Psychopharmacology — MCQs

Psychopharmacology Indian Medical PG Practice Questions and MCQs

Question 131: What is the treatment for tardive dyskinesia?

A. Dantrolene sodium
B. Clonazepam and vitamin E (Correct Answer)
C. Pacitine
D. Propranolol

Explanation: **Explanation:** **Tardive Dyskinesia (TD)** is a delayed-onset extrapyramidal side effect caused by long-term use of dopamine receptor blockers (antipsychotics). It is characterized by involuntary, choreoathetoid movements, most commonly involving the orofacial region (e.g., tongue protrusion, lip-smacking). **Why Option B is Correct:** The management of TD is challenging. The first step is usually to reduce the dose of the offending agent or switch to a second-generation antipsychotic like Clozapine. For symptomatic treatment: * **Vitamin E:** Acts as an antioxidant to combat free radical damage to striatal neurons caused by chronic dopamine blockade. * **Clonazepam:** A benzodiazepine that enhances GABAergic tone, which helps suppress involuntary movements. * *Note:* Modern gold-standard treatments now include VMAT2 inhibitors (Valbenazine, Deutetrabenazine), but in the context of standard NEET-PG options, Vitamin E and Clonazepam remain classic choices. **Why Other Options are Incorrect:** * **A. Dantrolene sodium:** This is a muscle relaxant used specifically for **Neuroleptic Malignant Syndrome (NMS)** and Malignant Hyperthermia. * **C. Pacitane (Trihexyphenidyl):** This is an anticholinergic used for *Acute Dystonia* and *Drug-induced Parkinsonism*. Crucially, anticholinergics often **worsen** TD symptoms. * **D. Propranolol:** This beta-blocker is the drug of choice for **Akathisia** (subjective restlessness). **High-Yield Clinical Pearls for NEET-PG:** 1. **Pathophysiology:** TD is thought to be due to **dopamine receptor supersensitivity** in the nigrostriatal pathway. 2. **Risk Factors:** Old age, female gender, and long-term use of typical antipsychotics (e.g., Haloperidol). 3. **AIMS Scale:** The Abnormal Involuntary Movement Scale is used for screening and monitoring TD. 4. **Clozapine:** The antipsychotic with the lowest risk of causing TD and often used to manage patients who develop it.

Question 132: Which medication is known to cause reversible lens granular deposits?

A. chlorpromazine (Correct Answer)
B. risperidone
C. paliperidone
D. olanzapine

Explanation: **Explanation** The correct answer is **Chlorpromazine**. **1. Why Chlorpromazine is correct:** Chlorpromazine is a low-potency typical antipsychotic known for its specific ocular side effects. Long-term use or high cumulative doses (typically >800 mg/day) lead to the deposition of drug-pigment complexes in the eye. These characteristically appear as **whitish-brown granular deposits** on the **anterior lens capsule** and the posterior surface of the cornea. These deposits are usually asymptomatic and do not significantly impair vision, though they can occasionally progress to "star-shaped" cataracts. Importantly, these lens changes are often **reversible** or stabilize upon discontinuation of the drug. **2. Why the other options are incorrect:** * **Risperidone, Paliperidone, and Olanzapine:** These are Second-Generation (Atypical) Antipsychotics. While they are associated with metabolic side effects (weight gain, dyslipidemia, and diabetes), they are **not** typically associated with granular lens deposits. Risperidone and Paliperidone are more frequently linked to hyperprolactinemia. **3. High-Yield Clinical Pearls for NEET-PG:** * **Chlorpromazine (CPZ):** Remember the mnemonic *"C for Chlorpromazine, C for Corneal/Lens deposits."* It is also associated with blue-grey skin discoloration and photosensitivity. * **Thioridazine:** Another low-potency antipsychotic, but it causes **Irreversible Retinitis Pigmentosa** (Browning of vision) at doses >800 mg/day. Remember: *"T for Thioridazine, T for Total blindness (Retina)."* * **Quetiapine:** Historically required baseline slit-lamp exams due to cataract concerns in animal studies, though this is rarely seen in humans. * **Monitoring:** Patients on long-term Chlorpromazine should undergo periodic slit-lamp examinations.

