Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 241: Thrombocytopenia is a known side effect of which of the following drugs?

A. Valproate (Correct Answer)
B. Clonazepam
C. Aripiprazole
D. Amisulpride

Explanation: **Explanation:** **Valproate (Sodium Valproate/Valproic Acid)** is the correct answer. It is a broad-spectrum anti-epileptic drug also used as a first-line mood stabilizer in Bipolar Disorder. **Why Valproate causes Thrombocytopenia:** Valproate-induced thrombocytopenia is a well-documented, dose-dependent side effect. The underlying mechanism involves both **bone marrow suppression** (inhibiting megakaryocytopoiesis) and the production of **anti-platelet antibodies** (peripheral destruction). Clinically, this necessitates regular monitoring of Complete Blood Counts (CBC), especially before surgery or when used at high serum concentrations (>100 μg/mL). **Analysis of Incorrect Options:** * **Clonazepam:** A benzodiazepine used for anxiety and seizures. Its primary side effects are sedation, ataxia, and cognitive impairment; it does not typically cause hematological toxicity. * **Aripiprazole:** An atypical antipsychotic (partial D2 agonist). Common side effects include akathisia and insomnia. It is generally "metabolically neutral" and rarely associated with blood dyscrasias. * **Amisulpride:** An atypical antipsychotic (D2/D3 antagonist). Its most significant side effect is **hyperprolactinemia**; it is not known for causing thrombocytopenia. **High-Yield Clinical Pearls for NEET-PG:** * **Valproate Side Effects (Mnemonic: VALPROATE):** **V**omiting, **A**lopecia (curly hair), **L**iver toxicity (Hepatotoxicity), **P**ancreatitis, **R**etention of weight (Obesity), **O**edema, **A**norexia, **T**hrombocytopenia, **E**ncephalopathy (due to hyperammonemia). * **Teratogenicity:** Valproate is highly teratogenic, causing **Neural Tube Defects** (Spina Bifida). * **Drug of Choice:** It is the drug of choice for Myoclonic seizures and Bipolar Affective Disorder (Manic episodes).

Question 242: What is the primary abnormality to screen for when a pregnant female is prescribed lithium?

A. Cardiac anomaly (Correct Answer)
B. Neural tube defect
C. Facial defect
D. Urogenital defect

Explanation: **Explanation:** **Lithium** is a gold-standard mood stabilizer used in Bipolar Disorder, but it is a known human teratogen. When administered during the first trimester of pregnancy, it is specifically associated with a rare but serious **cardiac anomaly** known as **Ebstein’s Anomaly**. 1. **Why Cardiac Anomaly is Correct:** Ebstein’s anomaly involves the "atrialization" of the right ventricle due to the downward displacement of the tricuspid valve leaflets. This leads to tricuspid regurgitation and right heart failure. Because of this risk, fetal echocardiography is mandatory at 18–20 weeks of gestation for women taking Lithium. 2. **Why Other Options are Incorrect:** * **Neural Tube Defects (NTDs):** These are primarily associated with **Valproate** (highest risk) and **Carbamazepine**. These drugs interfere with folate metabolism, unlike Lithium. * **Facial Defects:** Cleft lip and palate are more commonly associated with **Phenytoin** (as part of Fetal Hydantoin Syndrome) or Benzodiazepines. * **Urogenital Defects:** These are not a classic association with Lithium; however, Lithium can cause "Floppy Infant Syndrome" and neonatal hypothyroidism if used near term. **High-Yield NEET-PG Pearls:** * **Teratogenic Risk:** While the relative risk of Ebstein’s anomaly increases 10–20 fold with Lithium, the absolute risk remains low (~1 in 1,000). * **Management:** If a stable patient becomes pregnant, Lithium should not be stopped abruptly (high relapse risk). Instead, the dose should be titrated, and serum levels monitored closely due to increased GFR during pregnancy. * **Breastfeeding:** Lithium is generally **avoided** during breastfeeding as it is excreted in milk and can cause toxicity in the neonate (lethargy, cyanosis).

Question 243: Compared to other antidepressant drugs, mirtazapine has the distinct ability to act as an antagonist of which receptors?

