NR 546 Week 8 Final Exam Complete Questions
1-75 Actual Exam Screenshots 29 August 2025
Examplify Proctored NR546 Advanced
Psychopharmacology for The PMHNP Exam
Questions and Answers
Domain I: Foundational Neuroscience & Pharmacokinetics
(Questions 1-20)
1. A 45-year-old patient with major depressive disorder is started on
fluoxetine. After 4 weeks, the patient reports no improvement. The
PMHNP understands that the delayed onset of action is primarily
due to:
A) Rapid metabolism by CYP3A4
B) Desensitization of postsynaptic 5-HT1A autoreceptors
C) Upregulation of norepinephrine transporters
D) Antagonism of histamine H1 receptors
Rationale: The delayed onset of SSRIs is attributed to the time required
for somatodendritic 5-HT1A autoreceptors to desensitize, allowing for
increased serotonergic neurotransmission in the synapse .
2. A patient on phenelzine (Nardil) presents with a severe headache
and hypertension after eating aged cheese. This interaction is
mediated by:
,A) Direct release of norepinephrine
B) Irreversible inhibition of monoamine oxidase (MAO-A) in the gut
C) Antagonism of alpha-2 receptors
D) Inhibition of CYP2D6
Rationale: Phenelzine irreversibly inhibits MAO-A in the gut,
preventing the breakdown of tyramine, leading to hypertensive crisis .
3. The PMHNP is prescribing a medication that requires monitoring
of renal function. Which pharmacokinetic process is most impacted
by declining renal function?
A) Absorption
B) Distribution
C) Metabolism
D) Elimination
Rationale: Elimination (excretion) is primarily dependent on renal
function for many medications and their metabolites .
4. A patient with treatment-resistant schizophrenia is started on
clozapine. Which receptor affinity explains the low extrapyramidal
side effect (EPS) profile of this medication?
A) High D2 antagonism
B) High 5-HT2A antagonism relative to D2 antagonism
C) High muscarinic antagonism
D) High H1 antagonism
Rationale: The high ratio of 5-HT2A to D2 antagonism allows for
dopamine release in the nigrostriatal pathway, preventing EPS.
Clozapine's unique receptor profile (high 5-HT2A, low D2 occupancy at
therapeutic doses) explains its minimal EPS risk .
,5. Which cytochrome P450 enzyme is primarily responsible for the
metabolism of paroxetine and is also subject to auto-inhibition?
A) CYP1A2
B) CYP2C19
C) CYP2D6
D) CYP3A4
Rationale: Paroxetine is a potent inhibitor and substrate of CYP2D6,
exhibiting auto-inhibition that leads to nonlinear pharmacokinetics .
6. (Select All That Apply) A patient is prescribed lamotrigine.
Which of the following are critical counseling points?
A) Take with a full glass of grapefruit juice to enhance absorption.
B) Report any rash immediately, as Stevens-Johnson Syndrome is a
risk.
C) Double the dose if a dose is missed to catch up.
D) Use caution with valproate, as it doubles lamotrigine levels.
Rationale: Lamotrigine has a black box warning for Stevens-Johnson
syndrome (SJS) and toxic epidermal necrolysis (TEN). Valproate
inhibits lamotrigine glucuronidation, approximately doubling
lamotrigine levels, requiring dose reduction .
7. A patient with bipolar I disorder is stabilized on lithium
carbonate. The PMHNP notes a serum level of 1.4 mEq/L. The
patient reports nausea, coarse tremor, and mild confusion. The
PMHNP should:
A) Increase the dose to achieve therapeutic range for acute mania.
B) Hold the dose and recheck level, as this indicates early toxicity.
, C) Add haloperidol to manage the tremor.
D) Reassure the patient that this is normal at therapeutic levels.
Rationale: This level is in the toxicity range (>1.2 mEq/L for standard
maintenance) with neurological symptoms (coarse tremor, confusion,
nausea) indicating early lithium toxicity requiring dose hold and
reassessment .
8. The mechanism of action of ketamine/esketamine (Spravato) in
treatment-resistant depression involves:
A) Selective serotonin reuptake inhibition
B) NMDA receptor antagonism leading to increased glutamate and
BDNF release
C) Dopamine transporter blockade
D) GABA-A receptor potentiation
Rationale: Esketamine is an NMDA receptor antagonist that rapidly
increases glutamate and BDNF release, promoting synaptogenesis and
rapid antidepressant effects .
9. What are the three monoamine neurotransmitters?
A) Acetylcholine, GABA, Glutamate
B) Dopamine, Epinephrine, Melatonin
C) Dopamine, Norepinephrine, Serotonin
D) Norepinephrine, Histamine, Oxytocin
Rationale: These three are the classical monoamines involved in mood
regulation. The monoamine hypothesis posits that depression stems from
a deficiency in one or all of these, while mania may result from an
excess .
