Psychopharmacology — MCQs

A 25-year-old man with major depression discusses the potential benefits and side effects of various antidepressants with his psychiatrist. He clearly indicates that he does not want a medication that could decrease his libido or interfere with his ability to obtain and maintain an erection. Which of the listed antidepressants would be appropriate for this patient?

Q227Medium

Which of the following psychiatric disorders, apart from depression, are commonly treated with selective serotonin reuptake inhibitors?

Q228Easy

What is the toxic level of lithium?

Q229Easy

Which of the following is not a side effect of lithium?

Q230Medium

An appropriate pre-Lithium work-up includes all of the following, EXCEPT?

Psychopharmacology Indian Medical PG Practice Questions and MCQs

Question 221: Which of the following is given to a patient who is planned for ECT?

A. Diazepam
B. Phenytoin
C. Muscle relaxant (Correct Answer)
D. Barbiturate

Explanation: ### Explanation **Correct Option: C. Muscle relaxant** In modern Electroconvulsive Therapy (ECT), the procedure is performed under **modified** conditions, meaning general anesthesia and muscle relaxation are mandatory. The primary goal of using a muscle relaxant—most commonly **Succinylcholine** (a short-acting depolarizing agent)—is to prevent the peripheral musculoskeletal manifestations of the seizure. Without it, the intense muscle contractions could lead to bone fractures, joint dislocations, or tongue bites. By blocking the neuromuscular junction, the patient experiences a "modified" seizure where the brain activity (EEG) shows seizure patterns, but the body remains still. **Why other options are incorrect:** * **A. Diazepam & B. Phenytoin:** These are anticonvulsants. Since the therapeutic efficacy of ECT depends on inducing a generalized cerebral seizure of adequate duration (usually >20-25 seconds), drugs that **increase the seizure threshold** or shorten seizure duration are generally avoided or tapered before the procedure. * **D. Barbiturate:** While ultra-short-acting barbiturates (like **Methohexital** or Thiopental) are used as *anesthetic agents* in ECT, the question asks for what is "given" in the context of standard preparation. Between a sedative and a muscle relaxant, the muscle relaxant is the specific requirement to prevent the physical trauma of the fit. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug of Choice for Anesthesia:** Methohexital (due to its short recovery time and minimal effect on seizure threshold). 2. **Drug of Choice for Muscle Relaxation:** Succinylcholine. 3. **Pre-medication:** Atropine or Glycopyrrolate is often given to prevent vagally-mediated bradycardia and reduce secretions. 4. **Absolute Contraindication:** Increased intracranial pressure (ICP) is the only absolute contraindication for ECT. 5. **Most Common Side Effect:** Retrograde amnesia and post-ictal confusion.

Question 222: A patient with schizophrenia is responding well to haloperidol but has developed symptoms of parkinsonism. What is the drug of choice to treat this condition?

A. Levodopa
B. Bromocriptine
C. Tolcapone
D. Anticholinergic (Correct Answer)

Explanation: **Explanation:** The patient is experiencing **Drug-Induced Parkinsonism (DIP)**, a common Extrapyramidal Side Effect (EPS) of typical antipsychotics like Haloperidol. **1. Why Anticholinergics are the Drug of Choice:** Antipsychotics work by blocking Dopamine ($D_2$) receptors in the nigrostriatal pathway. In the basal ganglia, there is a functional balance between **Dopamine (inhibitory)** and **Acetylcholine (excitatory)**. When dopamine is blocked, acetylcholine becomes relatively overactive, leading to motor symptoms (tremor, rigidity, bradykinesia). **Anticholinergics** (e.g., **Benztropine, Trihexyphenidyl/Benzhexol, Biperiden**) restore this balance by reducing cholinergic activity. **2. Why other options are incorrect:** * **Levodopa (A) & Bromocriptine (B):** These are dopamine agonists used in idiopathic Parkinson’s disease. In schizophrenia, they are **contraindicated** because increasing dopamine levels can exacerbate or "rekindle" psychotic symptoms (the Dopamine Hypothesis of Schizophrenia). * **Tolcapone (C):** This is a COMT inhibitor used as an adjunct in Parkinson’s disease to prevent levodopa breakdown. It has no role in treating EPS and carries a risk of hepatotoxicity. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for Akathisia:** Beta-blockers (Propranolol). * **Drug of Choice for Acute Dystonia:** Intravenous/Intramuscular Anticholinergics (Promethazine or Benztropine). * **Tardive Dyskinesia:** Unlike other EPS, this is caused by dopamine receptor supersensitivity; anticholinergics can actually **worsen** it. Treatment involves Valbenazine or Deutetrabenazine (VMAT2 inhibitors). * **Amantadine:** An alternative for DIP if anticholinergics are poorly tolerated.

