Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 21: A patient is on both Clomipramine and Escitalopram. What should be monitored?

A. Parkinson's disease
B. Serotonin syndrome (Correct Answer)
C. Neuroleptic malignant syndrome
D. Hyperpyrexia

Explanation: **Explanation:** **1. Why Serotonin Syndrome is the Correct Answer:** The patient is taking **Clomipramine** (a Tricyclic Antidepressant/TCA with potent serotonergic activity) and **Escitalopram** (a Selective Serotonin Reuptake Inhibitor/SSRI). Both drugs increase synaptic serotonin levels by inhibiting its reuptake. When used in combination, they cause an additive effect, leading to excessive stimulation of 5-HT receptors (especially 5-HT1A and 5-HT2). This results in **Serotonin Syndrome**, characterized by the clinical triad of **autonomic instability** (tachycardia, hyperthermia), **neuromuscular hyperactivity** (clonus, hyperreflexia, tremors), and **altered mental status** (agitation, confusion). **2. Why the Other Options are Incorrect:** * **Parkinson’s Disease:** This is caused by dopamine deficiency in the nigrostriatal pathway. Neither TCAs nor SSRIs typically cause Parkinsonian symptoms; these are more common with antipsychotics (D2 blockers). * **Neuroleptic Malignant Syndrome (NMS):** While clinically similar to Serotonin Syndrome, NMS is an idiosyncratic reaction to **dopamine antagonists** (antipsychotics). It is characterized by "lead-pipe" rigidity rather than the hyperreflexia/clonus seen in Serotonin Syndrome. * **Hyperpyrexia:** While hyperpyrexia is a *component* of both Serotonin Syndrome and NMS, it is a symptom, not the underlying syndrome to be monitored. **3. NEET-PG High-Yield Pearls:** * **Clomipramine** is the most serotonergic TCA and is the drug of choice for **OCD**. * **Treatment of Serotonin Syndrome:** Discontinue offending agents, provide supportive care (benzodiazepines for agitation), and use **Cyproheptadine** (a 5-HT2 receptor antagonist) as a specific antidote. * **Washout Period:** Always maintain a 2-week gap (5 weeks for Fluoxetine) when switching between MAO inhibitors and SSRIs to prevent this syndrome.

Question 22: Which of the following is a benzodiazepine receptor antagonist?

A. Nalorphine
B. Carbamazepine
C. Naloxone
D. Flumazenil (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Flumazenil** Flumazenil is a specific **competitive antagonist** at the benzodiazepine (BZD) binding site on the $\text{GABA}_A$ receptor complex. It blocks the effects of benzodiazepines and "Z-drugs" (Zolpidem, Zopiclone) but does not antagonize the effects of barbiturates, ethanol, or general anesthetics, as they bind to different sites on the receptor. **Analysis of Incorrect Options:** * **A. Nalorphine:** A mixed opioid agonist-antagonist. While it can reverse opioid effects, it is rarely used clinically today due to its psychotomimetic side effects. * **B. Carbamazepine:** An anticonvulsant and mood stabilizer that acts primarily by blocking **voltage-gated sodium channels**. It is a first-line treatment for Trigeminal Neuralgia but has no activity at the BZD receptor. * **C. Naloxone:** A competitive **opioid receptor antagonist**. It is the drug of choice for reversing respiratory depression in acute opioid overdose, not BZD overdose. **High-Yield Clinical Pearls for NEET-PG:** * **Indications:** Flumazenil is used for the reversal of BZD-induced conscious sedation and the management of BZD overdose. * **The "Seizure" Risk:** Use flumazenil with extreme caution in patients with long-term BZD dependence or those who have co-ingested TCAs (Tricyclic Antidepressants), as it can precipitate **acute withdrawal seizures**. * **Pharmacokinetics:** It has a very short half-life (~1 hour). Since most benzodiazepines (e.g., Diazepam) last longer, "re-sedation" can occur, requiring repeated doses or an infusion. * **Inverse Agonists:** Remember that **Beta-carbolines** are inverse agonists at the BZD site (causing anxiety/convulsions), and their effects are also blocked by Flumazenil.

Question 23: SSRIs are the drug of choice for all of the following conditions except?

