Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 101: Which of the following is not a Selective Serotonin Reuptake Inhibitor (SSRI)?

A. Escitalopram
B. Sertraline
C. Paroxetine
D. Amitriptyline (Correct Answer)

Explanation: **Explanation:** The correct answer is **Amitriptyline** because it belongs to the class of **Tricyclic Antidepressants (TCAs)**, not SSRIs. **1. Why Amitriptyline is the correct choice:** Amitriptyline works by inhibiting the reuptake of both **Serotonin (5-HT) and Norepinephrine (NE)**. Unlike SSRIs, which are selective, TCAs also block several other receptors, including alpha-1 adrenergic, histaminergic (H1), and muscarinic (M1) receptors. This "shotgun" approach leads to its characteristic side-effect profile (sedation, dry mouth, constipation, and orthostatic hypotension). **2. Why the other options are incorrect:** * **Escitalopram:** The S-enantiomer of citalopram; it is considered the most selective SSRI and is widely used due to its minimal drug-drug interactions. * **Sertraline:** A potent SSRI frequently preferred in patients with recent myocardial infarction (MI) due to its proven safety profile in cardiac patients. * **Paroxetine:** A short-acting SSRI known for having the highest risk of "discontinuation syndrome" and potential teratogenic effects (congenital heart defects). **Clinical Pearls for NEET-PG:** * **First-line treatment:** SSRIs are the first-line drugs for Depression, OCD, Panic Disorder, and Social Phobia. * **Side Effects:** The most common side effects of SSRIs are GI upset (nausea/diarrhea) and **sexual dysfunction** (delayed ejaculation). * **TCA Overdose:** Amitriptyline overdose is characterized by the "3 Cs": **C**oma, **C**onvulsions, and **C**ardiotoxicity (arrhythmias due to sodium channel blockade). * **Drug of Choice:** Fluoxetine is the SSRI of choice for Bulimia Nervosa and Depression in children.

Question 102: What is the primary pharmacological classification of Buspirone?

A. Anxiolytic (Correct Answer)
B. Sedative
C. Treatment for acute panic attacks
D. Muscle relaxant

Explanation: **Explanation:** **Buspirone** is a unique non-benzodiazepine drug primarily classified as an **Anxiolytic**. Its mechanism of action involves acting as a **selective partial agonist at the 5-HT1A receptors**. Unlike benzodiazepines, it does not interact with the GABA-chloride channel complex, making it effective specifically for Generalized Anxiety Disorder (GAD). **Why the other options are incorrect:** * **B. Sedative:** Buspirone is notable for its **lack of sedative properties**. It does not cause drowsiness, cognitive impairment, or psychomotor depression, which is a major clinical advantage over benzodiazepines. * **C. Treatment for acute panic attacks:** Buspirone has a **slow onset of action** (taking 1–2 weeks to show effects). Therefore, it is ineffective for acute anxiety or panic attacks, which require rapid-acting agents like Alprazolam or Etizolam. * **D. Muscle relaxant:** Because it does not act on GABA receptors, Buspirone lacks anticonvulsant and muscle relaxant properties. **High-Yield Clinical Pearls for NEET-PG:** * **No Dependence:** It has no abuse potential and does not cause withdrawal symptoms or rebound anxiety upon discontinuation. * **No Interaction with Alcohol:** Unlike most psychotropic drugs, it does not potentiate the effects of CNS depressants like alcohol. * **Side Effects:** Most common side effects include dizziness, nausea, and headache. * **Metabolism:** It is metabolized by CYP3A4; concurrent use with rifampin (inducer) or erythromycin (inhibitor) requires dose adjustment.

