Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 121: Which of the following drugs is used in the treatment of Obsessive Compulsive Disorder (OCD)?

A. Clomipramine (Correct Answer)
B. Lithium
C. Olanzepine
D. None of the above

Explanation: **Explanation:** **Obsessive-Compulsive Disorder (OCD)** is primarily managed by enhancing serotonergic neurotransmission [1]. The first-line pharmacological treatment includes **Selective Serotonin Reuptake Inhibitors (SSRIs)** (e.g., Fluoxetine, Fluvoxamine, Sertraline) [1]. However, among the Tricyclic Antidepressants (TCAs), **Clomipramine** is the gold standard and the only TCA specifically indicated for OCD [2]. * **Clomipramine (Option A):** It is a tertiary amine TCA that acts as a potent and selective inhibitor of serotonin reuptake (SRI) [2]. Its efficacy in OCD is superior to other TCAs (like Imipramine or Amitriptyline) because those primarily affect norepinephrine rather than serotonin [2]. * **Lithium (Option B):** This is a mood stabilizer used as the drug of choice for **Bipolar Affective Disorder (BPAD)** and prophylaxis of manic-depressive illness. It has no primary role in treating OCD. * **Olanzapine (Option C):** This is an atypical antipsychotic used for **Schizophrenia** and Acute Mania. While atypical antipsychotics are sometimes used as "augmentation therapy" in treatment-resistant OCD, they are not the primary treatment. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC) for OCD:** SSRIs (due to a better safety profile) [1]. * **Most effective drug for OCD:** Clomipramine (often reserved for refractory cases due to side effects) [2]. * **OCD Dosing:** Treatment of OCD usually requires **higher doses** of SSRIs/Clomipramine and a **longer duration** (10–12 weeks) to see a clinical response compared to depression. * **Clomipramine Side Effects:** Notable for lowering the seizure threshold and causing significant anticholinergic effects [2].

Question 122: Which of the following is a primary use of 5-HT1 agonists?

A. Anti-anxiety drugs (Correct Answer)
B. Antipsychotic drugs
C. Gastroesophageal reflux disease (GERD)
D. Chemotherapy-induced vomiting

Explanation: **Explanation:** The correct answer is **A. Anti-anxiety drugs.** **Mechanism of Action:** The primary drug in this category is **Buspirone**, which acts as a **selective 5-HT1A partial agonist**. It is used for the treatment of Generalized Anxiety Disorder (GAD). Unlike benzodiazepines, it does not cause sedation, muscle relaxation, or physical dependence, making it an ideal choice for chronic anxiety management. Its effect typically takes 1–2 weeks to manifest. **Analysis of Incorrect Options:** * **B. Antipsychotic drugs:** Conventional antipsychotics primarily block **D2 receptors**. While some atypical antipsychotics (like Clozapine or Risperidone) involve 5-HT2A antagonism, 5-HT1 agonism is not their primary mechanism for treating psychosis. * **C. Gastroesophageal reflux disease (GERD):** Drugs used here include Proton Pump Inhibitors (PPIs) or H2 blockers. Prokinetic agents like Metoclopramide act via **5-HT4 agonism** and D2 antagonism, not 5-HT1. * **D. Chemotherapy-induced vomiting:** This is managed using **5-HT3 antagonists** (e.g., Ondansetron). Blocking 5-HT3 receptors in the Chemoreceptor Trigger Zone (CTZ) and the GI tract prevents the emetic reflex. **High-Yield NEET-PG Pearls:** * **Buspirone (5-HT1A):** "No Sedation, No Addiction, No Interaction with Alcohol." It is the "Safe" anxiolytic for elderly patients or those with a history of substance abuse. * **Sumatriptan (5-HT1B/1D):** Another class of 5-HT1 agonists used specifically for the **acute attack of Migraine** (causes vasoconstriction of cranial vessels). * **Tegaserod/Prucalopride (5-HT4):** Used for chronic constipation/IBS-C. * **Lorcaserin (5-HT2C):** Used as an appetite suppressant for obesity management.

Question 123: Lithium administration during pregnancy is associated with which of the following fetal abnormalities?

