Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 31: Which drug is used to treat extrapyramidal syndrome caused by phenothiazines?

A. Diphenhydramine
B. Benzhexol (Correct Answer)
C. Clonidine
D. Promethazine

Explanation: ### Explanation **Concept:** Phenothiazines (typical antipsychotics) cause Extrapyramidal Symptoms (EPS) by blocking dopamine ($D_2$) receptors in the nigrostriatal pathway. This creates a **cholinergic overactivity** because dopamine normally inhibits acetylcholine release. To restore the neurochemical balance, **central anticholinergics** are the treatment of choice. **Why Benzhexol is Correct:** **Benzhexol (Trihexyphenidyl)** is a potent central anticholinergic. It crosses the blood-brain barrier effectively to antagonize muscarinic receptors in the basal ganglia, thereby suppressing the cholinergic excess and relieving symptoms like drug-induced parkinsonism and acute dystonia. **Analysis of Incorrect Options:** * **Diphenhydramine:** While it has anticholinergic properties and can be used for EPS (especially in parenteral form for acute dystonia), **Benzhexol** is the more specific, standard oral maintenance therapy for drug-induced parkinsonism in clinical practice and exam scenarios. * **Clonidine:** An $\alpha_2$ agonist used primarily for hypertension and opioid withdrawal; it has no role in treating EPS. * **Promethazine:** An antihistamine with some anticholinergic effects, but it is itself a phenothiazine derivative. While it can occasionally treat mild dystonia, it is not the primary choice compared to dedicated anticholinergics like Benzhexol. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC) for Acute Dystonia:** Parenteral Promethazine or Benztropine. * **DOC for Akathisia:** Propranolol (Beta-blockers). * **DOC for Tardive Dyskinesia:** Valbenazine or Deutetrabenazine (VMAT2 inhibitors). *Note: Anticholinergics like Benzhexol worsen Tardive Dyskinesia.* * **L-Dopa** is contraindicated in drug-induced parkinsonism as it can worsen the underlying psychosis.

Question 32: Which of the following antidepressants is known to cause sedation and also provides pain relief?

A. Venlafaxine
B. Desipramine
C. Amitriptyline (Correct Answer)
D. Imipramine

Explanation: **Explanation:** **Amitriptyline** is a classic **Tricyclic Antidepressant (TCA)** belonging to the tertiary amine group. Its pharmacological profile makes it the correct choice for two primary reasons: 1. **Sedation:** It possesses potent **H1-receptor (histamine) blocking properties**, which leads to significant sedation. This makes it particularly useful for depressed patients suffering from insomnia. 2. **Pain Relief:** TCAs are first-line agents for **neuropathic pain** (e.g., diabetic neuropathy, post-herpetic neuralgia). They provide analgesia by inhibiting the reuptake of Serotonin and Norepinephrine, thereby enhancing the descending inhibitory pain pathways in the spinal cord. **Analysis of Incorrect Options:** * **Venlafaxine:** An SNRI. While it provides excellent pain relief, it is generally **activating** rather than sedating and can cause an increase in blood pressure. * **Desipramine:** A secondary amine TCA. It is a selective norepinephrine reuptake inhibitor and is significantly **less sedating** than tertiary amines like Amitriptyline because it has minimal antihistaminic activity. * **Imipramine:** While it is a tertiary amine TCA that can cause sedation and pain relief, **Amitriptyline is more potent** in its sedative and analgesic effects, making it the "prototypical" answer for this clinical combination. **High-Yield NEET-PG Pearls:** * **Anticholinergic Side Effects:** TCAs are notorious for the "3 Cs": Coma, Convulsions, and Cardiotoxicity (due to sodium channel blockade leading to QRS prolongation). * **Drug of Choice:** Amitriptyline is often the drug of choice for **prophylaxis of Migraine** and Tension-type headaches. * **Nocturnal Enuresis:** Imipramine is traditionally used for bedwetting in children (though non-pharmacological methods are preferred first).

