Drugs in Psychiatric Disorders Practice Questions

Q: Which of the following drugs can cause hyperprolactinemia?

Risperidone. **Explanation:** The correct answer is **Risperidone**. **Mechanism of Action:** Hyperprolactinemia in patients taking antipsychotics is caused by the blockade of **D2 receptors** in the **tuberoinfundibular pathway** of the brain. Under normal physiological conditions, dopamine acts as a "prolactin-inhibiting factor." When D2 receptors are blocked, the inhibition is removed, leading to increased prolactin secretion from the anterior pituitary. **Why Risperidone?** While Risperidone is classified as an atypical (second-generation) antipsychotic, it is unique because it has a very high affinity for D2 receptors and poor penetration of the blood-brain barrier in the pituitary region. Consequently, it behaves more like a typical antipsychotic regarding prolactin elevation. It is the **most common atypical antipsychotic** associated with significant hyperprolactinemia, often causing galactorrhea, amenorrhea, and gynecomastia. **Analysis of Incorrect Options:** * **Olanzapine:** While it can cause mild, transient elevations in prolactin, it is generally considered "prolactin-sparing" compared to Risperidone. * **Ziprasidone & Asenapine:** These are second-generation antipsychotics with low potential for prolactin elevation. They dissociate quickly from D2 receptors, minimizing the impact on the tuberoinfundibular pathway. **High-Yield Clinical Pearls for NEET-PG:** * **Highest Risk:** Typical antipsychotics (e.g., Haloperidol) and Risperidone/Paliperidone. * **Lowest Risk (Prolactin-sparing):** Aripiprazole (a D2 partial agonist), Quetiapine, and Clozapine. * **Management:** If hyperprolactinemia occurs, the drug of choice to add (if switching is not possible) is **Aripiprazole**, as its partial agonism helps lower prolactin levels. * **Clinical Features:** Look for "Amenorrhea-Galactorrhea syndrome" in females and "Gynecomastia/Sexual dysfunction" in males.

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

Premature ejaculation. Paroxetine is a Selective Serotonin Reuptake Inhibitor (SSRI). The core concept to understand here is that **SSRIs are notorious for causing sexual dysfunction** [1, 2], but they specifically **delay ejaculation** rather than causing it prematurely [2]. **Why Option A is the Correct Answer:** Paroxetine increases serotonin levels in the synaptic cleft. Serotonin has an inhibitory effect on ejaculation. Therefore, paroxetine causes **delayed ejaculation** (ejaculatory retardation) [2]. Because of this "side effect," paroxetine and other SSRIs (like Dapoxetine) are actually used therapeutically to treat premature ejaculation [4]. Thus, premature ejaculation is not a side effect; it is the condition the drug treats. **Analysis of Incorrect Options:** * **B & C (Erectile Dysfunction & Decreased Libido):** These are very common side effects of SSRIs. Increased serotonin stimulation of 5-HT2 receptors in the CNS leads to decreased sexual desire (libido) and difficulty maintaining an erection [2]. * **D (Diarrhea):** Approximately 90% of the body's serotonin is in the GI tract. SSRIs increase serotonergic activity in the gut, leading to increased motility, which commonly manifests as nausea, vomiting, or diarrhea [2]. **NEET-PG High-Yield Pearls:** * **Dapoxetine:** The specific SSRI approved for the "on-demand" treatment of premature ejaculation due to its rapid onset and short half-life. * **Most Sedating SSRI:** Paroxetine (also has significant anticholinergic properties). * **Discontinuation Syndrome:** Paroxetine has a short half-life, making it the SSRI most likely to cause withdrawal symptoms if stopped abruptly [3]. * **Drug of Choice for Sexual Dysfunction:** If a patient develops sexual side effects on SSRIs, switching to **Bupropion** (a NDRI) or **Mirtazapine** is the preferred clinical strategy.

Q: Which of the following is an extrapyramidal side effect of antipsychotics?

