Psychopharmacology — MCQs

Psychopharmacology Indian Medical PG Practice Questions and MCQs

Question 261: Raj Mohan has recently been on an increased regime of antipsychotics for Schizophrenia. Which of the following complications is NOT associated with the combined use of more than one antipsychotic?

A. Neuroleptic Malignant Syndrome
B. Renal Tubular Necrosis (Correct Answer)
C. Paralytic ileus
D. QTc Prolongation in ECG

Explanation: **Explanation:** The use of multiple antipsychotics (antipsychotic polypharmacy) significantly increases the risk of cumulative side effects due to additive pharmacodynamic and pharmacokinetic interactions. **Why Renal Tubular Necrosis (RTN) is the correct answer:** Renal Tubular Necrosis is **not** a recognized complication of antipsychotic therapy. While certain psychotropic drugs like Lithium are associated with nephrotoxicity (e.g., Nephrogenic Diabetes Insipidus), antipsychotics are primarily metabolized by the liver and excreted via the kidneys without causing direct tubular damage. If renal failure occurs in a psychiatric patient, it is usually secondary to **Rhabdomyolysis** (seen in NMS), not a direct toxic effect of the medication on the tubules. **Analysis of Incorrect Options:** * **Neuroleptic Malignant Syndrome (NMS):** This is a life-threatening idiosyncratic reaction. High doses or rapid escalation of multiple dopamine (D2) antagonists increase the risk of severe dopamine depletion in the nigrostriatal pathway and hypothalamus. * **Paralytic Ileus:** Many antipsychotics (especially low-potency typicals like Chlorpromazine and atypicals like Clozapine) have potent **anticholinergic** properties. Combining them leads to "anticholinergic overload," which can cause severe constipation or life-threatening paralytic ileus. * **QTc Prolongation:** Most antipsychotics (notably Thioridazine, Ziprasidone, and Haloperidol) block potassium channels in the heart. Polypharmacy increases the risk of Torsades de Pointes and sudden cardiac death. **High-Yield Clinical Pearls for NEET-PG:** * **NMS Pentad:** Muscle rigidity ("Lead-pipe"), Hyperthermia, Autonomic instability, Altered sensorium, and Elevated CPK levels. * **Treatment of NMS:** Stop the offending agent, provide supportive care, and use **Dantrolene** (muscle relaxant) or **Bromocriptine** (dopamine agonist). * **ECG Monitoring:** Mandatory when using high-dose antipsychotics or combining drugs like Ziprasidone and Pimozide.

Question 262: What is the common side effect associated with fluoxetine therapy?

A. Seizure
B. Anxiety
C. Hypotension
D. Loose stools (Correct Answer)

Explanation: **Explanation:** Fluoxetine is a Selective Serotonin Reuptake Inhibitor (SSRI). The mechanism involves increasing synaptic serotonin levels, which not only affects the brain but also acts on peripheral receptors. **Why "Loose Stools" is correct:** Approximately 90% of the body's serotonin is located in the **enterochromaffin cells of the GI tract**. SSRIs like fluoxetine increase serotonergic activity at **5-HT3 and 5-HT4 receptors** in the gut. This stimulates gastrointestinal motility and fluid secretion, leading to common side effects such as nausea, abdominal cramps, and **loose stools/diarrhea**. **Analysis of Incorrect Options:** * **A. Seizure:** While some antidepressants (like Bupropion or Maprotiline) significantly lower the seizure threshold, SSRIs are generally considered safe and have a very low risk of inducing seizures at therapeutic doses. * **B. Anxiety:** Although some patients experience "jitteriness" or transient activation syndrome during the first week of SSRI therapy, it is less common than GI side effects. Fluoxetine is actually used to *treat* chronic anxiety disorders. * **C. Hypotension:** SSRIs do not typically cause orthostatic hypotension. This side effect is more characteristic of Tricyclic Antidepressants (TCAs) due to alpha-1 adrenergic blockade. **High-Yield Clinical Pearls for NEET-PG:** * **Fluoxetine** has the **longest half-life** (4–6 days; its metabolite norfluoxetine lasts up to 16 days) among SSRIs, making it the least likely to cause discontinuation syndrome. * **Most common side effect of SSRIs:** GI upset (Nausea is #1, followed by diarrhea). * **Most common long-term side effect:** Sexual dysfunction (delayed ejaculation/anorgasmia). * **Drug of choice:** SSRIs are the first-line treatment for Depression, OCD, Panic Disorder, and Bulimia Nervosa (specifically Fluoxetine).

