NRNP 6665 WEEK 11 FINAL EXAM STUDY
GUIDE 2026 2027 QUESTIONS AND
VERIFIED ANSWERS
SECTION ONE: PSYCHOPHARMACOLOGY NEUROSCIENCE
Question 1
A patient with major depressive disorder is prescribed a Selective Serotonin Reuptake
Inhibitor (SSRI). What is the primary mechanism of action of this medication at the
synaptic cleft?
A. It blocks the presynaptic reuptake of serotonin and norepinephrine.
B. It directly stimulates the postsynaptic serotonin receptors.
C. It blocks the presynaptic reuptake of serotonin, initially increasing synaptic
serotonin, which eventually leads to postsynaptic receptor downregulation.
D. It inhibits the enzyme monoamine oxidase, preventing the breakdown of serotonin.
Answer: C
Rationale: SSRIs work by selectively blocking the serotonin transporter (SERT) on the
presynaptic neuron. This initially increases the concentration of serotonin in the
synaptic cleft. However, the therapeutic effect (which takes 2 to 4 weeks) is believed to
be caused by the downstream effect of chronically elevated serotonin, which leads to
the desensitization or downregulation of presynaptic autoreceptors and postsynaptic
,serotonin receptors, ultimately improving neuronal signal transduction. Option A
describes SNRIs. Option D describes MAOIs.
Question 2
What is the role of Brain-Derived Neurotrophic Factor (BDNF) in the pathophysiology
and treatment of major depressive disorder?
A. BDNF is elevated in depression and lowered by antidepressant therapy.
B. BDNF promotes neurogenesis and synaptic plasticity in the hippocampus, and
chronic stress decreases BDNF while effective antidepressant therapy increases it.
C. BDNF is exclusively responsible for the rapid onset of action of ketamine.
D. BDNF binds to dopamine receptors to improve mood.
Answer: B
Rationale: The neurotrophic hypothesis of depression states that chronic stress and
elevated cortisol levels decrease the expression of BDNF in the hippocampus, leading
to neuronal atrophy and cell death (decreased neuroplasticity). Effective
antidepressant treatments, including SSRIs and ketamine, ultimately increase BDNF
levels, promoting neurogenesis and repair of synaptic connections.
Question 3
A patient is prescribed an NMDA receptor antagonist for treatment-resistant
depression. Which medication fits this description, and what is a unique requirement
for its administration?
A. Bupropion; requires monitoring for seizures.
B. Esketamine (Spravato); must be administered in a certified healthcare setting under
a Risk Evaluation and Mitigation Strategy (REMS) program.
C. Mirtazapine; requires fasting before administration.
D. Dextromethorphan/bupropion (Auvelity); must be injected intramuscularly.
Answer: B
Rationale: Esketamine is an NMDA receptor antagonist that produces rapid
antidepressant effects by increasing glutamate release, which triggers a cascade of
, signaling leading to synaptogenesis. Due to risks of dissociation, sedation, and abuse, it
is strictly regulated under a REMS program and can only be administered in a certified
medical office where the patient must be observed for at least two hours after dosing.
SECTION TWO: ANTIDEPRESSANTS AND MOOD STABILIZERS
Question 4
A 28-year-old female patient is diagnosed with major depressive disorder and started
on Sertraline (Zoloft). She returns to the clinic in two weeks reporting that her
depression has not improved at all, but she is experiencing severe nausea, insomnia,
and sexual dysfunction. She is very discouraged. What is the best response by the
PMHNP?
A. Discontinue the Sertraline immediately due to intolerable side effects and switch to
a different class.
B. Reassure the patient that antidepressants take 4 to 6 weeks to reach full efficacy,
and the side effects often resolve in 1 to 2 weeks. Consider a temporary dose reduction
or symptomatic management if she can tolerate it.
C. Tell her that the medication is clearly not working and she will need to be referred
for electroconvulsive therapy.
D. Increase the dose of Sertraline to double the current amount to force a faster
response.
Answer: B
Rationale: A common clinical challenge in psychiatry is patient adherence during the
initial weeks of treatment. Antidepressants do not begin to show true therapeutic
efficacy for mood until 4 to 6 weeks (though sleep/appetite may improve earlier).
However, side effects occur immediately. Educating the patient about this timeline is
crucial to prevent premature discontinuation. If side effects are severe, a brief dose
reduction or symptomatic treatment (e.g., ondansetron for nausea) can be tried before
abandoning the medication.
