Psychopharmacology — MCQs
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Cardiac conduction defects seen with Tricyclic antidepressants are due to what mechanism?
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?
A patient of schizophrenia treated for 5 years develops perioral movements. What is the likely diagnosis?
Which of the following medications is NOT used in the treatment of schizophrenia?
Akathisia is characterized by which of the following?
Which drug has therapeutic benefit in Schizophrenia?
What is the best marker for electroconvulsive therapy?
Which antipsychotic has the least incidence of extrapyramidal symptoms?
Which of the following is not a symptom of neuroleptic malignant syndrome?
Which of the following is a disadvantage of mirtazapine?
Psychopharmacology Indian Medical PG Practice Questions and MCQs
Question 31: Cardiac conduction defects seen with Tricyclic antidepressants are due to what mechanism?
- A. Norepinephrine and serotonin reuptake inhibition
- B. Antimuscarinic action on the heart
- C. Only norepinephrine reuptake inhibition
- D. Both norepinephrine reuptake inhibition and antimuscarinic action on the heart (Correct Answer)
Explanation: ### Explanation Tricyclic Antidepressants (TCAs) have a complex pharmacological profile that affects multiple neurotransmitter systems, leading to both therapeutic effects and significant cardiovascular side effects. **Why Option D is Correct:** The cardiac conduction defects associated with TCAs are primarily mediated by two mechanisms: 1. **Norepinephrine Reuptake Inhibition:** By blocking the reuptake of norepinephrine at the synaptic cleft, TCAs increase sympathetic tone. This initially causes tachycardia and can predispose the heart to arrhythmias. 2. **Antimuscarinic (Anticholinergic) Action:** TCAs block M2 receptors in the heart. This inhibits the parasympathetic "braking" effect on the SA node, leading to sinus tachycardia and altered conduction velocity. **Analysis of Incorrect Options:** * **Option A & C:** While serotonin and norepinephrine reuptake inhibition are the primary mechanisms for treating depression, serotonin has a negligible direct effect on cardiac conduction compared to norepinephrine. Focusing "only" on norepinephrine ignores the potent anticholinergic effects that contribute to tachycardia. **High-Yield Clinical Pearls for NEET-PG:** * **The "3 Cs" of TCA Overdose:** **C**oma, **C**onvulsions, and **C**ardiotoxicity. * **Membrane Stabilizing Effect:** In toxic doses, TCAs block **fast sodium channels** (Quinidine-like effect) in the myocardium. This is the most dangerous mechanism, leading to QRS widening (>100ms), PR/QT interval prolongation, and Right Axis Deviation. * **ECG Hallmark:** A wide QRS complex and a prominent R wave in lead aVR are classic signs of TCA toxicity. * **Antidote:** **Sodium Bicarbonate** is the drug of choice for TCA-induced arrhythmias as it increases extracellular sodium and alkalinizes the blood, decreasing the drug's affinity for sodium channels.
Question 32: 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?
- A. Acute dystonia (Correct Answer)
- B. Akathisia
- C. Tardive dyskinesia
- D. Neuroleptic malignant syndrome
Explanation: ### 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.
Question 33: A patient of schizophrenia treated for 5 years develops perioral movements. What is the likely diagnosis?
- A. Tardive dyskinesia (Correct Answer)
- B. Muscular dystonia
- C. Akathisia
- D. Malignant neuroleptic syndrome
Explanation: ### 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.
Question 34: Which of the following medications is NOT used in the treatment of schizophrenia?
- A. Pemoline (Correct Answer)
- B. Olanzapine
- C. Sulpiride
- D. Chlorpromazine
Explanation: **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).
Question 35: Akathisia is characterized by which of the following?
- A. Restlessness, a persistent desire to move about, and fidgety or rocking movements. (Correct Answer)
- B. Tongue protrusion, stiffness, and abnormal posture of the trunk and limbs.
- C. Purposeless involuntary facial and limb movements.
- D. Perioral tremor.
