Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 181: Which of the following medications is not an antidepressant?

A. Amitriptyline
B. Fluoxetine
C. Imipramine
D. Chlorpromazine (Correct Answer)

Explanation: **Explanation:** The correct answer is **Chlorpromazine** because it belongs to the class of **Typical Antipsychotics** (First-generation antipsychotics), specifically the Low-Potency Phenothiazines. Its primary mechanism of action is the blockade of post-synaptic **D2 receptors** in the mesolimbic pathway, making it effective for treating schizophrenia and mania, rather than depression. **Analysis of Options:** * **Amitriptyline (Option A):** A classic **Tricyclic Antidepressant (TCA)**. It inhibits the reuptake of both Serotonin (5-HT) and Norepinephrine (NE). It is frequently used for depression, neuropathic pain, and migraine prophylaxis. * **Fluoxetine (Option B):** A prototype **Selective Serotonin Reuptake Inhibitor (SSRI)**. It is a first-line antidepressant due to its favorable side-effect profile and long half-life (due to its active metabolite, norfluoxetine). * **Imipramine (Option C):** Another **TCA** primarily used for major depressive disorder. It is also the historical "gold standard" for treating nocturnal enuresis (bed-wetting) in children. **NEET-PG High-Yield Pearls:** * **Chlorpromazine Side Effects:** It is notorious for causing significant sedation, orthostatic hypotension (alpha-blockade), and skin/ocular pigmentation. It has a lower risk of Extrapyramidal Symptoms (EPS) compared to Haloperidol. * **Drug of Choice:** SSRIs (like Fluoxetine) are the first-line treatment for most anxiety disorders and depression. * **TCA Overdose:** Characterized by the "3 Cs": Coma, Convulsions, and Cardiotoxicity (arrhythmias due to sodium channel blockade). Sodium bicarbonate is the antidote for TCA-induced arrhythmias.

Question 182: What is a primary use of phenothiazines?

A. To induce muscle relaxation.
B. To manage psychotic behavior. (Correct Answer)
C. To suppress coughing.
D. To provide analgesia.

Explanation: **Explanation:** **Phenothiazines** (e.g., Chlorpromazine, Fluphenazine) are a class of **First-Generation (Typical) Antipsychotics**. Their primary mechanism of action involves the **blockade of post-synaptic Dopamine (D2) receptors** in the mesolimbic and mesocortical pathways of the brain. By reducing dopaminergic neurotransmission, they effectively manage the "positive symptoms" of psychosis, such as hallucinations, delusions, and disorganized thinking. **Analysis of Options:** * **Option B (Correct):** As dopamine antagonists, phenothiazines are indicated for schizophrenia, acute mania, and other psychotic disorders. * **Option A (Incorrect):** Phenothiazines do not induce muscle relaxation; in fact, due to D2 blockade in the nigrostriatal pathway, they often cause **Extrapyramidal Symptoms (EPS)** like muscle rigidity and dystonia. * **Option C (Incorrect):** Antitussives (e.g., Codeine, Dextromethorphan) are used to suppress coughing. While some phenothiazines have antihistaminic properties, they are not primary antitussives. * **Option D (Incorrect):** Analgesia is provided by opioids or NSAIDs. Phenothiazines may potentiate the effects of analgesics but are not painkillers themselves. **High-Yield NEET-PG Pearls:** * **Chlorpromazine** is also used for the treatment of **intractable hiccups**. * **Side Effects:** They are notorious for causing **Hyperprolactinemia** (due to D2 blockade in the tuberoinfundibular pathway) and **Neuroleptic Malignant Syndrome (NMS)**. * **Low potency** phenothiazines (Chlorpromazine) cause more sedation and anticholinergic effects, while **high potency** ones (Fluphenazine) cause more EPS.

Question 183: Which of the following is not an atypical antipsychotic?

