Psychopharmacology — MCQs

Psychopharmacology Indian Medical PG Practice Questions and MCQs

Question 61: A patient with schizophrenia, who started haloperidol two days ago, presents with complaints of torticollis and orofaciolingual movements. What is the most likely diagnosis?

A. Acute dystonia (Correct Answer)
B. Tardive dyskinesia
C. Parkinsonism
D. Akathisia

Explanation: ### Explanation **1. Why Acute Dystonia is the Correct Answer:** Acute dystonia is an Extrapyramidal Side Effect (EPS) characterized by sudden, involuntary, and sustained muscle contractions. The key to this diagnosis lies in the **timeline** and the **presentation**. * **Timeline:** It is the earliest EPS to appear, typically occurring within **hours to a few days** (90% within the first 5 days) of starting or increasing the dose of a high-potency typical antipsychotic like Haloperidol. * **Presentation:** It commonly involves the neck (**torticollis**), eyes (oculogyric crisis), tongue (protrusion), or back (opisthotonus). The "orofaciolingual movements" in this acute setting represent lingual dystonia. **2. Why Other Options are Incorrect:** * **Tardive Dyskinesia (TD):** While it also involves orofaciolingual movements (e.g., lip-smacking), TD is a **late-onset** complication occurring after **months to years** of treatment. It would not occur two days after starting medication. * **Parkinsonism:** This typically presents within **weeks** (5–30 days) with a triad of tremors, rigidity, and bradykinesia/shuffling gait, rather than acute muscle spasms. * **Akathisia:** This presents as subjective **motor restlessness** (inability to sit still). It usually appears within **days to weeks** (5–60 days). **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Caused by a sudden blockade of D2 receptors in the nigrostriatal pathway, leading to a relative excess of Acetylcholine. * **Risk Factors:** Young males and those receiving high-potency typical antipsychotics (Haloperidol, Fluphenazine) are at highest risk. * **Management:** The drug of choice is an **intravenous or intramuscular anticholinergic** (e.g., **Promethazine**, Benztropine, or Trihexyphenidyl). * **Mnemonic for EPS Timeline:** "**ADAPT**" * **A**cute **D**ystonia (Hours/Days) * **A**kathisia (Days/Weeks) * **P**arkinsonism (Weeks/Months) * **T**ardive Dyskinesia (Months/Years)

Question 62: All of the following are true about antipsychotics except?

A. Haloperidol is a typical antipsychotic.
B. Asenapine can be administered sublingually.
C. The most common extrapyramidal symptom is acute dystonia. (Correct Answer)
D. Clozapine can lead to agranulocytosis.

Explanation: **Explanation:** The correct answer is **C**, as the statement is factually incorrect. While acute dystonia is a dramatic and early-onset extrapyramidal symptom (EPS), it is not the most common. **Akathisia** (a subjective feeling of inner restlessness and inability to sit still) is the **most common EPS** associated with antipsychotic use. **Analysis of Options:** * **Option A:** **Haloperidol** is a high-potency First-Generation Antipsychotic (FGA) or "typical" antipsychotic. It primarily acts via D2 receptor antagonism and has a high propensity for causing EPS. * **Option B:** **Asenapine** is a Second-Generation Antipsychotic (SGA) that has poor oral bioavailability due to extensive first-pass metabolism. Therefore, it is specifically formulated for **sublingual administration** to ensure systemic absorption. * **Option D:** **Clozapine** is the gold standard for treatment-resistant schizophrenia but is notorious for causing **agranulocytosis** (absolute neutrophil count <500/mm³). This necessitates mandatory periodic WBC monitoring (REMS protocol). **High-Yield Clinical Pearls for NEET-PG:** 1. **EPS Timeline:** * *Acute Dystonia:* Hours to days (Earliest; treat with Promethazine/Benztropine). * *Akathisia:* Days to weeks (Most common; treat with Beta-blockers like Propranolol). * *Drug-induced Parkinsonism:* Weeks to months. * *Tardive Dyskinesia:* Months to years (Choreiform movements; switch to Clozapine). 2. **Clozapine Side Effects:** It is the only antipsychotic that reduces suicide risk but carries risks of seizures, myocarditis, and significant weight gain, in addition to agranulocytosis. 3. **Hyperprolactinemia:** Most common with Typical antipsychotics and the atypical drug **Risperidone**.

