irritant, when urea breaks down in the presence of fecal urease it increases pH because ammonia is released, which in turn promotes the activity of fecal enzymes such as protease and lipase. These fecal enzymes increase the skins hydration and permeability to bile salts which also act as skin irritants.
There is no detectable difference in rates of diaper rash in conventional disposable diaper wearers and reusable cloth diaper wearers. "Babies wearing superabsorbent disposable diapers with a central gelling material have fewer episodes of diaper dermatitis compared with their counterparts wearing cloth diapers. However, keep in mind that superabsorbent diapers contain dyes that were suspected to cause allergic contact dermatitis (ACD)." Whether wearing cloth or disposable diapers they should be changed frequently to prevent diaper rash, even if they dont feel wet. To reduce the incidence of diaper rash, disposable diapers have been engineered to pull moisture away from the babys skin using synthetic non-biodegradable gel.  Today, cloth diapers use newly available superabsorbent microfiber cloth placed in a pocket with a layer of light permeable material that contacts the skin.  This design serves to pull moisture away from the skin in to the microfiber cloth.  This technology is used in most major pocket cloth diapers brands today.

Diet
The interaction between fecal enzyme activity and IDD explains the observation that infant diet and diaper rash are linked because fecal enzymes are in turn affected by diet. Breast-fed babies, for example, have a lower incidence of diaper rash, possibly because their stools have higher pH and lower enzymatic activity. Diaper rash is also most likely to be diagnosed in infants 8–12 months old, perhaps in response to an increase in eating solid foods and dietary changes around that age that affect fecal composition. Any time an infants diet undergoes a significant change (i.e. from breast milk to formula or from milk to solids) there appears to be an increased likelihood of diaper rash.The link between feces and IDD is also apparent in the observation that infants are more susceptible to developing diaper rash after treating with antibiotics, which affect the intestinal microflora. Also, there is an increased incidence of diaper rash in infants who have had diarrhea in the previous 48 hours, which may be because fecal enzymes such as lipase and protease are more active in feces which have passed rapidly through the gastrointestinal tract.

Secondary infections
The significance of secondary infection in IDD remains controversial. There seems to be no link between presence or absence of IDD and microbial counts. Although apparently healthy infants sometimes culture positive for Candida and other organisms without exhibiting any symptoms, there does seem to be a positive correlation between the severity of the diaper rash noted and the likelihood of secondary involvement. A wide variety of infections has been reported, including Staphylococcus aureus, Streptococcus pyogenes, Proteus mirabilis, enterococci and Pseudomonas aeruginosa, but it appears that Candida is the most common opportunistic invader in diaper areas.

Diagnosis
The diagnosis of IDD is made clinically, by observing the limitation of an erythematous eruption to the convex surfaces of the genital area and buttocks. If the diaper dermatitis occurs for greater than 3 days it may be colonized with Candida albicans, giving it the beefy red, sharply marginated, appearance of diaper candidiasis.

Differential diagnosis
Other rashes that  occur in the diaper area include seborrhoeic dermatitis and atopic dermatitis. Both Seborrheic and Atopic dermatitis require individualized treatment; they are not the subject of this article.

Seborrheic dermatitis, typified by oily, thick yellowish scales, is most commonly seen on the scalp (cradle cap) but can also appear in the inguinal folds.
Atopic dermatitis, or eczema, is associated with allergic reaction, often hereditary. This class of rashes may appear anywhere on the body and is characterized by intense itchiness.

Treatments
Possible treatments include minimizing diaper use, barrier creams, mild topical cortisones, and antifungal agents. A variety of other inflammatory and infectious processes can occur in the diaper area and an awareness of these secondary types of diaper dermatitis aids in the accurate diagnosis and treatment of patients.Overall, there is sparse evidence of sufficient quality to be certain of the effectiveness of the various treatments. Washcloths with cleansing, moisturising and protective properties may be better than soap and water, and skin cleansers may also be better than soap and water, but the certainty of evidence with regard other treatments is very low.

Diaper changing
The most effective treatment, although not the most practical one, is to discontinue use of diapers, allowing the affected skin to air out </s>


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


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pulmonary embolism and explain in detail? [/INST] Pulmonary embolism (PE) is a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream (embolism). Symptoms of a PE may include shortness of breath, chest pain particularly upon breathing in, and coughing up blood. Symptoms of a blood clot in the leg may also be present, such as a red, warm, swollen, and painful leg. Signs of a PE include low blood oxygen levels, rapid breathing, rapid heart rate, and sometimes a mild fever. Severe cases can lead to passing out, abnormally low blood pressure, obstructive shock, and sudden death.PE usually results from a blood clot in the leg that travels to the lung. The risk of blood clots is increased by cancer, prolonged bed rest, smoking, stroke, certain genetic conditions, estrogen-based medication, pregnancy, obesity, and after some types of surgery. A small proportion of cases are due to the embolization of air, fat, or amniotic fluid. Diagnosis is based on signs and symptoms in combination with test results. If the risk is low, a blood test known as a D-dimer may rule out the condition. Otherwise, a CT pulmonary angiography, lung ventilation/perfusion scan, or ultrasound of the legs may confirm the diagnosis. Together, deep vein thrombosis and PE are known as venous thromboembolism (VTE).Efforts to prevent PE include beginning to move as soon as possible after surgery, lower leg exercises during periods of sitting, and the use of blood thinners after some types of surgery. Treatment is with anticoagulants such as heparin, warfarin or one of the direct-acting oral anticoagulants (DOACs). These are recommended for at least three months. Severe cases may require thrombolysis using medication such as tissue plasminogen activator (tPA) given intravenously or through a catheter, and some may require surgery (a pulmonary thrombectomy). If blood thinners are not appropriate, a temporary vena cava filter may be used.Pulmonary emboli affect about 430,000 people each year in Europe. In the United States, between 300,000 and 600,000 cases occur each year, which contribute to at least 40,000 deaths. Rates are similar in males and females. They become more common as people get older.

Signs and symptoms
Symptoms of pulmonary embolism are typically sudden in onset and may include one or many of the following: dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a "pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability because of decreased blood flow through the lungs and into the left side of the heart. About 15% of all cases of sudden death are attributable to PE. While PE may present with syncope, less than 1% of syncope cases are due to PE.On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub may be audible over the affected area of the lung (mostly in PE with infarct). A pleural effusion is sometimes present that is exudative, detectable by decreased percussion note, audible breath sounds, and vocal resonance. Strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, and/or raised jugular venous pressure. A low-grade fever may be present, particularly if there is associated pulmonary hemorrhage or infarction.As smaller pulmonary emboli tend to lodge in more peripheral areas without collateral circulation, they are more likely to cause lung infarction and small effusions (both of which are painful), but not hypoxia, dyspnea, or hemodynamic instability such as tachycardia. Larger PEs, which tend to lodge centrally, typically cause dyspnea, hypoxia, low blood pressure, fast heart rate and fainting, but are often painless because there is no lung infarction due to collateral circulation. The classic presentation for PE with pleuritic pain, dyspnea, and tachycardia is likely caused by a large fragmented embolism causing both large and small PEs. Thus, small PEs are often missed because they cause pleuritic pain alone without any other findings and large PEs are often missed because they are painless and mimic other conditions often causing ECG changes and small rises in troponin and brain natriuretic peptide levels.PEs are sometimes described as massive, submassive, and nonmassive depending on the clinical signs and symptoms. Although the exact definitions of these are unclear, an accepted definition of massive PE is one in which there is hemodynamic instability. This is a cause of obstructive shock, which presents as sustained low blood pressure, slowed heart rate, or pulselessness.