Question 33: Buspirone is an:

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

Explanation: **Explanation:** **Buspirone** is a non-benzodiazepine drug used primarily in the management of **Generalized Anxiety Disorder (GAD)**. Its mechanism of action involves acting as a **selective partial agonist at the 5-HT1A receptors**. Unlike benzodiazepines, it does not act on the GABA receptor complex, which accounts for its unique clinical profile. * **Why Option A is correct:** Buspirone is classified as a pure **anxiolytic**. It effectively relieves the psychological symptoms of anxiety (worry, irritability) without causing significant psychomotor impairment. * **Why Options B, C, and D are incorrect:** Because Buspirone does not interact with GABA receptors, it lacks the classic side effects associated with benzodiazepines. It has **no muscle relaxant** properties, **no anticonvulsant** activity, and produces **minimal to no sedation**. Additionally, it does not cause cognitive impairment or physical dependence (no withdrawal symptoms). **High-Yield Clinical Pearls for NEET-PG:** 1. **Delayed Onset:** Unlike benzodiazepines, Buspirone has a slow onset of action; it takes **1–2 weeks** to show clinical effects. It is not useful for "PRN" (as-needed) use or acute panic attacks. 2. **Lack of Interaction:** It does not potentiate the effects of alcohol or other CNS depressants. 3. **Side Effects:** The most common side effects are dizziness, nausea, and headache. 4. **Metabolism:** It is metabolized by **CYP3A4**; therefore, its levels can be increased by grapefruit juice or erythromycin. 5. **Driving:** It is the preferred anxiolytic for patients who need to drive or operate machinery, as it does not impair motor skills.

Question 34: Which drug is used for cigarette smoking cessation?

A. Varenicline
B. Bupropion
C. Mecamylamine
D. All of the above (Correct Answer)

Explanation: **Explanation:** Smoking cessation involves targeting the neurobiological pathways of nicotine addiction, primarily the **α4β2 nicotinic acetylcholine receptors (nAChR)** in the brain's reward system. 1. **Varenicline:** This is a **selective partial agonist** at α4β2 nAChR. It provides a low level of dopamine release to reduce withdrawal symptoms (agonist action) while simultaneously blocking nicotine from binding to the receptor, thereby reducing the "reward" of smoking (antagonist action). It is currently considered the first-line pharmacological therapy. 2. **Bupropion:** Originally an atypical antidepressant, it acts as an **inhibitor of dopamine and norepinephrine reuptake**. By increasing dopamine levels in the nucleus accumbens, it mimics the reward effect of nicotine and significantly reduces the urge to smoke. 3. **Mecamylamine:** This is a **non-selective nicotinic antagonist**. While historically used as an antihypertensive (ganglion blocker), it is used off-label in smoking cessation to block the pharmacological effects of nicotine. It is often used in combination with nicotine patches to prevent the "hit" from a cigarette. **Clinical Pearls for NEET-PG:** * **Varenicline Side Effects:** Most common is nausea; most serious are **neuropsychiatric symptoms** (suicidal ideation, abnormal dreams). * **Bupropion Contraindication:** Must be avoided in patients with a history of **seizures or eating disorders** (bulimia/anorexia) as it lowers the seizure threshold. * **First-line agents:** Varenicline, Bupropion, and Nicotine Replacement Therapy (NRT). * **Cytisine:** Another partial agonist (similar to Varenicline) derived from plants, gaining importance as a cost-effective alternative.

Question 35: A patient with schizophrenia was started on a new antipsychotic medication. Three months later, the patient complains of significant weight gain. Which of the following medications is most likely responsible for this side effect?