Question 133: A patient diagnosed with schizophrenia presents a challenge for the use of clozapine as an antipsychotic drug. Which of the following acts as a limiting factor in its use?

A. Its potential to cause agranulocytosis (Correct Answer)
B. Its inability to benefit negative symptoms of schizophrenia
C. High incidence of extrapyramidal side effects
D. Production of hyperprolactinemia

Explanation: **Explanation:** Clozapine is a "Gold Standard" atypical antipsychotic, primarily reserved for **treatment-resistant schizophrenia** (failure of at least two other antipsychotic trials). Despite its superior efficacy, its clinical use is strictly limited by its side-effect profile. **1. Why Option A is Correct:** The most serious and life-threatening adverse effect of Clozapine is **agranulocytosis** (a severe decrease in white blood cell count, specifically neutrophils), occurring in approximately 1% of patients. Due to this risk, mandatory hematological monitoring (ANC - Absolute Neutrophil Count) is required—weekly for the first 6 months, biweekly for the next 6 months, and monthly thereafter. **2. Why Other Options are Incorrect:** * **Option B:** Incorrect. Unlike typical antipsychotics, Clozapine is highly effective against **both positive and negative symptoms** of schizophrenia. * **Option C:** Incorrect. Clozapine has the **lowest risk of Extrapyramidal Side Effects (EPS)** and Tardive Dyskinesia among all antipsychotics because of its low affinity for D2 receptors and high 5-HT2A antagonism. * **Option D:** Incorrect. Clozapine is "prolactin-sparing." It does not cause significant hyperprolactinemia, unlike Risperidone or Haloperidol. **High-Yield Clinical Pearls for NEET-PG:** * **Seizures:** Clozapine has a dose-dependent risk of seizures (highest among antipsychotics). * **Sialorrhea:** Paradoxical hypersalivation is a common, bothersome side effect. * **Myocarditis:** A rare but fatal side effect; monitor for chest pain or dyspnea in the first month. * **Metabolic Syndrome:** Significant weight gain, dyslipidemia, and diabetes are common. * **Smoking:** It induces CYP1A2; stopping smoking can lead to toxic levels of Clozapine.

Question 134: Which of the following is an absolute contraindication for the use of lithium?

A. Renal failure (Correct Answer)
B. Glaucoma
C. Epilepsy
D. Angina

Explanation: **Explanation:** **Lithium** is the gold standard mood stabilizer for Bipolar Affective Disorder (BPAD). Understanding its pharmacokinetics is crucial for NEET-PG: Lithium is a monovalent cation that is **exclusively excreted by the kidneys** and is not metabolized by the liver. 1. **Why Renal Failure is the Correct Answer:** Since Lithium is handled by the kidneys similarly to sodium (reabsorbed in the proximal tubule), any impairment in renal function leads to a drastic decrease in clearance. This results in rapid accumulation and **Lithium Toxicity**, which can be fatal or lead to permanent neurological damage (SILDCOR syndrome). Therefore, significant renal failure is an **absolute contraindication**. 2. **Analysis of Incorrect Options:** * **Glaucoma:** Unlike tricyclic antidepressants (TCAs) or antipsychotics with anticholinergic properties, Lithium does not significantly affect intraocular pressure. It is safe to use in glaucoma. * **Epilepsy:** Lithium is not contraindicated in epilepsy. While it can lower the seizure threshold at toxic levels, it is generally safe at therapeutic levels. In fact, some studies suggest it may have mild anticonvulsant properties. * **Angina:** While Lithium can cause EKG changes (like T-wave flattening/inversion), it is not an absolute contraindication for stable angina. However, it should be used with caution in patients with sick sinus syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Teratogenicity:** Causes **Ebstein’s Anomaly** (tricuspid valve displacement) if taken in the 1st trimester. * **Therapeutic Index:** Very narrow (0.6–1.2 mEq/L). Toxicity starts >1.5 mEq/L. * **Drug Interactions:** **NSAIDs, Thiazides, and ACE inhibitors** increase Lithium levels by decreasing renal clearance (High-yield mnemonic: **"NAT"**). * **Side Effects:** Nephrogenic Diabetes Insipidus, Hypothyroidism, and Fine Tremors.

