Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 141: Which of the following drugs is NOT associated with malignant neuroleptic syndrome?

A. Haloperidol
B. Metoclopramide
C. Domperidone
D. Amantadine (Correct Answer)

Explanation: ### Explanation **Neuroleptic Malignant Syndrome (NMS)** is a life-threatening idiosyncratic reaction characterized by the "FEVER" mnemonic: **F**ever, **E**ncephalopathy (altered mental status), **V**itals instability, **E**levated enzymes (CK), and **R**igidity ("lead-pipe"). #### Why Amantadine is the Correct Answer The underlying pathophysiology of NMS is a **profound deficiency of dopamine** in the central nervous system. * **Amantadine** is a dopaminergic agent (it increases dopamine release and inhibits reuptake). Therefore, it does **not** cause NMS. * **Crucial Concept:** While Amantadine doesn't cause NMS, the **abrupt withdrawal** of Amantadine (or Levodopa) in Parkinson’s patients can trigger a "Neuroleptic Malignant-like Syndrome" because it causes a sudden drop in dopamine levels. #### Why the Other Options are Incorrect NMS is primarily caused by **D2 receptor antagonism**. * **Haloperidol (Option A):** A high-potency typical antipsychotic and the most common culprit associated with NMS. * **Metoclopramide (Option B):** Though used as an antiemetic/prokinetic, it is a central D2 antagonist and is a well-documented cause of NMS. * **Domperidone (Option C):** While it primarily acts peripherally, it can cross the blood-brain barrier in small amounts (especially at high doses or in vulnerable patients), and cases of NMS have been reported. #### NEET-PG High-Yield Pearls 1. **Drug of Choice for NMS:** **Dantrolene** (a muscle relaxant that inhibits calcium release from the sarcoplasmic reticulum) or **Bromocriptine** (a D2 agonist). 2. **Distinction:** Unlike Serotonin Syndrome (which presents with hyperreflexia and myoclonus), NMS is characterized by **"Lead-pipe" rigidity** and bradyreflexia. 3. **Risk Factors:** Rapid dose escalation of antipsychotics, use of depot preparations, and dehydration.

Question 142: A person taking tricyclic antidepressants presents with blurred vision and dry mouth. These adverse effects result due to blockade of which receptors?

A. M3 muscarinic receptors (Correct Answer)
B. GABAA receptors
C. H1 histamine receptors
D. 5HT2 receptors

Explanation: **Explanation:** Tricyclic Antidepressants (TCAs), such as Amitriptyline and Imipramine, are known for their "dirty drug" profile, meaning they interact with multiple receptor systems beyond serotonin and norepinephrine reuptake inhibition. **1. Why Option A is Correct:** The symptoms of **blurred vision** (due to cycloplegia/mydriasis) and **dry mouth** (xerostomia) are classic **anticholinergic side effects**. TCAs act as competitive antagonists at muscarinic receptors. Specifically, the **M3 muscarinic receptors** are located on exocrine glands (salivary) and the ciliary/sphincter pupillae muscles of the eye. Blockade of these receptors inhibits parasympathetic signaling, leading to decreased secretions and loss of accommodation. **2. Why the Other Options are Incorrect:** * **Option B (GABA$_A$ receptors):** TCAs do not typically block GABA receptors. In overdose, TCAs actually inhibit GABAergic transmission (specifically at the chloride channel), which contributes to seizures, but this is not responsible for dry mouth or blurred vision. * **Option C (H$_1$ receptors):** Blockade of H$_1$ histamine receptors by TCAs results in **sedation** and **weight gain**, not anticholinergic symptoms. * **Option D (5HT$_2$ receptors):** While some TCAs have affinity for serotonin receptors, blockade here is often associated with antidepressant/anxiolytic effects or changes in sleep architecture, not autonomic side effects like dry mouth. **High-Yield Clinical Pearls for NEET-PG:** * **The "3 Cs" of TCA Toxicity:** Coma, Convulsions, and Cardiotoxicity (Arrhythmias due to Na+ channel blockade). * **Contraindication:** Due to their M3 blocking effects, TCAs are contraindicated in patients with **Narrow-Angle Glaucoma** and **Benign Prostatic Hyperplasia (BPH)**. * **Antidote:** Sodium bicarbonate is used to manage the cardiotoxicity (QRS widening) seen in TCA overdose.