Question 63: What is the treatment of choice for refractory schizophrenia?

A. Haloperidol
B. Flupenthixol
C. Trifluoperazine
D. Clozapine (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Clozapine** **Why it is the correct answer:** Refractory (treatment-resistant) schizophrenia is defined as a lack of clinical improvement despite at least two adequate trials of different antipsychotic medications (at least one being an atypical antipsychotic) for a duration of 4–6 weeks each. **Clozapine**, an atypical antipsychotic, is the **gold standard and treatment of choice** for this condition. Its unique efficacy is attributed to its complex receptor profile, particularly its low affinity for D2 receptors and high affinity for D4, 5-HT2A, and alpha-adrenergic receptors. It is the only antipsychotic proven to reduce suicidal behavior in schizophrenic patients. **Why the other options are incorrect:** * **A, B, and C (Haloperidol, Flupenthixol, Trifluoperazine):** These are all **First-Generation Antipsychotics (Typical Antipsychotics)**. They work primarily by potent D2 receptor antagonism. While effective for positive symptoms in non-resistant cases, they are associated with a high risk of Extrapyramidal Side Effects (EPS) and are generally not effective once a patient has failed initial antipsychotic therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Agranulocytosis:** The most dreaded side effect of Clozapine (occurs in ~1%). Mandatory **ANC (Absolute Neutrophil Count)** monitoring is required (Weekly for the first 6 months). * **Seizures:** Clozapine causes dose-dependent lowering of the seizure threshold. * **Sialorrhea:** Paradoxical hypersalivation is a common, highly specific side effect. * **Metabolic Syndrome:** Clozapine has the highest risk of weight gain and diabetes among antipsychotics. * **No EPS:** Clozapine has the lowest risk of Extrapyramidal Side Effects and does not cause Tardive Dyskinesia.

Question 64: Tardive dyskinesia is least commonly associated with which of the following drugs?

A. Thioridazine
B. Metoclopramide
C. Thiothixene
D. Clozapine (Correct Answer)

Explanation: **Explanation:** **Tardive Dyskinesia (TD)** is a late-onset extrapyramidal side effect (EPS) characterized by involuntary, choreoathetoid movements, typically involving the tongue, face, and jaw. It is caused by the **upregulation and supersensitivity of Dopamine D2 receptors** in the nigrostriatal pathway following chronic blockade. **Why Clozapine is the correct answer:** Clozapine is an atypical (second-generation) antipsychotic with a unique pharmacological profile. It has a **very low affinity for D2 receptors** and a high affinity for D4 and Serotonin (5-HT2A) receptors. It dissociates rapidly from D2 receptors ("loose binding"), which significantly minimizes the risk of nigrostriatal side effects. Clozapine is the only antipsychotic with a **near-zero risk** of causing TD and is, in fact, the drug of choice for managing patients who have already developed TD. **Analysis of Incorrect Options:** * **Thioridazine (A):** A low-potency typical antipsychotic. While it has some intrinsic anticholinergic activity that lowers acute EPS, it still carries a significant risk of TD with long-term use. * **Metoclopramide (B):** A prokinetic antiemetic that acts as a potent D2 receptor antagonist. It is a notorious non-psychiatric cause of TD, especially in elderly patients. * **Thiothixene (C):** A high-potency typical antipsychotic (thioxanthene class) with strong D2 blockade, making it highly associated with the development of TD. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment of choice for TD:** Valbenazine or Deutetrabenazine (VMAT2 inhibitors). * **Drug of choice for TD in a psychotic patient:** Clozapine. * **Risk Factor:** Long-term use of typical antipsychotics and advancing age. * **Note:** Anticholinergics (like Trihexyphenidyl) **worsen** TD, unlike other EPS.

Question 65: Coarse tremors, dysarthria, and ataxia are side effects of which medication?