Risk factors
About 90% of emboli are from proximal leg deep vein thrombosis (DVTs) or pelvic vein thromboses. The rare venous thoracic outlet syndrome can also be a cause of DVTs, especially in young men without significant risk factors. DVTs are at risk for dislodging and migrating to the lung circulation. The conditions are generally regarded as a continuum termed venous thromboembolism (VTE).VTE is much more common in immunocompromised individuals as well as individuals with comorbidities including:

Those that undergo orthopedic surgery at or below the hip without prophylaxis.This is due to immobility during or after the surgery, as well as venous damage during the surgery.
Pancreatic and colon cancer patients (other forms of cancer also can be factors, but these are the most common)This is due to the release of procoagulants.Risk of VTE is at its greatest during diagnosis and treatment, but lowers in remission.
Patients with high-grade tumors
Pregnant individualsAs the body puts itself into what is known as a "hypercoagulable state" the risk of a hemorrhage during childbirth is decreased and is regulated by increased expression of factors VII, VIII, X, Von Willebrand, and fibrinogen.
Those on estrogen medicationThe development of thrombosis is classically due to a group of causes named Virchows triad (alterations in blood flow, factors in the vessel wall, and factors affecting the properties of the blood). Often, more than one risk factor is present.
Alterations in blood flow: immobilization (after surgery, long-haul flight), injury, pregnancy (also procoagulant), obesity (also procoagulant), cancer (also procoagulant)
Factors in the vessel wall: surgery, catheterizations causing direct injury ("endothelial injury")
Factors affecting the properties of the blood (procoagulant state):
Estrogen-containing medication (transgender hormone therapy, menopausal hormone therapy and hormonal contraceptives)
Genetic thrombophilia (factor V Leiden, prothrombin mutation G20210A, protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia and plasminogen/fibrinolysis disorders)
Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria)
Cancer (due to secretion of pro-coagulants)Although most pulmonary embolisms are the result of proximal leg deep vein thrombosis (DVTs), there are still many other risk factors that can also result in a pulmonary embolism.

Risk factors include:
Varicose veins caused by vascular damage
Pulmonary hypertension
Diabetes
Traumatic hip fractures that immobilize the patient
Joint fixation (primarily in the legs)

Underlying causes
After a first PE, the search for secondary causes is usually brief. Only when a second PE occurs, and especially when this happens while still under anticoagulant therapy, a further search for underlying conditions is undertaken. This will include testing ("thrombophilia screen") for Factor V Leiden mutation, antiphospholipid antibodies, protein C and S and antithrombin levels, and later prothrombin mutation, MTHFR mutation, Factor VIII concentration and rarer inherited coagulation abnormalities.

Diagnosis
To diagnose a pulmonary embolism, a review of clinical criteria to determine the need for testing is recommended. In those who have low risk, age less than 50, heart rate less than 100 beats per minute, oxygen level more than 94% on room air, and no leg swelling, coughing up of blood, surgery or trauma in the last four weeks, previous blood clots, or estrogen use, further testing is not typically needed.In situations with more high risk individuals, further testing is needed.  A CT pulmonary angiogram (CTPA) is the preferred method for diagnosis of a pulmonary embolism due to its easy administration and accuracy. Although a CTPA is preferred, there are also other tests that can be done. For example, a proximal lower limb compression ultrasound (CUS) can be used. This is a test which is primarily used as a confirmatory test, meaning it confirms a previous analysis showing the presence or suspected presence of a pulmonary embolism. According to a cross-sectional study, CUS tests have a sensitivity of 41% and specificity of 96%.If there are concerns this is followed by testing to determine a likelihood of being able to confirm a diagnosis by imaging, followed by imaging if other tests have shown that there is a likelihood of a PE diagnosis.The diagnosis of PE is based primarily on validated clinical criteria combined with selective testing because the typical clinical presentation (shortness of breath, chest pain) cannot be definitively differentiated from other causes of chest pain and shortness of breath. The decision to perform medical imaging is based on clinical reasoning, that is, the medical history, symptoms, and findings on physical examination, followed by an assessment of clinical probability.

Probability testing
The most commonly used method to predict clinical probability, the Wells score, is a clinical prediction rule, whose use is complicated by multiple versions being available. In 1995, Philip Steven Wells, initially developed a prediction rule (based on a literature search) to predict the likelihood of PE, based on clinical criteria. The prediction rule was revised in 1998 This prediction rule was further revised when simplified during a validation by Wells et al. in 2000. In the 2000 publication, Wells proposed two different scoring systems using cutoffs of 2 or 4 with the same prediction rule. In 2001, Wells published results using the more conservative cutoff of 2 to create three categories. An additional version, the "modified extended version", using the more recent cutoff of 2 but including findings from Wellss initial studies were proposed. Most recently, a further study reverted to Wellss earlier use of a cutoff of 4 points to create only two categories.There are additional prediction rules for PE, such as the Geneva rule. More importantly, the use of any rule is associated with reduction in recurrent thromboembolism.The Wells score:
clinically suspected DVT – 3.0 points
alternative diagnosis is less likely than PE – 3.0 points
tachycardia (heart rate > 100) – 1.5 points
immobilization (≥ 3d)/surgery in previous four weeks – 1.5 points
history of DVT or PE – 1.5 points
hemoptysis – 1.0 points
malignancy (with treatment within six months) or palliative – 1.0 pointsTraditional interpretation
Score >6.0 – High (probability 59% based on pooled data)
Score 2.0 to 6.0 – Moderate (probability 29% based on pooled data)
Score <2.0 – Low (probability 15% based on pooled data)Alternative interpretation
Score > 4 – PE likely. Consider diagnostic imaging.
Score 4 or less – PE unlikely. Consider D-dimer to rule out PE.Recommendations for a diagnostic algorithm were published by the PIOPED investigators; however, these recommendations do not reflect research using 64 slice MDCT. These investigators recommended:

Low clinical probability. If negative D-dimer, PE is excluded. If positive D-dimer, obtain MDCT and base treatment on results.
Moderate clinical probability. If negative D-dimer, PE is excluded. However, the authors were not concerned that a negative MDCT with negative D-dimer in this setting has a 5% probability of being false. Presumably, the 5% error rate will fall as 64 slice MDCT is more commonly used. If positive D-dimer, obtain MDCT and base treatment on results.
High clinical probability. Proceed to MDCT. If positive, treat, if negative, more tests are needed to exclude PE. A D-dimer of less than 750 ug/L does not rule out PE in those who are at high risk.

Pulmonary embolism rule-out criteria
The pulmonary embolism rule-out criteria (PERC) helps assess people in whom pulmonary embolism is suspected, but unlikely. Unlike the Wells score and Geneva score, which are clinical prediction rules intended to risk stratify people with suspected PE, the PERC rule is designed to rule out the risk of PE in people when the physician has already stratified them into a low-risk category.People in this low risk category without any of these criteria may undergo no further testing for PE: low oxygen saturations – SaO2 <95%, unilateral leg swelling, coughing up blood, prior DVT or PE, recent surgery or trauma, age >50, hormone use, fast heart rate. The rationale behind this decision is that further testing (specifically CT angiogram of the chest) may cause more harm (from radiation exposure and contrast dye) than the risk of PE. The PERC rule has a sensitivity of 97.4% and specificity of 21.9% with a false negative rate of 1.0% (16/1666).

Blood tests
In people with a low or moderate suspicion of PE, a normal D-dimer level (shown in a blood test) is enough to exclude the possibility of thrombotic PE, with a three-month risk of thromboembolic events being 0.14%. D-dimer is highly sensitive but not specific (specificity around 50%). In other words, a positive D-dimer is not synonymous with PE, but a negative D-dimer is, with a good degree of certainty, an indication of absence of a PE. A low pretest probability is also valuable in ruling out PE. The typical cut off is 500 μg/L, although this varies based on the assay. However, in those over the age of 50, changing the cut-off value to the persons age multiplied by 10 μg/L (accounting for assay which has been used) is recommended as it decreases the number of falsely positive tests without missing any additional cases of PE.When a PE is being suspected, several blood tests are done in order to exclude important secondary causes of PE. This includes a full blood count, clotting status (PT, aPTT, TT), and some screening tests (erythrocyte sedimentation rate, kidney function, liver enzymes, electrolytes). If one of these is abnormal, further investigations might be warranted to the issue.Troponin levels are increased in between 16 and 47% with pulmonary embolism.

Imaging
In typical people who are not known to be at high risk of PE, imaging is helpful to confirm or exclude a diagnosis of PE after simpler first-line tests are used. Medical societies recommend tests such as the D-dimer to first provide supporting evidence for the need for imaging, and imaging would be done if other tests confirmed a moderate or high probability of finding evidence to support a diagnosis of PE.CT pulmonary angiography is the recommended first line diagnostic imaging test in most people.Ultrasound of the legs can confirm the presence of a PE but cannot rule it out.

