Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 61: Discontinuation of which of the following drugs can result in anxiety and insomnia?

A. Venlafaxine (Correct Answer)
B. Imipramine
C. Valproate
D. Olanzapine

Explanation: **Explanation:** The correct answer is **Venlafaxine**. This question tests the concept of **Antidepressant Discontinuation Syndrome (ADS)**, which is particularly severe with drugs that have a short half-life and potent mechanism of action. **1. Why Venlafaxine is correct:** Venlafaxine is a Serotonin-Norepinephrine Reuptake Inhibitor (SNRI). It has a very **short half-life** (approx. 5 hours for the parent drug). Abrupt withdrawal leads to a rapid drop in synaptic serotonin and norepinephrine levels, causing "FINISH" symptoms: **F**lu-like symptoms, **I**nsomnia, **N**ausea, **I**mbalance, **S**ensory disturbances (e.g., "brain zaps"), and **H**yperarousal (**Anxiety**). Among antidepressants, Venlafaxine and Paroxetine have the highest incidence of withdrawal symptoms. **2. Why the other options are incorrect:** * **Imipramine:** While TCAs can cause cholinergic rebound (nausea, sweating) upon discontinuation, they generally have longer half-lives and active metabolites, making the withdrawal less acute than Venlafaxine. * **Valproate:** This is a mood stabilizer/anticonvulsant. Discontinuation primarily risks seizure recurrence or mood relapse rather than a specific acute withdrawal syndrome characterized by insomnia and anxiety. * **Olanzapine:** An atypical antipsychotic. While abrupt cessation can cause rebound psychosis or cholinergic rebound, it is not the classic drug associated with the specific "anxiety and insomnia" withdrawal profile seen in antidepressant discontinuation. **Clinical Pearls for NEET-PG:** * **Longest half-life SSRI:** Fluoxetine (least likely to cause withdrawal symptoms). * **Shortest half-life SSRI:** Paroxetine (most likely to cause withdrawal). * **Management of ADS:** Reintroduce the drug and taper slowly. In severe cases, cross-tapering to a drug with a longer half-life (like Fluoxetine) is a strategy. * **Venlafaxine Side Effect:** Dose-dependent **Hypertension** (due to norepinephrine reuptake inhibition at higher doses).

Question 62: Which of the following substances is hallucinogenic?

A. Codeine
B. Cocaine (Correct Answer)
C. Papaverine
D. Steroid

Explanation: **Explanation:** **Cocaine** is a potent central nervous system (CNS) stimulant that acts by inhibiting the reuptake of dopamine, norepinephrine, and serotonin [2]. While primarily classified as a stimulant, high doses or chronic use can lead to **"Cocaine Psychosis,"** characterized by vivid visual, auditory, and tactile hallucinations (e.g., **Formication** or "Cocaine bugs"—the sensation of insects crawling under the skin). **Analysis of Options:** * **Codeine (Option A):** An opioid analgesic and antitussive. Its primary side effects are sedation, constipation, and respiratory depression, not hallucinations. * **Papaverine (Option B):** A non-opioid benzylisoquinoline alkaloid used as a vasodilator and smooth muscle relaxant. It has no significant CNS activity related to psychosis. * **Steroids (Option D):** While corticosteroids can cause "Steroid Psychosis" (mood swings, mania, or depression), they are not classified as primary hallucinogens. In the context of classic drugs of abuse, Cocaine is the more definitive answer for hallucinogenic potential. **High-Yield NEET-PG Pearls:** * **Formication (Magnan’s Symptom):** A classic tactile hallucination pathognomonic for cocaine toxicity. * **Mechanism:** Cocaine blocks the **DAT (Dopamine Transporter)**, leading to increased dopamine in the nucleus accumbens, causing euphoria and psychosis [2]. * **Other Hallucinogens to remember:** LSD (most potent), Psilocybin, Mescaline, and Phencyclidine (PCP) [1]. * **Management:** Acute cocaine toxicity is managed with **Benzodiazepines**; Beta-blockers are generally avoided due to the risk of unopposed alpha-adrenergic stimulation.