Question 135: Which of the following hormones is used in the adjuvant treatment of depression?

A. Progesterone
B. Cortisol
C. ACTH
D. Levothyroxine (Correct Answer)

Explanation: **Explanation:** **Levothyroxine (T4)** is the correct answer because thyroid hormones play a crucial role in modulating neurotransmitter systems (serotonin and norepinephrine) in the brain. In clinical psychiatry, T4 (and sometimes T3/Liothyronine) is used as an **augmentation strategy** for patients with Treatment-Resistant Depression (TRD), even in those who are euthyroid. It enhances the clinical response to standard antidepressants like SSRIs or TCAs by accelerating the onset of action and improving overall efficacy. **Analysis of Incorrect Options:** * **Progesterone (A):** While hormonal fluctuations (like those in postpartum or premenstrual periods) affect mood, progesterone is not a standard adjuvant for clinical depression. In fact, high levels of certain progesterone metabolites can sometimes induce depressive symptoms or sedation. * **Cortisol (B) & ACTH (C):** Elevated levels of cortisol and ACTH are actually associated with the *pathophysiology* of depression (Hypercortisolemia). Chronic activation of the HPA axis is a hallmark of melancholic depression; therefore, administering these would likely worsen the condition rather than treat it. **Clinical Pearls for NEET-PG:** * **T3 vs. T4:** While T4 is mentioned here, **Liothyronine (T3)** is historically more common in research for rapid augmentation due to its direct action on brain receptors. * **Other Augmentation Agents:** Common NEET-PG favorites for TRD augmentation include **Lithium** (most evidence), **Atypical Antipsychotics** (e.g., Aripiprazole, Quetiapine), and **Ketamine/Esketamine**. * **L-Methylfolate:** Another metabolic adjuvant used to enhance monoamine synthesis in depression.

Question 136: What is the prophylactic plasma concentration range of lithium in mEq that is generally NOT included?

A. 0.5 mEq
B. 0.8 mEq
C. 0.6 mEq
D. 1.0 mEq (Correct Answer)

Explanation: **Explanation:** Lithium is the gold standard mood stabilizer for Bipolar Affective Disorder (BPAD). It has a **narrow therapeutic index**, meaning the difference between a therapeutic dose and a toxic dose is very small. Consequently, monitoring serum lithium levels is mandatory. **Why 1.0 mEq is the correct answer:** The therapeutic window for lithium is divided into two distinct phases: 1. **Acute Manic Episode:** 0.8 to 1.2 mEq/L (up to 1.5 mEq/L in some guidelines). 2. **Prophylaxis (Maintenance):** **0.6 to 0.8 mEq/L.** While 1.0 mEq/L is within the therapeutic range for an *acute* episode, it is generally considered too high for long-term prophylaxis due to the increased risk of renal and thyroid toxicity. Therefore, it is not included in the standard prophylactic range. **Analysis of Incorrect Options:** * **A (0.5 mEq):** Often considered the lower threshold for maintenance. While 0.6 is ideal, some patients are maintained at 0.5 mEq/L to minimize side effects. * **B & C (0.8 & 0.6 mEq):** These represent the classic "sweet spot" for prophylaxis. Maintaining levels within this range effectively prevents relapse while minimizing long-term organ damage. **High-Yield Clinical Pearls for NEET-PG:** * **Sampling Time:** Serum levels should be checked **12 hours** after the last dose (Trough level). * **Steady State:** Achieved in **5 days** (5 half-lives). * **Toxicity:** Levels **>1.5 mEq/L** are toxic; **>2.0 mEq/L** require urgent intervention; **>4.0 mEq/L** usually require hemodialysis. * **Teratogenicity:** Ebstein’s Anomaly (tricuspid valve displacement). * **Drug Interactions:** Thiazides, NSAIDs, and ACE inhibitors increase lithium levels (Decreased clearance).

Question 137: At what serum lithium levels is permanent cerebellar damage typically observed?

