Drugs in Psychiatric Disorders Practice Questions

Q: Which drug possesses antidepressant and antipsychotic properties?

Amoxapine. **Explanation:** **Amoxapine** is a tetracyclic antidepressant (TeCA) and a metabolite of the antipsychotic drug loxapine. It is unique because it exhibits a dual pharmacological profile: 1. **Antidepressant Action:** It inhibits the reuptake of Norepinephrine (and to a lesser extent, Serotonin), similar to Tricyclic Antidepressants (TCAs). 2. **Antipsychotic Action:** Unlike other antidepressants, Amoxapine possesses significant **Postsynaptic Dopamine (D2) receptor blockade** activity. This makes it the drug of choice for **Psychotic Depression** (Major Depressive Disorder with psychotic features). **Analysis of Incorrect Options:** * **A. Buspirone:** An azapirone derivative used as a non-benzodiazepine anxiolytic. It acts as a selective 5-HT1A partial agonist. It does not have antipsychotic properties. * **C. Trazodone:** A SARI (Serotonin Antagonist and Reuptake Inhibitor). It is primarily used for depression with insomnia due to its highly sedative nature, but it lacks D2 blocking (antipsychotic) activity. * **D. Mianserine:** A tetracyclic compound that acts as an alpha-2 blocker. While it is an antidepressant, it does not possess significant D2 receptor antagonism. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** Because of its D2 blocking property, Amoxapine can cause **Extrapyramidal Side Effects (EPS)**, such as parkinsonism or tardive dyskinesia, and hyperprolactinemia—side effects typically associated with antipsychotics rather than antidepressants. * **Drug of Choice:** Always consider Amoxapine for "Psychotic Depression." * **Seizure Risk:** Like other tetracyclics, Amoxapine carries a risk of seizures in overdose.

Q: Which of the following is a non-selective MAO inhibitor?

Isocarboxazid. **Explanation:** Monoamine oxidase (MAO) inhibitors are classified based on their selectivity for the two isoforms of the enzyme: **MAO-A** (which degrades serotonin, norepinephrine, and melatonin) and **MAO-B** (which degrades dopamine). **1. Why Isocarboxazid is correct:** **Isocarboxazid** is a hydrazine derivative that acts as a **non-selective, irreversible MAO inhibitor**. It inhibits both MAO-A and MAO-B enzymes. Because it inhibits MAO-A, it carries a high risk of the "Cheese Reaction" (hypertensive crisis) when taken with tyramine-rich foods, as it prevents the breakdown of dietary tyramine. Other drugs in this class include Phenelzine and Tranylcypromine. **2. Analysis of Incorrect Options:** * **Moclobemide:** This is a **RIMA** (Reversible Inhibitor of MAO-A). It is selective for MAO-A and its reversible nature makes it safer regarding dietary tyramine interactions. * **Selegiline:** This is a **selective, irreversible MAO-B inhibitor** (at low doses). It is primarily used in Parkinson’s disease to increase dopamine levels. At higher doses, it loses selectivity and can inhibit MAO-A. * **Rasagiline:** Similar to Selegiline, this is a potent, **selective, irreversible MAO-B inhibitor** used in the management of Parkinson’s disease. **High-Yield Clinical Pearls for NEET-PG:** * **Cheese Reaction:** Occurs with non-selective MAOIs due to displacement of Norepinephrine by tyramine. Treatment of choice: **Phentolamine** (Alpha-blocker). * **Serotonin Syndrome:** A dangerous interaction when MAOIs are combined with SSRIs or Pethidine. * **Washout Period:** When switching from an MAOI to an SSRI (or vice versa), a gap of at least **14 days** is required to allow for enzyme regeneration.

Q: Akathisia is most commonly seen with the use of which of the following medications?

