Psychopharmacology Practice Questions

Q: A patient with acute psychosis, who is on haloperidol 20mg/day for the last 2 days, presents with an episode characterized by tongue protrusion, oculogyric crisis, stiffness, and abnormal posture of limbs and trunk without loss of consciousness for 20 minutes. The episode improved within a few minutes after administration of diphenhydramine HCl. What is the most likely diagnosis?

Acute dystonia. ### Explanation **Correct Answer: A. Acute dystonia** **Why it is correct:** Acute dystonia is an Extrapyramidal Side Effect (EPS) characterized by sudden, involuntary muscle spasms. This patient exhibits classic signs: **oculogyric crisis** (upward gaze deviation), **glossospasm** (tongue protrusion), and **torticollis/retrocollis** (abnormal posture). * **Mechanism:** It is caused by a sudden blockade of dopamine (D2) receptors in the nigrostriatal pathway, leading to a relative excess of acetylcholine. * **Timeline:** It typically occurs within hours to **days** (usually <5 days) of starting high-potency antipsychotics like Haloperidol. * **Management:** It is a medical emergency that responds rapidly to **anticholinergics** (e.g., Benztropine, Promethazine) or antihistamines with anticholinergic properties like **Diphenhydramine**. **Why the other options are wrong:** * **B. Akathisia:** Presents as subjective motor restlessness (inability to sit still). It does not involve muscle spasms or abnormal postures. * **C. Tardive dyskinesia:** Occurs after **long-term** (months to years) use of antipsychotics. It presents with choreoathetoid movements (e.g., lip-smacking), not acute sustained spasms. * **D. Neuroleptic malignant syndrome (NMS):** A life-threatening reaction characterized by "lead-pipe" rigidity, high fever, autonomic instability, and altered sensorium. The rapid reversal with diphenhydramine and lack of fever rule this out. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Young males and those receiving high-potency first-generation antipsychotics are at highest risk. * **The "Rule of 4" for EPS Timeline:** * **4 Hours:** Acute Dystonia * **4 Days:** Akathisia (can also occur in weeks) * **4 Weeks:** Parkinsonism * **4 Months:** Tardive Dyskinesia (usually >6 months) * **Drug of Choice:** Intravenous or Intramuscular **Promethazine** or Benztropine.

Q: A patient of schizophrenia treated for 5 years develops perioral movements. What is the likely diagnosis?

Tardive dyskinesia. ### Explanation **Correct Option: A. Tardive dyskinesia** Tardive dyskinesia (TD) is a late-onset extrapyramidal side effect (EPS) resulting from long-term blockade of dopamine (D2) receptors, typically occurring after months or years of antipsychotic use. The underlying pathophysiology is **dopamine receptor supersensitivity** in the nigrostriatal pathway. It characteristically presents as involuntary, choreoathetoid movements, most commonly involving the **orofacial region** (e.g., lip-smacking, tongue protrusion, or perioral tremors—often referred to as "Rabbit Syndrome" in its parkinsonian variant). **Why other options are incorrect:** * **B. Muscular dystonia:** This is an **acute** reaction occurring within hours to days of starting treatment. it involves sustained, painful muscle contractions (e.g., torticollis or oculogyric crisis). * **C. Akathisia:** This refers to a subjective feeling of **inner restlessness** and the inability to sit still. It usually develops within days to weeks of treatment. * **D. Malignant neuroleptic syndrome (NMS):** This is a life-threatening emergency characterized by the "tetrad" of fever, muscular rigidity ("lead-pipe"), autonomic instability, and altered mental status. It is not defined by localized perioral movements. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Old age, female gender, and long-term use of typical (1st generation) antipsychotics. * **Management:** The first step is to **taper/discontinue** the offending agent or switch to **Clozapine** (the antipsychotic with the lowest risk of TD). * **Newer Treatments:** VMAT-2 inhibitors like **Valbenazine** or Deutetrabenazine are now FDA-approved for TD. * **Note:** Unlike other EPS, anticholinergics (like Benztropine) can actually **worsen** tardive dyskinesia.