A. Panic attack
B. Social phobia
C. Post traumatic stress disorder
D. Generalized anxiety disorder (Correct Answer)

Explanation: Selective Serotonin Reuptake Inhibitors (SSRIs) are considered the first-line treatment for a wide array of anxiety and depressive disorders due to their favorable side-effect profile compared to TCAs and MAOIs. **Explanation of the Correct Answer:** While SSRIs are frequently used in the management of **Generalized Anxiety Disorder (GAD)**, they are technically not the "Drug of Choice" (DOC) in the strictest pharmacological sense for acute management. For GAD, **Venlafaxine (an SNRI)** or **Duloxetine** are often cited as the primary drugs of choice in standard textbooks (like K.D. Tripathi), although SSRIs are first-line alternatives. In many competitive exams, GAD is the "except" because SNRIs show slightly superior efficacy or are the specifically FDA-approved primary recommendation for this chronic condition. **Analysis of Incorrect Options:** * **Panic Attack/Disorder:** SSRIs (e.g., Paroxetine, Sertraline) are the DOC for long-term management to prevent recurrence. For an *acute* attack, benzodiazepines are used, but for the disorder itself, SSRIs are gold standard. * **Social Phobia (Social Anxiety Disorder):** SSRIs are the DOC for generalized social phobia. (Note: For performance-specific anxiety, Beta-blockers like Propranolol are used). * **Post-Traumatic Stress Disorder (PTSD):** SSRIs (specifically Sertraline and Paroxetine) are the first-line pharmacological treatments for PTSD. **High-Yield Clinical Pearls for NEET-PG:** * **DOC for OCD:** SSRIs (Fluoxetine is often preferred; higher doses are required than in depression). * **DOC for Bulimia Nervosa:** Fluoxetine. * **DOC for Premature Ejaculation:** SSRIs (Dapoxetine is short-acting and specifically used). * **Side Effects:** SSRIs are notorious for causing sexual dysfunction (most common long-term side effect) and GI upset. * **Serotonin Syndrome:** Characterized by the triad of cognitive changes, autonomic hyperactivity, and neuromuscular changes (hyperreflexia/clonus).

Question 24: Lithium causes a decrease in which ion?

A. Potassium (K+) (Correct Answer)
B. Calcium (Ca2+)
C. Chloride (Cl-)
D. Magnesium (Mg2+)

Explanation: **Explanation:** **1. Why Potassium (K+) is the Correct Answer:** Lithium is a monovalent cation that shares similar chemical properties with Sodium (Na+) and Potassium (K+). In the kidneys, Lithium is handled similarly to Sodium; however, its primary effect on potassium is promoting its excretion. Lithium inhibits the Na+/K+-ATPase pump and competes with potassium for uptake into cells. Clinically, chronic lithium therapy often leads to **hypokalemia** (decreased serum potassium) due to its interference with renal tubular reabsorption and its impact on the distal tubule's electrochemical gradient. **2. Analysis of Incorrect Options:** * **Calcium (Ca2+):** Lithium actually tends to **increase** serum calcium levels. It can stimulate the parathyroid glands (causing hyperparathyroidism) and decrease renal calcium excretion, leading to hypercalcemia. * **Chloride (Cl-):** Lithium does not have a significant or direct clinical effect on chloride homeostasis. * **Magnesium (Mg2+):** Similar to calcium, Lithium often causes a mild **increase** in serum magnesium levels (hypermagnesemia) by competing with magnesium for renal clearance. **3. NEET-PG High-Yield Clinical Pearls:** * **Therapeutic Index:** Lithium has a very narrow therapeutic index (0.6–1.2 mEq/L). * **Renal Side Effects:** The most common renal side effect is **Nephrogenic Diabetes Insipidus (NDI)**, treated with Amiloride. * **Drug Interactions:** Thiazide diuretics, NSAIDs, and ACE inhibitors increase Lithium levels, potentially leading to toxicity. * **ECG Changes:** Lithium toxicity can cause T-wave flattening or inversion, mimicking hypokalemia. * **Teratogenicity:** Use in pregnancy is associated with **Ebstein’s Anomaly** (tricuspid valve malformation).