Dystonia. **Explanation:** **Extrapyramidal Side Effects (EPS)** are drug-induced movement disorders caused by the blockade of dopamine (D2) receptors in the **nigrostriatal pathway** [1]. This is most commonly associated with First-Generation Antipsychotics (e.g., Haloperidol). **1. Why Dystonia is Correct:** **Acute Dystonia** is a classic EPS characterized by sudden, involuntary muscle spasms. Common presentations include torticollis (neck twisting), grimacing, and **oculogyric crisis** (upward deviation of eyes). It typically occurs within hours to days of starting treatment or increasing the dose. **2. Analysis of Incorrect Options:** * **Akathisia (Option B):** While Akathisia (subjective restlessness) is indeed an EPS [1], in the context of single-choice questions where "Dystonia" is the primary textbook example of an acute motor spasm, it serves as a distractor if Dystonia is the intended focus. *Note: In many clinical exams, both are EPS; however, Dystonia is the most "definitive" motor spasm.* * **Seizures (Option C):** This is a neurological side effect (lowering of seizure threshold), particularly with **Clozapine** [2], but it is not classified as an extrapyramidal motor symptom. * **Diarrhoea (Option D):** Antipsychotics typically have **anticholinergic** properties, which cause constipation, not diarrhoea. **High-Yield Clinical Pearls for NEET-PG:** * **Timeline of EPS:** 1. **Acute Dystonia:** Hours to days (Treatment: Promethazine or Benztropine) [1]. 2. **Akathisia:** Days to weeks (Treatment: Beta-blockers like Propranolol) [1]. 3. **Drug-induced Parkinsonism:** Weeks to months (Treatment: Trihexyphenidyl) [1]. 4. **Tardive Dyskinesia:** Months to years (Choreoathetoid movements; Treatment: Valbenazine) [1]. * **Pathophysiology:** EPS occurs when D2 blockade in the striatum leads to a relative **excess of Acetylcholine**. This is why anticholinergics are used for management [1].

Q: Concomitant use of valproic acid and lamotrigine increases the risk of which of the following conditions?

Stevens-Johnson syndrome. **Explanation:** The correct answer is **Stevens-Johnson syndrome (SJS)**. **Mechanism of Interaction:** Lamotrigine is primarily metabolized by the enzyme **UDP-glucuronosyltransferase (UGT)**. Valproic acid is a potent inhibitor of this enzyme. When used concomitantly, valproic acid inhibits the metabolism of lamotrigine, leading to a significant increase (up to two-fold) in its serum concentration and half-life. High levels of lamotrigine are strongly associated with life-threatening cutaneous adverse reactions, specifically **Stevens-Johnson syndrome (SJS)** and **Toxic Epidermal Necrolysis (TEN)**. To mitigate this risk, the starting dose of lamotrigine must be reduced by half when added to a regimen containing valproate. **Analysis of Incorrect Options:** * **A. Chondrodysplasia punctata:** This is a skeletal dysplasia associated with the use of **Warfarin** during pregnancy (Warfarin Embryopathy). * **B. Paroxysmal Nocturnal Hemoglobinuria (PNH):** This is an acquired hematopoietic stem cell disorder caused by a somatic mutation in the *PIGA* gene; it is not drug-induced. * **D. Floppy infant syndrome:** This refers to neonatal hypotonia, typically seen in infants born to mothers taking **Benzodiazepines** or **Lithium** near the time of delivery. **High-Yield Clinical Pearls for NEET-PG:** * **Valproate** is a broad-spectrum enzyme **inhibitor**, whereas Carbamazepine, Phenytoin, and Phenobarbital are enzyme **inducers**. * **Lamotrigine** is the preferred anti-epileptic for **bipolar depression** and is considered safe in pregnancy regarding major malformations, though it carries a risk of cleft lip/palate. * **SJS/TEN** is most commonly associated with sulfonamides, allopurinol, anticonvulsants (lamotrigine, carbamazepine, phenytoin), and NSAIDs.

Q: What is the most common cardiac adverse effect of lithium?

Bradycardia. **Explanation:** Lithium is the gold-standard mood stabilizer for Bipolar Disorder, but it has a narrow therapeutic index and significant multisystem side effects. **Why Bradycardia is the correct answer:** The most common cardiac manifestation of lithium therapy is **T-wave inversion or flattening** (similar to hypokalemia), which is usually benign. However, among the clinical cardiac adverse effects, **Sinus Bradycardia** and **Sinus Node Dysfunction (Sick Sinus Syndrome)** are the most frequently reported. Lithium interferes with the electrical conduction system of the heart by inhibiting the influx of sodium ions through the pacemaker channels, leading to a decrease in the firing rate of the sinoatrial (SA) node. **Analysis of Incorrect Options:** * **A. Arrhythmia:** While lithium can cause arrhythmias (like ventricular tachycardia) in cases of severe toxicity, they are less common than simple bradycardia at therapeutic or mildly toxic levels. * **B. Cardiomyopathy:** This is not a recognized side effect of lithium. Cardiomyopathy is more commonly associated with chronic alcohol use or certain antipsychotics (like Clozapine-induced myocarditis). * **D. Hypotension:** Lithium does not typically affect peripheral vascular resistance or blood pressure directly. **High-Yield NEET-PG Pearls:** * **ECG Changes:** T-wave flattening/inversion is the most common *electrocardiographic* finding (benign). * **Teratogenicity:** Lithium use in pregnancy is associated with **Ebstein’s Anomaly** (atrialization of the right ventricle). * **Monitoring:** Before starting lithium, baseline **ECG, Renal Function Tests (RFT), and Thyroid Function Tests (TFT)** are mandatory. * **Therapeutic Range:** 0.6–1.2 mEq/L (Prophylaxis: 0.6–0.8; Acute Mania: 0.8–1.2). Toxicity usually starts >1.5 mEq/L.

