Persius/hicric huggingface dataset:
Lamivudine zidovudine adverse reactions

# Adverse Reactions
The following adverse reactions are discussed in greater detail in other sections of the labeling:
- Hematologic toxicity, including neutropenia and anemia .
- Symptomatic myopathy .
- Lactic acidosis and hepatomegaly with steatosis .
- Acute exacerbations of hepatitis B .
- Hepatic decompensation in patients co-infected with HIV-1 and hepatitis C .
- Exacerbation of anemia in HIV-1/HCV co-infected patients receiving ribavirin and zidovudine .
- Pancreatitis .

## Clinical Trials Experience
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
Lamivudine Plus Zidovudine Administered As Separate Formulations: In 4 randomized, controlled trials of EPIVIR 300 mg per day plus RETROVIR 600 mg per day, the following selected adverse reactions and laboratory abnormalities were observed (see Tables 1 and 2).
Pancreatitis was observed in 9 of the 2,613 adult patients (0.3%) who received EPIVIR in controlled clinical trials .
Selected laboratory abnormalities observed during therapy are listed in Table 2.

## Postmarketing Experience
In addition to adverse reactions reported from clinical trials, the following reactions have been identified during post-approval use of EPIVIR, RETROVIR, and/or COMBIVIR. Because they are reported voluntarily from a population of unknown size, estimates of frequency cannot be made. These events have been chosen for inclusion due to a combination of their seriousness, frequency of reporting, or potential causal connection to EPIVIR, RETROVIR, and/or COMBIVIR.
Body as a Whole: Redistribution/accumulation of body fat .
Cardiovascular: Cardiomyopathy.
Endocrine and Metabolic: Gynecomastia, hyperglycemia.
Gastrointestinal: Oral mucosal pigmentation, stomatitis.
General: Vasculitis, weakness.
Hemic and Lymphatic: Anemia, (including pure red cell aplasia and anemias progressing on therapy), lymphadenopathy, splenomegaly.
Hepatic and Pancreatic: Lactic acidosis and hepatic steatosis, pancreatitis, posttreatment exacerbation of hepatitis B .
Hypersensitivity: Sensitization reactions (including anaphylaxis), urticaria.
Musculoskeletal: Muscle weakness, CPK elevation, rhabdomyolysis.
Nervous: Paresthesia, peripheral neuropathy, seizures.
Respiratory: Abnormal breath sounds/wheezing.
Skin: Alopecia, erythema multiforme, Stevens-Johnson syndrome.
Lamivudine zidovudine drug interactions

# Drug Interactions
No drug interaction studies have been conducted using COMBIVIR Tablets .

## Antiretroviral Agents
Lamivudine:Zalcitabine: Lamivudine and zalcitabine may inhibit the intracellular phosphorylation of one another. Therefore, use of COMBIVIR in combination with zalcitabine is not recommended.
Zidovudine:Stavudine: Concomitant use of COMBIVIR with stavudine should be avoided since an antagonistic relationship with zidovudine has been demonstrated in vitro.
Nucleoside Analogues Affecting DNA Replication: Some nucleoside analogues affecting DNA replication, such as ribavirin, antagonize the in vitro antiviral activity of zidovudine against HIV-1; concomitant use of such drugs should be avoided.

## Doxorubicin
Zidovudine: Concomitant use of COMBIVIR with doxorubicin should be avoided since an antagonistic relationship with zidovudine has been demonstrated in vitro.

## Hematologic/Bone Marrow Suppressive/Cytotoxic Agents
Zidovudine: Coadministration of ganciclovir, interferon alfa, ribavirin, and other bone marrow suppressive or cytotoxic agents may increase the hematologic toxicity of zidovudine.

## Interferon- and ribavirin-Based Regimens
Lamivudine: Although no evidence of a pharmacokinetic or pharmacodynamic interaction (e.g., loss of HIV-1/HCV virologic suppression) was seen when ribavirin was coadministered with lamivudine in HIV-1/HCV co-infected patients, hepatic decompensation (some fatal) has occurred in HIV-1/HCV co-infected patients receiving combination antiretroviral therapy for HIV-1 and interferon alfa with or without ribavirin .

