Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 211: Which of the following is a non-selective MAO inhibitor?

A. Moclobemide
B. Rasagiline
C. Selegiline
D. Isocarboxazid (Correct Answer)

Explanation: **Explanation:** Monoamine oxidase (MAO) inhibitors are classified based on their selectivity for the two isoforms of the enzyme: **MAO-A** (which degrades serotonin, norepinephrine, and melatonin) and **MAO-B** (which degrades dopamine). **1. Why Isocarboxazid is correct:** **Isocarboxazid** is a hydrazine derivative that acts as a **non-selective, irreversible MAO inhibitor**. It inhibits both MAO-A and MAO-B enzymes. Because it inhibits MAO-A, it carries a high risk of the "Cheese Reaction" (hypertensive crisis) when taken with tyramine-rich foods, as it prevents the breakdown of dietary tyramine. Other drugs in this class include Phenelzine and Tranylcypromine. **2. Analysis of Incorrect Options:** * **Moclobemide:** This is a **RIMA** (Reversible Inhibitor of MAO-A). It is selective for MAO-A and its reversible nature makes it safer regarding dietary tyramine interactions. * **Selegiline:** This is a **selective, irreversible MAO-B inhibitor** (at low doses). It is primarily used in Parkinson’s disease to increase dopamine levels. At higher doses, it loses selectivity and can inhibit MAO-A. * **Rasagiline:** Similar to Selegiline, this is a potent, **selective, irreversible MAO-B inhibitor** used in the management of Parkinson’s disease. **High-Yield Clinical Pearls for NEET-PG:** * **Cheese Reaction:** Occurs with non-selective MAOIs due to displacement of Norepinephrine by tyramine. Treatment of choice: **Phentolamine** (Alpha-blocker). * **Serotonin Syndrome:** A dangerous interaction when MAOIs are combined with SSRIs or Pethidine. * **Washout Period:** When switching from an MAOI to an SSRI (or vice versa), a gap of at least **14 days** is required to allow for enzyme regeneration.

Question 212: Which of the following is a feature of Haloperidol toxicity?

A. Weight loss
B. Sweating
C. Akathisia (Correct Answer)
D. Diarrhoea

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, particularly in the mesolimbic and nigrostriatal pathways. **Why Akathisia is correct:** Akathisia is a common **Extrapyramidal Side Effect (EPS)** resulting from D2 receptor blockade in the nigrostriatal pathway. It is characterized by a subjective feeling of inner restlessness and an inability to sit still. Among all antipsychotics, high-potency drugs like Haloperidol have the highest propensity to cause EPS, including acute dystonia, parkinsonism, and akathisia. **Why the other options are incorrect:** * **Weight loss:** Haloperidol is more likely to cause **weight gain**, though to a lesser extent than atypical antipsychotics like Olanzapine. * **Sweating & Diarrhea:** These are typically features of **cholinergic excess** or **Serotonin Syndrome**. Haloperidol actually possesses mild anticholinergic properties, which would more likely cause dry mouth, constipation, and decreased sweating. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for Akathisia:** Centrally acting beta-blockers (e.g., **Propranolol**). * **Neuroleptic Malignant Syndrome (NMS):** A life-threatening toxicity of Haloperidol characterized by "lead-pipe" rigidity, hyperthermia, and autonomic instability. Treatment involves **Dantrolene** or Bromocriptine. * **Hyperprolactinemia:** Due to D2 blockade in the tuberoinfundibular pathway, Haloperidol frequently causes galactorrhea and gynecomastia. * **QT Prolongation:** Haloperidol (especially IV) can increase the risk of Torsades de Pointes.

Question 213: Akathisia is most commonly seen with the use of which of the following medications?