Q: Which of the following medications is NOT used in the treatment of schizophrenia?

Pemoline. **Explanation:** The treatment of schizophrenia primarily involves **Antipsychotics**, which work by modulating dopaminergic pathways (specifically blocking D2 receptors). **Why Pemoline is the correct answer:** **Pemoline** is a sympathomimetic amine and a central nervous system (CNS) stimulant. It acts by increasing dopamine levels in the synaptic cleft. Because schizophrenia is associated with dopamine overactivity in the mesolimbic pathway, stimulants like Pemoline can actually **exacerbate or induce psychotic symptoms**. Historically, Pemoline was used for ADHD and narcolepsy, but it is not used for schizophrenia. (Note: It has been largely withdrawn globally due to hepatotoxicity). **Why the other options are incorrect:** * **Olanzapine:** An **Atypical (Second-Generation) Antipsychotic**. It blocks both D2 and 5-HT2A receptors and is a first-line treatment for schizophrenia due to its lower risk of extrapyramidal side effects (EPS). * **Sulpiride:** A **Substituted Benzamide** that acts as a selective D2 receptor antagonist. It is used as an antipsychotic, particularly effective in treating the negative symptoms of schizophrenia at lower doses. * **Chlorpromazine:** A **Typical (First-Generation) Antipsychotic** (Low potency). It was the first antipsychotic discovered (1952) and remains a standard treatment for schizophrenia. **High-Yield Clinical Pearls for NEET-PG:** * **Dopamine Hypothesis:** Schizophrenia is linked to *increased* dopamine in the mesolimbic pathway (positive symptoms) and *decreased* dopamine in the mesocortical pathway (negative symptoms). * **Chlorpromazine** is known for causing significant sedation and skin/eye pigmentation (corneal opacities). * **Olanzapine** is highly associated with metabolic syndrome (weight gain, dyslipidemia, and diabetes).

Q: What is the best marker for electroconvulsive therapy?

Brain-derived neurotrophic factor. **Explanation:** The correct answer is **Brain-derived neurotrophic factor (BDNF)**. **Why BDNF is the correct answer:** Electroconvulsive therapy (ECT) is the most effective treatment for severe, treatment-resistant depression. Modern research indicates that the therapeutic efficacy of ECT is closely linked to **neuroplasticity**. ECT significantly increases the expression of BDNF in the hippocampus and prefrontal cortex. BDNF is a protein that promotes the survival of existing neurons and encourages the growth and differentiation of new neurons and synapses (neurogenesis). Studies consistently show that serum BDNF levels rise following a course of ECT, making it the most reliable biological marker for the treatment's clinical response. **Why the other options are incorrect:** * **CSF 5-HIAA (A):** This is a metabolite of serotonin. While low levels of 5-HIAA in the CSF are associated with impulsive behavior and violent suicide attempts, it is not a specific marker for ECT response. * **CSF Serotonin (B):** Serotonin levels in the CSF do not reliably reflect the complex neurobiological changes or the neurotrophic effects induced by ECT. * **CSF Dopamine (D):** While ECT may influence dopaminergic transmission (relevant in treating Parkinson’s disease), dopamine levels are not used as a primary marker for ECT's antidepressant efficacy. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** The "Neurotrophic Hypothesis" (increased BDNF) is currently the most favored theory for ECT's action. * **Most Common Side Effect:** Retrograde amnesia (usually resolves over time). * **Absolute Contraindication:** There are no absolute contraindications, but **increased intracranial pressure (ICP)** is the most significant relative contraindication. * **Gold Standard:** ECT remains the gold standard for **Depressive Stupor** and **Catatonia**.

Q: Which antipsychotic has the least incidence of extrapyramidal symptoms?