Question 263: Who introduced lithium for the treatment of manic-depressive illness?

A. Benedict Morel
B. Delay and Deniker
C. John F. Cade (Correct Answer)
D. Bleuler

Explanation: **Explanation:** The correct answer is **John F. Cade**. In **1949**, Australian psychiatrist John Cade discovered the antimanic effects of lithium while researching the role of uric acid in psychotic patients. He observed that lithium urate had a calming effect on guinea pigs, leading him to successfully treat patients with chronic and acute mania. This discovery marked the beginning of the modern era of psychopharmacology. **Analysis of Incorrect Options:** * **Benedict Morel (A):** He is known for introducing the term *"Démence précoce"* (the precursor to the term Schizophrenia) to describe a condition of mental deterioration starting in adolescence. * **Delay and Deniker (B):** Jean Delay and Pierre Deniker are credited with discovering the antipsychotic properties of **Chlorpromazine** in 1952, which revolutionized the treatment of schizophrenia. * **Eugen Bleuler (D):** He coined the term **"Schizophrenia"** (replacing Morel’s term) and defined its core symptoms using the "4 As" (Ambivalence, Autism, Affective flattening, and Association looseness). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Lithium acts by inhibiting the **Inositol Monophosphatase (IMPase)** pathway and GSK-3 enzyme. * **Therapeutic Index:** It has a narrow therapeutic index. Target serum levels are **0.8–1.2 mEq/L** for acute mania and **0.6–0.8 mEq/L** for maintenance. * **Teratogenicity:** Use in pregnancy is associated with **Ebstein’s Anomaly** (tricuspid valve abnormality). * **Side Effects:** Common high-yield side effects include fine tremors, polyuria (nephrogenic diabetes insipidus), and hypothyroidism.

Question 264: Lithium use in pregnancy is associated with which of the following fetal defects?

A. Cardiovascular defects (Correct Answer)
B. Urogenital defects
C. Neural tube defects
D. Facial defects

Explanation: **Explanation:** **Lithium** is a gold-standard mood stabilizer used in Bipolar Disorder; however, it is a known teratogen. When used during the first trimester of pregnancy, it is specifically associated with **Cardiovascular defects**, most notably **Ebstein’s Anomaly**. This condition involves the downward displacement of the tricuspid valve into the right ventricle, leading to "atrialization" of the ventricle and severe tricuspid regurgitation. While the absolute risk is relatively low (approx. 1 in 1,000 to 2,000), it represents a 10-20 fold increase compared to the general population. **Analysis of Incorrect Options:** * **Urogenital defects:** These are not classically associated with Lithium. They are more commonly linked to maternal diabetes or specific genetic syndromes. * **Neural tube defects (NTDs):** These are the hallmark teratogenic effect of **Valproate** and **Carbamazepine** (due to interference with folate metabolism), not Lithium. * **Facial defects:** Cleft lip and palate are associated with anticonvulsants like Phenytoin (Fetal Hydantoin Syndrome) or Benzodiazepines, but are not the primary concern with Lithium. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** If Lithium must be used, fetal echocardiography is recommended at 18–22 weeks gestation. * **Dosage:** Lithium clearance increases during pregnancy (due to increased GFR) and drops abruptly at delivery; close serum monitoring is vital to prevent toxicity. * **Breastfeeding:** Lithium is generally discouraged during breastfeeding as it is excreted in milk and can cause "Floppy Baby Syndrome" (hypotonia, cyanosis). * **Alternative:** For NTDs (Valproate), the boards often ask about high-dose Folic acid supplementation (4mg/day).