Question 223: A patient with endogenous depression is administered imipramine. After what time interval is the therapeutic effect of imipramine likely to manifest?

A. 3 days
B. 1 week
C. 3 weeks (Correct Answer)
D. 3 months

Explanation: ### Explanation **Correct Answer: C. 3 weeks** **Mechanism and Rationale:** Imipramine is a **Tricyclic Antidepressant (TCA)**. While TCAs immediately block the reuptake of norepinephrine and serotonin at the synaptic cleft, the clinical antidepressant effect is not immediate. The therapeutic lag is attributed to the time required for **downregulation (desensitization) of post-synaptic beta-adrenergic receptors and presynaptic alpha-2 receptors**, as well as changes in gene expression (e.g., increased BDNF). In clinical practice, a noticeable improvement in mood typically manifests after **2 to 3 weeks** of continuous therapy. **Analysis of Incorrect Options:** * **A & B (3 days / 1 week):** These are too early for a therapeutic response. While patients may experience immediate side effects (like sedation or anticholinergic effects) or a slight improvement in sleep/anxiety, the core symptoms of depression do not lift within the first week. * **D (3 months):** This is far too long. If a patient shows no response by 4–6 weeks at an adequate dose, the treatment is usually considered a failure, and a switch to a different class of drugs is indicated. **High-Yield Clinical Pearls for NEET-PG:** * **The "Lag Period":** Always counsel patients that while side effects appear early, the "mood-lifting" effect takes 2–3 weeks. * **Suicide Risk:** During the first 1–2 weeks of treatment, physical energy (psychomotor activity) may improve before the depressive mood lifts. This creates a dangerous window where the patient may have the energy to act on suicidal ideation. * **Overdose Triad (The 3 C's):** Convulsions, Coma, and Cardiac arrhythmias (due to sodium channel blockade). * **Drug of Choice:** Imipramine is historically the drug of choice for **Enuresis (bed-wetting)** in children, though it is now a second-line option.

Question 224: Which of the following statements is FALSE regarding Neuroleptic Malignant Syndrome (NMS)?

A. Combining antipsychotics and antidepressants increases the risk of NMS.
B. An increase in Creatinine Phosphokinase (CPK) always indicates NMS. (Correct Answer)
C. First use of an injectable antipsychotic is a risk factor.
D. Catatonic symptoms and autonomic dysfunction are features of NMS.

Explanation: **Explanation:** **Neuroleptic Malignant Syndrome (NMS)** is a rare but life-threatening idiosyncratic reaction to dopamine antagonists (typically antipsychotics). **Why Option B is the Correct Answer (False Statement):** While an elevated **Creatinine Phosphokinase (CPK)** is a hallmark laboratory finding in NMS (due to intense muscle rigidity and rhabdomyolysis), it is **not pathognomonic**. CPK can be elevated in various other conditions such as myocardial infarction, strenuous exercise, intramuscular injections, status epilepticus, and other drug reactions (e.g., Serotonin Syndrome). Diagnosis of NMS is primarily clinical, based on the tetrad of fever, rigidity, altered mental status, and autonomic instability. **Analysis of Other Options:** * **Option A:** Polypharmacy, especially the combination of antipsychotics with lithium or certain antidepressants, significantly increases the risk of developing NMS. * **Option C:** High-potency neuroleptics, rapid dose escalation, and the use of **parenteral (injectable) forms** are well-established risk factors for NMS. * **Option D:** NMS is characterized by "lead-pipe" rigidity (a form of catatonic symptom) and profound **autonomic dysfunction** (tachycardia, labile blood pressure, and diaphoresis). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Massive dopamine (D2) blockade in the nigrostriatal pathway and hypothalamus. * **Drug of Choice:** **Dantrolene** (muscle relaxant) or **Bromocriptine** (dopamine agonist). * **NMS vs. Serotonin Syndrome:** NMS presents with "Lead-pipe" rigidity and bradyreflexia, whereas Serotonin Syndrome presents with hyperreflexia and myoclonus. * **First Step in Management:** Immediate discontinuation of the offending antipsychotic agent.