Thioridazine. **Explanation:** The incidence of **Extrapyramidal Symptoms (EPS)** in antipsychotics is inversely proportional to the drug's intrinsic **anticholinergic (M1 receptor) activity**. **Why Thioridazine is Correct:** Thioridazine is a low-potency typical antipsychotic. Among the options provided, it possesses the **strongest intrinsic anticholinergic activity**. In the nigrostriatal pathway, dopamine and acetylcholine exist in a reciprocal balance. While antipsychotics block D2 receptors (causing EPS), the potent anticholinergic effect of Thioridazine "re-balances" this system, significantly reducing the risk of motor side effects. Therefore, it has the lowest incidence of EPS among typical antipsychotics. **Analysis of Incorrect Options:** * **Haloperidol:** A high-potency typical antipsychotic with very low anticholinergic activity. It has the **highest risk** of EPS (especially acute dystonia and parkinsonism) among the choices. * **Thiothixene & Perphenazine:** These are high-to-medium potency typical antipsychotics. While they have lower EPS risks than Haloperidol, their anticholinergic profiles are much weaker than Thioridazine, making them more likely to cause movement disorders. **NEET-PG High-Yield Pearls:** * **The "Gold Standard":** If **Clozapine** (an atypical antipsychotic) were an option, it would be the overall correct answer for the "least EPS." * **Thioridazine Side Effects:** While low in EPS, it is high-yield for causing **Retinitis Pigmentosa** (at doses >800mg/day) and **QT interval prolongation** (Torsades de pointes). * **Potency Rule:** Generally, **Low Potency** = High Sedation, High Anticholinergic, Low EPS. **High Potency** = Low Sedation, Low Anticholinergic, High EPS.

Q: Which of the following is not a symptom of neuroleptic malignant syndrome?

Hypothermia. **Explanation:** Neuroleptic Malignant Syndrome (NMS) is a life-threatening idiosyncratic reaction to antipsychotic drugs (neuroleptics), primarily caused by potent dopamine (D2) receptor antagonism in the nigrostriatal pathway and hypothalamus. **Why Hypothermia is the correct answer:** The hallmark of NMS is **Hyperpyrexia (High-grade fever)**, not hypothermia. The blockade of dopamine receptors in the hypothalamus disrupts the body's thermoregulatory set-point, leading to uncontrolled heat production. This is further exacerbated by intense muscle contractions. **Analysis of Incorrect Options:** * **Autonomic dysregulation:** This is a core feature of NMS. Patients typically present with "autonomic instability," including tachycardia, labile blood pressure, profuse diaphoresis (sweating), and tachypnea. * **Muscle rigidity:** Often described as **"Lead-pipe rigidity,"** this is a classic diagnostic sign. It results from dopamine blockade in the basal ganglia and is often accompanied by elevated Creatine Kinase (CK) levels due to muscle breakdown (rhabdomyolysis). * **Catatonia and stupor:** Altered mental status is an early sign of NMS. It ranges from confusion and agitation to catatonic signs, mutism, and eventually stupor or coma. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic (FEVER):** **F**ever, **E**ncephalopathy (altered mental status), **V**itals unstable, **E**levated enzymes (CK), **R**igidity. * **Treatment of Choice:** Immediate discontinuation of the offending agent + Supportive care. Pharmacotherapy includes **Dantrolene** (muscle relaxant) or **Bromocriptine** (dopamine agonist). * **NMS vs. Serotonin Syndrome:** While both have fever and tachycardia, NMS is characterized by **"Lead-pipe" rigidity** and bradyreflexia, whereas Serotonin Syndrome features **hyperreflexia and myoclonus.**

Q: Which of the following is a disadvantage of mirtazapine?

