Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of nalorphine on eliciting symptoms of either alcohol or narcotic withdrawal was studied. Five male alcoholics were challenged with nalorphine and saline, both while sober and during alcohol ingestion. After nalorphine, pulse rate decreased in patients when sober, but increased when they were ingesting alcohol. Nalorphine administration resulted, during alcohol ingestion, but not in the sober state, in lacrimation, a symptom of narcotic withdrawal, in one patient, and in the following symptoms of alcohol or narcotic withdrawal in one or more patients: weakness, anorexia, insomnia, disorientation, and tremor. These findings suggest that morphine-like alkaloids play a role in the mediation of alcohol withdrawal symptoms.
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PMID:Induction of alcohol withdrawal symptoms by nalorphine in chronic alcoholic patients. 66 63

Twenty-four cases of Legionnaires' disease were diagnosed at the Wadsworth Veterans Administration Hospital during a 5-month period. All cases occurred in persons exposed to the hospital environment during the usual incubation period of Legionnaires' disease. The clinical illness was quite characteristic. All patients complained of weakness, malaise, anorexia, and cough. Rigors, diarrhea, and pleuritic pain were frequent symptoms. All patients had a maximum temperature of greater than or equal to 39.4 degrees C. Thirteen of 22 patients had relative bradycardia. Chest roentgenograms documented pneumonia in all patients. Leukocytosis, hyponatremia, hypophosphatemia, and abnormal liver-function test results were typical. Diagnosis was made by serologic criteria in 20 patients, postmortem examination of tissue in two, and both serology and tissue examination in two. Four patients in whom the disease was not suspected died of Legionnaires' disease. One patient died of unrelated causes. Fifteen of 19 survivors received erythromycin therapy. The presentation of Legionnaires' disease was characteristic enough to allow early, specific therapy.
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PMID:Legionnaires' disease: clinical features of 24 cases. 68 39

Naturally acquired Brucella canis infection is believed to be uncommon, but is not readily diagnosed. A 55-year-old woman developed fever, abdominal pain, malaise, weakness, and anorexia eight weeks after her dog delivered stillborn pups. Blood cultures yielded B canis. Specific B canis agglutinins were negative initially and remained negative during convalescence. Therapy with tetracycline and streptomycin was successful but was associated with a probable Jarisch-Herxheimer reaction.
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PMID:Case report. Brucella canis bacteremia: a case with negative B canis agglutinins. 72 14

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

Bacterial endocarditis caused by Actinobacillus actinomycetemcomitans is a rare disease. A 48-year-old man who had a Starr-Edwards aortic valve prosthesis inserted in 1972 was admitted for evaluation of confusion, headaches, anorexia, weight loss, diarrhea and weakness. Six blood cultures yielded gram-negative organisms which were subsequently identified as A. actinomycetemcomitans. Treatment with ampicillin and gentamicin resulted in cure which has been maintained after an observation period of eleven months. This represents the second report of A. actinomycetemcomitans endocarditis in a patient with a prosthetic valve.
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PMID:Actinobacillus actinomycetemcomitans endocarditis in a patient with a prosthetic aortic valve. 88 Dec 58

Each of two Desert Sheep was infected with 1500 cercariae of Schistosoma mansoni of Northern Sudan. Signs of infection were anorexia, soft faces, progressive weakness and loss of wool. The sheep were killed 254 and 269 days after infection. The findings were heavy infiltration of the lamina propria with inflammatory cells, numerous ova in the submucosa, hyperplasia of lymphoid tissue, oedema of the mesenteric lymph nodes, and focal pulmonary oedema and congestion. There were egg granulomas, focal necrosis, schistosomal pigment, fatty change, depletion of glycogen and reduction in the activity of adenosine triphosphatase, succinic tetrazolium reductase and glucose-6-phosphatase in the liver. In one sheep 1330 cercariae penetrated and 700 matured to produce males and females in a 5:2 ratio. In the other sheep, about one third of the cercariae penetrated and matured. The ratio of males to females was 3:1.
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PMID:Susceptibility of desert sheep to infection with Schistosoma mansoni of Northern Sudan. 93 26

