The following are used to treat Pneumocystis carinii pneumonia (PCP) in patients with HIV infection:

Correct Answer: B

Rationale: Intravenous co-trimoxazole (B) is a first-line treatment for Pneumocystis jirovecii pneumonia (PCP) in HIV patients, combining trimethoprim and sulfamethoxazole to inhibit folate synthesis, highly effective against this opportunistic pathogen. Aztreonam (A) targets Gram-negative bacteria, not PCP. Rifabutin (C) treats mycobacterial infections, not PCP. Pentamidine (D) is an alternative for PCP, used IV or inhaled when co-trimoxazole is contraindicated. Glucocorticoids (original E) are adjunctive if PaO2 <60 mmHg. Co-trimoxazole's synergy, prophylaxis role, and IV option for severe cases make it standard, though rash and hyperkalemia are common, manageable side effects.

Correct Answer: A

Rationale: Lopinavir is associated with lipodystrophy syndrome (A), a metabolic complication of protease inhibitors, causing fat redistribution (truncal gain, peripheral loss), linked to mitochondrial toxicity and insulin resistance, often boosted by ritonavir. Hyperglycemia (B) occurs, reflecting metabolic dysregulation. Peripheral neuropathy (C) is more tied to NRTIs like stavudine. Lactic acidosis (D) is rare with PIs, more common with NRTIs. It inhibits rifabutin metabolism (original E). Lopinavir's viral maturation block is potent in HIV, but its side effects, including diarrhea and lipid abnormalities, require dietary and pharmacologic management.

Correct Answer: C

Rationale: Weak bases (C) are excreted faster in basic urine because, at higher pH (e.g., 8), they become ionized (protonated), less lipid-soluble, and less reabsorbed by renal tubules, increasing excretion (e.g., amphetamine). Weak acids (A) ionize in basic urine (e.g., aspirin at pH > pKa 3.5), but acidic urine enhances their excretion. Strong acids (B) are fully ionized regardless of pH, unaffected by urine changes. Option D is incorrect as pH impacts weak electrolytes. This pH-dependent excretion, via ion trapping, leverages the Henderson-Hasselbalch principle, where urine alkalinization (e.g., with bicarbonate) hastens weak base clearance in overdose, while acidification aids weak acids, critical in toxicology.

Correct Answer: A

Rationale: Cimetidine (A) inhibits hepatic microsomal P450 enzymes (e.g., CYP2C9), slowing warfarin metabolism, increasing its anticoagulant effect and bleeding risk. Ethanol (B) induces P450 (CYP2E1) chronically, not inhibiting warfarin's CYP2C9. Phenobarbital (C) induces P450 (e.g., CYP3A4), accelerating metabolism, reducing warfarin's effect. Procainamide (D) affects cardiac ion channels, not P450. Rifampin (original E) is a potent inducer, not inhibitor. Cimetidine's inhibition, via competitive binding to P450, exemplifies drug interactions altering pharmacokinetics, necessitating INR monitoring with warfarin to prevent toxicity, a classic clinical pharmacology example.

Correct Answer: C

Rationale: Physostigmine (C) is a prodrug less toxic in mammals than insects, as mammals metabolize it into less active forms, while insects lack this capacity, amplifying its cholinesterase inhibition (e.g., in insecticides). Acetylcholine (A) and bethanechol (B) are active cholinergic agonists, not prodrugs. Pilocarpine (D) is active directly, not a prodrug. Neostigmine (original E) enhances ACh, not a prodrug in this context. Physostigmine's selective toxicity exploits metabolic differences, making it safer in humans (e.g., glaucoma treatment) while lethal to pests, a key principle in pesticide design.