Question 143: Which among the following are antipsychotics?

A. Resperidone
B. Lurasidone
C. Asenapine
D. All of the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. All of the above**. All three drugs listed belong to the class of **Atypical Antipsychotics** (Second-Generation Antipsychotics or SGAs). Unlike typical antipsychotics (e.g., Haloperidol), which primarily block Dopamine D2 receptors, atypical antipsychotics work by blocking both **D2 receptors and Serotonin (5-HT2A) receptors**. This dual mechanism helps in treating both the positive symptoms (hallucinations, delusions) and negative symptoms (social withdrawal, apathy) of schizophrenia while significantly reducing the risk of Extrapyramidal Side Effects (EPS). * **Risperidone:** A potent D2 and 5-HT2A antagonist. It is widely used but has a higher tendency to cause **hyperprolactinemia** compared to other atypicals. * **Lurasidone:** A newer SGA with high affinity for 5-HT7 receptors. It is notably used for **Bipolar Depression** and has a favorable metabolic profile (minimal weight gain). * **Asenapine:** Unique for its **sublingual administration** (due to high first-pass metabolism). It is used for schizophrenia and acute mania. **Clinical Pearls for NEET-PG:** 1. **Clozapine** is the "Gold Standard" for treatment-resistant schizophrenia but requires monitoring for **agranulocytosis**. 2. **Olanzapine** and **Clozapine** carry the highest risk of metabolic syndrome (weight gain, dyslipidemia, diabetes). 3. **Ziprasidone** is most notorious for **QT interval prolongation**. 4. **Aripiprazole** is a **partial D2 agonist**, often referred to as a "dopamine stabilizer."

Question 144: Escitalopram is a:

A. Selective serotonin reuptake inhibitor. (Correct Answer)
B. Nonspecific norepinephrine uptake inhibitor.
C. Atypical antidepressant.
D. MAO inhibitor.

Explanation: **Explanation:** **Escitalopram** is the S-enantiomer of citalopram and is classified as a **Selective Serotonin Reuptake Inhibitor (SSRI)**. It works by specifically inhibiting the serotonin transporter (SERT) at the presynaptic terminal, thereby increasing the concentration of serotonin (5-HT) in the synaptic cleft. It is considered the most "selective" of all SSRIs, with minimal effect on norepinephrine or dopamine reuptake. **Analysis of Options:** * **Option A (Correct):** Escitalopram belongs to the SSRI class (alongside Fluoxetine, Sertraline, Paroxetine, and Fluvoxamine). It is the first-line treatment for Major Depressive Disorder and Generalized Anxiety Disorder due to its high efficacy and favorable side-effect profile. * **Option B (Incorrect):** Nonspecific norepinephrine uptake inhibitors include Tricyclic Antidepressants (TCAs) like Amitriptyline or SNRIs like Venlafaxine (which affects both 5-HT and NE). * **Option C (Incorrect):** Atypical antidepressants include drugs with unique mechanisms, such as Bupropion (NDRI), Mirtazapine (α2-antagonist), or Trazodone (SARI). * **Option D (Incorrect):** MAO inhibitors (e.g., Phenelzine, Selegiline, Moclobemide) inhibit the enzyme monoamine oxidase rather than blocking reuptake transporters. **NEET-PG High-Yield Pearls:** * **Selectivity:** Escitalopram is the most potent and selective SSRI. * **Side Effects:** Common side effects include GI upset and sexual dysfunction (delayed ejaculation). It has a lower risk of drug-drug interactions compared to Fluoxetine. * **Drug of Choice:** SSRIs are the first-line treatment for Depression, OCD, Panic Disorder, Social Phobia, and PTSD. * **Safety:** They are preferred over TCAs because they lack anticholinergic side effects and are safer in overdose (low cardiotoxicity).

Question 145: Concomitant use of valproic acid and lamotrigine increases the risk of which of the following conditions?

