Psychopharmacology — MCQs

A 41-year-old man has been treated with haloperidol for his schizophrenia for the past 15 years. He begins to notice subtle involuntary movements of his hands, feet, lips, and tongue. Since he had been stable for over 1 year, his physician decided to decrease the dose. What would the physician tell the patient about the movement disorder?

Q50Easy

Which of the following is not an anxiolytic agent?

Psychopharmacology Indian Medical PG Practice Questions and MCQs

Question 41: Akathisia is treated by all except?

A. Trihexyphenidyl
B. Diazepam
C. Haloperidol (Correct Answer)
D. Promethazine

Explanation: **Explanation:** **Akathisia** is a common Extrapyramidal Side Effect (EPS) characterized by a subjective feeling of inner restlessness and an objective inability to sit still. **Why Haloperidol is the correct answer:** Haloperidol is a high-potency **Typical Antipsychotic** and a potent **D2 receptor antagonist**. Since akathisia is caused by the blockade of dopamine receptors in the nigrostriatal pathway, administering Haloperidol would **worsen** the condition rather than treat it. It is, in fact, one of the most common culprits behind the development of akathisia. **Analysis of Incorrect Options:** * **Trihexyphenidyl:** This is an anticholinergic agent. While Beta-blockers are the first-line treatment for akathisia, anticholinergics are frequently used as second-line agents to manage EPS. * **Diazepam:** Benzodiazepines are effective in reducing the subjective distress and motor restlessness associated with akathisia, especially when first-line treatments are insufficient. * **Promethazine:** This is an antihistamine with significant anticholinergic properties, making it a viable option for managing antipsychotic-induced movement disorders. **Clinical Pearls for NEET-PG:** 1. **Drug of Choice (DOC):** Propranolol (Beta-blocker) is the first-line treatment for Akathisia. 2. **Most Common EPS:** Akathisia is the most common extrapyramidal side effect of typical antipsychotics. 3. **Differential Diagnosis:** It is often misdiagnosed as worsening psychosis or agitation, leading to a dangerous "vicious cycle" if the antipsychotic dose is increased. 4. **Management Strategy:** The first step is usually to reduce the dose of the offending antipsychotic or switch to a Second Generation Antipsychotic (e.g., Quetiapine).

Question 42: Which of the following is a SARI?

A. Mianserin
B. Milnacipran
C. Clozapine
D. Nefazodone (Correct Answer)

Explanation: **Explanation:** **Nefazodone** is the correct answer because it belongs to the class of **SARIs (Serotonin Antagonist and Reuptake Inhibitors)**. The mechanism of action involves two primary pathways: it potently blocks post-synaptic **5-HT2A receptors** and inhibits the reuptake of serotonin (and to a lesser extent, norepinephrine). By blocking 5-HT2A, SARIs reduce common SSRI-induced side effects like agitation, insomnia, and sexual dysfunction. **Analysis of Incorrect Options:** * **A. Mianserin:** This is a **TeCA (Tetracyclic Antidepressant)**. It acts primarily as an alpha-2 adrenergic antagonist and H1 receptor antagonist, similar to Mirtazapine (NaSSA). * **B. Milnacipran:** This belongs to the **SNRI (Serotonin-Norepinephrine Reuptake Inhibitor)** class, commonly used in the management of fibromyalgia and depression. * **C. Clozapine:** This is an **Atypical Antipsychotic** (SDA - Serotonin-Dopamine Antagonist). While it has complex receptor binding, it is not classified as an antidepressant SARI. **Clinical Pearls for NEET-PG:** * **Trazodone** is the other major SARI. It is frequently used off-label for **insomnia** due to its sedative properties (H1 blockade). * **High-Yield Side Effect:** Nefazodone carries a **Black Box Warning for hepatotoxicity** (liver failure), which has limited its clinical use. * **Priapism:** A rare but classic side effect associated with Trazodone (remember the mnemonic: *"Trazodone causes a Trazo-bone"*). * Unlike SSRIs, SARIs generally do not cause weight gain or significant sexual dysfunction.

