Wilkes University NSG 552 Exam 3 (pdf) | 2026/2027 |
Psychopharmacology Q&A | Nursing
1. What is the primary mechanism of action of naloxone in reversing opioid overdose?
A) Partial mu receptor agonism that displaces full agonists
B) Competitive antagonism at mu, kappa, and delta opioid receptors
C) NMDA receptor blockade that reduces opioid tolerance
D) Dopamine reuptake inhibition that counteracts respiratory depression
Correct Answer: B) Competitive antagonism at mu, kappa, and delta opioid receptors
Rationale: Naloxone is a pure opioid antagonist with no intrinsic activity. It competitively binds mu,
kappa, and delta receptors, displacing opioids and rapidly reversing respiratory depression. Partial
agonism (A) describes buprenorphine, while NMDA antagonism (C) and dopamine effects (D) are
unrelated mechanisms.
2. Buprenorphine is classified as which type of opioid receptor agent?
A) Full mu receptor agonist
B) Partial mu receptor agonist
C) Pure opioid antagonist
D) Kappa receptor agonist
Correct Answer: B) Partial mu receptor agonist
Rationale: Buprenorphine binds mu receptors with high affinity but produces only partial activation,
creating a ceiling effect on respiratory depression. This property reduces overdose risk compared to
full agonists like methadone. It is not a pure antagonist (C), and its primary action is not at kappa
receptors (D).
3. Which medication for opioid use disorder is available as an extended-release implant?
A) Buprenorphine
B) Methadone
C) Naltrexone
D) Buprenorphine/naloxone combination
Correct Answer: C) Naltrexone
Rationale: Naltrexone is available as oral tablets, monthly injectable suspension, and a subdermal
implant for extended-release delivery. Buprenorphine (A, D) and methadone (B) are not
manufactured as implants. The implant provides sustained opioid blockade for months in selected
patients.
4. When buprenorphine is administered too soon after full opioid agonist use, what is the most
significant clinical risk?
,A) Severe respiratory depression
B) Euphoria and drug-seeking behavior
C) Intense precipitated withdrawal
D) Hypertensive crisis
Correct Answer: C) Intense precipitated withdrawal
Rationale: Buprenorphine has higher mu receptor affinity than full agonists. If administered while full
agonists remain bound, it displaces them and precipitates rapid, severe withdrawal. Patients must be
in moderate withdrawal before induction. Respiratory depression (A) is not the primary concern due
to the ceiling effect.
5. The classic clinical triad of Wernicke encephalopathy consists of which findings?
A) Confusion, ataxia, and nystagmus
B) Hallucinations, seizures, and coma
C) Hyperthermia, rigidity, and autonomic instability
D) Disorientation, tremor, and tachycardia
Correct Answer: A) Confusion, ataxia, and nystagmus
Rationale: Wernicke encephalopathy results from thiamine deficiency, commonly seen in alcohol use
disorder. The triad includes confusion, ataxia, and ophthalmoplegia or nystagmus. Option B describes
severe encephalopathy progression; C describes neuroleptic malignant syndrome; D is nonspecific.
6. A patient with alcohol use disorder develops confusion, ataxia, and ophthalmoplegia. What is
the priority intervention?
A) Administer IV lorazepam
B) Start oral naltrexone
C) Administer parenteral thiamine before glucose
D) Begin acamprosate therapy
Correct Answer: C) Administer parenteral thiamine before glucose
Rationale: Wernicke encephalopathy is a medical emergency requiring immediate thiamine
replacement. Glucose administration before thiamine can precipitate or worsen Wernicke syndrome
by consuming remaining thiamine stores. Lorazepam (A) treats withdrawal seizures, while naltrexone
(B) and acamprosate (D) are maintenance therapies.
7. Which antidepressant is contraindicated in patients with a history of seizure disorders or
eating disorders?
A) Bupropion
B) Fluoxetine
C) Sertraline
, D) Paroxetine
Correct Answer: A) Bupropion
Rationale: Bupropion lowers the seizure threshold and is contraindicated in epilepsy and
bulimia/anorexia nervosa due to electrolyte-related seizure risks. SSRIs (B, C, D) are generally safer in
these populations. Screening for eating disorders before initiating bupropion is essential.
8. Which medication is a non-stimulant treatment for ADHD that acts as a selective
norepinephrine reuptake inhibitor?
A) Lisdexamfetamine
B) Guanfacine
C) Atomoxetine
D) Clonidine
Correct Answer: C) Atomoxetine
Rationale: Atomoxetine selectively inhibits norepinephrine reuptake and is FDA-approved for ADHD as
a non-stimulant option. Lisdexamfetamine (A) is a stimulant prodrug. Guanfacine (B) and clonidine
(D) are alpha-2 agonists with different mechanisms.
9. When switching from fluoxetine to an MAOI, what is the required washout period?
A) 1 week
B) 2 weeks
C) 10 days
D) 5 weeks
Correct Answer: D) 5 weeks
Rationale: Fluoxetine and its active metabolite norfluoxetine have long half-lives requiring a 5-week
washout before MAOI initiation to prevent serotonin syndrome. Other SSRIs typically require 2 weeks.
This extended period ensures complete drug elimination and receptor normalization.
10. Which side effect of tricyclic antidepressants is most concerning in overdose situations?
A) Dry mouth
B) Weight gain
C) Cardiac arrhythmias
D) Constipation
Correct Answer: C) Cardiac arrhythmias
Rationale: TCAs are highly cardiotoxic in overdose, causing QTc prolongation and potentially lethal
arrhythmias such as torsades de pointes. Anticholinergic effects (A, D) and weight gain (B) are
bothersome but not immediately life-threatening. Emergency management includes sodium
bicarbonate for cardiac toxicity.
