Persius/hicric huggingface dataset:
Paroxysmal nocturnal dyspnea
Synonyms and keywords: Cardiac asthma; PND

# Overview
Paroxysmal nocturnal dyspnea (PND) is defined as sudden, severe shortness of breath at night that awakens a person from sleep, often with coughing and wheezing.  It is most closely associated with congestive heart failure. PND commonly occurs several hours after a person with heart failure has fallen asleep. PND is often relieved by sitting upright, but not as quickly as simple orthopnea. Also unlike orthopnea, it does not develop immediately upon lying down.

# Historical Perspective
It was first described by Charles Lepois in the 1500s.

# Pathophysiology
PND is caused by increasing amounts of fluid entering the lung during sleep and filling the small, air-filled sacs (alveoli) in the lung responsible for absorbing oxygen from the atmosphere. This fluid typically rests in the legs (peripheral edema) during the day when the individual is upright.  At night, when recumbent for an extended period, this fluid is reabsorbed, increasing total blood volume and blood pressure, leading to pulmonary hypertension in people with underlying heart failure.  The consequent  pulmonary hypertension leads to the accumulation of fluid in the lungs, or pulmonary edema.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Cardiac tamponade
- Pulmonary embolism

## Common Causes
- Congestive heart failure
- Left ventricular failure
- Mitral stenosis

## Causes by Organ System

## Causes in Alphabetical Order

# Diagnosis

## Symptoms
The experience of PND is often described as awakening suddenly to a feeling that one is suffocating, with wheezing respirations and coughing. It can be quite frightening.

# Treatment
Treatment depends upon the underlying cause.  The treatment of congestive heart failure can be found here.

# Related Chapters
- Dyspnea
- Trepopnea
- Congestive heart failure
Primary carnitine deficiency

# Overview
Primary carnitine deficiency is a condition that prevents the body from using fats for energy, particularly during periods without food.  Carnitine, a natural substance acquired mostly through diet, is used by cells to process fats and produce energy.  People with primary carnitine deficiency have defective proteins called carnitine transporters, which bring carnitine into cells and prevent its escape from the body.

# Historical Perspective
The current understanding of primary carnitine deficiency has been greatly influenced by the research of Doctors Susan C. Winter and Neil Buist.  Dr. Winter was one of the first doctors in the United States to begin treating inborn errors of metabolism with intravenous carnitine.

# Pathophysiology
There is a decrease in the transport function as a result carnitine is lost from the body.  Cells are not supplied with an adequate amount of carnitine. Without carnitine, fats cannot be processed correctly and are not converted into energy, which can lead to characteristic signs and symptoms of this disorder.

## Genetics
Mutations in the SLC22A5 gene lead to the production of defective carnitine transporters.  This condition is inherited in an autosomal recessive pattern.

# Differentiating Primary Carnitine Deficiency from other Diseases
This condition is sometimes mistaken for Reye syndrome, a severe disorder that develops in children while they appear to be recovering from viral infections such as chickenpox or flu.  Most cases of Reye syndrome are associated with the use of aspirin during these viral infections.

# Epidemiology and Demographics
On the average, primary carnitine deficiency affects 1 in every 40,000 live births in Japan and 1 in every 37,000 to 100,000 newborns in Australia.  The incidence of this condition in other populations is unknown, but is probably similar to that reported for Japan.

# Risk Factors
- Infections
- Fasting
- Malnutrition
- Strenuous physical work

# Natural History, Complications and Prognosis
Serious complications such as heart failure, liver problems, coma, and sudden unexpected death can occur.  Acute illness due to primary carnitine deficiency can be triggered by periods of fasting or illnesses such as viral infections, particularly when eating is reduced.

# Diagnosis

## Symptoms
- Confusion
- Vomiting
- Muscle weakness

## Physical Examination
Typically, initial signs  of this disorder occur during infancy or early childhood and often include brain function abnormalities

### Heart
- Cardiomyopathy

### Neuroloogic
- Encephalopathy

## Laboratory Findings

### Electrolyte and Biomarker Studies
- Hypoglycemia

# Treatment
Primary carnitine deficiency is sometimes diagnosed in adults and is then thought to be less severe both in symptoms and life expectation.  Treatment is usually done by supplementation of L-carnitine after assessing the severity of the deficiency after a muscular biopsy.

