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NSG 552 Exam 2 2026/2027 | Wilkes Psychopharmacology | Complete Review Q&A | Grade A

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Pass the NSG 552 Psychopharmacology Exam 2 at Wilkes University 2026/2027 with this complete review guide of verified questions and answers. This resource contains actual exam-style questions with accurate answers and detailed rationales covering psychopharmacology core concepts—including antidepressants (SSRIs, SNRIs, TCAs, MAOIs), antipsychotics (typical and atypical), mood stabilizers (lithium, anticonvulsants), anxiolytics and hypnotics (benzodiazepines, buspirone), stimulants for ADHD, and medications for substance use disorders. Topics also include pharmacokinetics and pharmacodynamics in psychiatric practice, drug interactions, adverse effect monitoring (serotonin syndrome, neuroleptic malignant syndrome, lithium toxicity, metabolic syndrome, tardive dyskinesia), and evidence-based prescribing for the PMHNP role. Each solution is verified and Grade A to mirror the official Wilkes NSG 552 exam format. With authentic content and our Pass Guarantee, you will ace your NSG 552 Exam 2 with confidence. Download now and excel in Psychopharmacology!

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NSG 552 Exam 2 - Psychopharmacology | Wilkes University | 2026/2027 Edition Page 1




NSG552 / NSG 552 EXAM 2 (LATEST UPDATE):
PSYCHOPHARMACOLOGY | COMPLETE REVIEW WITH
QUESTIONS AND VERIFIED ANSWERS | 100% CORRECT | GRADE
A - WILKES
Wilkes University School of Nursing | Advanced Practice Nursing Graduate Program | NSG 552
Psychopharmacology Course Examination
Wilkes University School of Nursing & Nursing Graduate Program | AACN Essentials of Master's Education Aligned |
Total Questions: 120 | Cognitive Mix: 20% Recall / 50% Application / 30% Analysis



Section 1: Principles of Psychopharmacology | Questions 1-18 | 18
Questions

*Q1: A graduate nursing student is studying cytochrome P450 (CYP) enzymes. Which CYP isoform is
the most abundantly expressed in the human liver and is responsible for metabolizing approximately
50% of clinically used medications, including many antipsychotics, benzodiazepines, and statins?
A. CYP2D6
B. CYP3A4 *[CORRECT]*
C. CYP2C19
D. CYP1A2
Correct Answer: B
Rationale:
CYP3A4 is the most abundant CYP enzyme in the human liver and intestines and handles ~50% of all
clinically used drugs. It metabolizes agents such as alprazolam, quetiapine, ziprasidone, carbamazepine, and
many SSRIs. CYP2D6 handles ~25% of drugs (notably codeine, atomoxetine, paroxetine) but is far less
abundant; CYP2C19 is prominent for clopidogrel, omeprazole, and citalopram; CYP1A2 is best known for
caffeine and clozapine.



*Q2: A 62-year-old patient with bipolar I disorder is prescribed oral lorazepam 1 mg for acute agitation.
The student knows the oral route is subject to first-pass hepatic metabolism. Compared with the
intravenous route, the oral bioavailability of lorazepam is approximately:
A. 10% due to extensive first-pass metabolism
B. 30% due to moderate first-pass metabolism
C. 90% because lorazepam undergoes glucuronidation, not oxidative CYP metabolism
*[CORRECT]*
D. 100% because lorazepam bypasses the portal circulation entirely
Correct Answer: C
Rationale:
Lorazepam is metabolized primarily by glucuronidation (UGT enzymes), which is not significantly impaired by
liver disease or first-pass effects; oral bioavailability is ~90%. Agents like morphine, propranolol, and
lidocaine undergo significant oxidative first-pass metabolism and have low oral bioavailability. Understanding
first-pass effect is critical for route selection and dose conversion in NSG 552 curriculum.




