Pharmacology Flashcards

Which drug is used to reverse the effects of benzodiazepine overdose?

Answer: Flumazenil

Flumazenil is a competitive benzodiazepine receptor antagonist that rapidly reverses sedation, but has a short half-life and may precipitate seizures in dependent patients.

Which antifungal mechanism involves disruption of ergosterol synthesis by inhibiting lanosterol 14-alpha-demethylase?

Answer: Azole antifungals (e.g., fluconazole)

Azoles inhibit CYP51 (lanosterol 14-alpha-demethylase), blocking ergosterol biosynthesis and disrupting fungal cell membrane integrity.

In a patient with renal failure, which pharmacokinetic parameter is most directly affected for renally-cleared drugs?

Answer: Clearance decreases, leading to prolonged half-life

Reduced GFR directly decreases renal clearance of drugs, prolonging their half-life and increasing the risk of accumulation and toxicity.

Which mechanism explains why aspirin irreversibly inhibits platelet aggregation?

Answer: Irreversible acetylation of cyclooxygenase (COX-1) preventing thromboxane A2 synthesis

Aspirin covalently acetylates a serine residue in COX-1, permanently blocking TXA2 production; since platelets lack nuclei, they cannot synthesize new COX.

A patient with gout is prescribed allopurinol. What is the mechanism of this drug?

Answer: Inhibits xanthine oxidase, reducing uric acid production

Allopurinol and its active metabolite oxypurinol inhibit xanthine oxidase, the enzyme that converts hypoxanthine and xanthine to uric acid.

Which receptor mechanism best explains the action of beta-blockers in reducing heart rate?

Answer: Block beta-1 adrenergic receptors in the SA node, reducing cAMP and slowing spontaneous depolarization

Beta-1 blockade at the sinoatrial node reduces adenylyl cyclase activity and cAMP, slowing the rate of phase 4 spontaneous depolarization.

Which drug used for type 2 diabetes carries the highest risk of lactic acidosis in patients with renal impairment?

Answer: Metformin

Metformin accumulates in renal failure, inhibiting mitochondrial complex I and increasing lactate production, leading to potentially fatal lactic acidosis.