A. Lithium (Correct Answer)
B. Haloperidol
C. Imipramine
D. None of the above

Explanation: **Explanation:** The correct answer is **Lithium**. The symptoms described—**coarse tremors, dysarthria (slurred speech), and ataxia (stumbling gait)**—are classic neurological hallmarks of **Lithium Toxicity**. 1. **Why Lithium is correct:** Lithium has a very narrow therapeutic index (0.6–1.2 mEq/L). While *fine* tremors are a common side effect at therapeutic levels, the progression to *coarse* tremors, along with cerebellar signs like ataxia and dysarthria, indicates toxicity (usually levels >1.5–2.0 mEq/L). These symptoms occur because lithium interferes with neurotransmission and can cause reversible or, in severe cases, permanent cerebellar damage (SILENT syndrome). 2. **Why other options are incorrect:** * **Haloperidol:** A typical antipsychotic primarily associated with **Extrapyramidal Side Effects (EPS)** such as acute dystonia, parkinsonism (resting tremors, not coarse), and akathisia. * **Imipramine:** A Tricyclic Antidepressant (TCA) characterized by **anticholinergic side effects** (dry mouth, blurred vision, constipation) and cardiotoxicity (prolonged QTc) in overdose, rather than ataxia and coarse tremors. **High-Yield Clinical Pearls for NEET-PG:** * **Therapeutic Range:** 0.6–1.2 mEq/L (Prophylaxis: 0.6–0.8; Acute Mania: 0.8–1.2). * **Early signs of toxicity:** Nausea, vomiting, and coarse tremors. * **Severe toxicity (>2.5 mEq/L):** Seizures, coma, and death. **Hemodialysis** is the treatment of choice for severe toxicity. * **Drug Interactions:** Thiazides, NSAIDs, and ACE inhibitors increase Lithium levels (decreasing clearance), potentially precipitating toxicity.

Question 66: Which of the following neurotransmitters/factors increases on Electroconvulsive therapy?

A. 5-hydroxy-indole-acetic acid
B. Dopamine
C. Serotonin
D. Brain derived neurotrophic factor (Correct Answer)

Explanation: **Explanation:** **Correct Answer: D. Brain-derived neurotrophic factor (BDNF)** The therapeutic efficacy of Electroconvulsive Therapy (ECT) is increasingly attributed to its **neuroplastic effects**. ECT significantly increases the levels of **Brain-derived neurotrophic factor (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). Chronic depression is associated with hippocampal atrophy and low BDNF levels; ECT reverses this by stimulating BDNF expression, which is considered a primary mechanism for its rapid antidepressant action. **Analysis of Incorrect Options:** * **A. 5-hydroxy-indole-acetic acid (5-HIAA):** This is the primary metabolite of serotonin. Studies show that ECT does not consistently increase 5-HIAA levels in the cerebrospinal fluid. * **B. Dopamine:** While ECT may increase postsynaptic dopamine receptor sensitivity, it does not consistently increase the overall levels of the neurotransmitter itself. * **C. Serotonin:** Similar to antidepressants, ECT modulates the serotonergic system (specifically increasing 5-HT2A receptor sensitivity), but it does not significantly increase the absolute concentration of serotonin. **Clinical Pearls for NEET-PG:** * **Gold Standard:** ECT remains the most effective treatment for **severe treatment-resistant depression** and **catatonia**. * **Mechanism:** The therapeutic effect requires a **generalized tonic-clonic seizure** lasting at least 25–30 seconds. * **Neurobiology:** Beyond BDNF, ECT is known to **decrease** hyperconnectivity in the "Default Mode Network" (DMN) of the brain. * **Contraindications:** There are no absolute contraindications, but **increased intracranial pressure (ICP)** is the most significant relative contraindication due to the risk of herniation.

Question 67: In Direct Electroconvulsive Therapy (ECT), what is the effect on intraocular tension?

