Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 151: A patient with Alzheimer's disease is on rivastigmine therapy and develops symptoms of depression. Which of the following drug classes, if used concurrently, would decrease the efficacy of rivastigmine?

A. Tricyclic antidepressants (TCAs) (Correct Answer)
B. Selective serotonin reuptake inhibitors (SSRIs)
C. Monoamine oxidase inhibitors (MAOIs)
D. Reversible inhibitors of monoamine oxidase A (RIMAs)

Explanation: **Explanation:**1. Why Tricyclic Antidepressants (TCAs) are correct:Rivastigmine is a **cholinesterase inhibitor** used in Alzheimer’s disease to increase synaptic levels of acetylcholine, thereby improving cognitive function [3]. Many TCAs (e.g., Amitriptyline, Imipramine) possess significant **anticholinergic (antimuscarinic) properties** [2]. When used concurrently, TCAs exert a pharmacological antagonism against rivastigmine. By blocking the muscarinic receptors that rivastigmine is trying to stimulate via increased acetylcholine, TCAs directly neutralize the therapeutic efficacy of the Alzheimer's medication and may worsen cognitive decline.2. Why other options are incorrect:* **SSRIs (e.g., Sertraline, Escitalopram):** These are the preferred antidepressants in Alzheimer’s patients because they lack significant anticholinergic activity and do not interfere with the mechanism of cholinesterase inhibitors.* **MAOIs and RIMAs (e.g., Moclobemide):** These drugs act on the metabolism of monoamines (Norepinephrine, Serotonin, Dopamine). They do not possess anticholinergic properties and therefore do not directly decrease the efficacy of rivastigmine.3. High-Yield Clinical Pearls for NEET-PG:* **Rivastigmine Unique Feature:** It is a "pseudo-irreversible" inhibitor of both **Acetylcholinesterase (AChE)** and **Butyrylcholinesterase (BuChE)** [1]. It is also available as a transdermal patch to reduce GI side effects.* **Drugs to Avoid in Dementia:** Always avoid drugs with "atropine-like" effects, including first-generation antihistamines (Diphenhydramine), bladder antispasmodics (Oxybutynin), and TCAs.* **Preferred Antidepressant:** SSRIs are the first-line treatment for depression in patients with dementia due to their favorable side-effect profile.

Question 152: Ebstein's anomaly is a known side effect of which medication?

A. Lithium (Correct Answer)
B. Carbamazepine
C. Valproate
D. Lamotrigine

Explanation: **Explanation:** **Lithium** is the correct answer. It is a classic mood stabilizer used in Bipolar Affective Disorder (BPAD). When taken during the first trimester of pregnancy, Lithium is associated with a specific cardiac teratogenic effect known as **Ebstein’s Anomaly**. This condition involves the "atrialization" of the right ventricle due to the downward displacement of the tricuspid valve leaflets, leading to severe tricuspid regurgitation and right heart failure. While the relative risk is increased, the absolute risk remains low (approx. 1 in 1,000–2,000 exposures). **Why the other options are incorrect:** * **Valproate:** This is the most teratogenic anti-epileptic. It is primarily associated with **Neural Tube Defects (NTDs)** like spina bifida due to interference with folate metabolism. * **Carbamazepine:** Also associated with **Neural Tube Defects** and craniofacial abnormalities (cleft lip/palate), but the risk is lower than with Valproate. * **Lamotrigine:** Generally considered one of the **safest** mood stabilizers/anti-epileptics during pregnancy, with a lower risk of major malformations compared to the others listed. **High-Yield Clinical Pearls for NEET-PG:** * **Therapeutic Index:** Lithium has a narrow therapeutic index (0.6–1.2 mEq/L). Toxicity occurs >1.5 mEq/L. * **L-Lithium, L-Lowering:** Lithium causes downward displacement of the valve (Ebstein's). * **Management:** If a pregnant woman must stay on Lithium, perform a fetal echocardiogram at 18–20 weeks to screen for cardiac defects. * **Other Lithium Side Effects:** Nephrogenic Diabetes Insipidus, Hypothyroidism, and Fine Tremors.

