A 45-year-old man with a history of chronic migraines is started on topiramate 100 mg daily for prophylaxis. Two weeks into treatment, his wife reports that he seems unusually forgetful, has difficulty concentrating at work, and has lost 3 kg despite unchanged appetite and no reported dietary changes. Vital signs are stable (BP 128/82 mmHg, HR 88 bpm, RR 16/min, Temp 37°C, SpO2 98% on room air). Laboratory studies show: serum bicarbonate 19 mEq/L (normal 22–26), chloride 108 mEq/L (normal 98–107), potassium 3.8 mEq/L (normal 3.5–5.0), and arterial pH 7.34. Urinalysis demonstrates an inappropriately high urine pH of 6.8 despite the systemic acidemia. Physical examination reveals no focal neurological deficits, and serum glucose is 95 mg/dL. Which of the following mechanisms best accounts for this patient's constellation of cognitive and metabolic findings?

  1. A)Carbonic anhydrase inhibition with resultant metabolic acidosis and altered CNS bicarbonate bufferingGABARITO
  2. B)Hyponatremia from the syndrome of inappropriate antidiuretic hormone secretion triggered by topiramate
  3. C)Acute hyperammonemia secondary to topiramate-induced hepatic enzyme inhibition
  4. D)Nephrolithiasis-induced acute kidney injury with hyperkalemia and uremia
  5. E)Enhanced GABA-A receptor activity causing excessive CNS depression and lethargy

Explicação

Topiramate is a weak carbonic anhydrase inhibitor that blocks renal bicarbonate reabsorption and hydrogen ion secretion. This causes a non-anion gap (hyperchloremic) metabolic acidosis, evidenced by the low serum bicarbonate (19), normal anion gap, and elevate... Ver explicação completa e trilha adaptativa →

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