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)

Acid-base terminology including the sue of SI units is reviewed. The historical reasons why nomograms have been particularly used in acid-base work are discussed. The theoretical basis of the Henderson-Hasselbalch equation is considered. It is emphasized that the solubility of CO2 in plasma and the apparent first dissociation constant of carbonic acid are not chemical constants when applied to media of uncertain and varying composition such as blood plasma. The use of the Henderson-Hasselbalch equation in making hypothermia corrections for PCO2 is discussed. The Astrup system for the in vitro determination of blood gases and derived parameters is described and the theoretical weakness of the base excess concept stressed. A more clinically-oriented approach to the assessment of acid-base problems is presented. Measurement of blood [H+] and PCO2 are considered to be primary data which should be recorded on a chart with in vivo CO2-titration lines (see below). Clinical information and results of other laboratory investigations such as plasma bicarbonate, PO2,P50 are then to be considered together with the primary data. In order to interpret this combined information it is essential to take into account the known ventilatory response to metabolic acidosis and alkalosis, and the renal response to respiratory acidosis and alkalosis. The use is recommended of a chart showing the whole-body CO2-titration points obtained when patients with different initial levels of non-respiratory [H+] are ventilated. A number of examples are given of the use of this [H+] and PCO2 in vivo chart in the interpretation of acid-base data. The aetiology, prognosis and treatment of metabolic alkalosis is briefly reviewed. Treatment with intravenous acid is recommended for established cases. Attention is drawn to the possibility of iatrogenic production of metabolic alkalosis. Caution is expressed over the use of intravenous alkali in all but the severest cases of metabolic acidosis. The role of 2,3-diphosphoglycerate on tissue oxygenation is stressed and use of intravenous sodium phosphate as an alternative to intravenous bicarbonate is mentioned.
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PMID:The physiological assessment of acid-base balance. 23 27

Analytical investigations were carried out on alteration crusts of "Pietra d'Istria" used for the construction of "Palazzo Papadopoli" in Venice. The chemical and mineralogical analyses of the microstructure showed that alteration process in mainly caused by the transformation of calcium carbonate into calcium sulphate and that the greatest damages are due to the subsequent detaching of sulphatic crusts according to a weakness surface. The isotopic analyses showed that sulphur present in the crust is mainly derived from the combustion of hydrocarbons. The investigations on the climatic conditions showed the meaningful importance of the climate parameters on described alterations.
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PMID:[Changes in the building stones of Venice: action of atmospheric sulfur on carbonic rocks]. 60 31

In summary, severe hyperchloremic acidosis developed in two patients as a late complication after jejunoileal bypass for morbid obesity. This acidosis was associated with episodes of dizziness, ataxia, headache, weakness, confusion and transient loss of consciousness. Recognition of this symptom complex in the patient with a jejunoileal bypass should suggest metabolic acidosis as a complication of this surgical procedure. Bicarbonate replacement provided prompt, but temporary, improvement in the symptoms and the acidosis. Revision of the intestinal bypass was required for correction. Special studies to rule out renal tubular acidosis were performed and definitely excluded the kidney as a source of the acidosis.
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PMID:Severe hyperchloremic acidosis complicating jejunoileal bypass. 63 46

A case of a 76-year-old man with the syndrome of inappropriate secretion of antidiuretic hormone (ADH) is discussed. The patient was initially treated with fluid restriction followed by the administration of hypertonic saline. After failure to achieve rapid correction of the condition and continued lethargy and muscle weakness in the patient, a trial with lithium carbonate 300 mg three times daily via nasogastric tube was initiated. This resulted in a prompt reversal of the hyperosmolar state and improvement in electrolyte balance. However, despite the apparent success in treating his inappropriate ADH, the patient expired as a result of a massive cerebral vascular accident. The potential benefit of using lithium in the treatment of the syndrome of inappropriate secretion of ADH, and possible mechanisms of action, are reviewed.
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PMID:Lithium carbonate treatment in the syndrome of inappropriate secretion of antidiuretic hormone. 92 Jul 46

In a patient with recurrent episodes of severe mania, classical manifestations of myasthenia gravis developed for the first time during treatment with lithium carbonate. Four episodes were recorded in which the appearance of progressive weakness coincided with subacute or long-term lithium carbonate administration during periods of psychiatric remission. In each instance, neurologic symptoms were ameliorated or disappeared shortly after the drug was discontinued or its dosage was reduced. There was no evidence of lithium carbonate toxicity or electrolyte disturbances at any time during treatment. Based on a literature review of animal studies and related clinical reports, a mechanism of peripherally mediated neuromuscular cholinergic insufficiency is proposed. In addition, the differential diagnosis of muscle weakness during lithium carbonate administration is discussed.
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PMID:Emergence of myasthenia gravis during treatment with lithium carbonate. 96 92

