Digestive loss of acid

Gastric alkalosis occurs when substantial amounts of acid gastric juice are eliminated from the organism by vomiting or gastric suction. Chloride is lost together with hydrogen ions. Bicarbonate generated during acid secretion is not neutralized by more distal buffering in the gut, and blood bicarbonate concentration increases above the renal reabsorption ability. Bicarbonaturia is associated with natriuria, kaliuria, and fluid excretion aggravating the gastric electrolyte and fluid losses. Whether, how, and how much the chloride, sodium, potassium, and fluid deficits individually contribute to the maintenance of the alkalosis has been the subject of much debate. The question is of considerable pathophysiological interest, but of less clinical importance because all the deficits can be corrected concomitantly to reverse the alkalosis.

Diarrhea due to metabolic defects and villous adenomas can cause metabolic alkalosis owing to failure of the the colonic mucosa to reabsorb chloride adequately. Diarrhea with normal chloride concentration can also cause metabolic alkalosis when large fluid, sodium, and potassium losses result in sodium and water retention at the expense of hydrogen ion and potassium excretion by the kidney.

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