Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year-old woman had been suffering from bulimia and habitual vomiting for about 7 years and was incidentally found to have right renal stones by computed tomography. She was referred to our hospital for the treatment of these caluculi. On admission, she presented with hypokalemia, hypochloremia and metabolic alkalosis and was diagnosed with anorexia nervosa. Following successful removal by percutaneous nephrolithotripsy and extracorporeal shockwave lithotripsy the stones were found to consist of pure ammonium urate. Since the urine of an anorexia nervosa patient tends to be rich in uric acid and ammonium, anorexia nervosa seems to be associated with ammonium urate urinary stones.
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PMID:[A case of ammonium urate urinary stones with anorexia nervosa]. 1110 33

Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation, mainly in the proximal tubule, and bicarbonate generation, predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na(+)-H(+) antiporter and to a smaller extent by the H(+)-ATPase (adenosine triphosphate-ase). The principal factors affecting HCO3(-) reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium. Bicarbonate regeneration is primarily affected by distal Na(+) delivery and reabsorption, aldosterone, arterial pH, and arterial partial pressure of carbon dioxide. To generate metabolic alkalosis, either a gain of base or a loss of acid must occur. The loss of acid may be via the gastrointestinal tract or via the kidney. Excess base may be gained by oral or parenteral HCO3(-) administration or by lactate, acetate, or citrate administration. Factors that help maintain metabolic alkalosis include decreased glomerular filtration rate, volume contraction, hypokalemia, hypochloremia, and aldosterone excess. Clinical states associated with metabolic alkalosis are vomiting, mineralocorticoid excess, the adrenogenital syndrome, licorice ingestion, diuretic administration, and Bartter's and Gitelman's syndromes. The effects of metabolic alkalosis on the body are variable and include effects on the central nervous system, myocardium, skeletal muscle, and liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors that are promoting the alkalosis and, in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.
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PMID:Metabolic alkalosis. 1126 55

Metabolic alkalosis (MA), defined as a primary increment in plasma bicarbonate concentration, is a common complication in hospitalized patients and is associated with high morbidity and mortality in severe cases. One of the major routes of compensation for MA (ie, the secretion of an alkaline urine) is lost in renal failure patients. We report three cases involving four episodes of extreme MA with an arterial pH value greater than 7.60, serum bicarbonate concentration greater than 55 mmol/L, and stupor or seizure. Profound vomiting or massive gastric drainage combined with concurrent oliguric renal failure was the underlying mechanism for severe MA. Hydration and normal central venous pressure failed to improve the MA. The extreme MA was reversed quickly and safely by conventional hemodialysis with normal bicarbonate dialysate of 25 to 28 mmol/L. To our knowledge, this is the first reported successful use of normal bicarbonate dialysate in the treatment of severe MA. We also found that either H(2) blockers or proton-pump inhibitors have a prophylactic effect on the formation of MA.
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PMID:Extreme metabolic alkalosis treated with normal bicarbonate hemodialysis. 1127 1

A maintenance hemodialysis patient developed metabolic alkalosis in the absence of vomiting or nasogastric suction. The cause of the metabolic alkalosis was ingestion of an exogenous alkali in the form of Bromoseltzer. The metabolic alkalosis improved with hemodialysis using a low-bicarbonate bath.
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PMID:Metabolic alkalosis in a hemodialysis patient after ingestion of a large amount of an antacid medication. 1131 61

A 39-year-old woman had been investigated elsewhere due to symptomatic hypokalaemia, renal potassium wasting and metabolic alkalosis. Vomiting was considered to be the underlying cause but the patient repeatedly denied this behaviour. After extensive investigations, Bartter's syndrome was finally diagnosed. Eighteen months later the patient was readmitted due to progressive renal insufficiency. On the basis of a very low urinary chloride excretion and the aforementioned laboratory results, it was concluded that the metabolic disturbances were due to vomiting and the diagnosis of Bartter's syndrome was rejected. Upon being confronted with these findings, the patient finally admitted to vomiting, but stated that this happened involuntarily after meals. She had a stenotic ulcer in the pylorus and a gastric biopsy demonstrated the presence of Helicobacter pylori associated gastritis. Eradication therapy was given and the symptoms disappeared. The renal insufficiency was partly accounted for by hypovolaemia and partly by tubulointerstitial nephropathy (demonstrated by kidney biopsy) which was probably due to the chronic hypokalaemia. This case illustrates the difficulty of establishing the differential diagnosis of hypokalaemia, especially in the case of denied vomiting. However, it also shows that in such cases the correct diagnosis can be made if objective parameters are used.
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PMID:[Clinical reasoning and decision-making in practice. A woman with hypokalaemia]. 1269 84

