Walden NURS 6630 Psychopharmacology
Final Exam ACTUAL EXAM 2026/2027 |
Psychopharmacology NURS 6630 | Verified
Q&A | Pass Guaranteed - A+ Graded
Section 1: Neurobiology & Neurotransmitter Systems (12 questions)
Q1: A patient with depression is started on an SSRI. The therapeutic effect is thought to involve
desensitization of which serotonin autoreceptor over 2-4 weeks?
A. 5-HT2A receptor
B. 5-HT1A autoreceptor
C. 5-HT3 receptor
D. 5-HT7 receptor
Correct Answer: B
Rationale: SSRIs initially increase synaptic serotonin, which stimulates 5-HT1A autoreceptors causing
negative feedback; chronic administration leads to desensitization of these autoreceptors, enhancing
serotonin neurotransmission and correlating with delayed clinical improvement.
Q2: Which neurotransmitter receptor antagonism is primarily responsible for the metabolic side effects
(weight gain, dyslipidemia) observed with second-generation antipsychotics?
A. D2 receptor
B. 5-HT2A receptor
C. Histamine H1 receptor
D. Muscarinic M3 receptor
Correct Answer: C
Rationale: H1 receptor antagonism increases appetite and weight gain; combined with 5-HT2C
antagonism (which affects satiety), these pharmacological properties drive the metabolic syndrome
associated with antipsychotics like olanzapine and clozapine.
Q3: Aripiprazole is classified as a dopamine system stabilizer due to which unique pharmacological
property?
,A. Pure D2 receptor antagonism
B. D2 receptor partial agonism
C. D1 receptor full agonism
D. D3 receptor inverse agonism
Correct Answer: B
Rationale: Aripiprazole acts as a partial agonist at D2 receptors, functioning as an agonist in
hypodopaminergic states (improving negative symptoms) and an antagonist in hyperdopaminergic
states (reducing positive symptoms), thereby stabilizing dopaminergic tone.
Q4: The NMDA receptor antagonist mechanism of ketamine is thought to produce rapid antidepressant
effects through which downstream neurobiological effect?
A. Immediate serotonin release
B. Increased BDNF release and synaptogenesis
C. Direct dopamine receptor stimulation
D. GABA-A receptor potentiation
Correct Answer: B
Rationale: Ketamine's NMDA antagonism triggers glutamate surge activating AMPA receptors, leading
to BDNF release, activation of TrkB receptors, and rapid synaptogenesis in prefrontal cortex, correlating
with its rapid antidepressant effects within hours to days.
Q5: Which receptor binding profile explains bupropion's efficacy for smoking cessation and lower risk of
sexual dysfunction compared to SSRIs?
A. SERT and NET inhibition
B. NET and DAT inhibition
C. 5-HT2A antagonism
D. Alpha-2 antagonism
Correct Answer: B
Rationale: Bupropion inhibits norepinephrine and dopamine reuptake (NDRI) without significant
serotonergic effects; dopaminergic enhancement in the mesolimbic pathway reduces nicotine craving
and withdrawal while preserving sexual function unlike serotonergic agents.
Q6: The therapeutic effect of vortioxetine on cognitive symptoms in depression is attributed to which
receptor activity?
A. 5-HT3 and 5-HT7 antagonism
B. 5-HT1A agonism and 5-HT1B partial agonism
C. SERT inhibition alone
,D. 5-HT2A inverse agonism
Correct Answer: B
Rationale: Vortioxetine's 5-HT1A agonism and 5-HT1B partial agonism enhance acetylcholine and
glutamate release in prefrontal cortex, improving executive function and processing speed independent
of its antidepressant effects.
Q7: Which neurotransmitter system dysfunction is most implicated in the pathophysiology of ADHD?
A. Serotonergic deficiency in the raphe nuclei
B. Dopaminergic and noradrenergic dysregulation in prefrontal cortex and striatum
C. GABAergic hyperactivity in the thalamus
D. Glutamatergic excess in the hippocampus
Correct Answer: B
Rationale: ADHD involves dysregulation of dopamine and norepinephrine circuits in the prefrontal
cortex (executive function) and striatum (reward processing, motor control), explaining the efficacy of
stimulants and norepinephrine reuptake inhibitors.
Q8: The "triptan" medications used for migraine work primarily through which serotonin receptor
agonism?
A. 5-HT1A
B. 5-HT1B and 5-HT1D
C. 5-HT2A
D. 5-HT3
Correct Answer: B
Rationale: Triptans are 5-HT1B/1D receptor agonists; 5-HT1B agonism causes vasoconstriction of cranial
blood vessels while 5-HT1D agonism inhibits trigeminal nerve peptide release and central pain
transmission.
Q9: Which second messenger system is primarily activated by 5-HT2A receptor stimulation?
