Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anorexia nervosa and bulimia nervosa are prevalent illnesses affecting between 1% and 10% of adolescent and college age women. Developmental, family dynamic, and biologic factors are all important in the cause of this disorder. Anorexia nervosa is diagnosed when a person refuses to maintain his or her body weight over a minimal normal weight for age and height, such as 15% below that expected, has an intense fear of gaining weight, has a disturbed body image, and, in women, has primary or secondary amenorrhea. A diagnosis of bulimia nervosa is made when a person has recurrent episodes of binge eating, a feeling of lack of control over behavior during binges, regular use of self-induced vomiting, laxatives, diuretics, strict dieting, or vigorous exercise to prevent weight gain, a minimum of 2 binge episodes a week for at least 3 months, and persistent overconcern with body shape and weight. Patients with eating disorders are usually secretive and often come to the attention of physicians only at the insistence of others. Practitioners also should be alert for medical complications including hypothermia, edema, hypotension, bradycardia, infertility, and osteoporosis in patients with anorexia nervosa and fluid or electrolyte imbalance, hyperamylasemia, gastritis, esophagitis, gastric dilation, edema, dental erosion, swollen parotid glands, and gingivitis in patients with bulimia nervosa. Treatment involves combining individual, behavioral, group, and family therapy with, possibly, psychopharmaceuticals. Primary care professionals are frequently the first to evaluate these patients, and their encouragement and support may help patients accept treatment. The treatment proceeds most smoothly if the primary care physician and psychiatrist work collaboratively with clear and frequent communication.
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PMID:Eating disorders. A review and update. 147 50

Totally-enclosed motor-propelled survival craft (TEMPSC) are used to evacuate the crews of mobile offshore drilling units in emergencies. The small size and flat bottom of the TEMPSC predispose most occupants to seasickness, even in relatively calm waters. This paper discusses efforts required to improve the well-being of occupants in terms of reducing seasickness, dehydration, hypothermia, anxiety, and the other factors that contribute to loss of comfort and the will to survive. Specific recommendations include the provision of climatic control to regulate temperature, remove odors and provide fresh air; potable water, electrolytes, and survival rations; and an ample supply of motion sickness bags. Overcrowding should be avoided. Anti-motion-sickness drug therapy to control vomiting should be administered in two ways: initial injection of intramuscular scopolamine for fast action followed by a transdermal ear patch for long-term protection. Leadership and seasickness management should be requisite survival training for all oil rig workers.
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PMID:Seasickness in totally-enclosed motor-propelled survival craft: remedial measures. 156 25

Natural PGF administered at a dose of at least 250 micrograms/kg twice daily subcutaneously for at least 4 days starting no earlier than day 5 of cytologic diestrus induces luteolysis and pregnancy termination in the mated bitch. The resulting shortening of the luteal phase is associated with a shortening of the interestrous interval from 1 to 4 months. Bitches treated with PGF show emesis, diarrhea, and panting within 5 minutes and transient hypothermia which lasts 2 to 3 hours but generally have no further reaction. Bitches with cardiac or respiratory dysfunctions are not considered safe patients for early pregnancy termination with PGF because of the cardiovascular effects of this drug. Bitches treated with this regime early in diestrus resorb their conceptuses; those treated after days 35 to 40 show clinical abortion of viable fetuses.
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PMID:Use of prostaglandin F2 alpha for early pregnancy termination in the mismated bitch. 185 44

N-(2,2-Diphenylethyl)adenosine (DPEA) has been identified as a potential antipsychotic agent acting via stimulation of adenosine receptors. The projected human therapeutic dose, based on animal studies, is 2-3 mg/kg. DPEA has been tested for potential toxicity in mice, rats, dogs and monkeys. Following single oral doses, median lethal dose values were approximately 10-fold greater in rats than in mice, although similar clinical signs including reduced activity, prostration, and necrosis of the tail were seen in both species. DPEA was well tolerated at daily doses up to 40 mg/kg in rats for 2 weeks. A no observed effect level (NOEL) was not identified in the dog or monkey studies. Reduced activity, dacryorrhea, ptosis, hypothermia, necrosis of the tail, and death occurred in rats given 120 and 160 mg/kg. Pathologic changes consisted of pancreatitis, gastric erosion/ulceration, lymphocyte depletion of the thymus, and pulmonary congestion and hemorrhage at 80 mg/kg or greater. In dogs, sporadic emesis was noted at 12.5 mg/kg and greater, and significant pathologic changes consisted of coronary arteritis associated with myocardial lesions and lymphocyte depletion at 25 and 50 mg/kg, pancreatic acinar necrosis at 50 mg/kg, and renal tubular degeneration at 12.5 mg/kg and greater. Emesis and depression were noted at 25 and 50 mg/kg in monkeys. Renal tubular dilatation and degeneration at 25 and 50 mg/kg were noted in the monkeys. These studies demonstrated that DPEA produced a range of adverse effects in common laboratory animal species.
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PMID:Preclinical toxicity studies of an adenosine agonist, N-(2,2-diphenylethyl) adenosine. 187 77