### Contraindicated medications
Carnitine deficiency is considered an absolute contraindication to the use of the following medications:
- Cefditoren
Cartilage associated protein
Cartilage associated protein is a protein that in humans is encoded by the CRTAP gene.

# Function
The protein encoded by this gene is similar to the chicken and mouse CRTAP genes. The encoded protein is a scaffolding protein that may influence the activity of at least one member of the cytohesin/ARNO family in response to specific cellular stimuli.

# Clinical significance
Mutations in the CRTAP gene are associated with osteogenesis imperfecta,  types VII and IIB, a connective tissue disorder characterized by bone fragility and low bone mass.
Crowdiagnosis project topics

# Overview
This section shows the list of topics available for the crowdiagnosis project and how to select a topic.  You can also update the status of your chosen topic here by going into the edit box for entering the details so that your work is not overlapped by the work of other editors.

# Select a Topic
- Select a topic from the below list.
- Click on the topic to make sure that the causes page of the topic is empty and not already worked.  Example of causes page: Empty causes page | Completed causes page
- To claim a topic, email WikiDoc  the name of the topic you are willing to choose for this project.
- Your active assignments can be viewed here.

# Topics

## List of Common Symptoms

## Lipoprotein Disorders

## High Priority Cardiology Topics

### Bradyarrhythmia

### List of Other Arrhythmia Topics

### List of Other Cardiology Topics

## List of All Topics
Cefadroxil adverse reactions

# Adverse Reactions

## Gastrointestinal
Onset of pseudomembranous colitis symptoms may occur during or after antibiotic treatment (see WARNINGS). Dyspepsia, nausea and vomiting have been reported rarely. Diarrhea has also occurred.

## Hypersensitivity
Allergies (in the form of rash, urticaria, angioedema, and pruritus) have been observed. These reactions usually subsided upon discontinuation of the drug. Anaphylaxis has also been reported.

## Other
Other reactions have included hepatic dysfunction including cholestasis and elevations in serum transaminase, genital pruritus, genital moniliasis, vaginitis, moderate transient neutropenia, fever. Agranulocytosis, thrombocytopenia, idiosyncratic hepatic failure, erythema multiforme, Stevens-Johnson syndrome, serum sickness, and arthralgia have been rarely reported.
In addition to the adverse reactions listed above which have been observed in patients treated with cefadroxil, the following adverse reactions and altered laboratory tests have been reported for cephalosporin-class antibiotics:
Toxic epidermal necrolysis, abdominal pain, superinfection, renal dysfunction, toxic nephropathy, aplastic anemia, hemolytic anemia, hemorrhage, prolonged prothrombin time, positive Coombs test, increased BUN, increased creatinine, elevated alkaline phosphatase, elevated aspartate aminotransferase (AST), elevated alanine aminotransferase (ALT), elevated bilirubin, elevated LDH, eosinophilia, pancytopenia, neutropenia.
Several cephalosporins have been implicated in triggering seizures, particularly in patients with renal impairment, when the dosage was not reduced (see DOSAGE AND ADMINISTRATION and OVERDOSAGE). If seizures associated with drug therapy occur, the drug should be discontinued. Anticonvulsant therapy can be given if clinically indicated.
Cefazolin sodium description