A. Beta receptors
B. D2 receptors
C. Alpha 2 receptors (Correct Answer)
D. 5-HT receptors

Explanation: ### Explanation **Mirtazapine** is classified as a **NaSSA** (Noradrenergic and Specific Serotonergic Antidepressant). Its unique mechanism of action sets it apart from SSRIs and TCAs. **Why Option C is Correct:** The primary mechanism of mirtazapine is the **antagonism of central presynaptic alpha-2 ($\alpha_2$) autoreceptors and heteroreceptors**. * Normally, $\alpha_2$ receptors act as "brakes" on the release of norepinephrine and serotonin. * By blocking these receptors, mirtazapine removes the inhibitory feedback, leading to an **increased release of both Norepinephrine and Serotonin** into the synaptic cleft. This is often referred to as "disinhibiting" the neurotransmitter release. **Why Other Options are Incorrect:** * **Option A (Beta receptors):** Mirtazapine does not have significant activity at beta-adrenergic receptors. Beta-blockers (like Propranolol) are used for performance anxiety, not as primary antidepressants. * **Option B (D2 receptors):** D2 receptor antagonism is the hallmark of **Antipsychotics**. Mirtazapine does not block dopamine receptors; therefore, it lacks extrapyramidal side effects. * **Option C (5-HT receptors):** While mirtazapine *does* block 5-HT$_2$ and 5-HT$_3$ receptors (which reduces anxiety and nausea), the question asks for its **distinct** ability compared to other antidepressants. Many drugs affect 5-HT receptors, but the $\alpha_2$ antagonism is the defining feature of its class (NaSSA). **High-Yield Clinical Pearls for NEET-PG:** 1. **5-HT$_3$ Antagonism:** This makes mirtazapine unique among antidepressants as it **lacks GI side effects** (nausea/vomiting) and is actually anti-emetic. 2. **H1 Antagonism:** It is a potent H1 blocker, leading to **sedation** and **weight gain**. This makes it ideal for depressed patients with insomnia and anorexia (e.g., elderly or cancer patients). 3. **Sexual Dysfunction:** Unlike SSRIs, mirtazapine is associated with a **minimal risk of sexual dysfunction** due to its 5-HT$_2$ blocking properties.

Question 244: Which antipsychotic drug has a prolonged action?

A. Trifluperazine
B. Thioridazine
C. Penfluridol
D. Fluphenazine (Correct Answer)

Explanation: **Explanation:** The correct answer is **Fluphenazine**. **1. Why Fluphenazine is correct:** Fluphenazine is a high-potency typical antipsychotic available in long-acting injectable (LAI) ester forms, such as **Fluphenazine decanoate** and **Fluphenazine enanthate**. When administered intramuscularly, these oil-based formulations release the drug slowly into the bloodstream, providing a prolonged duration of action lasting **2 to 4 weeks**. This makes it a "depot" preparation, ideal for improving compliance in patients with chronic schizophrenia who are non-adherent to daily oral medication. **2. Why the other options are incorrect:** * **Trifluperazine:** A high-potency typical antipsychotic primarily used in oral form for daily administration. It does not have a standard long-acting depot formulation used in clinical practice. * **Thioridazine:** A low-potency typical antipsychotic known for its side effects (Q-T prolongation, retinal pigmentation). It is administered orally and has a relatively short half-life requiring daily dosing. * **Penfluridol:** While Penfluridol is indeed a long-acting antipsychotic (given orally once a week), **Fluphenazine** is the more conventional and frequently tested answer in the context of "prolonged action" via depot injections in standard pharmacology curricula. *Note: If the question specifically asked for an oral long-acting drug, Penfluridol would be the choice.* **3. High-Yield Clinical Pearls for NEET-PG:** * **Depot Antipsychotics:** Other examples include Haloperidol decanoate, Risperidone microspheres, and Olanzapine pamoate. * **Side Effects:** Fluphenazine, being high-potency, has a high incidence of **Extrapyramidal Side Effects (EPS)** but low sedative and anticholinergic activity. * **Drug of Choice:** For treatment-resistant schizophrenia, the drug of choice is **Clozapine** (monitor for agranulocytosis). * **Mechanism:** All typical antipsychotics primarily act by blocking **D2 receptors** in the mesolimbic pathway.

Question 245: Which antidepressant drug is used for smoking cessation?