Question 63: Which of the following drugs does not activate opioid receptors, has been proposed as a drug in the management of opioid addiction, and with just a single dose blocks the action of injected heroin for up to 48 hours?

A. Amphetamine
B. Buspirone
C. Methadone
D. Naltrexone (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Naltrexone** **Mechanism and Rationale:** Naltrexone is a potent, long-acting **pure opioid antagonist** [1], [3]. Unlike methadone or buprenorphine, it has **zero agonist activity** (it does not activate opioid receptors) [3], [4]. It works by competitively binding to $\mu$-opioid receptors, thereby blocking the effects of exogenous opioids like heroin. * **Pharmacokinetics:** It has a significantly longer half-life than naloxone [4]. A single oral dose of 50 mg can effectively block the "high" and physical effects of injected heroin for **up to 48–72 hours**. This makes it an ideal agent for **relapse prevention** in highly motivated patients who have already undergone detoxification [5]. **Analysis of Incorrect Options:** * **A. Amphetamine:** A CNS stimulant that increases synaptic dopamine and norepinephrine. It has no role in opioid addiction management and is itself a drug of abuse. * **B. Buspirone:** A 5-HT$_{1A}$ partial agonist used as an anxiolytic. It does not interact with opioid receptors. * **C. Methadone:** While used in opioid addiction (maintenance therapy), it is a **full $\mu$-opioid agonist** [5]. It activates the receptors to prevent withdrawal symptoms, which contradicts the question's criteria. **High-Yield Clinical Pearls for NEET-PG:** * **Naltrexone vs. Naloxone:** Naltrexone is orally active and long-acting (used for maintenance/alcoholism); Naloxone is given parenterally and is short-acting (used for acute opioid overdose) [5]. * **Alcoholism:** Naltrexone is also FDA-approved for alcohol dependence as it reduces "craving" by blocking endogenous opioid-mediated reward pathways [2], [4]. * **Pre-requisite:** Naltrexone must **never** be started until a patient is opioid-free for at least 7–10 days; otherwise, it will precipitate severe, acute withdrawal.

Question 64: Which of the following medications is most associated with extrapyramidal side effects?

A. Haloperidol (Correct Answer)
B. Chlorpromazine
C. Imipramine
D. Clomipramine

Explanation: **Explanation:** The correct answer is **Haloperidol**. This question tests your understanding of the side effect profiles of typical antipsychotics based on their receptor potency. **1. Why Haloperidol is correct:** Haloperidol is a **High-Potency Typical Antipsychotic**. It acts as a potent antagonist at **D2 receptors** in the mesolimbic and nigrostriatal pathways. Because it has a very high affinity for D2 receptors and low anticholinergic activity, it is the drug most frequently associated with **Extrapyramidal Side Effects (EPS)**, such as acute dystonia, akathisia, and parkinsonism. **2. Why the other options are incorrect:** * **Chlorpromazine:** This is a **Low-Potency Typical Antipsychotic**. While it can cause EPS, it has significant **anticholinergic (M1) activity**. Since acetylcholine and dopamine exist in a reciprocal balance in the basal ganglia, the inherent anticholinergic effect of chlorpromazine partially "buffers" against EPS. It is more commonly associated with sedation and orthostatic hypotension. * **Imipramine & Clomipramine:** These are **Tricyclic Antidepressants (TCAs)**. Their primary side effects are related to muscarinic, alpha-1, and histaminic blockade (dry mouth, blurred vision, sedation). They do not primarily block D2 receptors and thus do not typically cause EPS. **High-Yield NEET-PG Pearls:** * **EPS Hierarchy:** High potency (Haloperidol, Fluphenazine) > Low potency (Chlorpromazine, Thioridazine) > Atypicals (Clozapine, Quetiapine). * **Treatment of Acute Dystonia:** Centrally acting anticholinergics like **Promethazine** or **Benztropine**. * **Neuroleptic Malignant Syndrome (NMS):** A severe side effect of Haloperidol; treated with **Dantrolene** or Bromocriptine. * **Rule of Thumb:** High potency = High EPS; Low potency = High Sedation/Autonomic effects.

Question 65: Which of the following is NOT a side effect of clozapine?

