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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A syndrome of metabolic acidosis of unknown etiology was diagnosed in twelve beef calves 7 to 31 days old. Principal clinical signs were unconsciousness or depression concomitant with weakness and ataxia. Other signs included weak or absent suckle and menace reflexes, succussable nontympanic fluid sounds in the anterior abdomen, and a slow, deep thoracic and abdominal pattern of respiration. The variation in clinical signs between calves was highly correlated (r = 0.87, P less than 0.001) with their acid-base (base deficit) status. Abnormal laboratory findings included reduced venous blood pH, pCO2 and bicarbonate ion concentration as well as hyperchloremia, elevated blood urea nitrogen, increased anion gap and neutrophilic leukocytosis with a left shift. Sodium bicarbonate solution administered intravenously effectively raised blood pH and improved demeanor, ambulation and appetite. All calves did well following a return to a normal acid-base status.
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PMID:Further studies on the clinical features and clinicopathological findings of a syndrome of metabolic acidosis with minimal dehydration in neonatal calves. 302 95

Toxic silo gases are a potential danger to livestock housed in close proximity to silos. On the fourth day of ensiling, five fattening pigs were found dead in a pen adjoining a grass silo. Post mortem examination revealed extensive lung damage and methaemoglobinaemia. A dense reddish-brown gas was concentrated at floor level to a height of 1 m in the pen and had diffused into adjoining pens, where dry and suckling sows and litters were showing signs of respiratory distress and weakness. The gas was identified as a mixture of nitrogen dioxide and dinitrogen tetroxide. These gases may be produced in the early stages of silage making. In this case, they had accumulated in a slurry channel below the silo and leaked through an adjoining wall into the piggery. The production and toxicological effects of silo gases are discussed.
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PMID:Nitrogen dioxide (silo gas) poisoning in pigs. 398 73

The metabolic response to human growth hormone (HGH) was studied in five obese subjects in the fed state and during prolonged (5-6 wk) starvation. In the fed state (three subjects), HGH induced an elevation in basal serum insulin concentration, a minimal increase in blood and urine ketone levels, and a marked reduction in urinary nitrogen and potassium excretion resulting in positive nitrogen and potassium balance. In prolonged fasting (four subjects), HGH administration resulted in a 2- to 3-fold increase in serum insulin which preceded a 50% elevation in blood glucose. Persistence of the lipolytic effects of HGH was indicated by a rise in free fatty acids and glycerol. The response differed markedly from the fed state in that blood beta-hydroxybutyrate and acetoacetate levels rose by 20-40%, resulting in total blood ketone acid concentrations of 10-12 mmoles/liter, ketonuria of 150-320 mmoles/day, and increased urinary potassium loss. The subjects complained of nausea, vomiting, weakness, and myalgias. Despite a 50% reduction in urea excretion during HGH administration, total nitrogen loss remained unchanged as urinary ammonia excretion rose by 50% and correlated directly with the degree of ketonuria. It is concluded that in prolonged starvation (a) HGH may have a direct insulinotropic effect on the beta cell independent of alterations in blood glucose concentration, (b) persistence of the lipolytic action of HGH results in severe exaggeration of starvation ketosis and interferes with its anticatabolic action by necessitating increased urinary ammonia loss, and (c) failure of HGH to reduce net protein catabolism in starvation suggests that this hormone does not have a prime regulatory role in conserving body protein stores during prolonged fasting.
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PMID:Metabolic response to human growth hormone during prolonged starvation. 554 Jan 76