Question 225: Which of the following medications is known to cause pancreatitis as a side effect?

A. Valproate (Correct Answer)
B. Clonazepam
C. Clozapine
D. Amisulpride

Explanation: **Explanation:** **Valproate (Sodium Valproate/Valproic Acid)** is a broad-spectrum antiepileptic and mood stabilizer. It is a well-documented, though rare, cause of **drug-induced acute pancreatitis**. The mechanism is thought to involve the depletion of free radical scavengers or the accumulation of toxic metabolites (like 4-pentenoic acid), leading to direct pancreatic acinar cell injury. This side effect is idiosyncratic, meaning it is not necessarily dose-dependent and can occur at any time during treatment. **Analysis of Incorrect Options:** * **Clonazepam:** A benzodiazepine primarily associated with sedation, ataxia, and cognitive impairment. It does not have a known association with pancreatitis. * **Clozapine:** An atypical antipsychotic known for severe side effects like **agranulocytosis**, seizures, and myocarditis. While it can cause metabolic syndrome and hypertriglyceridemia (which is a risk factor for pancreatitis), it is not the primary drug associated with direct pancreatic toxicity in this list. * **Amisulpride:** An atypical antipsychotic (substituted benzamide) mainly associated with **hyperprolactinemia** and extrapyramidal symptoms. It is not linked to pancreatitis. **High-Yield Clinical Pearls for NEET-PG:** * **Valproate Side Effects (Mnemonic: VALPROATE):** **V**omiting, **A**lopecia, **L**iver toxicity (Hepatotoxicity), **P**ancreatitis/PCOS, **R**etention of weight (Obesity), **O**edema, **A**terixis (due to hyperammonemia), **T**eratogenicity (Neural Tube Defects), **E**nzyme inhibitor. * **Monitoring:** If a patient on Valproate develops acute abdominal pain and vomiting, immediate serum **amylase and lipase** levels must be checked. * **Teratogenicity:** Valproate is the most teratogenic antiepileptic, specifically causing **Spina Bifida**.

Question 226: A 25-year-old man with major depression discusses the potential benefits and side effects of various antidepressants with his psychiatrist. He clearly indicates that he does not want a medication that could decrease his libido or interfere with his ability to obtain and maintain an erection. Which of the listed antidepressants would be appropriate for this patient?

A. Bupropion (Correct Answer)
B. Clomipramine
C. Amitriptyline
D. Sertraline

Explanation: **Explanation:** The correct answer is **Bupropion**. Sexual dysfunction (decreased libido, erectile dysfunction, and anorgasmia) is one of the most common reasons for non-compliance with antidepressant therapy. **Why Bupropion is correct:** Bupropion is an **Atypical Antidepressant** that acts as a **Norepinephrine-Dopamine Reuptake Inhibitor (NDRI)**. Unlike most other antidepressants, it does not have significant serotonergic activity. Sexual side effects are primarily mediated by the stimulation of 5-HT2 receptors; since Bupropion lacks this mechanism, it has a "neutral" effect on sexual function and is often used as an alternative or an adjunct to reverse SSRI-induced sexual dysfunction. **Why the other options are incorrect:** * **Sertraline (Option D):** As an **SSRI**, it is the class most frequently associated with sexual dysfunction (up to 60-70% of patients). It increases synaptic serotonin, which inhibits sexual desire and arousal. * **Clomipramine & Amitriptyline (Options B & C):** These are **Tricyclic Antidepressants (TCAs)**. They cause sexual dysfunction through multiple mechanisms, including serotonergic activity and strong anticholinergic effects (which can interfere with the parasympathetic-mediated erectile response). Clomipramine, specifically, is a potent serotonin reuptake inhibitor and has the highest rate of sexual side effects among TCAs. **NEET-PG High-Yield Pearls:** * **Weight Neutrality:** Bupropion is also preferred in patients concerned about weight gain. * **Contraindication:** It must be avoided in patients with **Seizure disorders** or **Eating disorders** (Bulimia/Anorexia) as it lowers the seizure threshold. * **Smoking Cessation:** It is also FDA-approved for smoking cessation. * **Other "Sexually Safe" Antidepressants:** Mirtazapine and Vilazodone.