Question 5
GUIDE 2026 2027 QUESTIONS AND
VERIFIED ANSWERS
SECTION ONE: PSYCHOPHARMACOLOGY NEUROSCIENCE
Question 1
A patient with major depressive disorder is prescribed a Selective Serotonin Reuptake
Inhibitor (SSRI). What is the primary mechanism of action of this medication at the
synaptic cleft?
A. It blocks the presynaptic reuptake of serotonin and norepinephrine.
B. It directly stimulates the postsynaptic serotonin receptors.
C. It blocks the presynaptic reuptake of serotonin, initially increasing synaptic
serotonin, which eventually leads to postsynaptic receptor downregulation.
D. It inhibits the enzyme monoamine oxidase, preventing the breakdown of serotonin.
Answer: C
Rationale: SSRIs work by selectively blocking the serotonin transporter (SERT) on the
presynaptic neuron. This initially increases the concentration of serotonin in the
synaptic cleft. However, the therapeutic effect (which takes 2 to 4 weeks) is believed to
be caused by the downstream effect of chronically elevated serotonin, which leads to
the desensitization or downregulation of presynaptic autoreceptors and postsynaptic
,serotonin receptors, ultimately improving neuronal signal transduction. Option A
describes SNRIs. Option D describes MAOIs.
Question 2
What is the role of Brain-Derived Neurotrophic Factor (BDNF) in the pathophysiology
and treatment of major depressive disorder?
A. BDNF is elevated in depression and lowered by antidepressant therapy.
B. BDNF promotes neurogenesis and synaptic plasticity in the hippocampus, and
chronic stress decreases BDNF while effective antidepressant therapy increases it.
C. BDNF is exclusively responsible for the rapid onset of action of ketamine.
D. BDNF binds to dopamine receptors to improve mood.
Answer: B
Rationale: The neurotrophic hypothesis of depression states that chronic stress and
elevated cortisol levels decrease the expression of BDNF in the hippocampus, leading
to neuronal atrophy and cell death (decreased neuroplasticity). Effective
antidepressant treatments, including SSRIs and ketamine, ultimately increase BDNF
levels, promoting neurogenesis and repair of synaptic connections.
Question 3
A patient is prescribed an NMDA receptor antagonist for treatment-resistant
depression. Which medication fits this description, and what is a unique requirement
for its administration?
A. Bupropion; requires monitoring for seizures.
B. Esketamine (Spravato); must be administered in a certified healthcare setting under
a Risk Evaluation and Mitigation Strategy (REMS) program.
C. Mirtazapine; requires fasting before administration.
D. Dextromethorphan/bupropion (Auvelity); must be injected intramuscularly.
Answer: B
Rationale: Esketamine is an NMDA receptor antagonist that produces rapid
antidepressant effects by increasing glutamate release, which triggers a cascade of
, signaling leading to synaptogenesis. Due to risks of dissociation, sedation, and abuse, it
is strictly regulated under a REMS program and can only be administered in a certified
medical office where the patient must be observed for at least two hours after dosing.
SECTION TWO: ANTIDEPRESSANTS AND MOOD STABILIZERS
Question 4
A 28-year-old female patient is diagnosed with major depressive disorder and started
on Sertraline (Zoloft). She returns to the clinic in two weeks reporting that her
depression has not improved at all, but she is experiencing severe nausea, insomnia,
and sexual dysfunction. She is very discouraged. What is the best response by the
PMHNP?
A. Discontinue the Sertraline immediately due to intolerable side effects and switch to
a different class.
B. Reassure the patient that antidepressants take 4 to 6 weeks to reach full efficacy,
and the side effects often resolve in 1 to 2 weeks. Consider a temporary dose reduction
or symptomatic management if she can tolerate it.
C. Tell her that the medication is clearly not working and she will need to be referred
for electroconvulsive therapy.
D. Increase the dose of Sertraline to double the current amount to force a faster
response.
Answer: B
Rationale: A common clinical challenge in psychiatry is patient adherence during the
initial weeks of treatment. Antidepressants do not begin to show true therapeutic
efficacy for mood until 4 to 6 weeks (though sleep/appetite may improve earlier).
However, side effects occur immediately. Educating the patient about this timeline is
crucial to prevent premature discontinuation. If side effects are severe, a brief dose
reduction or symptomatic treatment (e.g., ondansetron for nausea) can be tried before
abandoning the medication.
Question 5