Question 103: Buspirone is:

A. A 5HT-1 agonist (Correct Answer)
B. A 5HT-2 antagonist
C. An H1 agonist
D. A 5HT-2 antagonist

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, it inhibits the firing of serotonergic neurons, and by acting on postsynaptic receptors in the hippocampus, it modulates emotional responses. Unlike benzodiazepines, it does not interact with the GABA-A receptor complex. **2. Why the Other Options are Incorrect:** * **Options B & D (5-HT2 Antagonists):** Drugs that antagonize 5-HT2 receptors include atypical antipsychotics (e.g., Risperidone) and certain antidepressants like Mirtazapine or Trazodone. Buspirone has no significant affinity for 5-HT2 receptors. * **Option C (H1 Agonist):** There are no common psychiatric drugs used as H1 agonists. In fact, many psychotropic drugs (like Amitriptyline or Quetiapine) act as **H1 antagonists**, leading to side effects like sedation and weight gain. **3. NEET-PG High-Yield Clinical Pearls:** * **Slow Onset:** Unlike benzodiazepines, Buspirone takes **1–2 weeks** to show therapeutic effects. It is not useful for "PRN" (as-needed) use or acute panic attacks. * **Lack of Sedation:** It does not cause sedation, cognitive impairment, or psychomotor depression. * **No Dependence:** It lacks muscle relaxant or anticonvulsant properties and has **zero potential for abuse or withdrawal symptoms**. * **Interaction:** It should not be used with MAO inhibitors due to the risk of **Serotonin Syndrome** and hypertension.

Question 104: What is the most effective non-habit-forming sedative?

A. Lorazepam
B. Zolpidem (Correct Answer)
C. Flurazepam
D. Trazodone

Explanation: ### Explanation **Correct Answer: B. Zolpidem** **Why it is correct:** Zolpidem belongs to the **"Z-drugs"** (Non-benzodiazepine hypnotics), which also include Zaleplon and Eszopiclone. These drugs act selectively on the **α1 subunit** of the GABA-A receptor complex. Unlike traditional Benzodiazepines (BZDs), which bind non-selectively to various subunits, Zolpidem’s selectivity for α1 mediates primarily **sedative-hypnotic effects** without significant anxiolytic, muscle relaxant, or anticonvulsant properties. Crucially, Zolpidem has a much lower potential for tolerance, dependence, and "hangover" effects compared to BZDs, making it the most effective "non-habit-forming" (low abuse potential) sedative for short-term insomnia. **Why the other options are incorrect:** * **A. Lorazepam & C. Flurazepam:** These are classic Benzodiazepines. They bind non-selectively to GABA-A receptors. They are notorious for causing **rebound insomnia, tolerance, and physical dependence** (habit-forming). Flurazepam, in particular, has a very long half-life, leading to significant daytime sedation. * **D. Trazodone:** While used off-label for insomnia (especially in patients with depression), it is primarily an atypical antidepressant (SARI). It is less effective as a pure sedative compared to Zolpidem and is often associated with side effects like orthostatic hypotension and priapism. **High-Yield NEET-PG Pearls:** * **Antidote:** Flumazenil reverses the effects of both Benzodiazepines and Z-drugs. * **Z-drugs vs. BZDs:** Z-drugs do not significantly alter the sleep architecture (they preserve REM sleep better than BZDs). * **Zaleplon:** Has the shortest half-life among Z-drugs; useful for sleep-onset insomnia. * **Eszopiclone:** The only Z-drug approved for long-term use (up to 6 months).

Question 105: What is the mechanism of action of Mianserin?

A. Inhibits alpha-adrenergic, H1, and some types of 5-HT receptors (Correct Answer)
B. Inhibits alpha-adrenergic, H2, and some types of 5-HT receptors
C. Inhibits beta-adrenergic, H1, and some types of 5-HT receptors
D. Inhibits alpha-adrenergic and H1 receptors

