CARN Pharmacology of Addictive Substances 4 — Questions and Answers
Question 1: A patient with opioid use disorder on methadone maintenance is prescribed rifampin for tuberculosis. What pharmacokinetic interaction should the nurse anticipate?
- Rifampin inhibits CYP3A4, increasing methadone levels and risk of overdose
- Rifampin induces CYP3A4, reducing methadone levels and potentially precipitating withdrawal (Correct answer)
- Rifampin displaces methadone from protein-binding sites
- Rifampin enhances renal excretion of methadone
Correct answer: Rifampin induces CYP3A4, reducing methadone levels and potentially precipitating withdrawal
Rifampin is a potent CYP3A4 inducer; it accelerates methadone metabolism, significantly lowering plasma levels and triggering withdrawal symptoms.
Question 2: Which of the following best describes the pharmacological basis for using benzodiazepines to manage alcohol withdrawal?
- Benzodiazepines mimic alcohol's action at GABA-A receptors, preventing hyperexcitability (Correct answer)
- Benzodiazepines block NMDA receptors to prevent glutamate excitotoxicity
- Benzodiazepines enhance dopamine release to reduce craving
- Benzodiazepines inhibit alcohol dehydrogenase to slow withdrawal onset
Correct answer: Benzodiazepines mimic alcohol's action at GABA-A receptors, preventing hyperexcitability
Benzodiazepines are cross-tolerant with alcohol at GABA-A receptors, substituting for alcohol's CNS depressant effect and preventing seizures during withdrawal.
Question 3: MDMA (ecstasy) primarily causes serotonin syndrome risk when combined with which class of medications?
- Antipsychotics
- Monoamine oxidase inhibitors (MAOIs) (Correct answer)
- Beta-blockers
- Calcium channel blockers
Correct answer: Monoamine oxidase inhibitors (MAOIs)
MDMA causes massive serotonin release; MAOIs prevent serotonin breakdown, leading to life-threatening serotonin syndrome when combined.
Question 4: Varenicline (Chantix) reduces nicotine craving through which pharmacological mechanism?
- Full agonism at nicotinic acetylcholine receptors, continuously stimulating reward
- Partial agonism at α4β2 nicotinic receptors, providing modest dopamine release while blocking nicotine (Correct answer)
- Inhibition of dopamine reuptake in the mesolimbic pathway
- Antagonism of mu-opioid receptors that mediate nicotine reward
Correct answer: Partial agonism at α4β2 nicotinic receptors, providing modest dopamine release while blocking nicotine
Varenicline is a partial agonist at α4β2 nicotinic receptors, providing enough dopamine stimulation to reduce craving while competitively blocking nicotine's full effect.
Question 5: PCP (phencyclidine) produces its dissociative and psychotic effects primarily through which mechanism?
- Agonism at GABA-A receptors
- Antagonism of NMDA glutamate receptors (Correct answer)
- Stimulation of kappa-opioid receptors
- Blockade of serotonin 5-HT3 receptors
Correct answer: Antagonism of NMDA glutamate receptors
PCP blocks NMDA glutamate receptors (a dissociative mechanism), producing hallucinations, agitation, analgesia, and psychosis-like symptoms.
Question 6: A patient stabilized on buprenorphine presents requesting pain management for a dental procedure. Which analgesic approach is most appropriate?
- Discontinue buprenorphine and switch to full opioid agonist for 48 hours
- Continue buprenorphine and use non-opioid analgesics or regional anesthesia (Correct answer)
- Add a short-acting full opioid agonist without adjusting buprenorphine
- Administer naloxone to reverse buprenorphine before the procedure
Correct answer: Continue buprenorphine and use non-opioid analgesics or regional anesthesia
Buprenorphine's high receptor affinity blocks full opioids; continuing it with non-opioid analgesics or regional techniques provides analgesia without compromising addiction treatment.
Question 7: Which physiological effect explains why GHB (gamma-hydroxybutyrate) is particularly dangerous when combined with alcohol?
- Additive hepatotoxicity from shared metabolic pathways
- Synergistic CNS depression due to both agents enhancing GABA activity (Correct answer)
- Combined QTc prolongation causing fatal arrhythmias
- Competitive inhibition of alcohol dehydrogenase raising blood alcohol levels
Correct answer: Synergistic CNS depression due to both agents enhancing GABA activity
Both GHB and alcohol enhance GABAergic CNS depression; their combination produces synergistic respiratory depression and sedation, greatly increasing overdose risk.
CARN Pharmacology of Addictive Substances 4
A patient with opioid use disorder on methadone maintenance is prescribed rifampin for tuberculosis.
What pharmacokinetic interaction should the nurse anticipate?