A patient with protracted vomiting has metabolic alkalosis with pH 7.52, bicarbonate 38 mEq/L, urine sodium 15 mEq/L and urine chloride less than 10 mEq/L. The primary factor PERPETUATING the alkalosis in this setting is:
- A Volume contraction with aldosterone-driven hydrogen ion secretion in the collecting duct despite chloride depletion ✓
- B Respiratory compensation retaining carbon dioxide
- C Reduced proximal tubular bicarbonate reabsorption due to chloride excess
- D Increased anion gap from lactic acid production
Explanation
Chloride-depleted contracted extracellular volume stimulates the renin-angiotensin-aldosterone axis; under aldosterone with inadequate chloride delivery, distal sodium reabsorption proceeds via hydrogen secretion, so the kidney paradoxically maintains rather than excretes the alkali. The very low urine chloride confirms chloride-responsive alkalosis. Option B describes compensation, not perpetuation, and option D contradicts the normal anion gap expected here.
Reference: Ganong's Review of Medical Physiology, 27th ed.
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