Wilkes University School of Nursing | NSG 552 Advanced Psychopharmacology | AACN Essentials-Aligned

,NSG 552 Exam 2 - Psychopharmacology | Wilkes University | 2026/2027 Edition Page 2




*Q3: A patient with Parkinson's disease is prescribed levodopa-carbidopa rather than dopamine itself.
Which pharmacokinetic principle best explains why dopamine cannot be administered systemically to
treat Parkinson's?
A. Dopamine is rapidly destroyed by gastric acid and never reaches systemic circulation
B. Dopamine does not cross the blood-brain barrier due to its high polarity and large molecular
weight as a charged catecholamine *[CORRECT]*
C. Dopamine undergoes extensive first-pass metabolism yielding toxic metabolites
D. Dopamine is a Schedule II substance and cannot be prescribed outside hospital settings
Correct Answer: B
Rationale:
The blood-brain barrier (BBB) excludes circulating catecholamines such as dopamine, norepinephrine, and
serotonin because they are hydrophilic, charged molecules that lack specific carrier-mediated transport.
Levodopa, an amino acid precursor, crosses the BBB via the large neutral amino acid transporter (LAT1) and
is then decarboxylated to dopamine centrally. Carbidopa blocks peripheral decarboxylation, increasing CNS
availability.



*Q4: P-glycoprotein (P-gp), encoded by the ABCB1 gene, plays a clinically important role in
psychopharmacology. Which statement best describes P-gp's function at the blood-brain barrier?
A. It actively transports drugs from CSF back into brain tissue to enhance CNS effects
B. It is an efflux transporter that pumps certain drugs back into the bloodstream, limiting CNS
penetration *[CORRECT]*
C. It is a CYP450 enzyme responsible for metabolizing lipophilic psychotropics
D. It is a passive ion channel that controls potassium flux at the BBB
Correct Answer: B
Rationale:
P-glycoprotein is an ATP-dependent efflux transporter expressed at the luminal membrane of brain capillary
endothelial cells. It actively transports substrates such as risperidone, olanzapine, and many antidepressants
back into the blood, thereby limiting CNS penetration. P-gp polymorphisms and inhibitors (e.g., verapamil,
quinidine) can alter CNS drug levels and contribute to interindividual variability.




Wilkes University School of Nursing | NSG 552 Advanced Psychopharmacology | AACN Essentials-Aligned

,NSG 552 Exam 2 - Psychopharmacology | Wilkes University | 2026/2027 Edition Page 3




*Q5: A 7-year-old child is prescribed codeine after tonsillectomy. Genetic testing reveals the child is a
CYP2D6 poor metabolizer. What is the most appropriate clinical action based on pharmacogenomic
principles?
A. Increase the codeine dose to compensate for reduced metabolism
B. Switch to morphine because CYP2D6 poor metabolizers cannot convert codeine to morphine
effectively, risking inadequate analgesia *[CORRECT]*
C. Add a CYP2D6 inhibitor to prolong codeine half-life
D. Continue codeine but monitor for signs of opioid toxicity due to accumulation
Correct Answer: B
Rationale:
Codeine is a prodrug requiring CYP2D6 O-demethylation to morphine for analgesia. Poor metabolizers
produce inadequate morphine, leading to therapeutic failure. Conversely, ultrarapid metabolizers can
produce life-threatening morphine toxicity, prompting an FDA Boxed Warning and contraindication of codeine
in children <12 years. The AACN Essentials emphasize pharmacogenomic literacy in advanced nursing
practice.



*Q6: A 45-year-old patient stabilized on clopidogrel for recent stent placement is newly started on
omeprazole for GERD. The APRN should be concerned about which interaction?
A. Omeprazole induces CYP3A4, accelerating clopidogrel activation and increasing bleeding risk
B. Omeprazole inhibits CYP2C19, reducing clopidogrel activation to its active metabolite and
increasing thrombotic risk *[CORRECT]*
C. Omeprazole is a P-gp substrate that displaces clopidogrel from plasma proteins
D. There is no clinically meaningful interaction between these agents
Correct Answer: B
Rationale:
Clopidogrel is a prodrug activated by CYP2C19. Omeprazole, a CYP2C19 inhibitor, reduces active
metabolite formation and increases cardiovascular events. FDA recommends avoiding this combination or
using pantoprazole, which has minimal CYP2C19 inhibition. This scenario illustrates how pharmacogenomic
and drug-interaction knowledge must be integrated when managing complex polypharmacy.