A. 1-1.5 mEq/L
B. >2 mEq/L
C. >3 mEq/L (Correct Answer)
D. >4 mEq/L

Explanation: **Explanation:** Lithium has a very narrow therapeutic index, meaning the margin between a therapeutic dose and a toxic dose is slim. The risk of severe, irreversible neurological damage increases significantly as serum levels rise. * **Correct Answer (C): >3 mEq/L.** This level represents **severe lithium toxicity**. At concentrations exceeding 3 mEq/L, lithium becomes highly neurotoxic. It can lead to **SILNDA** (Syndrome of Irreversible Lithium-Effectuated Neurotoxicity), characterized by permanent cerebellar dysfunction (ataxia, dysarthria) and extrapyramidal symptoms. At this level, hemodialysis is usually mandatory to prevent permanent damage or death. * **Option A (1-1.5 mEq/L):** This range represents the upper limit of the **therapeutic window** for acute mania (0.8–1.2 mEq/L) or mild toxicity. Symptoms are usually limited to GI upset, fine tremors, and fatigue. * **Option B (>2 mEq/L):** This indicates **moderate toxicity**. Patients may exhibit gross tremors, ataxia, confusion, and slurred speech. While serious, these symptoms are often reversible if the drug is discontinued and hydration is started. * **Option D (>4 mEq/L):** While levels above 4 mEq/L certainly cause permanent damage, the threshold for irreversible cerebellar sequelae is clinically established at **>3 mEq/L**. Waiting for levels to reach 4 mEq/L would be fatal for many patients. **High-Yield Clinical Pearls for NEET-PG:** * **Therapeutic Range:** 0.6–1.2 mEq/L (Maintenance: 0.6–0.8; Acute Mania: 0.8–1.2). * **Sampling Time:** Blood should be drawn **12 hours** after the last dose (Trough level). * **Early Sign of Toxicity:** Coarse tremors (Fine tremors are a side effect). * **Pre-Lithium Workup:** Check Renal Function Tests (RFT), Thyroid Function Tests (TFT), and ECG (due to risk of Ebstein’s anomaly in pregnancy and T-wave flattening). * **Drug Interactions:** Thiazides, NSAIDs, and ACE inhibitors increase lithium levels (decreased clearance).

Question 138: A 40-year-old man with a psychiatric illness, on medication for the past two weeks, suddenly develops marked rigidity, immobility, fever, fluctuating blood pressure, and heart rate. What is the most likely diagnosis?

A. Akathisia
B. Parkinsonism
C. Malignant neuroleptic syndrome (Correct Answer)
D. Catatonic schizophrenia

Explanation: **Explanation:** The clinical presentation of **marked rigidity** ("lead-pipe" rigidity), **autonomic instability** (fluctuating BP and heart rate), **hyperpyrexia** (fever), and altered mental status (immobility/stupor) in a patient recently started on antipsychotics is a classic description of **Neuroleptic Malignant Syndrome (NMS)**. **1. Why the Correct Answer is Right:** NMS is a life-threatening idiosyncratic reaction to dopamine antagonists (typically first-generation antipsychotics like Haloperidol). It usually occurs within the first two weeks of treatment. The underlying mechanism is a massive **blockade of D2 receptors** in the nigrostriatal pathway (causing rigidity) and the hypothalamus (causing thermoregulatory failure/fever). **2. Why Incorrect Options are Wrong:** * **Akathisia:** Presents as subjective motor restlessness (inability to sit still). It does not involve fever or autonomic instability. * **Parkinsonism:** Characterized by tremors, bradykinesia, and cogwheel rigidity. While it involves rigidity, it lacks the life-threatening systemic features like high fever and tachycardia seen here. * **Catatonic Schizophrenia:** While it features immobility and rigidity (waxy flexibility), it is a primary psychiatric state and typically does not present with acute autonomic instability or high-grade fever unless complicated by "Lethal Catatonia." **3. NEET-PG High-Yield Pearls:** * **Key Lab Finding:** Significantly elevated **Creatine Phosphokinase (CPK)** levels due to muscle necrosis (rhabdomyolysis). * **Treatment of Choice:** Immediate drug discontinuation, aggressive cooling, and pharmacological intervention with **Dantrolene** (muscle relaxant) or **Bromocriptine** (D2 agonist). * **Mnemonic (FEVER):** **F**ever, **E**ncephalopathy, **V**itals unstable, **E**levated CPK, **R**igidity.

Question 139: Memory disturbance following electroconvulsive therapy (ECT) typically resolves within what timeframe?

