Drugs in Psychiatric Disorders — MCQs
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What is the drug of choice for antipsychotic-induced Parkinsonism?
Which of the following drugs has anxiolytic action with the least sedation?
True about anticonvulsants in pregnancy?
Methadone is used for opioid withdrawal because it functions as:
Which of the following is NOT a side effect of tricyclic antidepressants?
Which of the following antipsychotic medications has akathisia as a common side effect?
Which anxiolytic benzodiazepine also possesses antidepressant properties?
What is the new drug approved for the treatment of tardive dyskinesia?
Which of the following is not a selective serotonin reuptake inhibitor?
Which of the following is a non-selective serotonin and noradrenaline reuptake inhibitor?
Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs
Question 111: What is the drug of choice for antipsychotic-induced Parkinsonism?
- A. Pimavanserin
- B. Trihexyphenidyl (Correct Answer)
- C. Droxidopa
- D. Pramipexole
Explanation: **Explanation:** **Mechanism and Correct Answer:** Antipsychotic-induced Parkinsonism is a type of **Extrapyramidal Side Effect (EPS)** caused by the blockade of dopamine (D2) receptors in the nigrostriatal pathway. This blockade creates a relative **excess of cholinergic activity** (acetylcholine). To restore the balance between dopamine and acetylcholine, **centrally acting anticholinergics** are used. **Trihexyphenidyl (Benzhexol)** is the drug of choice because it effectively crosses the blood-brain barrier to antagonize muscarinic receptors, thereby alleviating tremors, rigidity, and bradykinesia. Other drugs in this class include Benztropine and Biperiden. **Analysis of Incorrect Options:** * **Pimavanserin:** This is a selective 5-HT2A inverse agonist. It is specifically used for **Parkinson’s disease psychosis** (hallucinations in patients who already have PD), not for treating drug-induced EPS. * **Droxidopa:** A synthetic precursor of norepinephrine used primarily for treating **neurogenic orthostatic hypotension**. * **Pramipexole:** A dopamine agonist used in idiopathic Parkinson’s disease and Restless Leg Syndrome. It is generally avoided in antipsychotic-induced Parkinsonism because it can worsen the underlying psychosis by stimulating dopamine receptors. **High-Yield NEET-PG Pearls:** * **Drug of Choice for Acute Dystonia:** Parenteral Promethazine or Benztropine. * **Drug of Choice for Akathisia:** Propranolol (Beta-blocker). * **Drug of Choice for Tardive Dyskinesia:** Valbenazine or Deutetrabenazine (VMAT-2 inhibitors). * **Note:** Levodopa is **contraindicated** in drug-induced Parkinsonism as it can precipitate or worsen psychosis.
Question 112: Which of the following drugs has anxiolytic action with the least sedation?
- A. Buspirone (Correct Answer)
- B. Triazolam
- C. Alprazolam
- D. Chlordiazepoxide
Explanation: **Explanation:** **Buspirone** is the correct answer because it is a non-benzodiazepine anxiolytic that belongs to the **Azapirone** class. Unlike benzodiazepines, it acts as a **selective 5-HT1A partial agonist**. Its unique pharmacological profile allows it to relieve anxiety without causing significant sedation, hypnosis, muscle relaxation, or anticonvulsant effects. It also lacks the potential for abuse or withdrawal symptoms, making it ideal for chronic generalized anxiety disorder (GAD). **Why the other options are incorrect:** * **Triazolam (Option B):** A short-acting benzodiazepine primarily used as a hypnotic. It causes significant sedation and has a high risk of rebound insomnia. * **Alprazolam (Option C):** A potent benzodiazepine used for panic disorders and anxiety. While effective, it causes dose-dependent sedation, psychomotor impairment, and carries a risk of dependence. * **Chlordiazepoxide (Option D):** A long-acting benzodiazepine commonly used for alcohol withdrawal. It produces active metabolites that cause prolonged sedation and "hangover" effects. **High-Yield Clinical Pearls for NEET-PG:** * **Latency of Action:** Buspirone has a slow onset of action (takes **1–2 weeks** to show effects). It is NOT useful for acute anxiety or panic attacks. * **No Interaction with Alcohol:** Unlike benzodiazepines, buspirone does not potentiate the CNS depressant effects of alcohol. * **Driving Safety:** Because it lacks sedative and psychomotor-impairing properties, it is the preferred anxiolytic for patients who need to drive or operate machinery. * **Side Effects:** Most common side effects include dizziness, nausea, and headache. It does not cause weight gain or sexual dysfunction (unlike SSRIs).