A. Chondrodysplasia punctata
B. Paroxysmal Nocturnal hemoglobinuria
C. Stevens-Johnson syndrome (Correct Answer)
D. Floppy infant syndrome

Explanation: **Explanation:** The correct answer is **Stevens-Johnson syndrome (SJS)**. **Mechanism of Interaction:** Lamotrigine is primarily metabolized by the enzyme **UDP-glucuronosyltransferase (UGT)**. Valproic acid is a potent inhibitor of this enzyme. When used concomitantly, valproic acid inhibits the metabolism of lamotrigine, leading to a significant increase (up to two-fold) in its serum concentration and half-life. High levels of lamotrigine are strongly associated with life-threatening cutaneous adverse reactions, specifically **Stevens-Johnson syndrome (SJS)** and **Toxic Epidermal Necrolysis (TEN)**. To mitigate this risk, the starting dose of lamotrigine must be reduced by half when added to a regimen containing valproate. **Analysis of Incorrect Options:** * **A. Chondrodysplasia punctata:** This is a skeletal dysplasia associated with the use of **Warfarin** during pregnancy (Warfarin Embryopathy). * **B. Paroxysmal Nocturnal Hemoglobinuria (PNH):** This is an acquired hematopoietic stem cell disorder caused by a somatic mutation in the *PIGA* gene; it is not drug-induced. * **D. Floppy infant syndrome:** This refers to neonatal hypotonia, typically seen in infants born to mothers taking **Benzodiazepines** or **Lithium** near the time of delivery. **High-Yield Clinical Pearls for NEET-PG:** * **Valproate** is a broad-spectrum enzyme **inhibitor**, whereas Carbamazepine, Phenytoin, and Phenobarbital are enzyme **inducers**. * **Lamotrigine** is the preferred anti-epileptic for **bipolar depression** and is considered safe in pregnancy regarding major malformations, though it carries a risk of cleft lip/palate. * **SJS/TEN** is most commonly associated with sulfonamides, allopurinol, anticonvulsants (lamotrigine, carbamazepine, phenytoin), and NSAIDs.

Question 146: Buspirone acts on which receptor subtype?

A. 5-HT1A (Correct Answer)
B. 5-HT1B
C. 5-HT2
D. 5-HT3

Explanation: **Explanation:** **Buspirone** is a non-benzodiazepine anxiolytic used primarily for the management of Generalized Anxiety Disorder (GAD). 1. **Why Option A is Correct:** Buspirone acts as a **selective partial agonist at the 5-HT1A receptors**. By stimulating these presynaptic autoreceptors in the raphe nuclei and postsynaptic receptors in the hippocampus, it modulates serotonin neurotransmission. Unlike benzodiazepines, it does not interact with GABA receptors, which explains its lack of sedative, anticonvulsant, or muscle relaxant properties. 2. **Why Other Options are Incorrect:** * **5-HT1B:** These receptors are primarily involved in cranial vessel vasoconstriction. Drugs like **Triptans** (e.g., Sumatriptan) act here to treat migraines. * **5-HT2:** This family (especially 5-HT2A) is the target for atypical antipsychotics (antagonists) and hallucinogens like LSD (agonists). * **5-HT3:** These are ionotropic receptors. Antagonists like **Ondansetron** are used as potent anti-emetics. **High-Yield Clinical Pearls for NEET-PG:** * **Latency of Action:** Buspirone has a slow onset of action, taking **1–2 weeks** to show effects. It is not useful for acute anxiety or panic attacks. * **Safety Profile:** It has **no potential for abuse or addiction** (no "buzz" or euphoria) and does not cause psychomotor impairment. It is safe for patients with a history of substance abuse. * **Interaction:** It does not potentiate the effects of alcohol or other CNS depressants. * **Side Effects:** Most common side effects include dizziness, nausea, and headache. It can cause a paradoxical increase in blood pressure if used with MAO inhibitors.

Question 147: Which of the following drugs causes hepatotoxicity?

