Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 221: Which of the following is not a Serotonin-Norepinephrine Reuptake Inhibitor (SNRI)?

A. Venlafaxine
B. Duloxetine
C. Milnacipram
D. Bupropion (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Bupropion**. **1. Why Bupropion is the correct answer:** Bupropion is classified as a **Norepinephrine-Dopamine Reuptake Inhibitor (NDRI)**. Unlike SNRIs, it does not significantly inhibit the reuptake of Serotonin. Its primary mechanism involves increasing the synaptic concentration of Dopamine and Norepinephrine. Clinically, this unique profile makes it useful for treating depression without the common serotonergic side effects like sexual dysfunction or weight gain. **2. Why the other options are incorrect:** * **Venlafaxine (Option A):** A prototypical SNRI. At low doses, it primarily acts on serotonin; at higher doses (>150 mg), it significantly inhibits norepinephrine reuptake. * **Duloxetine (Option B):** A potent SNRI used not only for depression but also for chronic pain conditions like diabetic neuropathy and fibromyalgia. * **Milnacipran (Option C):** An SNRI with a higher selectivity for norepinephrine reuptake compared to serotonin. It is frequently used in the management of fibromyalgia. **3. High-Yield NEET-PG Clinical Pearls:** * **Bupropion & Seizures:** Bupropion is strictly contraindicated in patients with **epilepsy** or eating disorders (bulimia/anorexia) as it lowers the seizure threshold. * **Smoking Cessation:** Bupropion is a first-line pharmacological aid for smoking cessation. * **SNRI Indications:** SNRIs are preferred over SSRIs in patients where depression is accompanied by chronic pain (e.g., Duloxetine). * **Desvenlafaxine:** This is the active metabolite of Venlafaxine and is also a common SNRI.

Question 222: Which food should not be consumed by a patient taking Monoamine Oxidase Inhibitors (MAOIs)?

A. Cheese
B. Beer
C. Fish
D. All of the above (Correct Answer)

Explanation: ### Explanation **The Underlying Concept: The "Cheese Reaction"** Monoamine Oxidase Inhibitors (MAOIs), such as Phenelzine and Tranylcypromine, inhibit the enzyme responsible for breaking down catecholamines and dietary amines. **Tyramine** is an indirect sympathomimetic amine found in fermented, aged, or spoiled foods. Normally, MAO-A in the gut and liver degrades dietary tyramine. When a patient takes a non-selective MAOI, tyramine escapes degradation, enters the systemic circulation, and displaces stored norepinephrine from nerve terminals. This massive release of norepinephrine leads to a **Hypertensive Crisis** (severe headache, palpitations, and potentially stroke), famously known as the "Cheese Reaction." **Analysis of Options:** * **A. Cheese:** Specifically aged cheeses (Cheddar, Swiss, Blue) are very high in tyramine. (Note: Fresh cottage cheese or cream cheese is generally safe). * **B. Beer:** Draught beers and certain wines (Chianti) contain significant tyramine levels due to fermentation processes. * **C. Fish:** While fresh fish is safe, dried, pickled, smoked, or fermented fish (like herring) are potent triggers for the hypertensive crisis. Since all these categories contain high-tyramine items that can trigger a life-threatening interaction, **Option D (All of the above)** is the correct choice. **High-Yield Clinical Pearls for NEET-PG:** * **The Antidote:** The drug of choice for managing an MAOI-induced hypertensive crisis is **Phentolamine** (an alpha-blocker). * **The Exception:** **Selegiline** (a selective MAO-B inhibitor) at low doses typically does not require strict dietary restrictions because MAO-A in the gut remains functional. * **Washout Period:** When switching from an MAOI to an SSRI, a **2-week washout period** is mandatory to prevent **Serotonin Syndrome**. (5 weeks for Fluoxetine due to its long half-life). * **Other Prohibited Foods:** Yeast extracts (Marmite), soy sauce, fava beans, and overripe avocados/bananas.

Question 223: Extrapyramidal side effects are commonly seen with which of the following drugs?