Question 113: True about anticonvulsants in pregnancy?
- A. Carbamazepine is safe in pregnancy.
- B. Lamotrigine is safe in pregnancy.
- C. Monotherapy is generally recommended. (Correct Answer)
- D. Newer anticonvulsant drugs are always safe in pregnancy.
Explanation: The management of epilepsy during pregnancy requires a delicate balance between controlling maternal seizures and minimizing teratogenic risks to the fetus [1]. **Why Option C is Correct:** **Monotherapy** (using a single drug at the lowest effective dose) is the gold standard in pregnancy [1]. The risk of congenital malformations increases significantly with **polytherapy** due to drug-drug interactions and cumulative toxicity. Most malformations are dose-dependent; hence, maintaining the patient on one drug reduces the overall teratogenic burden. **Analysis of Incorrect Options:** * **Option A:** Carbamazepine is **not "safe."** It is associated with a 2-3% risk of neural tube defects (spina bifida) and craniofacial abnormalities. While less teratogenic than Valproate, it still carries significant risk. * **Option B:** No anticonvulsant is strictly "safe." However, **Lamotrigine** and **Levetiracetam** are considered the *preferred* or *least teratogenic* options. Even so, "safe" is an absolute term that does not apply to AEDs in pregnancy. * **Option D:** Newer drugs are not "always safe." While drugs like Levetiracetam have better safety profiles, others like **Topiramate** are associated with an increased risk of oral clefts (cleft lip/palate). **High-Yield NEET-PG Pearls:** 1. **Most Teratogenic:** **Valproate** (causes Neural Tube Defects; highest risk among all AEDs). It should be avoided in women of childbearing age unless no alternative exists. 2. **Drug of Choice:** If a woman is already seizure-free on a specific drug, it is usually continued (except Valproate) because switching drugs during pregnancy can trigger breakthrough seizures. 3. **Prophylaxis:** All pregnant women on AEDs should take **High-dose Folic Acid (5 mg/day)** starting pre-conceptionally to reduce the risk of neural tube defects. 4. **Vitamin K:** Enzyme-inducing AEDs (Phenytoin, Carbamazepine) can cause neonatal hemorrhage; Vitamin K is often given to the mother in the last month of pregnancy [1].
Question 114: Methadone is used for opioid withdrawal because it functions as:
- A. An antagonist at the opioid receptor
- B. A partial antagonist at the opioid receptor
- C. An agonist at the opioid receptor (Correct Answer)
- D. A partial agonist at the opioid receptor
Explanation: **Explanation:** **1. Why Option C is Correct:** Methadone is a **long-acting synthetic μ (mu) opioid receptor agonist**. In the management of opioid use disorder, it is used for "Opioid Substitution Therapy" (OST). Because it is a full agonist with a long half-life (24–36 hours), it achieves two main goals: * **Prevents Withdrawal:** It stimulates the receptors enough to prevent the physical symptoms of withdrawal. * **Suppresses Craving:** It maintains a steady state in the blood, preventing the "rush" associated with heroin while blocking the cravings. **2. Why Other Options are Incorrect:** * **Option A (Antagonist):** Drugs like **Naloxone** and **Naltrexone** are antagonists. They block the receptor completely. Giving an antagonist to a dependent patient would precipitate immediate, severe withdrawal. * **Option B (Partial Antagonist):** This is not a standard pharmacological classification for opioid therapy. * **Option D (Partial Agonist):** **Buprenorphine** is the classic example of a partial μ-agonist. While it is also used for withdrawal, Methadone is distinct because it is a full agonist. **3. NEET-PG High-Yield Clinical Pearls:** * **NMDA Antagonism:** Apart from being a μ-agonist, Methadone also acts as an **NMDA receptor antagonist**, which may help in treating neuropathic pain and preventing opioid tolerance. * **Side Effect:** A critical "must-know" side effect of Methadone is **QT interval prolongation**, which can lead to Torsades de Pointes. * **Metabolism:** It is primarily metabolized by **CYP3A4**; therefore, inhibitors of this enzyme can lead to methadone toxicity. * **Gold Standard:** Methadone remains the gold standard for opioid maintenance therapy during **pregnancy**.
