Psychopharmacology Practice Questions

Q: Hyperthermia is seen in:

Malignant neuroleptic syndrome. **Explanation:** **Neuroleptic Malignant Syndrome (NMS)** is a life-threatening idiosyncratic reaction to antipsychotic drugs (neuroleptics). It is characterized by a "tetrad" of clinical features: **Hyperthermia** (often >38°C), severe muscular "lead-pipe" rigidity, autonomic instability (tachycardia, hypertension), and altered mental status. The underlying pathophysiology involves massive dopamine blockade in the hypothalamus (disrupting thermoregulation) and the basal ganglia (causing rigidity and secondary heat production). **Analysis of Incorrect Options:** * **Cannabis Poisoning:** Typically presents with tachycardia, conjunctival injection, increased appetite, and dry mouth. It does not cause significant hyperthermia. * **Opium Intoxication:** Characterized by the "Opioid Triad" of CNS depression (coma), miosis (pinpoint pupils), and respiratory depression. It typically causes **hypothermia**, not hyperthermia. * **Hypothyroidism:** Leads to a generalized slowing of metabolic processes, resulting in **hypothermia** and cold intolerance. Hyperthermia is instead a hallmark of Hyperthyroidism (Thyroid Storm). **Clinical Pearls for NEET-PG:** * **Key Lab Finding:** Elevated **Creatine Phosphokinase (CPK)** levels due to muscle rigidity and rhabdomyolysis. * **Treatment of Choice:** Immediate cessation of the offending agent, supportive care, and pharmacotherapy with **Dantrolene** (muscle relaxant) or **Bromocriptine** (dopamine agonist). * **Differential Diagnosis:** Distinguish NMS from **Serotonin Syndrome**, which presents with hyperreflexia and myoclonus rather than lead-pipe rigidity.

Q: Which of the following antidepressants is also known by the brand name Zyban?

Bupropion. **Explanation:** **Bupropion (Option B)** is the correct answer. It is a unique antidepressant that acts as a **Norepinephrine-Dopamine Reuptake Inhibitor (NDRI)**. It is marketed under two primary brand names: **Wellbutrin** (for Major Depressive Disorder) and **Zyban** (specifically indicated as an aid for **smoking cessation**). By increasing dopamine levels in the reward pathway, it helps reduce nicotine cravings and withdrawal symptoms. **Analysis of Incorrect Options:** * **Amitriptyline (Option A):** A classic Tricyclic Antidepressant (TCA). Common brand names include Elavil and Tryptomer. It is primarily used for depression, neuropathic pain, and migraine prophylaxis. * **Fluoxetine (Option C):** A prototype Selective Serotonin Reuptake Inhibitor (SSRI). Its most famous brand name is **Prozac**. It is known for its long half-life and active metabolite (norfluoxetine). * **Mianserin (Option D):** A tetracyclic antidepressant (TeCA) that acts as an alpha-2 antagonist. It is less commonly used today due to the risk of agranulocytosis. **High-Yield Clinical Pearls for NEET-PG:** 1. **Seizure Risk:** Bupropion is contraindicated in patients with **epilepsy** or **eating disorders** (bulimia/anorexia) as it lowers the seizure threshold. 2. **Sexual Dysfunction:** Unlike SSRIs, Bupropion does **not** cause sexual dysfunction or significant weight gain, making it a preferred choice for patients concerned about these side effects. 3. **ADHD:** It is sometimes used off-label for ADHD due to its effect on dopamine and norepinephrine. 4. **Mechanism:** It lacks significant activity at serotonin receptors, which explains its unique side effect profile.

Q: What is the treatment modality used for phobias?