A. Increased
B. Decreased (Correct Answer)
C. No change
D. Variable

Explanation: **Explanation:** The correct answer is **B. Decreased**. **1. Why it is correct:** Electroconvulsive Therapy (ECT) induces a generalized tonic-clonic seizure. During the seizure activity, there is a paradoxical and significant **decrease in intraocular pressure (IOP)**. This occurs primarily due to the contraction of extraocular muscles and the subsequent increase in the outflow of aqueous humor through the trabecular meshwork. Additionally, the autonomic changes during the seizure lead to a transient reduction in aqueous production. This makes ECT relatively safe for patients with controlled glaucoma. **2. Why other options are incorrect:** * **A. Increased:** While ECT causes a transient **increase** in heart rate, blood pressure, and **intracranial pressure (ICP)**, it does *not* increase intraocular pressure. Students often confuse the rise in ICP with IOP. * **C & D. No change/Variable:** These are incorrect because the physiological response to the seizure consistently leads to a measurable drop in IOP across clinical studies. **3. High-Yield Clinical Pearls for NEET-PG:** * **Direct vs. Modified ECT:** "Direct" ECT (without muscle relaxants) is rarely practiced today. Modern "Modified" ECT uses **Succinylcholine** (muscle relaxant) and **Thiopental/Propofol** (anesthetic). * **Cardiovascular effects:** The initial response is **Parasympathetic** (bradycardia/hypotension), followed by a more prolonged **Sympathetic** surge (tachycardia/hypertension). * **Absolute Contraindication:** There are no absolute contraindications to ECT, but **Increased Intracranial Pressure (ICP)** is the most significant relative contraindication (due to the risk of herniation). * **Glaucoma:** ECT is **not** contraindicated in glaucoma because it lowers IOP. However, caution is advised if using anticholinergic premedication (like Atropine), which can theoretically increase IOP in narrow-angle glaucoma.

Question 68: When compared to traditional antipsychotic medication, atypical antipsychotic medication is more likely to be helpful for which of the following symptoms?

A. Hallucinations
B. Delusions
C. Agitation
D. Social withdrawal (Correct Answer)

Explanation: ### Explanation The core distinction between traditional (Typical/First-generation) and Atypical (Second-generation) antipsychotics lies in their receptor profiles and their efficacy against the different symptom clusters of schizophrenia. **1. Why "Social Withdrawal" is correct:** Schizophrenia symptoms are categorized into **Positive** (hallucinations, delusions) and **Negative** (social withdrawal, apathy, flattened affect, alogia). * **Typical antipsychotics** (e.g., Haloperidol) primarily act via potent **D2 receptor antagonism** in the mesolimbic pathway, making them highly effective for positive symptoms but often ineffective (or even worsening) for negative symptoms. * **Atypical antipsychotics** (e.g., Olanzapine, Risperidone, Clozapine) provide **5-HT2A (Serotonin) receptor antagonism** in addition to D2 blockade. This serotonergic action increases dopamine release in the prefrontal cortex, which is hypothesized to improve **negative symptoms** like social withdrawal and cognitive deficits. **2. Analysis of Incorrect Options:** * **A & B (Hallucinations and Delusions):** These are "Positive Symptoms." Both typical and atypical antipsychotics are equally effective at treating these. Therefore, atypicals are not "more likely" to be helpful compared to typicals for these specific symptoms. * **C (Agitation):** Acute agitation is often managed effectively (and sometimes more rapidly) with high-potency typical antipsychotics or benzodiazepines. **3. NEET-PG High-Yield Pearls:** * **Mechanism:** Atypicals = "SDAs" (Serotonin-Dopamine Antagonists). They have a lower affinity for D2 receptors and "fast dissociation," leading to fewer Extrapyramidal Side Effects (EPS). * **Negative Symptoms:** Think of the **"5 A's"**: Affective flattening, Alogia, Avolition, Anhedonia, and Asociality (Social withdrawal). * **Drug of Choice:** Clozapine is the gold standard for **treatment-resistant schizophrenia**, but it requires monitoring for agranulocytosis. * **Side Effects:** While atypicals have lower EPS, they are more likely to cause **Metabolic Syndrome** (weight gain, dyslipidemia, diabetes), especially Olanzapine and Clozapine.

Question 69: Which of the following statements is NOT true regarding tricyclic antidepressants?

A. They are safe in bipolar depression as they do not cause a switch to mania. (Correct Answer)
B. They cause sedation.
C. They cause weight gain.
D. They cause giddiness.