Question 265: Which of the following conditions increases the chance of hyponatremia in a patient treated with an antidepressant?

A. Old age (Correct Answer)
B. Low weight
C. Cold climate
D. Obesity

Explanation: **Explanation:** The development of hyponatremia is a well-recognized side effect of antidepressant therapy, particularly with **Selective Serotonin Reuptake Inhibitors (SSRIs)** and **Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)**. **1. Why Old Age is Correct:** The primary mechanism is the **Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH)**. Antidepressants can stimulate the release of ADH or increase the sensitivity of the kidneys to it, leading to water retention and dilutional hyponatremia. **Old age** is the most significant risk factor because elderly patients often have decreased total body water, age-related changes in renal function, and are frequently on concomitant medications (like diuretics or NSAIDs) that further impair water excretion. **2. Analysis of Incorrect Options:** * **Low weight:** While some studies suggest low body mass index (BMI) might be a minor risk factor, it is not as clinically significant or consistently proven as advanced age. * **Cold climate:** Climate does not influence the pathophysiology of SIADH or antidepressant-induced hyponatremia. * **Obesity:** Obesity is not a recognized risk factor for SIADH; in fact, the risk is generally higher in those with lower body weight/frailty. **Clinical Pearls for NEET-PG:** * **Most Common Culprits:** SSRIs (Fluoxetine, Sertraline, Paroxetine) are the most frequently implicated. * **Timing:** Hyponatremia typically develops within the **first 2–4 weeks** of starting treatment. * **Monitoring:** Always check baseline and follow-up electrolytes in elderly patients starting SSRIs. * **Symptoms:** Range from lethargy and confusion to seizures and coma if sodium levels drop rapidly.

Question 266: Tardive dyskinesia is least common with which of the following medications?

A. Flupenthixol
B. Penfluridol
C. Olanzapine (Correct Answer)
D. None of the above

Explanation: **Explanation:** The risk of **Tardive Dyskinesia (TD)** is directly related to the potency of dopamine (D2) receptor blockade and the duration of treatment. **1. Why Olanzapine is correct:** Olanzapine is a **Second-Generation Antipsychotic (SGA)** or atypical antipsychotic. Atypical antipsychotics have a lower affinity for D2 receptors and a higher affinity for 5-HT2A receptors. They also exhibit "fast dissociation" from D2 receptors. These properties significantly reduce the risk of Extrapyramidal Side Effects (EPS) and long-term complications like Tardive Dyskinesia compared to First-Generation Antipsychotics (FGAs). Among the options provided, Olanzapine carries the lowest risk of inducing TD. **2. Why the other options are incorrect:** * **Flupenthixol (Option A):** This is a typical (First-Generation) antipsychotic of the thioxanthene class. It is a potent D2 receptor antagonist and is associated with a significantly higher risk of TD. * **Penfluridol (Option B):** This is a long-acting oral typical antipsychotic. Due to its high potency and long half-life, it maintains a sustained blockade of D2 receptors, making the risk of TD much higher than with atypical agents. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** TD is characterized by involuntary choreoathetoid movements, most commonly involving the orofacial region (e.g., tongue protrusion, lip-smacking). * **Pathophysiology:** It is thought to be caused by **dopamine receptor supersensitivity** in the nigrostriatal pathway following chronic blockade. * **Drug of Choice for TD:** If TD develops, the offending agent should be switched to **Clozapine** (the antipsychotic with the lowest overall risk of TD). * **FDA-Approved Treatment:** **VMAT-2 inhibitors** (e.g., Valbenazine, Deutetrabenazine) are now the standard treatment for managing TD symptoms. * **Risk Hierarchy:** Clozapine < Quetiapine < Olanzapine < Risperidone < Typical Antipsychotics (Haloperidol).