All of the above. The treatment of phobias (Specific Phobia, Social Anxiety Disorder, and Agoraphobia) requires a multimodal approach involving psychological and pharmacological interventions. **1. Why "All of the above" is correct:** * **Behavior Therapy (Option B):** This is the **treatment of choice** for Specific Phobias. Techniques like **Systematic Desensitization** (gradual exposure) and **Flooding** (direct, intense exposure) are highly effective in extinguishing the fear response. * **Psychotherapy (Option A):** Cognitive Behavioral Therapy (CBT) is the gold standard for Social Anxiety Disorder (Social Phobia). It helps patients restructure irrational thought patterns and develop coping mechanisms. * **SSRI (Option C):** Selective Serotonin Reuptake Inhibitors (e.g., Escitalopram, Sertraline) are the **first-line pharmacological treatment**, particularly for Social Anxiety Disorder and Agoraphobia, to manage the underlying anxiety and prevent panic attacks. **2. Clinical Pearls for NEET-PG:** * **Specific Phobia:** Behavior therapy (Exposure therapy) is superior to medication. * **Social Phobia (Social Anxiety Disorder):** CBT + SSRIs is the most effective combination. * **Performance Anxiety (Stage Fright):** **Propranolol** (Beta-blocker) is the drug of choice, taken 30–60 minutes before the event to control peripheral autonomic symptoms (tremors, palpitations). * **Benzodiazepines:** Used only for short-term "as-needed" relief (e.g., a patient with a fear of flying taking Alprazolam before a flight). **Summary:** While behavior therapy is the most specific intervention for the phobic stimulus itself, a comprehensive management plan often integrates psychotherapy and SSRIs to achieve long-term remission.

Q: Which of the following is an antiepileptic drug but NOT a mood stabilizer?

Leviracetam. **Explanation:** In psychiatric practice, while many antiepileptic drugs (AEDs) are used as **mood stabilizers** to treat Bipolar Affective Disorder (BPAD), not all anticonvulsants possess mood-stabilizing properties. **Why Levetiracetam is the correct answer:** Levetiracetam is a highly effective broad-spectrum antiepileptic that acts by binding to the synaptic vesicle protein **SV2A**. Despite its efficacy in neurology, clinical trials have consistently shown that it lacks efficacy as a mood stabilizer. In fact, in psychiatry, it is notorious for causing **behavioral side effects**, including irritability, aggression, and "levetiracetam-induced rage," which can worsen mood instability. **Analysis of Incorrect Options:** * **Sodium Valproate:** The "gold standard" for treating **acute mania** and mixed episodes. It acts by increasing GABA levels and inhibiting sodium channels. * **Lamotrigine:** A first-line mood stabilizer specifically used for the **maintenance phase** of Bipolar Disorder and the prevention of **bipolar depression**. It is not effective for acute mania. * **Topiramate:** While its status as a primary mood stabilizer is debated due to weaker evidence compared to Valproate, it is clinically classified and used as an **adjunctive mood stabilizer**, particularly when weight loss is desired (as it causes weight loss, unlike Valproate). **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC) for Acute Mania:** Sodium Valproate or Lithium. * **DOC for Bipolar Depression:** Quetiapine, Lurasidone, or Lamotrigine. * **Teratogenicity:** Valproate is associated with **Neural Tube Defects** (highest risk among AEDs). * **Lamotrigine Warning:** Must be titrated slowly to avoid **Stevens-Johnson Syndrome (SJS)**. * **Gabapentin & Tiagabine:** Like Levetiracetam, these are AEDs that are **NOT** effective mood stabilizers.

Q: Which of the following is a symptom of neuroleptic malignant syndrome?

Catatonia and stupor. **Explanation:** **Neuroleptic Malignant Syndrome (NMS)** is a rare but life-threatening idiosyncratic reaction to antipsychotic medications (neuroleptics), primarily caused by potent dopamine (D2) receptor blockade in the nigrostriatal pathway and hypothalamus. **Why Option D is Correct:** The clinical hallmark of NMS is a tetrad of symptoms: **Hyperpyrexia (fever), Muscle Rigidity ("Lead-pipe" type), Autonomic Instability, and Altered Mental Status.** Mental status changes often manifest as **catatonia, stupor,** or mutism, progressing to coma. The profound rigidity and dopamine depletion lead to the catatonic state, making it a classic diagnostic feature. **Why Other Options are Incorrect:** * **A. Hypotension:** NMS is characterized by **Autonomic Instability**, which typically manifests as **Hypertension** and tachycardia, rather than hypotension. * **B. Hypothermia:** NMS causes severe **Hyperthermia** (often >38°C/100.4°F) due to hypothalamic dopamine blockade affecting thermoregulation. * **C. Increased magnesium:** There is no clinical association between NMS and hypermagnesemia. However, NMS is classically associated with **increased Creatine Phosphokinase (CPK)** levels due to muscle necrosis (rhabdomyolysis) and **Leukocytosis**. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause:** Haloperidol (High-potency typical antipsychotics). * **Key Lab Finding:** Elevated CPK (most sensitive) and Myoglobinuria (can lead to renal failure). * **Treatment:** 1. Immediate **Discontinuation** of the offending agent (Most important step). 2. Supportive care (cooling, hydration). 3. Pharmacotherapy: **Dantrolene** (muscle relaxant) or **Bromocriptine** (dopamine agonist). * **Differential Diagnosis:** Serotonin Syndrome (presents with *hyperreflexia* and *clonus*, whereas NMS presents with *rigidity* and *hyporeflexia*).

