The following cytotoxic drugs are paired with a characteristic adverse effect:

Correct Answer: C

Rationale: Daunorubicin paired with cardiomyopathy (C) is correct, an anthracycline causing dose-dependent cardiotoxicity via oxidative stress and topoisomerase inhibition, common in leukemia treatment, mitigated by dexrazoxane. Etoposide (A) causes myelosuppression, not neuropathy (vincristine does). Paclitaxel (B) causes alopecia, a hallmark taxane effect. Irinotecan (D) causes diarrhea, due to cholinergic and mucosal damage. 6-Mercaptopurine with pulmonary fibrosis (original E) is incorrect; myelosuppression is typical. Daunorubicin's efficacy in acute leukemias is balanced by lifetime dose limits to protect cardiac function, monitored via echocardiography.

Correct Answer: D

Rationale: A chemical antagonist (D) best describes an antagonist that interacts directly with the agonist, not the receptor, by neutralizing or binding it (e.g., protamine with heparin). Pharmacological antagonists (A) block receptors directly (e.g., propranolol). Partial agonists (B) bind receptors but produce submaximal effects (e.g., buprenorphine). Physiological antagonists (C) oppose effects via different receptors (e.g., epinephrine vs. histamine). Noncompetitive antagonists (original E) bind irreversibly to receptors, reducing efficacy. Chemical antagonism, a rare but specific mechanism, alters the agonist's availability without receptor interaction, critical in overdose reversal or chelation therapies, distinct from receptor-based antagonism in pharmacodynamics.

Correct Answer: C

Rationale: The correct answer is that animal testing requires the submission of histopathologic slides and specimens to the FDA (C), part of preclinical data in the Investigational New Drug (IND) application, ensuring safety evaluation. Option A is false; testing duration varies (months to years), not fixed at 3 years. Option B is incorrect; two species (e.g., rodent and non-rodent like dog) are typical, not necessarily primates. Option D is wrong; allergy prediction is poor in animals due to immune differences. Option E (original) about abbreviation for toxic agents is true but less defining. This regulatory step validates toxicity and pharmacology data, bridging preclinical and human trials.

Correct Answer: C

Rationale: Propranolol, a non-selective beta-blocker, blocks norepinephrine-induced bradycardia (C). Norepinephrine's beta-1 stimulation increases heart rate, but high doses trigger reflex bradycardia via baroreceptors; propranolol prevents the beta-mediated component, attenuating this. Methacholine (A), a muscarinic agonist, causes tachycardia reflexively, unaffected by beta-blockade. Nicotine (B) induces hypertension via nicotinic receptors and catecholamine release, partially beta-mediated, but not fully blocked. Phenylephrine (D) causes mydriasis via alpha-1, not beta. Propranolol's beta-adrenergic antagonism is key in managing sympathetic overactivity, though alpha effects persist.

Correct Answer: C

Rationale: Hydrolysis (C) is the most common mechanism for chemical degradation, where water cleaves bonds (e.g., esters in aspirin to salicylic acid), accelerated by pH or enzymes. Racemization (A) alters chirality (e.g., thalidomide), less frequent. Photolysis (B) degrades via light (e.g., nitroprusside), context-specific. Decarboxylation (D) removes COâ‚‚ (e.g., levodopa), rarer. Oxidation (original E) affects drugs like morphine but is less universal. Hydrolysis's prevalence in aqueous environments drives stability testing, requiring protective packaging or formulation adjustments (e.g., dry powders) to extend shelf life.