Psychopharmacology Practice Questions

Q: What is the drug of choice for treating narcolepsy?

Modafinil. **Explanation:** **Narcolepsy** is a chronic neurological disorder characterized by excessive daytime sleepiness (EDS), cataplexy, and REM-sleep abnormalities. The primary goal of treatment is to manage debilitating daytime drowsiness. **Why Modafinil is the Correct Answer:** **Modafinil** is the **first-line drug of choice** for treating excessive daytime sleepiness in narcolepsy. It is a non-amphetamine wake-promoting agent. Its exact mechanism is not fully understood, but it is believed to inhibit dopamine reuptake and increase levels of hypothalamic **orexin (hypocretin)** and histamine. It is preferred over traditional stimulants because it has a lower risk of addiction, fewer sympathomimetic side effects (like tachycardia), and a lower potential for rebound hypersomnia. **Analysis of Incorrect Options:** * **B. Sildenafil:** A PDE-5 inhibitor used primarily for erectile dysfunction and pulmonary arterial hypertension; it has no role in sleep disorders. * **C. Disulfiram:** An aldehyde dehydrogenase inhibitor used as an aversive therapy in alcohol dependence (causes the Disulfiram-ethanol reaction). * **D. Dexmedetomidine:** A highly selective alpha-2 adrenergic agonist used for sedation in intensive care settings and during anesthesia; it promotes sleep rather than wakefulness. **High-Yield Clinical Pearls for NEET-PG:** * **Cataplexy Treatment:** While Modafinil treats sleepiness, **Sodium Oxybate** is the drug of choice for cataplexy (sudden loss of muscle tone). * **Pathophysiology:** Narcolepsy Type 1 is associated with a deficiency of **Hypocretin (Orexin)** in the cerebrospinal fluid. * **Classic Tetrad:** 1. Excessive daytime sleepiness, 2. Cataplexy, 3. Sleep paralysis, 4. Hypnagogic/Hypnopompic hallucinations. * **Diagnosis:** Confirmed via Polysomnography followed by a **Multiple Sleep Latency Test (MSLT)** showing a mean sleep latency <8 minutes and ≥2 REM periods.

Q: What is the current agent of choice for the treatment of bipolar affective disorder?

Lithium carbonate. **Explanation:** **Lithium carbonate** remains the "gold standard" and the agent of choice for the long-term maintenance treatment of Bipolar Affective Disorder (BPAD). Its primary mechanism involves the inhibition of the inositol monophosphatase pathway and modulation of G-proteins, leading to mood stabilization. It is uniquely effective in treating acute mania, preventing bipolar depression, and—most importantly for NEET-PG—it is the only drug proven to significantly **reduce the risk of suicide** in these patients. **Analysis of Incorrect Options:** * **Chlorpromazine & Haloperidol (Options A & B):** These are typical antipsychotics. While they are used for rapid tranquilization in cases of acute manic excitement or psychosis, they are not first-line for long-term mood stabilization. Prolonged use carries a high risk of Extrapyramidal Side Effects (EPS) and Tardive Dyskinesia. * **Diazepam (Option C):** This is a benzodiazepine used as an adjunct for sedation or to manage acute anxiety and insomnia. It has no mood-stabilizing properties and does not treat the underlying pathophysiology of BPAD. **High-Yield Clinical Pearls for NEET-PG:** * **Therapeutic Index:** Lithium has a narrow therapeutic index. Prophylactic levels are **0.6–1.2 mEq/L**, while levels >1.5 mEq/L indicate toxicity. * **Teratogenicity:** Use in pregnancy is associated with **Ebstein’s Anomaly** (atrialization of the right ventricle). * **Side Effects:** Common high-yield side effects include fine tremors, polyuria (Nephrogenic Diabetes Insipidus), hypothyroidism, and weight gain. * **Alternative:** Valproate is often preferred for "Rapid Cyclers" or "Mixed Episodes," but Lithium remains the overall classic answer for BPAD.