## Trimethoprim/Sulfamethoxazole (TMP/SMX)
Lamivudine: No change in dose of either drug is recommended. There is no information regarding the effect on lamivudine pharmacokinetics of higher doses of TMP/SMX such as those used to treat PCP.
Left anterior fascicular block overview

# Overview
Left anterior fascicular block is caused by interruption of the anterior division of the left bundle branch. This fascicle is fragile, easily  exposed to damage, and has a single blood supply (the left anterior descending coronary artery).

# Pathophysiology
Normal activation of the left ventricle proceeds down the left bundle branch, which consist of two fascicles the left anterior fascicle and left posterior fascicle. Left anterior fascicular block (LAFB), which is also known as left anterior hemiblock (LAHB), occurs when a cardiac impulse spreads first through the left posterior fascicle, causing a delay in activation of the anterior and lateral walls of the left ventricle which are normally activated via the left anterior fascicle. 
Although there is a delay or block in the activation of the left anterior fascicle there is still preservation of initial left to right septal activation as well as preservation of the inferior activation of the left ventricle (preservation of septal Q waves in I and aVL and small initial R wave in leads II, III, and aVF). The delayed and unopposed activation of the remainder of the left ventricle now results in a shift in the QRS axis leftward and superiorly, causing marked left axis deviation. This delayed activation also results in a widening of the QRS complex, although not to the extent of a complete LBBB. 

# Causes
Left anterior fascicular block, which is more common than left posterior fascicular block, may be due to damages to the left anterior fascicle as it passes through the left ventricular outflow tract, such causes include aortic stenosis, hypertensive heart disease and cardiomyopathy.  It can also be caused by congenital heart diseases such as Atrial septal defect, atrioventricular septal defect, single ventricle, e.t.c   However, life threatening conditions such as myocardial infarction must be promptly identified and treated accordingly.

# History and Symptoms
The symptoms depends on the degree of blockage of the conduction system of the heart.  Patients are usually asymptomatic but when symptoms do occur, they may experience some palpitations, intermittent chest pain, dizziness.  A thorough cardiovascular physical examination and an EKG is required in order to make a diagnosis.

# Electrocardiogram

### Criteria for LAHB
- Left axis deviation (usually between -45 and -90), some consider -30 to meet criteria
- QRS interval < 0.12 seconds
- qR complex in the lateral limb leads (I and aVL)
- rS pattern in the inferior leads (II, III, and aVF)
- Delayed intrinsicoid deflection in lead aVL (> 0.045 s)

# Medical therapy
Most isolated fascicular blocks are asymptomatic.  Therapy could only be considered in the presence of a persistent bifascicular block or trifascicular block.
Lipoprotein-associated phospholipase A2
Lipoprotein-associated phospholipase A2 (Lp-PLA2) also known as platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A2 enzyme that in humans is encoded by the PLA2G7 gene. Lp-PLA2 is a 45-kDa protein of 441 amino acids. It is one of several PAF acetylhydrolases.

# Function
In the blood it travels mainly with low-density lipoprotein (LDL). Less than 20% is associated with high-density lipoprotein HDL. Several lines of evidence suggest that HDL-associated Lp-PLA2 may substantially contribute to the HDL antiatherogenic activities. It is an enzyme produced by inflammatory cells and hydrolyzes oxidized phospholipids in LDL.
Lp-PLA2 is platelet-activating factor (PAF) acetylhydrolase (EC 3.1.1.47), a secreted enzyme that catalyzes the degradation of PAF to inactive products by hydrolysis of the acetyl group at the sn-2 position, producing the biologically inactive products LYSO-PAF and acetate.

# Clinical significance
Lp-PLA2 is involved in the development of atherosclerosis, an observation that has prompted interest as a possible therapeutic target (see, e.g. the investigational drug Darapladib). In human atherosclerotic lesions, 2 main sources of Lp-PLA2 can be identified, including that which is brought into the intima bound to LDL (from the circulation), and that which is synthesized de novo by plaque inflammatory cells (macrophages, T cells, mast cells)."
It is used as a marker for cardiac disease.
A meta-analysis involving a total of 79,036 participants in 32 prospective studies found that Lp-PLA2 levels are positively correlated with increased risk of developing coronary heart disease and stroke.
Management of Dead Bodies from COVID-19