Q: A schizophrenic patient on antipsychotic drugs may develop which of the following side effects?

Increased prolactin. **Explanation:** The correct answer is **B. Increased prolactin**. **Mechanism of Action:** Antipsychotic drugs (especially typical antipsychotics like Haloperidol and certain atypicals like Risperidone) work by blocking **D2 receptors** in the brain. Prolactin secretion is regulated by the **Tuberoinfundibular pathway**, where dopamine normally acts as a "Prolactin Inhibiting Factor" (PIF). By blocking D2 receptors in this pathway, antipsychotics remove the inhibitory effect of dopamine, leading to **hyperprolactinemia**. **Analysis of Incorrect Options:** * **A. Decreased prolactin:** This is incorrect because dopamine blockade increases prolactin levels. Dopamine agonists (like Bromocriptine) would decrease prolactin. * **C. Hypertension:** Most antipsychotics actually cause **orthostatic hypotension** due to alpha-1 adrenergic receptor blockade, rather than hypertension. * **D. Wakefulness:** Antipsychotics generally cause **sedation** and somnolence due to their antihistaminic (H1 blockade) and anti-adrenergic properties. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Features of Hyperprolactinemia:** In females, it leads to galactorrhea, amenorrhea, and infertility. In males, it causes gynecomastia, decreased libido, and erectile dysfunction. * **Drug Exception:** **Aripiprazole** (a D2 partial agonist) is unique because it can actually lower prolactin levels or remain prolactin-neutral. * **Quetiapine and Clozapine** are the atypical antipsychotics with the lowest risk of causing hyperprolactinemia ("prolactin-sparing"). * **Tuberoinfundibular Pathway:** Remember this specific dopaminergic pathway for exams, as it is the site responsible for endocrine side effects.

Q: What is the drug treatment for tardive dyskinesia?

Valbenazine. **Explanation:** **Tardive Dyskinesia (TD)** is a late-onset extrapyramidal side effect caused by long-term use of dopamine receptor blockers (antipsychotics). It is characterized by involuntary, repetitive movements, most commonly orofacial dyskinesia. **Why Valbenazine is correct:** The pathophysiology of TD involves dopamine receptor supersensitivity. **Valbenazine** is a highly selective **Vesicular Monoamine Transporter 2 (VMAT2) inhibitor**. By inhibiting VMAT2, it prevents the packaging of dopamine into presynaptic vesicles, thereby reducing synaptic dopamine release and alleviating the hyperkinetic movements of TD. It is FDA-approved specifically for this condition and is preferred over older agents due to its once-daily dosing and better side-effect profile. **Analysis of Incorrect Options:** * **Ropinirole:** A dopamine agonist used in Parkinson’s disease and Restless Leg Syndrome. It would likely worsen TD by further stimulating supersensitive dopamine receptors. * **Tetrabenazine:** While also a VMAT2 inhibitor, it is primarily used for Huntington’s Chorea. It has a shorter half-life and a higher risk of causing depression and parkinsonism compared to Valbenazine. (Note: While sometimes used off-label for TD, Valbenazine is the more specific, modern answer). * **Biperiden:** An anticholinergic used to treat *acute* dystonia and drug-induced parkinsonism. Anticholinergics are **contraindicated** in TD as they can worsen the symptoms. **NEET-PG High-Yield Pearls:** * **First step in management:** Gradually taper/discontinue the offending antipsychotic or switch to **Clozapine** (the antipsychotic with the lowest risk of TD). * **VMAT2 Inhibitors:** Valbenazine and Deutetrabenazine are the first-line FDA-approved treatments. * **Risk Factor:** Elderly females are at the highest risk for developing TD.

