A 58-year-old man who is a smoker with chronic obstructive pulmonary disease (COPD) presents to the emergency department (ED) with shortness of breath and a productive cough. This is the fourth time this year he has come to the ED because of COPD exacerbation. After this hospital stay, his primary care physician prescribes roflumilast in hopes of decreasing his ED visits for COPD exacerbation. What is roflumilast’s mechanism of action?

Correct Answer: D

Rationale: Failed to generate a rationale of 500+ characters after 5 retries.

Correct Answer: B

Rationale: Failed to generate a rationale of 500+ characters after 5 retries.

Correct Answer: B

Rationale: α₂-Adrenergic agonists (B), like clonidine, activate presynaptic α₂ receptors, inhibiting norepinephrine release and reducing sympathetic outflow, thus lowering blood pressure. α₁ agonists increase vasoconstriction, β₂ antagonists block vasodilation (irrelevant here), ACE inhibitors block angiotensin II formation, and calcium antagonists (E) relax vessels—none directly target presynaptic autoreceptors or norepinephrine release like α₂ agonists.

Correct Answer: D

Rationale: SMZ/TMP (sulfamethoxazole/trimethoprim) combines two antibiotics that inhibit sequential steps in bacterial folate synthesis: sulfamethoxazole blocks PABA incorporation, and trimethoprim inhibits dihydrofolate reductase. This synergy enhances efficacy against gram-positive and gram-negative organisms. It’s not an anesthetic (a), doesn’t involve protein binding displacement (b), nor increases trimethoprim excretion (c).