Question 43: A patient on haloperidol and clonazepam for psychotic symptoms presents with agitation, requiring both oral and intramuscular administration. The patient subsequently develops fever, rigidity, confusion, elevated CPK, and liver enzymes. What is the probable diagnosis?

A. Neuroleptic malignant syndrome (Correct Answer)
B. Malignant catatonia
C. Serotonin syndrome
D. Gegenhalten

Explanation: **Explanation:** The patient is presenting with the classic tetrad of **Neuroleptic Malignant Syndrome (NMS)**: fever (hyperpyrexia), muscle rigidity ("lead-pipe"), autonomic instability (agitation/tachycardia), and altered mental status (confusion). **Why NMS is the correct answer:** NMS is an idiosyncratic, life-threatening reaction to dopamine antagonists, most commonly **high-potency typical antipsychotics** like **Haloperidol**. The risk increases significantly with high doses or rapid escalation (e.g., combined oral and IM administration). Laboratory findings characteristically show **elevated Creatine Phosphokinase (CPK)** due to rhabdomyolysis from intense muscle rigidity and elevated liver enzymes. **Why the other options are incorrect:** * **Malignant Catatonia:** While it presents similarly with fever and rigidity, it is usually preceded by a prodrome of behavioral psychosis and is often *treated* with benzodiazepines/ECT, whereas NMS is *triggered* by neuroleptics. * **Serotonin Syndrome:** This occurs due to serotonergic agents (SSRIs/MAOIs). While it features fever and agitation, it is clinically distinguished by **hyperreflexia and myoclonus** rather than the "lead-pipe" rigidity seen in NMS. * **Gegenhalten (Paratonia):** This is a form of rigidity where the patient involuntarily resists passive movement in proportion to the force applied. It is associated with frontal lobe damage or dementia, not systemic symptoms like fever or elevated CPK. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for NMS (FEVER):** **F**ever, **E**ncephalopathy, **V**itals unstable, **E**levated enzymes (CPK), **R**igidity. * **Treatment of Choice:** Immediate discontinuation of the offending agent, supportive care, and pharmacotherapy with **Dantrolene** (muscle relaxant) or **Bromocriptine** (dopamine agonist). * **Key Lab:** Elevated CPK is the most sensitive laboratory indicator.

Question 44: A patient on antipsychotics presents with restlessness, an irresistible urge to move, and an inability to sit or stand in one position. What is the most likely diagnosis?

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

Explanation: **Explanation:** The patient is presenting with the classic triad of **Akathisia**: subjective restlessness, an irresistible urge to move, and objective motor hyperactivity (pacing, shifting weight, or inability to sit still). It is the most common Extrapyramidal Side Effect (EPS) associated with antipsychotics, particularly high-potency first-generation agents. **Why the other options are incorrect:** * **Acute Dystonia:** Characterized by sudden, involuntary, sustained muscle contractions (e.g., torticollis, oculogyric crisis). It usually occurs within hours to days of starting treatment, whereas akathisia typically appears within days to weeks. * **Tardive Dyskinesia:** A late-onset complication (months to years) involving involuntary choreoathetoid movements, most commonly orofacial (lip-smacking, tongue protrusion). Unlike akathisia, these movements are involuntary and the patient may be unaware of them. * **Rabbit Syndrome:** A rare, late-onset EPS characterized by fine, rhythmic tremors of the perioral muscles (mimicking a chewing rabbit). It does not involve generalized restlessness. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Result of dopamine (D2) blockade in the nigrostriatal pathway. * **Management:** The drug of choice for Akathisia is **Propranolol** (Beta-blocker). Centrally acting anticholinergics (e.g., Benztropine) or Benzodiazepines are second-line. * **Clinical Significance:** Akathisia is highly distressing and is a major cause of non-compliance and increased suicide risk in patients on antipsychotics. * **Rule of Thumb (Timing of EPS):** **A**cute Dystonia (4 hours) > **A**kathisia (4 days) > **P**arkinsonism (4 weeks) > **T**ardive Dyskinesia (4 months/years). *Mnemonic: ADAPT.*

Question 45: A patient on antipsychotics for 3 weeks presents with high-grade fever, elevated CPK, and myoglobinuria. What is the most probable diagnosis?