A. Aripiprazole
B. Amoxapine (Correct Answer)
C. Clozapine
D. Zotepine

Explanation: ### Explanation **Correct Answer: B. Amoxapine** **1. Why Amoxapine is the correct answer:** Amoxapine is a **Tricyclic Antidepressant (TCA)** belonging to the dibenzoxazepine class. While it is unique among antidepressants because its metabolite (7-hydroxyamoxapine) possesses significant **Dopamine D2 receptor blocking activity**—which can lead to extrapyramidal side effects—it is primarily classified and used as an antidepressant, not an atypical antipsychotic. **2. Analysis of Incorrect Options:** * **A. Aripiprazole:** A third-generation atypical antipsychotic. It is unique as a **partial agonist** at D2 and 5-HT1A receptors and an antagonist at 5-HT2A receptors (often called a "Dopamine System Stabilizer"). * **C. Clozapine:** The "prototype" atypical antipsychotic. It is the most effective drug for **treatment-resistant schizophrenia** but requires mandatory WBC monitoring due to the risk of **agranulocytosis**. * **D. Zotepine:** An atypical antipsychotic that blocks D2 and 5-HT2 receptors. It also inhibits norepinephrine reuptake, which may help with the negative symptoms of schizophrenia. **3. High-Yield Clinical Pearls for NEET-PG:** * **Atypical vs. Typical:** Atypical antipsychotics (Second Generation) are defined by a lower risk of Extrapyramidal Symptoms (EPS) and greater efficacy against **negative symptoms** compared to typicals (like Haloperidol). * **Mechanism:** Most atypicals act as **5-HT2A + D2 antagonists** (SDA - Serotonin Dopamine Antagonists). * **Metabolic Side Effects:** Remember the mnemonic **"COZ"** (Clozapine, Olanzapine, Zotepine) for drugs with the highest risk of weight gain and metabolic syndrome. * **Amoxapine Fact:** Because of its D2 blocking metabolite, it is the TCA most likely to cause **Tardive Dyskinesia** or Neuroleptic Malignant Syndrome.

Question 184: Buspirone is used as a:

A. Anxiolytic (Correct Answer)
B. Sedative
C. Muscle relaxant
D. Anticonvulsant

Explanation: **Explanation:** **Buspirone** is a non-benzodiazepine drug used primarily as an **anxiolytic** (Option A). Its mechanism of action involves acting as a **selective partial agonist at the 5-HT1A receptors**. Unlike benzodiazepines, it does not interact with the GABA-A receptor complex, which accounts for its unique clinical profile. **Why other options are incorrect:** * **Sedative (Option B):** Buspirone lacks significant sedative properties. It does not cause psychomotor impairment or drowsiness, making it preferable for patients who need to remain alert. * **Muscle relaxant (Option C) & Anticonvulsant (Option D):** These are classic features of Benzodiazepines (due to GABA-A modulation). Buspirone lacks these properties entirely; it has no effect on muscle tone and cannot be used to treat seizures. **High-Yield Clinical Pearls for NEET-PG:** 1. **Delayed Onset:** Unlike benzodiazepines, Buspirone has a slow onset of action. It takes **2–4 weeks** to show therapeutic effects, making it unsuitable for "as needed" (PRN) use or acute panic attacks. It is used for **Generalized Anxiety Disorder (GAD)**. 2. **Lack of Dependence:** It carries **no risk of tolerance, physical dependence, or withdrawal symptoms**. It is not a controlled substance. 3. **No Interaction with Alcohol:** It does not potentiate the CNS depressant effects of alcohol. 4. **Side Effects:** Most common side effects include dizziness, nausea, and headache. It does not cause significant weight gain or sexual dysfunction.

Question 185: Appetite is decreased by which of the following medications, except?