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

Tardive dyskinesia. **Explanation:** Extrapyramidal Side Effects (EPS) of antipsychotics are classified based on their time of onset. The key to this question lies in the word **"chronic."** **1. Why Tardive Dyskinesia is correct:** Tardive Dyskinesia (TD) is a **late-onset** (tardive means "late") movement disorder occurring after months or years of antipsychotic use. It is characterized by involuntary, choreoathetoid movements, most commonly involving the mouth and tongue (e.g., lip-smacking, tongue protrusion). The underlying pathophysiology is believed to be **dopamine receptor supersensitivity** in the nigrostriatal pathway following prolonged blockade. **2. Why the other options are incorrect:** * **Dystonia (Acute Dystonia):** This is the earliest EPS, occurring within hours to days of starting treatment. It involves sustained muscle contractions (e.g., torticollis, oculogyric crisis). * **Akathisia:** This typically occurs within days to weeks. It is characterized by subjective feelings of inner restlessness and an inability to sit still. It is the most common EPS. * **Parkinsonism (Drug-induced):** This usually develops within weeks to months. It mimics Parkinson’s disease with tremors, rigidity, and bradykinesia due to acute dopamine blockade. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment of TD:** The first step is to reduce the dose or switch to a second-generation antipsychotic (Clozapine is the drug of choice). VMAT-2 inhibitors (e.g., Valbenazine) are FDA-approved for treatment. * **Rule of Thumb for EPS Onset:** * **4 hours:** Acute Dystonia (Rx: Benztropine/Promethazine) * **4 days:** Akathisia (Rx: Propranolol) * **4 weeks:** Parkinsonism (Rx: Trihexyphenidyl) * **4 months/years:** Tardive Dyskinesia (Rx: Switch to Clozapine) * **Anticholinergics** (like Trihexyphenidyl) can **worsen** Tardive Dyskinesia and should be avoided in its management.

Q: Which group of drugs is considered first-line in the management of schizophrenia?

Dopamine antagonists. ### Explanation **Correct Answer: D. Dopamine Antagonists** The management of schizophrenia is primarily based on the **Dopamine Hypothesis**, which suggests that the positive symptoms of the disorder (hallucinations, delusions) are caused by overactivity of dopamine in the **mesolimbic pathway**. All standard antipsychotics (both Typical and Atypical) exert their primary therapeutic effect by blocking **D2 receptors**. * **Typical Antipsychotics** (e.g., Haloperidol) are potent D2 antagonists. * **Atypical Antipsychotics** (e.g., Risperidone, Olanzapine) block both D2 and 5-HT2A receptors, and are currently the preferred first-line agents due to a lower risk of Extrapyramidal Side Effects (EPS). **Why other options are incorrect:** * **A. Opioids:** These are primarily used for analgesia and anesthesia. They have no role in treating psychosis and can actually induce delirium or worsen mental status. * **B. Antiepileptics:** While drugs like Valproate or Carbamazepine are used as **mood stabilizers** in Bipolar Disorder or as adjuncts for aggression, they do not treat the core psychotic symptoms of schizophrenia. * **C. Serotonergic drugs:** While Atypical antipsychotics do have serotonin-blocking properties, "serotonergic drugs" usually refers to SSRIs/SNRIs used for depression and anxiety. Pure serotonergic stimulation can sometimes exacerbate psychotic symptoms. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for Resistant Schizophrenia:** Clozapine (requires mandatory WBC monitoring for agranulocytosis). * **Most Potent D2 Blocker:** Haloperidol (highest risk of EPS). * **Hyperprolactinemia:** A common side effect of D2 blockade in the tuberoinfundibular pathway (most common with Risperidone). * **Negative Symptoms:** Atypical antipsychotics are generally better than typical ones for treating negative symptoms (apathy, social withdrawal).

Q: A psychiatric patient on regular treatment presents with fundus findings of pigmented retinal epithelium. Which of the following drugs is most likely implicated?

