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NSG 533 Exam 3 – Wilkes Advanced Pharmacology (2026/2027) Q&A (A+ Guarantee)

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Wilkes NSG 533 Exam 3 Advanced Pharmacology study guide delivers real Q&A with detailed rationales covering endocrine drugs, psychotropic agents, GI pharmacology, and specialty prescribing. What You Will Get: verified practice questions, answer rationales, key concept breakdowns, and exam-focused review for guaranteed success.Wilkes NSG 533 exam 3 questions and answers, NSG 533 advanced pharmacology exam 3 study guide, Wilkes University NSG 533 exam 3 prep, NSG 533 exam 3 practice questions with rationales, advanced pharmacology NSG 533 exam 3 quizlet, NSG 533 exam 3 endocrine drugs questions, Wilkes NSG 533 exam 3 review, NSG 533 pharmacology practice test exam 3, NSG 533 exam 3 answers, Wilkes nursing NSG 533 study guide exam 3, NSG 533 psychotropic drugs quiz, NSG 533 GI pharmacology exam, NSG 533 thyroid and diabetes drugs test, NSG 533 corticosteroid therapy questions, NSG 533 antidepressant drugs exam, NSG 533 antipsychotic pharmacology quiz, Wilkes NSG 533 exam 3 review guide, NSG 533 advanced pharmacology prep exam 3#NSG533 #NSG533Exam3 #WilkesUniversity #WilkesNursing #AdvancedPharmacology #Pharmacology #NPStudent #FNPStudent #GraduateNursing #NursingExamPrep #ExamPrep #StudyGuide

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Wilkes University NSG 533 Exam 3 (pdf) | 2026/2027 |
Advanced Pharmacology Q&A | Nursing
1. What is the primary mechanism of action of ethosuximide in treating absence
seizures?
A) Blockade of voltage-gated sodium channels

B) Inhibition of T-type calcium channels in thalamic neurons

C) Enhancement of GABA-A receptor activity

D) Antagonism of NMDA glutamate receptors

Correct Answer: Inhibition of T-type calcium channels in thalamic neurons

Rationale: Ethosuximide selectively blocks T-type calcium channels in thalamic
neurons, which reduces the abnormal oscillatory activity that generates absence
seizures. Sodium channel blockade is the mechanism of carbamazepine and
phenytoin. GABA enhancement and NMDA antagonism are mechanisms of other
anticonvulsant classes not specific to absence seizures.

2. A patient with newly diagnosed generalized tonic-clonic seizures is being started
on phenytoin. Which pharmacokinetic property of phenytoin requires careful
monitoring?
A) Linear first-order elimination

B) Zero-order kinetics at therapeutic concentrations

C) Renal excretion of unchanged drug

D) Half-life of 4-6 hours

Correct Answer: Zero-order kinetics at therapeutic concentrations

Rationale: Phenytoin follows Michaelis-Menten (saturable) kinetics at therapeutic
concentrations, meaning small dose increases can produce disproportionately large
serum level increases. This nonlinear behavior necessitates therapeutic drug
monitoring to avoid toxicity. It is not primarily excreted unchanged, and its half-life is
longer and dose-dependent.

3. Which antiepileptic drug is associated with metabolic acidosis and
nephrolithiasis as unique adverse effects?
A) Levetiracetam

B) Gabapentin

C) Topiramate

,D) Lamotrigine

Correct Answer: Topiramate

Rationale: Topiramate inhibits carbonic anhydrase in the kidneys, which can cause non-
anion gap metabolic acidosis and promote calcium phosphate kidney stone formation.
Levetiracetam is associated with behavioral changes. Gabapentin binds calcium
channels but does not cause acidosis. Lamotrigine carries a risk of serious rash.

4. A patient on levetiracetam reports new-onset irritability and mood lability. What
is the most appropriate interpretation of these symptoms?
A) An allergic reaction requiring immediate discontinuation

B) A common dose-dependent behavioral adverse effect

C) Evidence of drug-induced psychosis requiring hospitalization

D) An unrelated psychiatric disorder

Correct Answer: A common dose-dependent behavioral adverse effect

Rationale: Levetiracetam is associated with behavioral changes including irritability,
aggression, and mood lability in up to 10-15% of patients. These effects are dose-
dependent and often improve with dose reduction. They do not represent an allergic
reaction or necessarily indicate a primary psychiatric disorder.