Dyslipidemia. **Explanation:** **Mirtazapine** is a Noradrenergic and Specific Serotonergic Antidepressant (NaSSA). Its unique mechanism involves blocking presynaptic $\alpha_2$-autoreceptors and heteroreceptors, which increases the release of both norepinephrine and serotonin. **Why Dyslipidemia is the correct answer:** Mirtazapine is notorious for causing metabolic side effects. It has a high affinity for **$H_1$ histamine receptors**, which leads to significant sedation and **increased appetite/weight gain**. Clinically, this is frequently associated with an increase in serum cholesterol and triglyceride levels (**dyslipidemia**). Monitoring the lipid profile is recommended for patients on long-term mirtazapine therapy. **Analysis of Incorrect Options:** * **A. Seizures:** While many antidepressants lower the seizure threshold, this is a classic "high-yield" disadvantage associated primarily with **Bupropion** (especially in eating disorders) and **Maprotiline**. * **B. Cheese reaction:** This is a hypertensive crisis caused by the interaction of tyramine-rich foods with **Non-selective MAO inhibitors** (e.g., Phenelzine, Tranylcypromine). Mirtazapine does not inhibit MAO. * **C. Premature ejaculation:** Mirtazapine actually has a **low incidence of sexual dysfunction** because it blocks $5-HT_2$ and $5-HT_3$ receptors. In fact, SSRIs (which cause delayed ejaculation) are used to *treat* premature ejaculation; mirtazapine is often an alternative for patients who cannot tolerate SSRI-induced sexual side effects. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** $\alpha_2$ antagonist + $5-HT_2$ & $5-HT_3$ antagonist. * **The "Sleep & Eat" Drug:** Ideal for elderly depressed patients with insomnia and weight loss. * **Side Effects:** Sedation, weight gain, dyslipidemia, and rarely, **agranulocytosis**. * **Unique Benefit:** It is one of the few antidepressants that does not typically cause nausea (due to $5-HT_3$ blockade).

Question 1

Cardiac conduction defects seen with Tricyclic antidepressants are due to what mechanism?

Accepted Answer

Both norepinephrine reuptake inhibition and antimuscarinic action on the heart

Answer

Norepinephrine and serotonin reuptake inhibition

Answer

Antimuscarinic action on the heart

Answer

Only norepinephrine reuptake inhibition

Question 2

A patient with acute psychosis, who is on haloperidol 20mg/day for the last 2 days, presents with an episode characterized by tongue protrusion, oculogyric crisis, stiffness, and abnormal posture of limbs and trunk without loss of consciousness for 20 minutes. The episode improved within a few minutes after administration of diphenhydramine HCl. What is the most likely diagnosis?

Accepted Answer

Acute dystonia

Answer

Akathisia

Answer

Tardive dyskinesia

Answer

Neuroleptic malignant syndrome

Question 3

A patient of schizophrenia treated for 5 years develops perioral movements. What is the likely diagnosis?

Accepted Answer

Tardive dyskinesia

Answer

Muscular dystonia

Answer

Akathisia

Answer

Malignant neuroleptic syndrome

Question 4

Which of the following medications is NOT used in the treatment of schizophrenia?

Accepted Answer

Pemoline

Answer

Olanzapine

Answer

Sulpiride

Answer

Chlorpromazine

Question 5

Akathisia is characterized by which of the following?

Accepted Answer

Restlessness, a persistent desire to move about, and fidgety or rocking movements.

Answer

Tongue protrusion, stiffness, and abnormal posture of the trunk and limbs.

Answer

Purposeless involuntary facial and limb movements.

Answer

Perioral tremor.

Question 6

Which drug has therapeutic benefit in Schizophrenia?

Accepted Answer

Fluphenazine

Answer

Lithium

Answer

Doxepin

Answer

Imipramine

Question 7

What is the best marker for electroconvulsive therapy?

Accepted Answer

Brain-derived neurotrophic factor

Answer

CSF 5-HIAA

Answer

CSF serotonin

Answer

CSF dopamine

Question 8

Which antipsychotic has the least incidence of extrapyramidal symptoms?

Accepted Answer

Thioridazine

Answer

Haloperidol

Answer

Thiothixene

Answer

Perphenazine

Question 9

Which of the following is not a symptom of neuroleptic malignant syndrome?

Accepted Answer

Hypothermia

Answer

Autonomic dysregulation

Answer

Muscle rigidity

Answer

Catatonia and stupor

Question 10

Which of the following is a disadvantage of mirtazapine?

Accepted Answer

Dyslipidemia

Answer

Seizures

Answer

Cheese reaction

Answer

Premature ejaculation

Psychopharmacology — MCQs

Psychopharmacology — MCQs

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