Persius/hicric huggingface dataset:
Mafenide dosage and administration

# Dosage & Administration

## Mafenide Acetate, USP For 5% Topical Solution

## Directions for Preparation of the Solution
Mafenide Acetate for 5% Topical Solution is supplied as a sterile powder and is to be reconstituted with Sterile Water for Irrigation, USP or 0.9% Sodium Chloride Irrigation, USP. Aseptic techniques should be observed during preparation of the solution. Pre-measured quantities of 50 g of Mafenide Acetate powder are provided in sterile packets. The entire quantity of Mafenide Acetate, USP For 5% Topical Solution should be emptied into a suitable container which contains 1000 mL of Sterile Water for Irrigation, USP or 0.9% Sodium Chloride Irrigation, USP and mixed until completely dissolved. The reconstituted solution may be held up to 28 days after preparation if stored in unopened containers. ONCE A CONTAINER IS OPENED, ANY UNUSED PORTION SHOULD BE DISCARDED AFTER 48 HOURS. Store the reconstituted solution at 20 to 25C (68 to 77F). Limited storage periods at 15 to 30C (59 to 86F) are acceptable. Not for Injection -For Topical Use Only.

## Directions for Use of the Solution
The grafted area should be covered with one layer of fine mesh gauze. An eight-ply burn dressing should be cut to the size of the graft and wetted with Mafenide Acetate ,USP for 5% solution using an irrigation syringe and/or irrigation tubing until leaking is noticeable. If irrigation tubing is used, the tubing should be placed over the burn dressing in contact with the wound and covered with a second piece of eight-ply dressing. The irrigation dressing should be secured with a bolster dressing and wrapped as appropriate. The gauze dressing should be kept wet. In clinical studies, this has been accomplished by irrigating with a syringe or injecting the solution into the irrigation tubing every 4 hours or as necessary. If irrigation tubing is not used, the gauze dressing may be moistened every 68 hours or as necessary to keep wet.
Wound dressings may be left undisturbed, except for the irrigations, for up to five days. Additional soaks may be initiated until graft take is complete. Maceration of skin may result from wet dressings applied for intervals as short as 24 hours. Treatment is usually continued until autograft vascularization occurs and healing is progressing (typically occurring in about 5 days). Safety and effectiveness have not been established for longer than 5 days for an individual grafting procedure.
If allergic manifestations occur during treatment with Mafenide Acetate ,USP for 5% solution, discontinuation of treatment should be considered. If acidosis occurs and becomes difficult to control, particularly in patients with pulmonary dysfunction, discontinuing the soaks with the mafenide acetate solution for 24 to 48 hours may aid in restoring acid-base balance (see PRECAUTIONS section). Dressing changes and monitoring the site for bacterial growth during this interruption should be adjusted accordingly.
Methenamine mandelate how supplied

# How Supplied
Methenamine Mandelate Tablets, USP 500 mg are supplied as:
NDC 42799-105-01 Bottles of 100
Each tablet is blue, film coated, and bears the product code 105.
Methenamine Mandelate Tablets, USP 1000 mg are supplied as:
NDC 42799-106-01 Bottles of 100
Each tablet is pink, film coated, and bears the product code 106.
Store at controlled room temperature between 15-30C (59-86F).
Dispense in a tight, light-resistant container as defined in the USP.
Manufactured for:
Edenbridge Pharmaceuticals, LLC
Parsippany, NJ 07054
Methysergide indications and usage

# Indications
For the prevention or reduction of intensity and frequency of vascular headaches in the following kinds of patients:
- Patients suffering from one or more severe vascular headaches per week.
- Patients suffering from vascular headaches that are uncontrollable or so severe that preventive therapy is indicated regardless of the frequency of the attack.
Metipranolol clinical pharmacology