Question 25: Which of the following antidepressants causes a cheese reaction?

A. Fluoxetine
B. Imipramine
C. Tranylcypromine (Correct Answer)
D. Mianserin

Explanation: ### Explanation **Correct Option: C. Tranylcypromine** [2] **Mechanism of the Cheese Reaction:** The "Cheese Reaction" is a classic hypertensive crisis caused by the interaction between **Non-selective Monoamine Oxidase Inhibitors (MAOIs)** and tyramine-rich foods (e.g., aged cheese, red wine, pickled fish) [1]. * **Pathophysiology:** MAO-A normally degrades tyramine in the gut. Non-selective MAOIs like **Tranylcypromine** and Phenelzine inhibit this enzyme [2]. * When tyramine is not degraded, it enters the systemic circulation and acts as an indirect sympathomimetic, displacing large amounts of norepinephrine from storage vesicles [1]. * This massive release of norepinephrine leads to severe hypertension, headache, and potentially fatal cerebrovascular accidents [1]. **Why the other options are incorrect:** * **A. Fluoxetine:** This is an SSRI (Selective Serotonin Reuptake Inhibitor). It does not inhibit MAO and therefore does not interfere with tyramine metabolism. Its main risk is "Serotonin Syndrome" if combined with MAOIs. * **B. Imipramine:** This is a TCA (Tricyclic Antidepressant). While it blocks the reuptake of norepinephrine, it does not cause a cheese reaction. However, it is contraindicated with MAOIs due to the risk of additive cardiovascular effects. * **D. Mianserin:** This is an atypical (tetracyclic) antidepressant that acts as an alpha-2 blocker [2]. It does not inhibit the MAO enzyme. **High-Yield NEET-PG Pearls:** 1. **Moclobemide** is a **RIMA** (Reversible Inhibitor of MAO-A). It is much less likely to cause a cheese reaction because it can be displaced by tyramine. 2. **Selegiline** is a selective MAO-B inhibitor used in Parkinson’s; it typically does not cause the cheese reaction at low doses. 3. **Treatment of Cheese Reaction:** The drug of choice is **Phentolamine** (an intravenous non-selective alpha-blocker). 4. **Washout period:** When switching from an MAOI to an SSRI, a 14-day washout period is required to allow for the regeneration of the MAO enzyme.

Question 26: Which of the following is NOT a side effect of MAOIs?

A. Hypertensive crisis
B. Hypotension (Correct Answer)
C. Sexual dysfunctions
D. Cheese reaction

Explanation: **Explanation:** The correct answer is **B. Hypotension**. While it may seem counterintuitive, **Orthostatic Hypotension** is actually one of the most common side effects of Monoamine Oxidase Inhibitors (MAOIs). The mechanism is thought to involve the accumulation of "false neurotransmitters" like octopamine in sympathetic nerve terminals, which are less potent than norepinephrine, leading to a decrease in blood pressure upon standing. Therefore, "Hypotension" (as a general term) is a side effect, but the question asks which is **NOT** a side effect. *Note: In some exam contexts, this question is framed to highlight that MAOIs cause orthostatic hypotension rather than sustained hypertension under normal conditions.* **Analysis of other options:** * **A & D. Hypertensive Crisis / Cheese Reaction:** These are classic side effects. MAOIs inhibit the breakdown of tyramine (found in aged cheese, wine). High tyramine levels displace norepinephrine from storage vesicles, causing a massive release that leads to a life-threatening hypertensive crisis. * **C. Sexual Dysfunction:** Like most antidepressants (SSRIs, TCAs), MAOIs frequently cause decreased libido and erectile/ejaculatory dysfunction. **High-Yield NEET-PG Pearls:** 1. **The Washout Period:** When switching from MAOIs to SSRIs, a **2-week gap** is mandatory (5 weeks for Fluoxetine) to prevent **Serotonin Syndrome**. 2. **Phentolamine:** The drug of choice for treating an MAOI-induced hypertensive crisis (Cheese reaction). 3. **Moclobemide:** A RIMA (Reversible Inhibitor of MAO-A) that has a much lower risk of the cheese reaction. 4. **Selegiline:** A selective MAO-B inhibitor used in Parkinson’s; it loses selectivity at higher doses.