Violent shaking causes severe injury in infants, but the diagnosis of shaken baby syndrome is often difficult to make because of the lack of obvious external signs. Consultations by other specialists may not be helpful, since the findings of most organ systems, taken in isolation, are usually nonspecific. Shaken baby syndrome should be considered in infants presenting with seizures, failure to thrive, vomiting associated with lethargy or drowsiness, hypothermia, bradycardia, hypertension or hypotension, respiratory irregularities, coma or death. Shaken babies are usually less than one year old, and most are under six months of age. Head injury (notably subdural hemorrhage) and retinal hemorrhages are the hallmarks of the syndrome.
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PMID:Shaken baby syndrome. 218 31

A 14-year-old male presented with a one week history of weakness, lightheadedness and vomiting. Bilateral pleural effusions were evident on chest radiography; electrocardiogram revealed decreased voltages. Echocardiogram, abdominal ultrasound and magnetic resonance imaging revealed a mass in an hepatic vein and the inferior vena cava extending up to and filling the right atrium. Under deep hypothermia and extracorporeal circulation the mass was removed en bloc. It originated from the hepatic vein. Pathology revealed a smooth muscle tumour intermediate between benign and malignant (atypical leiomyoma). This is the first reported pediatric primary leiomyoma of the hepatic vein. It caused the Budd-Chiari syndrome, a rare pediatric entity.
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PMID:Atypical hepatic vein leiomyoma extending into the right atrium: an unusual cause of the Budd-Chiari syndrome. 218 75

In the attempt to correlate clinical findings with serum levels of aldrin, sixteen patients were followed-up after acute intoxication by this agent. Eight of them, males and females, aged from 1 to 37 years, presented no or light symptoms (some discomfort and nausea). The serum of one of these patients was found to contain 16.6 ppb of aldrin and that of another, 1.41 ppb of dieldrin. A group of five patients, aged from two to 30 years, showed symptoms of moderate severity, reporting nausea, vomiting, drowsiness, dyspnea, sweating, mild jerking, rise in blood pressure and convulsions. Of these cases, two were accidental and three were attempted suicides, the majority achieving complete recovery within 24 hours. Serum levels of aldrin were between 6.98 ppb and 26.3 ppb and of dieldrin between 82.00 and 314.18 ppb. We found three severe cases, aged from 21 to 35 years, two attempted suicides and one occupational case. Two of these patients died and one of them presented hypothermia, coma, absence of reflexes and generalized convulsions, and another presented abdominal pain, paleness, sweating, cold extremities, dyspnea, hyperthermia and generalized convulsions. In the first one that died the serum levels were: of aldrin 30.00 ppb and of dieldrin 720 ppb. In the other levels of 747.3 ppb of aldrin and 1,314.00 ppb of dieldrin were found. The third had less serious symptoms and presented serum levels of aldrin of 31.05 ppb and of dieldrin 147.11 ppb.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute poisoning by aldrin: relationship between serum levels and toxic effects in humans]. 221 74

A breast-fed boy, born to first-cousin parents, had been vomiting since birth; his general condition remained good until age 6 weeks when vomiting became more frequent, and his status suddenly worsened, with polypnea, shock, hypothermia, jaundice, presence of blood in urine, gastric juice, stool, and bleeding tendency during veno-punctures. There was an huge hepatomegaly and a splenomegaly. Hypoglycaemia, metabolic acidosis, severe blood coagulation disturbances, elevated liver enzymes, hypoalbuminemia, pointed to an acute liver failure. He was resuscitated with current supportive measures, and was given a wide spectrum antibiotherapy. Because serologic tests for syphilis were positive in the child and his mother, including the presence of specific IgM the infant was then given Penicillin G therapy only, which resulted in a complete recovery. One month later, a needle liver biopsy showed residual signs of hepatitis. Other possible infectious or metabolic causes of acute liver failure occurring early in life had been excluded.
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PMID:[Acute hepatic insufficiency disclosing congenital syphilis]. 240 70

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

The effects of mafoprazine, a new phenylpiperazine derivative, on the central dopaminergic system were studied. Mafoprazine, like chlorpromazine and haloperidol, reduced the apomorphine-induced cage-climbing behavior in mice, emesis in dogs and stereotyped behavior in monkeys; methamphetamine-induced hyperlocomotion and group toxicity in mice; and agitation in rats. Mafoprazine inhibited the unilateral circling behavior induced by methamphetamine and apomorphine in rats with 6-hydroxydopamine-induced lesions in the unilateral nigrostriatal neuronal tract. The potency of mafoprazine in these experiments was almost equal to that of chlorpromazine and about one-tenth that of haloperidol. The cataleptogenic activity of mafoprazine was lower than those of chlorpromazine and haloperidol. Mafoprazine potentiated clonidine-induced hypothermia. These results suggest that mafoprazine has a relatively selective postsynaptic dopamine D2-receptor blocking action in the nucleus accumbens compared with chlorpromazine and haloperidol and suggest that mafoprazine also has alpha 2-adrenoceptor-stimulating actions.
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PMID:Effects of mafoprazine, a phenylpiperazine derivative, on the central dopaminergic system. 256 44


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