A patient with pyloric stenosis from peptic ulcer disease presents with vomiting of 3 weeks' duration. ABG shows pH 7.55, PaCO2 50 mmHg, HCO3- 42 mEq/L. The paradoxical aciduria in this setting results from:
- A Hypokalaemia causing K+ to exit cells in exchange for H+ entry, acidifying urine
- B Hypovolaemia activating aldosterone, driving H+ secretion in the collecting duct despite alkalosis ✓
- C Metabolic alkalosis directly stimulating H+ secretion by the proximal tubule
- D Compensatory respiratory acidosis causing renal H+ excretion
Explanation
Loss of HCl from repeated vomiting causes hypochloraemic, hypokalaemic metabolic alkalosis. Hypovolaemia strongly activates the renin-angiotensin-aldosterone system. Aldosterone stimulates H+ secretion by alpha-intercalated cells and Na+/H+ exchange in collecting ducts; despite systemic alkalosis, the kidney excretes an acid urine ('paradoxical aciduria') because volume conservation takes precedence over pH correction. Hypokalaemia contributes by shifting K+/H+ exchanges but volume depletion is the primary driver.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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