Question 227: Which of the following psychiatric disorders, apart from depression, are commonly treated with selective serotonin reuptake inhibitors?

A. Phobias
B. Obsessive compulsive disorder
C. Post-traumatic stress disorder
D. All of the above (Correct Answer)

Explanation: **Explanation:** Selective Serotonin Reuptake Inhibitors (SSRIs) are the first-line pharmacological treatment for a wide spectrum of psychiatric conditions beyond Major Depressive Disorder. Their primary mechanism involves inhibiting the presynaptic reuptake of serotonin (5-HT), thereby increasing its availability in the synaptic cleft and modulating downstream neurocircuitry involved in anxiety and impulse control. * **Obsessive-Compulsive Disorder (OCD):** SSRIs (e.g., Fluoxetine, Fluvoxamine, Sertraline) are the gold standard. Note that OCD typically requires **higher doses** of SSRIs and a longer duration (10–12 weeks) to show a clinical response compared to depression. * **Phobias:** SSRIs are highly effective for **Social Anxiety Disorder (Social Phobia)** and Panic Disorder (with or without agoraphobia). They help reduce the limbic system's hypersensitivity to perceived threats. * **Post-Traumatic Stress Disorder (PTSD):** SSRIs (specifically Sertraline and Paroxetine) are FDA-approved first-line agents. They address the core symptoms of intrusive thoughts, avoidance, and hyperarousal. **Why "All of the above" is correct:** Since SSRIs are the first-line treatment for OCD, PTSD, and various Phobias/Anxiety disorders, all listed options are clinically accurate. **High-Yield Clinical Pearls for NEET-PG:** * **First-line for most:** SSRIs are the first-line for Depression, OCD, PTSD, Panic Disorder, GAD, and Bulimia Nervosa (specifically Fluoxetine). * **Side Effects:** Most common acute side effect is **GI upset** (nausea/diarrhea); most common long-term side effect is **sexual dysfunction** (delayed ejaculation). * **Drug of choice for OCD in children:** Sertraline or Fluvoxamine. * **Shortest half-life:** Fluvoxamine; **Longest half-life:** Fluoxetine (least likely to cause discontinuation syndrome).

Question 228: What is the toxic level of lithium?

A. 0.6 mEq/L
B. 1.2 mEq/L
C. 2.6 mEq/L (Correct Answer)
D. <0.6 mEq/L

Explanation: ### Explanation Lithium is a mood stabilizer with a **narrow therapeutic index**, meaning the margin between a therapeutic dose and a toxic dose is very small. Regular Therapeutic Drug Monitoring (TDM) is essential for patient safety. **1. Why Option C (2.6 mEq/L) is Correct:** Lithium toxicity is generally categorized into three levels based on serum concentration: * **Mild to Moderate:** 1.5 – 2.0 mEq/L * **Moderate to Severe:** 2.0 – 2.5 mEq/L * **Life-threatening:** **>2.5 mEq/L** At **2.6 mEq/L**, the patient is in the range of severe toxicity, which can manifest as seizures, coma, cardiac arrhythmias, and permanent neurological damage. Hemodialysis is often indicated when levels exceed 2.5 mEq/L in acute-on-chronic poisoning. **2. Why Other Options are Incorrect:** * **Option A (0.6 mEq/L):** This is the **lower limit** of the therapeutic range for maintenance therapy in Bipolar Disorder. * **Option B (1.2 mEq/L):** This is the **upper limit** of the therapeutic range. Levels between 0.8 and 1.2 mEq/L are typically targeted during acute manic episodes. * **Option D (<0.6 mEq/L):** This is considered a **sub-therapeutic level**, where the drug is unlikely to be effective in preventing mood episodes. **3. 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 Signs of Toxicity:** Coarse tremors (fine tremors are a side effect), vomiting, diarrhea, and ataxia. * **Drug Interactions:** **NSAIDs, Thiazides, and ACE inhibitors** increase lithium levels (by decreasing renal clearance), while high sodium intake or caffeine can decrease levels. * **Ebstein’s Anomaly:** The classic teratogenic risk associated with Lithium use in the first trimester.

Question 229: Which of the following is not a side effect of lithium?

