Drugs in Psychiatric Disorders — MCQs
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Which of the following drugs can cause toxic epidermal necrolysis as an adverse effect?
Which 5-HT1A agonist drug acts as an anxiolytic agent?
Which of the following drugs are used in the treatment of ADHD?
Propranolol is useful in the management of which of the following side effects of a typical neuroleptic?
Tricyclic antidepressants are contraindicated in which of the following conditions?
Drug-induced psychosis occurs due to all the following drugs except?
Which of the following typical antipsychotic drugs is not available in depot form?
Which was the first type of antidepressant that was introduced?
A patient on antidepressant therapy developed sudden hypertension on consuming cheese. Which of the following drugs is probably responsible for this condition?
Which drug is known to cause agranulocytosis?
Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs
Question 81: Which of the following drugs can cause toxic epidermal necrolysis as an adverse effect?
- A. Felbamate
- B. Gabapentin
- C. Lamotrigine (Correct Answer)
- D. Vigabatrin
Explanation: **Explanation:** **Lamotrigine** is a broad-spectrum antiepileptic drug (AED) that acts by blocking voltage-gated sodium channels and inhibiting glutamate release. Its most significant and life-threatening adverse effect is a severe hypersensitivity reaction manifesting as **Stevens-Johnson Syndrome (SJS)** or **Toxic Epidermal Necrolysis (TEN)**. The risk is highest during the first 8 weeks of treatment and is significantly increased if the drug is started at a high dose or escalated rapidly. **Analysis of Options:** * **Lamotrigine (Correct):** Known for causing severe skin rashes. To minimize this risk, clinicians follow a "low and slow" titration schedule. * **Felbamate:** Primarily associated with **aplastic anemia** and **severe hepatotoxicity**, which limits its clinical use. * **Gabapentin:** Generally well-tolerated; its main side effects are sedation, dizziness, and peripheral edema. It is not typically associated with life-threatening dermatological reactions. * **Vigabatrin:** Notorious for causing **permanent visual field defects** (concentric contraction) due to retinal toxicity, requiring regular perimetry monitoring. **High-Yield Clinical Pearls for NEET-PG:** * **Drug Interaction:** Valproate inhibits the metabolism of Lamotrigine, doubling its half-life and significantly increasing the risk of SJS/TEN. * **Other Drugs causing SJS/TEN:** Remember the mnemonic **SAPP**: **S**ulfonamides, **A**ntiepileptics (Phenytoin, Carbamazepine, Phenobarbital, Lamotrigine), **P**enicillins, and **P**iroxicam (NSAIDs). * **HLA Link:** HLA-B*1502 is strongly associated with SJS/TEN caused by Carbamazepine, particularly in Asian populations.
Question 82: Which 5-HT1A agonist drug acts as an anxiolytic agent?
- A. Diazepam
- B. Zolpidem
- C. Cinnarizine
- D. Buspirone (Correct Answer)
Explanation: **Explanation:** **Buspirone** is the correct answer as it is a selective **5-HT1A partial agonist** used primarily for the management of Generalized Anxiety Disorder (GAD). Unlike traditional anxiolytics, it does not interact with the GABA-A receptor complex. Its primary mechanism involves stimulating presynaptic 5-HT1A receptors (inhibiting serotonin release) and postsynaptic 5-HT1A receptors in the hippocampus and cortex. **Analysis of Incorrect Options:** * **Diazepam:** A Benzodiazepine (BZD) that acts as a positive allosteric modulator of the **GABA-A receptor**. While it is an anxiolytic, it works via chloride channel opening, not 5-HT receptors. * **Zolpidem:** A "Z-drug" used as a hypnotic. It selectively binds to the **alpha-1 subunit of the GABA-A receptor**. It lacks significant anxiolytic or muscle relaxant properties. * **Cinnarizine:** An **H1-receptor antagonist** and calcium channel blocker used primarily for vertigo and motion sickness; it has no role as a 5-HT1A-mediated anxiolytic. **High-Yield NEET-PG Pearls:** 1. **Delayed Onset:** Buspirone takes **2–4 weeks** to show therapeutic effects, making it unsuitable for acute anxiety or panic attacks. 2. **"3 No’s" of Buspirone:** **No** sedation, **No** muscle relaxation/anticonvulsant activity, and **No** potential for abuse/dependence (unlike BZDs). 3. **No Interaction with Alcohol:** It does not potentiate the effects of CNS depressants. 4. **Metabolism:** It is metabolized by **CYP3A4**; concurrent use with rifampicin (inducer) or erythromycin (inhibitor) requires dose adjustment.