A. Olanzapine (Correct Answer)
B. Amisulpride
C. Risperidone
D. Haloperidol

Explanation: **Explanation:** The correct answer is **Olanzapine**. Weight gain and metabolic syndrome are significant adverse effects of Second-Generation Antipsychotics (SGAs), primarily due to their potent antagonism of **Histamine (H1)** and **Serotonin (5-HT2C)** receptors, which increases appetite and disrupts glucose metabolism. **Why Olanzapine is correct:** Among all antipsychotics, **Clozapine** and **Olanzapine** carry the highest risk of significant weight gain, dyslipidemia, and Type 2 Diabetes Mellitus. Patients on Olanzapine can gain several kilograms within the first few months of treatment, necessitating regular monitoring of BMI, waist circumference, and blood glucose levels. **Why other options are incorrect:** * **Amisulpride:** This is a D2/D3 selective antagonist. It is considered "weight-neutral" or associated with low weight gain compared to Olanzapine. * **Risperidone:** While Risperidone does cause weight gain and hyperprolactinemia, its metabolic impact is moderate—significantly less than Olanzapine but more than Aripiprazole. * **Haloperidol:** As a First-Generation Antipsychotic (FGA), Haloperidol is primarily associated with Extrapyramidal Side Effects (EPS). It has a very low risk of weight gain or metabolic disturbances. **High-Yield Clinical Pearls for NEET-PG:** * **Highest Weight Gain Risk:** Clozapine > Olanzapine. * **Lowest Weight Gain Risk (Weight Neutral):** Ziprasidone, Aripiprazole, and Lurasidone. * **Monitoring:** The **ATP III guidelines** recommend monitoring fasting lipid profiles and blood glucose for patients on SGAs. * **Mechanism:** H1 receptor blockade is the strongest predictor of antipsychotic-induced weight gain.

Question 36: Which of the following extrapyramidal effects is seen on chronic use of antipsychotics?

A. Dystonia
B. Akathisia
C. Tardive dyskinesia (Correct Answer)
D. Parkinsonism

Explanation: **Explanation:** Extrapyramidal Side Effects (EPS) of antipsychotics are classified based on their time of onset following the initiation of therapy. **Why Tardive Dyskinesia is correct:** **Tardive dyskinesia (TD)** is a **late-onset** (chronic) extrapyramidal syndrome, typically occurring after months or years of treatment with typical antipsychotics (e.g., Haloperidol). It is characterized by involuntary, repetitive movements of the face, tongue (fly-catching movements), and extremities. The underlying pathophysiology is believed to be **dopamine receptor supersensitivity** in the nigrostriatal pathway following prolonged blockade. **Why the other options are incorrect:** * **A. Dystonia:** This is an **acute** reaction occurring within hours to days of starting treatment. It involves sustained muscle contractions (e.g., torticollis, oculogyric crisis). * **B. Akathisia:** This is the most common EPS and usually occurs within days to weeks. It presents as subjective motor restlessness (inability to sit still). * **D. Parkinsonism:** This typically develops within weeks to months (subacute). It presents with the classic triad of tremors, rigidity, and bradykinesia due to dopamine blockade. **NEET-PG High-Yield Pearls:** * **Treatment of Choice (TOC):** For Acute Dystonia and Parkinsonism, use **central anticholinergics** (e.g., Benztropine, Promethazine). * **TOC for Akathisia:** **Propranolol** (Beta-blocker) is the first-line treatment. * **Management of TD:** Anticholinergics often worsen TD. Management involves switching to **Clozapine** or using VMAT-2 inhibitors like **Valbenazine** or **Deutetrabenazine**. * **Rule of thumb for onset:** Dystonia (4 hours) $\rightarrow$ Akathisia (4 days) $\rightarrow$ Parkinsonism (4 weeks) $\rightarrow$ Tardive Dyskinesia (4 months/years).

Question 37: Which of the following drugs has the least extrapyramidal symptoms?

A. Aripiprazole (Correct Answer)
B. Loxapine
C. Fluphenazine
D. Chlorpromazine

Explanation: **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).

Question 38: A child with schizophrenia, who was on antipsychotic medications, suddenly developed neck stiffness and spasm. What is the best treatment for this condition?