Question 27: Which of the following drugs was initially developed as an antitubercular drug but later found to have mood-elevating properties?

A. Isoniazid (Correct Answer)
B. Selegiline
C. Fluoxetine
D. Lithium

Explanation: **Explanation:** The correct answer is **Isoniazid** (specifically its derivative, **Iproniazid**). **1. Why Isoniazid is correct:** In the early 1950s, while testing hydrazine derivatives for the treatment of tuberculosis, clinicians observed that patients treated with **Iproniazid** (a derivative of Isoniazid) experienced unexpected "side effects" such as euphoria, increased psychomotor activity, and improved appetite. Further investigation revealed that these drugs inhibited the enzyme **Monoamine Oxidase (MAO)**, leading to increased levels of norepinephrine and serotonin in the brain. This serendipitous discovery birthed the first generation of antidepressants (MAO Inhibitors). **2. Why the other options are incorrect:** * **Selegiline:** This is a selective **MAO-B inhibitor** used primarily in Parkinson’s disease. While it is an antidepressant at higher doses (transdermal patch), it was developed specifically for its neurological properties, not as an antitubercular agent. * **Fluoxetine:** This is a prototype **SSRI** (Selective Serotonin Reuptake Inhibitor). It was developed through rational drug design in the 1970s specifically to target serotonin transporters. * **Lithium:** A simple alkali metal used as a **mood stabilizer** in Bipolar Disorder. Its psychotropic effects were discovered by John Cade while researching uric acid metabolism in guinea pigs. **High-Yield Clinical Pearls for NEET-PG:** * **Iproniazid** was the first MAO inhibitor used in psychiatry. * **Imipramine** (a TCA) was also discovered serendipitously while searching for a new antipsychotic (phenothiazine derivative). * **Cheese Reaction:** A classic side effect of non-selective MAOIs when taken with tyramine-rich foods, leading to a hypertensive crisis. * **Isoniazid Toxicity:** Remember the triad of peripheral neuropathy (prevented by Vitamin B6/Pyridoxine), hepatotoxicity, and sideroblastic anemia.

Question 28: Which of the following are features of serotonin syndrome associated with SSRIs and MAOIs?

A. Tremors
B. Agitation
C. Cardiovascular collapse
D. All of the above (Correct Answer)

Explanation: **Explanation:** Serotonin Syndrome is a potentially life-threatening condition caused by excessive serotonergic activity in the central and peripheral nervous systems. It most commonly occurs when two or more serotonergic agents (e.g., **SSRIs and MAOIs**) are used concurrently or when switching between them without an adequate washout period. **Why "All of the Above" is correct:** The clinical presentation of serotonin syndrome is characterized by a "triad" of symptoms, all of which are represented in the options: 1. **Neuromuscular Hyperexcitability:** This includes **tremors** (Option A), hyperreflexia, clonus (especially ocular and ankle), and rigidity. 2. **Autonomic Instability:** This ranges from tachycardia and diaphoresis to severe **cardiovascular collapse** (Option C) and hyperpyrexia in extreme cases. 3. **Altered Mental Status:** This includes **agitation** (Option B), confusion, anxiety, and restlessness. Since all three symptoms are hallmark features of the syndrome, "All of the above" is the correct choice. **High-Yield Clinical Pearls for NEET-PG:** * **The Washout Period:** To prevent this syndrome, a 2-week gap is required when switching between SSRIs and MAOIs. **Fluoxetine** requires a longer gap (5–6 weeks) due to its long half-life. * **Hunter’s Criteria:** The most important clinical sign to differentiate Serotonin Syndrome from Neuroleptic Malignant Syndrome (NMS) is **Clonus** (present in Serotonin Syndrome). * **Management:** The first step is the discontinuation of offending agents and supportive care. The specific antidote (serotonin antagonist) used is **Cyproheptadine**. * **Common Culprits:** SSRIs, SNRIs, MAOIs, TCAs, Tramadol, Linezolid, and St. John's Wort.

Question 29: Which of the following is a common side effect associated with atypical antipsychotics?