CT pulmonary angiography
CT pulmonary angiography (CTPA) is a pulmonary angiogram obtained using computed tomography (CT) with radiocontrast rather than right heart catheterization. Its advantages are that it is accurate, it is non-invasive, it is more often available, and it may identifying other lung disorders in case there is no pulmonary embolism. The accuracy and non-invasive nature of CTPA also make it advantageous for people who are pregnant.

Assessing the accuracy of CT pulmonary angiography is hindered by the rapid changes in the number of rows of detectors available in multidetector CT (MDCT) machines. According to a cohort study, single-slice spiral CT may help diagnose detection among people with suspected pulmonary embolism. In this study, the sensitivity was 69% and specificity was 84%. In this study which had a prevalence of detection was 32%, the positive predictive value of 67.0% and negative predictive value of 85.2%. However, this studys results may be biased due to possible incorporation bias, since the CT scan was the final diagnostic tool in people with pulmonary embolism. The authors noted that a negative single slice CT scan is insufficient to rule out pulmonary embolism on its own. A separate study with a mixture of 4 slice and 16 slice scanners reported a sensitivity of 83% and a specificity of 96%, which means that it is a good test for ruling out a pulmonary embolism if it is not seen on imaging and that it is very good at confirming a pulmonary embolism is present if it is seen. This study noted that additional testing is necessary when the clinical probability is inconsistent with the imaging results. CTPA is non-inferior to VQ scanning, and identifies more emboli (without necessarily improving the outcome) compared to VQ scanning.

Ventilation/perfusion scan
A ventilation/perfusion scan (or V/Q scan or lung scintigraphy) shows that some areas of the lung are being ventilated but not perfused with blood (due to obstruction by a clot). This type of examination is as accurate as multislice CT, but is less used, due to the greater availability of CT technology.  It is particularly useful in people who have an allergy to iodinated contrast, impaired kidney function, or are pregnant (due to its lower radiation exposure as compared to CT). The test can be performed with planar two-dimensional imaging, or single photon emission computed tomography (SPECT) which enables three-dimensional imaging. Hybrid devices combining SPECT and CT (SPECT/CT) further enable anatomic characterization of any abnormality.

Low probability diagnostic tests/non-diagnostic tests
Tests that are frequently done that are not sensitive for PE, but can be diagnostic.

Chest X-rays are often done on people with shortness of breath to help rule-out other causes, such as congestive heart failure and rib fracture. Chest X-rays in PE are rarely normal, but usually lack signs that suggest the diagnosis of PE (for example, Westermark sign, Hamptons hump).
Ultrasonography of the legs, also known as leg doppler, in search of deep venous thrombosis (DVT). The presence of DVT, as shown on ultrasonography of the legs, is in itself enough to warrant anticoagulation, without requiring the V/Q or spiral CT scans (because of the strong association between DVT and PE). This may be a valid approach in pregnancy, in which the other modalities would increase the risk of birth defects in the unborn child. However, a negative scan does not rule out PE, and low-radiation dose scanning may be required if the mother is deemed at high risk of having a pulmonary embolism. The main use of ultrasonography of the legs is therefore in those with clinical symptoms suggestive of deep vein thrombosis.

Fluoroscopic pulmonary angiography
Historically, the gold standard for diagnosis was pulmonary angiography by fluoroscopy, but this has fallen into disuse with the increased availability of non-invasive techniques that offer similar diagnostic accuracy.

Electrocardiogram
The primary use of the ECG is to rule out other causes of chest pain.  An electrocardiogram (ECG) is routinely done on people with chest pain to quickly diagnose myocardial infarctions (heart attacks), an important differential diagnosis in an individual with chest pain. While certain ECG changes may occur with PE, none are specific enough to confirm or sensitive enough to rule out the diagnosis. An ECG may show signs of right heart strain or acute cor pulmonale in cases of large PEs – the classic signs are a large S wave in lead I, a large Q wave in lead III, and an inverted T wave in lead III (S1Q3T3), which occurs in 12–50% of people with the diagnosis, yet also occurs in 12% without the diagnosis.This is occasionally present (occurring in up to 20% of people), but may also occur in other acute lung conditions, and, therefore, has limited diagnostic value.  The most commonly seen signs in the ECG are sinus tachycardia, right axis deviation, and right bundle branch block.  Sinus tachycardia, however, is still only found in 8–69% of people with PE.ECG findings associated with pulmonary emboli may suggest worse prognosis since the six findings identified with RV strain on ECG (heart rate > 100 beats per minute, S1Q3T3, inverted T waves in leads V1-V4, ST elevation in aVR, complete right bundle branch block, and atrial fibrillation) are associated with increased risk of circulatory shock and death.Cases with inverted T in leads V1-3 are suspected with PE or inferior myocardial infarction. PE cases show inverted T waves in leads II and aVF, but inferior myocardial infarction cases do not show inverted T waves in II and aVF.

Echocardiography
In massive and submassive PE, dysfunction of the right side of the heart may be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the right ventricle, a low-pressure pump, is unable to match the pressure. Some studies (see below) suggest that this finding may be an indication for thrombolysis. Not every person with a (suspected) pulmonary embolism requires an echocardiogram, but elevations in cardiac troponins or brain natriuretic peptide may indicate heart strain and warrant an echocardiogram, and be important in prognosis.The specific appearance of the right ventricle on echocardiography is referred to as the McConnells sign. This is the finding of akinesia of the mid-free wall but a normal motion of the apex. This phenomenon has a 77% sensitivity and a 94% specificity for the diagnosis of acute pulmonary embolism in the setting of right ventricular dysfunction.

Prevention
Pulmonary embolism may be preventable in those with risk factors. People admitted to hospital may receive preventative medication, including unfractionated heparin, low molecular weight heparin (LMWH), or fondaparinux, and anti-thrombosis stockings to reduce the risk of a DVT in the leg that could dislodge and migrate to the lungs.Following the completion of anticoagulation in those with prior PE, long-term aspirin is useful to prevent recurrence.

Treatment
Anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments, such as oxygen or analgesia, may be required. People are often admitted to hospital in the early stages of treatment, and tend to remain under inpatient care until the INR has reached therapeutic levels (if warfarin is used). Increasingly, however, low-risk cases are managed at home in a fashion already common in the treatment of DVT. Evidence to support one approach versus the other is weak.

Anticoagulation
Anticoagulant therapy is the mainstay of treatment. For many years, vitamin K antagonists (warfarin or less commonly acenocoumarol or phenprocoumon) have been the cornerstone. As vitamin K antagonists do not act immediately, initial treatment is with rapidly acting injectable anticoagulants: unfractionated heparin (UFH), low molecular weight heparin (LMWH), or fondaparinux, while oral vitamin K antagonists are initiated and titrated (usually as part of inpatient hospital care) to the international normalized ratio, a test that determines the dose. In terms of injectable treatments, LMWH may reduce bleeding among people with pulmonary embolism as compared to UFH. According to the same review, LMWH reduced the incidence of recurrent thrombotic complications and reduced thrombus size when compared to heparin. There was no difference in overall mortality between participants treated with LMWH and those treated with unfractionated heparin. Vitamin K antagonists require frequent dose adjustment and monitoring of the international normalized ratio (INR). In PE, INRs between 2.0 and 3.0 are generally considered ideal. If another episode of PE occurs under warfarin treatment, the INR window may be increased to e.g. 2.5–3.5 (unless there are contraindications) or anticoagulation may be changed to a different anticoagulant e.g. LMWH.In recent years, many anticoagulants have been introduced that offer similar to warfarin but without a need for titration to the INR. Known as the directly acting oral anticoagulants, these treatments are now preferred over vitamin K antagonists by American professional guidelines. Two of these (rivaroxaban and apixaban) do not require initial heparin or fondaparinux treatment, whereas dabigatran and edoxaban do. A Cochrane review found that there is no evidence of a difference between oral DTIs (dabigatran, rivaroxaban, edoxaban, apixaban) and standard anticoagulation in the prevention of recurrent pulmonary embolism.In people with cancer who develop pulmonary embolism, therapy with a course of LMWH is favored over warfarin or other oral anticoagulants. Similarly, pregnant women are treated with low molecular weight heparin until after delivery to avoid the known teratogenic effects of warfarin, especially in the early stages of pregnancy, but it can be used while breastfeeding.Anticoagulation therapy is usually continued for 3–6 months, or "lifelong" if there have been previous DVTs or PEs, or none of the usual transient risk factors is present. In those without a known cause that can be reversed 2 years of treatment may be better than 6 months. For those with small PEs (known as subsegmental PEs) the effects of anticoagulation is unknown as it has not been properly studied as of 2020.