# Management of Dead Bodies from COVID-19

### Do any special procedures exist for the management of bodies of persons who died from COVID-19?
- The health worker attending to the dead body should perform hand hygiene, ensure proper use of PPE (water-resistant apron, goggles, N95 mask, gloves).
- Plug Oral, nasal orifices of the dead body to prevent leakage of body fluids. If the family of the patient wishes to view the body at the time of removal from the isolation room or area, they may be allowed to do so with the application of standard precautions.
- Place the dead body in a leak-proof plastic body bag.
- The exterior of the body bag can be decontaminated with 1% hypochlorite. The body bag can be wrapped with a mortuary sheet or sheet provided by the family members.
- All used/ soiled linen should be handled with standard precautions, put in a biohazard bag and the outer surface of the bag disinfected with hypochlorite
solution.
- Used equipment should be autoclaved or decontaminated with disinfectant solutions in accordance with established infection prevention control
practices.
- All medical waste must be handled and disposed of in accordance with Biomedical waste management rules.
Mannheim's Peritoneal index score (MPI)

# Overview
Mannheim's Peritoneal index score (MPI) is used for risk stratifying patients with peritonitis based on age, sex, peritoneal fluid analysis and comorbidities.

# Mannheim's Peritoneal index score (MPI)
Mannheim's Peritoneal index score (MPI) is used for risk stratifying patients with peritonitis based on age, sex, peritoneal fluid analysis and comorbidities.

## Assessment of the prognosis of patients with peritonitis using Mannheim Peritonitis Index (MPI)
- For a score of 27, the sensitivity was 66.67%, specificity was 100%, and positive predictive value for mortality is 100% at an accuracy of 94%.
Mediastinal mass differential diagnosis

# Overview
The mediastinum is a non-delineated group of structures in the thorax (chest), surrounded by loose connective tissue. It is the central compartment of the thoracic cavity. It contains the heart, the great vessels of the heart, esophagus, trachea, thymus, and lymph nodes of the central chest. A wide variety of diseases involving mediastinal structures may present as a mediastinal mass or widening of the mediastinum on imaging studies. Mediastinal widening is diagnosed by the mediastinum measuring greater than 8 cm in width on PA chest x-ray. The mediastinal mass may present with symptoms or even without any symptoms. Mediastinal mass may cause a variety of symptoms by the mass pressing against surrounding mediastinal structures, collectively known as mediastinal syndrome. Mediastinal may can be differentiated depending on their location in mediastinal cavity into: Anterior mediastinal mass, middle mediastinal mass, or posterior mediastinal mass. Mediastinal mass may also be differentiated according to the content of the mass such as: cystic, fatty or solid (tumor).

# Mediastinal Mass Differential Diagnosis
Wide variety of medical conditions can present as a mediastinal mass on radiological imaging.
- Mediastinal mass may cause obstruction, entrapment or infiltration of other mediastinal organs such as: trachea, bronchi, esophagus, aorta, superior vena cava (SVC), or heart.
- Symptoms caused by any kind of mediastinal mass is collectively known as: Mediastinal syndrome
- Mediastinal syndrome includes:
Symptoms caused by compression of the trachea: Dyspnea and respiratory insufficiency.
Symptoms caused by compression of the esophagus: Dysphagia.
Symptoms caused by compression of SVC causes superior vena cava syndrome: Vein distention, edema of the face or upper extremities and a positive Pemberton's sign.
Pemberton's sign: Development of suffusion, plethora, or duskiness upon elevation of the arms above the head in patient
Superior vena cava syndrome is the most severe complication of mediastinal syndrome and a medical emergency.
- Symptoms caused by compression of the trachea: Dyspnea and respiratory insufficiency.
- Symptoms caused by compression of the esophagus: Dysphagia.
- Symptoms caused by compression of SVC causes superior vena cava syndrome: Vein distention, edema of the face or upper extremities and a positive Pemberton's sign.
Pemberton's sign: Development of suffusion, plethora, or duskiness upon elevation of the arms above the head in patient
Superior vena cava syndrome is the most severe complication of mediastinal syndrome and a medical emergency.
- Pemberton's sign: Development of suffusion, plethora, or duskiness upon elevation of the arms above the head in patient
- Superior vena cava syndrome is the most severe complication of mediastinal syndrome and a medical emergency.
Medically unexplained physical symptoms
Medically unexplained physical symptoms or MUPS is a term used in health care to describe a situation where an individual suffers from multiple physical symptoms for which the physician or other healthcare provider has found no physical cause. Up to 30% of all primary care consultations are patients with medically unexplained symptoms. The term is commonly used to refer to Gulf War illness and more occasionally to other symptom-based diagnoses such as fibromyalgia, chronic fatigue syndrome, and multiple chemical sensitivity.
The term does not imply that a physical cause does not exist, and as more becomes known about a disorder (as is the case with chronic fatigue syndrome) it may be applied less often.

