ranitidine

Ranitidine competitively blocks histamine H2 receptors on gastric parietal cells, reducing cAMP-mediated activation of the H+/K+ ATPase (proton pump), thereby decreasing basal and stimulated gastric acid secretion. It was historically used for peptic ulcer disease, gastroesophageal reflux disease (GERD), Zollinger-Ellison syndrome, and stress ulcer prophylaxis. Compared to PPIs, H2 blockers provide less potent acid suppression but faster onset for symptomatic relief. Mechanistically, ranitidine is class-related to cimetidine and famotidine but had fewer drug interactions than cimetidine (which inhibits cytochrome P450 enzymes) and did not cause the antiandrogenic effects seen with cimetidine (gynecomastia, impotence). In April 2020, the FDA requested removal of all ranitidine products from the market due to unacceptable levels of NDMA, a probable human carcinogen, found in some formulations—this contamination could increase over time and with improper storage. Clinically, this case is a good example of pharmacovigilance and drug recall processes tested on Step 1/2. Students should know the H2 blocker class mechanism, compare to PPIs (irreversible inhibition of H+/K+ ATPase), and understand adverse effects of the class: confusion (especially in elderly), and cimetidine-specific effects (CYP450 inhibition, antiandrogenic effects). Famotidine has now largely replaced ranitidine clinically as the preferred H2 blocker.