Thioridazine. **Explanation:** The correct answer is **Thioridazine**. This is a classic high-yield association in psychopharmacology regarding ocular side effects of antipsychotics. **1. Why Thioridazine is correct:** Thioridazine, a low-potency typical antipsychotic, is uniquely associated with **Retinitis Pigmentosa** (pigmentary retinopathy). This occurs due to the accumulation of the drug and its metabolites in the uveal tract, leading to melanin-related toxicity. Clinically, this presents as "brownish" vision and can lead to permanent visual loss if the dose exceeds the safe threshold (typically **>800 mg/day**). Fundus examination reveals characteristic pigmentary deposits on the retinal epithelium. **2. Why other options are incorrect:** * **Chlorpromazine:** While it also causes ocular side effects, it typically causes **lenticular and corneal opacities** (whitish-brown granular deposits) rather than retinal pigmentation. It is often described as "star-shaped" cataracts. * **Haloperidol:** A high-potency antipsychotic that is more commonly associated with Extrapyramidal Side Effects (EPS) and has a negligible risk of significant ocular toxicity. * **Clozapine:** An atypical antipsychotic primarily known for agranulocytosis and seizures; it does not cause pigmentary retinopathy. **Clinical Pearls for NEET-PG:** * **Thioridazine:** Remember the "800 mg rule"—never exceed this dose to avoid irreversible retinopathy. It is also the antipsychotic most associated with **QT interval prolongation**. * **Mnemonic:** **C**hlorpromazine = **C**ornea/Lens; **T**hioridazine = **T**errible **R**etina. * **Quetiapine:** Historically linked to cataracts in animal studies (requires periodic eye exams in some protocols).

Q: Which of the following drugs, when combined with electroconvulsive therapy, is most likely to lead to postictal delirium?

Lithium. **Explanation:** **Lithium** is the correct answer because it significantly lowers the seizure threshold and prolongs the effects of neuromuscular blocking agents. When combined with Electroconvulsive Therapy (ECT), Lithium can lead to **postictal delirium**, prolonged seizures (status epilepticus), and increased neurotoxicity. The underlying mechanism involves Lithium’s interference with electrolyte balance and neurotransmission, which sensitizes the brain to the electrical stimulus, leading to delayed recovery of consciousness. **Analysis of Incorrect Options:** * **Succinylcholine (Option A):** This is a depolarizing neuromuscular blocker routinely used in "Modified ECT" to prevent bone fractures and muscle injuries. While it causes muscle relaxation, it does not cross the blood-brain barrier and does not cause delirium. * **Desipramine (Option B):** This is a Tricyclic Antidepressant (TCA). While TCAs can lower the seizure threshold, they are generally considered safe to continue during ECT and are not specifically associated with postictal delirium. * **Clozapine (Option D):** Although Clozapine significantly lowers the seizure threshold, it is sometimes used intentionally in combination with ECT for treatment-resistant schizophrenia. While it increases seizure risk, it is not the classic drug associated with postictal delirium in the same way Lithium is. **High-Yield Clinical Pearls for NEET-PG:** * **Management:** It is standard clinical practice to **discontinue or taper Lithium** at least 24–48 hours before initiating ECT to minimize the risk of delirium. * **Benzodiazepines & Anticonvulsants:** These drugs *increase* the seizure threshold, making it harder to induce a therapeutic seizure during ECT. They should be tapered if possible. * **Theophylline:** This drug should be avoided during ECT as it can lead to status epilepticus (prolonged seizures).

Q: A patient on antipsychotics presents with muscle rigidity, fever, and tachycardia. Investigations reveal an elevated WBC count and increased creatinine phosphokinase levels. What is the drug of choice for this patient?