Question 83: Which of the following drugs are used in the treatment of ADHD?
- A. Amphetamine
- B. Modafinil
- C. Methylphenidate
- D. All of the above (Correct Answer)
Explanation: Attention-Deficit Hyperactivity Disorder (ADHD) is primarily managed by increasing the synaptic concentrations of dopamine and norepinephrine in the prefrontal cortex, which improves focus and impulse control [2]. * **Methylphenidate (Option C):** This is the **first-line drug of choice** for ADHD [1, 2]. It acts by inhibiting the reuptake of dopamine and norepinephrine (NDRI). It is preferred due to its efficacy and relatively lower potential for abuse compared to pure amphetamines [1, 2]. * **Amphetamines (Option A):** These are potent CNS stimulants that both inhibit reuptake and promote the release of catecholamines from storage vesicles [3]. They are highly effective and FDA-approved for ADHD [1, 2, 3]. * **Modafinil (Option B):** While primarily used as a first-line agent for **Narcolepsy**, Modafinil is used **off-label** in the treatment of ADHD, particularly in patients who do not respond well to or cannot tolerate conventional stimulants. It acts as a weak dopamine reuptake inhibitor and modulates the orexin system. Since all three drugs are utilized in clinical practice for managing ADHD, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** 1. **Non-Stimulant of Choice:** **Atomoxetine** (a selective Norepinephrine Reuptake Inhibitor) is the preferred non-stimulant for ADHD, especially in patients with a history of substance abuse or tics. 2. **Side Effects:** Stimulants can cause growth retardation (monitor height/weight), insomnia, and appetite suppression [1]. 3. **Alpha-2 Agonists:** Clonidine and Guanfacine are also used as adjunctive treatments for ADHD. 4. **Drug Holiday:** Often recommended during weekends or school vacations to minimize growth suppression in children.
Question 84: Propranolol is useful in the management of which of the following side effects of a typical neuroleptic?
- A. Parkinsonism
- B. Acute muscle dystonia
- C. Tardive dyskinesia
- D. Akathisia (Correct Answer)
Explanation: **Explanation:** **Akathisia** is characterized by a subjective feeling of inner restlessness and an inability to sit still. It is one of the most common and distressing Extrapyramidal Side Effects (EPS) of typical antipsychotics (neuroleptics). **Propranolol**, a non-selective beta-blocker, is the **drug of choice** for akathisia. It works by crossing the blood-brain barrier and blocking beta-adrenergic receptors, which helps alleviate the peripheral and central manifestations of restlessness. **Analysis of Incorrect Options:** * **A. Parkinsonism:** Drug-induced parkinsonism (rigidity, tremors, bradykinesia) is caused by dopamine (D2) blockade in the nigrostriatal pathway. It is managed with **central anticholinergics** like Benztropine or Trihexyphenidyl (Benzhexol). * **B. Acute Muscle Dystonia:** This involves sudden, painful muscle spasms (e.g., torticollis, oculogyric crisis). It is a medical emergency treated with **parenteral anticholinergics** (Promethazine or Benztropine). * **C. Tardive Dyskinesia:** This is a late-onset EPS characterized by involuntary choreoathetoid movements (e.g., lip-smacking). Propranolol is ineffective here. Management involves switching to Clozapine or using VMAT-2 inhibitors like **Valbenazine**. **High-Yield Clinical Pearls for NEET-PG:** * **Akathisia** is often misdiagnosed as worsening psychosis/agitation; increasing the neuroleptic dose will worsen it, while Propranolol will improve it. * **Benzodiazepines** (like Lorazepam) are second-line agents for akathisia. * **Neuroleptic Malignant Syndrome (NMS):** Remember the "FEVER" mnemonic (Fever, Encephalopathy, Vitals unstable, Elevated CPK, Rigidity). The drug of choice is **Dantrolene** or Bromocriptine.