Thrombolysis
Massive PE causing hemodynamic instability (shock and/or low blood pressure, defined as a systolic blood pressure <90 mmHg or a pressure drop of 40 mmHg for >15 min if not caused by new-onset arrhythmia, hypovolemia or sepsis) is an indication for thrombolysis, the enzymatic destruction of the clot with medication. In this situation, it is the best available treatment in those without contraindications and is supported by clinical guidelines. It is also recommended in those in cardiac arrest with a known PE. Catheter-directed thrombolysis (CDT) is a new technique found to be relatively safe and effective for massive PEs. This involves accessing the venous system by placing a catheter into a vein in the groin and guiding it through the veins by using fluoroscopic imaging until it is located next to the PE in the lung circulation. Medication that breaks up blood clots is released through the catheter so that its highest concentration is directly next to the pulmonary embolus. CDT is performed by  interventional radiologists or vascular surgeons, and in medical centers that offer CDT, it may be offered as a first-line treatment. Catheter-based ultrasound-assisted thrombolysis is being investigated.The use of thrombolysis in non-massive PEs is still debated. Some have found that the treatment decreases the risk of death and increases the risk of bleeding including intracranial hemorrhage. Others have found no decrease in the risk of death.

Inferior vena cava filter
There are two situations when an inferior vena cava filter is considered advantageous, and those are if anticoagulant therapy is contraindicated (e.g. shortly after a major operation), or a person has a pulmonary embolus in spite of being anticoagulated. In these instances, it may be implanted to prevent new or existing DVTs from entering the pulmonary artery and combining with an existing blockage. In spite of the devices theoretical advantage of preventing pulmonary emboli, there is a lack of evidence supporting its effectiveness.Inferior vena cava filters should be removed as soon as it becomes safe to start using anticoagulation. Although modern filters are meant to be retrievable, complications may prevent some from being removed. The long-term safety profile of permanently leaving a filter inside the body is not known.

Surgery
Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes. However, recently, it has gone through a resurgence with the revision of the surgical technique and is thought to benefit certain people. Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy.

Epidemiology
There are roughly 10 million cases of pulmonary embolisms per year. In the United States, pulmonary embolisms are the primary cause of at least 10,000 to 12,000 deaths per year and a contributing cause in at least 30,000 to 40,000 deaths per year. True incidence involving pulmonary embolisms is unknown because they often go undiagnosed or unnoticed until autopsy. From 1993 to 2012, there have been an increased number of admissions in hospitals due to pulmonary embolisms, jumping from 23 cases per 100,000 people to 65 cases per 100,000 people. Despite this increase, there has been a decrease in mortality during that same time period due to medical advances that have occurred.Venous thromboembolism (VTE), a common risk factor, is present at much higher rates in those over the age of 70 (three times higher compared to those aged 45 to 69). This is likely due to there being a generally lower level of activity among the elderly, resulting in higher rates of immobility and obesity. VTE has a large, and continuously rising, case fatality rate. This rate is roughly 10% after 30 days, 15% after three months and up to 20% after one year. Pulmonary embolisms alone (when resulting in hospitalizations) have a case fatality rate of about 5% to 10% so VTE can play a large factor in the severity of the embolisms.When looking at all cases, the rate of fatal pulmonary emboli has declined from 6% to 2% over the last 25 years in the United States. In Europe, an average of approximately 40,000 deaths per year with pulmonary embolism as the primary cause were reported between 2013 and 2015, a conservative estimate because of potential underdiagnosis.

Prognosis
Less than 5 to 10% of symptomatic PEs are fatal within the first hour of symptoms.There are several markers used for risk stratification and these are also independent predictors of adverse outcomes. These include hypotension, cardiogenic shock, syncope, evidence of right heart dysfunction, and elevated cardiac enzymes. Some ECG changes including S1Q3T3 also correlate with a worse short-term prognosis. There have been other patient-related factors such as COPD and chronic heart failure thought to also play a role in prognosis.Prognosis depends on the amount of lung that is affected and on the co-existence of other medical conditions; chronic embolisation to the lung can lead to pulmonary hypertension. After a massive PE, the embolus must be resolved somehow if the patient is to survive. In thrombotic PE, the blood clot may be broken down by fibrinolysis, or it may be organized and recanalized so that a new channel forms through the clot. Blood flow is restored most rapidly in the first day or two after a PE. Improvement slows thereafter and some deficits may be permanent. There is controversy over whether small subsegmental PEs need treatment at all and some evidence exists that patients with subsegmental PEs may do well without treatment.Once anticoagulation is stopped, the risk of a fatal pulmonary embolism is 0.5% per year.Mortality from untreated PEs was said to be 26%. This figure comes from a trial published in 1960 by Barrit and Jordan, which compared anticoagulation against placebo for the management of PE. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957 </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Metabolic alkalosis and explain in detail? [/INST] Metabolic alkalosis is a metabolic condition in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations. The condition typically cannot last long if the kidneys are functioning properly.

Signs and symptoms
Mild cases of metabolic alkalosis often cause no symptoms. Typical manifestations of moderate to severe metabolic alkalosis include abnormal sensations, neuromuscular irritability, tetany, abnormal heart rhythms (usually due to accompanying electrolyte abnormalities such as low levels of potassium in the blood), coma, seizures, and temporary waxing and waning confusion.

Causes
The causes of metabolic alkalosis can be divided into two categories, depending upon urine chloride levels.

Chloride-responsive (Urine chloride < 25 mEq/L)
Loss of hydrogen ions – Most often occurs via two mechanisms, either vomiting or via the kidney.
Vomiting results in the loss of hydrochloric acid (hydrogen and chloride ions) with the stomach contents. In the hospital setting this can commonly occur from nasogastric suction tubes.
Severe vomiting also causes loss of potassium (hypokalemia) and sodium (hyponatremia). The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions (sparing sodium/potassium pumps to prevent further loss of potassium), leading to metabolic alkalosis.
Congenital chloride diarrhea – rare for being a diarrhea that causes alkalosis instead of acidosis.
 Contraction alkalosis – This results from a loss of water in the extracellular space, such as from dehydration. Decreased extracellular volume triggers the renin-angiotensin-aldosterone system, and aldosterone subsequently stimulates reabsorption of sodium (and thus water) within the nephron of the kidney. However, a second action of aldosterone is to stimulate renal excretion of hydrogen ions (while retaining bicarbonate), and it is this loss of hydrogen ions that raises the pH of the blood.
Diuretic therapy – loop diuretics and thiazides can both initially cause increase in chloride, but once stores are depleted, urine excretion will be below < 25 mEq/L. The loss of fluid from sodium excretion causes a contraction alkalosis. Diuretic abuse among athletes and people with eating disorders may present with metabolic alkalosis.
Posthypercapnia – Hypoventilation (decreased respiratory rate) causes hypercapnia (increased levels of CO2), which results in respiratory acidosis. Renal compensation with excess bicarbonate retention occurs to lessen the effect of the acidosis. Once carbon dioxide levels return to base line, the higher bicarbonate levels reveal themselves putting the patient into metabolic alkalosis.
Cystic fibrosis – excessive loss of sodium chloride in the sweat leads to contraction of the extracellular volume in the same way as contraction alkalosis, as well chloride depletion.
Alkalotic agents – Alkalotic agents, such as bicarbonate (administrated in cases of peptic ulcer or hyperacidity) or antacids, administered in excess can lead to an alkalosis.