A. Neuroleptic malignant syndrome (Correct Answer)
B. Tardive dyskinesia
C. Acute dystonia
D. Akathisia

Explanation: ### Explanation **Neuroleptic Malignant Syndrome (NMS)** is a rare but life-threatening idiosyncratic reaction to antipsychotic medications (neuroleptics). The clinical presentation in this patient—**high-grade fever (hyperpyrexia)**, **elevated Creatine Phosphokinase (CPK)**, and **myoglobinuria**—is the classic triad of NMS. * **Why Option A is correct:** NMS is caused by potent dopamine (D2) receptor blockade in the nigrostriatal pathway and hypothalamus. This leads to severe "lead-pipe" muscle rigidity, which causes muscle breakdown (rhabdomyolysis), resulting in elevated CPK levels and myoglobinuria (which can lead to renal failure). Autonomic instability and altered mental status are also hallmark features. * **Why other options are incorrect:** * **Tardive Dyskinesia:** A late-onset (months to years) extrapyramidal side effect characterized by involuntary choreoathetoid movements, typically of the tongue and face. It does not present with fever or elevated CPK. * **Acute Dystonia:** An early-onset reaction (hours to days) involving sudden, sustained muscle contractions (e.g., torticollis, oculogyric crisis). It lacks systemic symptoms like fever. * **Akathisia:** A subjective feeling of inner restlessness and an inability to sit still. It is the most common extrapyramidal side effect but does not cause lab abnormalities or hyperpyrexia. **High-Yield NEET-PG Pearls:** * **Treatment of NMS:** Immediate discontinuation of the offending drug, aggressive cooling, and pharmacological intervention with **Dantrolene** (muscle relaxant) or **Bromocriptine** (dopamine agonist). * **NMS vs. Serotonin Syndrome:** Both have fever and autonomic instability, but NMS is characterized by **"Lead-pipe rigidity"** and bradyreflexia, whereas Serotonin Syndrome presents with **hyperreflexia and myoclonus.** * **Risk Factor:** High-potency first-generation antipsychotics (e.g., Haloperidol) are most commonly implicated.

Question 46: Which of the following SSRIs is used in the management of pathological emotions?

A. Escitalopram (Correct Answer)
B. Paroxetine
C. Clomipramine
D. Fluoxetine

Explanation: **Explanation:** **Pathological emotions**, also known as **Pseudobulbar Affect (PBA)** or emotional lability, is a clinical condition characterized by involuntary, sudden, and inappropriate episodes of laughing or crying. It is commonly seen in neurological disorders like Amyotrophic Lateral Sclerosis (ALS), Multiple Sclerosis (MS), and post-stroke states. **1. Why Escitalopram is correct:** Selective Serotonin Reuptake Inhibitors (SSRIs) are the first-line pharmacological treatment for pathological emotions. Among the options provided, **Escitalopram** is specifically documented and frequently utilized in clinical practice for this indication due to its high selectivity for the serotonin transporter and its favorable side-effect profile in neurologically compromised patients. It helps stabilize the emotional threshold, reducing the frequency and severity of outbursts. **2. Analysis of Incorrect Options:** * **Paroxetine:** While an SSRI, it is generally avoided in patients with neurological comorbidities due to its mild anticholinergic effects and higher risk of withdrawal symptoms. * **Clomipramine:** This is a **Tricyclic Antidepressant (TCA)**, not an SSRI. While TCAs can be used for PBA, they are second-line due to significant side effects (sedation, arrhythmias, and anticholinergic toxicity). * **Fluoxetine:** Although an SSRI, its long half-life and active metabolites make it less ideal for rapid titration in the elderly or neurologically ill compared to Escitalopram. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for PBA:** Traditionally, the combination of **Dextromethorphan and Quinidine** (Nuedexta) is the only FDA-approved specific treatment. However, among antidepressants, SSRIs (like Escitalopram) are the standard of care. * **Escitalopram** is the S-enantiomer of Citalopram and is considered the most "selective" SSRI. * **Pathological emotions** result from a "disconnection syndrome" involving the prefrontal cortex and the cerebellum/brainstem.

