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Nr 546 Advanced Pharmacology Chamberlain College Of Nursing Week 2026 Plus Rationales| Instant Download

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This study guide covers advanced pharmacology topics including antidepressants, antipsychotics, MAOIs, and neuropathic pain agents. It features multiple-choice questions with correct answers and detailed rationales, helping you understand drug mechanisms, interactions, and clinical applications. Perfect for Chamberlain College of Nursing students preparing for exams in the academic year.

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, Question 1
A patient with treatment-resistant depression is prescribed a drug that
combines serotonin reuptake inhibition with 5-HT1A partial agonism and
5-HT3 antagonism. Which agent's mechanism most closely matches this
profile?
A. Vortioxetine
B. Vilazodone
C. Trazodone
D. Mirtazapine
Correct Answer: B - Vilazodone


RATIONALE
Vilazodone acts as an SSRI plus 5-HT1A partial agonist, enhancing
serotonergic transmission while mitigating sexual dysfunction.
Vortioxetine also modulates multiple 5-HT receptors but is not a
5-HT1A partial agonist. Trazodone is a 5-HT2 antagonist and reuptake
inhibitor, and mirtazapine is an alpha-2 antagonist/5-HT2/3 antagonist
without reuptake inhibition.

Question 2
Which statement best explains why low-potency typical antipsychotics are
more likely to cause anticholinergic delirium than high-potency agents?
A. High-potency agents have greater affinity for muscarinic receptors.
B. Low-potency agents require higher doses, saturating muscarinic
receptors.
C. Low-potency agents have intrinsic anticholinergic activity at
therapeutic doses.
D. High-potency agents induce CYP3A4, reducing anticholinergic
metabolites.
Correct Answer: C - Low-potency agents have intrinsic
anticholinergic activity at therapeutic doses.


Page 2

, RATIONALE
Low-potency phenothiazines (e.g., chlorpromazine) have significant
muscarinic antagonism, causing anticholinergic effects. High-potency
agents (e.g., haloperidol) have minimal muscarinic affinity, so they
cause more extrapyramidal symptoms but less delirium. The other
options misstate receptor pharmacology or metabolic pathways.

Question 3
A patient on chronic MAO-B inhibitor therapy for Parkinson's disease
develops severe hypertension after eating aged cheese. Which mechanism best
explains this hypertensive crisis?
A. Inhibition of peripheral monoamine oxidase A allows tyramine to
displace stored norepinephrine.
B. MAO-B inhibition in the gut increases tyramine absorption, causing
direct alpha-1 agonism.
C. Central MAO-B inhibition increases dopamine, leading to sympathetic
overactivity.
D. Tyramine acts as a direct serotonin agonist at 5-HT2A receptors in the
periphery.
Correct Answer: A - Inhibition of peripheral monoamine oxidase
A allows tyramine to displace stored norepinephrine.


RATIONALE
Selegiline, a selective MAO-B inhibitor, loses selectivity at higher
doses, inhibiting MAO-A in the gut. This allows dietary tyramine to
enter systemic circulation, displacing norepinephrine and triggering
hypertensive crisis. The other options incorrectly describe tyramine's
mechanism or MAO-B's role.




Page 3

, Question 4
Which property of clozapine most directly accounts for its unique efficacy in
treatment-resistant schizophrenia while also necessitating regular ANC
monitoring?
A. High D2 receptor occupancy with rapid dissociation
B. Broad receptor antagonism including 5-HT2A, D4, and muscarinic
receptors
C. Selective D3 receptor partial agonism with low D2 affinity
D. Irreversible inhibition of monoamine oxidase type B
Correct Answer: B - Broad receptor antagonism including
5-HT2A, D4, and muscarinic receptors


RATIONALE
Clozapine's efficacy in treatment-resistant schizophrenia is linked to
its broad receptor profile (5-HT2A, D4, muscarinic, alpha-adrenergic),
but its risk of agranulocytosis requires ANC monitoring. The other
options describe other antipsychotics or incorrect mechanisms.

Question 5
A patient with neuropathic pain is started on duloxetine. Which
neurotransmitter system's dual modulation is primarily responsible for its
analgesic effect?
A. Serotonin and norepinephrine reuptake inhibition in descending pain
pathways
B. GABA-A receptor potentiation and glutamate antagonism
C. Dopamine D2 and mu-opioid receptor agonism
D. Voltage-gated sodium channel blockade and NMDA antagonism
Correct Answer: A - Serotonin and norepinephrine reuptake
inhibition in descending pain pathways




Page 4

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