A. Ebstein anomaly (Correct Answer)
B. Transposition of great vessels
C. Truncus arteriosus
D. Tetralogy of Fallot

Explanation: **Explanation:** Lithium is a classic teratogen when administered during the first trimester of pregnancy. It is specifically associated with **Ebstein anomaly**, a rare congenital heart defect characterized by the downward displacement of the tricuspid valve leaflets into the right ventricle. This "atrialization" of the right ventricle leads to tricuspid regurgitation and right-sided heart failure. While the absolute risk is relatively low (approx. 1 in 1,000 to 2,000 exposures), it represents a significant increase compared to the general population. **Analysis of Options:** * **Ebstein Anomaly (Correct):** The hallmark cardiovascular malformation linked to Lithium. * **Transposition of Great Vessels (B), Truncus Arteriosus (C), and Tetralogy of Fallot (D):** These are cyanotic congenital heart diseases (Right-to-Left shunts) but are not specifically associated with Lithium use. They are more commonly linked to maternal diabetes or specific genetic syndromes (e.g., DiGeorge syndrome for Truncus Arteriosus). **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** Lithium has a narrow therapeutic index (0.6–1.2 mEq/L). Toxicity occurs >1.5 mEq/L. * **Pregnancy Management:** If a bipolar patient is on Lithium, fetal echocardiography is recommended at 18–20 weeks. * **Floppy Baby Syndrome:** Lithium use near term can cause neonatal hypotonia, cyanosis, and lethargy. * **Excretion:** Lithium is excreted in breast milk; hence, breastfeeding is generally discouraged while on this medication. * **Alternative:** Lamotrigine is often considered a safer mood stabilizer during pregnancy.

Question 124: Which of the following drugs does not cause sedation?

A. Buspirone (Correct Answer)
B. Nitrazepam
C. Zopiclone
D. Diazepam

Explanation: **Explanation:** The correct answer is **Buspirone**. **1. Why Buspirone is correct:** Buspirone is a non-benzodiazepine anxiolytic that belongs to the **Azapirone** class. Its primary mechanism of action is as a **selective 5-HT1A partial agonist**. Unlike Benzodiazepines (BZDs), it does not interact with the GABA-A receptor complex. Consequently, it lacks the sedative, hypnotic, anticonvulsant, and muscle relaxant properties associated with BZDs. It is specifically used for Generalized Anxiety Disorder (GAD) where daytime alertness is required. **2. Why the other options are incorrect:** * **Nitrazepam & Diazepam:** These are classic **Benzodiazepines** that act as positive allosteric modulators of the GABA-A receptor. They increase the frequency of chloride channel opening, leading to CNS depression, which manifests as significant sedation and hypnosis. * **Zopiclone:** This is a **"Z-drug"** (non-benzodiazepine hypnotic). Although it is chemically different from BZDs, it acts on the same BZ1 (α1 subunit) site of the GABA-A receptor. It is specifically indicated for the short-term treatment of insomnia because of its potent sedative-hypnotic effects. **3. NEET-PG High-Yield Pearls:** * **Buspirone Lag Time:** Unlike BZDs, Buspirone has a slow onset of action (takes 2–4 weeks for full effect); thus, it is not useful for acute anxiety or panic attacks. * **No Abuse Potential:** Buspirone does not cause physical dependence, withdrawal symptoms, or cognitive impairment, making it "driving-friendly." * **Z-drugs (Zolpidem, Zopiclone, Zaleplon):** These are preferred for insomnia as they do not significantly alter the sleep architecture (minimal effect on REM sleep).

Question 125: Buspirone is a:

A. Antianxiety drug (Correct Answer)
B. Antipsychotic drug
C. Antidepressant drug
D. None of the above

Explanation: **Explanation:** **Buspirone** is a non-benzodiazepine **anxiolytic (antianxiety)** drug. Unlike traditional benzodiazepines, it does not act on the GABA receptor complex. Instead, its primary mechanism of action is as a **selective partial agonist at the 5-HT1A receptors**. **Why Option A is correct:** Buspirone is specifically indicated for the management of **Generalized Anxiety Disorder (GAD)**. It effectively relieves anxiety without causing significant sedation, hypnosis, or muscle relaxation. A key characteristic is its slow onset of action; it typically takes 1–2 weeks to show therapeutic effects, making it unsuitable for acute anxiety or panic attacks. **Why other options are incorrect:** * **Option B (Antipsychotic):** Antipsychotics (e.g., Haloperidol, Risperidone) primarily act by blocking Dopamine (D2) receptors. Buspirone lacks significant D2 receptor antagonism and does not treat psychosis. * **Option C (Antidepressant):** While some antidepressants (like SSRIs) are used to treat anxiety, Buspirone itself is not classified as a primary antidepressant, though it is sometimes used as an "augmentation" agent in treatment-resistant depression. **High-Yield Clinical Pearls for NEET-PG:** 1. **No Abuse Potential:** Unlike benzodiazepines, Buspirone does not cause physical dependence, withdrawal symptoms, or cognitive impairment. 2. **No Interaction with Alcohol:** It does not potentiate the effects of CNS depressants like alcohol. 3. **Side Effects:** Common side effects include dizziness, nausea, and headache. 4. **Metabolism:** It is metabolized by **CYP3A4**; therefore, its levels increase when taken with grapefruit juice or erythromycin.