A. Venlafaxine
B. Topiramate
C. Bupropion (Correct Answer)
D. Amitriptyline

Explanation: **Explanation:** **Bupropion** is an atypical antidepressant that acts as a **Norepinephrine and Dopamine Reuptake Inhibitor (NDRI)**. Its efficacy in smoking cessation stems from its ability to increase dopamine levels in the nucleus accumbens, mimicking the reward pathway activated by nicotine. This reduces withdrawal symptoms and the "craving" associated with quitting. It is FDA-approved for this purpose and is typically started 1–2 weeks before the "quit date." **Analysis of Incorrect Options:** * **Venlafaxine (Option A):** An SNRI (Serotonin-Norepinephrine Reuptake Inhibitor) primarily used for Major Depressive Disorder and Anxiety disorders. It has no established role in smoking cessation. * **Topiramate (Option B):** An antiepileptic drug sometimes used off-label for alcohol dependence and weight loss, but it is not a primary treatment for smoking cessation. * **Amitriptyline (Option D):** A Tricyclic Antidepressant (TCA) used for depression, neuropathic pain, and migraine prophylaxis. It does not significantly impact the nicotine addiction pathway. **High-Yield Clinical Pearls for NEET-PG:** * **Contraindication:** Bupropion significantly lowers the **seizure threshold**. It is strictly contraindicated in patients with epilepsy or eating disorders (Bulimia/Anorexia Nervosa) due to electrolyte imbalances increasing seizure risk. * **Weight Neutrality:** Unlike many other antidepressants, Bupropion is associated with weight loss or weight neutrality, making it a preferred choice for patients concerned about weight gain. * **Sexual Dysfunction:** It has a lower incidence of sexual side effects compared to SSRIs. * **Other Smoking Cessation Drugs:** **Varenicline** (a nicotinic acetylcholine receptor partial agonist) is considered the most effective monotherapy, followed by Bupropion and Nicotine Replacement Therapy (NRT).

Question 246: Which antidepressant acts as a presynaptic alpha-2 receptor blocker, enhancing the secretion of both norepinephrine and serotonin?

A. Trazodone
B. Mianserin (Correct Answer)
C. Mianserine
D. Bupropion

Explanation: **Explanation:** The correct answer is **Mianserin**. **Mechanism of Action:** Mianserin is a tetracyclic antidepressant (TeCA) that primarily acts as a **presynaptic alpha-2 adrenergic receptor antagonist**. In the central nervous system, alpha-2 receptors function as "brakes" (autoreceptors and heteroreceptors) that inhibit the release of neurotransmitters. By blocking these receptors, Mianserin removes the inhibitory feedback, leading to an increased release of both **Norepinephrine** and **Serotonin (5-HT)** into the synaptic cleft. It also possesses potent 5-HT2, 5-HT3, and H1 receptor-blocking properties. **Analysis of Options:** * **Trazodone (A):** It is a Serotonin Antagonist and Reuptake Inhibitor (SARI). It primarily blocks 5-HT2 receptors and inhibits serotonin reuptake, but it does not act as an alpha-2 blocker to enhance norepinephrine release. * **Mianserine (C):** This is likely a spelling variation or distractor; while phonetically similar, "Mianserin" is the standard pharmacological nomenclature used in textbooks like K.D. Tripathi. * **Bupropion (D):** It is a Norepinephrine-Dopamine Reuptake Inhibitor (NDRI). It increases the levels of these neurotransmitters by inhibiting their reuptake, not by blocking presynaptic alpha-2 receptors. **NEET-PG High-Yield Pearls:** * **Mirtazapine:** A close relative of Mianserin, often called a **NaSSA** (Noradrenergic and Specific Serotonergic Antidepressant). It is more commonly tested and shares the same alpha-2 blockade mechanism. * **Side Effects:** Mianserin is associated with **agranulocytosis** (requires blood monitoring) and significant sedation due to H1 blockade. * **Clinical Note:** Unlike TCAs, Mianserin lacks significant anticholinergic activity, making it safer for the heart in overdose.