Dantrolene. ### Explanation **Diagnosis: Neuroleptic Malignant Syndrome (NMS)** The clinical triad of **muscle rigidity** ("lead-pipe" rigidity), **autonomic instability** (fever, tachycardia, hypertension), and **altered mental status** in a patient taking antipsychotics is diagnostic of NMS. Laboratory findings typically show **elevated Creatinine Phosphokinase (CPK)** due to muscle necrosis (rhabdomyolysis) and **leukocytosis** (elevated WBC). **Why Dantrolene is the Correct Answer:** Dantrolene is a direct-acting skeletal muscle relaxant. It works by binding to the **ryanodine receptor (RyR1)** on the sarcoplasmic reticulum, inhibiting the release of calcium. This reduces muscle rigidity and heat production, addressing the core pathophysiology of the hypermetabolic state in NMS. **Analysis of Incorrect Options:** * **A & D (Paracetamol, IV Fluids, Penicillin):** While supportive care (IV fluids for hydration and cooling blankets) is essential, Paracetamol is insufficient to treat the underlying muscle-driven hyperthermia. Penicillin is irrelevant as the fever is not due to a bacterial infection. * **C (Neostigmine):** This is an acetylcholinesterase inhibitor used in Myasthenia Gravis or to reverse neuromuscular blockade. It has no role in NMS and could potentially worsen autonomic instability. **NEET-PG High-Yield Pearls:** 1. **Mechanism of NMS:** Primarily due to potent **D2 receptor blockade** in the nigrostriatal pathway and hypothalamus. 2. **Drug of Choice (Pharmacological):** **Dantrolene** is the specific muscle relaxant. **Bromocriptine** or **Amantadine** (Dopamine agonists) are also used to restore dopaminergic tone. 3. **First Step in Management:** Immediately **discontinue** the offending antipsychotic agent. 4. **Differential Diagnosis:** Unlike Serotonin Syndrome, NMS is characterized by "lead-pipe" rigidity and bradyreflexia, whereas Serotonin Syndrome presents with hyperreflexia and myoclonus.

Q: Polycystic ovarian syndrome is a potential side effect of which mood stabilizer?

Valproate. **Explanation:** **Valproate (Sodium Valproate)** is the correct answer. It is a broad-spectrum antiepileptic and mood stabilizer frequently associated with endocrine and metabolic side effects. The association with **Polycystic Ovarian Syndrome (PCOS)** is significant, particularly in young women. Valproate can cause hyperinsulinemia and weight gain, which disrupts the hypothalamic-pituitary-ovarian axis, leading to hyperandrogenism (hirsutism, acne), menstrual irregularities, and polycystic ovaries on ultrasound. **Analysis of Incorrect Options:** * **B. Carbamazepine:** While it can cause weight gain and is an enzyme inducer (leading to oral contraceptive failure), it is not classically associated with the development of PCOS. * **C. Lithium:** The most high-yield side effects for Lithium are **hypothyroidism**, nephrogenic diabetes insipidus, and Ebstein’s anomaly (teratogenicity). It does not cause PCOS. * **D. Lamotrigine:** Generally considered "weight-neutral" and has a favorable side-effect profile regarding endocrine function, making it a preferred choice for women of childbearing age. **Clinical Pearls for NEET-PG:** * **Monitoring:** Baseline and periodic monitoring of weight, menstrual cycle, and BMI is essential for female patients on Valproate. * **Teratogenicity:** Valproate is highly teratogenic, causing **Neural Tube Defects** (specifically Spina Bifida). * **Other Side Effects:** Remember the mnemonic **"VALPROATE"**: **V**omit, **A**lopecia (transient), **L**iver toxicity (Hepatotoxicity), **P**ancreatitis, **R**etention of fat (Weight gain), **O**edema, **A**norexia, **T**remor/Thrombocytopenia, **E**ncephalopathy (due to hyperammonemia).

Q: What is the most useful drug in the management of enuresis?