Explanation: **Explanation:** **Mianserin** is a tetracyclic antidepressant (TeCA) that belongs to the class of **Atypical Antidepressants**. Its mechanism of action is unique as it does not significantly inhibit the reuptake of norepinephrine or serotonin, unlike TCAs. 1. **Why Option A is Correct:** Mianserin acts primarily as an antagonist at multiple receptors: * **Alpha-adrenergic receptors:** It blocks **presynaptic $\alpha_2$-receptors**, which increases the release of norepinephrine in the synaptic cleft (disinhibition). It also has $\alpha_1$-blocking properties. * **H1 receptors:** It is a potent **Histamine (H1) antagonist**, which accounts for its significant sedative properties. * **5-HT receptors:** It antagonizes various serotonin receptors, specifically **5-HT$_{2A}$, 5-HT$_{2C}$, and 5-HT$_3$**. 2. **Why Other Options are Incorrect:** * **Option B:** Mianserin targets **H1 receptors**, not H2. H2-receptor antagonism is associated with gastric acid reduction (e.g., Ranitidine), not antidepressant action. * **Option C:** Mianserin does not inhibit beta-adrenergic receptors; its adrenergic activity is focused on **alpha-blockade**. * **Option D:** This is incomplete. While it blocks alpha and H1 receptors, its **5-HT receptor antagonism** is a crucial component of its pharmacological profile and clinical effect. **NEET-PG High-Yield Pearls:** * **Mirtazapine Connection:** Mianserin is the parent compound of Mirtazapine (a NaSSA). Both share the $\alpha_2$-blockade mechanism. * **Clinical Advantage:** Due to its lack of significant anticholinergic activity and low cardiotoxicity, it is often preferred over TCAs in elderly patients. * **Side Effects:** The most serious side effect to remember for exams is **agranulocytosis** (requires monitoring of CBC). It also causes significant weight gain and sedation due to H1 blockade.

Question 106: Which of the following is a tricyclic antidepressant?

A. Sertraline
B. Bupropion
C. Fluoxetine
D. Imipramine (Correct Answer)

Explanation: **Explanation:** **Imipramine** is the correct answer as it is a prototype **Tricyclic Antidepressant (TCA)**. TCAs are characterized by a three-ring chemical structure and work primarily by inhibiting the reuptake of Norepinephrine (NE) and Serotonin (5-HT) from the synaptic cleft. Imipramine is a non-selective inhibitor, often used clinically for nocturnal enuresis in children due to its anticholinergic properties. **Analysis of Incorrect Options:** * **Sertraline (A) and Fluoxetine (C):** These belong to the **Selective Serotonin Reuptake Inhibitors (SSRIs)** class. They are currently the first-line treatment for depression and anxiety disorders due to their superior safety profile and lack of significant anticholinergic or cardiotoxic side effects compared to TCAs. * **Bupropion (B):** This is an **Atypical Antidepressant** that acts as a Norepinephrine-Dopamine Reuptake Inhibitor (NDRI). It is notably used for smoking cessation and has a lower risk of causing sexual dysfunction or weight gain. **High-Yield NEET-PG Pearls:** * **Mechanism of TCA Toxicity:** TCAs block sodium channels in the heart, leading to QRS prolongation and arrhythmias. The "3 Cs" of TCA overdose are **C**oma, **C**onvulsions, and **C**ardiotoxicity. * **Antidote:** Sodium bicarbonate is used to treat TCA-induced cardiotoxicity. * **Secondary Amines vs. Tertiary Amines:** Imipramine and Amitriptyline are tertiary amines (more sedative), while Desipramine and Nortriptyline are secondary amines (more potent for NE reuptake).

Question 107: Which of the following drugs, when given along with serotonergic drugs, can lead to serotonin syndrome?

