Drugs in Psychiatric Disorders Practice Questions

Q: Which of the following drugs has the least extrapyramidal symptoms?

Aripiprazole. **Explanation:** The risk of Extrapyramidal Symptoms (EPS) in antipsychotic therapy is directly proportional to the degree of **D2 receptor antagonism** in the nigrostriatal pathway. **Why Aripiprazole is correct:** Aripiprazole is a **Third-Generation Atypical Antipsychotic**. Its unique mechanism of action is **D2 Partial Agonism**. Unlike traditional antagonists that completely block dopamine, aripiprazole binds to the D2 receptor and provides a low level of "intrinsic activity." This stabilizes dopamine levels—reducing activity in the mesolimbic pathway (treating positive symptoms) while maintaining enough dopaminergic tone in the nigrostriatal pathway to significantly minimize EPS. **Why the other options are incorrect:** * **Fluphenazine:** A high-potency Typical Antipsychotic (FGA). It has the strongest D2 blockade among the options and, therefore, the **highest risk** of EPS. * **Loxapine:** A mid-potency Typical Antipsychotic. While it has some 5-HT2A antagonism, it still behaves primarily like a first-generation drug with a significant risk of EPS. * **Chlorpromazine:** A low-potency Typical Antipsychotic. While it causes fewer EPS than Fluphenazine (due to inherent anticholinergic properties), it still carries a higher risk than Atypical agents like Aripiprazole. Its main side effects are sedation and orthostatic hypotension. **High-Yield NEET-PG Pearls:** 1. **Clozapine** has the absolute lowest risk of EPS but is reserved for resistant cases due to agranulocytosis. 2. **Quetiapine** is the preferred antipsychotic in patients with Parkinson’s disease who develop psychosis. 3. **Hyperprolactinemia** is common with FGAs and Risperidone but rare with Aripiprazole (due to partial agonism). 4. **Metabolic Syndrome** (weight gain, dyslipidemia) is the primary concern with Atypical antipsychotics (highest with Clozapine and Olanzapine).

Q: Which of the following drugs is least associated with extra-pyramidal side effects?

Carbamazepine. ### Explanation The core concept behind this question is the distinction between **Antipsychotics** (which act on dopamine receptors) and **Antiepileptics/Mood Stabilizers**. **Why Carbamazepine is the correct answer:** Carbamazepine is primarily an **Antiepileptic** drug also used as a **Mood Stabilizer** in Bipolar Disorder. Its mechanism of action involves blocking voltage-gated sodium channels. Unlike antipsychotics, it does not have significant antagonist activity at the Dopamine D2 receptors in the nigrostriatal pathway. Therefore, it is **not associated with Extra-Pyramidal Side Effects (EPS)**. **Why the other options are incorrect:** * **Haloperidol & Fluphenazine:** These are **Typical (First-generation) Antipsychotics** belonging to the Butyrophenone and Piperazine-phenothiazine classes, respectively. They are "High Potency" drugs with very strong D2 receptor blockade, making them the most likely to cause severe EPS (dystonia, akathisia, parkinsonism). * **Chlorpromazine:** This is a "Low Potency" typical antipsychotic. While it has more sedative and anticholinergic effects, it still blocks D2 receptors and is significantly associated with EPS compared to non-antipsychotic drugs. **NEET-PG High-Yield Pearls:** * **EPS Mechanism:** Caused by D2 blockade in the **Nigrostriatal pathway**. * **Potency vs. EPS:** High-potency typical antipsychotics (Haloperidol, Fluphenazine) have the **highest** risk of EPS. * **Atypical Antipsychotics:** Drugs like **Clozapine** and **Quetiapine** have the **lowest** risk of EPS among antipsychotics due to rapid D2 dissociation and 5HT2A antagonism. * **Carbamazepine Side Effects:** Watch for Diplopia, Ataxia, **SIADH**, and life-threatening **Stevens-Johnson Syndrome** (associated with HLA-B*1502).

