GI Pharmacology

By completing this question set, you will be able to explain the PPI prodrug activation mechanism and predict the consequences of long-term acid suppression, including reduced B12 absorption, calcium malabsorption, hypomagnesemia, and the CYP2C19/clopidogrel interaction. You will distinguish PPIs from H2 blockers by their binding type (irreversible vs reversible), potency, and adverse effect profiles — and identify cimetidine as uniquely dangerous among H2 blockers due to broad CYP inhibition and anti-androgenic effects. You will explain how sucralfate requires an acidic environment to exert its protective effect and why its administration timing relative to PPIs matters. You will predict the teratogenic mechanism of misoprostol and apply its contraindication in pregnancy. You will identify metoclopramide's full adverse effect profile from its dopamine receptor blockade mechanism — including the irreversible tardive dyskinesia risk — and explain why it is contraindicated in Parkinson's disease. You will apply the thiopurine metabolism pathway (AZA → 6-MP → 6-TGN via TPMT and XO) to predict the consequence of TPMT deficiency and the allopurinol drug interaction, and explain why TPMT testing is mandatory before initiating thiopurines. You will distinguish the three anti-TNF agents by their molecular structure (certolizumab = PEGylated Fab, no Fc) and apply this to pregnancy safety, and explain why vedolizumab's gut selectivity eliminates the systemic immunosuppression risks of anti-TNF agents — including the absence of PML and TB reactivation risk. You will explain the JAK inhibitor VTE/MACE black box mechanism and identify the pre-treatment screenings required. You will distinguish TDF from TAF by their intracellular activation pattern, apply the renal and bone toxicity implications, and explain the amiodarone-sofosbuvir cardiac black box. You will explain octreotide's somatostatin receptor mechanism and predict its gallstone and glucose dysregulation adverse effects from that mechanism.