A. Methylphenidate
B. Olanzapine (Correct Answer)
C. Fluoxetine
D. Sertraline

Explanation: ### Explanation The correct answer is **Olanzapine**. **1. Why Olanzapine is the correct answer:** Olanzapine is a **Second-Generation (Atypical) Antipsychotic**. One of its most significant and notorious side effects is **significant weight gain and increased appetite (hyperphagia)** [1]. This occurs primarily due to its potent antagonism at **H1 (histamine)** and **5-HT2C (serotonin)** receptors, which are key regulators of the satiety center in the hypothalamus. Among atypical antipsychotics, Olanzapine and Clozapine carry the highest risk for metabolic syndrome, dyslipidemia, and Type 2 Diabetes Mellitus [1], [3]. Olanzapine has also shown clinical efficacy in improving weight gain in patients with eating disorders or psychogenic vomiting [2]. **2. Why the other options are incorrect:** * **Methylphenidate (Option A):** This is a CNS stimulant used in ADHD. It increases norepinephrine and dopamine levels, which suppresses the appetite center. Growth monitoring is essential in children on this medication due to potential weight loss. * **Fluoxetine & Sertraline (Options C & D):** These are **SSRIs**. While some SSRIs can be weight-neutral in the long term, **Fluoxetine** is specifically known for causing initial weight loss and decreased appetite [2]. It is, in fact, the only FDA-approved drug for Bulimia Nervosa because it helps reduce binge-eating episodes. **3. High-Yield NEET-PG Pearls:** * **Weight Gain Hierarchy:** Clozapine > Olanzapine > Quetiapine > Risperidone > Ziprasidone/Aripiprazole (Weight neutral) [1]. * **Drug of choice for Bulimia Nervosa:** Fluoxetine (High dose: 60mg). * **Anorexiant agents:** Sibutramine (withdrawn), Lorcaserin (withdrawn), and Phentermine. * **Metabolic Monitoring:** Patients on Olanzapine must have regular monitoring of BMI, waist circumference, fasting blood glucose, and lipid profile.

Question 186: Which of the following medications is NOT used for the treatment of heroin detoxification?

A. Disulfiram (Correct Answer)
B. Buprenorphine
C. Clonidine
D. Lofexidine

Explanation: **Explanation:** The correct answer is **A. Disulfiram**. **Why Disulfiram is the correct answer:** Disulfiram is an aldehyde dehydrogenase inhibitor used exclusively in the treatment of **Alcohol Use Disorder**, not opioid/heroin detoxification. It acts as an "aversion therapy" agent by causing the accumulation of acetaldehyde if alcohol is consumed, leading to the unpleasant "Disulfiram-like reaction" (flushing, tachycardia, nausea). It has no pharmacological role in managing opioid withdrawal or detoxification. **Analysis of incorrect options (Drugs used in Heroin Detoxification):** * **Buprenorphine:** A partial μ-opioid agonist and κ-antagonist. It is a mainstay in opioid detoxification as it relieves withdrawal symptoms and reduces cravings with a lower risk of overdose due to its "ceiling effect." * **Clonidine:** An $\alpha_2$-adrenergic agonist. During heroin withdrawal, there is a massive surge in central sympathetic activity (noradrenergic storm). Clonidine helps suppress autonomic symptoms like sweating, tachycardia, hypertension, and restlessness. * **Lofexidine:** Similar to clonidine, this is a selective $\alpha_2$-adrenergic agonist. It is specifically FDA-approved for the mitigation of opioid withdrawal symptoms and often preferred over clonidine due to a lower risk of hypotension. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard for Opioid Detoxification:** Methadone (Full agonist) or Buprenorphine (Partial agonist). * **Non-Opioid Management:** $\alpha_2$ agonists (Clonidine/Lofexidine) are used for symptomatic relief of autonomic hyperactivity. * **Opioid Overdose:** Naloxone (Short-acting antagonist). * **Opioid Relapse Prevention:** Naltrexone (Long-acting antagonist). * **Disulfiram-like reaction** can also be caused by drugs like Metronidazole, Griseofulvin, and certain Cephalosporins (e.g., Cefotetan).

Question 187: Antipsychotic drug-induced Parkinsonism is treated by which of the following drug classes?

