Quinine sulfate:

Correct Answer: A

Rationale: Quinine sulfate is the drug of choice in chloroquine-resistant falciparum malaria (A), used IV or orally for severe Plasmodium falciparum infections, acting as a blood schizonticide to reduce parasitemia. It's available IV and orally (B), critical for flexibility in severe cases. It doesn't eradicate hepatic P. vivax parasites (C); primaquine is needed for hypnozoites. It's not contraindicated in renal failure (D), though dose adjustment is advised. Large doses cause tinnitus (original E), part of cinchonism. Quinine's efficacy in multidrug-resistant malaria, via heme polymerization disruption, remains vital, though cardiotoxicity (QT prolongation) requires ECG monitoring.

Correct Answer: B

Rationale: Aqueous hydrolysis is the correct answer because it is not a mechanism of drug permeation across biological membranes. Permeation refers to the process by which drugs move across cell membranes to reach their site of action, and it includes aqueous diffusion (A), where drugs pass through aqueous channels or pores; lipid diffusion (C), where lipophilic drugs dissolve into the lipid bilayer; and pinocytosis or endocytosis (D), where cells engulf drugs in vesicles. Special carrier transport (original E) involves specific proteins facilitating drug movement. Aqueous hydrolysis (B), however, is a chemical degradation process where a drug reacts with water, breaking chemical bonds (e.g., in esters or amides), not a physical movement across membranes. This distinction is critical in pharmacology, as permeation mechanisms determine bioavailability and tissue distribution, while hydrolysis affects drug stability, often in the gastrointestinal tract or plasma, not membrane crossing.

Correct Answer: B

Rationale: The most correct statement is that spare receptors will be detected if the intracellular effect of drug-receptor interaction lasts longer than the drug-receptor interaction itself (B). Spare receptors exist when maximal response occurs before all receptors are occupied (e.g., histamine on H2 receptors), detectable when downstream signaling (e.g., cAMP) persists post-dissociation. Option A is false; spare receptors are membrane-bound, not cytoplasmic. Option C is incorrect; maximal efficacy is set by receptor-effector coupling, not spare receptor number. Option D is wrong; receptors need agonists for activation. Option E (original) is incorrect; EC50 < Kd indicates spare receptors, not the reverse. This phenomenon increases sensitivity, explaining why low agonist doses can achieve full effects in systems like beta-adrenergic signaling.

Correct Answer: A

Rationale: Phase I involves the study of a small number of normal volunteers by highly trained clinical pharmacologists (A), assessing safety, pharmacokinetics, and tolerability (e.g., 20-100 subjects) in controlled settings. Phase II (B) tests efficacy in patients (100-300), not thousands. Phase III (C) compares efficacy and safety in larger populations (300-3000), not inducing toxicity for therapeutic index. Option D is irrelevant. Phase II with controls (original E) is true but less defining than A. Phase I's focus on healthy subjects establishes safe dosing, critical for advancing drug development, balancing risk and scientific rigor.

Correct Answer: A

Rationale: Phenylephrine causes constriction of vessels in the nasal mucosa (A), an alpha-1 agonist shrinking mucosal blood vessels, reducing congestion (e.g., in decongestants). It doesn't increase gastric secretion/motility (B), a cholinergic effect. It decreases skin temperature (C is incorrect) by vasoconstriction. It causes mydriasis (D is incorrect), not miosis, via pupil dilation. Option E (original) is false. This selective alpha-adrenergic action underlies its topical/systemic use, with minimal beta effects, though reflex bradycardia or hypertension may occur, requiring cautious use in cardiovascular patients.