Pharmacology and Therapeutics Flashcards
7 cards from real KAPS practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 7 Pharmacology and Therapeutics flashcards as text
A patient taking warfarin is started on fluconazole. What is the most likely pharmacokinetic mechanism behind the increased bleeding risk?
Answer: Inhibition of CYP2C9, reducing warfarin metabolism
Fluconazole inhibits CYP2C9, the primary enzyme responsible for S-warfarin metabolism, leading to elevated warfarin levels and increased anticoagulation.
Which receptor mechanism is responsible for the therapeutic effect of beta-2 agonists in asthma?
Answer: Gs-coupled receptor activation increasing cAMP and causing bronchodilation
Beta-2 agonists activate Gs-coupled receptors, elevating intracellular cAMP, which activates protein kinase A and relaxes bronchial smooth muscle.
A patient with stage 3 chronic kidney disease is prescribed metformin. What is the primary concern?
Answer: Lactic acidosis due to metformin accumulation
Metformin is renally cleared, and accumulation in CKD increases the risk of lactic acidosis, especially when eGFR falls below 30 mL/min/1.73m².
Which pharmacodynamic principle explains why combining two opioid agonists rarely doubles the analgesic effect?
Answer: Receptor saturation at the mu-opioid receptor
Once mu-opioid receptors are saturated, adding a second full agonist produces little additional effect because the maximum receptor occupancy has been reached.
A 70-year-old patient receives gentamicin for a gram-negative infection. Which dosing strategy best reduces nephrotoxicity?
Answer: Once-daily extended-interval dosing exploiting concentration-dependent killing
Extended-interval (once-daily) dosing achieves high bactericidal peaks while allowing trough levels to fall, reducing aminoglycoside accumulation in renal tubular cells.
Which mechanism best explains the hepatotoxicity seen with acetaminophen overdose?
Answer: Accumulation of NAPQI depleting glutathione and binding hepatic proteins
CYP2E1 converts excess acetaminophen to the reactive metabolite NAPQI; when glutathione stores are depleted, NAPQI covalently binds hepatic macromolecules, causing necrosis.
A patient on phenytoin for epilepsy is also prescribed rifampin for tuberculosis. What dosing adjustment is expected?
Answer: Increase phenytoin dose to compensate for rifampin-induced CYP3A4/2C9 induction
Rifampin is a potent inducer of multiple CYP enzymes including CYP2C9 and CYP3A4, accelerating phenytoin metabolism and requiring higher doses to maintain therapeutic levels.