# Description
Cefazolin for Injection, USP, Pharmacy Bulk Package bag SmartPak should be used only in patients who require a 1 gram dose and not any fraction thereof.
Cefazolin for Injection USP, Pharmacy Bulk Package bag SmartPak should not be used in patients who require less than the 1 gram dose of cefazolin.
Cefazolin for Injection, USP, is a sterile, lyophilized, semisynthetic cephalosporin for intravenous administration. It is the sodium salt of 3-{-methyl}-8-oxo-7- -5-thia-1-azabicyclo oct-2-ene-2-carboxylic acid. Each Pharmacy Bulk Package contains 48 mg (2.1 mEq) of sodium per 1 gram of cefazolin sodium. Cefazolin for Injection, USP, is supplied in 100 grams and 300 grams SmartPak Pharmacy Bulk Packages bags equivalent. Each SmartPak Pharmacy Bulk Package bag contains cefazolin sodium equivalent to 100 grams or 300 grams of cefazolin.
BEFORE ADMINISTRATION, THIS PHARMACY BULK PACKAGE REQUIRES RECONSTITUTION USING STERILE WATER FOR INJECTION, USP TO A CONCENTRATION OF 100 mg per mL AND FURTHER DILUTION IN 50 mL OF A COMPATIBLE SOLUTION AND INFUSED INTRAVENOUSLY.
THIS PRODUCT IS NOT INTENDED TO BE USED IN PEDIATRIC AND RENALLY IMPAIRED PATIENTS WHO REQUIRE LESS THAN A 1 GRAM DOSE.
A Pharmacy Bulk Package is a container of a sterile preparation for intravenous use that contains many single doses. The contents are intended for use in a pharmacy admixture service and are restricted to the preparation of admixtures for intravenous infusion.
The molecular formula is C14H13N8NaO4S3. The molecular weight is 476.49.
The structural formula is as follows:
The pH of the reconstituted solution is between 4 and 6.
Cefditoren contraindications

# Contraindications
SPECTRACEF is contraindicated in patients with known allergy to the cephalosporin class of antibiotics or any of its components.
SPECTRACEF is contraindicated in patients with carnitine deficiency or inborn errors of metabolism that may result in clinically significant carnitine deficiency, because use of SPECTRACEF causes renal excretion of carnitine. (See PRECAUTIONS, General.)
SPECTRACEF tablets contain sodium caseinate, a milk protein. Patients with milk protein hypersensitivity (not lactose intolerance) should not be administered SPECTRACEF.
Cefditoren drug interactions

# Drug Interactions

### Oral Contraceptives
Multiple doses of cefditoren pivoxil had no effect on the pharmacokinetics of ethinyl estradiol, the estrogenic component in most oral contraceptives.

### Antacids
Co-administration of a single dose of an antacid which contained both magnesium (800 mg) and aluminum (900 mg) hydroxides reduced the oral absorption of a single 400 mg dose of cefditoren pivoxil administered following a meal, as evidenced by a 14% decrease in mean Cmax and an 11% decrease in mean AUC. Although the clinical significance is not known, it is not recommended that cefditoren pivoxil be taken concomitantly with antacids.

### H2-Receptor Antagonists
Co-administration of a single dose of intravenously administered famotidine (20 mg) reduced the oral absorption of a single 400 mg dose of cefditoren pivoxil administered following a meal, as evidenced by a 27% decrease in mean Cmax and a 22% decrease in mean AUC. Although the clinical significance is not known, it is not recommended that cefditoren pivoxil be taken concomitantly with H2 receptor antagonists.

### Probenecid
As with other -lactam antibiotics, co-administration of probenecid with cefditoren pivoxil resulted in an increase in the plasma exposure of cefditoren, with a 49% increase in mean Cmax, a 122% increase in mean AUC, and a 53% increase in t1/2.

### Drug/Laboratory Test Interactions
Cephalosporins are known to occasionally induce a positive direct Coombs test. A false-positive reaction for glucose in the urine may occur with copper reduction tests (Benedicts or Fehlings solution or with CLINITEST tablets), but not with enzyme-based tests for glycosuria (e.g., CLINISTIX, TES-TAPE). As a false-negative result may occur in the ferricyanide test, it is recommended that either the glucose oxidase or hexokinase method be used to determine blood/plasma glucose levels in patients receiving cefditoren pivoxil.
Cefpodoxime clinical studies

# Cystitis
In two double-blind, 2:1 randomized, comparative trials performed in adults in the United States, cefpodoxime proxetil was compared to other beta-lactam antibiotics. In these studies, the following bacterial eradication rates were obtained at 5 to 9 days after therapy:
In these studies, clinical cure rates and bacterial eradication rates for cefpodoxime proxetil were comparable to the comparator agents; however, the clinical cure rates and bacteriologic eradication rates were lower than those observed with some other classes of approved agents for cystitis.