A. A few days to a few weeks
B. A few weeks to a few months (Correct Answer)
C. A few months to a few years
D. Permanent

Explanation: **Explanation:** Memory impairment is the most common side effect of Electroconvulsive Therapy (ECT). The correct answer is **B (A few weeks to a few months)** because while acute cognitive deficits appear immediately after treatment, they are transient. **1. Why Option B is Correct:** ECT-induced memory loss typically involves two types: **Anterograde amnesia** (difficulty forming new memories), which usually resolves within 1–2 weeks post-treatment, and **Retrograde amnesia** (loss of past memories), which takes longer. Most patients return to their cognitive baseline within **1 to 6 months** after the final session. Long-term follow-up studies show that objective memory performance often improves beyond baseline levels as the underlying depression resolves. **2. Why Other Options are Incorrect:** * **Option A:** A few days is too short; while the post-ictal confusion clears in hours, the formal memory deficits persist longer. * **Option C & D:** While some patients subjectively report "gaps" in their memory for events surrounding the treatment period (permanent focal retrograde amnesia), global memory disturbance lasting years or being permanent is not the clinical norm and contradicts standard psychiatric data. **High-Yield Clinical Pearls for NEET-PG:** * **Type of ECT:** Bilateral ECT causes more memory impairment than Unilateral ECT. * **Electrode Placement:** Brief-pulse stimuli and Right Unilateral (RUL) placement (d'Elia placement) are used to minimize cognitive side effects. * **Pre-medication:** Atropine or Glycopyrrolate is used to prevent vagal bradycardia; Methohexital (gold standard) or Propofol is used for anesthesia; Succinylcholine is the muscle relaxant of choice. * **Mortality:** Extremely low (approx. 0.002% per treatment), usually due to cardiovascular complications.

Question 140: Which antidepressant is best for a patient with hypotension and cardiac disease?

A. Venlafaxine
B. Mianserin (Correct Answer)
C. Duloxetine
D. Citalopram

Explanation: **Explanation:** The correct answer is **Mianserin**. **Why Mianserin is the correct choice:** Mianserin is a tetracyclic antidepressant (TeCA) that acts as an alpha-2 adrenergic receptor antagonist. Unlike Tricyclic Antidepressants (TCAs), Mianserin is notably **devoid of anticholinergic effects** and has **minimal cardiovascular toxicity**. It does not inhibit the reuptake of norepinephrine to a significant degree at the cardiac level and does not cause orthostatic hypotension or conduction delays. This makes it one of the safest options for elderly patients or those with pre-existing cardiac disease and hypotension. **Analysis of Incorrect Options:** * **Venlafaxine & Duloxetine (SNRIs):** These agents inhibit the reuptake of norepinephrine. A common side effect, especially with Venlafaxine, is a **dose-dependent increase in blood pressure** (hypertension) and heart rate, making them less ideal for unstable cardiac patients. * **Citalopram (SSRI):** While SSRIs are generally cardiac-safe, Citalopram is specifically associated with **dose-dependent QTc interval prolongation**. In patients with structural cardiac disease, this increases the risk of fatal arrhythmias like Torsades de Pointes. **NEET-PG High-Yield Pearls:** * **Mianserin vs. Mirtazapine:** Both are alpha-2 antagonists. Mianserin is associated with a rare risk of **agranulocytosis** (requires CBC monitoring), whereas Mirtazapine is known for weight gain and sedation. * **Drug of Choice:** For a post-Myocardial Infarction (MI) patient with depression, **Sertraline** is often considered the gold standard due to its extensive safety data. * **Avoid TCAs:** In cardiac patients, TCAs are contraindicated as they are "quinidine-like" and cause PR/QT prolongation and orthostatic hypotension.

Practice by Chapter

Principles of Psychopharmacology

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Antipsychotic Medications

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Antidepressant Medications

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Mood Stabilizers

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Anxiolytics and Hypnotics

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Stimulants and Cognitive Enhancers

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Pharmacokinetics and Pharmacodynamics

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Drug Interactions

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Adverse Effects and Management

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Pharmacogenomics in Psychiatry

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Special Populations Considerations

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Treatment Algorithms and Guidelines

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