Master of Pharmacy: Pharmacology and Therapeutics Flashcards
7 cards from real MPharm Master of Pharmacy practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 7 Master of Pharmacy: Pharmacology and Therapeutics flashcards as text
A patient with rheumatoid arthritis on methotrexate and naproxen develops toxicity. Which pharmacokinetic interaction is responsible?
Answer: NSAIDs reduce renal blood flow and tubular secretion, impairing methotrexate clearance
NSAIDs reduce renal prostaglandin synthesis, decreasing GFR and inhibiting organic anion transporters, impairing methotrexate excretion and causing toxicity.
Which mechanism distinguishes selective COX-2 inhibitors (coxibs) from non-selective NSAIDs regarding cardiovascular risk?
Answer: COX-2 inhibition reduces prostacyclin without reducing platelet thromboxane A2, shifting balance toward thrombosis
COX-2 in vascular endothelium produces antithrombotic prostacyclin; selective COX-2 inhibition reduces prostacyclin but spares platelet COX-1-derived thromboxane A2, promoting thrombosis.
A patient with treatment-resistant depression fails SSRIs and SNRIs. Ketamine is considered. What is its proposed antidepressant mechanism?
Answer: NMDA receptor antagonism promoting rapid BDNF-mediated synaptogenesis
Ketamine blocks NMDA receptors, leading to a glutamate surge that activates AMPA receptors, promoting BDNF release and rapid synaptogenesis in the prefrontal cortex.
A patient on amiodarone develops hypothyroidism after 18 months. Which mechanism is primarily responsible?
Answer: Amiodarone's high iodine content causes Wolff-Chaikoff effect blocking thyroid hormone synthesis
Amiodarone contains ~37% iodine by weight; the iodine load triggers the Wolff-Chaikoff effect, suppressing thyroid hormone synthesis and causing hypothyroidism in susceptible patients.
In a patient with chronic kidney disease, why does the dosing interval for aminoglycosides need to be extended rather than reducing individual doses?
Answer: Reduced renal clearance extends half-life; maintaining peak concentrations preserves concentration-dependent killing
Aminoglycosides are concentration-dependent antibiotics; high peak/MIC ratios drive efficacy, so maintaining peak concentrations while extending intervals accommodates reduced clearance in CKD.
Which drug interaction occurs when P-glycoprotein (P-gp) inhibitors are combined with digoxin?
Answer: Increased digoxin plasma levels due to reduced P-gp-mediated efflux and renal secretion
P-gp normally limits digoxin absorption in the gut and facilitates renal tubular secretion; P-gp inhibitors (e.g., amiodarone, verapamil) increase digoxin bioavailability and reduce its elimination.
A patient develops pseudomembranous colitis after clindamycin therapy. What is the pathophysiological mechanism?
Answer: C. difficile overgrowth producing toxins A and B that disrupt colonic epithelial tight junctions
Antibiotic disruption of normal gut flora allows C. difficile overgrowth; its toxins A and B cause glucosylation of Rho GTPases, disrupting tight junctions and triggering colitis.