Question 153: Tianeptine acts by which of the following mechanisms?

A. MAO inhibitor
B. Serotonin uptake inhibitor
C. Serotonin uptake enhancer (Correct Answer)
D. 5-HT agonist

Explanation: **Explanation:** **Tianeptine** is a unique antidepressant that defies the traditional "monoamine hypothesis" of depression. While most conventional antidepressants (like SSRIs) work by inhibiting the reuptake of serotonin to increase its synaptic concentration, Tianeptine acts as a **Selective Serotonin Reuptake Enhancer (SSRE)**. It increases the presynaptic uptake of serotonin (5-HT), thereby decreasing 5-HT levels in the synaptic cleft. Despite this paradoxical mechanism, it effectively exerts antidepressant and anxiolytic effects, likely through its downstream modulation of glutamate receptors (NMDA and AMPA) and its role in neuroplasticity. **Analysis of Options:** * **Option A (MAO Inhibitor):** MAOIs (e.g., Phenelzine, Selegiline) prevent the breakdown of monoamines. Tianeptine does not inhibit the Monoamine Oxidase enzyme. * **Option B (Serotonin uptake inhibitor):** This is the mechanism of **SSRIs** (e.g., Fluoxetine, Sertraline). Tianeptine acts in the exact opposite manner by *enhancing* uptake. * **Option D (5-HT agonist):** Drugs like Buspirone (5-HT1A partial agonist) act here. Tianeptine does not have significant direct affinity for serotonin receptors. **High-Yield Clinical Pearls for NEET-PG:** * **Neuroprotection:** Tianeptine is known to prevent stress-induced atrophy of dendrites in the hippocampus. * **Opioid Link:** Recent studies show Tianeptine also acts as a **full agonist at μ-opioid receptors**, which may contribute to its mood-elevating effects. * **Pharmacokinetics:** It is primarily metabolized by the liver (beta-oxidation) rather than the Cytochrome P450 system, leading to fewer drug-drug interactions. * **Side Effects:** Unlike SSRIs, it typically **does not cause sexual dysfunction** or significant sedation.

Question 154: Which of the following psychiatric medications are available as depot preparations?

A. Haloperidol
B. Risperidone
C. Olanzapine
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Depot preparations** are long-acting injectable (LAI) formulations designed to release the drug slowly over weeks or months. They are primarily used in psychiatric practice to improve treatment adherence in patients with chronic conditions like schizophrenia. 1. **Haloperidol (Option A):** This is a typical (first-generation) antipsychotic. It is available as **Haloperidol Decanoate**, administered intramuscularly every 4 weeks. It is one of the most commonly used depot preparations in clinical practice. 2. **Risperidone (Option B):** An atypical (second-generation) antipsychotic available as **Risperidone microspheres**. It is typically administered every 2 weeks. 3. **Olanzapine (Option C):** Also an atypical antipsychotic, it is available as **Olanzapine Pamoate**. While effective, it requires strict monitoring due to the risk of Post-injection Delirium Sedation Syndrome (PDSS). Since all three medications have established long-acting injectable formulations, **Option D (All of the above)** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Depot formulations are usually esterified with long-chain fatty acids (like decanoate or palmitate) in an oil vehicle (sesame or castor oil), slowing absorption from the injection site. * **Other Depot Antipsychotics:** Fluphenazine decanoate, Zuclopenthixol decanoate, and Paliperidone palmitate (available as 1-month and 3-month formulations). * **Aripiprazole** is another atypical antipsychotic frequently asked about that is available as a once-monthly depot. * **Contraindication:** Depot preparations should **never** be given intravenously; they are strictly for deep intramuscular (IM) injection.

Question 155: Which of the following is NOT an atypical antipsychotic?