The utility and side effects of sustained-release lithium carbonate (Priadel) in a once-per-day dose regimen was investigated with 66 male delinquents, ages 17-24 years, in a double-blind study comparing the antiaggressive effect of lithium carbonate with placebo. Serum lithium levels and symptoms were determined weekly for up to eight drug-free and 12 on-medication weeks. Average daily doses of 1500-1700 mg Priadel gave 24-hour serum lithium levels in the range 0.7-0.9 mEq/liter. Principal side effects were polyuria and shakiness, with other important side effects bring hand tremor, dryness of mouth, nausea, and weakness. No lithium toxicity was observed, and diarrhea was reported infrequently. Placebo response data are presented.
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PMID:Sustained-release lithium carbonate in double-blind study: serum lithium levels, side effects, and placebo response. 126 38

Cardiopulmonary function was examined in 18 dogs with serious chronic heartworm disease showing ascites, subcutaneous edema, prostration, weakness, jaundice and so on. After surgical heartworm removal from the pulmonary arteries, 10 dogs recovered (surviving group), and 8 dogs died or were euthanatized because of poor prognosis (nonsurviving group). The number of live heartworms residing in the pulmonary arteries of the surviving group tended to be larger than that in the nonsurviving group. At necropsy, severe pulmonary arterial lesions such as thromboembolism including dead heartworms, proliferative and villous lesions and intimal hyperplasia were noticed in all dogs examined, and tended to be severer in the nonsurviving group. Heartworm-coiling around the tricuspid valve chord was found in 1 dog of the surviving group and 4 dogs of the nonsurviving group. Before heartworm removal, there was no significant difference in the mean pulmonary arterial pressure (MPAP) between the surviving and nonsurviving group. Right atrial pressure (v-wave) was higher, and the cardiac index (CI) was lower in the nonsurviving group. Arterial oxygen tension was lower in the surviving group than in the heartworm-free group, and it was lower in the nonsurviving group than in the surviving group. Carbon dioxide tension was lower in the surviving group than in the heartworm-free group. Bicarbonate concentration (HCO3-) was lower both in the surviving and nonsurviving groups than in the heartworm-free group. One week after heartworm removal, MPAP decreased (P less than 0.05), and CI and HCO3- tended to increase in the surviving group.
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PMID:Cardiopulmonary function in dogs with serious chronic heartworm disease. 139 Nov 87

We describe a neonate with distal renal tubular acidosis with secondary hyperparathyroidism manifesting as hyperchloraemia, hypercalcaemia, elevated serum parathyroid hormone (PTH) and life-threatening metabolic acidosis. He exhibited general weakness, tachypnoea, dry skin and weight loss. Urinary excretion of titratable acid and ammonium was decreased. Daily alkali (2.5 mEq/kg body weight) was required to maintain a normal plasma bicarbonate (HCO3-). With alkali therapy, the fractional excretion of HCO3- was below 5%. Serum calcium and PTH were restored to normal promptly on initiation of alkali therapy. After 5 months of alkali therapy, normal growth and urine acidifying ability were restored and alkali therapy was discontinued. The acidification defect in this patient was transient. We consider this patient to be consistent with Lightwood's syndrome of "transient infantile renal tubular acidosis".
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PMID:Transient neonatal distal renal tubular acidosis with secondary hyperparathyroidism. 161 37

Barium intoxication, a rare cause of hypokalemia, can sometimes result in respiratory paralysis and ventricular tachyarrhythmia. Herein, we report one such case. A 29-year-old man swallowed barium-contaminated fried flour-coated sweet potatoes. Then, abdominal discomfort, vomiting, diarrhea, progressive muscular weakness, apnea and ventricular tachycardia developed and laboratory data revealed profound hypokalemia. He regained his health after mechanical ventilation, anti-arrhythmic agent and aggressive potassium chloride supplement. Analysis of blood, urine and contaminated flour showed the presence of barium carbonate. Barium intoxication is a medical emergency which requires rapid therapy to prevent mortality.
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PMID:[Barium intoxication: a case report]. 168 96

A 59-year-old female patient was admitted because of muscle weakness in all four limbs for a period of 5 days. She had been found to have Graves' disease 4 years ago previous to this, and had received a subtotal thyroidectomy 1 year later. Hypothyroidism supervened and she had been receiving levothyroxine replacement in recent years. She also had non-insulin-dependent diabetes, which was controlled with diet only. During the 5 days prior to admission, she developed muscle weakness which finally worsened to complete paralysis of all four limbs. Physical examination showed tenderness and weakness of the extremity muscles. Abnormal laboratory data included serum K, 1.6 mEq/L; P, 1.2 mg/dl; uric acid, 1.6 mg/dl; fasting glucose, 267 mg/dl; T3, 36.65 ng/dl; T4, 4.0 micrograms/dl; TSH, 5.35 mu u/ml; free T4, 0.57 ng/dl; and metabolic acidosis with pH, 7.298; PCO2, 27.0 mmHg; and HCO3, 12.8 mEq/L. An EKG showed a prominent U wave, and urinalysis revealed renal glucosuria and massive aminoaciduria. An oral sodium bicarbonate loading test showed an increasing loss of bicarbonate through the urine, while the plasma bicarbonate level was elevated. Clinical manifestations improved after the administration of sodium bicarbonate, potassium chloride and neutral phosphate.
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PMID:Fanconi syndrome: report of a case. 198 86


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