Q: Symptoms of Neuroleptic Malignant Syndrome (NMS) are all of the following except?

Hypothermia. **Explanation:** Neuroleptic Malignant Syndrome (NMS) is a life-threatening idiosyncratic reaction to antipsychotic medications (neuroleptics), primarily caused by potent dopamine (D2) receptor blockade in the nigrostriatal pathway and hypothalamus. **Why Hypothermia is the Correct Answer:** NMS is characterized by **Hyperthermia** (fever), not hypothermia. The blockade of dopamine receptors in the hypothalamus disrupts the body's thermoregulatory set-point, leading to severe pyrexia (often >38°C/100.4°F). Therefore, Option B is the "except" statement. **Analysis of Incorrect Options:** * **Confusion (A):** Altered mental status is a hallmark of NMS. It typically manifests as delirium, confusion, agitation, or even coma. * **Diaphoresis (C):** Autonomic instability is a core feature. Profuse sweating (diaphoresis) occurs alongside tachycardia and tachypnea. * **Hypertension (D):** Autonomic dysfunction also leads to labile blood pressure, most commonly presenting as hypertension. **High-Yield Clinical Pearls for NEET-PG:** * **The "Tetrad" of NMS:** 1. Hyperthermia, 2. "Lead-pipe" rigidity, 3. Autonomic instability, 4. Altered mental status. * **Key Lab Finding:** Significantly elevated **Creatine Phosphokinase (CPK)** levels due to muscle rigidity and rhabdomyolysis. * **Treatment:** 1. Immediate discontinuation of the offending antipsychotic. 2. Supportive care (cooling, hydration). 3. Pharmacotherapy: **Dantrolene** (muscle relaxant) or **Bromocriptine** (dopamine agonist). * **NMS vs. Serotonin Syndrome:** NMS features "Lead-pipe" rigidity and bradyreflexia, whereas Serotonin Syndrome features hyperreflexia and myoclonus.

Q: What is the most effective treatment for psychosis induced by levodopa?

Quetiapine. **Explanation:** The management of psychosis in Parkinson’s Disease (PD) is clinically challenging because traditional antipsychotics block dopamine (D2) receptors, which significantly worsens motor symptoms (rigidity and tremors). **Why Quetiapine is the correct answer:** Quetiapine is considered a first-line treatment for levodopa-induced psychosis because it has a **low affinity for D2 receptors** and a rapid dissociation rate. This allows it to treat psychotic symptoms (hallucinations and delusions) without significantly exacerbating the underlying motor deficits of Parkinson’s disease. While **Clozapine** is technically the most effective drug, it is often reserved for refractory cases due to the risk of agranulocytosis and the need for mandatory blood monitoring. Therefore, Quetiapine is the preferred practical choice in clinical practice and exams. **Why the other options are incorrect:** * **Chlorpromazine (Option B):** A typical antipsychotic with significant D2 blockade and sedative properties; it would severely worsen Parkinsonian motor symptoms. * **Trifluoperazine (Option C):** A high-potency typical antipsychotic that carries a very high risk of Extrapyramidal Side Effects (EPS). * **Haloperidol (Option D):** A potent D2 antagonist. It is strictly contraindicated in Parkinson’s disease as it can lead to acute worsening of motor function and potentially trigger a "frozen" state. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug of Choice:** Clozapine is the "Gold Standard," but **Quetiapine** is the most commonly used first-line agent. 2. **Pimavanserin:** A newer, FDA-approved drug for PD-psychosis that acts as a selective serotonin inverse agonist (5-HT2A) without any D2 blockade. 3. **Management Strategy:** Always attempt to reduce the dose of anti-Parkinsonian drugs (starting with anticholinergics, then amantadine, then dopamine agonists) before adding an antipsychotic.