Chloride-indeterminate alkalosis
Milk alkali syndrome
Blood product administration since this contains sodium citrate which is then metabolized into sodium bicarbonate. Typically, this is seen with large volume transfusions such as more than 8 units.
Decreases in albumin and phosphate will cause metabolic alkalosis.

Chloride-resistant (Urine chloride > 40 mEq/L)
Retention of bicarbonate – Retention of bicarbonate would lead to alkalosis.
Shift of hydrogen ions into intracellular space – Seen in hypokalemia.  Due to a low extracellular potassium concentration, potassium shifts out of the cells </s>


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


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


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Esophageal rupture and explain in detail? [/INST] Esophageal rupture  is a rupture of the esophageal wall. Iatrogenic causes account for approximately 56% of esophageal perforations, usually due to medical instrumentation such as an endoscopy or paraesophageal surgery. In contrast, the term Boerhaave syndrome is reserved for the 10% of esophageal perforations which occur due to vomiting.Spontaneous perforation of the esophagus most commonly results from a full-thickness tear in the esophageal wall due to a sudden increase in intraesophageal pressure combined with relatively negative intrathoracic pressure caused by straining or vomiting (effort rupture of the esophagus or Boerhaaves syndrome). Other causes of spontaneous perforation include caustic ingestion, pill esophagitis, Barretts esophagus, infectious ulcers in patients with AIDS, and following dilation of esophageal strictures.In most cases of Boerhaaves syndrome, the tear occurs at the left postero-lateral aspect of the distal esophagus and extends for several centimeters. The condition is associated with high morbidity and mortality and is fatal without treatment. The occasionally nonspecific nature of the symptoms may contribute to a delay in diagnosis and a poor outcome. Spontaneous effort rupture of the cervical esophagus, leading to localized cervical perforation, may be more common than previously recognized and has a generally benign course. Preexisting esophageal disease is not a prerequisite for esophageal perforation but it contributes to increased mortality.This condition was first documented by the 18th-century physician Herman Boerhaave, after whom it is named. A related condition is Mallory-Weiss syndrome which is only a mucosal tear.
In case of iatrogenic perforation common site is cervical esophagus just above the upper sphincter whereas spontaneous rupture as seen in Boerhaaves syndrome perforation commonly occurs in the lower one-third of esophagus.

Signs and symptoms
The classic history of esophageal rupture is one of severe retching and vomiting followed by excruciating retrosternal chest and upper abdominal pain. Odynophagia, tachypnea, dyspnea, cyanosis, fever, and shock develop rapidly thereafter.Physical examination is usually not helpful, particularly early in the course.  Subcutaneous emphysema (crepitation) is an important diagnostic finding but is not very sensitive, being present in only 9 of 34 patients (27 percent) in one series. A pleural effusion may be detected.Macklers triad includes chest pain, vomiting, and subcutaneous emphysema, and while it is a classical presentation, it is only present in 14% of people.Pain can occasionally radiate to the left shoulder, causing physicians to confuse an esophageal perforation with a myocardial infarction.It may also be audibly recognized as Hammans sign.

Pathophysiology
Esophageal rupture,  in Boerhaave syndrome, is thought to be the result of a sudden rise in internal esophageal pressure produced during vomiting, as a result of neuromuscular incoordination causing failure of the cricopharyngeus muscle (a sphincter within the pharynx) to relax. As the intra-oesophageal pressure increases, the bolus within the oesophagus has nowhere to go superiorly (as the cricopharyngeus fails to relax) which causes the oesophagus to rupture.   The syndrome is commonly associated with the consumption of excessive food and/or alcohol as well as eating disorders such as bulimia.The most common anatomical location of the tear in Boerhaave syndrome is at  left posterolateral wall  of the lower third of the esophagus, 2–3 cm before the stomach.Currently, the most common cause of esophageal perforation is iatrogenic. However, iatrogenic perforations, while still constituting a serious medical condition, are easier to treat and less prone to complications, particularly mediastinitis and sepsis. This is because they usually do not involve contamination of the mediastinum with gastric contents.

Diagnosis
The diagnosis of Boerhaaves syndrome is suggested on the plain chest radiography and confirmed by chest CT scan. The initial plain chest radiograph is almost always abnormal in patients with Boerhaaves syndrome and usually reveals mediastinal or free peritoneal air as the initial radiologic manifestation. With cervical esophageal perforations, plain films of the neck show air in the soft tissues of the prevertebral space.Hours to days later, pleural effusion(s) with or without pneumothorax, widened mediastinum, and subcutaneous emphysema is typically seen. CT scan may show esophageal wall edema and thickening, extraesophageal air, periesophageal fluid with or without gas bubbles, mediastinal widening, and air and fluid in the pleural spaces, retroperitoneum or lesser sac.The diagnosis of esophageal perforation could also be confirmed by water-soluble contrast esophagram (Gastrografin), which reveals the location and extent of extravasation of contrast material. Although barium is superior in demonstrating small perforations, the spillage of barium sulfate into the mediastinal and pleural cavities can cause an inflammatory response and subsequent fibrosis and is therefore not used as the primary diagnostic study. If, however, the water-soluble study is negative, a barium study should be performed for better definition.Endoscopy has no role in the diagnosis of spontaneous esophageal perforation. Both the endoscope and insufflation of air can extend the perforation and introduce air into the mediastinum.Patients may also have a pleural effusion high in amylase (from saliva), low pH, and may contain particles of food.

Differential diagnosis
Common misdiagnoses include myocardial infarction, pancreatitis, lung abscess, pericarditis, and spontaneous pneumothorax. If esophageal perforation is suspected, even in the absence of physical findings, chest xray, water soluble contrast radiographic studies of the esophagus and a CT scan should be promptly obtained.  In most cases, non-operative management is administered based on radiological evidence contained in mediastinal collection.

Treatment
With the exception of a few case reports describing survival without surgery, the mortality of untreated Boerhaave syndrome is  100%. Its treatment includes immediate antibiotic therapy to prevent mediastinitis and sepsis, surgical repair of the perforation, and if there is significant fluid loss it should be replaced with IV fluid therapy since oral rehydration is not possible.  Even with early surgical intervention (within 24 hours) the risk of death is 25%.

References
Further reading
Radiology  Esophageal rupture
Arens, Ann; Ben-Youssef, Leila; Hayashi, Sandra; Smollin, Craig (2016). "Esophageal Rupture After Ghost Pepper Ingestion". The Journal of Emergency Medicine. 51 (6): e141–e143. doi:10.1016/j.jemermed.2016.05.061. PMID 27693067.
Henderson, John A.M.; Péloquin, AndréJ.M. (1989). "Boerhaave revisited: Spontaneous esophageal perforation as a diagnostic masquerader". The American Journal of Medicine. 86 (5): 559–67. doi:10.1016/0002-9343(89)90385-9. PMID 2653030.
Larrieu, AJ; Kieffer, R (1975). "Boerhaave syndrome: report of a case treated non-operatively". Annals of Surgery. 181 (4): 452–4. doi:10.1097/00000658-197504000-00015. PMC 1343787. PMID 1130863.
Patton, Anthony S.; Lawson, Dexter W.; Shannon, James M.; Risley, Thomas S.; Bixby, Frank E. (1979). "Reevaluation of the Boerhaave syndrome" </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Leukorrhea and explain in detail? [/INST] Leukorrhea or (leucorrhoea British English), also known as fluor albus, is a thick, whitish, yellowish or greenish vaginal discharge.
It has also been referred to as "the whites".
There are many causes of leukorrhea, the usual one being estrogen imbalance. The amount of discharge may increase due to vaginal infection, and it may disappear and reappear from time to time. This discharge can keep occurring for years, in which case it becomes more yellow and strong-smelling. It is usually a non-pathological symptom secondary to inflammatory conditions of the vagina or cervix.Leukorrhea can be confirmed by finding >10 WBC per high-power field under a microscope when examining vaginal fluid.Vaginal discharge is normal, and causes of change in discharge include infection, malignancy, and hormonal changes </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Crackles and explain in detail? [/INST] Crackles are the clicking, rattling, or crackling noises that may be made by one or both lungs of a human with a respiratory disease during inhalation. They are usually heard only with a stethoscope ("on auscultation"). Pulmonary crackles are abnormal breath sounds that were formerly referred to as rales.Bilateral crackles refers to the presence of crackles in both lungs. Basal crackles are crackles apparently originating in or near the base of the lung. Bibasal crackles refer to crackles at the bases of both the left and right lungs. Bilateral basal crackles also refers to the presence of basal crackles in both lungs.
Crackles are caused by the "popping open" of small airways and alveoli collapsed by fluid, exudate, or lack of aeration during expiration.
Crackles can be heard in patients with pneumonia, atelectasis, pulmonary fibrosis, acute bronchitis, bronchiectasis, acute respiratory distress syndrome (ARDS), interstitial lung disease or post thoracotomy or metastasis ablation. Pulmonary edema secondary to left-sided congestive heart failure can also cause crackles.