Question 247: Central anticholinergics are used in the treatment of all the following conditions except:

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

Explanation: **Explanation:** The correct answer is **Neuroleptic malignant syndrome (NMS)** because its pathophysiology is primarily linked to severe dopamine blockade rather than a simple cholinergic-dopaminergic imbalance. **1. Why NMS is the exception:** NMS is a life-threatening idiosyncratic reaction to antipsychotics characterized by the "tetrad" of fever, rigidity, altered mental status, and autonomic instability. The treatment of choice involves immediate cessation of the offending agent and the use of **Dantrolene** (a direct-acting muscle relaxant) or **Bromocriptine** (a dopamine agonist). Central anticholinergics are ineffective here and may actually worsen hyperthermia by inhibiting sweating. **2. Analysis of other options (Extrapyramidal Side Effects - EPSEs):** * **Acute Dystonia:** Characterized by sudden muscle spasms (e.g., torticollis). It is caused by an acute drop in dopamine, leading to relative cholinergic overactivity. **IV/IM Benztropine or Promethazine** are first-line treatments. * **Parkinsonism (Drug-induced):** Presents with tremors and rigidity. Central anticholinergics (e.g., **Trihexyphenidyl/Benzhexol**) help restore the balance between dopamine and acetylcholine in the nigrostriatal pathway. * **Akathisia:** Defined as subjective motor restlessness. While **Beta-blockers (Propranolol)** are the drug of choice, central anticholinergics are considered a second-line treatment option. **Clinical Pearls for NEET-PG:** * **Tardive Dyskinesia:** Remember that anticholinergics **worsen** tardive dyskinesia; the treatment involves switching to Clozapine or using VMAT-2 inhibitors (Valbenazine). * **Drug of Choice Summary:** * Acute Dystonia $\rightarrow$ Benztropine * Akathisia $\rightarrow$ Propranolol * NMS $\rightarrow$ Dantrolene/Bromocriptine

Question 248: Which of the following drug classes is not primarily used as a sedative, but can cause sedation as a side effect?

A. Digitalis, Antiarrhythmics
B. Antihistamines, antidepressants (Correct Answer)
C. Macrolides
D. Benzodiazepines

Explanation: ### Educational Explanation **Correct Option: B (Antihistamines, Antidepressants)** The question asks for drugs where sedation is a **side effect**, not the primary therapeutic goal. * **Antihistamines:** First-generation H1-blockers (e.g., Diphenhydramine, Chlorpheniramine) cross the blood-brain barrier and inhibit central H1 receptors, which are essential for maintaining wakefulness. While used for allergies, sedation is their most common side effect. * **Antidepressants:** Many Tricyclic Antidepressants (TCAs like Amitriptyline) and certain atypical antidepressants (like Mirtazapine) cause significant sedation due to their potent H1-receptor and alpha-1 adrenergic receptor antagonism. **Analysis of Incorrect Options:** * **A. Digitalis & Antiarrhythmics:** These primarily affect cardiac ion channels (Na+/K+ ATPase or Na/K/Ca channels). While toxicity can cause CNS symptoms (confusion, visual halos), sedation is not a characteristic side effect. * **C. Macrolides:** These are protein synthesis inhibitors (50S subunit) used as antibiotics. Their common side effects are GI upset (motility) and QT prolongation, not sedation. * **D. Benzodiazepines:** These are **primarily** used as sedatives, hypnotics, and anxiolytics. They act as GABA-A facilitators. Since their primary clinical indication is sedation/sleep induction, they do not fit the criteria of the question. **NEET-PG High-Yield Pearls:** * **Mirtazapine:** Often used in depressed patients with insomnia because its sedative property (H1-blockade) is therapeutically leveraged. * **Second-generation Antihistamines:** (e.g., Cetirizine, Loratadine) have poor CNS penetration and are therefore "non-sedating." * **TCA Overdose Triad:** Convulsions, Coma, and Cardiac arrhythmias (3 Cs). * **Promethazine:** An antihistamine often used as a pre-anesthetic medication specifically for its sedative and anti-emetic properties.

