Pharmacology and Therapeutics Flashcards

A patient with HIV is started on ritonavir. Beyond its antiviral activity, why is ritonavir often used in 'boosted' regimens at low doses?

Answer: It inhibits CYP3A4, raising plasma levels of co-administered protease inhibitors

At sub-therapeutic antiviral doses, ritonavir potently inhibits CYP3A4, acting as a pharmacokinetic 'booster' to dramatically increase the AUC of co-administered protease inhibitors.

Which mechanism explains the increased risk of tendon rupture with fluoroquinolone antibiotics?

Answer: Chelation of magnesium in tendon extracellular matrix, impairing tenocyte function

Fluoroquinolones chelate divalent cations such as magnesium, disrupting tendon extracellular matrix homeostasis and impairing tenocyte metabolism, predisposing to rupture.

In the context of digoxin toxicity, which electrolyte imbalance greatly potentiates the risk?

Answer: Hypokalemia

Hypokalemia increases digoxin binding to the Na⁺/K⁺-ATPase pump (their binding site is shared with potassium), enhancing toxicity at otherwise therapeutic digoxin concentrations.

A patient prescribed clozapine requires which routine monitoring due to a potentially life-threatening adverse effect?

Answer: Absolute neutrophil count for agranulocytosis

Clozapine carries a black-box warning for agranulocytosis (~1-2% risk), requiring mandatory ANC monitoring through the REMS program before each prescription.

Which pharmacokinetic property of vancomycin makes therapeutic drug monitoring essential in critically ill patients?

Answer: Narrow therapeutic index combined with variable renal clearance

Vancomycin has a narrow therapeutic index and is almost entirely renally eliminated, so AUC/MIC-guided TDM is essential to ensure efficacy while minimizing nephrotoxicity.

A patient experiences bronchospasm, urticaria, and hypotension within minutes of receiving IV penicillin. What is the first-line treatment?

Answer: Intramuscular epinephrine 1:1000 concentration

IM epinephrine (1:1000, 0.3–0.5 mg in adults) is the first-line treatment for anaphylaxis because it reverses vasodilatation, bronchospasm, and prevents further mediator release.

Which drug class inhibits the final step of bacterial cell wall synthesis by binding to the D-Ala-D-Ala terminus of peptidoglycan precursors?

Answer: Glycopeptide antibiotics (e.g., vancomycin)

Vancomycin and other glycopeptides bind the D-Ala-D-Ala dipeptide terminus, preventing transglycosylation and transpeptidation steps in peptidoglycan cross-linking.