Pharmacology · NSAIDs and Autocoids (Histamine, Serotonin, Eicosanoids, Gout Drugs)

A 16-year-old girl presents 8 hours after ingesting a large quantity of aspirin tablets. She has tachypnoea, tinnitus, sweating, and vomiting. Arterial blood gas shows pH 7.48, PaCO2 28 mmHg, bicarbonate 20 mEq/L. The primary reason for the initial respiratory alkalosis in salicylate poisoning is:

  • A Uncoupling of oxidative phosphorylation causing lactic acidosis with compensatory hyperventilation
  • B Salicylate directly stimulates the medullary respiratory centre, increasing ventilation
  • C Inhibition of carbonic anhydrase leading to renal bicarbonate loss
  • D Pulmonary oedema causing hypoxaemic drive to breathe
Correct answer: B. Salicylate directly stimulates the medullary respiratory centre, increasing ventilation

Explanation

Salicylates directly stimulate the respiratory centre in the medulla, producing hyperventilation, a fall in PaCO2 and a pure respiratory alkalosis early in poisoning. Uncoupling of oxidative phosphorylation occurs later and produces the metabolic (high anion gap) acidosis seen as toxicity progresses. Carbonic anhydrase inhibition is a property of acetazolamide, not aspirin.

Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.

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