Mechanism of penicillins’ antibacterial effect is:

Correct Answer: A

Rationale: The correct answer is A: Inhibition of transpeptidation in the bacterial cell wall. Penicillins work by inhibiting the enzyme transpeptidase, which is involved in the cross-linking of peptidoglycan chains in the bacterial cell wall. This leads to weakened cell walls, causing bacterial cell lysis. Choices B, C, and D are incorrect because penicillins do not inhibit beta-lactamase (choice B), activate endogenous proteases to destroy the cell wall (choice C), or activate endogenous phospholipases altering cell membrane permeability (choice D). The primary mechanism of action of penicillins is through interfering with cell wall synthesis, making choice A the correct answer.

Correct Answer: B

Rationale: The correct answer is B: Rimantadine. Rimantadine inhibits the uncoating of viral RNA by preventing the release of viral RNA into the host cell. This disrupts the replication process of the virus. Vidarabine (A) inhibits viral DNA polymerase, not viral RNA uncoating. Acyclovir (C) inhibits viral DNA polymerase as well. Didanozine (D) is an antiretroviral drug used in HIV treatment, not for inhibiting viral RNA uncoating.

Correct Answer: C

Rationale: The correct answer is C: Increased capacitance of systemic veins. Nitrates cause vasodilation, leading to increased venous capacitance, reducing preload and myocardial oxygen demand. Decreased ejection time (A) and decreased arterial pressure (D) are actually beneficial effects of nitrates, as they reduce cardiac workload. Increased cardiac rate (B) is not a common adverse effect of nitrates in the treatment of exertional angina.

Correct Answer: A

Rationale: The correct answer is A: Inhibition of phosphodiesterase. Milrinone is a phosphodiesterase inhibitor, which increases cAMP levels, leading to enhanced cardiac contractility. This occurs through the inhibition of the breakdown of cAMP, resulting in increased intracellular calcium levels and improved myocardial function. Choice B is incorrect because while protein kinase can increase cytoplasmic Ca2+, it is not the primary mechanism of milrinone's positive inotropic action. Choice C is incorrect as milrinone does not directly inhibit the Ca2+/Na+ exchanger. Choice D is incorrect as activation of phospholipase A2 is not the mechanism through which milrinone exerts its positive inotropic effects.

Correct Answer: D

Rationale: In the context of cardiovascular drugs, understanding the regulation of aldosterone release is crucial. The correct answer is D) Both (b) and (c) because both Angiotensin and Angiotensin III stimulate aldosterone release. Angiotensin, which is converted from Angiotensin I through the action of ACE (Angiotensin-Converting Enzyme), directly stimulates the release of aldosterone from the adrenal cortex. This hormone plays a key role in regulating blood pressure and electrolyte balance in the body. Angiotensin III, a metabolite of Angiotensin II, also has the ability to stimulate aldosterone release. It binds to specific receptors in the adrenal gland, leading to aldosterone secretion. Option A, Angiotensin I, is incorrect because Angiotensin I itself does not directly stimulate aldosterone release. It needs to be converted to Angiotensin II to exert its effects on aldosterone secretion. Option C, Angiotensin III alone, is also incorrect as it is not the sole stimulator of aldosterone release. While Angiotensin III does have some aldosterone-stimulating activity, it is not as potent as Angiotensin II. Understanding the interactions between the renin-angiotensin-aldosterone system and how different components regulate hormone release is essential in pharmacology and clinical practice. This knowledge helps healthcare professionals in managing conditions like hypertension and heart failure effectively by targeting specific points in this pathway with medications like ACE inhibitors or angiotensin receptor blockers.