A. cAMP accumulation
B. Phosphoinositide hydrolysis (IP3/DAG)
C. Ion channel opening
D. Tyrosine kinase activation
Correct Answer: B
Rationale: 5-HT2A receptors are Gq-coupled, activating phospholipase C to hydrolyze
phosphatidylinositol bisphosphate into IP3 (calcium release) and DAG (protein kinase C activation),
distinct from Gi/o-coupled 5-HT1A receptors that inhibit cAMP.
, Q10: The sedating effects of mirtazapine at lower doses (7.5-15mg) are primarily due to antagonism of
which receptor?
A. Alpha-2 adrenergic
B. 5-HT2A
C. Histamine H1
D. 5-HT3
Correct Answer: C
Rationale: Mirtazapine's potent H1 antagonism causes sedation and appetite stimulation; at higher
doses (30-45mg), noradrenergic enhancement via alpha-2 antagonism becomes more prominent,
paradoxically reducing sedation through increased histamine release.
Q11: Which neurobiological mechanism explains why benzodiazepines have rapid anxiolytic effects but
antidepressants require weeks?
A. Benzodiazepines increase GABA synthesis; antidepressants decrease serotonin metabolism
B. Benzodiazepines allosterically modulate GABA-A receptors immediately; antidepressants require
neuroplasticity and receptor adaptation
C. Benzodiazepines block glutamate receptors; antidepressants stimulate BDNF immediately
D. Benzodiazepines inhibit norepinephrine reuptake; antidepressants modulate gene expression
Correct Answer: B
Rationale: Benzodiazepines produce immediate allosteric potentiation of GABA-A receptor chloride
conductance, while antidepressants require weeks for receptor desensitization, downstream signaling
changes, and neuroplasticity (BDNF, synaptogenesis) to achieve clinical effects.
Q12: The prokinetic effect of low-dose quetiapine and mirtazapine's antiemetic properties are mediated
through which receptor antagonism?
A. D2 receptor
B. 5-HT3 receptor
C. 5-HT2A receptor
D. Muscarinic M1 receptor
Correct Answer: B
Rationale: 5-HT3 receptor antagonism in the gastrointestinal tract and chemoreceptor trigger zone
reduces nausea and vomiting; mirtazapine's potent 5-HT3 blockade explains its antiemetic properties,
while 5-HT3 agonists (e.g., chemotherapy) induce vomiting.
Final Exam ACTUAL EXAM 2026/2027 |
Psychopharmacology NURS 6630 | Verified
Q&A | Pass Guaranteed - A+ Graded
Section 1: Neurobiology & Neurotransmitter Systems (12 questions)
Q1: A patient with depression is started on an SSRI. The therapeutic effect is thought to involve
desensitization of which serotonin autoreceptor over 2-4 weeks?
A. 5-HT2A receptor
B. 5-HT1A autoreceptor
C. 5-HT3 receptor
D. 5-HT7 receptor
Correct Answer: B
Rationale: SSRIs initially increase synaptic serotonin, which stimulates 5-HT1A autoreceptors causing
negative feedback; chronic administration leads to desensitization of these autoreceptors, enhancing
serotonin neurotransmission and correlating with delayed clinical improvement.
Q2: Which neurotransmitter receptor antagonism is primarily responsible for the metabolic side effects
(weight gain, dyslipidemia) observed with second-generation antipsychotics?
A. D2 receptor
B. 5-HT2A receptor
C. Histamine H1 receptor
D. Muscarinic M3 receptor
Correct Answer: C
Rationale: H1 receptor antagonism increases appetite and weight gain; combined with 5-HT2C
antagonism (which affects satiety), these pharmacological properties drive the metabolic syndrome
associated with antipsychotics like olanzapine and clozapine.
Q3: Aripiprazole is classified as a dopamine system stabilizer due to which unique pharmacological
property?
,A. Pure D2 receptor antagonism
B. D2 receptor partial agonism
C. D1 receptor full agonism
D. D3 receptor inverse agonism
Correct Answer: B
Rationale: Aripiprazole acts as a partial agonist at D2 receptors, functioning as an agonist in
hypodopaminergic states (improving negative symptoms) and an antagonist in hyperdopaminergic
states (reducing positive symptoms), thereby stabilizing dopaminergic tone.
Q4: The NMDA receptor antagonist mechanism of ketamine is thought to produce rapid antidepressant
effects through which downstream neurobiological effect?
A. Immediate serotonin release
B. Increased BDNF release and synaptogenesis
C. Direct dopamine receptor stimulation
D. GABA-A receptor potentiation
Correct Answer: B
Rationale: Ketamine's NMDA antagonism triggers glutamate surge activating AMPA receptors, leading
to BDNF release, activation of TrkB receptors, and rapid synaptogenesis in prefrontal cortex, correlating
with its rapid antidepressant effects within hours to days.