Question 115: Which of the following is NOT a side effect of tricyclic antidepressants?
- A. Weight loss (Correct Answer)
- B. Weight gain
- C. Giddiness
- D. Sedation
Explanation: **Explanation:** Tricyclic Antidepressants (TCAs), such as Amitriptyline and Imipramine, are known for their broad pharmacological profile, acting on multiple receptors including muscarinic (M1), histaminergic (H1), and alpha-adrenergic (α1) receptors. **Why Weight Loss is the Correct Answer:** TCAs are notorious for causing **Weight Gain**, not weight loss. This occurs primarily due to the potent blockade of **H1 (Histamine)** receptors, which increases appetite and cravings for carbohydrates. Therefore, weight loss is not a side effect of TCAs; in fact, it is more commonly associated with certain SSRIs (like Fluoxetine) or Bupropion. **Analysis of Incorrect Options:** * **Weight Gain:** As mentioned, H1 receptor antagonism leads to significant weight gain, making it a common reason for patient non-compliance. * **Giddiness:** This is a result of **Orthostatic Hypotension** caused by the blockade of **alpha-1 (α1) adrenergic receptors**. Patients often experience dizziness or giddiness when standing up suddenly. * **Sedation:** This is another direct consequence of **H1 receptor blockade**. TCAs like Amitriptyline are highly sedative and are often administered at bedtime to aid sleep. **NEET-PG High-Yield Pearls:** 1. **Anticholinergic Side Effects:** TCAs cause the "3 Ds": Dry mouth, Dilated pupils (blurred vision), and Difficulty in micturition (due to M1 blockade). 2. **Cardiotoxicity:** The most dangerous side effect in overdose is cardiac arrhythmia due to **Sodium (Na+) channel blockade**, leading to QRS prolongation. 3. **Treatment of Overdose:** Sodium bicarbonate is the specific antidote used to manage TCA-induced arrhythmias. 4. **Drug of Choice:** Imipramine is the DOC for Nocturnal Enuresis in children (though non-pharmacological methods are preferred first).
Question 116: Which of the following antipsychotic medications has akathisia as a common side effect?
- A. Fluoxetine
- B. Olanzapine
- C. Haloperidol (Correct Answer)
- D. Risperidone
Explanation: **Explanation:** **Correct Answer: C. Haloperidol** **Mechanism and Concept:** Akathisia is a common **Extrapyramidal Side Effect (EPS)** characterized by subjective feelings of inner restlessness and an inability to sit still. It is primarily caused by the potent blockade of **D2 receptors** in the nigrostriatal pathway. **Haloperidol** is a high-potency, first-generation (typical) antipsychotic. Because it binds very strongly and non-selectively to D2 receptors, it has the highest propensity among the given options to cause EPS, including akathisia, dystonia, and parkinsonism. **Analysis of Incorrect Options:** * **A. Fluoxetine:** This is an SSRI (Selective Serotonin Reuptake Inhibitor) used for depression. While SSRIs can occasionally cause "jitteriness" or "activation syndrome" early in treatment, they are not classified as antipsychotics and are not the classic cause of D2-mediated akathisia. * **B. Olanzapine:** This is a second-generation (atypical) antipsychotic. It has a higher affinity for 5-HT2A receptors than D2 receptors and dissociates rapidly from D2 receptors, leading to a significantly lower risk of akathisia compared to Haloperidol. * **D. Risperidone:** While Risperidone is an atypical antipsychotic that can cause EPS at higher doses (>6mg), its risk profile for akathisia is generally lower than that of high-potency typicals like Haloperidol. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment of Akathisia:** The drug of choice is **Propranolol** (Beta-blocker). Benzodiazepines or anticholinergics (like Benztropine) are second-line options. * **Potency Rule:** High-potency typical antipsychotics (Haloperidol, Fluphenazine) = High EPS risk, Low sedative/anticholinergic risk. * **Aripiprazole Note:** Among atypical antipsychotics, Aripiprazole is uniquely associated with a relatively higher incidence of akathisia due to its partial D2 agonism.
