Cases reported "Alkalosis"

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1/67. Saline-resistant metabolic alkalosis, severe hypokalemia and hypertension in a 74-year-old woman.

    The case of a 74-year-old woman with past history of hypertension and cerebrovascular accident admitted with pneumonia, dehydration, hypernatremia and severe hypokalemic alkalosis is presented. After correction of the hypertonic dehydration, the hypokalemia and alkalosis persisted in spite of aggressive potassium supplementation and the patient became hypertensive. Mineralocorticoid excess was suspected and excluded after extensive endocrinological testing. The use of aldactone failed to revert the abnormalities. triamterene administration corrected the electrolytes and acid base aberrations, and dramatically improved the blood pressure control. This clinical picture is compatible with the diagnosis of Liddle's syndrome. Our patient exemplifies the unique occurrence of hypokalemic metabolic alkalosis in association with volume contraction at the start of the hospitalization and volume expansion later on her course.
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2/67. Metabolic alkalosis in a hemodialysis patient after ingestion of a large amount of an antacid medication.

    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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keywords = acid
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3/67. Postoperative metabolic alkalosis and acute renal failure: rationale for the use of hydrochloric acid.

    Metabolic alkalosis secondary to chloride depletion, especially following gastrointestinal surgery and associated with acute renal failure, is a frequent clinical occurrence. Management of the resultant acid-base disturbance mandates chloride replacement. The presence of oliguria limits the choice of accompanying cation. The use of intravenous hydrochloric acid to correct and maintain proper chloride balance, secondary to external gastric fluid losses, is recommended as a straightforward approach. Two brief case synopses are presented. Both patients, florid examples of profound chloride depletion, required large amounts of intravenous hydrochloric acid. The options regarding the choice of chloride solution, hazards involved, and a simplified schema of replacement therapy are presented. Combined gastrointestinal and renal dysfunction create unusual biochemical and clinical alterations and may result in a complex management problem.
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keywords = hydrochloric acid, acid
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4/67. liddle syndrome in a newborn infant.

    A 10-week-old female infant developed hypertension. The elevated blood pressure was associated with metabolic alkalosis and urinary chloride wastage. The family history was unremarkable. Her urinalysis, blood urea nitrogen (BUN), and serum creatinine concentrations were all normal. A renal ultrasound was normal. A technetium-99m diethylenetriaminopentoacetic acid (DTPA) renal scan with captopril showed normal blood flow bilaterally. The head ultrasound and echocardiogram were normal. Blood epinephrine, norepinephrine, catecholamines, thyroxine, and steroid levels were also normal. Treatment with various combinations of labetalol, hydralazine, captopril, methyldopa, nifedipine, and spironolactone, all at high doses, failed to control the elevated blood pressure. serum aldosterone level and peripheral plasma renin activity were low. The lack of therapeutic response to spironolactone, with a good response to amiloride and recurrence of hypertension and metabolic alkalosis after amiloride cessation that was subsequently treated with amiloride, established the diagnosis of liddle syndrome. To our knowledge, this is the youngest patient with liddle syndrome that has been reported in the literature.
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5/67. A frameshift mutation of beta subunit of epithelial sodium channel in a case of isolated liddle syndrome.

    BACKGROUND: liddle syndrome is an autosomal dominant form of salt-sensitive hypertension caused by mutations in the epithelial sodium channel expressed in the distal nephron playing an essential role in Na absorption. All reported mutations in liddle syndrome are either missense mutations or frameshift mutations destroying the PY motif closer to the C-terminus of the beta or gamma subunits causing the situation that the epithelial sodium channels are not degraded and sodium is pooled and thus hypertension and hypokalemia are caused. methods: We sequenced the C-terminus of the beta or gamma subunits of the epithelial sodium channel in a Japanese family of a patient clinically diagnosed as having liddle syndrome. RESULTS: As a result, we found in the proband, a frameshift mutation of the beta subunit caused by a single cytosine insertion at the codon 595, introducing a new stop codon at 605 and deleting the last 34 amino acids from the normally encoded protein. CONCLUSION: This mutation is carried by neither parent (with paternity proven) and hence confirms this has occurred as a event within this family.
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6/67. Hypokalaemia and paralysis.

    A patient with a severe degree of hypokalaemia (1.8 mmol/l) and paralysis was brought to the emergency department. Hypokalaemic periodic paralysis was an unlikely diagnosis, because an acid-base disorder (metabolic alkalosis) and a high rate of potassium (K( )) excretion were present. During an imaginary consultation with Professor McCance, the combination of emphasis on principles of integrative physiology, a deductive analysis, common sense, and clinical skills led to an obvious diagnosis. Nevertheless, a surprise was in store, because renal K( ) wasting persisted for almost 2 weeks after removal of the causative agent. Possible explanations for the continued kaliuresis, as well as therapeutic strategies to avoid potential complications, were considered. This case illustrates the value of applying principles of physiology in a quantitative fashion at the bedside.
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7/67. Metabolic alkalosis and myoclonus.

    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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8/67. Metabolic alkalosis in a patient with renal failure: role of antacids.

    A 75-year-old patient with anuric renal failure developed a significant metabolic alkalosis thought to be due to the enteral absorption of "nonsystemic" antacid administered in large daily doses for prevention of recurrent peptic ulcer disease.
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keywords = acid
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9/67. myoclonus and metabolic alkalosis from licorice in antacid.

    A 90-year-old woman with hypertension developed metabolic alkalosis and myoclonus. Her medications included diltiazem hydrochloride, benidipine hydrochloride, kallidinogenase, procaterol hydrochloride, sennoside, dihydrocodeine phosphate, and KM powder antacid that contained 354 mg of licorice and 900 mg of sodium bicarbonate per 3.9 g of powder. Endocrinological studies showed slightly reduced plasma renin activity and normal plasma aldosterone concentration. A provisional diagnosis of licorice-induced metabolic alkalosis was established and the patient was successfully treated after correction of serum pH and cessation of the medications. Licorice-induced metabolic alkalosis must be considered in the differential diagnosis of myoclonus.
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ranking = 5
keywords = acid
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10/67. Severe hypotension during hemofiltration in an uremic patient with metabolic alkalosis.

    We describe a case of medication induced metabolic alkalosis in a maintenance dialysis patient who developed severe hypotension while undergoing a lactate hemofiltration procedure. A 73-year-old man with ESRD due to renovascular disease was used to ingesting up to 30 grams per day of a non-prescription medication (Effervescent granulare 250 grams, CRASTAN, Pisa italy) consisting of sodium bicarbonate, citric acid, glucose and lemon flavor. For technical problem lactate hemofiltration was performed and thirty minutes after dialysis was started a severe symptomatic hypotension occurred (blood pressure 65/35 mmHg). Lactate hemofiltration was suspended and one-hour later standard bicarbonate dialysis was performed without any clinical problem. The different mechanisms in acidosis buffering occurring in lactate and bicarbonate hemofiltration were discussed.
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