# Acute Otitis Media Studies
In controlled studies of acute otitis media performed in the United States, where significant rates of beta-lactamase-producing organisms were found, cefpodoxime proxetil was compared to cefixime. In these studies, using very strict evaluability criteria and microbiologic and clinical response criteria at the 4 to 21 day post-therapy follow-up, the following presumptive bacterial eradication/clinical success outcomes (cured and improved) were obtained.
Ceftriaxone clinical studies
Clinical Trials in Pediatric Patients With Acute Bacterial Otitis Media: In two adequate and well-controlled U.S. clinical trials a single IM dose of ceftriaxone was compared with a 10 day course of oral antibiotic in pediatric patients between the ages of 3 months and 6 years. The clinical cure rates and statistical outcome appear in the table below:
An open-label bacteriologic study of ceftriaxone without a comparator enrolled 108 pediatric patients, 79 of whom had positive baseline cultures for one or more of the common pathogens. The results of this study are tabulated as follows:
Week 2 and 4 Bacteriologic Eradication Rates in the Per Protocol Analysis in the Roche Bacteriologic Study by pathogen:
File:Cftr.png
Cefuroxime adverse reactions
ZINACEF is generally well tolerated. The most common adverse effects have been local reactions following IV administration. Other adverse reactions have been encountered only rarely.
Local Reactions
Thrombophlebitis has occurred with IV administration in 1 in 60 patients.
Gastrointestinal
Gastrointestinal symptoms occurred in 1 in 150 patients and included diarrhea (1 in 220 patients) and nausea (1 in 440 patients). The onset of pseudomembranous colitis may occur during or after antibacterial treatment (see WARNINGS).
Hypersensitivity Reactions
Hypersensitivity reactions have been reported in fewer than 1% of the patients treated with ZINACEF and include rash (1 in 125). Pruritus, urticaria, and positive Coombs' test each occurred in fewer than 1 in 250 patients, and, as with other cephalosporins, rare cases of anaphylaxis, drug fever, erythema multiforme, interstitial nephritis, toxic epidermal necrolysis, and Stevens-Johnson syndrome have occurred.
Blood
A decrease in hemoglobin and hematocrit has been observed in 1 in 10 patients and transient eosinophilia in 1 in 14 patients. Less common reactions seen were transient neutropenia (fewer than 1 in 100 patients) and leukopenia (1 in 750 patients). A similar pattern and incidence were seen with other cephalosporins used in controlled studies. As with other cephalosporins, there have been rare reports of thrombocytopenia.
Hepatic
Transient rise in SGOT and SGPT (1 in 25 patients), alkaline phosphatase (1 in 50 patients), LDH (1 in 75 patients), and bilirubin (1 in 500 patients) levels has been noted.
Kidney
Elevations in serum creatinine and/or blood urea nitrogen and a decreased creatinine clearance have been observed, but their relationship to cefuroxime is unknown.
Postmarketing Experience with ZINACEF
In addition to the adverse events reported during clinical trials, the following events have been observed during clinical practice in patients treated with ZINACEF and were reported spontaneously. Data are generally insufficient to allow an estimate of incidence or to establish causation.
Immune System Disorders
Cutaneous vasculitis.
Neurologic
Seizure.
Non-site specific
Angioedema.
Cephalosporin-class Adverse Reactions
In addition to the adverse reactions listed above that have been observed in patients treated with cefuroxime, the following adverse reactions and altered laboratory tests have been reported for cephalosporin-class antibiotics:
Adverse Reactions
Vomiting, abdominal pain, colitis, vaginitis including vaginal candidiasis, toxic nephropathy, hepatic dysfunction including cholestasis, aplastic anemia, hemolytic anemia, hemorrhage.
Several cephalosporins, including ZINACEF, have been implicated in triggering seizures, particularly in patients with renal impairment when the dosage was not reduced (see DOSAGE AND ADMINISTRATION). If seizures associated with drug therapy should occur, the drug should be discontinued. Anticonvulsant therapy can be given if clinically indicated.
Altered Laboratory Tests
Prolonged prothrombin time, pancytopenia, agranulocytosis.
Cefuroxime direction for use