A. Agranulocytosis
B. Hypersalivation
C. Myocarditis
D. Hyperprolactinemia (Correct Answer)

Explanation: **Explanation:** Clozapine is a prototype **Atypical Antipsychotic** (Second Generation). The correct answer is **Hyperprolactinemia** because clozapine is unique among antipsychotics for its minimal effect on prolactin levels. 1. **Why Hyperprolactinemia is NOT a side effect:** Most typical antipsychotics block $D_2$ receptors in the **tuberoinfundibular pathway**, leading to increased prolactin. However, Clozapine has low affinity for $D_2$ receptors and rapidly dissociates from them. Consequently, it does not cause significant hyperprolactinemia, making it a preferred drug in patients experiencing galactorrhea or gynecomastia from other agents. 2. **Analysis of Incorrect Options:** * **Agranulocytosis:** This is the most dreaded side effect (1% of patients). It requires mandatory weekly WBC monitoring for the first 6 months. * **Hypersalivation (Sialorrhea):** Paradoxically, despite having anticholinergic properties, clozapine causes significant nighttime drooling, likely due to $M_4$ receptor agonism or impairment of the swallowing reflex. * **Myocarditis:** A rare but potentially fatal idiosyncratic reaction, usually occurring within the first 2 months of treatment. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Clozapine is the gold standard for **Treatment-Resistant Schizophrenia** and schizophrenia associated with suicidality. * **Seizures:** It carries a dose-dependent risk of seizures (highest among antipsychotics). * **Metabolic Syndrome:** It causes significant weight gain, dyslipidemia, and Type 2 Diabetes. * **No EPS:** It has the lowest risk of Extrapyramidal Side-effects (EPS) and Tardive Dyskinesia.

Question 66: Which of the following antipsychotic drugs is available as a depot injection?

A. Fluphenazine (Correct Answer)
B. Ziprasidone
C. Trifluoperazine
D. Aripiprazole

Explanation: **Explanation:** **1. Why Fluphenazine is Correct:** Fluphenazine is a high-potency typical antipsychotic. It is available as **Fluphenazine decanoate**, an esterified formulation in a sesame oil vehicle. When administered intramuscularly, it is released slowly into the bloodstream, providing a therapeutic effect for 2–4 weeks. This "depot" preparation is primarily used to improve treatment adherence in patients with chronic schizophrenia who are non-compliant with oral medications. **2. Analysis of Incorrect Options:** * **Ziprasidone:** An atypical antipsychotic available in oral and **short-acting** IM forms (used for acute agitation), but it does not have a long-acting depot formulation. * **Trifluoperazine:** A high-potency typical antipsychotic used orally for schizophrenia and anxiety; however, it is not available as a depot injection. * **Aripiprazole:** While Aripiprazole *does* have a depot form (Aripiprazole Maintena), in the context of standard medical examinations like NEET-PG, **Fluphenazine** and **Haloperidol** are the classic, high-yield examples of depot injections. In this specific MCQ, Fluphenazine is the established traditional answer. **3. High-Yield Clinical Pearls for NEET-PG:** * **Common Depot Drugs:** The most frequently tested depot antipsychotics are **Fluphenazine decanoate** and **Haloperidol decanoate**. * **Atypical Depots:** Newer long-acting injectables (LAIs) include Risperidone, Paliperidone, and Olanzapine (though Olanzapine carries a risk of Post-injection Delirium Sedation Syndrome). * **Mechanism:** Esterification with long-chain fatty acids (like decanoate) increases lipophilicity, allowing slow release from the muscle site. * **Side Effects:** Depot injections of typical antipsychotics carry a high risk of **Extrapyramidal Side Effects (EPS)** due to their high potency and long duration of action.

Question 67: Dry mouth during antidepressant therapy is caused by blockade of which receptors?

