Pharmacology · patient case question

Omeprazole reduces gastric acid by acting on which target?

Patient case: Polypharmacy — Cardiovascular & GI

demo: 68-year-old male

chief: “I need a crown on my lower left molar.”

history: Hypertension, gastroesophageal reflux disease, atrial fibrillation, hyperlipidemia, gout. Non-smoker.

meds: Lisinopril, omeprazole, verapamil, apixaban, rosuvastatin, allopurinol

findings: BP 132/84 mmHg. Generalized attrition. Tooth #19 with fractured MOD amalgam, no pulpal symptoms. No active periodontal disease.

  1. The H₂ histamine receptor on parietal cells
  2. Gastrin receptors on enterochromaffin-like cells
  3. Muscarinic M3 receptors on parietal cells
  4. The H⁺/K⁺-ATPase proton pump of gastric parietal cells
Show answer and explanation

Correct answer: D. The H⁺/K⁺-ATPase proton pump of gastric parietal cells

  • A. That is the mechanism of ranitidine and famotidine, which are H₂ blockers, not PPIs.
  • B. Gastrin receptor antagonism is not a clinically used mechanism for this drug class.
  • C. Anticholinergics reduce acid through M3 blockade, but that is not omeprazole.
  • D. Correct. Omeprazole is a proton pump inhibitor; it irreversibly binds the H⁺/K⁺-ATPase, the final common step of acid secretion.

Note: Dental relevance: PPIs raise gastric pH and therefore reduce absorption of azole antifungals (ketoconazole, itraconazole) and ampicillin, and they increase serum levels of benzodiazepines, phenytoin, and warfarin.

Practice Pharmacology questions Pharmacology study notes

More Pharmacology practice questions