Q: Weight gain caused by antipsychotics is due to antagonism of which receptor subtype?

5-HT2C. **Explanation:** The correct answer is **D. 5-HT2C**. **Mechanism of Weight Gain:** Antipsychotic-induced weight gain is a complex metabolic side effect primarily mediated by the antagonism of two specific receptors: **5-HT2C (Serotonin 2C)** and **H1 (Histamine 1)**. * **5-HT2C receptors** are located in the hypothalamus and play a crucial role in regulating satiety and energy homeostasis. When these receptors are blocked, the "satiety signal" is inhibited, leading to hyperphagia (increased appetite) and subsequent weight gain. * **H1 antagonism** further exacerbates this by causing sedation and increasing cravings for high-calorie carbohydrates. **Analysis of Incorrect Options:** * **A. 5-HT3:** These receptors are primarily involved in the emetic reflex (nausea/vomiting). Antagonists (like Ondansetron) are used as anti-emetics, not associated with metabolic changes. * **B. 5-HT2A:** Antagonism of 5-HT2A is the hallmark of Second Generation (Atypical) Antipsychotics. It helps reduce Extrapyramidal Side Effects (EPS) and improves negative symptoms, but it is not the primary driver of weight gain. * **C. 5-HT2B:** These receptors are mainly found in the heart and GI tract. Agonism of 5-HT2B is associated with cardiac valvulopathy (e.g., with Fenfluramine). **High-Yield Clinical Pearls for NEET-PG:** * **Highest Risk of Weight Gain/Metabolic Syndrome:** Clozapine (most potent) > Olanzapine. * **Lowest Risk/Weight Neutral:** Ziprasidone, Aripiprazole, and Lurasidone. * **Monitoring:** Patients on Atypical Antipsychotics must have regular monitoring of BMI, waist circumference, fasting blood glucose, and lipid profile (Metabolic Monitoring). * **Management:** Metformin is often the first-line pharmacological intervention for antipsychotic-induced weight gain.

Q: A patient on antidepressant therapy developed sudden hypertension on consuming cheese. The antidepressant is possibly:

Tranylcypromine. **Explanation:** The clinical scenario describes a **"Cheese Reaction"** (Hypertensive Crisis), a classic adverse interaction associated with **Non-selective Monoamine Oxidase Inhibitors (MAOIs)**. **1. Why Tranylcypromine is Correct:** Tranylcypromine is an irreversible, non-selective MAO inhibitor. MAO enzymes (specifically MAO-A) are responsible for breaking down **Tyramine** in the gut. When a patient on MAOIs consumes tyramine-rich foods (like aged cheese, red wine, or smoked meats), tyramine escapes degradation, enters the systemic circulation, and acts as an indirect sympathomimetic. It displaces stored norepinephrine from synaptic vesicles, leading to a massive release of catecholamines, resulting in sudden, severe hypertension, headache, and potential stroke. **2. Why Other Options are Incorrect:** * **Amitriptyline:** A Tricyclic Antidepressant (TCA). While it has side effects like anticholinergic symptoms and arrhythmias, it does not cause a hypertensive crisis with tyramine. * **Fluoxetine & Sertraline:** These are Selective Serotonin Reuptake Inhibitors (SSRIs). Their main risk is "Serotonin Syndrome" if combined with other serotonergic drugs, but they do not interact with dietary tyramine. **Clinical Pearls for NEET-PG:** * **Antidote for Cheese Reaction:** Phentolamine (an alpha-blocker) is the drug of choice. * **MAOI Examples:** Phenelzine, Isocarboxazid, and Tranylcypromine (Non-selective); Selegiline (MAO-B selective at low doses); Moclobemide (RIMA - Reversible Inhibitor of MAO-A). * **Washout Period:** When switching from an MAOI to an SSRI (or vice versa), a **2-week washout period** is required (5 weeks for Fluoxetine due to its long half-life) to prevent Serotonin Syndrome.

