Drugs in Psychiatric Disorders Practice Questions

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

Serotonin syndrome. **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.

Q: Which of the following is a benzodiazepine receptor antagonist?

Flumazenil. ### 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.

Q: Lithium causes a decrease in which ion?

Potassium (K+). **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).

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

Hypotension. **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.

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

Isoniazid. **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.

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

All of the above. **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.

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

Weight gain. **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.

Q: 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?

Amitriptyline. ### 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).

Question 1

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

Accepted Answer

Serotonin syndrome

Answer

Parkinson's disease

Answer

Neuroleptic malignant syndrome

Answer

Hyperpyrexia

Question 2

Which of the following is a benzodiazepine receptor antagonist?

Accepted Answer

Flumazenil

Answer

Nalorphine

Answer

Carbamazepine

Answer

Naloxone

Question 3

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

Accepted Answer

Generalized anxiety disorder

Answer

Panic attack

Answer

Social phobia

Answer

Post traumatic stress disorder

Question 4

Lithium causes a decrease in which ion?

Accepted Answer

Potassium (K+)

Answer

Calcium (Ca2+)

Answer

Chloride (Cl-)

Answer

Magnesium (Mg2+)

Question 5

Which of the following antidepressants causes a cheese reaction?

Accepted Answer

Tranylcypromine

Answer

Fluoxetine

Answer

Imipramine

Answer

Mianserin

Question 6

Which of the following is NOT a side effect of MAOIs?

Accepted Answer

Hypotension

Answer

Hypertensive crisis

Answer

Sexual dysfunctions

Answer

Cheese reaction

Question 7

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

Accepted Answer

Isoniazid

Answer

Selegiline

Answer

Fluoxetine

Answer

Lithium

Question 8

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

Accepted Answer

All of the above

Answer

Tremors

Answer

Agitation

Answer

Cardiovascular collapse

Question 9

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

Accepted Answer

Weight gain

Answer

Miosis

Answer

Akathisia

Answer

Dystonia

Question 10

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?

Accepted Answer

Amitriptyline

Answer

Lithium

Answer

Selegiline

Answer

Dextroamphetamine

Drugs in Psychiatric Disorders — MCQs

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