Question 85: Tricyclic antidepressants are contraindicated in which of the following conditions?
- A. Glaucoma (Correct Answer)
- B. Brain tumor
- C. Bronchial asthma
- D. Hypertension
Explanation: **Explanation:** The correct answer is **Glaucoma**. Tricyclic Antidepressants (TCAs), such as Amitriptyline and Imipramine, possess significant **potent anticholinergic (antimuscarinic) properties**. These drugs block $M_3$ receptors, leading to mydriasis (dilation of the pupil) and cycloplegia. In patients with narrow-angle glaucoma, mydriasis causes the iris to block the drainage angle, preventing the outflow of aqueous humor and leading to a dangerous increase in intraocular pressure. **Analysis of Options:** * **Brain Tumor:** While TCAs lower the seizure threshold (caution in epilepsy), they are not strictly contraindicated in brain tumors unless the patient has uncontrolled intracranial pressure or active seizures. * **Bronchial Asthma:** Anticholinergics generally cause bronchodilation, not bronchoconstriction. Therefore, TCAs do not worsen asthma (unlike Beta-blockers). * **Hypertension:** TCAs can cause orthostatic hypotension (due to $\alpha_1$ blockade). While they should be used cautiously with certain antihypertensives (like Guanethidine), hypertension itself is not a primary contraindication. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effect Profile:** Remember the mnemonic "3 Cs" for TCA toxicity: **C**onvulsions, **C**oma, and **C**ardiotoxicity (Arrhythmias due to Na+ channel blockade). * **Cardiac Warning:** TCAs are strictly contraindicated in patients with recent **Myocardial Infarction** or pre-existing **Heart Block** (due to prolonged QT interval). * **Other Anticholinergic Contraindications:** Due to their atropine-like effects, TCAs should also be avoided in **Benign Prostatic Hyperplasia (BPH)** as they can precipitate acute urinary retention.
Question 86: Drug-induced psychosis occurs due to all the following drugs except?
- A. Isoniazid
- B. Para-amino salicylic acid
- C. Lysergic acid derivatives
- D. Para-aminophenol (Correct Answer)
Explanation: **Explanation:** The correct answer is **Para-aminophenol (Option D)**. **1. Why Para-aminophenol is correct:** Para-aminophenol is the parent chemical class of **Paracetamol (Acetaminophen)**. Paracetamol is a non-opioid analgesic and antipyretic that acts primarily by inhibiting prostaglandin synthesis in the CNS. It does not have any significant dopaminergic or serotonergic activity in the brain and is **not** associated with drug-induced psychosis. **2. Why the other options are incorrect:** * **Isoniazid (INH):** This anti-tubercular drug is a well-known cause of "INH psychosis." It interferes with Vitamin B6 (Pyridoxine) metabolism, which is a cofactor for the synthesis of GABA. A deficiency in GABA can lead to CNS excitation, seizures, and psychotic symptoms. * **Para-amino salicylic acid (PAS):** Another second-line anti-tubercular agent, PAS is known to cause various neuropsychiatric side effects, including acute psychosis and encephalopathy, though less frequently than INH. * **Lysergic acid derivatives (LSD):** LSD is a potent hallucinogen that acts as a partial agonist at **5-HT2A receptors**. It is a classic cause of drug-induced psychosis, characterized by vivid hallucinations and sensory distortions. **High-Yield Clinical Pearls for NEET-PG:** * **Dopamine Hypothesis:** Most drugs that cause psychosis (like Amphetamines, Cocaine, or Levodopa) increase dopamine levels in the mesolimbic pathway. * **Anticholinergic Psychosis:** Drugs like Atropine and Datura can cause "madness" (delirium/psychosis) due to central muscarinic blockade. * **Steroid Psychosis:** Glucocorticoids are a frequent cause of organic psychosis in clinical practice. * **Ketamine:** Acts as an NMDA receptor antagonist and can mimic the negative and positive symptoms of schizophrenia.
