Indicate cholinesterase activator:

Correct Answer: A

Rationale: The correct answer is A, Pralidoxime, as it is a cholinesterase reactivator used to treat organophosphate poisoning by reactivating inhibited acetylcholinesterase. Edrophonium (B) is a cholinesterase inhibitor used for diagnostic purposes. Pilocarpine (C) is a muscarinic agonist used to treat glaucoma and dry mouth. Isoflurophate (D) is an irreversible cholinesterase inhibitor used as an insecticide. Therefore, Pralidoxime is the only cholinesterase activator among the options provided.

Correct Answer: D

Rationale: Step-by-step rationale: 1. Norepinephrine is a direct-acting sympathomimetic that stimulates alpha1, alpha2, and beta1 receptors. 2. Activation of alpha1 receptors causes vasoconstriction. 3. Activation of alpha2 receptors inhibits norepinephrine release. 4. Activation of beta1 receptors increases heart rate and contractility. Summary: A. Isoproterenol is a non-selective beta agonist. B. Ephedrine acts mainly by releasing norepinephrine. C. Dobutamine is a beta1-selective agonist. D. Norepinephrine is the correct choice as it stimulates alpha1, alpha2, and beta1 receptors.

Correct Answer: D

Rationale: The correct answer is D: Αlfa-receptor antagonists. Alpha-receptor antagonists, such as phenoxybenzamine and phentolamine, are used in the management of pheochromocytoma to block the effects of excess catecholamines released by the tumor. These agents help control hypertension and other symptoms associated with pheochromocytoma. A: Selective beta2-receptor antagonists are not typically used in the management of pheochromocytoma because they do not target the alpha-receptors responsible for the symptoms. B: Nonselective beta-receptor antagonists may be used as adjunct therapy in pheochromocytoma to control tachycardia, but they do not directly address the alpha-receptor effects. C: Indirect-acting adrenoreceptor antagonist drugs do not specifically target the alpha-receptors involved in pheochromocytoma symptoms. In summary,

Correct Answer: D

Rationale: The correct answer is D because barbiturates act by increasing the duration, frequency, and direct activation of GABA-gated Cl- channels. This leads to hyperpolarization of neurons, resulting in sedative and hypnotic effects. Choice A is correct as barbiturates prolong the opening of Cl- channels. Choice B is incorrect as barbiturates enhance, not directly activate, the Cl- channels. Choice C is incorrect as barbiturates increase the duration, not frequency, of Cl- channel opening events. Therefore, the correct answer is D as it encompasses all the mechanisms of barbiturate action.

Correct Answer: B

Rationale: The correct answer is B: Inhibition of GABA aminotransferase. Vigabatrin increases GABA levels by inhibiting GABA aminotransferase enzyme, which is responsible for GABA breakdown. This leads to enhanced GABAergic inhibition in the brain. A: Direct action on the GABA receptor-chloride channel complex is incorrect as vigabatrin does not directly bind to GABA receptors. C: NMDA receptor blockade via the glycine binding site is incorrect as vigabatrin does not affect NMDA receptors. D: Inhibition of GABA neuronal reuptake from synapses is incorrect as vigabatrin does not affect GABA reuptake mechanisms.