This is the first case reported of vomiting-induced metabolic alkalosis associated with myoclonus. The report describes an unusual presentation of myoclonus secondary to acid-base disturbance caused by recreational drug-induced vomiting. The severe derangement of hyponatraemia, hypokalaemia, and alkalosis appears to have been reasonably well tolerated due to the gradual onset and relatively long history. The causes, mechanism, and management of metabolic alkalosis are discussed.
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PMID:Metabolic alkalosis and myoclonus. 1289 23

Bartter's syndrome is characterized by hypochloremia, hypokalemia, metabolic alkalosis associated with renal potassium leakage, and normal blood pressure despite increased plasma renin activity. Although association of empty sella with Gitelman syndrome has been reported, no association has been reported with Bartter's syndrome. Here we report a patient with Bartter's syndrome and empty sella. A 12 month-old male patient presented with a history of nausea, vomiting, abdominal distension, constipation, and edema in the lower extremities that had begun in the early postnatal period. The patient was born at 32 weeks gestation by operative delivery for polyhydramnios. Blood pressure was normal. Serum sodium, potassium, calcium, phosphate, chloride, albumin and alkaline phosphatase levels were 129 mEq/l, 2.5 mEq/l, 9 mg/dl, 3.8 mg/dl, 72 mg/dl, 4.2 g/dl and 1285 IU/l, respectively. Serum magnesium level was normal. Arterial blood gas levels revealed pH 7.55 (normal, 7.35-7.45), PCO2 33.6 mm/Hg (36-46), base excess +7.1 (+/- 2.3), and total CO2 33.6 mmol/l (23-27). Renin and aldosterone levels were elevated. Urine had pH 8.0 and specific gravity 1.010. Urinary calcium excretion was 22.8 kg/day (urine calcium/creatinine ratio 0.46). Urinary potassium and chloride levels were elevated. MRI of the brain was normal except for partially empty sella. We present the first pediatric patient with the association of Bartter's syndrome and empty sella.
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PMID:Association of Bartter's syndrome and empty sella. 1451 87

This study was designed to evaluate possible organ and system disorders associated with experimentally induced levamisole poisoning in dogs. For this purpose, twelve clinically healthy dogs of different ages, sexes and breeds were used. They were divided into two equal groups (Group A and Group B) and given levamisole orally at a dose of 25 mg/kg of body weight daily for three days. The dogs in Group B were also injected with atropin sulphate (0.04 mg/kg of body weight) subcutaneously (sc) 1 hour after each administration of levamisole. Routine clinical examinations were made and some haematological, biochemical and blood gas parameters were established at various times after administration of levamisole. The dogs in Group A developed severe neurological signs, gastric haemorrhage, bloody vomiting, colic, anaemia and four dogs died. In Group B these signs were mild and only one dog died. Levamisole poisoning was characterised by a significant reduction in the total number of red blood cells (RBCs), concentration of haemoglobin (Hb) and packed cell volume (PCV), and by anaemia. Peripheral blood pH, actual bicarbonate of plasma (HCO3), actual base excess (BE), partial pressure of oxygen (pO2) and saturated oxygen (O2SAT) increased in both groups of animals and these dogs developed metabolic alkalosis 48 hours after the first administration of levamisole. The results of the study also show that levamisole poisoning in dogs causes a significant increase in the activity of serum alanine aminotransferase (ALT) and of alkaline phosphatase (AP) and in the concentration of urea in both Group A and Group B. In the study, atropin sulphate reduced the severity of the clinical signs and the number of deaths, but it was not alone sufficient to remedy levamisole poisoning in dogs.
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PMID:The effects of levamisole poisoning on the haematological and biochemical parameters in dogs. 1503 67

A 32-year-old morbidly obese woman with an obstructing dislocated gastric band is presented. Because of prolonged vomiting, a metabolic alkalosis would be expected, but instead an impressive high anion gap acidosis was observed. Because of a highly positive urine ketone test and a high serum concentration of beta-hydroxybutyrate, a ketoacidosis caused by starvation appears to be the primary cause of this metabolic acidosis. This type of acidosis was treated successfully with intravenous administration of glucose and insulin as well as sodium bicarbonate, with urgent removal of the band.
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PMID:Severe metabolic acidosis resulting from a dislocated gastric band. 1513 Feb 38

A 42-year-old woman with eating disorder underwent electroconvulsive therapy (ECT) under general anesthesia with thiamylal 150 mg and suxamethonium 60 mg. On her fourth ECT procedure, premature ventricular contraction (PVC) occurred immediately after the treatment. We speculate that increased release of catecholamine by ECT and hypokalemia caused PVC. It seems that she repeated self-vomiting, because she had hypokalemia, metabolic alkalosis, and weight loss of 3 kg in two weeks before arrhythmia episode. We conclude that in the anesthetic management of patients undergoing ECT a careful attention should be given to body weight change and serum electrolyte care before ECT because it is easy to develop electrolyte abnormality by eating disorder of self-emetic type.
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PMID:[Case of premature ventricular contraction immediately after electroconvulsive therapy in a depressive patient]. 1571 68


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