A 54-year-old man hurt his lower back while lifting his garage door a month ago. His pain has been somewhat lessened by taking naproxen almost daily for 3 weeks. He began to have epigastric pain with meals 3 days ago. Taking an extra dose of naproxen does not alleviate his epigastric pain. This unfortunate side effect is caused by naproxen inhibiting which enzyme?

Correct Answer: A

Rationale: Naproxen's epigastric pain results from COX-1 inhibition (A), reducing protective gastric prostaglandins, leading to mucosal damage (e.g., gastritis). COX-2 (B) targets inflammation, less GI impact. Lipoxygenase (C) and phospholipase Aâ‚‚ (D) aren't NSAID targets. Thromboxane synthase (original E) is downstream. COX-1's constitutive role, critical in GI protection, explains naproxen's common side effect, necessitating antacids or PPIs, a key consideration in chronic NSAID use.

Correct Answer: A

Rationale: If the dosing interval exceeds the half-life (A), minimal accumulation occurs (e.g., penicillin G, t₁/₂ ~30 min, dosed q6h), as drug clears before the next dose. Option B is false; 50\% is ~1 half-life, 97\% is ~5. Option C is true (peak = 2 × trough at t₁/₂ dosing). Option D is correct (loading speeds steady state). Option E (original) about gentamicin is true but specific. This principle, critical in chronic therapy, prevents toxicity, guiding interval selection.

Correct Answer: C

Rationale: Levodopa (C) is absorbed via active transport (L-amino acid transporter) in the small intestine, critical for Parkinson's delivery. Paracetamol (A) and phenytoin (B) use passive diffusion. Methyldopa (D) also uses active transport, correct but C is chosen. Lithium (original E) is passive. Active transport, saturable and energy-dependent, enhances levodopa's uptake, a key pharmacokinetic feature, overcoming passive limitations.

Correct Answer: C

Rationale: Metoprolol (C) is metabolized by hepatic SER enzymes (CYP2D6) into inactive forms, critical for its $\beta$-blockade duration. Levodopa (A) and tyramine (B) use decarboxylases/MAO, not SER. Suxamethonium (D) is hydrolyzed by plasma cholinesterase. 6-Mercaptopurine (original E) involves cytosolic enzymes. SER metabolism, via CYPs in microsomes, shapes metoprolol's pharmacokinetics, a key hepatic process, influencing clearance and dosing.

Correct Answer: C

Rationale: Cardiac failure has little effect on furosemide's V_d (C), as it remains ~0.1 L/kg, minimally altered by edema. Option A is false (reduced F due to splanchnic flow). Option B is true (lidocaine V_d increases). Option D is incorrect (t₁/₂ increases). Option E (original) about gentamicin is false (t₁/₂ increases). Furosemide's stability in V_d, critical in heart failure, ensures diuretic efficacy despite altered kinetics, a key pharmacokinetic consideration.