A. Haloperidol (Correct Answer)
B. Clozapine
C. Tetracycline
D. Ketoconazole

Explanation: **Explanation:** **Haloperidol** is a high-potency, typical (first-generation) antipsychotic. Its primary mechanism of action is the potent blockade of **D2 receptors** in the brain. Extrapyramidal side effects (EPS) occur due to the blockade of D2 receptors in the **nigrostriatal pathway**, which disrupts the balance between dopamine and acetylcholine. High-potency drugs like Haloperidol have a high affinity for these receptors and low anticholinergic activity, making them the most common culprits for EPS. **Analysis of Incorrect Options:** * **Clozapine:** This is an atypical (second-generation) antipsychotic. It has a higher affinity for 5-HT2A receptors than D2 receptors and dissociates rapidly from D2 receptors. Consequently, it has a very low risk of EPS and is often the drug of choice when EPS occurs with other agents. * **Tetracycline:** This is a broad-spectrum antibiotic that inhibits protein synthesis (30S subunit). It is not associated with dopaminergic pathways or EPS. * **Ketoconazole:** This is an antifungal agent (imidazole) that inhibits ergosterol synthesis. While it can cause endocrine side effects (due to inhibition of cytochrome P450 enzymes), it does not cause EPS. **High-Yield Clinical Pearls for NEET-PG:** * **EPS Spectrum:** Includes Acute Dystonia (earliest), Akathisia (most common), Parkinsonism, and Tardive Dyskinesia (late-onset/potentially irreversible). * **Treatment of Acute Dystonia:** Centrally acting anticholinergics like **Benztropine** or **Promethazine**. * **Drug of Choice for Akathisia:** Propropanol (Beta-blockers). * **Hyperprolactinemia:** Also caused by D2 blockade in the tuberoinfundibular pathway, common with Haloperidol and Risperidone.

Question 224: Which of the following is true regarding tricyclic antidepressants?

A. Tricyclic antidepressants increase the antihypertensive effect of guanethidine.
B. Tricyclic antidepressants have anticonvulsant activity.
C. Tricyclic antidepressants should not be used in patients with glaucoma. (Correct Answer)
D. Tricyclic antidepressants may increase oral absorption of levodopa.

Explanation: **Explanation:** Tricyclic Antidepressants (TCAs) like Amitriptyline and Imipramine are known for their complex pharmacological profile, involving the inhibition of Norepinephrine (NE) and Serotonin (5-HT) reuptake, as well as significant blockade of muscarinic, histaminergic, and alpha-adrenergic receptors [1]. **Why Option C is Correct:** TCAs possess potent **antimuscarinic (atropine-like) properties** [1]. Blockade of muscarinic receptors in the eye leads to mydriasis (dilation of the pupil). In patients with narrow-angle glaucoma, this can cause the iris to block the drainage angle of the eye, acutely increasing intraocular pressure and potentially precipitating an attack of **acute angle-closure glaucoma**. Therefore, they are contraindicated in such patients. **Analysis of Incorrect Options:** * **Option A:** TCAs **block the antihypertensive effect** of guanethidine. Guanethidine requires the neuronal uptake pump (NET) to reach its site of action; TCAs inhibit this pump, preventing the drug from entering the neuron. * **Option B:** TCAs actually **lower the seizure threshold**. They possess pro-convulsant activity rather than anticonvulsant activity, making them risky for patients with epilepsy. * **Option C:** TCAs **decrease the oral absorption** of levodopa. Due to their anticholinergic effect, they delay gastric emptying, leading to increased degradation of levodopa in the stomach before it reaches its absorption site in the small intestine. **High-Yield Clinical Pearls for NEET-PG:** * **Overdose Triad (The 3 C’s):** **C**onvulsions, **C**oma, and **C**ardiotoxicity (Arrhythmias due to Sodium channel blockade). * **Antidote for Cardiotoxicity:** Sodium Bicarbonate (to overcome sodium channel blockade). * **Most Sedating TCA:** Amitriptyline (due to high H1 receptor affinity). * **Least Sedating/Least Anticholinergic:** Desipramine or Nortriptyline [1].