Explanation: **Explanation:** **1. Why Option A is the Correct Answer (The "Not True" Statement):** Tricyclic Antidepressants (TCAs) are notorious for having the **highest risk of inducing a "manic switch"** among all antidepressant classes when used in patients with Bipolar Disorder. In Bipolar Depression, TCAs can trigger a rapid transition from a depressive episode to a manic or hypomanic episode. Therefore, they are generally avoided or used with extreme caution (and always with a mood stabilizer) in bipolar patients. Modern antidepressants like SSRIs or Bupropion have a lower risk of this switch compared to TCAs. **2. Why the Other Options are Incorrect (They are True Statements):** * **Option B (Sedation):** TCAs cause significant sedation due to their potent **antihistaminic (H1 receptor) blockade**. This is why drugs like Amitriptyline are often administered at bedtime. * **Option C (Weight Gain):** Weight gain is a common side effect of TCAs, primarily mediated through **H1 receptor antagonism** and 5-HT2C receptor blockade, which increases appetite. * **Option D (Giddiness):** TCAs cause giddiness and orthostatic hypotension due to **alpha-1 adrenergic receptor blockade**. This increases the risk of falls, especially in the elderly. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** TCAs inhibit the reuptake of Serotonin (5-HT) and Norepinephrine (NE). * **The "3 Cs" of Toxicity:** In overdose, TCAs cause **C**oma, **C**onvulsions, and **C**ardiotoxicity (arrhythmias due to sodium channel blockade). * **ECG Finding:** Widening of the QRS complex (>100ms) is a hallmark of TCA toxicity. * **Antidote:** Intravenous **Sodium Bicarbonate** is used to manage TCA-induced cardiotoxicity. * **Anticholinergic Side Effects:** Dry mouth, blurred vision, constipation, and urinary retention (due to M1 receptor blockade).

Question 70: Which medication class is used in the medical treatment of paraphilias?

A. Selective Serotonin Reuptake Inhibitors (SSRIs) (Correct Answer)
B. Benzodiazepines
C. Opioids
D. Barbiturates

Explanation: **Explanation:** The medical management of paraphilic disorders primarily focuses on reducing the intensity of deviant sexual urges and improving impulse control. **Selective Serotonin Reuptake Inhibitors (SSRIs)** are considered a first-line pharmacological intervention for non-dangerous paraphilias. **Why SSRIs are correct:** SSRIs work through two main mechanisms in this context: 1. **Impulse Control:** By increasing synaptic serotonin, they help modulate the frontal cortex, reducing compulsive behaviors and intrusive sexual fantasies. 2. **Side Effect Profile:** A common side effect of SSRIs is decreased libido and delayed ejaculation/orgasm. In the treatment of paraphilias, this "side effect" is utilized therapeutically to dampen sexual drive and arousal. **Why other options are incorrect:** * **Benzodiazepines:** These are GABA-A agonists used for anxiety and insomnia. They have no specific effect on sexual drive and may actually cause disinhibition, potentially worsening paraphilic behaviors. * **Opioids:** These are analgesics. While chronic opioid use can lower testosterone, they are not a standard or indicated treatment for paraphilias due to high addiction potential. * **Barbiturates:** These are CNS depressants used for anesthesia or epilepsy. They do not target the neurobiology of sexual deviance. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-androgens:** For severe or "high-risk" paraphilias, hormonal therapy is used. **Medroxyprogesterone acetate** and **Cyproterone acetate** reduce testosterone levels. * **GnRH Agonists:** Drugs like **Leuprolide** are the most potent hormonal treatments (chemical castration) used for refractory cases. * **Comorbidity:** Paraphilias often co-occur with OCD or Depression; SSRIs are particularly useful in these dual-diagnosis cases. * **Psychotherapy:** Pharmacotherapy is most effective when combined with **Cognitive Behavioral Therapy (CBT)**.

Practice by Chapter

Principles of Psychopharmacology

Practice Questions

Antipsychotic Medications

Practice Questions

Antidepressant Medications

Practice Questions

Mood Stabilizers

Practice Questions

Anxiolytics and Hypnotics

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Stimulants and Cognitive Enhancers

Practice Questions

Pharmacokinetics and Pharmacodynamics

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Drug Interactions

Practice Questions

Adverse Effects and Management

Practice Questions

Pharmacogenomics in Psychiatry

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Special Populations Considerations

Practice Questions

Treatment Algorithms and Guidelines

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