A. Anticholinergics (Correct Answer)
B. Levodopa
C. Selegiline
D. Amantadine

Explanation: ### Explanation **Mechanism of Action (Why A is Correct):** Antipsychotic-induced Parkinsonism (a type of Extrapyramidal Side Effect or EPS) occurs due to the blockade of **D2 receptors** in the **nigrostriatal pathway** [1]. In the striatum, there is a physiological balance between inhibitory **Dopamine** and excitatory **Acetylcholine (ACh)**. When antipsychotics block dopamine receptors, it leads to a relative cholinergic overactivity [3]. To restore this balance, **central anticholinergics** (e.g., Benztropine, Trihexyphenidyl/Benzhexol, Biperiden) are used [4]. **Why Other Options are Incorrect:** * **B. Levodopa:** While it is the gold standard for idiopathic Parkinson’s disease, it is contraindicated here [2]. Increasing dopamine levels can worsen the underlying psychosis (the "Dopamine Hypothesis" of schizophrenia). * **C. Selegiline:** This is an MAO-B inhibitor used in idiopathic Parkinson’s. Like Levodopa, it increases synaptic dopamine and can exacerbate psychotic symptoms. * **D. Amantadine:** Although Amantadine is sometimes used as a second-line agent for EPS due to its weak NMDA antagonism and dopaminergic effects, **Anticholinergics** remain the primary, first-line drug class of choice for drug-induced Parkinsonism in standard clinical guidelines and exams [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for Acute Dystonia:** Intravenous/Intramuscular Promethazine or Benztropine. * **Akathisia:** The most common EPS; the drug of choice is **Propranolol** (Beta-blocker). * **Tardive Dyskinesia:** Occurs due to dopamine receptor supersensitivity after long-term use [3]. Anticholinergics **worsen** Tardive Dyskinesia. Treatment involves switching to Clozapine or using VMAT-2 inhibitors (e.g., Valbenazine). * **Rule of Thumb:** If the question asks for the treatment of any *early-onset* EPS (except Akathisia), think Anticholinergics.

Question 188: The selective MAO-B inhibitor among the following is

A. Selegiline (Correct Answer)
B. Clorgyline
C. Moclobemide
D. Tranylcypromine

Explanation: **Explanation:** Monoamine oxidase (MAO) is an enzyme responsible for the oxidative deamination of biogenic amines. It exists in two isoforms: **MAO-A** (preferentially degrades serotonin, norepinephrine, and dopamine) and **MAO-B** (preferentially degrades dopamine). **1. Why Selegiline is Correct:** **Selegiline** is a selective, irreversible inhibitor of **MAO-B**. By inhibiting the breakdown of dopamine in the striatum, it increases dopamine levels without significantly affecting systemic norepinephrine or serotonin. This selectivity makes it highly effective in the management of **Parkinson’s disease** (often as an adjunct to Levodopa) and, at higher doses, for depression. **2. Analysis of Incorrect Options:** * **Clorgyline:** This is a selective and irreversible inhibitor of **MAO-A**. It is primarily used in research and is not a standard clinical treatment for Parkinson's. * **Moclobemide:** This is a **RIMA** (Reversible Inhibitor of MAO-A). It is used as an antidepressant and is safer than older MAOIs because it carries a lower risk of the "cheese reaction." * **Tranylcypromine:** This is a **non-selective**, irreversible inhibitor of both MAO-A and MAO-B. It is an older antidepressant associated with significant dietary restrictions. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cheese Reaction (Hypertensive Crisis):** Occurs when patients on non-selective MAOIs or MAO-A inhibitors consume tyramine-rich food (aged cheese, wine). Tyramine displaces NE, leading to massive sympathetic discharge. * **Selectivity Loss:** Selegiline loses its MAO-B selectivity at higher doses (>10 mg/day), increasing the risk of hypertensive crisis. * **Rasagiline:** Another potent, irreversible MAO-B inhibitor used in Parkinson’s, often preferred over Selegiline as it is not metabolized into amphetamine derivatives. * **Drug Interaction:** Never combine MAOIs with SSRIs/SNRIs due to the risk of **Serotonin Syndrome**.

Question 189: What is the primary site of action for disulfiram?