Explanation: **Explanation:** **Akathisia** is the most common Extrapyramidal Side Effect (EPS) associated with antipsychotic medications (especially first-generation antipsychotics). The term is derived from the Greek word for "unable to sit." 1. **Why Option A is Correct:** Akathisia is characterized by a subjective feeling of inner restlessness and an objective need to move. Patients often exhibit "fidgety" behavior, such as pacing, rocking from foot to foot, or crossing and uncrossing their legs. Unlike other movement disorders, it has a significant **psychological component** (the distressing urge to move). 2. **Analysis of Incorrect Options:** * **Option B (Acute Dystonia):** This describes sudden, involuntary muscle contractions causing abnormal postures, such as torticollis (neck twisting) or oculogyric crisis. * **Option C (Tardive Dyskinesia):** This refers to delayed-onset, involuntary choreoathetoid movements, typically involving the face (lip-smacking, tongue protrusion) and limbs, resulting from long-term dopamine blockade. * **Option D (Rabbit Syndrome):** This is a specific, late-onset EPS characterized by fine, rhythmic tremors of the perioral muscles, mimicking a rabbit's chewing motion. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment of Choice:** **Propranolol** (Beta-blocker) is the first-line treatment for Akathisia. Benzodiazepines or anticholinergics (like Benztropine) are second-line. * **Clinical Significance:** Akathisia is highly associated with increased **suicidality** and non-compliance because the sensation is extremely distressing to the patient. * **Timeline:** It typically develops within days to weeks of starting or increasing the dose of an antipsychotic.
Question 36: Which drug has therapeutic benefit in Schizophrenia?
- A. Lithium
- B. Doxepin
- C. Imipramine
- D. Fluphenazine (Correct Answer)
Explanation: **Explanation:** The correct answer is **Fluphenazine**. **1. Why Fluphenazine is correct:** Fluphenazine is a **First-Generation Antipsychotic (FGA)**, specifically belonging to the high-potency **Piperazine** subclass of Phenothiazines. Its primary mechanism of action involves the potent blockade of **Postsynaptic Dopamine D2 receptors** in the mesolimbic pathway, which effectively treats the "positive symptoms" of Schizophrenia (hallucinations and delusions). Because it is high-potency, it is often administered as a long-acting injectable (Decanoate) for patients with poor treatment compliance. **2. Why the other options are incorrect:** * **Lithium (Option A):** This is the gold-standard **Mood Stabilizer**. It is the first-line treatment for Bipolar Affective Disorder (BPAD) and acute mania, but it does not possess primary antipsychotic properties. * **Doxepin (Option B):** This is a **Tricyclic Antidepressant (TCA)**. It is primarily used for depression, anxiety, and insomnia (due to its strong antihistaminic properties). It has no role in treating the core symptoms of Schizophrenia. * **Imipramine (Option C):** This is also a **TCA** (the first one discovered). It is used for Major Depressive Disorder and specifically for **Nocturnal Enuresis** in children. Like Doxepin, it does not treat psychosis. **3. NEET-PG High-Yield Pearls:** * **Potency vs. Side Effects:** High-potency FGAs like Fluphenazine and Haloperidol have a higher risk of **Extrapyramidal Side Effects (EPS)** but a lower risk of sedation and anticholinergic effects compared to low-potency drugs like Chlorpromazine. * **Depot Preparations:** Fluphenazine decanoate is a "Depot" injection, providing therapeutic coverage for 2–4 weeks. * **Drug of Choice:** While FGAs are effective, **Atypical Antipsychotics** (e.g., Risperidone, Olanzapine) are generally preferred first-line today due to lower EPS risk. **Clozapine** remains the drug of choice for *Treatment-Resistant Schizophrenia*.
Question 37: What is the best marker for electroconvulsive therapy?
- A. CSF 5-HIAA
- B. CSF serotonin
- C. Brain-derived neurotrophic factor (Correct Answer)
- D. CSF dopamine
Explanation: **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**.
Question 38: Which antipsychotic has the least incidence of extrapyramidal symptoms?
- A. Haloperidol
- B. Thiothixene
- C. Thioridazine (Correct Answer)
- D. Perphenazine
Explanation: **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.
Question 39: Which of the following is not a symptom of neuroleptic malignant syndrome?
- A. Autonomic dysregulation
- B. Hypothermia (Correct Answer)
- C. Muscle rigidity
- D. Catatonia and stupor
Explanation: **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.**
Question 40: Which of the following is a disadvantage of mirtazapine?
- A. Seizures
- B. Cheese reaction
- C. Dyslipidemia (Correct Answer)
- D. Premature ejaculation
Explanation: **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).
Practice by Chapter
Principles of Psychopharmacology
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Antipsychotic Medications
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Antidepressant Medications
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Mood Stabilizers
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Anxiolytics and Hypnotics
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Stimulants and Cognitive Enhancers
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Pharmacokinetics and Pharmacodynamics
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Drug Interactions
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Adverse Effects and Management
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Pharmacogenomics in Psychiatry
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Special Populations Considerations
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Treatment Algorithms and Guidelines
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