Question 225: True about Imipramine is:

A. Antiepileptic
B. Antidepressant (Correct Answer)
C. Anxiolytic
D. Antipsychotic

Explanation: **Explanation:**1. Why Option B is Correct:Imipramine is a prototype drug belonging to the **Tricyclic Antidepressants (TCAs)** class [1, 2]. Its primary mechanism of action involves the non-selective inhibition of the reuptake of norepinephrine (NE) and serotonin (5-HT) from the synaptic cleft into the presynaptic nerve terminals [1, 2]. By increasing the concentration of these monoamines in the brain, it effectively alleviates the symptoms of clinical depression [2].2. Why Other Options are Incorrect:* **Option A (Antiepileptic):** Imipramine actually **lowers the seizure threshold**. It is contraindicated in patients with epilepsy as it can precipitate seizures.* **Option C (Anxiolytic):** While TCAs may be used for panic disorders, they are not classified as primary anxiolytics (like Benzodiazepines). In fact, initial doses can sometimes worsen agitation.* **Option D (Antipsychotic):** Antipsychotics (e.g., Haloperidol, Risperidone) primarily act by blocking Dopamine (D2) receptors. Imipramine does not possess significant antipsychotic properties.3. Clinical Pearls & High-Yield Facts for NEET-PG:* **Nocturnal Enuresis:** Imipramine is the drug of choice for bedwetting in children (above 5 years) due to its anticholinergic effect, which increases bladder capacity.* **Side Effect Profile:** TCAs are notorious for "3Cs": **C**oma, **C**onvulsions, and **C**ardiotoxicity (arrhythmias due to Na+ channel blockade).* **Anticholinergic Effects:** Common side effects include dry mouth, blurred vision, constipation, and urinary retention [1].* **Metabolism:** It is a tertiary amine that is metabolized into **Desipramine** (an active metabolite) [1, 2].

Question 226: Which of the following antidepressants is used for smoking cessation?

A. Fluoxetine
B. Bupropion (Correct Answer)
C. Reboxetine
D. Venlafaxine

Explanation: **Bupropion** is an atypical antidepressant that acts as a **Norepinephrine-Dopamine Reuptake Inhibitor (NDRI)** [2]. It is the only antidepressant FDA-approved for smoking cessation [1]. Its efficacy lies in its ability to increase dopamine levels in the nucleus accumbens (the brain's reward center), which mimics the effect of nicotine and reduces withdrawal symptoms and the urge to smoke [1].**Analysis of Options:** * **Fluoxetine (Option A):** An SSRI (Selective Serotonin Reuptake Inhibitor) primarily used for Depression, OCD, and Bulimia. It has no proven efficacy in smoking cessation.* **Reboxetine (Option C):** A Selective Norepinephrine Reuptake Inhibitor (SNRI) used for depression; it does not play a role in nicotine addiction management.* **Venlafaxine (Option D):** A Serotonin-Norepinephrine Reuptake Inhibitor (SNRI) used for Major Depressive Disorder and Anxiety disorders, but not for smoking cessation.**High-Yield Clinical Pearls for NEET-PG:** * **Mechanism in Smoking:** Bupropion (Sustained Release) is typically started 1–2 weeks *before* the patient's "quit date."* **Contraindication (Must Know):** Bupropion lowers the seizure threshold. It is strictly contraindicated in patients with **Seizure disorders** or **Eating disorders** (Anorexia/Bulimia) due to increased risk of convulsions [1].* **Weight Neutrality:** Unlike many other antidepressants, Bupropion is associated with weight loss or is weight-neutral, making it a preferred choice in obese patients [1].* **Sexual Dysfunction:** It does not cause sexual dysfunction (unlike SSRIs), making it useful for patients experiencing SSRI-induced side effects [1].* **Other Smoking Cessation Drugs:** **Varenicline** (Partial agonist at α4β2 nicotinic receptors) is currently considered the most effective pharmacological agent for smoking cessation.