# Clinical Pharmacology
Metipranolol blocks beta1 and beta2 (non-selective) adrenergic receptors. It does not have significant intrinsic sympathomimetic activity, and has only weak local anesthetic (membrane-stabilizing) and myocardial depressant activity.
Orally administered beta-adrenergic blocking agents reduce cardiac output in both healthy subjects and patients with heart disease. In patients with severe impairment of myocardial function, beta-adrenergic receptor antagonists may inhibit the sympathetic stimulatory effect necessary to maintain adequate cardiac output.
Beta-adrenergic receptor blockade in the bronchi and bronchioles may result in significantly increased airway resistance from unopposed para-sympathetic activity. Such an effect is potentially dangerous in patients with asthma or other bronchospastic conditions (see CONTRAINDICATIONS and WARNINGS).
Metipranolol when applied topically in the eye, has the action of reducing elevated as well as normal intraocular pressure (IOP), whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss. The higher the level of intraocular pressure, the greater the likelihood of glaucomatous visual field loss and optic nerve damage.
The primary mechanism of the ocular hypotensive action of metipranolol is most likely due to reduction in aqueous humor production. A slight increase in outflow may be an additional mechanism. Metipranolol reduces IOP with little or no effect on pupil size or accommodation.
In controlled studies of patients with intraocular pressure greater than 24 mmHg at baseline, metipranolol ophthalmic solution reduced the average intraocular pressure approximately 20 - 26%.
The onset of action of metipranolol ophthalmic solution, as measured by a reduction in intraocular pressure, occurs within 30 minutes after a single administration. The maximum effect occurs at about 2 hours. A reduction in intraocular pressure can be demonstrated 24 hours after a single dose. Clinical studies in patients with glaucoma treated for up to two years indicate that an intraocular pressure lowering effect is maintained.

### Animal Pharmacology
In rabbits administered metipranolol in one eye at 2 to 4 fold increased concentrations, multi-focal interstitial nephritis was observed in male animals, and lympho-hystiocytic and heterophilic interstitial pneumonia was observed in female animals. The clinical relevance of these findings is unknown.
Mine Safety and Health Act of 1977
The Federal Mine Safety and Health Act of 1977 (Public Law 95-164) amended the Coal Mine Safety and Health Act of 1969.  It can be found in the United States Code under Title 30, Mineral Lands and Mining, Chapter 22, Mine Safety and Health.  Enacted November 9, 1977, it took effect 120 days later.

# Main provisions
- combination of coal, metal and non metal mines under single legislation
- retention of separate health and safety standards for coal mining
- transfer of enforcement from the Department of Interior to the Department of Labor
- renaming of the Mine Enforcement Safety Administration (MESA) as Mine Safety and Health Administration (MSHA)
- four annual inspections of underground coal mines
- two annual inspections of all surface mines
- elimination of advisory standards for metal and nonmetal mines
- discontinuation of state enforcement plans
- mandating of miner training
- requirement of mine rescue teams for all underground mines
- provision of increased involvement of miners and their representatives in health and safety activities
Mitral Regurgitation vetriculogram

# Left Ventriculographic Evaluation of Mitral Regurgitation
Both the RAO and LAO/Cranial projections can be used to identify significant mitral regurgitation.  Grading the amount of regurgitation is based on the amount of opacification of the atrium compared to the ventricular opacification, atrial size and the number of cycles required for maximal opacification. Elevation of left atrial pressure in acute regurgitation and dilation of the left atrium from chronic regurgitation can both interfere with the use of this grading system.
1+  Brief and incomplete atrial opacification over several cycles. Clears rapidly. No atrial enlargement.
8237703398893439012&hl=en 1+ MR
-8044287213933915863&hl=en 1+ MR LAO with SAM
2+  Moderate opacification of the atria with each cycle. Never greater than LV opacification. No significant LA enlargement.
-3259427927007644054&hl=en 2+ MR
3+ Atrial opacification equal to ventricular opacification.  Delayed clearing of atria over several cycles. Significant enlargement of the LA.
-8295323872088090226&hl=en 3-4+ MR
2584010676245016071&hl=en 3+ MR
4+ Atrial Opacification immediate and greater than that of the ventricle.  Severe enlagement of the LA.  Opacification of the pulmonary veins.
-5531059825466069834&hl=en 4+ Paravalvular MR
7527640933077169571&hl=en 4+ MR

# Severe Mitral Regurgitation by Ventriculogram
Mitral stenosis treatment overview

# Overview
Medical therapy for mitral stenosis includes anticoagulation and rate control in patients with atrial fibrillation. Medical therapy can relieve symptoms, but the patient may need surgery to relieve the blood flow obstruction by mitral stenosis.   The interventional and surgical treatments for mitral stenosis include: percutaneous mitral balloon valvotomy (PMBV), closed commissurotomy, open commissurotomy (valve repair), and mitral valve replacement.