Previous studies have shown that high-altitude hypoxic hypoxia is associated with reduced ventilatory capacity that may be related to skeletal muscle weakness. In the present investigation, ascent to high altitude (4,000 m) was simulated experimentally by exposure of male rats (Sprague-Dawley, 250-350 g), anesthetized with thiopental sodium (25 mg/kg, i.p.), to a breathing gas mixture of 12% oxygen diluted in 88% nitrogen (FiO2 = 0.12). Determinations of oxygen saturation on microsamples (250 ul) of arterial and central venous blood were made spectrophotometrically. Neuromuscular conduction latency was measured following electrostimulation of the sciatic nerve (1-5 V, 0.5 msec duration, 1-40 Hz) and recording of the electromyogram from the gastrocnemius muscle. Experimental hypoxia (FiO2 = 0.12) produced a highly significant increase in conduction latency from a control value (mean +/- SEM) of 3.06 +/- 0.16 msec to 4.02 +/- 0.31 msec (n = 10, P less than 0.001). Conduction latency increased with decreasing arterial oxygen saturation from a control value of 92.9% +/- 0.18% to 83.2% +/- 0.76% (P less than 0.001) in the absence of statistically significant changes in central venous oxygen saturation, central venous pressure, arterial and central venous pH, and heart rate. A significant decrement in the mean arterial blood pressure from a control value of 85 +/- 1.5 mm Hg to 69 +/- 1.5 mm Hg suggests that local ischemia may be a component of this model. These responses were accompanied by marked reduction in uptake of 3,3'-diaminobenzidine (DAB) by gastrocnemius muscle mitochondria, suggesting decreased intracellular activity of cytochrome oxidase. It was concluded that exposure of rodents to hypoxic gas mixtures may provide a suitable model for studying the mechanism of skeletal muscle weakness associated with ascent to high altitude and of other conditions wherein the supply of oxygen to tissues is limited.
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PMID:Relationship between intracellular oxygenation and neuromuscular conduction during hypoxic hypoxia. 609 57

Diuretic therapy is the most common cause of potassium deficiency. Although the extent of potassium deficiency usually does not exceed 200 or 300 mEq, under appropriate circumstances such modest deficiency may have important consequences. Factors that tend to increase the incidence or severity of potassium deficiency in patients who take diuretics include high salt diets, large urine volumes, metabolic alkalosis, increased aldosterone production, and the simultaneous use of two diuretics that act on different sites in the renal tubule. There are many serious complications of potassium deficiency, including cardiac arrhythmias, muscle weakness, rhabdomyolysis, glucose intolerance, and several complications that result directly from increased ammonia production, such as protein and nitrogen wasting and hepatic coma. Emphasized herein are those conditions that impose potential danger in patients with mild hypokalemia. Important factors that identify specific causes of potassium deficiency and its treatment are discussed briefly.
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PMID:Diuretic-induced hypokalemia. 649 56

A 44-year-old black male presented with fever, myalgia and weakness. He had elevated blood urea nitrogen, creatine phosphokinase and serum glutamic-oxaloacetic transaminase. During the first 6 days of this undiagnosed illness azotemia increased, a pericardial friction rub occurred, and hematuria was present. On the 7th day bilateral subconjunctival hemorrhages, anterior uveitis, and peripapillary cotton-wool spots were noted. This combination of findings suggested leptospirosis, which was subsequently confirmed by specific antibody titers. Therapeutic response was achieved with high-dose systemic steroids.
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PMID:Cotton-wool spots as a sign in leptospirosis (Weil's disease). 663 59

The toxic effects of PR toxin were observed in mice, rats, anesthetized cats and isolated rat auricle preparations. In mice and rats the toxic effects included abdominal writhing, decrease of motor activity and respiratory rate, weakness of hindleg and ataxia. In mice, the i.p. LD50 was 5.8 mg/kg. In mice, rats and cats PR toxin given i.p. caused ascites fluid an edema in the scrotum and lungs, and i.v. injection caused edema in the lungs, giving rise to a large volume of pleural and pericardial fluid. In rats, at the LD50 dose level (11.6 mg/kg, i.p. and 8.2 mg/kg, i.v.), the water content in the lungs was increased, but in the skin it was decreased. Blood K+, hematocrit, red blood cell, white blood cell, hemoglobin, uric acid, cholesterol, blood urea nitrogen and alkaline phosphatase concentrations were all increased, while the total protein and albumin contents were decreased after i.p. injection of PR toxin. High content of protein was found in the pleural fluid and fluid due to ascites. In anesthetized cats the blood pressure and respiratory rate were progressively decreased and the heart rate was reflexly increased after i.p. injection. The i.v. injection produced a multiple response on the arterial blood pressure, but with a progressively decreasing heart rate. Arrhythmias were observed in the late shock stage in the case of i.p. or i.v. injection. In the isolated rat auricle preparations contractile force was more affected that heart rate. We conclude that PR toxin produced acute toxic effects in animals via an increase of capillary permeability and a direct damage to the lungs, heart, liver and kidney.
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PMID:Acute toxicity of PR toxin, a mycotoxin from Penicillium roqueforti. 708 52