A. Blood dyscrasias (Correct Answer)
B. Polyuria
C. Hypothyroidism
D. Weight gain

Explanation: **Explanation:** Lithium is the gold-standard mood stabilizer for Bipolar Affective Disorder (BPAD), but it has a narrow therapeutic index and a wide range of systemic side effects. **Why Blood Dyscrasias is the Correct Answer:** Lithium does **not** cause blood dyscrasias (like agranulocytosis or aplastic anemia). In fact, it causes the opposite effect: **Leukocytosis** (specifically neutrophilia). It stimulates granulopoiesis in the bone marrow. This is a benign side effect, though it can sometimes be used therapeutically to treat Felty’s syndrome or chemotherapy-induced neutropenia. **Analysis of Incorrect Options:** * **Polyuria:** Lithium inhibits the action of Antidiuretic Hormone (ADH) on the distal tubules, leading to **Nephrogenic Diabetes Insipidus**. This results in polyuria and compensatory polydipsia. * **Hypothyroidism:** Lithium interferes with iodine organification and thyroid hormone release. It is a common cause of goiter and hypothyroidism, necessitating regular TSH monitoring. * **Weight Gain:** This is a very common metabolic side effect of Lithium, often leading to poor patient compliance. **High-Yield Clinical Pearls for NEET-PG:** * **L-I-T-H-I-U-M Mnemonic for Side Effects:** **L**eukocytosis, **I**nsipidus (Diabetes), **T**remors (Fine)/Teratogenicity (Ebstein's Anomaly), **H**ypothyroidism, **I**ncreased Weight, **U**nder-active heart (Sinus bradycardia), **M**others (Pregnancy contraindication). * **Therapeutic Range:** 0.6–1.2 mEq/L (Prophylaxis: 0.6–0.8; Acute Mania: 0.8–1.2). * **Toxicity:** Occurs >1.5 mEq/L; characterized by **coarse tremors**, ataxia, and seizures. * **Drug Interactions:** Thiazides, NSAIDs, and ACE inhibitors increase Lithium levels (Decreased clearance).

Question 230: An appropriate pre-Lithium work-up includes all of the following, EXCEPT?

A. Erythrocyte sedimentation rate (Correct Answer)
B. Serum creatinine
C. Thyroid-stimulating hormone (TSH)
D. Serum electrolytes

Explanation: Lithium is the gold-standard mood stabilizer for Bipolar Affective Disorder (BPAD), but its narrow therapeutic index and multi-organ side effects necessitate a rigorous baseline work-up. **Explanation of the Correct Answer:** **A. Erythrocyte sedimentation rate (ESR):** This is the correct answer because ESR is a non-specific marker of inflammation. Lithium does not affect the inflammatory cascade or connective tissues in a way that requires baseline ESR monitoring. It has no clinical utility in predicting Lithium toxicity or monitoring its side effects. **Explanation of Incorrect Options:** * **B. Serum Creatinine:** Lithium is almost exclusively excreted by the kidneys. Baseline renal function tests (RFTs) are mandatory because pre-existing renal impairment increases the risk of toxicity. Long-term use can also cause nephrogenic diabetes insipidus or interstitial nephritis. * **C. Thyroid-stimulating hormone (TSH):** Lithium inhibits the release of thyroid hormones. It is a common cause of drug-induced hypothyroidism and goiter. Baseline TSH is essential to distinguish pre-existing thyroid dysfunction from Lithium-induced effects. * **D. Serum Electrolytes:** Lithium is handled by the proximal tubule similarly to sodium. Hyponatremia (due to diuretics or dehydration) leads to increased Lithium reabsorption, precipitating toxicity. Baseline levels help monitor this balance. **High-Yield Clinical Pearls for NEET-PG:** * **The "Lithium Checklist":** Before starting, check **RFT** (Creatinine/BUN), **Thyroid** (TSH), **Electrolytes**, **ECG** (for patients >40 or with cardiac history), and **Pregnancy Test** (risk of Ebstein’s Anomaly). * **CBC:** Lithium causes benign **leukocytosis** (increased WBC count), which is a common "trick" question. * **Therapeutic Range:** 0.6–1.2 mEq/L (Prophylaxis: 0.6–0.8; Acute Mania: 0.8–1.2). * **Toxicity:** Usually occurs at levels >1.5 mEq/L. Dialysis is indicated if levels >4.0 mEq/L (acute) or >2.5 mEq/L (chronic with symptoms).

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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