A. Sertraline
B. Fluoxetine
C. Nefazodone (Correct Answer)
D. Amitriptyline

Explanation: **Explanation:** **Nefazodone** is a Serotonin-2 Antagonist and Reuptake Inhibitor (SARI). While it is effective for depression and anxiety, its clinical use has been severely restricted due to a **Black Box Warning** regarding life-threatening **hepatotoxicity**. The drug can cause a rapid increase in hepatic enzymes leading to fulminant hepatic failure, often requiring liver transplantation. Because of this risk, it has been withdrawn from the market in several countries (e.g., USA, Canada). **Analysis of Incorrect Options:** * **Sertraline & Fluoxetine (SSRIs):** These are the first-line treatments for depression. While all drugs undergo hepatic metabolism, SSRIs are generally considered safe for the liver. Idiosyncratic liver injury is extremely rare with these agents. * **Amitriptyline (TCA):** Tricyclic antidepressants are primarily associated with anticholinergic side effects (dry mouth, constipation), sedation, and cardiotoxicity (arrhythmias due to sodium channel blockade). While they can occasionally cause a mild, transient rise in transaminases, they do not carry the high risk of severe hepatotoxicity seen with Nefazodone. **Clinical Pearls for NEET-PG:** * **Nefazodone vs. Trazodone:** Both are SARIs. While Nefazodone is hepatotoxic, **Trazodone** is famously associated with **priapism** and is frequently used off-label for insomnia due to its sedative properties. * **Mechanism:** Nefazodone also acts as a potent inhibitor of the **CYP3A4** enzyme, leading to numerous drug-drug interactions. * **Mnemonic:** Remember **"N"** for Nefazodone = **"N"**ecrosis of the liver.

Question 148: Which drug is used in the prophylaxis of nicotine addiction?

A. Diazepam
B. Naloxone
C. Bupropion (Correct Answer)
D. Acamprosate

Explanation: **Explanation:** **Bupropion** is an atypical antidepressant that acts as a selective **norepinephrine and dopamine reuptake inhibitor (NDRI)**. It is FDA-approved for smoking cessation (prophylaxis of nicotine addiction) because it mimics some of the neurochemical effects of nicotine. By increasing dopamine levels in the brain's reward pathway (nucleus accumbens), it reduces the intensity of nicotine withdrawal symptoms and the urge to smoke. **Analysis of Incorrect Options:** * **Diazepam:** A benzodiazepine used for acute alcohol withdrawal and anxiety. It has no role in treating nicotine addiction and carries its own risk of dependence. * **Naloxone:** An opioid antagonist used primarily for the emergency reversal of opioid overdose. It does not significantly impact the nicotinic acetylcholine receptors involved in smoking. * **Acamprosate:** Used specifically for maintaining abstinence in **alcohol dependence** by modulating glutamate and GABA neurotransmission; it is ineffective for nicotine addiction. **High-Yield Clinical Pearls for NEET-PG:** * **Varenicline** (a partial agonist at $\alpha_4\beta_2$ nicotinic receptors) is considered the most effective monotherapy for smoking cessation, followed by Bupropion and Nicotine Replacement Therapy (NRT). * **Contraindication:** Bupropion is strictly contraindicated in patients with **seizure disorders** or eating disorders (bulimia/anorexia) as it lowers the seizure threshold. * **Weight Neutrality:** Unlike many antidepressants, Bupropion is often associated with weight loss, making it a preferred choice for smokers concerned about post-cessation weight gain. * **Clonidine** and **Nortriptyline** are considered second-line agents for smoking cessation.

Question 149: Which of the following is a typical antidepressant drug?

