Drug Interactions Flashcards
7 cards from real PSA practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 7 Drug Interactions flashcards as text
A patient on simvastatin drinks large amounts of grapefruit juice daily and develops muscle pain. What is the mechanism?
Answer: Furanocoumarins in grapefruit irreversibly inhibit intestinal CYP3A4 and reduce P-glycoprotein efflux, markedly increasing simvastatin bioavailability
Furanocoumarins (e.g., bergamottin) in grapefruit irreversibly inhibit gut-wall CYP3A4, substantially increasing the oral bioavailability of CYP3A4-metabolized statins and raising myopathy risk.
A chronic heavy alcohol user takes regular doses of acetaminophen (paracetamol) for pain. What interaction increases hepatotoxicity risk?
Answer: Alcohol induces CYP2E1, increasing production of the hepatotoxic NAPQI metabolite beyond glutathione's neutralizing capacity
Chronic alcohol use induces CYP2E1, accelerating conversion of acetaminophen to NAPQI; this toxic metabolite depletes glutathione stores and causes hepatocellular necrosis even at therapeutic doses.
A patient on warfarin substantially increases their intake of green leafy vegetables (kale, spinach). The INR unexpectedly falls. What is the mechanism?
Answer: Pharmacodynamic antagonism: increased dietary vitamin K provides more substrate for vitamin K epoxide reductase, restoring clotting factor synthesis
Warfarin blocks vitamin K epoxide reductase; increased dietary vitamin K overcomes this blockade by providing more substrate, driving clotting factor gamma-carboxylation and reducing the INR.
Valproate is added to a patient's existing lamotrigine regimen for epilepsy. The lamotrigine dose must be halved because:
Answer: Valproate inhibits UGT1A4-mediated glucuronidation of lamotrigine, approximately doubling its half-life and plasma levels
Valproate is a potent inhibitor of UGT1A4, the enzyme responsible for lamotrigine's primary glucuronidation pathway, reducing lamotrigine clearance by approximately 50% and requiring dose adjustment.
A renally impaired patient on digoxin starts verapamil for rate control. The digoxin level rises to a toxic concentration. What is the primary mechanism?
Answer: Verapamil inhibits P-glycoprotein-mediated renal and biliary excretion of digoxin, reducing its elimination
Verapamil inhibits P-glycoprotein in the renal tubule and biliary epithelium, the primary secretory pathways for digoxin; renal impairment compounds this by independently reducing filtration-based elimination.
A patient maintained on warfarin begins taking St. John's Wort (Hypericum perforatum) for low mood. The INR drops from 2.5 to 1.4 within 4 weeks. What is the mechanism?
Answer: Decreased INR due to hyperforin-mediated induction of CYP2C9, CYP3A4, and P-glycoprotein, accelerating warfarin clearance
Hyperforin in St. John's Wort activates the pregnane X receptor (PXR), potently inducing CYP2C9, CYP3A4, and intestinal P-glycoprotein, all of which increase warfarin clearance and reduce anticoagulation.
Probenecid is co-administered with penicillin to prolong its plasma half-life. Which pharmacokinetic mechanism is exploited?
Answer: Probenecid competitively inhibits renal OAT (organic anion transporter) proteins, blocking tubular secretion of penicillin
OAT1 and OAT3 in the proximal renal tubule normally actively secrete penicillin; probenecid competes at these transporters, dramatically slowing penicillin renal elimination and doubling its half-life.