Q: Which of the following drugs causes hepatotoxicity?

Nefazodone. **Explanation:** **Nefazodone** is a Serotonin-2 Antagonist and Reuptake Inhibitor (SARI). While it is effective for depression and anxiety, its clinical use has been severely restricted due to a **Black Box Warning** regarding life-threatening **hepatotoxicity**. The drug can cause a rapid increase in hepatic enzymes leading to fulminant hepatic failure, often requiring liver transplantation. Because of this risk, it has been withdrawn from the market in several countries (e.g., USA, Canada). **Analysis of Incorrect Options:** * **Sertraline & Fluoxetine (SSRIs):** These are the first-line treatments for depression. While all drugs undergo hepatic metabolism, SSRIs are generally considered safe for the liver. Idiosyncratic liver injury is extremely rare with these agents. * **Amitriptyline (TCA):** Tricyclic antidepressants are primarily associated with anticholinergic side effects (dry mouth, constipation), sedation, and cardiotoxicity (arrhythmias due to sodium channel blockade). While they can occasionally cause a mild, transient rise in transaminases, they do not carry the high risk of severe hepatotoxicity seen with Nefazodone. **Clinical Pearls for NEET-PG:** * **Nefazodone vs. Trazodone:** Both are SARIs. While Nefazodone is hepatotoxic, **Trazodone** is famously associated with **priapism** and is frequently used off-label for insomnia due to its sedative properties. * **Mechanism:** Nefazodone also acts as a potent inhibitor of the **CYP3A4** enzyme, leading to numerous drug-drug interactions. * **Mnemonic:** Remember **"N"** for Nefazodone = **"N"**ecrosis of the liver.

Q: Which drug is used in the prophylaxis of nicotine addiction?

Bupropion. **Explanation:** **Bupropion** is an atypical antidepressant that acts as a selective **norepinephrine and dopamine reuptake inhibitor (NDRI)**. It is FDA-approved for smoking cessation (prophylaxis of nicotine addiction) because it mimics some of the neurochemical effects of nicotine. By increasing dopamine levels in the brain's reward pathway (nucleus accumbens), it reduces the intensity of nicotine withdrawal symptoms and the urge to smoke. **Analysis of Incorrect Options:** * **Diazepam:** A benzodiazepine used for acute alcohol withdrawal and anxiety. It has no role in treating nicotine addiction and carries its own risk of dependence. * **Naloxone:** An opioid antagonist used primarily for the emergency reversal of opioid overdose. It does not significantly impact the nicotinic acetylcholine receptors involved in smoking. * **Acamprosate:** Used specifically for maintaining abstinence in **alcohol dependence** by modulating glutamate and GABA neurotransmission; it is ineffective for nicotine addiction. **High-Yield Clinical Pearls for NEET-PG:** * **Varenicline** (a partial agonist at $\alpha_4\beta_2$ nicotinic receptors) is considered the most effective monotherapy for smoking cessation, followed by Bupropion and Nicotine Replacement Therapy (NRT). * **Contraindication:** Bupropion is strictly contraindicated in patients with **seizure disorders** or eating disorders (bulimia/anorexia) as it lowers the seizure threshold. * **Weight Neutrality:** Unlike many antidepressants, Bupropion is often associated with weight loss, making it a preferred choice for smokers concerned about post-cessation weight gain. * **Clonidine** and **Nortriptyline** are considered second-line agents for smoking cessation.

Q: Dryness of mouth is caused by antipsychotics due to their:

Anticholinergic action. **Explanation:** The correct answer is **A. Anticholinergic action**. **Mechanism of Action:** Antipsychotics (especially first-generation agents like Chlorpromazine and low-potency neuroleptics) often possess significant affinity for **Muscarinic (M1) receptors**. By blocking these receptors, they inhibit the parasympathetic nervous system's stimulation of the salivary glands. Since acetylcholine is the primary neurotransmitter responsible for inducing salivation, its antagonism leads to **Xerostomia** (dryness of mouth). **Analysis of Incorrect Options:** * **B. Antiadrenergic action:** Blockade of alpha-1 adrenergic receptors primarily leads to orthostatic hypotension, reflex tachycardia, and nasal congestion, rather than dry mouth. * **C. Antidopaminergic action:** This is the primary therapeutic mechanism of antipsychotics (D2 blockade). It is responsible for the antipsychotic effect and extrapyramidal side effects (EPS) like parkinsonism and dystonia, but not autonomic side effects like dry mouth. * **D. Antihistaminic action:** Blockade of H1 receptors is primarily associated with sedation and weight gain. **NEET-PG High-Yield Clinical Pearls:** * **Low-potency vs. High-potency:** Low-potency antipsychotics (e.g., Chlorpromazine, Thioridazine) have **higher** anticholinergic activity compared to high-potency drugs (e.g., Haloperidol). * **The "Anti-SLUDGE" Effect:** Anticholinergic side effects can be remembered by the mnemonic: Dry mouth, blurred vision (cycloplegia), constipation, and urinary retention. * **Clozapine Paradox:** While most antipsychotics cause dry mouth, **Clozapine** is unique because it often causes **Sialorrhea** (excessive salivation), likely due to its agonist action at M4 receptors or impairment of the swallowing reflex. * **Management:** Patients are often advised to use sugarless gum or frequent sips of water to manage xerostomia.