Question 47: Which of the following conditions is characterized by twisting and protrusion of the tongue, and chewing of the lips?

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

Explanation: **Explanation:** The clinical presentation of twisting and protrusion of the tongue (fly-catcher’s tongue) and repetitive chewing movements of the lips (bucco-linguo-masticatory movements) is a classic description of **Tardive Dyskinesia (TD)**. **1. Why Tardive Dyskinesia is correct:** TD is a delayed-onset extrapyramidal side effect (EPS) resulting from long-term blockade of dopamine (D2) receptors by antipsychotics. The underlying pathophysiology is **dopamine receptor supersensitivity** in the nigrostriatal pathway. It is characterized by involuntary, choreoathetoid movements, most commonly affecting the face, mouth, and tongue. **2. Why other options are incorrect:** * **Acute Akathisia:** Presents as subjective motor restlessness (e.g., inability to sit still, pacing). It does not involve involuntary orofacial movements. * **Acute Dystonia:** Characterized by sudden, sustained, and painful muscle contractions (e.g., torticollis, oculogyric crisis). It typically occurs within hours to days of starting medication, unlike the delayed onset of TD. * **Chronic Dystonia:** While persistent, dystonia involves sustained posturing rather than the rhythmic, repetitive "chewing" or "twisting" movements seen in dyskinesia. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Old age, female gender, and long-term use of typical antipsychotics (e.g., Haloperidol). * **Management:** The first step is to **taper/discontinue** the offending agent or switch to **Clozapine** (the antipsychotic with the lowest risk of TD). * **Specific Treatments:** VMAT-2 inhibitors like **Valbenazine** or **Deutetrabenazine** are FDA-approved for TD. * **Warning:** Anticholinergics (like Trihexyphenidyl) **worsen** Tardive Dyskinesia, whereas they help in Acute Dystonia.

Question 48: Weight gain caused by antipsychotics is due to antagonism of which receptor subtype?

A. 5-HT3
B. 5-HT2A
C. 5-HT2B
D. 5-HT2C (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. 5-HT2C**. **Mechanism of Weight Gain:** Antipsychotic-induced weight gain is a complex metabolic side effect primarily mediated by the antagonism of two specific receptors: **5-HT2C (Serotonin 2C)** and **H1 (Histamine 1)**. * **5-HT2C receptors** are located in the hypothalamus and play a crucial role in regulating satiety and energy homeostasis. When these receptors are blocked, the "satiety signal" is inhibited, leading to hyperphagia (increased appetite) and subsequent weight gain. * **H1 antagonism** further exacerbates this by causing sedation and increasing cravings for high-calorie carbohydrates. **Analysis of Incorrect Options:** * **A. 5-HT3:** These receptors are primarily involved in the emetic reflex (nausea/vomiting). Antagonists (like Ondansetron) are used as anti-emetics, not associated with metabolic changes. * **B. 5-HT2A:** Antagonism of 5-HT2A is the hallmark of Second Generation (Atypical) Antipsychotics. It helps reduce Extrapyramidal Side Effects (EPS) and improves negative symptoms, but it is not the primary driver of weight gain. * **C. 5-HT2B:** These receptors are mainly found in the heart and GI tract. Agonism of 5-HT2B is associated with cardiac valvulopathy (e.g., with Fenfluramine). **High-Yield Clinical Pearls for NEET-PG:** * **Highest Risk of Weight Gain/Metabolic Syndrome:** Clozapine (most potent) > Olanzapine. * **Lowest Risk/Weight Neutral:** Ziprasidone, Aripiprazole, and Lurasidone. * **Monitoring:** Patients on Atypical Antipsychotics must have regular monitoring of BMI, waist circumference, fasting blood glucose, and lipid profile (Metabolic Monitoring). * **Management:** Metformin is often the first-line pharmacological intervention for antipsychotic-induced weight gain.

