Cases reported "Alkalosis"

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1/7. diabetic ketoacidosis with alkalemia.

    A case of diabetic ketoacidosis presenting with alkalemia (pH, 7.61) instead of acidemia (pH less than 7.35) is discussed. Severe vomiting results in electrolyte depletion and hypovolemia, which in turn results in bicarbonate reabsorption and an alkalemia state despite the presence of ketoacids. Severe respiratory alkalosis can also result in alkalemia. Recognition of the alkalemia and its cause will lead to the institution of appropriate therapy.
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keywords = ketoacidosis
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2/7. Mechanisms in hypokalemia: clinical correlation.

    hypokalemia is seen most often with the use of diuretics and in patients with emesis. Other common clinical settings in which it may be significant include corticosteroid therapy, antibiotic usage, diarrhea, diabetic ketoacidosis, or psychiatric illness. Occasionally the cause may be obscure. In such situations the determination of urine potassium and arterial pH may prove helpful. Subclassification of hypokalemia into such categories as "acidosis", "alkalosis", "extra-renal", or "renal" loss is then possible. The cases discussed demonstrate the utilization of these methods to define the etiology and to understand the pathophysiology in hypokalemia.
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keywords = ketoacidosis
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3/7. Ketoalkalosis as a result of triple derangement of acid-base equilibrium in a diabetic patient.

    A diabetic patient presented with weight loss, ketosis, and hyperventilation, thus mimicking the clinical picture of diabetic ketoacidosis. Laboratory investigations revealed alkalemia and a pattern consistent with a triple derangement of acid-base equilibrium: respiratory alkalosis, metabolic acidosis and metabolic alkalosis. High cortisol level suggested a genesis of ketosis different from diabetes mellitus. The patient died suddenly from acute gastrointestinal bleeding. autopsy showed a carcinoma of the head of the pancreas with secondary portal hypertension and rupture of varices. Pulmonary micrometastases were demonstrated. It is suggested that stress hormones were the main cause of the 'ketoalkalotic' pattern observed.
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keywords = ketoacidosis
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4/7. Lactic acidosis and ketoacidosis: biochemical and clinical implications.

    A case of lactic acidosis presented the opportunity for review of the association between lactic acidosis and ketoacidosis. The diagnosis of lactic acidosis or the combination of lactic acidosis and ketoacidosis is established clinically by the detection of a metabolic acidosis of the "unmeasured anion gap" type in the absence of significant renal failure, poison intake or a strongly positive clinical test for ketones. Before treatment can be planned the biochemical basis of lactic acidosis and ketoacidosis must be understood -- especially the fact that lactic acidosis is not a single disease entity but has many possible causes. Among important considerations is the relation between the blood concentrations of bicarbonate and organic acid anions. After recovery from metabolic acidosis of the unmeasured anion gap type, metabolic alkalosis is common. Decreased bicarbonate excretion plays an important role in the pathogenesis of the latter and may be the result of potassium or chloride loss, or both. The deficits, if present, should be corrected with appropriate therapy.
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ranking = 1.4
keywords = ketoacidosis
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5/7. Diabetic ketoalkalosis.

    The usual metabolic derangement in uncontrolled diabetes mellitus is metabolic acidosis, with an increase in the anion gap because of increased ketoacids and lactate. However, diabetic ketoalkalosis may occasionally be encountered, the prominent clinical feature of which is vomiting, with depletion of potassium, chloride, and hydrogen ions. Self-medication with absorbabe alkali may also contribute to the alkalosis. It would be dangerous to treat hyperlgycemic patients with alkali if their condition is ketoalkalosis instead of ketoacidosis.
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ranking = 0.2
keywords = ketoacidosis
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6/7. Alkalemia in diabetic ketoacidosis.

    A patient with a history of diabetes mellitus and congestive heart failure was taking furosemide and metolazone as diuretics. diabetic ketoacidosis developed, and the patient became lethargic and confused. Initial biochemical determinations showed an alkalemic pH, serum and urine ketones with an anion gap, and hyperventilation. The hyperventilation was appropriate for the degree of ketoacidosis but it was grossly inappropriate for the alkalemia. This could be explained by a direct effect of ketones on the respiratory center or a sudden increase in hydrogen ion concentration superimposed on previously chronic alkalemic pH due to the potent combination of furosemide and metolazone.
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ranking = 1.2
keywords = ketoacidosis
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7/7. Metabolic alkalosis in diabetic ketosis: a case report.

    A mixed metabolic alkalosis and metabolic acidosis, resulting in an alkalemic state, occurred in a hyperlipemic patient with previously diagnosed non insulin dependent diabetes. The metabolic alkalosis, due to large loss of gastric HCl, was more severe than the diabetic acidosis and resulted in an alkaline blood pH. Initially the metabolic acidosis was due to ketoacidosis and coexistent lactic acidosis. During the improvement of the alkalemic and hyperglycemic state, lactic acidosis disappeared but a paradoxical rise of plasma NEFA and ketone body concentrations supervened so that the high anion gap metabolic acidosis was virtually unchanged. The rise of plasma NEFA was probably related to the marked removal of plasma triglycerides, by insulin activation of lipoprotein lipase, and consequent saturation of the pathways of fatty acid incorporation into adipose tissue.
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ranking = 0.2
keywords = ketoacidosis
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