A. Clozapine
B. Propranolol
C. Benztropine
D. Haloperidol (Correct Answer)

Explanation: **Explanation:** **1. Why Haloperidol is the Correct Answer:** Akathisia is a common **Extrapyramidal Side Effect (EPS)** characterized by a subjective feeling of inner restlessness and an inability to sit still [2]. It is most frequently associated with **First-Generation Antipsychotics (Typical Antipsychotics)** like **Haloperidol** [1]. The underlying mechanism is the potent, non-selective blockade of **Dopamine D2 receptors** in the nigrostriatal pathway. High-potency neuroleptics like Haloperidol have a high affinity for these receptors, making them the most common culprits for EPS, including akathisia, dystonia, and parkinsonism [1]. **2. Why the Other Options are Incorrect:** * **A. Clozapine:** This is an atypical (Second-Generation) antipsychotic. It has a low affinity for D2 receptors and a higher affinity for 5-HT2A receptors. It is specifically known for having the **lowest risk of EPS** among antipsychotics. * **B. Propranolol:** This is a non-selective beta-blocker. It is actually the **drug of choice (DOC) for treating akathisia**, not a cause of it [1]. * **C. Benztropine:** This is a centrally acting anticholinergic drug. It is used to treat acute dystonia and drug-induced parkinsonism. While it can be used in akathisia, it is generally less effective than beta-blockers. **3. High-Yield Clinical Pearls for NEET-PG:** * **Management of Akathisia:** First-line treatment is **Propranolol**. Benzodiazepines (like Diazepam) are second-line [1]. * **Timeline of EPS:** 1. **Acute Dystonia:** Hours to days (DOC: Promethazine or Benztropine). 2. **Akathisia:** Days to weeks (DOC: Propranolol). 3. **Parkinsonism:** Weeks to months (DOC: Benztropine). 4. **Tardive Dyskinesia:** Months to years (DOC: Valbenazine/Deutetrabenazine; *Note: Anticholinergics worsen this*). * **Clozapine Warning:** Always monitor for **agranulocytosis** (absolute neutrophil count) and seizures.

Question 214: Extrapyramidal adverse effects are commonly caused by which class of drugs?

A. Antidepressants
B. Antipsychotics (Correct Answer)
C. Antimanics
D. Antiepileptics

Explanation: **Explanation:** **Why Antipsychotics are the correct answer:** Extrapyramidal symptoms (EPS) are primarily caused by the blockade of **Dopamine (D2) receptors** in the **Nigrostriatal pathway** of the brain. Typical (First-generation) antipsychotics, such as Haloperidol and Fluphenazine, are potent D2 antagonists. When dopamine is blocked in the striatum, the normal inhibitory balance between dopamine and acetylcholine is disrupted, leading to cholinergic overactivity and the manifestation of movement disorders. **Analysis of Incorrect Options:** * **Antidepressants:** While some (like SSRIs) can rarely cause tremors, they primarily modulate Serotonin and Norepinephrine, not the nigrostriatal dopamine pathway. * **Antimanics:** Lithium (the gold standard) commonly causes fine tremors, but these are not classified as classical extrapyramidal symptoms. * **Antiepileptics:** These drugs generally act on GABA receptors or Ion channels (Sodium/Calcium). While some (like Phenytoin) cause cerebellar ataxia, they do not typically cause EPS. **NEET-PG High-Yield Clinical Pearls:** 1. **Types of EPS (Chronological Order):** * **Acute Dystonia:** Earliest onset (hours); characterized by muscle spasms (e.g., torticollis). Rx: Central anticholinergics (Benztropine, Promethazine). * **Akathisia:** Most common EPS; subjective feeling of restlessness. Rx: Beta-blockers (Propranolol). * **Drug-Induced Parkinsonism:** Rigidity, tremors, and bradykinesia. Rx: Central anticholinergics (Trihexyphenidyl). * **Tardive Dyskinesia:** Late-onset (months/years); involuntary choreoathetoid movements (e.g., lip-smacking). Rx: Switch to Clozapine or use VMAT-2 inhibitors (Valbenazine). 2. **Atypical Antipsychotics** (e.g., Quetiapine, Clozapine) have a lower risk of EPS because they dissociate rapidly from D2 receptors and have 5-HT2A antagonist properties.

Question 215: Which of the following effects is unlikely to occur during treatment with imipramine?