*Q7: A patient on long-term warfarin therapy is started on fluconazole for a fungal infection. Three days
later, the INR rises to 5.2. Which pharmacokinetic mechanism best explains this finding?
A. Fluconazole induces CYP2C9, increasing warfarin clearance
B. Fluconazole is a potent CYP2C9 inhibitor, reducing warfarin metabolism and increasing
anticoagulant effect *[CORRECT]*
C. Fluconazole displaces warfarin from plasma proteins only
D. Fluconazole antagonizes warfarin action at vitamin K epoxide reductase
Correct Answer: B
Rationale:
Warfarin's S-enantiomer is metabolized by CYP2C9. Fluconazole is a potent CYP2C9 inhibitor; concurrent
therapy markedly increases INR and bleeding risk. This is a classic example of CYP-mediated inhibition.
While protein-binding displacement occurs transiently, the sustained INR rise reflects impaired metabolic
clearance. Therapeutic drug monitoring (INR) and dose adjustment are essential in this scenario.




Wilkes University School of Nursing | NSG 552 Advanced Psychopharmacology | AACN Essentials-Aligned

, NSG 552 Exam 2 - Psychopharmacology | Wilkes University | 2026/2027 Edition Page 4




*Q8: Which of the following statements best describes the therapeutic drug monitoring (TDM) of
lithium?
A. Lithium levels are drawn 12 hours post-dose (trough), with a target range of 0.6-1.0 mEq/L for
acute mania and 0.6-0.8 mEq/L for maintenance *[CORRECT]*
B. Lithium levels are drawn 2 hours post-dose (peak), with a target range of 1.5-2.5 mEq/L
C. Lithium levels are not monitored because the drug has a wide therapeutic index
D. Lithium levels are drawn at random times because lithium has a flat concentration-response curve
Correct Answer: A
Rationale:
Lithium has a narrow therapeutic index and requires TDM. Standard practice is a 12-hour post-dose trough
level. Acute mania target is 0.6-1.0 mEq/L (sometimes up to 1.2 mEq/L); maintenance is 0.6-0.8 mEq/L.
Toxicity emerges above 1.5 mEq/L. Levels are obtained twice weekly during initiation and every 3-6 months
once stable. Renal function, thyroid function, and electrolytes must also be monitored.



*Q9: Pharmacodynamics describes the relationship between drug concentration and drug effect. Which
of the following best defines 'affinity' in receptor pharmacology?
A. The maximum effect a drug can produce at full receptor occupancy
B. The strength of binding between a drug and its receptor *[CORRECT]*
C. The dose required to produce 50% of maximal effect (ED50)
D. The ability of a drug to produce a response once bound
Correct Answer: B
Rationale:
Affinity refers to the strength of drug-receptor binding and is reflected in the Kd (dissociation constant); lower
Kd = higher affinity. Efficacy (option A) is the maximum response at full occupancy; potency (option C) is
reflected in ED50; intrinsic activity (option D) describes the ability to produce a response upon binding. A
drug can have high affinity but low intrinsic activity (antagonist) or high affinity and high intrinsic activity (full
agonist).



*Q10: Which signal transduction mechanism is most commonly associated with the actions of typical
antipsychotics and many antidepressants acting at monoamine receptors?
A. Ligand-gated ion channel receptors (e.g., NMDA, GABA-A)
B. G-protein coupled receptors coupled to second messenger systems such as cAMP or IP3/DAG
*[CORRECT]*
C. Intracellular nuclear receptors that alter gene transcription
D. Tyrosine kinase receptors that activate the MAP kinase cascade
Correct Answer: B
Rationale:
Most monoamine neurotransmitter receptors (dopamine D1-D5, serotonin 5-HT1A/2A/2C/6/7,
alpha-adrenergic, muscarinic) are GPCRs that signal through cAMP, IP3/DAG, or inwardly rectifying K+
channels (GIRK). GABA-A and NMDA are ligand-gated ion channels; steroid and thyroid hormones act via
nuclear receptors; insulin and growth factors act through tyrosine kinases. Understanding transduction aids in
predicting onset, duration, and tolerability of psychotropics.




Wilkes University School of Nursing | NSG 552 Advanced Psychopharmacology | AACN Essentials-Aligned

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