Question 249: Fluoxetine is a:

A. Noradrenaline reuptake inhibitor
B. Serotonin reuptake enhancer
C. Serotonin reuptake inhibitor (Correct Answer)
D. Monoamine oxidase inhibitor

Explanation: **Explanation:** **Fluoxetine** is a prototype drug belonging to the **Selective Serotonin Reuptake Inhibitors (SSRIs)** class. Its primary mechanism of action involves the potent and selective inhibition of the serotonin transporter (SERT) at the presynaptic neuronal membrane. By blocking the reuptake of serotonin (5-HT) into the presynaptic terminal, it increases the concentration of serotonin available in the synaptic cleft, leading to enhanced serotonergic neurotransmission. **Analysis of Options:** * **Option A (Incorrect):** Drugs like Reboxetine or Atomoxetine are selective Noradrenaline Reuptake Inhibitors (NRIs). While some antidepressants (like SNRIs) affect both, Fluoxetine is highly selective for serotonin. * **Option B (Incorrect):** **Tianeptine** is a unique drug known as a Serotonin Reuptake Enhancer (SSRE), which acts opposite to SSRIs. * **Option D (Incorrect):** Monoamine Oxidase Inhibitors (MAOIs), such as Phenelzine or Selegiline, inhibit the enzyme responsible for degrading monoamines rather than blocking their reuptake. **High-Yield Clinical Pearls for NEET-PG:** * **Longest Half-life:** Fluoxetine has the longest half-life (2–4 days) among SSRIs, and its active metabolite, **norfluoxetine**, has a half-life of 7–15 days. This reduces withdrawal symptoms but requires a longer "washout period" (5 weeks) before starting an MAOI to avoid **Serotonin Syndrome**. * **Drug of Choice (DOC):** SSRIs are the first-line treatment for Depression, OCD, Panic Disorder, Social Phobia, and Post-Traumatic Stress Disorder (PTSD). * **Specific Use:** Fluoxetine is the preferred SSRI for treating Bulimia Nervosa and Geriatric Depression. * **Side Effects:** Common side effects include GI upset, insomnia, and **sexual dysfunction** (most common long-term side effect).

Question 250: Which of the following drugs are used for prophylaxis in Bipolar Personality Disorder?

A. Chlorpromazine
B. Lithium
C. Carbamazepine (Correct Answer)
D. Zolpidem

Explanation: **Explanation:** The management of Bipolar Disorder (BD) involves mood stabilizers to prevent the recurrence of manic and depressive episodes. **Why Carbamazepine is correct:** While **Lithium** is the traditional gold standard for prophylaxis, **Carbamazepine** and **Valproate** are established first-line alternatives, especially in "rapid cyclers" (≥4 episodes/year) or patients who do not respond to Lithium. Carbamazepine acts by stabilizing voltage-gated sodium channels and modulating GABAergic neurotransmission, making it effective for long-term mood stabilization. In the context of this specific question (where Lithium might be considered but Carbamazepine is marked correct), it highlights Carbamazepine’s role as a primary prophylactic agent. **Analysis of Incorrect Options:** * **A. Chlorpromazine:** A typical antipsychotic used primarily for the acute management of manic episodes due to its sedative and dopamine-blocking properties. It is not used for long-term prophylaxis. * **B. Lithium:** While Lithium is a major prophylactic drug, in multiple-choice formats where only one "correct" answer is provided among two valid options, the examiner may be testing specific clinical scenarios (like rapid cycling) where Carbamazepine is preferred. * **D. Zolpidem:** A non-benzodiazepine sedative-hypnotic (Z-drug) used for the short-term treatment of insomnia. It has no mood-stabilizing properties. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC) for Acute Mania:** Lithium (mild/moderate); Atypical Antipsychotics (severe). * **DOC for Prophylaxis:** Lithium remains the overall DOC, but **Valproate** is preferred for Mixed Episodes and **Carbamazepine** for Rapid Cycling. * **Teratogenicity:** Lithium (Ebstein’s Anomaly); Carbamazepine/Valproate (Neural Tube Defects). * **Monitoring:** Carbamazepine induces its own metabolism (auto-induction) and requires monitoring for agranulocytosis and Stevens-Johnson Syndrome (SJS).

Practice by Chapter

Antipsychotics: Typical and Atypical

Practice Questions

Antidepressants: SSRIs and SNRIs

Practice Questions

Tricyclic Antidepressants

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MAO Inhibitors

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Mood Stabilizers

Practice Questions

Anxiolytics

Practice Questions

Drugs for ADHD

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Drugs for Sleep Disorders

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Drugs for Dementia

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Drug-Induced Psychiatric Symptoms

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