Aciclovir:

Correct Answer: A

Rationale: Aciclovir inhibits viral DNA polymerase (A), a key mechanism in treating herpes simplex virus (HSV) and varicella-zoster virus (VZV) infections, activated by viral thymidine kinase to halt replication. It's indicated in herpetic keratitis (B), effectively treating ocular HSV. It's safe in pregnancy (C is incorrect), with no clear teratogenic risk, often used for severe HSV/VZV. It's indicated in herpetic meningoencephalitis (D), critical for HSV encephalitis. It's effective in chickenpox (original E is incorrect), reducing severity. Aciclovir's specificity for virally infected cells minimizes host toxicity, making it a cornerstone antiviral, though resistance in immunocompromised patients is a challenge.

Correct Answer: A

Rationale: Infection is the commonest life-threatening complication during cancer chemotherapy (A), due to myelosuppression reducing neutrophils, increasing sepsis risk from opportunistic pathogens. It's often from the patient's gut flora (B), like E. coli, translocating during mucositis. Pyrexia is usually present (C is incorrect), a key sign of febrile neutropenia. Conception must be avoided (D), due to teratogenic risks. Second malignancies (original E) are a long-term risk, not immediate. Chemotherapy's immunosuppression, especially with alkylating agents or antimetabolites, disrupts immune barriers, necessitating prompt antibiotic therapy and G-CSF in high-risk cases.

Correct Answer: D

Rationale: Filgrastim stimulates proliferation and differentiation of myeloid progenitor cells (D), a G-CSF boosting neutrophil production, used post-chemotherapy to reduce neutropenia duration and infection risk. It's given subcutaneously (A), the standard route. It causes a transient neutrophil increase, not neutropenia (B is incorrect). It's not used in myeloid leukemia (C) treatment; it supports recovery. It causes bone pain (original E), from marrow expansion. Filgrastim's role in accelerating granulopoiesis is critical in oncology, shortening neutropenic periods, though leukocytosis and rare splenic rupture are concerns.

Correct Answer: A

Rationale: Quantal dose-response curves are often used for determining the therapeutic index of a drug (A), the ratio of TD50 (toxic dose in 50% of subjects) to ED50 (effective dose in 50%), assessing safety (e.g., penicillin's high TI). Option B is incorrect; maximal efficacy is derived from graded curves, measuring continuous responses (e.g., blood pressure). Option C is false; inhibitors shift curves (e.g., rightward with competitive antagonists) but don't invalidate them. Option D is wrong; quantal curves apply to both intact subjects and tissues (e.g., lethality studies). Option E (original) about statistical variation fits graded curves better. Quantal curves, plotting all-or-none responses (e.g., survival), are key in toxicology and clinical trials for balancing efficacy and toxicity.

Correct Answer: A

Rationale: Acetylation (A) is a phase II drug-metabolizing reaction, conjugating drugs (e.g., isoniazid) with acetyl-CoA to increase water solubility and excretion, catalyzed by N-acetyltransferases. Deamination (B), hydrolysis (C), oxidation (D), and reduction (original E) are phase I reactions, modifying drug structure (e.g., CYP450 oxidation of diazepam) to expose functional groups. Phase II reactions, like acetylation, glucuronidation, or sulfation, typically follow, enhancing elimination. Acetylation's polymorphic nature (fast vs. slow acetylators) affects drug toxicity (e.g., isoniazid neuropathy), a key consideration in personalized medicine, distinguishing it from phase I's oxidative processes.