Question 126: Which of the following drugs is associated with the stated adverse drug reaction?

A. Haloperidol (Correct Answer)
B. Aripiprazole
C. Benztropine
D. Milnacipran

Explanation: ***Haloperidol*** - **Typical antipsychotic** that blocks **dopamine D2 receptors**, leading to **receptor upregulation** and **tardive dyskinesia** with chronic use. - Long-term **D2 receptor blockade** causes compensatory changes resulting in **involuntary choreiform movements** of face, tongue, and extremities. *Aripiprazole* - Acts as a **partial D2 agonist** rather than complete antagonist, providing **dopamine system stabilization**. - Actually **FDA-approved to treat tardive dyskinesia** due to its unique mechanism that doesn't cause receptor upregulation. *Benztropine* - **Anticholinergic agent** used to treat **acute extrapyramidal symptoms** but does not prevent or treat **tardive dyskinesia**. - Can actually **worsen tardive dyskinesia** by further disrupting the **dopamine-acetylcholine balance** in the brain. *Milnacipran* - **SNRI antidepressant** that inhibits **serotonin and norepinephrine reuptake** without affecting dopamine receptors. - Has **no association** with tardive dyskinesia as it doesn't interfere with **dopaminergic pathways** in the basal ganglia.

Question 127: Tardive dyskinesia is produced by which of the following drugs, except?

A. Fluphenazine
B. Haloperidol
C. Chlorpromazine
D. Clozapine (Correct Answer)

Explanation: **Explanation:** **Tardive Dyskinesia (TD)** is a late-onset extrapyramidal side effect (EPS) characterized by involuntary, repetitive movements (e.g., lip-smacking, tongue protrusion). It results from the **upregulation and supersensitivity of Dopamine D2 receptors** in the nigrostriatal pathway following chronic blockade. **Why Clozapine is the correct answer:** Clozapine is an **Atypical (Second-Generation) Antipsychotic**. It has a unique pharmacological profile characterized by: * **Low affinity for D2 receptors:** It dissociates rapidly from D2 receptors ("loose binding"). * **High 5-HT2A antagonism:** This increases dopamine release in the striatum, counteracting excessive D2 blockade. Because it does not cause significant D2 receptor upregulation, Clozapine carries a **negligible risk** of causing Tardive Dyskinesia. In fact, it is the drug of choice for patients who have already developed TD. **Why the other options are incorrect:** * **A, B, and C (Fluphenazine, Haloperidol, Chlorpromazine):** These are **Typical (First-Generation) Antipsychotics**. They act via potent and sustained blockade of D2 receptors. Chronic use of these agents leads to compensatory receptor supersensitivity, making them the primary culprits behind Tardive Dyskinesia. Haloperidol (High potency) carries a higher risk than Chlorpromazine (Low potency). **High-Yield Clinical Pearls for NEET-PG:** 1. **Treatment of TD:** The first step is to stop the offending drug or switch to **Clozapine** or **Quetiapine**. 2. **FDA-approved drugs for TD:** **Valbenazine** and **Deutetrabenazine** (VMAT2 inhibitors). 3. **The "Holiday" Myth:** Drug holidays do not prevent TD; they may actually unmask or worsen the symptoms. 4. **Anticholinergics:** Drugs like Trihexyphenidyl **worsen** Tardive Dyskinesia, unlike other EPS (like Parkinsonism) where they are used for treatment.

Question 128: Fluoxetine is a potent reuptake blocker of which neurotransmitter?

A. Morphine
B. Serotonin (Correct Answer)
C. Norepinephrine
D. Cholecystokinin

Explanation: **Explanation:** **Fluoxetine** is the prototype drug of 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)**, it increases the concentration of this neurotransmitter in the synaptic cleft, leading to enhanced serotonergic neurotransmission. This is the fundamental basis for its use in treating depression, OCD, and panic disorders. **Analysis of Incorrect Options:** * **Morphine (A):** This is an exogenous opioid analgesic that acts on mu-opioid receptors; it is not a neurotransmitter subject to reuptake inhibition by antidepressants. * **Norepinephrine (C):** While drugs like SNRIs (e.g., Venlafaxine) or TCAs (e.g., Amitriptyline) block norepinephrine reuptake, SSRIs like Fluoxetine have negligible affinity for the norepinephrine transporter (NET). * **Cholecystokinin (D):** This is a gastrointestinal peptide hormone and neuropeptide; it is not the target of standard antidepressant therapy. **NEET-PG High-Yield Pearls:** * **Longest Half-life:** Fluoxetine has the longest half-life among SSRIs (2–3 days), and its active metabolite, **norfluoxetine**, stays in the body for 7–10 days. * **Washout Period:** Due to its long half-life, a 5-week washout period is required before starting an MAO inhibitor to avoid **Serotonin Syndrome**. * **Drug of Choice:** It is often considered the DOC for **Bulimia nervosa** and is preferred in children/adolescents for depression. * **Side Effects:** Common issues include GI upset, insomnia, and sexual dysfunction (e.g., delayed ejaculation).