Q: All of the following are side effects of Clozapine except?

Weight loss. **Explanation:** Clozapine is a unique "atypical" antipsychotic reserved for treatment-resistant schizophrenia. The correct answer is **Weight loss** because Clozapine is actually associated with significant **weight gain** and metabolic syndrome. 1. **Why Weight Loss is the Correct Answer:** Clozapine has a high affinity for $H_1$ (histamine) and $5-HT_{2C}$ receptors. Blockade of these receptors leads to increased appetite and profound weight gain. It also carries the highest risk among antipsychotics for causing dyslipidemia and Type 2 Diabetes Mellitus. 2. **Analysis of Incorrect Options:** * **Agranulocytosis:** This is the most dreaded side effect (occurring in ~1%). It requires mandatory WBC and ANC (Absolute Neutrophil Count) monitoring. * **Myocarditis:** A rare but potentially fatal idiosyncratic reaction, usually occurring within the first 4–8 weeks of treatment. * **Seizures:** Clozapine reduces the seizure threshold in a dose-dependent manner. The risk is significantly higher at doses above 600 mg/day. **High-Yield Clinical Pearls for NEET-PG:** * **Sialorrhea (Drooling):** Paradoxically, though it has anticholinergic properties, Clozapine commonly causes excessive salivation (often nocturnal). * **Constipation:** It can cause life-threatening paralytic ileus due to potent anticholinergic effects. * **No EPS/Hyperprolactinemia:** Clozapine is unique because it rarely causes Extrapyramidal Side Effects or increases prolactin levels. * **DOC (Drug of Choice):** For treatment-resistant schizophrenia and schizophrenia with persistent suicidal behavior.

Question 1

Which of the following drugs can cause hyperprolactinemia?

Accepted Answer

Risperidone

Answer

Olanzapine

Answer

Ziprasidone

Answer

Asenapine

Question 2

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

Accepted Answer

Premature ejaculation

Answer

Erectile dysfunction

Answer

Decreased libido

Answer

Diarrhea

Question 3

Which of the following is an extrapyramidal side effect of antipsychotics?

Accepted Answer

Dystonia

Answer

Akathisia

Answer

Seizures

Answer

Diarrhoea

Question 4

Concomitant use of valproic acid and lamotrigine increases the risk of which of the following conditions?

Accepted Answer

Stevens-Johnson syndrome

Answer

Chondrodysplasia punctata

Answer

Paroxysmal Nocturnal hemoglobinuria

Answer

Floppy infant syndrome

Question 5

What is the most common cardiac adverse effect of lithium?

Accepted Answer

Bradycardia

Answer

Arrhythmia

Answer

Cardiomyopathy

Answer

Hypotension

Question 6

Which of the following drugs causes hepatotoxicity?

Accepted Answer

Nefazodone

Answer

Sertraline

Answer

Fluoxetine

Answer

Amitriptyline

Question 7

Which drug is used in the prophylaxis of nicotine addiction?

Accepted Answer

Bupropion

Answer

Diazepam

Answer

Naloxone

Answer

Acamprosate

Question 8

Dryness of mouth is caused by antipsychotics due to their:

Accepted Answer

Anticholinergic action

Answer

Antiadrenergic action

Answer

Antidopaminergic action

Answer

Antihistaminic action

Question 9

An 8-year-old boy is evaluated for fatigue. Auscultation reveals a holosystolic murmur best heard at the lower sternal border. Echocardiography reveals apical displacement of the tricuspid valve leaflets, decreased right ventricular volume and atrialisation of the right ventricle. Moderate to severe tricuspid regurgitation is present. This patient's condition is believed to be a teratogenic effect of a drug taken during pregnancy. Which one of the following could not have been a side effect of that drug on the biological mother?

Accepted Answer

Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH)

Answer

Hypothyroidism

Answer

Acneiform eruptions

Answer

Leukocytosis

Question 10

All of the following are side effects of Clozapine except?

Accepted Answer

Weight loss

Answer

Agranulocytosis

Answer

Myocarditis

Answer

Seizures

Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders — MCQs

On this page

Practice by Chapter

Want unlimited practice?