A. Aldehyde dehydrogenase (Correct Answer)
B. Alcohol dehydrogenase
C. G6PD
D. Acetate dehydrogenase

Explanation: **Explanation:**1. Mechanism of Action (Why A is correct):Disulfiram is used as an aversion therapy for chronic alcoholism. Its primary site of action is the irreversible inhibition of the enzyme Aldehyde Dehydrogenase (ALDH) [1]. Normally, alcohol is metabolized into acetaldehyde by alcohol dehydrogenase, and then acetaldehyde is converted into acetic acid by ALDH. By blocking ALDH, disulfiram causes a toxic accumulation of acetaldehyde in the blood. This leads to the Disulfiram-Ethanol Reaction (DER), characterized by flushing, tachycardia, nausea, vomiting, and hypotension, which discourages the patient from consuming alcohol [1].2. Analysis of Incorrect Options:B. Alcohol Dehydrogenase: This enzyme converts ethanol to acetaldehyde. It is inhibited by Fomepizole, which is used in methanol or ethylene glycol poisoning, not disulfiram.C. G6PD: Glucose-6-phosphate dehydrogenase is an enzyme in the pentose phosphate pathway. Its deficiency leads to hemolytic anemia; it is not a target for alcohol-related drugs.D. Acetate Dehydrogenase: This is not a primary target in human ethanol metabolism. Acetic acid (acetate) is typically converted to Acetyl-CoA by acetyl-CoA synthetase.3. NEET-PG High-Yield Clinical Pearls:Disulfiram-like reaction: Several other drugs can cause a similar reaction when taken with alcohol. High-yield examples include Metronidazole (most common), Cefotetan, Tinidazole, and Sulfonylureas (Chlorpropamide).Contraindication: Disulfiram should never be administered if the patient has consumed alcohol within the last 12 hours or is in a state of intoxication [2].Acamprosate vs. Naltrexone: While Disulfiram is for aversion, Acamprosate is used to maintain abstinence (NMDA antagonist), and Naltrexone (Opioid antagonist) is used to reduce cravings [1].

Question 190: What is the primary mechanism of action of Fluoxetine?

A. GABA inhibition
B. Adrenergic neuron blocking agent
C. Inhibition of axonal uptake of 5-HT (Correct Answer)
D. Alpha adrenergic stimulation

Explanation: **Explanation:** **Fluoxetine** is a prototype drug belonging to the **Selective Serotonin Reuptake Inhibitors (SSRIs)** class. 1. **Why Option C is Correct:** The primary mechanism of Fluoxetine is the potent and selective inhibition of the serotonin transporter (SERT) located on the presynaptic axonal membrane. By blocking the **axonal uptake of 5-HT (Serotonin)**, it increases the concentration of serotonin in the synaptic cleft, leading to enhanced serotonergic neurotransmission. This is the mainstay treatment for Major Depressive Disorder, OCD, and Panic Disorder. 2. **Why Other Options are Incorrect:** * **Option A (GABA inhibition):** GABA is an inhibitory neurotransmitter. Drugs like Benzodiazepines modulate GABA, but Fluoxetine has no direct effect on GABAergic pathways. * **Option B (Adrenergic neuron blocking agent):** These drugs (e.g., Guanethidine) prevent the release of norepinephrine. Fluoxetine specifically targets serotonin, not the release mechanism of adrenergic neurons. * **Option D (Alpha adrenergic stimulation):** Alpha-agonists (like Phenylephrine) stimulate the sympathetic nervous system. SSRIs like Fluoxetine lack significant affinity for alpha-adrenergic receptors, which is why they have fewer cardiovascular side effects compared to TCAs. **High-Yield Clinical Pearls for NEET-PG:** * **Longest Half-life:** Fluoxetine has the longest half-life (2–4 days) among SSRIs, and its active metabolite, **Norfluoxetine**, has a half-life of 7–10 days. * **Washout Period:** Due to its long half-life, a 5-week washout period is required before starting an MAO inhibitor to avoid **Serotonin Syndrome**. * **Drug of Choice:** SSRIs are the first-line treatment for Depression, OCD, Panic Disorder, Social Phobia, and Post-Traumatic Stress Disorder (PTSD). * **Side Effects:** Common side effects include GI upset, sexual dysfunction, and insomnia. Unlike TCAs, they do not cause significant sedation or anticholinergic effects.

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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