Psychopharmacology Q&A | Nursing
1. What is the primary mechanism of action of naloxone in reversing opioid overdose?
A) Partial mu receptor agonism that displaces full agonists
B) Competitive antagonism at mu, kappa, and delta opioid receptors
C) NMDA receptor blockade that reduces opioid tolerance
D) Dopamine reuptake inhibition that counteracts respiratory depression
Correct Answer: B) Competitive antagonism at mu, kappa, and delta opioid receptors
Rationale: Naloxone is a pure opioid antagonist with no intrinsic activity. It competitively binds mu,
kappa, and delta receptors, displacing opioids and rapidly reversing respiratory depression. Partial
agonism (A) describes buprenorphine, while NMDA antagonism (C) and dopamine effects (D) are
unrelated mechanisms.
2. Buprenorphine is classified as which type of opioid receptor agent?
A) Full mu receptor agonist
B) Partial mu receptor agonist
C) Pure opioid antagonist
D) Kappa receptor agonist
Correct Answer: B) Partial mu receptor agonist
Rationale: Buprenorphine binds mu receptors with high affinity but produces only partial activation,
creating a ceiling effect on respiratory depression. This property reduces overdose risk compared to
full agonists like methadone. It is not a pure antagonist (C), and its primary action is not at kappa
receptors (D).
3. Which medication for opioid use disorder is available as an extended-release implant?
A) Buprenorphine
B) Methadone
C) Naltrexone
D) Buprenorphine/naloxone combination
Correct Answer: C) Naltrexone
Rationale: Naltrexone is available as oral tablets, monthly injectable suspension, and a subdermal
implant for extended-release delivery. Buprenorphine (A, D) and methadone (B) are not
manufactured as implants. The implant provides sustained opioid blockade for months in selected
patients.
4. When buprenorphine is administered too soon after full opioid agonist use, what is the most
significant clinical risk?
,A) Severe respiratory depression
B) Euphoria and drug-seeking behavior
C) Intense precipitated withdrawal
D) Hypertensive crisis
Correct Answer: C) Intense precipitated withdrawal
Rationale: Buprenorphine has higher mu receptor affinity than full agonists. If administered while full
agonists remain bound, it displaces them and precipitates rapid, severe withdrawal. Patients must be
in moderate withdrawal before induction. Respiratory depression (A) is not the primary concern due
to the ceiling effect.
5. The classic clinical triad of Wernicke encephalopathy consists of which findings?
A) Confusion, ataxia, and nystagmus
B) Hallucinations, seizures, and coma
C) Hyperthermia, rigidity, and autonomic instability
D) Disorientation, tremor, and tachycardia
Correct Answer: A) Confusion, ataxia, and nystagmus
Rationale: Wernicke encephalopathy results from thiamine deficiency, commonly seen in alcohol use
disorder. The triad includes confusion, ataxia, and ophthalmoplegia or nystagmus. Option B describes
severe encephalopathy progression; C describes neuroleptic malignant syndrome; D is nonspecific.
6. A patient with alcohol use disorder develops confusion, ataxia, and ophthalmoplegia. What is
the priority intervention?
A) Administer IV lorazepam
B) Start oral naltrexone
C) Administer parenteral thiamine before glucose
D) Begin acamprosate therapy
Correct Answer: C) Administer parenteral thiamine before glucose
Rationale: Wernicke encephalopathy is a medical emergency requiring immediate thiamine
replacement. Glucose administration before thiamine can precipitate or worsen Wernicke syndrome
by consuming remaining thiamine stores. Lorazepam (A) treats withdrawal seizures, while naltrexone
(B) and acamprosate (D) are maintenance therapies.
7. Which antidepressant is contraindicated in patients with a history of seizure disorders or
eating disorders?
A) Bupropion
B) Fluoxetine
C) Sertraline
, D) Paroxetine
Correct Answer: A) Bupropion
Rationale: Bupropion lowers the seizure threshold and is contraindicated in epilepsy and
bulimia/anorexia nervosa due to electrolyte-related seizure risks. SSRIs (B, C, D) are generally safer in
these populations. Screening for eating disorders before initiating bupropion is essential.
8. Which medication is a non-stimulant treatment for ADHD that acts as a selective
norepinephrine reuptake inhibitor?
A) Lisdexamfetamine
B) Guanfacine
C) Atomoxetine
D) Clonidine
Correct Answer: C) Atomoxetine
Rationale: Atomoxetine selectively inhibits norepinephrine reuptake and is FDA-approved for ADHD as
a non-stimulant option. Lisdexamfetamine (A) is a stimulant prodrug. Guanfacine (B) and clonidine
(D) are alpha-2 agonists with different mechanisms.
9. When switching from fluoxetine to an MAOI, what is the required washout period?
A) 1 week
B) 2 weeks
C) 10 days
D) 5 weeks
Correct Answer: D) 5 weeks
Rationale: Fluoxetine and its active metabolite norfluoxetine have long half-lives requiring a 5-week
washout before MAOI initiation to prevent serotonin syndrome. Other SSRIs typically require 2 weeks.
This extended period ensures complete drug elimination and receptor normalization.
10. Which side effect of tricyclic antidepressants is most concerning in overdose situations?
A) Dry mouth
B) Weight gain
C) Cardiac arrhythmias
D) Constipation
Correct Answer: C) Cardiac arrhythmias
Rationale: TCAs are highly cardiotoxic in overdose, causing QTc prolongation and potentially lethal
arrhythmias such as torsades de pointes. Anticholinergic effects (A, D) and weight gain (B) are
bothersome but not immediately life-threatening. Emergency management includes sodium
bicarbonate for cardiac toxicity.