Question 87: Which of the following typical antipsychotic drugs is not available in depot form?
- A. Haloperidol
- B. Risperidone
- C. Olanzapine
- D. Chlorpromazine (Correct Answer)
Explanation: **Explanation:** The correct answer is **Chlorpromazine**. **1. Why Chlorpromazine is the correct answer:** Chlorpromazine is a low-potency typical antipsychotic. Depot formulations (Long-Acting Injectables or LAIs) are designed for sustained release over weeks to improve compliance in chronic schizophrenia. These are typically created by esterifying high-potency drugs with fatty acids (like decanoate or enanthate) in an oil vehicle. Chlorpromazine is not available in a depot form; it is administered orally or via short-acting intramuscular injection for acute agitation. **2. Analysis of Incorrect Options:** * **Haloperidol (Option A):** This is a high-potency typical antipsychotic available as **Haloperidol Decanoate**. It is one of the most commonly used first-generation depot preparations, administered every 4 weeks. * **Risperidone (Option B):** An atypical antipsychotic available as a long-acting injection (e.g., Risperdal Consta). It uses microsphere technology for sustained release. * **Olanzapine (Option C):** An atypical antipsychotic available as **Olanzapine Pamoate**. Note: It carries a risk of "Post-injection Delirium Sedation Syndrome" (PDSS), requiring mandatory 3-hour observation. **3. High-Yield Clinical Pearls for NEET-PG:** * **Typical Antipsychotics available as Depots:** Haloperidol, Fluphenazine, Flupentixol, and Zuclopenthixol. * **Atypical Antipsychotics available as Depots:** Risperidone, Olanzapine, Paliperidone, and Aripiprazole. * **Mechanism:** Depot forms are usually prodrugs. The ester bond is slowly hydrolyzed by plasma esterases to release the active drug. * **Key Contraindication:** Depot preparations should **never** be given intravenously; they are strictly for deep intramuscular (IM) use.
Question 88: Which was the first type of antidepressant that was introduced?
- A. Monoamine oxidase inhibitor (MAOI) (Correct Answer)
- B. Selective serotonin reuptake inhibitor (SSRI)
- C. Norepinephrine-dopamine reuptake inhibitor (NDRI)
- D. Serotonin-norepinephrine reuptake inhibitor (SNRI)
Explanation: ### Explanation The correct answer is **Monoamine oxidase inhibitor (MAOI)**. **1. Why MAOIs are the correct answer:** The history of modern antidepressants began in the early 1950s with the accidental discovery of **Iproniazid** [2]. Originally developed as an anti-tubercular drug, clinicians observed that patients experienced significant mood elevation [2]. Iproniazid was identified as a Monoamine Oxidase Inhibitor (MAOI), making this class the first pharmacological intervention for depression [3]. Shortly thereafter, the first Tricyclic Antidepressant (TCA), Imipramine, was developed in 1957 [2]. **2. Why the other options are incorrect:** * **SSRI (Selective Serotonin Reuptake Inhibitors):** These were developed much later (late 1970s/1980s) to improve the safety profile and reduce the side effects associated with MAOIs and TCAs. * **SNRI (Serotonin-Norepinephrine Reuptake Inhibitors):** These are "dual-action" antidepressants (e.g., Venlafaxine) introduced in the 1990s. * **NDRI (Norepinephrine-Dopamine Reuptake Inhibitor):** Bupropion is the primary drug in this class, introduced in the mid-1980s [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** MAOIs inhibit the enzyme responsible for the mitochondrial degradation of catecholamines (NE, DA, 5-HT), thereby increasing their bioavailability in the synaptic cleft. * **Cheese Reaction:** A classic exam topic. Patients on non-selective MAOIs (like Tranylcypromine) must avoid tyramine-rich foods (aged cheese, red wine) to prevent a **hypertensive crisis** due to the displacement of norepinephrine. * **Drug Interaction:** Never combine MAOIs with SSRIs/SNRIs due to the risk of **Serotonin Syndrome**. A "washout period" of at least 14 days is required when switching between these classes. * **Moclobemide:** A RIMA (Reversible Inhibitor of MAO-A) that has a lower risk of the cheese reaction.