A. Buspirone
B. Fluoxetine (Correct Answer)
C. Penfluridol
D. Clozapine

Explanation: **Explanation:** **Serotonin Syndrome** is a potentially life-threatening condition caused by excessive serotonergic activity in the central and peripheral nervous systems [1]. It typically occurs when two or more drugs that increase serotonin levels are administered concurrently. **Why Fluoxetine is Correct:** **Fluoxetine** is a Selective Serotonin Reuptake Inhibitor (SSRI). It works by inhibiting the serotonin transporter (SERT), preventing the reuptake of serotonin into the presynaptic neuron [1]. When combined with other serotonergic agents (like MAO inhibitors, SNRIs, or Tramadol), it leads to a synergistic increase in synaptic serotonin, precipitating serotonin syndrome [1]. Fluoxetine is particularly high-risk due to its **long half-life** and active metabolite (norfluoxetine), which can persist in the body for weeks [2]. **Why Other Options are Incorrect:** * **Buspirone:** While it is a partial agonist at 5-HT1A receptors used for generalized anxiety, it has a much lower risk of inducing serotonin syndrome compared to SSRIs. * **Penfluridol:** This is a long-acting **typical antipsychotic** (diphenylbutylpiperidine class) that primarily blocks Dopamine D2 receptors. It does not significantly increase serotonin levels. * **Clozapine:** An **atypical antipsychotic** that actually acts as an antagonist at several serotonin receptors (especially 5-HT2A). It is more commonly associated with Neuroleptic Malignant Syndrome (NMS) or agranulocytosis rather than serotonin syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Cognitive effects (confusion, agitation), Autonomic hyperactivity (hyperthermia, tachycardia, diaphoresis), and Somatic effects (myoclonus, hyperreflexia) [1]. * **Key Differentiator:** Hyperreflexia and **clonus** are characteristic of Serotonin Syndrome, whereas "lead-pipe" rigidity is characteristic of NMS. * **Management:** Discontinue offending agents, supportive care (cooling), and the specific antidote **Cyproheptadine** (5-HT2 receptor antagonist).

Question 108: Which drug is most useful in treating an episode of antipsychotic-induced acute dystonia?

A. Haloperidol
B. Promethazine (Correct Answer)
C. Phenobarbitone
D. Lorazepam

Explanation: **Explanation:** **Mechanism and Correct Answer:** Acute dystonia is an Extrapyramidal Side Effect (EPS) caused by a blockade of dopamine (D2) receptors in the nigrostriatal pathway, leading to a relative **excess of cholinergic activity**. To restore the neurochemical balance, drugs with potent **central anticholinergic properties** are required. **Promethazine (Option B)** is a first-generation antihistamine with significant anticholinergic activity, making it highly effective for reversing acute dystonic reactions (such as torticollis, grimacing, or oculogyric crisis). Other parenteral options frequently used include Benztropine or Trihexyphenidyl. **Analysis of Incorrect Options:** * **A. Haloperidol:** This is a high-potency typical antipsychotic and a potent D2 blocker. It is a common *cause* of acute dystonia; administering it would worsen the condition. * **C. Phenobarbitone:** This is a barbiturate used for seizures or sedation. It has no anticholinergic activity and does not address the underlying dopamine-acetylcholine imbalance. * **D. Lorazepam:** While benzodiazepines can provide sedation and mild muscle relaxation, they are not the primary treatment of choice for dystonia. They are generally reserved for Akathisia or as adjunctive therapy if anticholinergics are insufficient. **NEET-PG High-Yield Pearls:** * **Acute Dystonia:** The earliest EPS to appear (within hours to days). * **Drug of Choice (DOC):** Central anticholinergics (Promethazine, Benztropine). * **Akathisia:** Most common EPS; DOC is **Propranolol**. * **Drug-Induced Parkinsonism:** DOC is **Trihexyphenidyl** (Centrally acting anticholinergic). * **Tardive Dyskinesia:** Occurs after long-term use; characterized by "fly-catcher tongue." Treatment involves switching to Clozapine or using VMAT-2 inhibitors (Valbenazine).

Question 109: Which of the following antidepressants causes paresthesia due to pyridoxine deficiency?