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

Explanation: **Explanation** Antipsychotics are broadly classified into two categories: **Typical (First Generation)** and **Atypical (Second Generation)**. The primary distinction lies in their mechanism of action and side-effect profile. **Why Thioridazine is the correct answer:** **Thioridazine** is a **Typical Antipsychotic** belonging to the Phenothiazine class (specifically the piperidine subgroup). It acts primarily by blocking **D2 receptors** in the mesolimbic pathway. Unlike atypical agents, it has a higher propensity for causing extrapyramidal symptoms (EPS), though less than haloperidol, and is notorious for its specific side effects like retinal pigmentation and cardiotoxicity. **Why the other options are incorrect:** * **Clozapine:** The prototype atypical antipsychotic. It has a low affinity for D2 receptors and high affinity for D4 and 5-HT2A receptors. It is the gold standard for treatment-resistant schizophrenia. * **Olanzapine:** A common atypical agent associated with significant metabolic side effects like weight gain and hyperglycemia. * **Risperidone:** An atypical antipsychotic that blocks both D2 and 5-HT2A receptors. At higher doses, it is the atypical agent most likely to cause EPS and hyperprolactinemia. **High-Yield Clinical Pearls for NEET-PG:** * **Thioridazine Warning:** It is associated with **QT interval prolongation** (Torsades de pointes) and **retinitis pigmentosa** (if dose >800mg/day). * **Atypical Advantage:** Atypical antipsychotics are preferred because they treat both **positive and negative symptoms** of schizophrenia and have a lower risk of Extrapyramidal Side Effects (EPS). * **Clozapine Monitoring:** Requires mandatory WBC count monitoring due to the risk of **agranulocytosis**. It is also the only antipsychotic proven to reduce suicide risk in schizophrenia.

Question 156: Which of the following statements about extrapyramidal side effects of antipsychotic drugs is FALSE?

A. Caused by blockade of dopamine receptors
B. Less likely to be produced by clozapine than by chlorpromazine
C. Can be countered to some degree by antimuscarinic drugs
D. Haloperidol does not cause extrapyramidal syndrome (Correct Answer)

Explanation: ### Explanation **1. Why Option D is the Correct (False) Statement:** Haloperidol is a **high-potency, first-generation (typical) antipsychotic**. It has a very high affinity for **D2 receptors** in the nigrostriatal pathway. Because it lacks significant intrinsic anticholinergic activity, it is one of the drugs **most likely** to cause severe Extrapyramidal Symptoms (EPS), including acute dystonia, parkinsonism, and akathisia. **2. Analysis of Incorrect Options:** * **Option A (True):** EPS is primarily caused by the blockade of D2 receptors in the **nigrostriatal pathway**. When dopamine is inhibited here, the balance between dopamine and acetylcholine is disrupted, leading to motor symptoms. * **Option B (True):** **Clozapine** is an atypical antipsychotic with low D2 affinity and high 5-HT2A antagonism. It is considered the "gold standard" for having the **lowest risk of EPS**, whereas chlorpromazine (a low-potency typical antipsychotic) has a higher risk, though less than haloperidol. * **Option C (True):** EPS results from a relative **excess of cholinergic activity** due to dopamine blockade. Therefore, centrally acting antimuscarinic drugs (e.g., **Benztropine, Trihexyphenidyl**) are used to restore the neurochemical balance and alleviate symptoms like parkinsonism and dystonia. **3. High-Yield Clinical Pearls for NEET-PG:** * **Acute Dystonia:** Earliest onset (hours); treat with IV/IM anticholinergics. * **Akathisia:** Most common EPS; characterized by motor restlessness; treat with **Beta-blockers (Propranolol)**. * **Tardive Dyskinesia:** Late-onset (months/years); caused by D2 receptor supersensitivity; **anticholinergics worsen it**. * **Drug of Choice for EPS:** Central anticholinergics (Trihexyphenidyl/Benzhexol). * **Atypical Antipsychotics (SGA):** Lower EPS risk because they dissociate rapidly from D2 receptors ("hit and run" hypothesis).

Question 157: Which of the following is NOT a monoamine oxidase (MAO) inhibitor?