# History and usage
The term medically unexplained physical symptoms was first used in 1987 by D.I. Melville.
MUPS is not synonymous with somatization disorder or psychosomatic illness where the cause or perception of symptoms is mental in origin.  Instead, MUPS refers to the clinical situation where the cause of the symptoms cannot be determined, but might include somatic, physical or environmental causes.
However, several definitions of both somatization and MUPS exist, and the usage of both terms is not consistent in medical literature and practice.  MUPS is sometimes used interchangeably with both somatization and functional somatic symptoms. 

# Contested causation
The lack of etiology diagnosis in MUPS cases can lead to conflict between patient and health-care provider over the diagnosis and treatment of MUPS.  This conflict can occur in the public arena and may involve media controversy, advocacy groups, scientific and political debate and even legal proceedings .
Diagnosis of MUPS is seldom a satisfactory situation for the patient, as many patients feel this implies it is "all in their head." This can lead to an adversarial doctor-patient relationship, which can develop into an iatrogenic neurosis, thus complicating the situation.
According to psychiatrist Simon Wessely, "Various names have been given to medically unexplained symptoms. These include somatisation, somatoform disorders and functional somatic symptoms." He continues to claim "that a substantial overlap exists between the individual syndromes and that the similarities between them outweigh the differences". In another publication, Wessely warns that "the conferring of an illness label is not a neutral act, since specific labels are associated with specific beliefs and attitudes", and "even when organic illness is certain, the illness label can result in adverse behaviour changes".
Wessely's views have been met with considerable criticism.
Bell and Lapp argue that "the existence of an illness is not dependent on a reliable, objective marker to identify the condition, or upon knowledge of aetiology".

# Differential Diagnosis of Medically unexplained physical symptoms

# Treatment
A randomized controlled trial found improvement using multi-faceted, collaborative care.
Methylprednisolone detailed information
Methylprednisolone (molecular weight 374.48) is a synthetic glucocorticoid drug taken orally or administered intraveinously.  Its chemical name is pregna-1,4-diene-3,20 -dione, 11,17,21-trihydroxy-6-methyl-,(6, 11)- and its chemical formula is C22H30O5. Methylprednisolone is sold in the USA and Canada under the brand name Medrol.
Like most adrenocortical steroids, methylprednisolone is typically used for its anti-inflammatory purposes.  However, glucocorticoids have a wide range of effects, including changes to metabolism and immune responses.  The list of medical conditions for which methlyprednisolone is prescribed is rather large, and is similar to other corticosteroids such as prednisolone.  Common uses include arthritis therapy and short-term treatment of bronchial inflammation or acute bronchitis due to various respiratory diseases. It is used both in the treatment of acute periods and long-term controlling of autoimmune diseases, most notably SLE.
Methylprednisolone has serious side effects if taken long-term, including weight gain, glaucoma, osteoporosis and psychosis, especially when overdosed.  The most serious side effect occurs after the adrenal glands cease natural production of cortisone, which methylprednisolone will replace.  Abrupt cessation of the drug after this occurs can result in a condition known as Addisonian crisis, which can be fatal.  To prevent this, the drug is usually prescribed with a tapering dosage, including a pre-dosed "dose pack" detailing a specific number of pills to take at designated times over a six day period.
Alternative treatments to many of the conditions currently indicated for methlyprednisolone are actively being researched.  Additionally, new drugs such as budesonide are being created, which provide similar benefits but without the adrenal suppression problems.
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Metronidazole dosage and administration

# DOSAGE AND ADMINISTRATION

## Trichomoniasis
- In the Female: Seven-day course of treatment (375 mg two times daily for seven consecutive days).
A seven-day course of treatment may minimize reinfection by protecting the patient long enough for the sexual contacts to obtain treatment. Pregnant patients should not be treated during the first trimester (see Contraindications and Precautions).
When repeat courses of the drug are required, it is recommended that an interval of four to six weeks elapse between courses and that the presence of the trichomonad be reconfirmed by appropriate laboratory measures. Total and differential leukocyte counts should be made before and after re-treatment.
- In the Male: Treatment should be individualized as it is for the female.