A. Benzatropine (Correct Answer)
B. Lorazepam
C. Diphenhydramine
D. Propranolol

Explanation: ### Explanation **Diagnosis: Acute Dystonia** The clinical presentation of sudden neck stiffness (torticollis) and muscle spasms in a patient taking antipsychotics is classic for **Acute Dystonia**. This is an Extrapyramidal Side Effect (EPS) caused by a sudden blockade of dopamine (D2) receptors in the nigrostriatal pathway, leading to a relative excess of cholinergic (acetylcholine) activity. **1. Why Benzatropine is the Correct Answer:** To restore the balance between dopamine and acetylcholine, a **centrally acting anticholinergic** drug is required. **Benzatropine** is the drug of choice (along with Trihexyphenidyl) because it effectively antagonizes muscarinic receptors in the basal ganglia, providing rapid relief from spasms. **2. Analysis of Incorrect Options:** * **Lorazepam (B):** A benzodiazepine used for Acute Akathisia (restlessness) or status epilepticus. While it has muscle-relaxant properties, it does not address the underlying cholinergic imbalance in dystonia. * **Diphenhydramine (C):** Although this antihistamine has significant anticholinergic properties and *can* be used to treat dystonia, **Benzatropine** is generally preferred in clinical guidelines and exam scenarios as the more specific first-line agent for drug-induced EPS. * **Propranolol (D):** This is a beta-blocker and is the **drug of choice for Akathisia**, not acute dystonia. **3. NEET-PG High-Yield Pearls:** * **Timeline of EPS:** Acute Dystonia (hours to days) → Akathisia (days to weeks) → Parkinsonism (weeks to months) → Tardive Dyskinesia (months to years). * **Acute Dystonia:** Most common in young males and those taking high-potency first-generation antipsychotics (e.g., Haloperidol). * **Tardive Dyskinesia:** The only EPS where anticholinergics are **contraindicated** (they worsen the condition). It is treated by switching to Clozapine or using VMAT-2 inhibitors (e.g., Valbenazine).

Question 39: Malignant neuroleptic hyperthermia (NMS) is seen with all of the following drugs except:

A. Haloperidol
B. Metoclopramide
C. Domperidone
D. Amantadine (Correct Answer)

Explanation: **Explanation:** **Neuroleptic Malignant Syndrome (NMS)** is a life-threatening idiosyncratic reaction characterized by the clinical tetrad of **muscle rigidity (lead-pipe), hyperthermia, autonomic instability, and altered mental status.** **1. Why Amantadine is the Correct Answer:** The underlying pathophysiology of NMS is a **massive decrease in central dopaminergic activity**, specifically at the D2 receptors in the hypothalamus and corpus striatum. * **Amantadine** is a dopaminergic agonist (it increases dopamine release). Therefore, it does not cause NMS. * **Crucial Point:** While Amantadine doesn't *cause* NMS, the **abrupt withdrawal** of dopaminergic drugs like Amantadine or Levodopa can actually *trigger* NMS. **2. Why the other options are incorrect:** * **Haloperidol (Option A):** This is a high-potency typical antipsychotic and the most common culprit associated with NMS due to its potent D2 receptor blockade. * **Metoclopramide (Option B):** Although used as an antiemetic, it is a central D2 receptor antagonist. It can cross the blood-brain barrier and is a well-known cause of NMS and extrapyramidal symptoms. * **Domperidone (Option C):** While Domperidone primarily acts peripherally, it can occasionally cause NMS in susceptible individuals or at high doses, as it still possesses D2 antagonist properties. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for NMS:** **Dantrolene** (a direct-acting muscle relaxant) or **Bromocriptine** (a dopamine agonist). * **Biochemical Marker:** Elevated **Creatine Phosphokinase (CPK)** levels due to intense muscle rigidity. * **Differential Diagnosis:** Unlike Serotonin Syndrome (which presents with hyperreflexia/myoclonus), NMS presents with **"Lead-pipe" rigidity** and hyporeflexia.

Question 40: Which of the following drugs is least associated with extra-pyramidal side effects?

A. Chlorpromazine
B. Fluphenazine
C. Carbamazepine (Correct Answer)
D. Haloperidol

Explanation: ### 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).

Practice by Chapter

Antipsychotics: Typical and Atypical

Practice Questions

Antidepressants: SSRIs and SNRIs

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Tricyclic Antidepressants

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MAO Inhibitors

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Mood Stabilizers

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Anxiolytics

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Drugs for ADHD

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Drugs for Sleep Disorders

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Drugs for Dementia

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Drug-Induced Psychiatric Symptoms

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