Chemical Dependency Counselor License Exam Pharmacology of Substance Use 4 — Questions and Answers
Question 1: Disulfiram (Antabuse) produces its aversive effect by inhibiting which enzyme?
- Alcohol dehydrogenase (ADH)
- Aldehyde dehydrogenase (ALDH) (Correct answer)
- CYP2E1
- Monoamine oxidase (MAO)
Correct answer: Aldehyde dehydrogenase (ALDH)
Disulfiram blocks ALDH, the enzyme that converts acetaldehyde to acetate; acetaldehyde accumulates and causes flushing, nausea, vomiting, and cardiovascular symptoms.
Question 2: Which cannabinoid receptor subtype mediates most of THC's psychoactive effects?
- CB2 receptors in peripheral immune tissue
- CB1 receptors in the central nervous system (Correct answer)
- Opioid mu receptors in the limbic system
- TRP vanilloid channels in sensory neurons
Correct answer: CB1 receptors in the central nervous system
THC is a partial agonist at CB1 receptors concentrated in the basal ganglia, hippocampus, cerebellum, and prefrontal cortex, producing its psychoactive, amnestic, and motor effects.
Question 3: Acamprosate's therapeutic mechanism in alcohol use disorder involves:
- Blocking opioid reward pathways to reduce craving
- Modulating glutamate and GABA activity to reduce post-acute withdrawal symptoms (Correct answer)
- Producing aversive reactions when alcohol is consumed
- Replacing alcohol at GABA-A receptors to prevent withdrawal seizures
Correct answer: Modulating glutamate and GABA activity to reduce post-acute withdrawal symptoms
Chronic alcohol use upregulates NMDA glutamate receptors; acamprosate reduces glutamate hyperactivity during abstinence and stabilizes GABAergic tone, alleviating protracted withdrawal discomfort.
Question 4: Phencyclidine (PCP) produces its distinctive dissociative effects primarily by:
- Agonizing sigma receptors in the limbic cortex
- Noncompetitively antagonizing NMDA glutamate receptors (Correct answer)
- Releasing large amounts of serotonin like MDMA
- Blocking dopamine reuptake similar to cocaine
Correct answer: Noncompetitively antagonizing NMDA glutamate receptors
PCP binds within the ion channel of the NMDA receptor and blocks glutamate-mediated transmission, producing analgesia, dissociation, and psychosis-like symptoms.
Question 5: A client on buprenorphine maintenance presents with acute severe pain after a car accident. The MOST appropriate analgesic strategy is:
- Discontinue buprenorphine and start full agonist opioids
- Continue buprenorphine and add non-opioid analgesics plus, if needed, high-dose full agonist opioids (Correct answer)
- Switch to methadone immediately for better analgesic coverage
- Administer naloxone to clear receptors before opioid analgesia
Correct answer: Continue buprenorphine and add non-opioid analgesics plus, if needed, high-dose full agonist opioids
Buprenorphine's high mu-receptor affinity means full agonists must compete, but continuing buprenorphine prevents withdrawal and addiction relapse; multimodal analgesia with high-dose opioids can still provide pain relief.
Question 6: Inhalant intoxication leading to 'sudden sniffing death' is most commonly caused by:
- Hypoxic brain injury from displaced oxygen
- Cardiac arrhythmia triggered by catecholamine sensitization of the myocardium (Correct answer)
- Acute liver necrosis from chlorinated solvent metabolites
- Pulmonary edema from direct alveolar toxicity
Correct answer: Cardiac arrhythmia triggered by catecholamine sensitization of the myocardium
Halogenated hydrocarbons sensitize cardiac tissue to endogenous catecholamines; sudden exertion or fright after inhalation can trigger fatal ventricular fibrillation within minutes.
Question 7: Which statement about nicotine pharmacology is MOST accurate?
- Nicotine acts solely on mu-opioid receptors to produce dependence
- Nicotine stimulates nicotinic acetylcholine receptors, ultimately increasing mesolimbic dopamine (Correct answer)
- Nicotine's half-life is approximately 24 hours, explaining daily cravings
- Nicotine replacement therapy delivers nicotine faster than cigarettes
Correct answer: Nicotine stimulates nicotinic acetylcholine receptors, ultimately increasing mesolimbic dopamine
Nicotine binds neuronal nAChRs on VTA dopamine neurons, stimulating dopamine release in the nucleus accumbens through the same reward pathway as other drugs of abuse.