Q: Which of the following drugs causes diastolic hypertension as a side effect?

Venlafaxine. **Explanation:** **Venlafaxine** is a Serotonin-Norepinephrine Reuptake Inhibitor (SNRI). At higher doses (>150 mg/day), it significantly inhibits the reuptake of norepinephrine (NE) in addition to serotonin. Increased synaptic NE levels lead to peripheral vasoconstriction and increased peripheral vascular resistance, which clinically manifests as a **dose-dependent increase in blood pressure**, specifically **diastolic hypertension**. Monitoring BP is mandatory for patients on high-dose Venlafaxine. **Analysis of Incorrect Options:** * **Amitriptyline (TCA):** While it also inhibits NE reuptake, its potent **alpha-1 adrenergic blockade** typically causes **orthostatic hypotension** rather than hypertension. * **Nefazodone (SARI):** This drug acts as a 5-HT2 receptor antagonist and weak reuptake inhibitor. It is more commonly associated with sedation and hepatotoxicity; it does not cause hypertension. * **Mianserin (Atypical Antidepressant):** It is an alpha-2 adrenoceptor antagonist. Like TCAs, it is more likely to cause postural hypotension and sedation rather than a sustained rise in diastolic BP. **High-Yield Clinical Pearls for NEET-PG:** * **SNRI Class Effect:** Both Venlafaxine and Desvenlafaxine are notorious for causing hypertension. Duloxetine (another SNRI) has a lesser effect on BP. * **Venlafaxine Withdrawal:** It has a very short half-life; abrupt discontinuation leads to severe "discontinuation syndrome" (flu-like symptoms, electric shock sensations). * **TCA Overdose:** Remember the "3 Cs": Coma, Convulsions, and Cardiotoxicity (arrhythmias due to Na+ channel blockade).

Q: Which of the following is not an adverse effect of clomipramine?

Bradycardia. **Explanation:** **Clomipramine** is a Tricyclic Antidepressant (TCA) primarily used in the management of Obsessive-Compulsive Disorder (OCD). Understanding its side effect profile requires knowledge of its multi-receptor blockade. **Why Bradycardia is the correct answer:** TCAs, including clomipramine, are notorious for their **cardiotoxicity**. They exert a "quinidine-like" effect on the heart, blocking fast sodium channels. This leads to slowed conduction, prolonged PR and QRS intervals, and most importantly, **Tachycardia** (due to potent muscarinic blockade and inhibition of norepinephrine reuptake). Therefore, **Bradycardia** is not a feature of TCA action; rather, tachycardia and arrhythmias are expected. **Analysis of Incorrect Options:** * **Dryness of mouth:** This is a classic **anticholinergic (antimuscarinic)** side effect. TCAs block M1 receptors, leading to "red as a beet, dry as a bone" symptoms like xerostomia, blurred vision, and constipation. * **Seizures:** TCAs **lower the seizure threshold**. Clomipramine and Maprotiline are particularly associated with a higher risk of seizures, especially in overdose or in patients with pre-existing epilepsy. * **Metabolic acidosis:** In cases of severe TCA overdose, tissue hypoxia and seizures can lead to **lactic acidosis (metabolic acidosis)**. This is a critical complication managed with Sodium Bicarbonate (which also helps reverse cardiotoxicity). **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Clomipramine is the gold standard for **OCD**, though SSRIs are preferred first-line due to a better safety profile. * **TCA Overdose Triad (3 C’s):** **C**oma, **C**onvulsions, and **C**ardiotoxicity (widened QRS is the most reliable marker). * **Antidote:** Intravenous **Sodium Bicarbonate** is used to treat QRS widening and arrhythmias in TCA poisoning.

Q: Which of the following drugs can cause hyponatremia?