Question 227: Which of the following is a short-acting benzodiazepine?

A. Diazepam
B. Flurazepam
C. Lorazepam (Correct Answer)
D. Chlordiazepoxide

Explanation: **Explanation:** Benzodiazepines (BZDs) are classified based on their elimination half-life into short, intermediate, and long-acting agents. This classification is clinically significant for determining their use in insomnia, anxiety, or anesthesia. **Why Lorazepam is Correct:** **Lorazepam** is categorized as an **intermediate to short-acting** benzodiazepine (half-life approx. 10–20 hours). Unlike many other BZDs, it does not undergo phase I oxidative metabolism in the liver; instead, it is directly conjugated (Phase II) to inactive glucuronides. This lack of active metabolites prevents cumulative effects, making it relatively shorter-acting compared to the other options provided. **Analysis of Incorrect Options:** * **Diazepam (A):** A classic **long-acting** BZD (half-life >30 hours). It is converted into active metabolites like desmethyldiazepam, which has an extremely long half-life (up to 100 hours). * **Flurazepam (B):** A **long-acting** BZD primarily used for insomnia. Its active metabolite, desalkylflurazepam, remains in the system for a prolonged duration, often causing "daytime hangover." * **Chlordiazepoxide (D):** The first BZD synthesized, it is **long-acting** and frequently used in alcohol withdrawal due to its smooth tapering effect. **NEET-PG High-Yield Pearls:** * **Mnemonic for Short-Acting BZDs:** **ATOMS** (Alprazolam, Triazolam, Oxazepam, Midazolam, Temazepam). *Note: Lorazepam is often grouped here in exams due to its lack of active metabolites.* * **Safe in Liver Failure:** Use **LOT** (Lorazepam, Oxazepam, Temazepam) as they undergo direct glucuronidation and do not rely on hepatic microsomal enzymes. * **Ultra-short acting:** **Midazolam** (used for conscious sedation) and **Triazolam** (highest risk for rebound insomnia). * **Drug of Choice:** Lorazepam is the preferred BZD for **Status Epilepticus** (IV) due to its lower lipid solubility compared to Diazepam, allowing it to remain in the vascular compartment longer.

Question 228: Which of the following drugs is considered to have dual reuptake inhibition?

A. Clomipramine
B. Amitriptyline
C. Venlafaxine
D. All of the above (Correct Answer)

Explanation: ### Explanation The term **"Dual Reuptake Inhibition"** refers to the pharmacological action of inhibiting the reuptake of both **Serotonin (5-HT)** and **Norepinephrine (NE)** from the synaptic cleft. This increases the concentration of both neurotransmitters, providing a potent antidepressant effect. **Why "All of the above" is correct:** 1. **Clomipramine:** Although classified as a Tricyclic Antidepressant (TCA), it is unique because it is the most potent serotonin reuptake inhibitor among TCAs, while its active metabolite (desmethylclomipramine) strongly inhibits norepinephrine reuptake. 2. **Amitriptyline:** A classic Tertiary Amine TCA. It non-selectively inhibits the reuptake of both 5-HT and NE. 3. **Venlafaxine:** This drug belongs to the **SNRI (Serotonin-Norepinephrine Reuptake Inhibitor)** class. At lower doses, it primarily inhibits serotonin reuptake, but at medium to higher doses, it significantly inhibits norepinephrine reuptake as well. **Clinical Pearls for NEET-PG:** * **Clomipramine** is the drug of choice (DOC) for **Obsessive-Compulsive Disorder (OCD)**. * **Venlafaxine** is known for causing **dose-dependent hypertension** due to its noradrenergic activity. * **TCAs vs. SNRIs:** While both provide dual reuptake inhibition, SNRIs (like Venlafaxine and Duloxetine) are preferred in modern practice because they lack the "dirty" side-effect profile of TCAs (i.e., they do not significantly block alpha-1, H1-histamine, or muscarinic receptors). * **Duloxetine** (another SNRI) is frequently asked as the DOC for **Diabetic Neuropathy** and Fibromyalgia.