Question 117: Which anxiolytic benzodiazepine also possesses antidepressant properties?
- A. Alprazolam (Correct Answer)
- B. Oxazepam
- C. Lorazepam
- D. Chlordiazepoxide
Explanation: **Explanation:** **Alprazolam** is a unique triazolo-benzodiazepine. While all benzodiazepines (BZDs) share common properties (anxiolytic, sedative-hypnotic, muscle relaxant, and anticonvulsant), Alprazolam is the only one in this list that possesses significant **antidepressant properties**. This is attributed to its ability to modulate central monoaminergic systems and its high potency at the GABA-A receptor complex. It is specifically indicated for anxiety associated with depression and is highly effective in treating **Panic Disorder**. **Analysis of Incorrect Options:** * **Oxazepam:** A short-to-intermediate acting BZD. It is a direct metabolite of Diazepam and is preferred in patients with liver failure (as it undergoes direct glucuronidation), but it lacks antidepressant efficacy. * **Lorazepam:** A high-potency BZD used primarily for status epilepticus, acute anxiety, and pre-anesthetic medication. It does not have inherent antidepressant activity. * **Chlordiazepoxide:** The first BZD discovered. It has a long half-life and active metabolites. Its primary clinical use today is in the management of **Alcohol Withdrawal Syndrome**. **High-Yield Clinical Pearls for NEET-PG:** * **DOC for Panic Disorder:** Alprazolam (along with SSRIs for long-term management). * **BZD for Liver Failure:** Remember the mnemonic **LOT** (Lorazepam, Oxazepam, Temazepam) as they do not require hepatic oxidation. * **Antidote:** Flumazenil is a competitive BZD receptor antagonist used for overdose. * **Mechanism:** BZDs increase the **frequency** of chloride channel opening (GABA-facilitatory), whereas Barbiturates increase the **duration**.
Question 118: What is the new drug approved for the treatment of tardive dyskinesia?
- A. Safinamide
- B. Tetrabenazine
- C. Valbenazine (Correct Answer)
- D. Deutetrabenazine
Explanation: **Explanation:** **Valbenazine** is the first drug specifically FDA-approved for the treatment of **Tardive Dyskinesia (TD)**. TD is a movement disorder caused by long-term use of dopamine receptor blockers (antipsychotics), characterized by upregulation of dopamine receptors. Valbenazine acts as a highly selective **Vesicular Monoamine Transporter 2 (VMAT2) inhibitor**. By inhibiting VMAT2, it prevents the packaging of dopamine into presynaptic vesicles, thereby reducing dopamine release into the synaptic cleft and alleviating the hyperkinetic movements of TD. **Analysis of Options:** * **Safinamide (Option A):** This is a reversible MAO-B inhibitor used as an add-on treatment for Parkinson’s disease to manage "off" episodes. It has no role in treating TD. * **Tetrabenazine (Option B):** While it is a VMAT2 inhibitor used for Huntington’s Chorea, it is not specifically preferred for TD due to its short half-life and significant side effects like depression and parkinsonism. * **Deutetrabenazine (Option D):** This is a deuterated form of tetrabenazine. While it is also approved for TD, **Valbenazine** is often highlighted in exams as the "first" or "novel" specific agent with a superior pharmacokinetic profile (once-daily dosing and less risk of depression). **High-Yield Clinical Pearls for NEET-PG:** 1. **VMAT2 Inhibitors:** Valbenazine and Deutetrabenazine are the current drugs of choice for TD. 2. **Mechanism:** They decrease dopamine levels without blocking the D2 receptor directly, avoiding the worsening of TD. 3. **Historical Context:** Previously, Vitamin E and Benzodiazepines were used, but they lacked robust efficacy. 4. **Pro-tip:** If a patient develops TD, the first step is to taper/stop the offending antipsychotic or switch to **Clozapine** (the antipsychotic with the lowest risk of TD).
