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NSG 552 Psychopharmacology Exam 2026–2027 | 300
Case-Based Questions & Answers with Rationales
1. Explain the dopamine hypothesis of schizophrenia and identify which
pathway is primarily responsible for positive symptoms.
Answer:
The dopamine hypothesis proposes that schizophrenia involves dysregulated dopamine
transmission. Hyperactivity in the mesolimbic pathway produces positive symptoms
(hallucinations, delusions).
Rationale:
Antipsychotics reduce positive symptoms by blocking D2 receptors in the mesolimbic tract.
However, dopamine blockade in other pathways produces side effects (EPS, prolactin elevation).
2. A patient on haloperidol develops muscle rigidity and tremor. Identify the
mechanism and treatment.
Answer:
Mechanism: Dopamine D2 blockade in the nigrostriatal pathway, leading to extrapyramidal
symptoms (drug-induced parkinsonism).
Treatment: Anticholinergic agents such as benztropine or diphenhydramine.
Rationale:
Dopamine normally balances acetylcholine in the basal ganglia. Blocking dopamine allows
acetylcholine to dominate, causing rigidity and tremor.
3. Describe the pathophysiology of serotonin syndrome.
Answer:
Serotonin syndrome results from excessive serotonergic activity in the CNS, typically from
combining serotonergic agents.
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Clinical triad:
• Mental status changes
• Autonomic instability
• Neuromuscular hyperactivity
Rationale:
Excess serotonin overstimulates 5-HT receptors, especially 5-HT1A and 5-HT2A.
4. A patient on lithium develops vomiting, ataxia, and confusion. What level
suggests severe toxicity and why does dehydration worsen toxicity?
Answer:
Levels above approximately 2.0 mEq/L indicate severe toxicity.
Dehydration reduces renal perfusion, decreasing lithium clearance, leading to accumulation.
Rationale:
Lithium is excreted renally and competes with sodium reabsorption.
5. Explain why MAOIs require dietary restrictions.
Answer:
MAOIs inhibit monoamine oxidase, preventing breakdown of tyramine.
Tyramine ingestion leads to massive norepinephrine release, causing hypertensive crisis.
Rationale:
Tyramine-rich foods bypass metabolism when MAO is blocked.
6. Describe the difference between first-generation and second-generation
antipsychotics in receptor activity.
Answer:
First-generation: Strong D2 antagonism.
Second-generation: Moderate D2 blockade plus significant 5-HT2A antagonism.
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Rationale:
Serotonin antagonism in atypicals reduces EPS risk.
7. Identify the mechanism behind antipsychotic-induced hyperprolactinemia.
Answer:
Dopamine blockade in the tuberoinfundibular pathway removes inhibition of prolactin
release.
Rationale:
Dopamine suppresses prolactin under normal conditions.
8. Why does bupropion have lower sexual side effects than SSRIs?
Answer:
Bupropion primarily increases norepinephrine and dopamine without significant serotonin
reuptake inhibition.
Rationale:
Sexual dysfunction is linked to excess serotonergic activity.
9. Explain why tricyclic antidepressants are dangerous in overdose.
Answer:
They block cardiac sodium channels, causing arrhythmias, and have strong anticholinergic and
antihistaminic effects.
Rationale:
Cardiac toxicity is the primary lethal risk.
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10. Describe neuroleptic malignant syndrome and its mechanism.
Answer:
A life-threatening reaction to dopamine blockade characterized by hyperthermia, rigidity,
autonomic instability, and elevated CK.
Mechanism:
Sudden severe dopamine suppression in CNS.
11. Why is fluoxetine less likely to cause discontinuation syndrome?
Answer:
It has a long half-life and active metabolites, leading to gradual decline in plasma levels.
12. Explain how benzodiazepines enhance GABA function.
Answer:
They increase the frequency of chloride channel opening at GABA-A receptors.
Rationale:
This enhances inhibitory neurotransmission.
13. Why must lamotrigine be titrated slowly?
Answer:
Rapid titration increases risk of Stevens-Johnson syndrome.
14. Which mood stabilizer has proven anti-suicidal benefit and why is this
clinically significant?
Answer:
Lithium.
It significantly reduces suicide risk in bipolar disorder.