Question 229: Which antipsychotic drug has the longest elimination half-life?

A. Aripiprazole (Correct Answer)
B. Loxapine
C. Quetiapine
D. Ziprasidone

Explanation: **Explanation:** The correct answer is **Aripiprazole**. **1. Why Aripiprazole is correct:** Aripiprazole is a third-generation atypical antipsychotic characterized by a unique mechanism of action as a **D2 partial agonist**. Among the oral antipsychotics, it possesses an exceptionally long elimination half-life, averaging approximately **75 hours** (extending up to 94 hours in poor metabolizers of CYP2D6). This long half-life allows for once-daily dosing and provides a "buffer" against missed doses, as plasma levels decline slowly. **2. Why the other options are incorrect:** * **Loxapine:** A typical (first-generation) antipsychotic of the dibenzoxazepine class. It has a relatively short half-life of approximately **4 to 8 hours**. * **Quetiapine:** An atypical antipsychotic known for rapid dissociation from D2 receptors. It has one of the shortest half-lives among second-generation drugs, approximately **6 to 7 hours**, often requiring twice-daily dosing or extended-release formulations. * **Ziprasidone:** An atypical antipsychotic with a short half-life of approximately **7 hours**. It must be taken with food (at least 500 calories) to ensure adequate absorption. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Aripiprazole acts as a "Dopamine Stabilizer" (Partial agonist at D2 and 5-HT1A; antagonist at 5-HT2A). * **Side Effect Profile:** It has the lowest risk of weight gain, hyperprolactinemia, and sedation among atypical antipsychotics. However, it is frequently associated with **Akathisia**. * **Long-acting Injectable (LAI):** Aripiprazole is also available as a monthly depot (Aripiprazole Maintena), but even in its **oral form**, it has the longest half-life of the options provided. * **Metabolism:** It is primarily metabolized by **CYP2D6** and **CYP3A4**.

Question 230: Which of the following drugs is not associated with an increase in prolactin levels?

A. Haloperidol
B. Chlorpromazine
C. Hydroxysulpiride
D. Quetiapine (Correct Answer)

Explanation: **Explanation:** The regulation of prolactin secretion is primarily controlled by the **Tuberoinfundibular pathway** in the brain. In this pathway, dopamine acts as a "Prolactin Inhibiting Factor" by stimulating **D2 receptors** on lactotroph cells in the anterior pituitary. Antipsychotic drugs that block these D2 receptors remove this inhibition, leading to **hyperprolactinemia**. **Why Quetiapine is the correct answer:** Quetiapine is a **Second-Generation (Atypical) Antipsychotic**. It is characterized by "loose" binding and rapid dissociation from D2 receptors. Because it does not maintain prolonged blockade of D2 receptors in the pituitary, it is considered **prolactin-sparing**. Along with Aripiprazole and Clozapine, Quetiapine is least likely to cause prolactin elevation. **Analysis of incorrect options:** * **Haloperidol & Chlorpromazine:** These are **First-Generation (Typical) Antipsychotics**. They are potent D2 receptor antagonists with high affinity. They significantly block the tuberoinfundibular pathway, frequently causing side effects like galactorrhea, amenorrhea, and gynecomastia. * **Hydroxysulpiride (and Sulpiride/Amisulpiride):** These are substituted benzamides. Despite being classified as atypical in some contexts, they are notorious for causing the **highest** increases in prolactin levels because they do not cross the blood-brain barrier well and concentrate in the pituitary (which lies outside the BBB). **NEET-PG High-Yield Pearls:** 1. **Highest Prolactin Elevation:** Risperidone, Paliperidone, and Amisulpiride. 2. **Lowest Prolactin Elevation:** Aripiprazole (D2 partial agonist), Quetiapine, and Clozapine. 3. **Clinical Sign:** Hyperprolactinemia can lead to decreased bone mineral density (osteoporosis) due to suppressed GnRH/estrogen.

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

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Drugs for Dementia

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Drug-Induced Psychiatric Symptoms

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