Hepatic microsomal drug-metabolizing enzyme induction leads to:

Correct Answer: A

Rationale: Step-by-step rationale for choice A being correct: Hepatic microsomal drug-metabolizing enzyme induction increases the metabolism of drugs like barbiturates. This leads to decreased drug levels, resulting in tolerance - requiring higher doses for the same effect. Choices B, C, and D are incorrect because cumulative effects refer to increased drug levels due to impaired metabolism, physical dependence is related to behavioral aspects, and hangover effects are due to drug toxicity or residual effects, not enzyme induction.

Correct Answer: D

Rationale: The correct answer is D because all three drugs (Reserpine, Haloperidol, Chlorpromazine) antagonize the effects of levodopa by different mechanisms, leading to a junctional blockade of dopamine action. Reserpine depletes dopamine stores, Haloperidol blocks dopamine receptors, and Chlorpromazine inhibits dopamine release. Therefore, all of these drugs can reduce the effectiveness of levodopa in treating Parkinson's disease by interfering with dopamine function. Choices A, B, and C are incorrect because each of them individually, not collectively, antagonizes the effects of levodopa and leads to a junctional blockade of dopamine action.

Correct Answer: C

Rationale: Rationale: 1. Nalbuphine is a strong kappa receptor agonist: It primarily activates kappa receptors, providing analgesia. 2. Nalbuphine is a mu receptor antagonist: It blocks mu receptors, reducing the risk of mu receptor-associated side effects. 3. Naltrexone (A) is a mu receptor antagonist but not a kappa agonist. 4. Methadone (B) is a mu receptor agonist and NMDA receptor antagonist. 5. Buprenorphine (D) is a partial mu receptor agonist and kappa receptor agonist, not a mu antagonist like nalbuphine.

Correct Answer: B

Rationale: Rationale for Choice B (Hyperactive dopaminergic state in the presence of dopamine blockers): 1. Dopamine blockers disrupt the balance of dopamine in the brain. 2. Dopamine blockers lead to an increase in dopamine receptor activity. 3. Hyperactive dopaminergic state causes abnormal movements seen in tardive dyskinesia. 4. This choice directly correlates with the pathophysiology of tardive dyskinesia. Summary of why other choices are incorrect: A: Degeneration of dopaminergic and cholinergic fibers - Tardive dyskinesia is not primarily caused by degeneration of these fibers. C: Degeneration of histaminergic fibers - Histaminergic fibers are not implicated in the development of tardive dyskinesia. D: Supersensitivity of cholinergic receptors in the caudate-putamen - While cholinergic dysfunction is involved, it is not the primary cause of tardive dyskinesia.

Correct Answer: C

Rationale: Rationale: Choice C is correct because fluoxetine has minimal binding to cholinergic, histaminic, and alpha-adrenergic receptors, reducing the likelihood of adverse effects compared to drugs that bind strongly to these receptors. Choices A and B are incorrect because fluoxetine specifically inhibits serotonin reuptake, not norepinephrine, and it does not deplete neurotransmitter stores. Choice D is incorrect because not all the statements in A and B are true for fluoxetine.