Acetazolamide acts by inhibiting carbonic anhydrase in the proximal tubule. Which acid-base disturbance is a predictable consequence of prolonged acetazolamide use?
- A Metabolic alkalosis from bicarbonate retention
- B Respiratory acidosis from CNS respiratory centre depression
- C Respiratory alkalosis from stimulation of peripheral chemoreceptors
- D Metabolic acidosis from urinary bicarbonate wasting ✓
Explanation
Carbonic anhydrase in the proximal tubule catalyses H+ secretion and HCO3- reabsorption. Acetazolamide inhibition prevents this reabsorption, causing bicarbonate to be lost in urine (bicarbonaturia). This progressive urinary HCO3- loss depletes serum bicarbonate, resulting in a non-anion-gap hyperchloraemic metabolic acidosis. This self-limiting acidosis also reduces acetazolamide's effectiveness (alkaline urine is required for CA inhibitor diuresis). Conversely, acetazolamide is used clinically to treat metabolic alkalosis and altitude sickness (where it induces mild acidosis to stimulate breathing).
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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