The objective of this paper is to characterize the fat cow syndrome. This condition refers to a combination of metabolic, digestive, infectious, and reproductive conditions which affects the obese periparturient cow. The condition develops primarily due to faulty feed management which permits excessive consumption of unbalanced diets. The syndrome is frequently a herd problem characterized by a high morbidity and mortality due to an increase in disease in periparturient cows. Clinical signs include depression, anorexia, ketonuria, marked decrease in production, progressive debilitation, weakness, nervous signs, and an elevation in temperature due to infectious disease. The obesity is generalized throughout the body with extensive fatty metamorphosis in the liver. Histological changes are primarily in the liver and kidney. Treatment of the condition consists of feeding a balanced diet, symptomatic treatment, and good supportive care. The condition can be prevented by feeding a balanced diet according to nutrient requirements of the National Research Council.
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PMID:Fat cow syndrome. 96 40

An autopsy case of Cronkhite-Canada's syndrome characterized by diffuse gastrointestinal polyposis, alopetia, onychodystrophia and pigmentation of the skin is reported. The patient, 51 year-old-male, died with general weakness and pneumonia at 6 months after the first notice of alopetia anorexia and weight loss. Numerous and various sized polyps and polypoid lesions were revealed in the gastrointestinal tracts at the autopsy. The microscopic pictures of the lesions were composed of hyperplastic or papillary adenomatous polyps with hyperplasia of mucosa epithelium. In some of the lesions, the glands are cystically dilated containing mucous. Lymph vessels of thelamina propria and the submucosa benerked chronic inflammatory infiltrate was noted. The present report is described the histopathological findings of the gastrointestinal lesions with Cronkhite-Canada syndrome and discussed with literature.
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PMID:An autopsy case of Cronkhite-Canada syndrome. 99 57

Eight 5-to 8-week-old Beagle pups were allotted to 4 groups of 2 dogs each. For 55 to 70 days, they were fed either a semisynthetic basal diet (BD) deficient in vitamin E and selenium (Se) (group 1) or the BD supplemented with either 30 IU alpha-tocopherol/kg (group 2), 0.5 ppm Se as selenite (group 3), or 1.0 ppm Se as selenite (group 4). In the dogs fed the BD, clinical signs of vitamin E-Se deficiency developed after 40 to 60 days. These signs were accompanied by increased plasma activity of creatine phosphokinase (CPK) and glutamic oxalacetic transaminase (GOT). The dogs were euthanatized after 10 to 15 days of progressive clinical signs, including muscular weakness, subcutaneous edema, anorexia, depression, dyspnea, and eventual coma. Gross lesions seen at necropsy included ventral subcutaneous edema, generalized skeletal muscular pallor and edema with scattered white longitudinal streaking, prominent brownish yellow discoloration of the intestinal musculature, and a layer of white chalky material at the renal corticomedullary junction. Microscopically, there was evidence of extensive skeletal muscular degeneration and regeneration, focal subendocardial necrosis in the ventricular myocardium, intestinal lipofuscinosis, and renal mineralization. Mean hepatic Se content in the dogs fed the BD was 0.10 ppm (wet weight basis) at necropsy. In the dogs fed the 3 supplemented diets, clinical signs of deficiency did not develop. At necropsy, mild skeletal myopathy was evident histologically in the dogs fed BD and 0.5 ppm Se (group 3) but not in the dogs fed the other supplemented diets. Intestinal lipofuscinosis was found in the dogs fed the 3 supplemented diets but was less severe in the dogs fed the diet supplemented with vitamin E than in those fed diets supplemented with Se.
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PMID:Experimentally induced vitamin E-selenium deficiency in the growing dog. 112 Jul 35


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