Q5: Which receptor binding profile explains bupropion's efficacy for smoking cessation and lower risk of
sexual dysfunction compared to SSRIs?
A. SERT and NET inhibition
B. NET and DAT inhibition
C. 5-HT2A antagonism
D. Alpha-2 antagonism
Correct Answer: B
Rationale: Bupropion inhibits norepinephrine and dopamine reuptake (NDRI) without significant
serotonergic effects; dopaminergic enhancement in the mesolimbic pathway reduces nicotine craving
and withdrawal while preserving sexual function unlike serotonergic agents.
Q6: The therapeutic effect of vortioxetine on cognitive symptoms in depression is attributed to which
receptor activity?
A. 5-HT3 and 5-HT7 antagonism
B. 5-HT1A agonism and 5-HT1B partial agonism
C. SERT inhibition alone
,D. 5-HT2A inverse agonism
Correct Answer: B
Rationale: Vortioxetine's 5-HT1A agonism and 5-HT1B partial agonism enhance acetylcholine and
glutamate release in prefrontal cortex, improving executive function and processing speed independent
of its antidepressant effects.
Q7: Which neurotransmitter system dysfunction is most implicated in the pathophysiology of ADHD?
A. Serotonergic deficiency in the raphe nuclei
B. Dopaminergic and noradrenergic dysregulation in prefrontal cortex and striatum
C. GABAergic hyperactivity in the thalamus
D. Glutamatergic excess in the hippocampus
Correct Answer: B
Rationale: ADHD involves dysregulation of dopamine and norepinephrine circuits in the prefrontal
cortex (executive function) and striatum (reward processing, motor control), explaining the efficacy of
stimulants and norepinephrine reuptake inhibitors.
Q8: The "triptan" medications used for migraine work primarily through which serotonin receptor
agonism?
A. 5-HT1A
B. 5-HT1B and 5-HT1D
C. 5-HT2A
D. 5-HT3
Correct Answer: B
Rationale: Triptans are 5-HT1B/1D receptor agonists; 5-HT1B agonism causes vasoconstriction of cranial
blood vessels while 5-HT1D agonism inhibits trigeminal nerve peptide release and central pain
transmission.
Q9: Which second messenger system is primarily activated by 5-HT2A receptor stimulation?
A. cAMP accumulation
B. Phosphoinositide hydrolysis (IP3/DAG)
C. Ion channel opening
D. Tyrosine kinase activation
Correct Answer: B
Rationale: 5-HT2A receptors are Gq-coupled, activating phospholipase C to hydrolyze
phosphatidylinositol bisphosphate into IP3 (calcium release) and DAG (protein kinase C activation),
distinct from Gi/o-coupled 5-HT1A receptors that inhibit cAMP.
, Q10: The sedating effects of mirtazapine at lower doses (7.5-15mg) are primarily due to antagonism of
which receptor?
A. Alpha-2 adrenergic
B. 5-HT2A
C. Histamine H1
D. 5-HT3
Correct Answer: C
Rationale: Mirtazapine's potent H1 antagonism causes sedation and appetite stimulation; at higher
doses (30-45mg), noradrenergic enhancement via alpha-2 antagonism becomes more prominent,
paradoxically reducing sedation through increased histamine release.
Q11: Which neurobiological mechanism explains why benzodiazepines have rapid anxiolytic effects but
antidepressants require weeks?
A. Benzodiazepines increase GABA synthesis; antidepressants decrease serotonin metabolism
B. Benzodiazepines allosterically modulate GABA-A receptors immediately; antidepressants require
neuroplasticity and receptor adaptation
C. Benzodiazepines block glutamate receptors; antidepressants stimulate BDNF immediately
D. Benzodiazepines inhibit norepinephrine reuptake; antidepressants modulate gene expression
Correct Answer: B
Rationale: Benzodiazepines produce immediate allosteric potentiation of GABA-A receptor chloride
conductance, while antidepressants require weeks for receptor desensitization, downstream signaling
changes, and neuroplasticity (BDNF, synaptogenesis) to achieve clinical effects.
Q12: The prokinetic effect of low-dose quetiapine and mirtazapine's antiemetic properties are mediated
through which receptor antagonism?
A. D2 receptor
B. 5-HT3 receptor
C. 5-HT2A receptor
D. Muscarinic M1 receptor
Correct Answer: B
Rationale: 5-HT3 receptor antagonism in the gastrointestinal tract and chemoreceptor trigger zone
reduces nausea and vomiting; mirtazapine's potent 5-HT3 blockade explains its antiemetic properties,
while 5-HT3 agonists (e.g., chemotherapy) induce vomiting.