A. tranylcypromine (Correct Answer)
B. amitriptyline
C. duloxetine
D. milnacipran

Explanation: ### Explanation **Correct Option: A. Tranylcypromine** Tranylcypromine is a non-selective, irreversible **Monoamine Oxidase Inhibitor (MAOI)**. Certain MAOIs, particularly those belonging to the hydrazine group (like phenelzine) and occasionally non-hydrazines like tranylcypromine, can interfere with pyridoxine (Vitamin B6) metabolism. These drugs can bind to and inhibit **pyridoxine kinase**, the enzyme responsible for converting pyridoxine into its active form, pyridoxal-5-phosphate (PLP). A deficiency in PLP impairs the synthesis of neurotransmitters (like GABA) and leads to axonal degeneration, manifesting clinically as **peripheral neuropathy and paresthesia**. This is similar to the mechanism seen with Isoniazid (INH) in tuberculosis treatment. **Incorrect Options:** * **B. Amitriptyline:** A Tricyclic Antidepressant (TCA). Its primary side effects are anticholinergic (dry mouth, constipation), antihistaminic (sedation), and alpha-blocking (orthostatic hypotension). It does not affect pyridoxine levels. * **C. Duloxetine & D. Milnacipran:** These are Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs). They are actually used to *treat* neuropathic pain (especially Duloxetine for diabetic neuropathy) rather than causing it. Common side effects include nausea, hypertension, and insomnia. **High-Yield Clinical Pearls for NEET-PG:** * **MAOI + Tyramine (Cheese Reaction):** Leads to hypertensive crisis due to displacement of norepinephrine. * **MAOI + SSRI:** Risk of **Serotonin Syndrome** (hyperthermia, muscle rigidity, cardiovascular collapse). * **Drug of Choice for Atypical Depression:** MAOIs are often considered highly effective for atypical depression (characterized by mood reactivity and hyperphagia). * **Management:** Paresthesia caused by MAOIs can be reversed or prevented by supplemental **Pyridoxine (10-50 mg/day)**.

Question 110: Which of the following antidepressants is a selective serotonin reuptake inhibitor (SSRI)?

A. Fluoxetine (Correct Answer)
B. Imipramine
C. Desipramine
D. Amitriptyline

Explanation: **Explanation:** The correct answer is **Fluoxetine**. Selective Serotonin Reuptake Inhibitors (SSRIs) are the first-line treatment for depression due to their favorable side-effect profile compared to older antidepressants. **1. Why Fluoxetine is correct:** Fluoxetine is a prototype **SSRI**. It works by selectively inhibiting the presynaptic reuptake transporter for serotonin (5-HT), thereby increasing the concentration of serotonin in the synaptic cleft. It is unique for its exceptionally long half-life (due to its active metabolite, norfluoxetine), which reduces withdrawal symptoms if a dose is missed. **2. Why the other options are incorrect:** * **Imipramine, Desipramine, and Amitriptyline** all belong to the **Tricyclic Antidepressant (TCA)** class. * **Amitriptyline and Imipramine** are non-selective, inhibiting the reuptake of both Serotonin (5-HT) and Norepinephrine (NE). They also block muscarinic, histaminergic, and alpha-adrenergic receptors, leading to significant side effects (dry mouth, sedation, orthostatic hypotension). * **Desipramine** is a secondary amine TCA that is relatively selective for **Norepinephrine** reuptake inhibition rather than serotonin. **High-Yield Clinical Pearls for NEET-PG:** * **SSRI Mnemonic:** "Effective For Compulsions, Panic, & Depression" (**E**scitalopram, **F**luoxetine/Fluvoxamine, **C**italopram, **P**aroxetine, **S**ertraline). * **Drug of Choice:** SSRIs are the DOC for Depression, OCD, Panic Disorder, Social Phobia, and PTSD. * **Side Effects:** Sexual dysfunction is the most common long-term side effect of SSRIs. * **Safety:** Unlike TCAs, SSRIs have a low risk of cardiotoxicity in overdose (TCAs cause QRS prolongation).

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

Practice Questions

Drug-Induced Psychiatric Symptoms

Practice Questions

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