# Instructions for Constitution of ADD-Vantage Vials
To Open Diluent Container:
Peel the corner of the ADD-Vantage diluent overwrap and remove flexible diluent container. Some opacity of the plastic flexible container due to moisture absorption during the sterilization process may be observed. This is normal and does not affect the solution quality or safety. The opacity will diminish gradually.
To Assemble Vial and Flexible DiluentContainer(Use Aseptic Technique):
1. Remove the protective covers from the top of the vial and the vial port on the diluent container as follows:
a. To remove the breakaway vial cap, swing the pull ring over the top of the vial and pull down far enough to start the opening (see Figure 1), then pull straight up to remove the cap (see Figure 2). Note: Once the breakaway cap has been removed, do not access vial with syringe.
b. To remove the vial port cover, grasp the tab on the pull ring, pull up to break the 3 tie strings, then pull back to remove the cover (see Figure 3).
2. Screw the vial into the vial port until it will go no further. THE VIAL MUST BE SCREWED IN TIGHTLY TO ASSURE A SEAL. This occurs approximately one-half turn (180) after the first audible click (see Figure 4). The clicking sound does not assure a seal; the vial must be turned as far as it will go. Note:Once vial is seated, do not attempt to remove (see Figure 4).
3. Recheck the vial to assure that it is tight by trying to turn it further in the direction of assembly.
4. Label appropriately.
To Prepare Admixture:
1. Squeeze the bottom of the diluent container gently to inflate the portion of the container surrounding the end of the drug vial.
2. With the other hand, push the drug vial down into the container, telescoping the walls of the container. Grasp the inner cap of the vial through the walls of the container (see Figure 5).
3. Pull the inner cap from the drug vial (see Figure 6). Verify that the rubber stopper has been pulled out, allowing the drug and diluent to mix.
4. Mix container contents thoroughly and use within the specified time.
Preparation for Administration (Use Aseptic Technique):
1. Confirm the activation and admixture of vial contents.
2. Check for leaks by squeezing container firmly. If leaks are found, discard unit as sterility may be impaired.
3. Close flow control clamp of administration set.
4. Remove cover from outlet port at bottom of container.
5. Insert piercing pin of administration set into port with a twisting motion until the pin is firmly seated. Note: See full directions on administration set carton.
6. Lift the free end of the hanger loop on the bottom of the vial, breaking the 2 tie strings. Bend the loop outward to lock it in the upright position, then suspend container from hanger.
7. Squeeze and release drip chamber to establish proper fluid level in chamber.
8. Open flow control clamp and clear air from set. Close clamp.
9. Attach set to venipuncture device. If device is not indwelling, prime and make venipuncture.
10. Regulate rate of administration with flow control clamp.
WARNING: Do not use flexible container in series connections.
Center for Scientific Review
The Center for Scientific Review or CSR is the portal for United States National Institutes of Health (NIH) grant applications and their review for scientific merit. The CSR organizes the peer review groups or study sections that evaluate the majority (70%) of the research grant applications sent to NIH. It also receives all grant applications for NIH, as well as for some other components of the United States Department of Health and Human Services (DHHS). Since 1946, its mission has remained clear and timely: to see that NIH grant applications receive fair, independent, expert, and timely reviews -- free from inappropriate influences -- so NIH can fund the most promising research.
CSR receives nearly 80,000 applications a year and recruits over 18,000 external experts to review its portion of them in its study sections, which often meet three times during the year. Additional scientists serve on other NIH advisory councils, which provide a second level of peer review and make funding recommendations based on priorities set by the United States Congress, DHHS, and the public.

# Current initiatives
- Shorten the review process so applicants can revise and resubmit their applications in the next review round if necessary and NIH can more timely fund the best research. Shortening the review process by 45 days could thus reduce the time to resubmit by four months.
- Recruit and retain the best reviewers so NIH and applicants receive the best advice.
- Foster a culture more favorable to innovative applications, so that NIH can fund research that promises larger advances in science and health.
- Address the concern that clinical research is not properly evaluated, so this important research is well represented in the NIH program.
- Increase the transparency, accountability, and uniformity of NIH peer review.