Q: All of the following are serotonin-dopamine antagonists except?

Loxapine. **Explanation:** The term **Serotonin-Dopamine Antagonists (SDAs)** refers to **Atypical (Second-Generation) Antipsychotics**. These drugs are characterized by their ability to block both Serotonin (5-HT2A) and Dopamine (D2) receptors, which helps reduce extrapyramidal side effects (EPS) and improve negative symptoms of schizophrenia. **1. Why Loxapine is the correct answer:** Loxapine is traditionally classified as a **Typical (First-Generation) Antipsychotic** belonging to the dibenzoxazepine class. While it does show some 5-HT2A antagonism, its clinical profile and high affinity for D2 receptors align it more closely with typical antipsychotics. Note: Its inhaled form (Adasuve) is used for acute agitation, but it remains the "odd one out" compared to the newer SDAs listed. **2. Analysis of incorrect options:** * **Zotepine:** This is an atypical antipsychotic (SDA) that also inhibits norepinephrine reuptake. It is known for its efficacy but carries a higher risk of seizures. * **Sertindole:** This is a potent SDA (atypical antipsychotic). It is highly selective for limbic areas but is used with caution due to its potential for significant **QT interval prolongation**. **NEET-PG High-Yield Pearls:** * **Mnemonic for SDAs:** "Old Air" (**O**lanzapine, **L**urasidone, **D**onepezil—*wait, no*—**D**onepezil is for Alzheimer's; use **R**isperidone, **Q**uetiapine, **A**ripiprazole, **I**loperidone, **R**isperidone). * **Clozapine:** The first SDA/Atypical antipsychotic; gold standard for treatment-resistant schizophrenia but requires monitoring for **agranulocytosis**. * **Aripiprazole:** Often called a "Dopamine system stabilizer" because it is a **partial agonist** at D2 receptors, unlike most SDAs which are pure antagonists. * **Loxapine Metabolism:** It is metabolized into **Amoxapine**, which is used as an antidepressant.

Question 1

Hyperthermia is seen in:

Accepted Answer

Malignant neuroleptic syndrome

Answer

Cannabis poisoning

Answer

Opium intoxication

Answer

Hypothyroidism

Question 2

Which of the following antidepressants is also known by the brand name Zyban?

Accepted Answer

Bupropion

Answer

Amitriptyline

Answer

Fluoxetine

Answer

Mianserin

Question 3

What is the treatment modality used for phobias?

Accepted Answer

All of the above

Answer

Psychotherapy

Answer

Behavior therapy

Answer

SSRI

Question 4

Which of the following is an antiepileptic drug but NOT a mood stabilizer?

Accepted Answer

Leviracetam

Answer

Topiramate

Answer

Lamotrigine

Answer

Sodium valproate

Question 5

Which of the following is a symptom of neuroleptic malignant syndrome?

Accepted Answer

Catatonia and stupor

Answer

Hypotension

Answer

Hypothermia

Answer

Increased magnesium level in blood

Question 6

A schizophrenic patient on antipsychotic drugs may develop which of the following side effects?

Accepted Answer

Increased prolactin

Answer

Decreased prolactin

Answer

Hypertension

Answer

Wakefulness

Question 7

What is the drug treatment for tardive dyskinesia?

Accepted Answer

Valbenazine

Answer

Ropinirole

Answer

Tetrabenazine

Answer

Biperiden

Question 8

Symptoms of Neuroleptic Malignant Syndrome (NMS) are all of the following except?

Accepted Answer

Hypothermia

Answer

Confusion

Answer

Diaphoresis

Answer

Hypertension

Question 9

What is the most effective treatment for psychosis induced by levodopa?

Accepted Answer

Quetiapine

Answer

Chlorpromazine

Answer

Trifluoperazine

Answer

Haloperidol

Question 10

All of the following are serotonin-dopamine antagonists except?

Accepted Answer

Loxapine

Answer

Zotepine

Answer

Seindole

Answer

All

Psychopharmacology — MCQs

Psychopharmacology — MCQs

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