1-75 Actual Exam Screenshots 29 August 2025
Examplify Proctored NR546 Advanced
Psychopharmacology for The PMHNP Exam
Questions and Answers
Domain I: Foundational Neuroscience & Pharmacokinetics
(Questions 1-20)
1. A 45-year-old patient with major depressive disorder is started on
fluoxetine. After 4 weeks, the patient reports no improvement. The
PMHNP understands that the delayed onset of action is primarily
due to:
A) Rapid metabolism by CYP3A4
B) Desensitization of postsynaptic 5-HT1A autoreceptors
C) Upregulation of norepinephrine transporters
D) Antagonism of histamine H1 receptors
Rationale: The delayed onset of SSRIs is attributed to the time required
for somatodendritic 5-HT1A autoreceptors to desensitize, allowing for
increased serotonergic neurotransmission in the synapse .
2. A patient on phenelzine (Nardil) presents with a severe headache
and hypertension after eating aged cheese. This interaction is
mediated by:
,A) Direct release of norepinephrine
B) Irreversible inhibition of monoamine oxidase (MAO-A) in the gut
C) Antagonism of alpha-2 receptors
D) Inhibition of CYP2D6
Rationale: Phenelzine irreversibly inhibits MAO-A in the gut,
preventing the breakdown of tyramine, leading to hypertensive crisis .
3. The PMHNP is prescribing a medication that requires monitoring
of renal function. Which pharmacokinetic process is most impacted
by declining renal function?
A) Absorption
B) Distribution
C) Metabolism
D) Elimination
Rationale: Elimination (excretion) is primarily dependent on renal
function for many medications and their metabolites .
4. A patient with treatment-resistant schizophrenia is started on
clozapine. Which receptor affinity explains the low extrapyramidal
side effect (EPS) profile of this medication?
A) High D2 antagonism
B) High 5-HT2A antagonism relative to D2 antagonism
C) High muscarinic antagonism
D) High H1 antagonism
Rationale: The high ratio of 5-HT2A to D2 antagonism allows for
dopamine release in the nigrostriatal pathway, preventing EPS.
Clozapine's unique receptor profile (high 5-HT2A, low D2 occupancy at
therapeutic doses) explains its minimal EPS risk .
,5. Which cytochrome P450 enzyme is primarily responsible for the
metabolism of paroxetine and is also subject to auto-inhibition?
A) CYP1A2
B) CYP2C19
C) CYP2D6
D) CYP3A4
Rationale: Paroxetine is a potent inhibitor and substrate of CYP2D6,
exhibiting auto-inhibition that leads to nonlinear pharmacokinetics .
6. (Select All That Apply) A patient is prescribed lamotrigine.
Which of the following are critical counseling points?
A) Take with a full glass of grapefruit juice to enhance absorption.
B) Report any rash immediately, as Stevens-Johnson Syndrome is a
risk.
C) Double the dose if a dose is missed to catch up.
D) Use caution with valproate, as it doubles lamotrigine levels.
Rationale: Lamotrigine has a black box warning for Stevens-Johnson
syndrome (SJS) and toxic epidermal necrolysis (TEN). Valproate
inhibits lamotrigine glucuronidation, approximately doubling
lamotrigine levels, requiring dose reduction .
7. A patient with bipolar I disorder is stabilized on lithium
carbonate. The PMHNP notes a serum level of 1.4 mEq/L. The
patient reports nausea, coarse tremor, and mild confusion. The
PMHNP should:
A) Increase the dose to achieve therapeutic range for acute mania.
B) Hold the dose and recheck level, as this indicates early toxicity.
, C) Add haloperidol to manage the tremor.
D) Reassure the patient that this is normal at therapeutic levels.
Rationale: This level is in the toxicity range (>1.2 mEq/L for standard
maintenance) with neurological symptoms (coarse tremor, confusion,
nausea) indicating early lithium toxicity requiring dose hold and
reassessment .
8. The mechanism of action of ketamine/esketamine (Spravato) in
treatment-resistant depression involves:
A) Selective serotonin reuptake inhibition
B) NMDA receptor antagonism leading to increased glutamate and
BDNF release
C) Dopamine transporter blockade
D) GABA-A receptor potentiation
Rationale: Esketamine is an NMDA receptor antagonist that rapidly
increases glutamate and BDNF release, promoting synaptogenesis and
rapid antidepressant effects .
9. What are the three monoamine neurotransmitters?
A) Acetylcholine, GABA, Glutamate
B) Dopamine, Epinephrine, Melatonin
C) Dopamine, Norepinephrine, Serotonin
D) Norepinephrine, Histamine, Oxytocin
Rationale: These three are the classical monoamines involved in mood
regulation. The monoamine hypothesis posits that depression stems from
a deficiency in one or all of these, while mania may result from an
excess .