A. Tranylcypromine
B. Isocarboxazide
C. Phenelzine
D. Maprotiline (Correct Answer)

Explanation: **Explanation:** The correct answer is **Maprotiline**. **1. Why Maprotiline is the correct answer:** Maprotiline is a **Tetracyclic Antidepressant (TeCA)**, not an MAO inhibitor. Its primary mechanism of action is the selective inhibition of norepinephrine reuptake. It is chemically and pharmacologically similar to Tricyclic Antidepressants (TCAs). It is specifically known for its high selectivity for the norepinephrine transporter (NET) and is often associated with a higher risk of seizures compared to other antidepressants. **2. Why the other options are incorrect:** Options A, B, and C are all classic examples of **Non-selective, Irreversible MAO Inhibitors**. * **Tranylcypromine:** A non-hydrazine MAO inhibitor. It is the most potent agent in this class and has a structure similar to amphetamine. * **Isocarboxazid:** A hydrazine-derivative MAO inhibitor used primarily for treatment-resistant depression. * **Phenelzine:** Another hydrazine-derivative MAO inhibitor. Like the others, it inhibits both MAO-A and MAO-B. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cheese Reaction:** Patients on non-selective MAOIs (like A, B, and C) must avoid tyramine-rich foods (aged cheese, red wine) to prevent a hypertensive crisis. * **Moclobemide:** A **RIMA** (Reversible Inhibitor of MAO-A); it carries a much lower risk of the cheese reaction. * **Selegiline:** A selective **MAO-B inhibitor** used in Parkinson’s disease (at low doses). * **Drug Interaction:** Never combine MAOIs with SSRIs or Pethidine due to the risk of **Serotonin Syndrome**. A washout period of 14 days is typically required when switching between these classes.

Question 158: Which drug, when given to a patient with alcohol dependence, can cause an adverse drug reaction if the patient consumes alcohol due to a drug interaction?

A. Disulfiram (Correct Answer)
B. Acamprosate
C. Naloxone
D. Naltrexone

Explanation: **Explanation:** The correct answer is **Disulfiram**. This drug is used as **Aversion Therapy** in alcohol dependence. **1. Why Disulfiram is correct:** Disulfiram inhibits the enzyme **Aldehyde Dehydrogenase (ALDH)**. Normally, alcohol is metabolized into Acetaldehyde, which ALDH then converts into Acetic Acid. By blocking ALDH, Disulfiram causes a toxic accumulation of **Acetaldehyde** in the blood if alcohol is consumed. This leads to the **Disulfiram-Ethanol Reaction (DER)**, characterized by flushing, throbbing headache, nausea, vomiting, tachycardia, and hypotension. The fear of this unpleasant reaction deters the patient from drinking. **2. Why other options are incorrect:** * **Acamprosate:** It is an NMDA receptor antagonist used to maintain abstinence by reducing "protracted withdrawal" symptoms (craving). It does not cause a reaction with alcohol. * **Naltrexone:** An opioid antagonist that reduces the "reward" or euphoria associated with drinking by blocking mu-opioid receptors. It is the drug of choice for reducing cravings but has no interaction reaction. * **Naloxone:** An intravenous opioid antagonist used primarily for acute opioid overdose, not for the long-term management of alcohol dependence. **Clinical Pearls for NEET-PG:** * **Drug of Choice for Alcohol Withdrawal:** Benzodiazepines (e.g., Chlordiazepoxide, Diazepam). * **Drug of Choice to Reduce Craving:** Naltrexone. * **Other drugs causing Disulfiram-like reactions:** Metronidazole (most common), Cefotetan, Cefoperazone, Chlorpropamide, and Griseofulvin. * **Contraindication:** Disulfiram should never be administered if the patient has consumed alcohol within the last 12 hours or is in a state of intoxication.

Question 159: True regarding bupropion is?