A. Elevation of seizure threshold (Correct Answer)
B. Mydriasis
C. Sedation
D. Urinary retention

Explanation: **Explanation:** **Imipramine** is a prototype **Tricyclic Antidepressant (TCA)**. Understanding its pharmacological profile is crucial for NEET-PG, as it involves multiple receptor systems. **Why Option A is the correct answer:** Imipramine, like most TCAs and antipsychotics, **lowers the seizure threshold** rather than elevating it. This means it makes the brain more susceptible to seizures, especially in patients with pre-existing epilepsy or in overdose situations. Therefore, "elevation of seizure threshold" is the incorrect statement regarding its effects. **Analysis of Incorrect Options:** * **B. Mydriasis:** TCAs have potent **anticholinergic (muscarinic blockade)** properties. This leads to pupillary dilation (mydriasis), blurred vision, and can potentially precipitate narrow-angle glaucoma. * **C. Sedation:** Imipramine possesses **H1-antihistaminic** properties. Sedation is a common side effect, particularly during the initiation of therapy. * **D. Urinary Retention:** This is another manifestation of its **anticholinergic** action (detrusor relaxation and sphincter contraction). It is a significant concern in elderly patients with prostatic hypertrophy. **High-Yield Clinical Pearls for NEET-PG:** 1. **Mechanism of Action:** TCAs inhibit the reuptake of Norepinephrine (NE) and Serotonin (5-HT). 2. **The "3 Cs" of TCA Toxicity:** Coma, Convulsions (due to lowered seizure threshold), and Cardiotoxicity (arrhythmias due to sodium channel blockade). 3. **ECG Changes:** TCA overdose characteristically shows **QRS widening** and QT prolongation. 4. **Specific Use:** Imipramine is a first-line drug for **Nocturnal Enuresis** in children (due to its anticholinergic effect and alteration of sleep patterns).

Question 216: Antipsychotic drugs primarily act through blockade of which of the following receptors?

A. Dopamine D1 receptor
B. Dopamine D2 receptor (Correct Answer)
C. Dopamine D3 receptor
D. Dopamine D4 receptor

Explanation: **Explanation:** The therapeutic efficacy of antipsychotic drugs (neuroleptics) is primarily attributed to the **blockade of Dopamine D2 receptors** in the mesolimbic and mesocortical pathways of the brain. This is known as the **Dopamine Hypothesis of Schizophrenia**, which suggests that overactivity of dopamine in these regions leads to positive symptoms like hallucinations and delusions. * **Dopamine D2 receptor (Correct):** All conventional (typical) antipsychotics, such as Haloperidol and Chlorpromazine, are potent D2 antagonists. Their clinical potency is directly proportional to their affinity for the D2 receptor. Even atypical antipsychotics (e.g., Risperidone) maintain a degree of D2 blockade alongside serotonin (5-HT2A) antagonism. * **Dopamine D1 receptor:** While some drugs (like Phenothiazines) may show minor binding to D1, it is not the primary mechanism for antipsychotic action. * **Dopamine D3 receptor:** These receptors are located mainly in the limbic system. While some newer drugs like Cariprazine act here, D3 blockade is not the "primary" mechanism for the class as a whole. * **Dopamine D4 receptor:** This receptor gained interest because **Clozapine** has a high affinity for it. However, selective D4 antagonists have failed to show antipsychotic efficacy in clinical trials, confirming that D2 remains the essential target. **High-Yield Clinical Pearls for NEET-PG:** 1. **Nigrostriatal Pathway:** Blockade of D2 receptors here leads to **Extrapyramidal Side Effects (EPS)**. 2. **Tuberoinfundibular Pathway:** D2 blockade here causes **Hyperprolactinemia** (galactorrhea, gynecomastia). 3. **Threshold:** Antipsychotic effects typically require **60-80%** D2 receptor occupancy; exceeding 80% significantly increases the risk of EPS.

Question 217: Which of the following drugs are used in the management of schizophrenia?