Question 89: A patient on antidepressant therapy developed sudden hypertension on consuming cheese. Which of the following drugs is probably responsible for this condition?
- A. Amitriptyline
- B. Tranylcypramine (Correct Answer)
- C. Fluoxetine
- D. Sertraline
Explanation: ### Explanation The clinical scenario describes the **"Cheese Reaction,"** a classic hypertensive crisis associated with the use of **Monoamine Oxidase Inhibitors (MAOIs)**. **Why Tranylcypramine is correct:** Tranylcypramine is a non-selective, irreversible MAO inhibitor. MAO-A is responsible for metabolizing dietary **Tyramine** in the gut and liver. When a patient on MAOIs consumes tyramine-rich foods (like aged cheese, red wine, or fermented meat), tyramine escapes degradation and enters the systemic circulation. It acts as an indirect sympathomimetic, displacing stored norepinephrine from nerve endings. This massive release of norepinephrine leads to severe vasoconstriction, resulting in a sudden, life-threatening increase in blood pressure (hypertensive crisis). **Why the other options are incorrect:** * **Amitriptyline:** This is a Tricyclic Antidepressant (TCA). While it can cause side effects like sedation and anticholinergic symptoms, it does not interact with dietary tyramine to cause hypertension. * **Fluoxetine and Sertraline:** These are Selective Serotonin Reuptake Inhibitors (SSRIs). Their primary risk is "Serotonin Syndrome" when combined with other serotonergic drugs, but they do not cause the cheese reaction. **High-Yield NEET-PG Pearls:** * **Antidote:** The drug of choice for treating a hypertensive crisis due to the cheese reaction is **Phentolamine** (an alpha-blocker). * **Moclobemide:** A Reversible Inhibitor of MAO-A (RIMA) which has a much lower risk of the cheese reaction compared to Tranylcypramine. * **Selegiline:** At low doses, it selectively inhibits MAO-B and usually does not require dietary restrictions; however, at high doses, it loses selectivity. * **Washout Period:** When switching from MAOIs to other antidepressants, a 2-week washout period is required (5 weeks for Fluoxetine due to its long half-life).
Question 90: Which drug is known to cause agranulocytosis?
- A. Pimozide
- B. Clozapine (Correct Answer)
- C. Risperidone
- D. Olanzapine
Explanation: **Explanation:** **Clozapine** is the correct answer. It is a prototype **Atypical Antipsychotic** (Second Generation) primarily used for treatment-resistant schizophrenia. The most serious and life-threatening adverse effect associated with Clozapine is **agranulocytosis** (a severe decrease in the absolute neutrophil count <500/mm³), occurring in approximately 1% of patients. This is an idiosyncratic reaction, necessitating mandatory weekly blood monitoring (CBC) for the first six months of treatment. **Analysis of Incorrect Options:** * **Pimozide (Option A):** A typical antipsychotic primarily used for Tourette’s syndrome. Its major concern is QT interval prolongation and sudden cardiac death, not agranulocytosis. * **Risperidone (Option C):** An atypical antipsychotic known for causing significant hyperprolactinemia and extrapyramidal symptoms at higher doses, but it does not carry a significant risk of bone marrow suppression. * **Olanzapine (Option D):** While structurally similar to Clozapine, it is most notorious for causing significant **metabolic side effects** (weight gain, dyslipidemia, and Type 2 Diabetes) rather than agranulocytosis. **High-Yield Clinical Pearls for NEET-PG:** * **Clozapine** is the only antipsychotic proven to reduce the risk of **suicidal behavior** in schizophrenia. * It has the **least potential** for causing Extrapyramidal Symptoms (EPS) and Tardive Dyskinesia. * Other side effects include **seizures** (dose-dependent), **sialorrhea** (excessive salivation), and myocarditis. * **Contraindication:** Do not co-administer with **Carbamazepine**, as it also causes bone marrow suppression, increasing the risk of agranulocytosis synergistically.
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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