ATI RN
Central Nervous System Stimulants and Related Drugs NCLEX Style Questions Questions
Question 1 of 5
Acute opium poisoning is treated by intravenous administration of
Correct Answer: A
Rationale: Naloxone is an opioid antagonist that rapidly reverses respiratory depression in opioid overdose.
Question 2 of 5
Pharmacologic actions of acetylsalicylic acid include all of the following EXCEPT:
Correct Answer: C
Rationale: Acetylsalicylic acid (aspirin) inhibits COX enzymes, reducing prostaglandin synthesis (choice D), yielding analgesic (choice A) and antipyretic (choice B) effects by decreasing pain mediators and hypothalamic heat regulation, respectively. However, it inhibits, not promotes, platelet aggregation (choice C) by blocking thromboxane A2 production, a pro-aggregatory prostaglandin, making it antiplatelet, used in cardiovascular prophylaxis. Promotion of aggregation would contradict its mechanism. This exception tests understanding of aspirin's unique antiplatelet action among NSAIDs, critical for its clinical applications.
Question 3 of 5
A 57-year-old man with a seizure disorder takes anti-epileptic medications. His physician would like to use a medicine that is metabolized only by the CYP1A2 receptor. Which of the following agents would be preferred?
Correct Answer: C
Rationale: Felbamate is primarily metabolized by the CYP1A2 enzyme, making it a suitable choice for patients where CYP1A2 metabolism is desired.
Question 4 of 5
N-acetylcysteine is beneficial in acute paracetamol poisoning because
Correct Answer: D
Rationale: N-acetylcysteine restores glutathione levels, preventing hepatotoxicity from toxic paracetamol metabolites.
Question 5 of 5
Benzodiazepines produce their actions on CNS by:
Correct Answer: B
Rationale: Benzodiazepines (e.g., diazepam, lorazepam) are CNS depressants used for anxiety, seizures, and insomnia. They exert effects by binding to a specific allosteric site on the GABAa receptor, enhancing GABA's inhibitory action. GABA, the primary inhibitory neurotransmitter, opens chloride (Clâ») channels, hyperpolarizing neurons and reducing excitability. Benzodiazepines increase the frequency of channel opening, potentiating this effect, leading to sedation and anxiolysis. Blocking Clâ» channels (choice A) would oppose inhibition, contrary to their purpose. Acting as direct agonists (choice C) is incorrect—they don't activate the receptor alone but amplify GABA's action. Antagonizing GABAb receptors (choice D) is irrelevant, as benzodiazepines target GABAa specifically. This potentiation mechanism underlies their therapeutic utility and risks like tolerance. Understanding this is key to distinguishing benzodiazepines from other CNS drugs and managing their clinical use effectively.