A. Chlorpromazine
B. Haloperidol
C. Olanzapine
D. All of the above (Correct Answer)

Explanation: **Explanation:** Schizophrenia is a chronic psychotic disorder primarily managed with **Antipsychotics** (Neuroleptics). These drugs work by modulating dopaminergic pathways in the brain, specifically by blocking **D2 receptors** in the mesolimbic system to alleviate "positive symptoms" (delusions and hallucinations). * **Chlorpromazine (Option A):** This is a prototypical **Low-potency Typical Antipsychotic** (Phenothiazine). It was the first antipsychotic discovered. Due to its low potency, it requires higher doses and is associated with significant sedation and alpha-blocking (orthostatic hypotension) side effects. * **Haloperidol (Option B):** This is a **High-potency Typical Antipsychotic** (Butyrophenone). It is highly effective against positive symptoms but has a high propensity for causing **Extrapyramidal Side Effects (EPS)** like acute dystonia and parkinsonism due to potent D2 blockade. * **Olanzapine (Option C):** This is a **Second-Generation (Atypical) Antipsychotic**. Unlike typical drugs, it blocks both **5-HT2A and D2 receptors**. It is preferred for treating "negative symptoms" (apathy, social withdrawal) and has a lower risk of EPS, though it is notorious for causing significant **weight gain and metabolic syndrome**. Since all three drugs belong to different classes of antipsychotics used in clinical practice for schizophrenia, **Option D (All of the above)** is correct. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug of Choice for Resistant Schizophrenia:** Clozapine (monitor for agranulocytosis). 2. **Hyperprolactinemia:** Most common with Haloperidol and Risperidone. 3. **Neuroleptic Malignant Syndrome (NMS):** A rare, fatal side effect characterized by "lead-pipe" rigidity, hyperthermia, and autonomic instability. Treatment: **Dantrolene** or Bromocriptine. 4. **Tardive Dyskinesia:** A late-onset EPS characterized by involuntary choreoathetoid movements (e.g., lip-smacking).

Question 218: Which of the following statements regarding Lithium is false?

A. Maximum plasma concentration is avoided due to its low therapeutic index.
B. It is contraindicated in pregnancy.
C. There is no individual variation in the rate of excretion. (Correct Answer)
D. 80% is reabsorbed in the proximal convoluted tubule.

Explanation: ### Explanation **1. Why Option C is the correct (false) statement:** Lithium is excreted almost entirely by the kidneys [3]. Its excretion rate is **highly variable** among individuals because it depends on factors like glomerular filtration rate (GFR), age, and sodium balance. Since Lithium is handled by the kidneys similarly to sodium, any variation in renal function or hydration status significantly alters its clearance. Therefore, the statement that there is "no individual variation" is incorrect. **2. Analysis of other options:** * **Option A (True):** Lithium has a very **narrow therapeutic index** (0.6–1.2 mEq/L) [5]. High peak plasma concentrations (Cmax) can lead to acute toxicity; hence, sustained-release formulations or divided doses are often used to avoid sharp peaks [2]. * **Option B (True):** Lithium is generally contraindicated in pregnancy, especially during the first trimester, due to its teratogenic potential—specifically **Ebstein’s Anomaly** (tricuspid valve malformation) [1]. * **Option D (True):** Lithium is filtered by the glomerulus, and approximately **80% is reabsorbed in the proximal convoluted tubule (PCT)**. It competes with sodium for reabsorption; thus, states of sodium depletion (like dehydration or use of thiazide diuretics) lead to increased Lithium reabsorption and toxicity [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Therapeutic Drug Monitoring (TDM):** Essential for Lithium. Blood samples should be drawn **12 hours after the last dose** (trough levels). * **Drug Interactions:** "The Deadly Trio"—**Diuretics (Thiazides), NSAIDs, and ACE inhibitors**—all increase Lithium levels by decreasing its renal clearance [5]. * **Side Effects:** Nephrogenic Diabetes Insipidus (treated with Amiloride), Hypothyroidism, and fine tremors [4], [5]. * **L-I-T-H-I-U-M Mnemonic:** **L**eukocytosis, **I**nsipidus (Diabetes), **T**remors/Teratogenicity, **H**ypothyroidism, **I**ncreased **U**rine, **M**others (Ebstein's) [1].

Question 219: Which of the following is a non-sedating antidepressant?