Question 129: The secretion of which of the following hormones increases with chlorpromazine therapy?

A. Prolactin (Correct Answer)
B. Gonadotropin
C. Corticotropin
D. Antidiuretic hormone

Explanation: **Explanation:** The correct answer is **Prolactin**. **Mechanism of Action:** Chlorpromazine is a typical (first-generation) antipsychotic that acts primarily by blocking **Dopamine (D2) receptors**. In the brain, dopamine is the primary physiological inhibitor of prolactin secretion from the anterior pituitary (acting via the **tuberoinfundibular pathway**). By blocking D2 receptors in this pathway, chlorpromazine removes the "inhibitory brake" on lactotrophs, leading to hyperprolactinemia. **Analysis of Incorrect Options:** * **B. Gonadotropin (FSH/LH):** High prolactin levels exert negative feedback on the hypothalamus, inhibiting the release of Gonadotropin-Releasing Hormone (GnRH). This leads to a **decrease** in FSH and LH, often resulting in amenorrhea or infertility. * **C. Corticotropin (ACTH):** Chlorpromazine generally suppresses the hypothalamic-pituitary-adrenal (HPA) axis, leading to a potential **decrease** in ACTH secretion, rather than an increase. * **D. Antidiuretic hormone (ADH):** While some psychotropic drugs can cause SIADH, chlorpromazine does not typically increase ADH as a primary endocrine side effect. **NEET-PG High-Yield Pearls:** * **Clinical Manifestations:** Hyperprolactinemia presents as galactorrhea, gynecomastia, and sexual dysfunction. * **Pathway Specificity:** Antipsychotic efficacy (positive symptoms) is due to D2 blockade in the **mesolimbic** pathway; extrapyramidal side effects (EPS) are due to blockade in the **nigrostriatal** pathway. * **Exceptions:** **Clozapine** and **Quetiapine** have a lower risk of increasing prolactin compared to typical antipsychotics and Risperidone. * **Growth Hormone:** Chlorpromazine also tends to **decrease** Growth Hormone secretion (dopamine normally stimulates GH in healthy individuals).

Question 130: Newer MAO inhibitors are useful in the treatment of?

A. Mania
B. Schizophrenia
C. Hypertension
D. Depression (Correct Answer)

Explanation: ### **Explanation** **Correct Answer: D. Depression** **Mechanism of Action:** Monoamine Oxidase Inhibitors (MAOIs) work by inhibiting the enzyme responsible for the metabolic breakdown of biogenic amines (Norepinephrine, Serotonin, and Dopamine). By blocking this degradation, MAOIs increase the synaptic concentration of these neurotransmitters. Since the **"Monoamine Hypothesis"** of depression suggests that the condition results from a deficiency of these amines in the brain, MAOIs effectively alleviate depressive symptoms. **Why the other options are incorrect:** * **A. Mania:** Mania is characterized by an *excess* of monoamines. MAOIs would exacerbate this condition. The mainstay of treatment for mania includes mood stabilizers (Lithium) and antipsychotics. * **B. Schizophrenia:** This disorder is primarily linked to overactive dopamine pathways. Increasing dopamine levels via MAOIs could worsen psychotic symptoms. Antipsychotics (D2 receptor antagonists) are the treatment of choice. * **C. Hypertension:** Older, non-selective MAOIs are notorious for causing **Hypertensive Crisis** (the "Cheese Reaction") when taken with tyramine-rich foods. They are never used to treat hypertension. **NEET-PG High-Yield Pearls:** * **Classification:** * *Non-selective (Irreversible):* Phenelzine, Tranylcypromine, Isocarboxazid. * *MAO-A Selective (Reversible):* **Moclobemide** (RIMA - Reversible Inhibitor of MAO-A). These are the "newer" MAOIs that carry a much lower risk of hypertensive crisis. * *MAO-B Selective:* Selegiline, Rasagiline (primarily used in **Parkinson’s Disease**). * **The Cheese Reaction:** Occurs when tyramine (found in aged cheese, wine, beer) displaces stored norepinephrine. Because MAO-A is inhibited, the excess norepinephrine is not degraded, leading to a massive sympathetic surge and stroke risk. * **Drug Interaction:** Never combine MAOIs with SSRIs due to the risk of **Serotonin Syndrome**. A washout period of 2–5 weeks is required when switching between them.

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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