A. Amitriptyline (Correct Answer)
B. Clozapine
C. Olanzapine
D. Trazodone

Explanation: **Amitriptyline** is the correct answer because it is a classic example of a **Tricyclic Antidepressant (TCA)** [1]. TCAs are considered "typical" or first-generation antidepressants [1]. They work by inhibiting the reuptake of both Norepinephrine (NE) and Serotonin (5-HT) into the presynaptic neurons, thereby increasing their concentration in the synaptic cleft [3].**Analysis of Options:*** **Amitriptyline (Option A):** A tertiary amine TCA [1]. It is highly effective but associated with significant side effects due to its blockade of muscarinic (anticholinergic), alpha-adrenergic, and histaminergic receptors [3].* **Clozapine & Olanzapine (Options B & C):** These are **Atypical Antipsychotics** (Second-generation antipsychotics). They are used primarily in the treatment of Schizophrenia and Bipolar Disorder, not as primary antidepressants. Clozapine is specifically reserved for treatment-resistant schizophrenia.* **Trazodone (Option D):** This is an **Atypical Antidepressant** (specifically a SARI – Serotonin Antagonist and Reuptake Inhibitor) [3]. While it treats depression [2], it is classified as "atypical" because its mechanism and side-effect profile (e.g., prominent sedation and risk of priapism) differ from the classic TCAs or SSRIs.**High-Yield Clinical Pearls for NEET-PG:*** **TCA Overdose Triad:** Coma, Convulsions, and Cardiac arrhythmias (due to sodium channel blockade). The antidote is **Sodium Bicarbonate**.* **Amitriptyline** is also a first-line agent for **Neuropathic pain** and **Prophylaxis of Migraine**.* **Clozapine** requires mandatory WBC monitoring due to the risk of **Agranulocytosis**.* **Trazodone** is frequently used off-label for insomnia due to its highly sedative nature.

Question 150: MAO inhibitors are contraindicated in all the following conditions EXCEPT:

A. With tricyclic antidepressants
B. With indirectly acting sympathomimetics
C. Cheese
D. Aspirin (Correct Answer)

Explanation: **Explanation:** Monoamine Oxidase Inhibitors (MAOIs) are potent antidepressants that prevent the breakdown of biogenic amines (Norepinephrine, Serotonin, and Dopamine). Their contraindications are primarily based on preventing two life-threatening crises: **Hypertensive Crisis** and **Serotonin Syndrome**. **Why Aspirin is the Correct Answer:** Aspirin (Acetylsalicylic acid) is a Non-Steroidal Anti-inflammatory Drug (NSAID) that inhibits cyclooxygenase. It does not interfere with monoamine metabolism or the adrenergic/serotonergic systems. Therefore, there is no clinically significant interaction between MAOIs and Aspirin, making it safe to use. **Why the other options are contraindicated:** * **Tricyclic Antidepressants (TCAs):** Combining MAOIs with TCAs (especially Clomipramine or Imipramine) can lead to **Serotonin Syndrome** (hyperthermia, rigidity, myoclonus) or severe cardiovascular instability due to excessive synaptic monoamine levels. * **Indirectly acting sympathomimetics (e.g., Ephedrine, Tyramine, Amphetamines):** These drugs displace stored catecholamines into the synaptic cleft. Since MAOIs prevent the degradation of these catecholamines, a massive release occurs, leading to a **Hypertensive Crisis**. * **Cheese:** Aged cheese is rich in **Tyramine** (an indirect sympathomimetic). Normally, GI-based MAO-A degrades tyramine. MAOIs block this "first-pass" metabolism, allowing tyramine to reach systemic circulation and trigger the **"Cheese Reaction"** (severe hypertension, headache, and potential stroke). **High-Yield Clinical Pearls for NEET-PG:** * **The "Washout Period":** When switching from an MAOI to an SSRI (or vice versa), a gap of **at least 14 days** is required to allow for the regeneration of the MAO enzyme. * **Pethidine Interaction:** MAOIs are strictly contraindicated with Pethidine, as it can trigger excitatory reactions (hyperpyrexia and seizures). * **Moclobemide:** A RIMA (Reversible Inhibitor of MAO-A) that carries a much lower risk of the cheese reaction compared to non-selective, irreversible MAOIs like Phenelzine.

Practice by Chapter

Antipsychotics: Typical and Atypical

Practice Questions

Antidepressants: SSRIs and SNRIs

Practice Questions

Tricyclic Antidepressants

Practice Questions

MAO Inhibitors

Practice Questions

Mood Stabilizers

Practice Questions

Anxiolytics

Practice Questions

Drugs for ADHD

Practice Questions

Drugs for Sleep Disorders

Practice Questions

Drugs for Dementia

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Drug-Induced Psychiatric Symptoms

Practice Questions

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