A. Fluoxetine (Correct Answer)
B. Mianserine
C. Amoxapine
D. Imipramine

Explanation: Fluoxetine is a **Selective Serotonin Reuptake Inhibitor (SSRI)**. Unlike older antidepressants, SSRIs have minimal affinity for histamine ($H_1$), atarget="_blank" href="https://www.ncbi.nlm.nih.gov/books/NBK538466/" alpha-adrenergic, and muscarinic receptors. The lack of $H_1$ receptor blockade makes SSRIs generally non-sedating. In fact, Fluoxetine is often described as **"activating"** or CNS-stimulating [1], which can cause insomnia or agitation in some patients. For this reason, it is typically administered in the morning. **Analysis of Incorrect Options:** * **B. Mianserine:** An atypical antidepressant (Tetracyclic) that is highly sedating due to its potent **$H_1$ receptor antagonism**. It is often used in depressed patients with significant insomnia. * **C. Amoxapine:** A tetracyclic antidepressant (a metabolite of the antipsychotic loxapine) that possesses significant sedative properties and potential extrapyramidal side effects due to $D_2$ blockade [2]. * **D. Imipramine:** A classic **Tricyclic Antidepressant (TCA)**. TCAs cause significant sedation because they block $H_1$ histamine receptors and $\alpha_1$-adrenergic receptors. **NEET-PG High-Yield Pearls:** * **Fluoxetine** has the longest half-life among SSRIs (due to its active metabolite, **norfluoxetine**), requiring a 5-week washout period before starting an MAO inhibitor to avoid **Serotonin Syndrome**. * **Drug of Choice (DOC):** SSRIs are the first-line treatment for Depression, OCD, Panic Disorder, Social Phobia, and Bulimia Nervosa (specifically Fluoxetine) [2]. * **Side Effects:** While non-sedating, SSRIs are frequently associated with **sexual dysfunction** (most common long-term side effect) and GI upset. * **Weight Neutrality:** Fluoxetine is generally weight-neutral compared to TCAs or Mirtazapine, which cause weight gain.

Question 220: Inhibitors of serotonin (5-HT) uptake, such as paroxetine, can cause clinically significant drug interactions with which of the following?

A. Diazepam
B. Digoxin
C. Halothane
D. Tranylcypromine (Correct Answer)

Explanation: **Explanation:** The correct answer is **Tranylcypromine**. **1. Why Tranylcypromine is correct:** Paroxetine is a Selective Serotonin Reuptake Inhibitor (SSRI), while Tranylcypromine is a non-selective Monoamine Oxidase Inhibitor (MAOI). When these two classes are combined, they cause an excessive accumulation of serotonin in the synaptic cleft. This leads to **Serotonin Syndrome**, a potentially fatal condition characterized by the "triad" of cognitive effects (confusion, agitation), autonomic hyperactivity (hyperthermia, tachycardia), and somatic effects (myoclonus, rigidity). To avoid this, a "washout period" of at least 14 days is required when switching between these drugs. **2. Why the other options are incorrect:** * **Diazepam:** This is a benzodiazepine. While SSRIs and benzodiazepines are often co-prescribed for anxiety disorders, they do not have a life-threatening pharmacodynamic interaction. * **Digoxin:** Digoxin metabolism is not significantly affected by SSRIs like paroxetine. Interactions are more common with drugs affecting P-glycoprotein or renal clearance. * **Halothane:** This is an inhaled anesthetic. While halothane can sensitize the myocardium to catecholamines, it does not have a direct, clinically significant interaction with serotonin uptake inhibitors. **High-Yield Clinical Pearls for NEET-PG:** * **Serotonin Syndrome vs. NMS:** Remember that Serotonin Syndrome presents with **hyperreflexia and myoclonus**, whereas Neuroleptic Malignant Syndrome (NMS) presents with **"lead-pipe" rigidity** and is caused by dopamine antagonists. * **The Fluoxetine Exception:** Most SSRIs require a 2-week washout period before starting an MAOI, but **Fluoxetine** requires a **5-week** washout due to its long-acting metabolite (norfluoxetine). * **Drug of Choice:** SSRIs are currently the first-line treatment for Depression, OCD, Panic Disorder, and Social Phobia.

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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