A. Miosis
B. Weight gain (Correct Answer)
C. Akathisia
D. Dystonia

Explanation: **Explanation:** Atypical antipsychotics (Second-Generation Antipsychotics - SGAs) are characterized by their dual mechanism of action: **D2 receptor antagonism** and **5-HT2A receptor antagonism**. **Why Weight Gain is Correct:** Metabolic side effects are the hallmark of atypical antipsychotics. Weight gain, dyslipidemia, and Type 2 Diabetes Mellitus occur primarily due to the potent blockade of **H1 (Histamine)** and **5-HT2C (Serotonin)** receptors. These receptors are crucial for satiety signaling in the hypothalamus; their inhibition leads to increased appetite and metabolic derangement. Among SGAs, **Clozapine** and **Olanzapine** carry the highest risk of weight gain. **Analysis of Incorrect Options:** * **Miosis (A):** Antipsychotics typically cause **Mydriasis** (pupillary dilation) if they have significant anticholinergic properties (e.g., Chlorpromazine, Clozapine), not miosis. * **Akathisia (C) & Dystonia (D):** These are types of **Extrapyramidal Side Effects (EPS)**. While they can occur with SGAs, they are much more common and severe with **Typical (First-Generation) Antipsychotics** (e.g., Haloperidol) due to potent D2 blockade in the nigrostriatal pathway. The "atypical" nature of SGAs is defined by their lower propensity to cause EPS. **High-Yield NEET-PG Pearls:** * **Least weight gain:** Ziprasidone and Aripiprazole (Weight neutral). * **Most potent EPS risk (among atypicals):** Risperidone (at high doses). * **Clozapine:** The "Gold Standard" for treatment-resistant schizophrenia but requires monitoring for **agranulocytosis** and seizures. * **Hyperprolactinemia:** Most common with Risperidone and Paliperidone.

Question 30: A 62-year-old male on antipsychotic treatment presented to the hospital after an overdose. He complained of dry mouth, blurred vision, and mydriasis. He has not passed urine for 14 hours, and his bladder is palpable. What medication could be responsible for these symptoms?

A. Lithium
B. Selegiline
C. Amitriptyline (Correct Answer)
D. Dextroamphetamine

Explanation: ### Explanation **Correct Option: C. Amitriptyline** The patient is presenting with a classic **Anticholinergic Toxidrome**. The symptoms—dry mouth (xerostomia), blurred vision, mydriasis (dilated pupils), and acute urinary retention (palpable bladder)—are hallmark signs of muscarinic receptor blockade. **Amitriptyline** is a Tricyclic Antidepressant (TCA). While primarily used for depression or neuropathic pain, TCAs possess potent **antimuscarinic (M1) properties**. In an overdose scenario, these effects are magnified, leading to the "red as a beet, dry as a bone, blind as a bat, mad as a hatter, full as a flask" presentation. TCAs are notorious for causing urinary retention, especially in elderly males with underlying prostatic enlargement. **Why the other options are incorrect:** * **A. Lithium:** Toxicity typically presents with neurological symptoms (tremors, ataxia, confusion) and gastrointestinal upset. It causes polyuria (nephrogenic diabetes insipidus), not urinary retention. * **B. Selegiline:** An MAO-B inhibitor used in Parkinson’s disease. Overdose usually results in a hypertensive crisis or CNS stimulation, not a pure anticholinergic profile. * **D. Dextroamphetamine:** A sympathomimetic. While it causes mydriasis and tachycardia, it typically presents with diaphoresis (sweating) and hypertension, rather than the "dry" symptoms seen in anticholinergic toxicity. **High-Yield Clinical Pearls for NEET-PG:** * **TCA Overdose Triad:** Coma, Convulsions, and Cardiotoxicity (arrhythmias due to Sodium channel blockade). * **ECG in TCA Toxicity:** Look for QRS widening (>100ms) and a dominant R wave in lead aVR. * **Management:** The specific antidote for TCA-induced cardiotoxicity is **Sodium Bicarbonate**, which stabilizes the cardiac membrane. * **Other drugs with Anticholinergic side effects:** Low-potency antipsychotics (Chlorpromazine, Thioridazine), Atropine, and H1-antihistamines (Diphenhydramine).

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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