5. A patient with epilepsy is being transitioned to lamotrigine. Which titration
strategy is essential to minimize the risk of serious adverse effects?
A) Rapid titration to therapeutic dose within 48 hours

B) Slow titration over several weeks

C) Loading dose followed by maintenance

D) Every-other-day dosing initially

Correct Answer: Slow titration over several weeks

Rationale: Lamotrigine requires slow titration over several weeks to reduce the risk of
Stevens-Johnson syndrome and toxic epidermal necrolysis. Rapid titration significantly
increases this risk. A loading dose approach is not used, and every-other-day dosing is
not a standard strategy for this medication.

6. Which medication is considered first-line for status epilepticus in adults?
A) Oral phenytoin

B) Intravenous lorazepam

C) Oral valproic acid

,D) Intravenous levetiracetam

Correct Answer: Intravenous lorazepam

Rationale: Benzodiazepines, particularly intravenous lorazepam, are the first-line
treatment for status epilepticus due to their rapid onset of action. Phenytoin, valproic
acid, and levetiracetam are second-line agents used if seizures persist after
benzodiazepine administration.

7. What is the mechanism of action of levodopa in Parkinson's disease?
A) Direct stimulation of dopamine receptors

B) Conversion to dopamine in the central nervous system

C) Inhibition of dopamine metabolism

D) Blockade of acetylcholine receptors

Correct Answer: Conversion to dopamine in the central nervous system

Rationale: Levodopa is a dopamine precursor that crosses the blood-brain barrier and is
converted to dopamine by aromatic amino acid decarboxylase, replenishing depleted
dopamine stores. Direct receptor stimulation is the mechanism of dopamine agonists.
Metabolism inhibition is the mechanism of MAO-B and COMT inhibitors.

8. What is the primary role of carbidopa when administered with levodopa?
A) It directly stimulates dopamine receptors

B) It inhibits peripheral dopa decarboxylase

C) It blocks dopamine reuptake

D) It inhibits central MAO-B

Correct Answer: It inhibits peripheral dopa decarboxylase

Rationale: Carbidopa inhibits dopa decarboxylase in the periphery, preventing the
conversion of levodopa to dopamine outside the brain. This increases the amount of
levodopa that reaches the central nervous system and reduces peripheral side effects
like nausea and vomiting. It does not cross the blood-brain barrier.

9. A patient with Parkinson's disease is started on pramipexole. Which adverse
effect class is uniquely associated with dopamine agonists?
A) Dyskinesias

B) Impulse control disorders

C) Hepatotoxicity

D) Hypertensive crisis

, Correct Answer: Impulse control disorders

Rationale: Dopamine agonists such as pramipexole are associated with impulse control
disorders including pathological gambling, hypersexuality, and compulsive shopping.
Dyskinesias are more commonly associated with levodopa therapy. Hepatotoxicity and
hypertensive crisis are not characteristic of this drug class.

10. Which agent is a COMT inhibitor used to prolong the action of levodopa in
Parkinson's disease?
A) Selegiline

B) Amantadine

C) Entacapone

D) Trihexyphenidyl

Correct Answer: Entacapone

Rationale: Entacapone is a catechol-O-methyltransferase (COMT) inhibitor that blocks
peripheral metabolism of levodopa, prolonging its duration of action and reducing "off"
time. Selegiline is an MAO-B inhibitor. Amantadine is used for dyskinesias.
Trihexyphenidyl is an anticholinergic.

11. Which adverse effect is most commonly associated with interferon beta-1a
therapy for multiple sclerosis and often requires premedication?
A) Depression

B) Flu-like symptoms

C) Hepatotoxicity

D) Cardiotoxicity

Correct Answer: Flu-like symptoms

Rationale: Interferon beta-1a commonly causes flu-like symptoms such as fever, chills,
myalgias, and fatigue, particularly at the start of therapy. Premedication with NSAIDs or
acetaminophen and evening dosing can improve tolerability. Depression and
hepatotoxicity are possible but less common.

12. What is the mechanism of action of glatiramer acetate in multiple sclerosis?
A) Depletion of B lymphocytes

B) Blockade of alpha-4 integrin

C) Immunomodulation by altering T-cell function

D) Sphingosine-1-phosphate receptor modulation

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