Trimipramine. ### Explanation **Correct Answer: C. Trimipramine** **Medical Concept:** Enuresis (bedwetting) is often managed pharmacologically using **Tricyclic Antidepressants (TCAs)** when behavioral interventions fail. While **Imipramine** is the most commonly cited TCA for this condition, **Trimipramine** belongs to the same class and shares the same therapeutic mechanism. TCAs work in enuresis through a triple action: 1. **Anticholinergic effect:** Increases bladder capacity by relaxing the detrusor muscle. 2. **Alpha-adrenergic stimulation:** Increases internal sphincter tone. 3. **Alteration of sleep architecture:** Lightens sleep, allowing the child to wake up when the bladder is full. **Analysis of Incorrect Options:** * **A. Haloperidol:** A typical antipsychotic (D2 blocker) used for schizophrenia or Tourette’s. It has no role in bladder control and may cause extrapyramidal side effects. * **B. Diazepam:** A benzodiazepine used for anxiety or seizures. It can actually worsen enuresis by deepening sleep, making it harder for the child to wake up to void. * **D. Chlorpromazine:** A low-potency antipsychotic. While it has some anticholinergic properties, it is not indicated for enuresis and carries a high side-effect profile (sedation, hypotension). **NEET-PG High-Yield Pearls:** * **First-line treatment:** Behavioral therapy (Enuresis Alarms/Pad and Bell) is the gold standard. * **Drug of Choice (DOC):** **Desmopressin (DDAVP)**, an ADH analogue, is the preferred pharmacological agent due to its safety profile. * **TCAs (Imipramine/Trimipramine):** Used as second-line therapy. They have a high relapse rate once discontinued and carry a risk of cardiotoxicity in overdose. * **Diagnosis:** Enuresis is diagnosed only after the **chronological age of 5 years** (developmental age).

Question 1

What is the drug of choice for treating narcolepsy?

Accepted Answer

Modafinil

Answer

Sildenafil

Answer

Disulfiram

Answer

Dexmedetomidine

Question 2

What is the current agent of choice for the treatment of bipolar affective disorder?

Accepted Answer

Lithium carbonate

Answer

Chlorpromazine

Answer

Haloperidol

Answer

Diazepam

Question 3

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

Accepted Answer

Tardive dyskinesia

Answer

Dystonia

Answer

Akathisia

Answer

Parkinsonism

Question 4

Which group of drugs is considered first-line in the management of schizophrenia?

Accepted Answer

Dopamine antagonists

Answer

Opioids

Answer

Antiepileptics

Answer

Serotonergic drugs

Question 5

A 21-year-old woman presents with complaints of constricting chest pain and difficulty breathing. She reports three similar episodes in the past month and believes she is having a heart attack. Her past medical history is unremarkable, but her father died of a myocardial infarction at age 47. ECG shows sinus tachycardia, and cardiac enzymes and urine drug screen are normal. What is the next best step in the management of this patient?

Accepted Answer

Alprazolam

Answer

Reassurance

Answer

Escitalopram

Answer

Cognitive behavioural therapy

Question 6

A psychiatric patient on regular treatment presents with fundus findings of pigmented retinal epithelium. Which of the following drugs is most likely implicated?

Accepted Answer

Thioridazine

Answer

Haloperidol

Answer

Chlorpromazine

Answer

Clozapine

Question 7

Which of the following drugs, when combined with electroconvulsive therapy, is most likely to lead to postictal delirium?

Accepted Answer

Lithium

Answer

Succinylcholine

Answer

Desipramine

Answer

Clozapine

Question 8

A patient on antipsychotics presents with muscle rigidity, fever, and tachycardia. Investigations reveal an elevated WBC count and increased creatinine phosphokinase levels. What is the drug of choice for this patient?

Accepted Answer

Dantrolene

Answer

Paracetamol and IV Fluids

Answer

Neostigmine

Answer

Paracetamol and Penicillin

Question 9

Polycystic ovarian syndrome is a potential side effect of which mood stabilizer?

Accepted Answer

Valproate

Answer

Carbamazepine

Answer

Lithium

Answer

Lamotrigine

Question 10

What is the most useful drug in the management of enuresis?

Accepted Answer

Trimipramine

Answer

Haloperidol

Answer

Diazepam

Answer

Chlorpromazine

Psychopharmacology — MCQs

Psychopharmacology — MCQs

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