Fluoxetine. **Explanation:** **Fluoxetine** is a Selective Serotonin Reuptake Inhibitor (SSRI). The most common mechanism by which psychotropic drugs cause hyponatremia is the **Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH)**. SSRIs are the most frequently implicated class of antidepressants in this condition, particularly in elderly patients or those taking diuretics. Serotonin is believed to stimulate the release of ADH (Vasopressin) from the posterior pituitary, leading to water retention and dilutional hyponatremia. **Analysis of Options:** * **Fluoxetine (Option A):** As an SSRI, it carries the highest risk of SIADH among the choices. It is a classic NEET-PG "high-yield" cause of drug-induced hyponatremia. * **Amitriptyline (Option B):** This is a Tricyclic Antidepressant (TCA). While TCAs can rarely cause SIADH, the risk is significantly lower compared to SSRIs. * **Mianserin (Option C):** An atypical tetracyclic antidepressant that acts as an alpha-2 antagonist. It is not typically associated with hyponatremia. * **Milnacipran (Option D):** A Serotonin-Norepinephrine Reuptake Inhibitor (SNRI). While SNRIs can cause SIADH, Fluoxetine (SSRI) is the more established and frequently tested culprit in this context. **Clinical Pearls for NEET-PG:** * **Risk Factors:** Elderly age, female gender, and concomitant use of diuretics (e.g., Thiazides) increase the risk of SSRI-induced hyponatremia. * **Timing:** It usually occurs within the first 2–4 weeks of starting therapy. * **Other drugs causing SIADH:** Carbamazepine (very common), Cyclophosphamide, Vincristine, and Chlorpropamide. * **Management:** Fluid restriction and discontinuation of the offending drug.

Q: Which antidepressant drug can cause neuroleptic malignant syndrome and tardive dyskinesia?

Amoxapine. **Explanation:** The correct answer is **Amoxapine**. **1. Why Amoxapine is correct:** Amoxapine is a secondary amine tricyclic antidepressant (TCA). Its unique pharmacological profile lies in its metabolism: it is metabolized to **7-hydroxyamoxapine**, which possesses potent **dopamine D2 receptor blocking activity**. This makes it structurally and functionally similar to loxapine (an antipsychotic). Because it blocks dopamine receptors in the nigrostriatal and mesolimbic pathways, it can cause side effects typically associated with antipsychotics, such as **Extrapyramidal Symptoms (EPS)**, **Tardive Dyskinesia**, and the life-threatening **Neuroleptic Malignant Syndrome (NMS)** [1]. **2. Why other options are incorrect:** * **Amineptine:** It is an atypical antidepressant that acts as a dopamine reuptake inhibitor. It does not block D2 receptors and is not associated with NMS or tardive dyskinesia. * **Fluoxetine:** This is a Selective Serotonin Reuptake Inhibitor (SSRI). While it can rarely cause Serotonin Syndrome, it does not have significant D2 blocking activity to cause tardive dyskinesia. * **Trazodone:** A Serotonin Antagonist and Reuptake Inhibitor (SARI). Its most notorious high-yield side effect is **priapism**, not dopamine-related movement disorders. **Clinical Pearls for NEET-PG:** * **Amoxapine** is often the drug of choice for **Psychotic Depression** due to its dual antidepressant and antipsychotic-like properties [1]. * **NMS vs. Serotonin Syndrome:** Remember that NMS presents with "lead-pipe" rigidity and hyporeflexia, whereas Serotonin Syndrome presents with hyperreflexia and myoclonus. * Other antidepressants with unique side effects: **Bupropion** (seizures), **Mirtazapine** (weight gain/sedation), and **Duloxetine** (used for neuropathic pain).