## Amebiasis

### Adults
For acute intestinal amebiasis (acute amebic dysentery): 750 mg orally three times daily for 5 to 10 days.
For amebic liver abscess: 750 mg orally three times daily for 5 to 10 days.

### Pediatric patients
35 to 50 mg/kg/24 hours, divided into three doses, orally for 10 days.

## Anaerobic Bacterial Infections
In the treatment of most serious anaerobic infections, intravenous metronidazole is usually administered initially.
The usual adult oral dosage is 7.5 mg/kg every 6 hours (approximately 500 mg for a 70 kg adult). A maximum of 4 g should not be exceeded during a 24-hour period.
The usual duration of therapy is 7 to 10 days; however, infections of the bone and joint, lower respiratory tract, and endocardium may require longer treatment.

## Dosage Adjustments

### Patients with Severe Hepatic impairment
For amebiasis patients with severe (Child-Pugh C) hepatic impairment, pharmacokinetic modeling and simulation indicate that the FLAGYL 375 capsules dose should be reduced by 50%. Therefore, the dosage regimen of FLAGYL 375 capsules inChild Pugh C patients with amebiasis is 375 mg q8h for 5 to 10 days (see Clinical Pharmacology and Precautions).
For trichomoniasis patients with severe (Child-Pugh C) hepatic impairment, pharmacokinetic modeling and simulation indicate that the frequency of metronidazole administration should be reduced from every12 hours to every 24 hours. Therefore, the dosage regiment of FLAYGL 375 capsules in Child Pugh C patients with trichomoniasis is 375 mg q24h for 7 days (see Clinical Pharmacology and Precautions).

### Patients Undergoing Hemodialysis
Hemodialysis removes significant amounts of metronidazole and its metabolites from systemic circulation. The clearance of metronidazole will depend on the type of dialysis membrane used, the duration of the dialysis session, and other factors. If the administration of metronidazole cannot be separated from a hemodialysis session, supplementation of metronidazole dosage following the hemodialysis session should be considered, depending on the patient's clinical situation (see Clinical Pharmacology).
Mitral regurgitation treatment overview

# Overview
Vasodilator therapy with ACE inhibitors and hydralazine is the foundation of medical therapy and once the patient becomes symptomatic, mitral valve surgery is the definitive therapy.  This chapter reviews general treatment measures for the patient with mitral regurgitation.

# Afterload Reduction
- Afterload reduction should be instituted with the use of vasodilators such as ACE inhibitors and hydralazine.

# Diuretics
- Diuretics are useful in reducing left ventricular volumes to improve functional mitral regurgitation and to improve pulmonary edema.

# Digitalis
- Digitalis may be used to strengthen contractility, and potentially reduce hospitalization in patients with congestive heart failure.

# Diet
- A low-sodium diet may be helpful.

# Activity
- Most patients with chronic compensated mitral regurgitation have no symptoms; but if a person develops symptoms, activity should be restricted.

# Beta Blockers
Beta blockers are generally not recommended as they would slow the compensatory tachycardia and would allow greater time over which the regurgitation could occur and increase the regurgitant volume.

# Calcium Channel Blockers
- In the presence of atrial fibrillation, a calcium channel blocker or digoxin can be administered to slow the heart rate down and improve left ventricular filling.

# Cardioversion
Cardioversion should be considered in the patient with atrial fibrillation or flutter who is hemodynamically unstable.

# Anticoagulation
- Anti-coagulation therapy should be considered in patients with atrial fibrillation and in patients with prosthetic mitral valve replacement surgery.

# Antibiotic Prophylaxis
- Prophylactic antibiotics prior to a periodontal procedure which involves manipulation of gingival tissue, the periapical region of a tooth, or perforation of oral mucosa is recommended in patients with previous infective endocarditis, patients who have a prosthetic mitral valve implanted and in those with congentital heart disease.