In chronic metabolic alkalosis secondary to prolonged vomiting, the kidney retains HCO₃⁻ rather than excreting it. The 'contraction alkalosis' is perpetuated by which renal mechanism?
- A Volume depletion activates RAAS; aldosterone increases H⁺ secretion and HCO₃⁻ reabsorption in the collecting duct ✓
- B Low serum Cl⁻ directly inhibits the HCO₃⁻ filter at the glomerulus
- C Elevated serum HCO₃⁻ directly stimulates proximal tubule H⁺ secretion
- D Reduced GFR decreases filtered HCO₃⁻ load, making excretion impossible
Correct answer: A. Volume depletion activates RAAS; aldosterone increases H⁺ secretion and HCO₃⁻ reabsorption in the collecting duct
Explanation
Vomiting causes HCl loss (alkalosis), volume depletion (activating RAAS), and hypochloremia/hypokalemia. Volume depletion stimulates aldosterone, which increases apical ENaC activity creating a lumen-negative potential that drives H⁺ secretion via H⁺-ATPase and H⁺-K⁺-ATPase in the collecting duct. Hypokalemia shifts K⁺ out of cells and H⁺ in, promoting intracellular acidosis that further stimulates proximal tubule NHE3. These mechanisms 'maintain' alkalosis. Treatment requires NaCl and KCl repletion (saline-responsive alkalosis).
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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