Acetazolamide inhibits carbonic anhydrase in the proximal convoluted tubule. The metabolic consequence of prolonged acetazolamide use is:

• A Metabolic alkalosis due to bicarbonate retention
• B Hyperchloraemic normal anion gap metabolic acidosis due to bicarbonate wasting in urine ✓
• C Hypokalaemic metabolic alkalosis similar to loop diuretics
• D Metabolic acidosis with raised anion gap due to lactic acid accumulation

Explanation

Carbonic anhydrase in proximal tubule cells catalyzes the conversion of filtered bicarbonate (via carbonic acid) to CO2 and water, which are reclaimed by the cell. Acetazolamide blocks this reclamation, causing bicarbonate, sodium, potassium, and water to be lost in urine. The resulting reduction in plasma bicarbonate produces hyperchloraemic (normal anion gap) metabolic acidosis. As urinary bicarbonate is excreted, chloride is retained to maintain electroneutrality. Paradoxically, the acidosis self-limits acetazolamide's effect — once plasma bicarbonate falls, less is filtered and less is available to block.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.