Question 267: A young patient with schizophrenia is intolerant to antipsychotic medications. Which drug is most preferred for such a patient?

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

Explanation: **Explanation:** The correct answer is **Clozapine (Option A)**. In clinical psychiatry, **Clozapine** is the gold-standard treatment for **Treatment-Resistant Schizophrenia (TRS)**. It is indicated when a patient has failed to respond to at least two different antipsychotic trials (one of which must be an atypical antipsychotic) or, as mentioned in the question, when a patient is **intolerant** to the side effects of other medications (particularly Extrapyramidal Symptoms or EPS). Clozapine is unique because it has a very low affinity for D2 receptors in the striatum, making it the drug of choice for patients who cannot tolerate the motor side effects of other agents. **Why other options are incorrect:** * **Haloperidol (Option D):** A high-potency typical antipsychotic with a high risk of EPS (dystonia, parkinsonism). It is usually the *least* preferred in intolerant patients. * **Risperidone (Option C) & Olanzapine (Option B):** These are first-line atypical antipsychotics. While they have a lower risk of EPS than Haloperidol, they are still associated with significant side effects (Risperidone: Hyperprolactinemia; Olanzapine: Metabolic syndrome). If a patient is "intolerant" to standard therapy, Clozapine is the next logical step. **High-Yield NEET-PG Pearls:** * **Clozapine** is the only antipsychotic proven to reduce **suicidal behavior** in schizophrenia. * **Most serious side effect:** Agranulocytosis (requires mandatory WBC monitoring). * **Most common side effect:** Sialorrhea (excessive salivation). * **Other risks:** Lowers seizure threshold (dose-dependent) and causes myocarditis. * **Mechanism:** Potent 5-HT2A and weak D2 blockade.

Question 268: A patient diagnosed with depression, currently on treatment, presents to the emergency department with altered sensorium, seizures, and palpitations. ECG shows sinus tachycardia. How do you treat this patient?

A. Aspirin + clopidogrel
B. IV Lorazepam
C. IV Sodium bicarbonate (Correct Answer)
D. IV Haloperidol

Explanation: ### Explanation The clinical presentation of **altered sensorium, seizures, and sinus tachycardia** in a patient being treated for depression is a classic description of **Tricyclic Antidepressant (TCA) overdose** (e.g., Amitriptyline). **Why IV Sodium Bicarbonate is the Correct Answer:** TCAs cause cardiotoxicity primarily by blocking **fast sodium channels** in the myocardium, leading to QRS prolongation, arrhythmias, and hypotension. * **Mechanism:** IV Sodium Bicarbonate increases extracellular sodium concentration and raises serum pH. The alkaline pH decreases the affinity of the TCA molecule for the sodium channel, while the sodium load helps overcome the channel blockade. This stabilizes the cardiac membrane and prevents fatal arrhythmias. **Analysis of Incorrect Options:** * **A. Aspirin + clopidogrel:** These are antiplatelets used for Acute Coronary Syndrome (ACS). While the patient has tachycardia, the underlying cause is toxicological, not thrombotic. * **B. IV Lorazepam:** While benzodiazepines are the first-line treatment for TCA-induced **seizures**, they do not address the life-threatening cardiac conduction delays, which is the priority in management. * **D. IV Haloperidol:** This is contraindicated. Antipsychotics can lower the seizure threshold and further prolong the QT interval, worsening the clinical state. **NEET-PG High-Yield Pearls:** * **The "3 Cs" of TCA Poisoning:** **C**oma, **C**onvulsions, and **C**ardiotoxicity. * **ECG Hallmark:** QRS duration **>100 ms** is predictive of seizures; **>160 ms** is highly predictive of ventricular arrhythmias. Look for a terminal R wave in lead aVR. * **Anticholinergic Toxidrome:** Patients often present with "dry as a bone, red as a beet, hot as a hare, blind as a bat, and mad as a hatter."

Question 269: Which of the following SSRIs is considered safe?