A. Dopamine reuptake stimulator
B. It is an antianxiety drug
C. No precipitation of seizures
D. Nicotinic receptor antagonist (Correct Answer)

Explanation: **Explanation:** **Bupropion** is an atypical antidepressant with a unique mechanism of action compared to SSRIs or TCAs. 1. **Why Option D is correct:** Bupropion acts as a **non-competitive antagonist at nicotinic acetylcholine receptors (nAChR)**. This specific action is responsible for its effectiveness in **smoking cessation**, as it reduces the rewarding effects of nicotine and minimizes withdrawal symptoms. 2. **Why other options are incorrect:** * **Option A:** Bupropion is a **Dopamine and Norepinephrine Reuptake Inhibitor (DNRI)**, not a stimulator. It increases the synaptic concentration of these neurotransmitters. * **Option B:** Bupropion is primarily an **antidepressant**. Unlike SSRIs, it is generally not effective for anxiety disorders and may occasionally worsen anxiety or agitation due to its stimulating properties. * **Option C:** Bupropion is notorious for **lowering the seizure threshold**. It is contraindicated in patients with seizure disorders, eating disorders (bulimia/anorexia), or those undergoing alcohol withdrawal. **High-Yield Clinical Pearls for NEET-PG:** * **Sexual Dysfunction:** Unlike SSRIs, Bupropion does **not** cause sexual dysfunction or weight gain, making it a preferred choice for patients concerned about these side effects. * **Smoking Cessation:** It is FDA-approved for smoking cessation (often marketed as Zyban). * **Contraindications:** Always avoid in patients with a history of seizures or head injury. * **Active Metabolite:** Hydroxybupropion is its major active metabolite.

Question 160: Absolute contraindication to lithium therapy is:

A. Pregnancy (Correct Answer)
B. Angioma
C. Glaucoma
D. Epilepsy

Explanation: **Explanation:** **1. Why Pregnancy is the Correct Answer:** Lithium is a known **teratogen** and is classified under FDA Pregnancy Category D. Its use during the first trimester is strongly associated with **Ebstein’s Anomaly**, a congenital cardiac defect characterized by the downward displacement of the tricuspid valve into the right ventricle ("atrialization" of the ventricle). While some modern guidelines suggest lithium can be used in severe refractory cases with close monitoring, for the purpose of NEET-PG, it remains an absolute contraindication in early pregnancy due to this specific morphological risk. **2. Analysis of Incorrect Options:** * **Angioma:** There is no clinical or pharmacological correlation between lithium therapy and the progression or occurrence of angiomas. * **Glaucoma:** Unlike Tricyclic Antidepressants (TCAs) or Antipsychotics with anticholinergic properties, lithium does not affect intraocular pressure and is safe to use in glaucoma patients. * **Epilepsy:** Lithium is not contraindicated in epilepsy. In fact, it can sometimes be used in patients with comorbid mood disorders, though caution is required as lithium toxicity can lower the seizure threshold. **3. High-Yield Clinical Pearls for NEET-PG:** * **Therapeutic Index:** Lithium has a narrow therapeutic index (0.6–1.2 mEq/L). Toxicity starts >1.5 mEq/L. * **Renal Function:** Since lithium is excreted 100% by the kidneys, **Renal Failure** is a major contraindication. * **Drug Interactions:** Thiazides, NSAIDs, and ACE inhibitors increase lithium levels (decreasing clearance), leading to toxicity. * **Side Effects:** Remember the mnemonic **LITHIUM**: **L**eukocytosis, **I**nsipidus (Diabetes Insipidus), **T**remors/Teratogenicity, **H**ypothyroidism, **I**ncreased Weight, **U**nderactive heart (Sinus node dysfunction), **M**others (Ebstein’s).

Practice by Chapter

Antipsychotics: Typical and Atypical

Practice Questions

Antidepressants: SSRIs and SNRIs

Practice Questions

Tricyclic Antidepressants

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MAO Inhibitors

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Mood Stabilizers

Practice Questions

Anxiolytics

Practice Questions

Drugs for ADHD

Practice Questions

Drugs for Sleep Disorders

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Drugs for Dementia

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Drug-Induced Psychiatric Symptoms

Practice Questions

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