Foscarnet:

Correct Answer: A

Rationale: Foscarnet is indicated in CMV retinitis in AIDS patients (A), a key treatment for this vision-threatening infection, directly inhibiting viral DNA polymerase without needing activation, unlike aciclovir. It treats aciclovir-resistant HSV (B), particularly in immunocompromised patients. It's nephrotoxic (C), requiring hydration and monitoring due to renal tubular damage. It causes fits (D), linked to electrolyte imbalances like hypocalcemia. It's not usually oral/topical (original E is incorrect), given IV. Foscarnet's broad antiviral activity, including against ganciclovir-resistant CMV, makes it vital in advanced HIV, though its toxicity profile demands careful management.

Correct Answer: B

Rationale: Cyclophosphamide is an alkylating agent (B), cross-linking DNA to halt cancer cell division, widely used in lymphomas, leukemias, and solid tumors. It's typically combined with other agents (A) in regimens like CHOP for synergy. It causes granulocytopenia (C), a dose-limiting toxicity increasing infection risk. It causes nausea and vomiting (D), moderately to highly emetogenic. Alopecia (original E) is common. Its activation by CYP450 to active metabolites like phosphoramide mustard enhances efficacy, but hemorrhagic cystitis (prevented by mesna) and cardiotoxicity at high doses require careful monitoring.

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.