Terminology
René Laennec adopted the existing word râles (which has been translated as "rattles", groans" and otherwise) to describe the added breath sounds that are now referred to as "crackles". He described them using unusual daily examples, such as "whistling of little birds", "crackling of salt on a heated dish", "cooing of the woodpidgeon", etc., but he soon realized that he was unable to use the term in front of his patients because it conjured the association of le râle de la mort, which translates to " the death rattle", the noise that people who are about to die make when they can no longer clear secretions. Therefore, at the bedside, he used the Latin word rhonchus, which originally meant a snore. That was not clearly understood by his translator, John Forbes, and the terminology became very confusing after the publication in the 1830s of Forbess English translation of Laennecs De LAuscultation Mediate. The difficulty of translating râle itself had been remarked upon in a British review of Laennecs work in 1820.The terminology of "rales" and "rhonchi" in English remained variable until 1977, when a standardization was established by the American Thoracic Society and American College of Chest Physicians. As a result, the term râles was abandoned, and "crackles" became its recommended substitute. The term "rales" is still common in English-language medical literature, but cognizance of the ATS/CHEST guidelines calls for "crackles".
In 2016, the European Respiratory Society reported on a study of various physicians listening to audiovisual recordings of auscultation findings and interobserver variation was analyzed. The study found that broad descriptions agreed better than detailed descriptions.

Sound
Crackles are caused by explosive opening of small airways and are discontinuous, nonmusical, and brief </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sciatica and explain in detail? [/INST] Sciatica is pain going down the leg from the lower back. This pain may go down the back, outside, or front of the leg. Onset is often sudden following activities like heavy lifting, though gradual onset may also occur. The pain is often described as shooting. Typically, symptoms are only on one side of the body. Certain causes, however, may result in pain on both sides. Lower back pain is sometimes present. Weakness or numbness may occur in various parts of the affected leg and foot.About 90% of sciatica is due to a spinal disc herniation pressing on one of the lumbar or sacral nerve roots. Spondylolisthesis, spinal stenosis, piriformis syndrome, pelvic tumors, and pregnancy are other possible causes of sciatica. The straight-leg-raising test is often helpful in diagnosis. The test is positive if, when the leg is raised while a person is lying on their back, pain shoots below the knee. In most cases medical imaging is not needed. However, imaging may be obtained if bowel or bladder function is affected, there is significant loss of feeling or weakness, symptoms are long standing, or there is a concern for tumor or infection. Conditions that may present similarly are diseases of the hip and infections such as early shingles (prior to rash formation).Initial treatment typically involves pain medications. However, evidence for pain medication and muscle relaxants is lacking. It is generally recommended that people continue with normal activity to the best of their abilities. Often all that is required for sciatica resolution is time; in about 90% of people symptoms resolve in less than six weeks. If the pain is severe and lasts for more than six weeks, surgery may be an option. While surgery often speeds pain improvement, its long term benefits are unclear. Surgery may be required if complications occur, such as loss of normal bowel or bladder function. Many treatments, including corticosteroids, gabapentin, pregabalin, acupuncture, heat or ice, and spinal manipulation, have limited or poor evidence for their use.Depending on how it is defined, less than 1% to 40% of people have sciatica at some point in time. Sciatica is most common between the ages of 40 and 59, and men are more frequently affected than women. The condition has been known since ancient times. The first known use of the word sciatica dates from 1451.

Definition
The term "sciatica" usually describes a symptom—pain along the sciatic nerve pathway—rather than a specific condition, illness, or disease. Some use it to mean any pain starting in the lower back and going down the leg. The pain is characteristically described as shooting or shock-like, quickly traveling along the course of the affected nerves. Others use the term as a diagnosis (i.e. an indication of cause and effect) for nerve dysfunction caused by compression of one or more lumbar or sacral nerve roots from a spinal disc herniation. Pain typically occurs in the distribution of a dermatome and goes below the knee to the foot. It may be associated with neurological dysfunction, such as weakness and numbness.

Causes
Risk factors
Modifiable risk factors for sciatica include smoking, obesity, occupation, and physical sports where back muscles and heavy weights are involved. Non-modifiable risk factors include increasing age, being male, and having a personal history of low back pain.

Spinal disc herniation
Spinal disc herniation pressing on one of the lumbar or sacral nerve roots is the most frequent cause of sciatica, being present in about 90% of cases. This is particularly true in those under age 50. Disc herniation most often occurs during heavy lifting. Pain typically increases when bending forward or sitting, and reduces when lying down or walking.

Spinal stenosis
Other compressive spinal causes include lumbar spinal stenosis, a condition in which the spinal canal, the space the spinal cord runs through, narrows and compresses the spinal cord, cauda equina, or sciatic nerve roots. This narrowing can be caused by bone spurs, spondylolisthesis, inflammation, or a herniated disc, which decreases available space for the spinal cord, thus pinching and irritating nerves from the spinal cord that become the sciatic nerve. This is the most frequent cause after age 50. Sciatic pain due to spinal stenosis is most commonly brought on by standing, walking, or sitting for extended periods of time, and reduces when bending forward. However, pain can arise with any position or activity in severe cases. The pain is most commonly relieved by rest.

Piriformis syndrome
Piriformis syndrome is a condition that, depending on the analysis, varies from a "very rare" cause to contributing up to 8% of low back or buttock pain. In 17% of people, the sciatic nerve runs through the piriformis muscle rather than beneath it. When the piriformis shortens or spasms due to trauma or overuse, it is posited that this causes compression of the sciatic nerve. Piriformis syndrome has colloquially been referred to as "wallet sciatica" since a wallet carried in a rear hip pocket compresses the buttock muscles and sciatic nerve when the bearer sits down. Piriformis syndrome may be suspected as a cause of sciatica when the spinal nerve roots contributing to the sciatic nerve are normal and no herniation of a spinal disc is apparent.

Endometriosis
Sciatic endometriosis, also called catamenial or cyclical sciatica, is a sciatica whose cause is endometriosis. Its incidence is unknown. Diagnosis is usually made by an MRI or CT-myelography.

Pregnancy
Sciatica may also occur during pregnancy, especially during later stages, as a result of the weight of the fetus pressing on the sciatic nerve during sitting or during leg spasms. While most cases do not directly harm the woman or the fetus, indirect harm may come from the numbing effect on the legs, which can cause loss of balance and falls. There is no standard treatment for pregnancy-induced sciatica.

Other
Pain that does not improve when lying down suggests a nonmechanical cause, such as cancer, inflammation, or infection. Sciatica can be caused by tumors impinging on the spinal cord or the nerve roots. Severe back pain extending to the hips and feet, loss of bladder or bowel control, or muscle weakness may result from spinal tumors or cauda equina syndrome. Trauma to the spine, such as from a car accident or hard fall onto the heel or buttocks, may also lead to sciatica. A relationship has been proposed with a latent Cutibacterium acnes infection in the intervertebral discs, but the role it plays is not yet clear.