# Treatment Algorithm
Shown below is an algorithm depicting the indications for mitral stenosis intervention according to the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease.
Abbreviations: AF: atrial fibrillation; MR: mitral regurgitation; MS: mitral stenosis; MVA: mitral valve area ; PCWP: pulmonary capillary wedge pressure; PMBC: percutaneous mitral balloon commissurotomy; T1/2: pressure half-time
Mouth ulcers (patient information)
For the WikiDoc page for this topic, click here

# Overview
Mouth ulcers are sores or open lesions in the mouth.

# What are the symptoms of Mouth ulcers?
Symptoms vary and depend on the specific cause of the mouth ulcer. In general, symptoms may include:
- Open sores in the mouth
- Pain or discomfort in the mouth

# What causes Mouth ulcers?
Mouth ulcers are caused by many disorders. These include:
- Canker sores
- Gingivostomatitis
- Herpes simplex (fever blister)
- Leukoplakia
- Oral cancer
- Oral lichen planus
- Oral thrush
The skin lesion of histoplasmosis may also appear as a mouth ulcer.

# Who is at highest risk?
Individuals who have been diagnosed with these conditions may have a higher risk:
- Canker sores
- Gingivostomatitis
- Herpes simplex (fever blister)
- Leukoplakia
- Oral cancer
- Oral lichen planus
- Oral thrush

# Diagnosis
A health care provider or dentist usually diagnoses the type of mouth ulcer, based on its appearance and location. Blood tests or a biopsy of the ulcer may be needed to confirm the cause.

# When to seek urgent medical care?
Call for an appointment with your health care provider if your mouth ulcers don't go away after 3 weeks. Call for an appointment with your health care provider if mouth ulcers return frequently, or if new symptoms develop.

# Treatment options
The goal of treatment is to relieve symptoms. The cause, if known, should be treated.
Gentle, thorough oral hygiene may relieve some of the symptoms. Topical (rubbed on) antihistamines, antacids, corticosteroids, or other soothing preparations may be recommended for applying directly to the ulcer.
Avoid hot or spicy foods, which often increase the pain of mouth ulcers.

# Where to find medical care for Mouth ulcers?
Directions to Hospitals Treating Mouth ulcers

# What to expect (Outlook/Prognosis)?
The outcome varies depending on the cause of the ulcer. Many mouth ulcers are harmless and heal without treatment.
There are types of cancer, however, that may first appear as a mouth ulcer that does not heal. See: Squamous cell carcinoma

# Possible complications
- Cellulitis of the mouth, from secondary bacterial infection of ulcers
- Dental infections (tooth abscesses)
- Oral cancer
- Spread of contagious disorders to other people

# Prevention of Mouth ulcers
Good oral hygiene may help prevent some types of mouth ulcers, as well as some complications from mouth ulcers. Good oral hygiene includes brushing the teeth at least twice per day, flossing at least daily, and getting regular professional dental cleanings and examinations.