A. Muscarinic acetylcholine receptors (Correct Answer)
B. Serotonergic receptors
C. Dopaminergic receptors
D. GABA receptors

Explanation: **Explanation:** Dry mouth (xerostomia) is a classic side effect of several antidepressant classes, most notably **Tricyclic Antidepressants (TCAs)** like Amitriptyline and certain SSRIs/SNRIs. **1. Why Muscarinic Acetylcholine Receptors are correct:** The salivary glands are primarily under the control of the parasympathetic nervous system. Stimulation of **M3 muscarinic receptors** by acetylcholine normally triggers watery salivation. Many antidepressants possess potent **anticholinergic (antimuscarinic)** properties. By blocking these receptors, the drugs inhibit parasympathetic signaling, leading to decreased secretions, resulting in dry mouth, blurred vision, urinary retention, and constipation. **2. Analysis of Incorrect Options:** * **Serotonergic receptors:** Blockade or stimulation of these receptors (e.g., 5-HT2) is associated with side effects like sexual dysfunction, GI upset, or serotonin syndrome, but not typically dry mouth. * **Dopaminergic receptors:** Blockade of D2 receptors (common in antipsychotics) leads to Extrapyramidal Symptoms (EPS) and hyperprolactinemia. * **GABA receptors:** These are inhibitory receptors in the CNS. Drugs acting here (like Benzodiazepines) cause sedation and anxiolysis, not peripheral autonomic side effects like xerostomia. **High-Yield Clinical Pearls for NEET-PG:** * **TCAs** are the biggest culprits of "Anti-SLUDGE" effects (Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis—all of which are decreased). * **Amitriptyline** has the highest anticholinergic potency among TCAs. * **Management:** Patients are often advised to use sugarless gum or frequent sips of water. * **Contraindication:** Due to their muscarinic blockade, these drugs should be used with caution in patients with **narrow-angle glaucoma** and **benign prostatic hyperplasia (BPH)**.

Question 68: Which of the following drugs has the least anticholinergic side effects?

A. Clomipramine
B. Desipramine (Correct Answer)
C. Imipramine
D. Trimipramine

Explanation: **Explanation:** The question tests your knowledge of the side effect profiles of **Tricyclic Antidepressants (TCAs)**. All options listed belong to the TCA class, which typically block muscarinic (M1), histamine (H1), and alpha-1 adrenergic receptors, leading to their characteristic side effect profile. **Why Desipramine is Correct:** TCAs are broadly divided into **Tertiary Amines** and **Secondary Amines**. * **Secondary Amines** (e.g., Desipramine, Nortriptyline) are metabolites of tertiary amines. * They are more selective for inhibiting Norepinephrine reuptake and, crucially, have a **significantly lower affinity** for muscarinic, histaminic, and alpha-adrenergic receptors compared to their parent compounds. * **Desipramine** is the most potent norepinephrine reuptake inhibitor among TCAs and possesses the **least anticholinergic and sedative activity** in this group. **Why Other Options are Incorrect:** * **A, C, and D (Clomipramine, Imipramine, Trimipramine):** These are all **Tertiary Amines**. Tertiary amines are potent inhibitors of both Serotonin and Norepinephrine reuptake but also have a high affinity for muscarinic receptors. This results in significant anticholinergic effects such as dry mouth, blurred vision, urinary retention, and constipation. Among these, **Amitriptyline** (not listed) and **Clomipramine** are often cited as having the highest anticholinergic potency. **High-Yield NEET-PG Pearls:** 1. **Most Anticholinergic TCA:** Amitriptyline. 2. **Least Anticholinergic/Least Sedating TCA:** Desipramine. 3. **Least Arrhythmogenic/Safest in Elderly:** Nortriptyline (a secondary amine with a better safety profile). 4. **Drug of Choice for OCD:** Clomipramine (due to high serotonin selectivity). 5. **TCA Overdose Triad:** Coma, Convulsions, and Cardiac arrhythmias (prolonged QRS/QT intervals). The antidote for cardiotoxicity is Sodium Bicarbonate.

Question 69: Which of the following drugs belongs to the NaSSA group?