Pathophysiology
Sciatica is generally caused by the compression of lumbar nerves L4 or L5 or sacral nerve S1. Less commonly, sacral nerves S2 or S3 or compression of the sciatic nerve itself may cause sciatica. In 90% of sciatica cases, this can occur as a result of a spinal disc bulge or herniation. Intervertebral spinal discs consist of an outer anulus fibrosus and an inner nucleus pulposus. The anulus fibrosus forms a rigid ring around the nucleus pulposus early in human development, and the gelatinous contents of the nucleus pulposus are thus contained within the disc. Discs separate the spinal vertebrae, thereby increasing spinal stability and allowing nerve roots to properly exit through the spaces between the vertebrae from the spinal cord. As an individual ages, the anulus fibrosus weakens and becomes less rigid, making it at greater risk for tear. When there is a tear in the anulus fibrosus, the nucleus pulposus may extrude through the tear and press against spinal nerves within the spinal cord, cauda equina, or exiting nerve roots, causing inflammation, numbness, or excruciating pain. Inflammation of spinal tissue can then spread to adjacent facet joints and cause facet syndrome, which is characterized by lower back pain and referred pain in the posterior thigh.Other causes of sciatica secondary to spinal nerve entrapment include the roughening, enlarging, or misalignment (spondylolisthesis) of vertebrae, or disc degeneration that reduces the diameter of the lateral foramen through which nerve roots exit the spine.  When sciatica is caused by compression of a dorsal nerve root, it is considered a lumbar radiculopathy or radiculitis when accompanied by an inflammatory response. Sciatica-like pain prominently focused in the buttocks can also be caused by compression of peripheral sections of the sciatic nerve usually from soft tissue tension in the piriformis or related muscles.

Diagnosis
Sciatica is typically diagnosed by physical examination, and the history of the symptoms.

Physical tests
Generally, if a person reports the typical radiating pain in one leg, as well as one or more neurological indications of nerve root tension or neurological deficit, sciatica can be diagnosed.The most frequently used diagnostic test is the straight leg raise to produce Lasègues sign, which is considered positive if pain in the distribution of the sciatic nerve is reproduced with passive flexion of the straight leg between 30 and 70 degrees. While this test is positive in about 90% of people with sciatica, approximately 75% of people with a positive test do not have sciatica. Straight leg raising of the leg unaffected by sciatica may produce sciatica in the leg on the affected side; this is known as the Fajersztajn sign. The presence of the Fajersztajn sign is a more specific finding for a herniated disc than Lasègues sign. Maneuvers that increase intraspinal pressure, such as coughing, flexion of the neck, and bilateral compression of the jugular veins, may transiently worsen sciatica pain.

Medical imaging
Imaging modalities such as computerised tomography or magnetic resonance imaging can help with the diagnosis of lumbar disc herniation. The utility of MR neurography in the diagnosis of piriformis syndrome is controversial.Discography could be considered to determine a specific discs role in an individuals pain. Discography involves the insertion of a needle into a disc to determine the pressure of disc space. Radiocontrast is then injected into the disc space to assess for visual changes that may indicate an anatomic abnormality of the disc. The reproduction of an individuals pain during discography is also diagnostic.

Differential diagnosis
Cancer should be suspected if there is previous history of it, unexplained weight loss, or unremitting pain. Spinal epidural abscess is more common among those who have diabetes mellitus or immunodeficiency, or who have had spinal surgery, injection or catheter; it typically causes fever, leukocytosis and increased erythrocyte sedimentation rate. If cancer or spinal epidural abscess is suspected, urgent magnetic resonance imaging is recommended for confirmation. Proximal diabetic neuropathy typically affects middle aged and older people with well-controlled type-2 diabetes mellitus; onset is sudden, causing pain, usually in multiple dermatomes, quickly followed by weakness. Diagnosis typically involves electromyography and lumbar puncture. Shingles is more common among the elderly and immunocompromised; typically, pain is followed by the appearance of a rash with small blisters along a single dermatome. Acute Lyme radiculopathy may follow a history of outdoor activities during warmer months in likely tick habitats in the previous 1–12 weeks. In the U.S., Lyme is most common in New England and Mid-Atlantic states and parts of Wisconsin and Minnesota, but it is expanding to other areas. The first manifestation is usually an expanding rash possibly accompanied by flu-like symptoms. Lyme can also cause a milder, chronic radiculopathy an average of 8 months after the acute illness.

Management
Sciatica can be managed with a number of different treatments with the goal of restoring a persons normal functional status and quality of life. When the cause of sciatica is lumbar disc herniation (90% of cases), most cases resolve spontaneously over weeks to months. Initially treatment in the first 6–8 weeks should be conservative. More than 75% of sciatica cases are managed without surgery. In persons that smoke who also have sciatica, smoking cessation should be strongly considered, in order to promote healing. Treatment of the underlying cause of nerve compression is needed in cases of epidural abscess, epidural tumors, and cauda equina syndrome.

Physical activity
Physical activity is often recommended for the conservative management of sciatica for persons who are physically able. However, the difference in outcomes between physical activity compared to bed rest have not been fully elucidated. The evidence for physical therapy in sciatica is unclear though such programs appear safe. Physical therapy is commonly used. Nerve mobilization techniques for sciatic nerve is supported by tentative evidence.

Medication
There is no one medication regimen used to treat sciatica. Evidence supporting the use of opioids and muscle relaxants is poor. Low-quality evidence indicates that NSAIDs do not appear to improve immediate pain, and all NSAIDs appear to be nearly equivalent in their ability to relieve sciatica. Nevertheless, NSAIDs are commonly recommended as a first-line treatment for sciatica. In those with sciatica due to piriformis syndrome, botulinum toxin injections may improve pain and function. While there is little evidence supporting the use of epidural or systemic steroids, systemic steroids may be offered to individuals with confirmed disc herniation if there is a contraindication to NSAID use. Low-quality evidence supports the use of gabapentin for acute pain relief in those with chronic sciatica </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Casting defect and explain in detail? [/INST] A casting defect is an undesired irregularity in a metal casting process. Some defects can be tolerated while others can be repaired, otherwise they must be eliminated. They are broken down into five main categories: gas porosity, shrinkage defects, mould material defects, pouring metal defects, and metallurgical defects.

Terminology
The terms "defect" and "discontinuity" refer to two specific and separate things in castings. Defects are defined as conditions in a casting that must be corrected or removed, or the casting must be rejected. Discontinuities, also known as "imperfections", are defined as "interruptions in the physical continuity of the casting". Therefore, if the casting is less than perfect, but still useful and in tolerance, the imperfections should be deemed "discontinuities".

Types
There are many types of defects which result from many different causes. Some of the solutions to certain defects can be the cause for another type of defect.The following defects can occur in sand castings. Most of these also occur in other casting processes.

Shrinkage defects
Shrinkage defects
can occur when standard feed metal is not available to compensate for shrinkage as the thick metal solidifies.  Shrinkage defects will have jagged or linear appearance. Shrinkage defects usually occur in either the cope or drag portion of the casting. Shrinkage defects can be split into two different types: open shrinkage defects and closed shrinkage defects. Open shrinkage defects are open to the atmosphere, therefore as the shrinkage cavity forms, air compensates. There are two types of open air defects: pipes and caved surfaces. Pipes form at the surface of the casting and burrow into the casting, while caved surfaces are shallow cavities that form across the surface of the casting.Closed shrinkage defects, also known as shrinkage porosity, are defects that form within the casting. Isolated pools of liquid form inside solidified metal, which are called hot spots. The shrinkage defect usually forms at the top of the hot spots. They require a nucleation point, so impurities and dissolved gas can induce closed shrinkage defects. The defects are broken up into macroporosity and microporosity (or micro shrinkage), where macroporosity can be seen by the naked eye and microporosity cannot.