# Sources
Multisystem Developmental Disorder

# Background
Multisystem Developmental Disorder, also known as MSDD, is a term coined by Dr. Stanley Greenspan to diagnose children under the age of 3 who exhibit signs of impaired communication as in autism, but with strong emotional attachments atypical of autism. Multisystem Developmental Disorder should not be confused with multiplex developmental disorder (MDD).
MSDD is not listed in DSM-IV or ICD-10, but rather is described in the DC:0-3 diagnostic manual, a manual intended to supplement the standard manuals when diagnosing infants and children under the age of three . DC:0-3 (1994) was published by Zero to Three (ISBN 0-943657-32-6) and is currently under revision.
Though MSDD appears very similar to disorders on the autism spectrum, it is thought to be a secondary impairment, in which difficulties in communicating and relating, characteristic of autism, are in fact a secondary result of motor and sensory processing difficulties. It is thought to be related to sensory integration disorder. MSDD presents as milder than pervasive developmental disorders: children with MSDD tend to respond better to treatment, are less likely to have severe delays in mental ability, and are less likely to have severe rituals or repetitive behaviors. But the differences are very slight, and some would argue that they are in the eyes of the observer. Parents should be aware that the same child, diagnosed by a different practitioner, might very well receive the diagnosis PDD or PDD-NOS.
Little is known about the long term outcomes of children diagnosed with MSDD, though generally their prognosis is considered to be better than most children diagnosed with PDD, given adequate treatment.
As with PDD-NOS, some clinicians use MSDD as a "temporary" diagnosis for children under the age of 3, when for whatever reason there is a reluctance to diagnose autism or PDD. There are several justifications for this: very young children have limited social interaction and communication skills to begin with, therefore it can be tricky to diagnose milder cases in toddlerhood. However, some parents view the MSDD label as no more than a euphemism for autistic spectrum disorders, and one that makes it more difficult for parents to understand the importance of early intervention and treatment and to receive fincancial aid for such intervention.
Treatment for MSDD is similar to treatment for PDD, with more focus on sensory integration. Speech and language therapy, occupational therapy and behavioral therapy all have their benefits. Given that the practitioners who diagnose MSDD in the first place are those who are influenced by Greenspan, they are probably more likely to recommend Greenspan's favored "floortime" treatment.
Nafcillin sodium adverse reactions

# Adverse Reactions

## Body as a Whole
The reported incidence of allergic reactions to penicillins ranges from 0.7 to 10 percent (see WARNINGS). Sensitization is usually the result of treatment but some individuals have had immediate reactions to penicillin when first treated. In such cases, it is thought that the patients may have had prior exposure to the drug via trace amounts present in milk or vaccines.
Two types of allergic reactions to penicillin are noted clinically, immediate and delayed.
Immediate reactions usually occur within 20 minutes of administration and range in severity from urticaria and pruritus to angioneurotic edema, laryngospasm, bronchospasm, hypotension, vascular collapse, and death. Such immediate anaphylactic reactions are very rare (see WARNINGS) and usually occur after parenteral therapy but have occurred in patients receiving oral therapy. Another type of immediate reaction, an accelerated reaction, may occur between 20 minutes and 48 hours after administration and may include urticaria, pruritus, and fever. Although laryngeal edema, laryngospasm, and hypotension occasionally occur, fatality is uncommon.
Delayed allergic reactions to penicillin therapy usually occur after 48 hours and sometimes as late as 2 to 4 weeks after initiation of therapy. Manifestations of this type of reaction include serum sickness-like symptoms (i.e., fever, malaise, urticaria, myalgia, arthralgia, abdominal pain) and various skin rashes. Nausea, vomiting, diarrhea, stomatitis, black or hairy tongue, and other symptoms of gastrointestinal irritation may occur, especially during oral penicillin therapy.

## Local Reactions
Pain, swelling, inflammation, phlebitis, thrombophlebitis, and occasional skin sloughing at the injection site have occurred with intravenous administration of nafcillin (see DOSAGE AND ADMINISTRATION). Severe tissue necrosis with sloughing secondary to subcutaneous extravasation of nafcillin has been reported.

## Nervous System Reactions
Neurotoxic reactions similar to those observed with penicillin G could occur with large intravenous or intraventricular doses of nafcillin especially in patients with concomitant hepatic insufficiency and renal dysfunction (see PRECAUTIONS).

## Urogenital Reactions
Renal tubular damage and interstitial nephritis have been associated infrequently with the administration of nafcillin. Manifestations of this reaction may include rash, fever, eosinophilia, hematuria, proteinuria, and renal insufficiency.

## Gastrointestinal Reactions
Pseudomembranous colitis has been reported with the use of nafcillin. The onset of pseudomembranous colitis symptoms may occur during or after antibiotic treatment (see WARNINGS).