Question 49: A 41-year-old man has been treated with haloperidol for his schizophrenia for the past 15 years. He begins to notice subtle involuntary movements of his hands, feet, lips, and tongue. Since he had been stable for over 1 year, his physician decided to decrease the dose. What would the physician tell the patient about the movement disorder?

A. It will disappear as soon as the medication is decreased.
B. It will increase initially as the medication is decreased. (Correct Answer)
C. It will remain unchanged.
D. It will disappear in his hands but not his feet as soon as the medication is decreased.

Explanation: **Explanation:** The patient is presenting with **Tardive Dyskinesia (TD)**, a late-onset extrapyramidal side effect caused by long-term use of first-generation antipsychotics like Haloperidol. **Why Option B is correct:** The underlying pathophysiology of TD involves **dopamine receptor supersensitivity**. Chronic blockade of $D_2$ receptors by haloperidol leads to an upregulation (increase in number and sensitivity) of these receptors in the nigrostriatal pathway. When the antipsychotic dose is decreased or discontinued, the "masking" effect of the drug is removed. This allows dopamine to act on these supersensitive receptors, which paradoxically **worsens or unmasks** the involuntary movements initially. This phenomenon is sometimes referred to as "withdrawal dyskinesia." **Why other options are incorrect:** * **Option A & D:** These are incorrect because decreasing the dose does not lead to immediate disappearance. In fact, symptoms often persist for months or may become permanent (irreversible) in many patients. * **Option C:** The movements rarely remain unchanged; they typically fluctuate in intensity following dosage adjustments due to the change in receptor occupancy. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Old age, female gender, and long-term use of typical antipsychotics. * **Clinical Feature:** Characterized by orofacial dyskinesia (tongue protrusion, lip-smacking, chewing) and choreoathetoid movements of limbs. * **Management:** 1. Prevention is key (use lowest effective dose). 2. Switch to **Clozapine** (the antipsychotic with the lowest risk of TD). 3. **VMAT-2 inhibitors** (e.g., Valbenazine, Deutetrabenazine) are now the first-line FDA-approved treatments for TD. * **Note:** Anticholinergics (like Trihexyphenidyl) **worsen** Tardive Dyskinesia, unlike other extrapyramidal symptoms.

Question 50: Which of the following is not an anxiolytic agent?

A. Risperidone (Correct Answer)
B. SSRI
C. Clonazepam
D. Buspirone

Explanation: **Explanation:** The core of this question lies in distinguishing between drugs that primarily treat psychosis versus those that manage anxiety disorders. **1. Why Risperidone is the Correct Answer:** **Risperidone** is a **Second-Generation (Atypical) Antipsychotic**. Its primary mechanism involves potent antagonism of Dopamine (D2) and Serotonin (5-HT2A) receptors. It is indicated for Schizophrenia, Bipolar Disorder, and irritability in Autism. While it may have secondary calming effects, it is not classified as an anxiolytic agent. **2. Analysis of Incorrect Options:** * **SSRI (Selective Serotonin Reuptake Inhibitors):** These are currently the **first-line pharmacological treatment** for most chronic anxiety disorders, including Panic Disorder, GAD, and Social Anxiety Disorder. * **Clonazepam:** This is a **Benzodiazepine** (BZD). BZDs act as GABA-A receptor agonists, providing rapid relief of acute anxiety symptoms. They are the most commonly used "classical" anxiolytics. * **Buspirone:** This is a **non-benzodiazepine anxiolytic** that acts as a partial agonist at the **5-HT1A receptor**. It is specifically used for Generalized Anxiety Disorder (GAD) and lacks the sedative or addictive potential of BZDs. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC) for GAD:** SSRIs (Long-term); Benzodiazepines (Short-term/Acute). * **Buspirone** takes 2–4 weeks to show anxiolytic effects; it is ineffective for "as-needed" (PRN) use. * **Propranolol** (Beta-blocker) is the drug of choice for **Performance Anxiety** (Stage fright). * **Antidote for Benzodiazepine overdose:** Flumazenil (Competitive antagonist).

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Principles of Psychopharmacology

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Antipsychotic 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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