Gas porosity
Gas porosity is the formation of bubbles within the casting after it has cooled. This occurs because most liquid materials can hold a large amount of dissolved gas, but the solid form of the same material cannot, so the gas forms bubbles within the material as it cools. Gas porosity may present itself on the surface of the casting as porosity or the pore may be trapped inside the metal, which reduces strength in that vicinity. Nitrogen, oxygen and hydrogen are the most encountered gases in cases of gas porosity. In aluminium castings, hydrogen is the only gas that dissolves in significant quantity, which can result in hydrogen gas porosity. For casting that are a few kilograms in weight the pores are usually 0.01 to 0.5 mm (0.00039 to 0.01969 in) in size. In larger casting, they can be up to a millimetre (0.040 in) in diameter.To prevent gas porosity the material may be melted in a vacuum, in an environment of low-solubility gases, such as argon or carbon dioxide, or under a flux that prevents contact with the air. To minimize gas solubility the superheat temperatures can be kept low. Turbulence from pouring the liquid metal into the mould can introduce gases, so the moulds are often streamlined to minimize such turbulence. Other methods include vacuum degassing, gas flushing, or precipitation. Precipitation involves reacting the gas with another element to form a compound that will form a dross that floats to the top. For instance, oxygen can be removed from copper by adding phosphorus; aluminium or silicon can be added to steel to remove oxygen. A third source consists of reactions of the molten metal with grease or other residues in the mould.
Hydrogen is produced by the reaction of the metal with humidity or residual moisture in the mould. Drying the mould can eliminate this source of hydrogen formation.Gas porosity can sometimes be difficult to distinguish from micro shrinkage because microshrinkage cavities can contain gases as well. In general, microporosities will form if the casting is not properly risered or if a material with a wide solidification range is cast. If neither of these are the case then most likely the porosity is due to gas formation.

Tiny gas bubbles are called porosities, but larger gas bubbles are called blowholes or blisters. Such defects can be caused by air entrained in the melt, steam or smoke from the casting sand, or other gasses from the melt or mould. (Vacuum holes caused by metal shrinkage (see above) may also be loosely referred to as blowholes). Proper foundry practices, including melt preparation and mould design, can reduce the occurrence of these defects. Because they are often surrounded by a skin of sound metal, blowholes may be difficult to detect, requiring harmonic, ultrasonic, magnetic, or X-ray (e.g., industrial CT scanning) analysis.

Pouring metal defects
Pouring metal defects include misruns, cold shuts, and inclusions. A misrun occurs when the liquid metal does not completely fill the mould cavity, leaving an unfilled portion. Cold shuts occur when two fronts of liquid metal do not fuse properly in the mould cavity, leaving a weak spot. Both are caused by either a lack of fluidity in the molten metal or cross-sections that are too narrow. The fluidity can be increased by changing the chemical composition of the metal or by increasing the pouring temperature. Another possible cause is back pressure from improperly vented mould cavities.Misruns and cold shuts are closely related and both involve the material freezing before it completely fills the mould cavity. These types of defects are serious because the area surrounding the defect is significantly weaker than intended. The castability and viscosity of the material can be important factors with these problems. Fluidity affects the minimum section thickness that can be cast, the maximum length of thin sections, fineness of feasibly cast details, and the accuracy of filling mould extremities. There are various ways of measuring the fluidity of a material, although it usually involves using a standard mould shape and measuring the distance the material flows. Fluidity is affected by the composition of the material, freezing temperature or range, surface tension of oxide films, and, most importantly, the pouring temperature. The higher the pouring temperature, the greater the fluidity; however, excessive temperatures can be detrimental, leading to a reaction between the material and the mould; in casting processes that use a porous mould material the material may even penetrate the mould material.The point at which the material cannot flow is called the coherency point. The point is difficult to predict in mould design because it is dependent on the solid fraction, the structure of the solidified particles, and the local shear strain rate of the fluid. Usually this value ranges from 0.4 to 0.8.An inclusion is a metal contamination of dross, if solid, or slag, if liquid. These usually are impurities in the pour metal (generally oxides, less frequently nitrides, carbides, or sulfides), material that is eroded from furnace or ladle linings, or contaminates from the mould. In the specific case of aluminium alloys, it is important to control the concentration of inclusions by measuring them in the liquid aluminium and taking actions to keep them to the required level.
There are a number of ways to reduce the concentration of inclusions. In order to reduce oxide formation the metal can be melted with a flux, in a vacuum, or in an inert atmosphere. Other ingredients can be added to the mixture to cause the dross to float to the top where it can be skimmed off before the metal is poured into the mould. If this is not practical, then a special ladle that pours the metal from the bottom can be used. Another option is to install ceramic filters into the gating system. Otherwise swirl gates can be formed which swirl the liquid metal as it is poured in, forcing the lighter inclusions to the center and keeping them out of the casting. If some of the dross or slag is folded into the molten metal then it becomes an entrainment defect.

Metallurgical defects
There are two defects in this category: hot tears and hot spots. Hot tears, also known as hot cracking, are failures in the casting that occur as the casting cools. This happens because the metal is weak when it is hot and the residual stresses in the material can cause the casting to fail as it cools. Proper mould design prevents this type of defect.Hot spots are sections of casting which have cooled down more slowly than the surrounding material due to higher volume than its surrounding. This causes abnormal shrinkage in this region, which can lead to porosity and cracks.  This type of defect can be avoided by proper cooling practices or by changing the chemical composition of the metal.
Additional methods of minimising hot tears are not overheating the casting material and increasing the temperature of the mould.

Process specific defects
Die casting
In die casting the most common defects are misruns and cold shuts. These defects can be caused by cold dies, low metal temperature, dirty metal, lack of venting, or too much lubricant. Other possible defects are gas porosity, shrinkage porosity, hot tears, and flow marks. Flow marks are marks left on the surface of the casting due to poor gating, sharp corners, or excessive lubricant.

Continuous casting
A longitudinal facial crack is a specialized type of defect that only occurs in continuous casting processes. This defect is caused by uneven cooling, both primary cooling and secondary cooling, and includes molten steel qualities, such as the chemical composition being out of specification, cleanliness of the material, and homogeneity.

Sand casting
Sand casting has many defects that can occur due to the mould failing. The mould usually fails because of one of two reasons: the wrong material is used or it is improperly rammed.The first type is mould erosion, which is the wearing away of the mould as the liquid metal fills the mould. This type of defect usually only occurs in sand castings because most other casting processes have more robust moulds. The castings produced have rough spots and excess material. The moulding sand becomes incorporated into the casting metal and decreases the ductility, fatigue strength, and fracture toughness of the casting. This can be caused by a sand with too little strength or a pouring velocity that is too fast. The pouring velocity can be reduced by redesigning the gating system to use larger runners or multiple gates. A related source of defects are drops, in which part of the moulding sand from the cope drops into the casting while it is still a liquid. This also occurs when the mould is not properly rammed.The second type of defect is metal penetration, which occurs when the liquid metal penetrates into the moulding sand. This causes a rough surface finish. This is caused by sand particles which are too coarse, lack of mould wash, or pouring temperatures that are too high. An alternative form of metal penetration into the mould known as veining is caused by cracking of the sand.
If the pouring temperature is too high or a sand of low melting point is used then the sand can fuse to the casting. When this happens the surface of the casting produced has a brittle, glassy appearance.A run out occurs when the liquid metal leaks out of the mould because of a faulty mould or flask.Scabs are a thin layer of metal that sits proud of the casting. They are easy to remove and always reveal a buckle underneath, which is an indentation in the casting surface. Rattails are similar to buckles, except they are thin line indentations and not associated with scabs. Another similar defect is pulldowns, which are buckles that occur in the cope of sand castings. All of these defects are visual in nature and are no reason to scrap the workpiece. These defects are caused by overly high pouring temperatures or deficiencies of carbonaceous material.A swell occurs when the mould wall gives way across a whole face, and is caused by an improperly rammed mould.Burn-on occurs when metallic oxides interact with impurities in silica sands. The result is sand particles embedded in the surface of the finished casting. This defect can be avoided by reducing the temperature of the liquid metal, by using a mould wash, and by using various additives in the sand mixture.

See also
Hydrogen gas porosity
Inclusions in aluminium alloys
Non-metallic inclusions for inclusions in steel
Porosity sealing

References
Bibliography
Avedesian, M. M.; Baker, Hugh; ASM International (1999). Magnesium and magnesium alloys (2nd ed.). ASM International. ISBN 978-0-87170-657-7..
Campbell, John (2003). Castings. Butterworth-Heinemann. ISBN 978-0-7506-4790-8..
Degarmo, E. Paul; Black, J T.; Kohser, Ronald A. (2003). Materials and Processes in Manufacturing (9th ed.). Wiley </s>