Q: Moclobemide is:

Monoamine oxidase (MAO) inhibitor. **Explanation:** **Moclobemide** is a **Reversible Inhibitor of MAO-A (RIMA)**. Monoamine oxidase (MAO) is an enzyme responsible for the oxidative deamination of neurotransmitters. MAO-A primarily metabolizes serotonin, norepinephrine, and dopamine. By inhibiting this enzyme, Moclobemide increases the synaptic concentration of these monoamines, thereby exerting its antidepressant effect. **Why the other options are incorrect:** * **Option A (SSRI):** Drugs like Fluoxetine, Sertraline, and Escitalopram belong to this class. They specifically inhibit the serotonin transporter (SERT) rather than the MAO enzyme. * **Option B (Antipsychotic):** These drugs (e.g., Haloperidol, Risperidone) primarily act by blocking Dopamine (D2) receptors or Serotonin (5-HT2A) receptors, not by inhibiting MAO. * **Option C (Tricyclic Antidepressant):** TCAs like Amitriptyline and Imipramine work by inhibiting the reuptake of both Norepinephrine and Serotonin (NET and SERT) and possess significant anticholinergic properties. **High-Yield Clinical Pearls for NEET-PG:** 1. **Cheese Reaction:** Unlike older, irreversible non-selective MAO inhibitors (e.g., Phenelzine), Moclobemide has a **lower risk of the "Cheese Reaction"** (hypertensive crisis caused by tyramine). This is because it is reversible; high levels of tyramine can displace Moclobemide from the enzyme, allowing tyramine metabolism to continue. 2. **Selectivity:** MAO-**A** inhibitors (Moclobemide) are used for **Depression**, while MAO-**B** inhibitors (Selegiline, Rasagiline) are used for **Parkinson’s Disease**. 3. **Serotonin Syndrome:** Even though it is a RIMA, Moclobemide should not be combined with SSRIs or TCAs due to the fatal risk of Serotonin Syndrome.

Question 1

Which of the following drugs has the least extrapyramidal symptoms?

Accepted Answer

Aripiprazole

Answer

Loxapine

Answer

Fluphenazine

Answer

Chlorpromazine

Question 2

Which of the following drugs is least associated with extra-pyramidal side effects?

Accepted Answer

Carbamazepine

Answer

Chlorpromazine

Answer

Fluphenazine

Answer

Haloperidol

Question 3

Weight gain caused by antipsychotics is due to antagonism of which receptor subtype?

Accepted Answer

5-HT2C

Answer

5-HT3

Answer

5-HT2A

Answer

5-HT2B

Question 4

A patient on antidepressant therapy developed sudden hypertension on consuming cheese. The antidepressant is possibly:

Accepted Answer

Tranylcypromine

Answer

Amitriptyline

Answer

Fluoxetine

Answer

Sertraline

Question 5

Which of the following drugs causes diastolic hypertension as a side effect?

Accepted Answer

Venlafaxine

Answer

Amitriptyline

Answer

Nefazodone

Answer

Mianserin

Question 6

All of the following are true about Clozapine except?

Accepted Answer

Blood level below 350 ng/ml should be maintained to avoid agranulocytosis.

Answer

More potently blocks D2 as compared to D1 receptors.

Answer

Should not be used along with Carbamazepine.

Answer

Should be discontinued if the WBC count is below 3,000/mm³ cells.

Question 7

Which of the following is not an adverse effect of clomipramine?

Accepted Answer

Bradycardia

Answer

Dryness of mouth

Answer

Seizures

Answer

Metabolic acidosis

Question 8

Which of the following drugs can cause hyponatremia?

Accepted Answer

Fluoxetine

Answer

Amitriptyline

Answer

Mianserin

Answer

Milnacipran

Question 9

Which antidepressant drug can cause neuroleptic malignant syndrome and tardive dyskinesia?

Accepted Answer

Amoxapine

Answer

Amineptin

Answer

Fluoxetine

Answer

Trazodone

Question 10

Moclobemide is:

Accepted Answer

Monoamine oxidase (MAO) inhibitor

Answer

Selective serotonin reuptake inhibitor (SSRI)

Answer

Antipsychotic drug

Answer

Tricyclic antidepressant

Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders — MCQs

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