Hyperparathyroid crisis is a rare disease manifested by elevated serum calcium, weakness, nausea and vomiting, altered states of consciousness, and elevated circulating parathormone. This hypercalcemic state is noted for a frequently acute presentation and associated high mortality rate, approaching 60% in some series. Ten patients in parathyroid crisis were observed in a consecutive personal series of 325 cases of operatively proved hyperparthyroidism. All 10 patients were successfully treated. Each patient remained or lapsed into persistent coma despite extensive medical management and normalization of serum calcium in some instances. An emergency parathyroidectomy was performed in all cases. Reversal of the comatose state was noted in all patients within 24 hours, followed by gradual normalization of serum calcium. Serum calcium ranged from 15 to 19.6 mg/dl. The blood urea nitrogen level was elevated in six patients. A single adenoma was found in nine patients and multiglandular disease involving the neck and the mediastinum in one. All patients survived. The successful treatment of this disease demands prompt and accurate diagnosis coupled with vigorous medical therapy and emergency parathyroidectomy if the patient's status continues to deteriorate.
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PMID:Hyperparathyroid crisis. Successful treatment of ten comatose patients. 728 Oct 12

Two of 80 cynomolgus monkeys, Macaca fascicularis, imported from Indonesia showed weakness, anorexia, paralysis of extremities and dysstasia. The blood test conducted at the time of autopsy proved that the white blood cell count markedly decreased in both cases and the blood urea nitrogen content increased in Case No. 1. In Case No. 2, a high blood sugar value, a low red blood cell count and a low hematocrit value were recognized. Histologic examinations revealed the presence of fragments of a nematode in the subarachnoid space of the cerebrum, granular layer of the cerebellum and gray matter of the cervical spinal cord. The findings of eosinophilic meningitis, necrosis, foreign body giant cells and cellular infiltration predominantly with eosinophils were also noted there. Morphological features of the nematode found in the tissue sections were identical, in all respects, with those described by predecessors who made morphological observations on the cross sections of Angiostrongylus cantonensis. Immunoelectrophoretic analyses of sera from these monkeys demonstrated the presence of band "a", which has been described to be highly specific to human A. cantonensis infection. Based on the above-mentioned evidences, the parasite fragments found in the histological sections from the monkeys were identified as A. cantonensis. The cases of natural infection reported herein represent the first, to our knowledge, in which migration of A. cantonensis larvae in the central nervous system of monkey was demonstrated. The present observation suggests applicability of simian angiostrongyliasis as a model for infections in man.
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PMID:[Two cases of natural infection of Angiostrongylus cantonensis in cynomolgus monkeys (Macaca fascicularis) (author's transl)]. 731 30

A 78-year-old man was hospitalized because of muscular weakness and acute renal failure. He had been taking glycyrrhizin (280 mg/day) for the last 7 years. Hypertension was noted in his history. Serum potassium was 1.9 mEq/l with metabolic alkalosis. There was hyporeninemic hypoaldosteronism. Serum enzymes, including GOT, LDH and CPK were markedly elevated. In addition, serum myoglobin was as high as 46 micrograms/ml with massive myoglobinuria. Oliguria occurred and blood urea nitrogen and serum creatinine rapidly elevated from 20.9 to 87 mg/dl and from 1.3 to 6.7 mg/dl, respectively. Profound calcium deposition was found in the damaged skeletal muscles, including the quadriceps femoris, axillar, neck, and cardiac muscles. These results indicate that licorice-induced pseudoaldosteronism produces hypokalemic rhabdomyolysis, resulting in acute renal failure and profound deposition of calcium into the damaged skeletal and cardiac muscles.
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PMID:An autopsy case of licorice-induced hypokalemic rhabdomyolysis associated with acute renal failure: special reference to profound calcium deposition in skeletal and cardiac muscle. 785 65


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