A. escitalopram (Correct Answer)
B. clomipramine
C. fluoxetine
D. amitriptyline

Explanation: **Explanation:** The question asks to identify the safe **SSRI (Selective Serotonin Reuptake Inhibitor)** among the given options. **1. Why Escitalopram is Correct:** Escitalopram is the S-enantiomer of citalopram and is considered the **most selective** SSRI. It has a very favorable safety profile due to its minimal effect on the Cytochrome P450 enzyme system, leading to fewer drug-drug interactions. It is also known for having the lowest potential for causing QTc prolongation among the SSRIs (unlike its parent compound, citalopram, which is dose-restricted). **2. Why the Other Options are Incorrect:** * **Clomipramine (Option B):** This is a **Tricyclic Antidepressant (TCA)**, not an SSRI. While it is the gold standard for OCD, it carries a high risk of side effects, including sedation, anticholinergic effects, and cardiotoxicity in overdose. * **Fluoxetine (Option C):** Although fluoxetine is an SSRI, it has a very long half-life (and an active metabolite, norfluoxetine) and is a potent inhibitor of CYP2D6. This makes it less "safe" in terms of drug interactions and management of side effects compared to escitalopram. * **Amitriptyline (Option D):** This is a **TCA**. It is highly cardiotoxic and has significant sedative and anticholinergic properties, making it much less safe than any SSRI. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** SSRIs are the first-line treatment for Depression, Panic Disorder, GAD, and OCD. * **Safest SSRI Post-MI:** Sertraline is generally preferred in patients with recent myocardial infarction. * **Longest Half-life:** Fluoxetine (useful in patients with poor compliance). * **Shortest Half-life:** Fluvoxamine/Paroxetine (highest risk of discontinuation syndrome). * **Side Effects:** The most common side effect of SSRIs is **GI upset** (nausea/diarrhea), and the most common long-term side effect is **sexual dysfunction**.

Question 270: What are the therapeutic serum levels of lithium in a patient with acute mania?

A. 0.4–0.8 mEq/L
B. 0.8–1.2 mEq/L (Correct Answer)
C. 1.2–1.6 mEq/L
D. 1.6–2.0 mEq/L

Explanation: **Explanation:** Lithium is the gold-standard mood stabilizer used for both the treatment of acute manic episodes and the long-term prophylaxis of Bipolar Affective Disorder (BPAD). Because Lithium has a **narrow therapeutic index**, monitoring serum levels is critical for both efficacy and safety. 1. **Why Option B is Correct:** In the **acute phase of mania**, higher serum concentrations are required to control symptoms effectively. The established therapeutic range for acute mania is **0.8–1.2 mEq/L**. Levels are typically measured 12 hours after the last dose (trough levels). 2. **Why Other Options are Incorrect:** * **Option A (0.4–0.8 mEq/L):** This is the range for **maintenance therapy** (prophylaxis). Once the acute episode subsides, the dose is usually lowered to minimize long-term side effects. * **Option C & D (>1.2 mEq/L):** These levels approach the toxic range. Toxicity generally begins at levels **>1.5 mEq/L**. Levels above 2.0 mEq/L are considered severe toxicity and may require hemodialysis. **High-Yield Clinical Pearls for NEET-PG:** * **Steady State:** Lithium levels should be checked after **5 days** of starting or changing the dose (5 half-lives). * **Side Effects:** Look for "LITHIUM" mnemonic: **L**eukocytosis, **I**nsipidus (Diabetes Insipidus), **T**remors/Teratogenicity (Ebstein’s Anomaly), **H**ypothyroidism, **I**ncreased **U**rine, **M**others (Pregnancy concerns). * **Drug Interactions:** Thiazides, NSAIDs, and ACE inhibitors increase Lithium levels (by decreasing renal clearance), potentially leading to toxicity. * **Monitoring:** Baseline Thyroid Function Tests (TFTs) and Renal Function Tests (RFTs) are mandatory.

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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