A. Amoxetine
B. Mirtazapine (Correct Answer)
C. Duloxetine
D. Venlafaxine

Explanation: **Explanation:** **Mirtazapine** is the correct answer as it is the prototype drug of the **NaSSA** (Noradrenergic and Specific Serotonergic Antidepressant) class. ### Why Mirtazapine is correct: Mirtazapine works through a unique dual mechanism: 1. **Alpha-2 ($\alpha_2$) Antagonism:** It blocks presynaptic $\alpha_2$ autoreceptors (on noradrenergic neurons) and heteroreceptors (on serotonergic neurons). This "disinhibits" the neurons, leading to increased release of both Norepinephrine and Serotonin. 2. **Specific Serotonergic Action:** It blocks **$5-HT_2$** and **$5-HT_3$** receptors. By blocking these, it directs serotonin to specifically stimulate the **$5-HT_1A$** receptor, which mediates antidepressant effects while avoiding side effects like anxiety ($5-HT_2$) or nausea ($5-HT_3$). ### Why other options are incorrect: * **Amoxetine (Atomoxetine):** A selective **NRI** (Norepinephrine Reuptake Inhibitor) primarily used in ADHD. * **Duloxetine & Venlafaxine:** These belong to the **SNRI** (Serotonin-Norepinephrine Reuptake Inhibitor) class. They work by inhibiting the reuptake transporters (SERT and NET) rather than blocking $\alpha_2$ receptors. ### High-Yield Clinical Pearls for NEET-PG: * **Side Effect Profile:** Mirtazapine is a potent **$H_1$ blocker**, leading to significant **sedation** and **weight gain**. * **Clinical Utility:** It is the drug of choice for depressed patients suffering from **insomnia** and **underweight/anorexia**. * **Sexual Dysfunction:** Unlike SSRIs, Mirtazapine has a very low incidence of sexual dysfunction due to its $5-HT_2$ blockade. * **The "California Rocket Fuel":** A high-yield combination of Venlafaxine + Mirtazapine used for treatment-resistant depression.

Question 70: Which of the following statements is NOT true for the therapy with lithium?

A. It is used in bipolar disorder.
B. Amiloride is useful in treating lithium-induced diabetes insipidus.
C. Regular measurements of blood concentration of lithium are necessary.
D. Sodium ion is a specific antidote for lithium clearance. (Correct Answer)

Explanation: ### Explanation **1. Why Option D is the correct answer (The False Statement):** While sodium intake influences lithium excretion, **sodium ion is NOT a specific antidote** for lithium toxicity. Lithium is handled by the kidneys similarly to sodium; however, there is no pharmacological "antidote" that specifically neutralizes lithium. In cases of severe toxicity, the definitive treatment for clearance is **Hemodialysis**. While saline diuresis (Normal Saline) is used to restore volume and promote excretion, it is a supportive measure, not a specific antidote [4]. **2. Analysis of Incorrect Options (True Statements):** * **Option A:** Lithium remains the **gold standard** for the long-term prophylaxis and treatment of Bipolar Affective Disorder (BPAD), especially for manic episodes [3]. * **Option B:** Lithium causes Nephrogenic Diabetes Insipidus (NDI) by inhibiting ADH-induced cAMP production. **Amiloride** is the drug of choice because it blocks the ENaC channels in the collecting duct, preventing lithium from entering the cells and interfering with ADH action [1]. * **Option C:** Lithium has a **narrow therapeutic index** (0.6–1.2 mEq/L) [1, 4]. Regular Therapeutic Drug Monitoring (TDM) is mandatory to prevent toxicity, which typically occurs at levels >1.5 mEq/L [4]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** Blood samples for TDM should be drawn **12 hours after the last dose** (trough level). Before starting treatment, ensuring normal functioning of kidneys and thyroid is essential [3]. * **Drug Interactions:** **"D-A-N-T-E"** (Diuretics like Thiazides, ACE inhibitors, NSAIDs, Tetracyclines, and Ethacrynic acid) can increase lithium levels and precipitate toxicity [1]. * **Teratogenicity:** Use in pregnancy is associated with **Ebstein’s Anomaly** (atrialization of the right ventricle). * **Side Effects:** L-I-T-H: **L**eukocytosis, **I**nsipidus (NDI), **T**remors/Teratogenicity, **H**ypothyroidism [2].

Practice by Chapter

Antipsychotics: Typical and Atypical

Practice Questions

Antidepressants: SSRIs and SNRIs

Practice Questions

Tricyclic Antidepressants

Practice Questions

MAO Inhibitors

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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

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