## Metabolic Reactions
Agranulocytosis, neutropenia, and bone marrow depression have been associated with the use of nafcillin.
To report SUSPECTED ADVERSE EVENTS, contact FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
National Resident Matching Program

# About the NRMP
The National Resident Matching Program (NRMP) is a private, non-profit corporation established in 1952 to provide a uniform date of appointment to positions in graduate medical education (GME) in the United States.
Each year, approximately 16,000 U.S. allopathic medical school students participate in the NRMP residency match for post-medical school residency positions. In addition, another 18,000 "independent" applicants compete for the approximately 24,000 available residency positions. Independent applicants include former graduates of U.S. allopathic medical schools, U.S. osteopathic students, Canadian students, and graduates of foreign medical schools.
The NRMP also conducts matches for fellowship positions in 34 sub-specialties, through its Specialties Matching Service. Those positions involve further training after completion of the initial residency program and lead to certification in a specialty. 
The USMLE score is just one of many factors considered by residency programs in selecting applicants.  The median USMLE Step 1 scores for graduates of U.S. Medical Schools for various residencies are charted in Figure 4 on page 11 of "Charting Outcomes in the Match" available at 
The NRMP is sponsored by five medical / medical education organizations:
- American Board of Medical Specialties (ABMS)
- American Medical Association (AMA)
- Association of American Medical Colleges (AAMC)
- American Hospital Association (AHA),
- Council of Medical Specialty Societies (CMSS)
The NRMP governed by its Board of Directors, chosen from candidates nominated by participating and allied organizations. These include ten physicians; two residency program directors; three resident physician members; three medical student members, and one at-large public member. NRMP policy is shaped by policy directives from its sponsoring and allied organizations.
Necrotising enterocolitis overview

# Overview
Necrotizing enterocolitis (NEC) is a medical condition primarily seen in premature infants, where portions of the bowel undergo necrosis (tissue death).

# Causes
NEC has no definitive known cause.  An infectious agent has been suspected, as cluster outbreaks in neonatal intensive care units (NICUs) have been seen, but no common organism has been idenitfied.  A combination of intestinal flora, inherent weakness in the neonatal immune system, alterations in mesenteric blood flow and milk feeding may be factors.  NEC is almost never seen in infants before oral feedings are initiated.

# Diagnosis

## History and Symptoms
The condition is typically seen in premature infants, and the timing of its onset is generally inversely proportional to the gestational age of the baby at birth.  i.e. the earlier a baby is born, the later signs of NEC are typically seen.  Initial symptoms include feeding intolerance, increased gastric residuals, abdominal distension and bloody stools.  Symptoms may progress rapidly to abdominal discoloration with intestinal perforation and peritonitis and systemic hypotension requiring intensive medical support.

## Abdominal X Ray
The diagnosis is usually suspected clinically but often requires the aid of diagnostic imaging modalities. Plain radiographs of the abdomen are useful by showing evidence of extraluminal gas (pneumatosis, portal venous gas or pneumoperitoneum) or an abnormal bowel gas pattern, particularly a persistently unaltered gas-filled dilated loop of bowel on serial radiographs (fixed loop). Monitoring is clinical, although serial supine and left lateral decubitus abdominal roentgenograms should be performed every 6 hours.  Signs of radiographic worsening of NEC include dilated bowel loops, pneumatosis intestinalis, portal venous gas, and pneumoperitoneum.

## Ultrasound
More recently ultrasonography has proven to be useful as it may detect signs and complications of NEC before they are evident on radiographs.

# Treatment

## Medical Therapy
Treatment consists primarily of supportive care including providing bowel rest by stopping enteral feeds, gastric decompression with intermittent suction, fluid repletion to correct electrolyte abnormalities and third space losses, parenteral nutrition, and prompt antibiotic therapy.

## Surgery
Where the disease is not halted through medical treatment alone, or when the bowel perforates, immediate emergency surgery to resect the dead bowel is required.  This may require a colostomy, which may be able to be reversed at a later time.  Some children may suffer later as a result of short bowel syndrome if extensive portions of the bowel had to be removed.