Question 119: Which of the following is not a selective serotonin reuptake inhibitor?
- A. Fluoxetine
- B. Fluvoxamine
- C. Paroxetine
- D. Amoxapine (Correct Answer)
Explanation: ### Explanation The correct answer is **D. Amoxapine**. **1. Why Amoxapine is the correct answer:** Amoxapine is a **Tricyclic Antidepressant (TCA)** belonging to the dibenzoxazepine class. Unlike Selective Serotonin Reuptake Inhibitors (SSRIs), its primary mechanism involves inhibiting the reuptake of norepinephrine and, to a lesser extent, serotonin. Crucially, it is a metabolite of the antipsychotic loxapine and possesses significant **Dopamine (D2) receptor blocking activity**, giving it unique antipsychotic properties among antidepressants. **2. Why the other options are incorrect:** * **A. Fluoxetine:** The prototype SSRI with the longest half-life (due to its active metabolite norfluoxetine) [2]. It is commonly used for depression and OCD [3]. * **B. Fluvoxamine:** An SSRI primarily indicated for Obsessive-Compulsive Disorder (OCD) and social anxiety disorder [3]. * **C. Paroxetine:** A potent SSRI known for having the shortest half-life among the group and a higher risk of discontinuation syndrome [2]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Amoxapine Side Effects:** Due to D2 blockade, it can cause **Extrapyramidal Symptoms (EPS)** and hyperprolactinemia, unlike other antidepressants. * **SSRI Drug of Choice:** SSRIs are currently the first-line treatment for Depression, OCD, Panic Disorder, Social Phobia, and Post-Traumatic Stress Disorder (PTSD). * **Serotonin Syndrome:** A critical complication when SSRIs are combined with MAO inhibitors; characterized by cognitive effects, autonomic hyperactivity, and somatic effects (hyperreflexia/clonus) [2]. * **Mnemonic for SSRIs:** **F**lashbacks **P**aralyze **S**enior **C**itizens (**F**luoxetine, **F**luvoxamine, **P**aroxetine, **S**ertraline, **C**italopram/Escitalopram) [1].
Question 120: Which of the following is a non-selective serotonin and noradrenaline reuptake inhibitor?
- A. Sertraline
- B. Citalopram
- C. Venlafaxine (Correct Answer)
- D. Paroxetine
Explanation: The question tests the classification of antidepressant drugs based on their mechanism of action. **Correct Option: C. Venlafaxine** Venlafaxine belongs to the class of **Serotonin and Noradrenaline Reuptake Inhibitors (SNRIs)** [1]. These drugs are "non-selective" because they inhibit the reuptake of both serotonin (5-HT) and noradrenaline (NE) by binding to their respective transporters (SERT and NET) [1]. This dual action increases the synaptic concentration of both neurotransmitters. Other drugs in this class include Duloxetine, Milnacipran, and Desvenlafaxine [1, 2]. **Incorrect Options:** * **A, B, and D (Sertraline, Citalopram, Paroxetine):** These drugs belong to the **Selective Serotonin Reuptake Inhibitors (SSRIs)** class [1]. As the name suggests, they selectively inhibit the reuptake of serotonin (5-HT) with minimal to no effect on noradrenaline or dopamine reuptake [1]. SSRIs are currently the first-line treatment for most anxiety and depressive disorders due to their better safety profile. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-Dependent Action:** At low doses, Venlafaxine acts primarily as an SSRI; its noradrenergic effect becomes significant only at higher doses (>150 mg/day) [2]. * **Side Effects:** Due to its noradrenergic activity, Venlafaxine can cause a **dose-dependent increase in blood pressure** (diastolic hypertension). * **Duloxetine:** Another SNRI frequently asked about; it is the drug of choice for **diabetic neuropathy** and fibromyalgia. * **Discontinuation Syndrome:** Venlafaxine has a short half-life, making it more likely to cause severe withdrawal symptoms if stopped abruptly compared to SSRIs like Fluoxetine.
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
Practice Questions
Drugs for Dementia
Practice Questions
Drug-Induced Psychiatric Symptoms
Practice Questions
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