Haloperidol. **Explanation:** **1. Why Haloperidol is the Correct Answer:** Akathisia is a common **Extrapyramidal Side Effect (EPS)** characterized by a subjective feeling of inner restlessness and an inability to sit still [2]. It is most frequently associated with **First-Generation Antipsychotics (Typical Antipsychotics)** like **Haloperidol** [1]. The underlying mechanism is the potent, non-selective blockade of **Dopamine D2 receptors** in the nigrostriatal pathway. High-potency neuroleptics like Haloperidol have a high affinity for these receptors, making them the most common culprits for EPS, including akathisia, dystonia, and parkinsonism [1]. **2. Why the Other Options are Incorrect:** * **A. Clozapine:** This is an atypical (Second-Generation) antipsychotic. It has a low affinity for D2 receptors and a higher affinity for 5-HT2A receptors. It is specifically known for having the **lowest risk of EPS** among antipsychotics. * **B. Propranolol:** This is a non-selective beta-blocker. It is actually the **drug of choice (DOC) for treating akathisia**, not a cause of it [1]. * **C. Benztropine:** This is a centrally acting anticholinergic drug. It is used to treat acute dystonia and drug-induced parkinsonism. While it can be used in akathisia, it is generally less effective than beta-blockers. **3. High-Yield Clinical Pearls for NEET-PG:** * **Management of Akathisia:** First-line treatment is **Propranolol**. Benzodiazepines (like Diazepam) are second-line [1]. * **Timeline of EPS:** 1. **Acute Dystonia:** Hours to days (DOC: Promethazine or Benztropine). 2. **Akathisia:** Days to weeks (DOC: Propranolol). 3. **Parkinsonism:** Weeks to months (DOC: Benztropine). 4. **Tardive Dyskinesia:** Months to years (DOC: Valbenazine/Deutetrabenazine; *Note: Anticholinergics worsen this*). * **Clozapine Warning:** Always monitor for **agranulocytosis** (absolute neutrophil count) and seizures.

Q: Which of the following effects is unlikely to occur during treatment with imipramine?

Elevation of seizure threshold. **Explanation:** **Imipramine** is a prototype **Tricyclic Antidepressant (TCA)**. Understanding its pharmacological profile is crucial for NEET-PG, as it involves multiple receptor systems. **Why Option A is the correct answer:** Imipramine, like most TCAs and antipsychotics, **lowers the seizure threshold** rather than elevating it. This means it makes the brain more susceptible to seizures, especially in patients with pre-existing epilepsy or in overdose situations. Therefore, "elevation of seizure threshold" is the incorrect statement regarding its effects. **Analysis of Incorrect Options:** * **B. Mydriasis:** TCAs have potent **anticholinergic (muscarinic blockade)** properties. This leads to pupillary dilation (mydriasis), blurred vision, and can potentially precipitate narrow-angle glaucoma. * **C. Sedation:** Imipramine possesses **H1-antihistaminic** properties. Sedation is a common side effect, particularly during the initiation of therapy. * **D. Urinary Retention:** This is another manifestation of its **anticholinergic** action (detrusor relaxation and sphincter contraction). It is a significant concern in elderly patients with prostatic hypertrophy. **High-Yield Clinical Pearls for NEET-PG:** 1. **Mechanism of Action:** TCAs inhibit the reuptake of Norepinephrine (NE) and Serotonin (5-HT). 2. **The "3 Cs" of TCA Toxicity:** Coma, Convulsions (due to lowered seizure threshold), and Cardiotoxicity (arrhythmias due to sodium channel blockade). 3. **ECG Changes:** TCA overdose characteristically shows **QRS widening** and QT prolongation. 4. **Specific Use:** Imipramine is a first-line drug for **Nocturnal Enuresis** in children (due to its anticholinergic effect and alteration of sleep patterns).

Q: Antipsychotic drugs primarily act through blockade of which of the following receptors?

Dopamine D2 receptor. **Explanation:** The therapeutic efficacy of antipsychotic drugs (neuroleptics) is primarily attributed to the **blockade of Dopamine D2 receptors** in the mesolimbic and mesocortical pathways of the brain. This is known as the **Dopamine Hypothesis of Schizophrenia**, which suggests that overactivity of dopamine in these regions leads to positive symptoms like hallucinations and delusions. * **Dopamine D2 receptor (Correct):** All conventional (typical) antipsychotics, such as Haloperidol and Chlorpromazine, are potent D2 antagonists. Their clinical potency is directly proportional to their affinity for the D2 receptor. Even atypical antipsychotics (e.g., Risperidone) maintain a degree of D2 blockade alongside serotonin (5-HT2A) antagonism. * **Dopamine D1 receptor:** While some drugs (like Phenothiazines) may show minor binding to D1, it is not the primary mechanism for antipsychotic action. * **Dopamine D3 receptor:** These receptors are located mainly in the limbic system. While some newer drugs like Cariprazine act here, D3 blockade is not the "primary" mechanism for the class as a whole. * **Dopamine D4 receptor:** This receptor gained interest because **Clozapine** has a high affinity for it. However, selective D4 antagonists have failed to show antipsychotic efficacy in clinical trials, confirming that D2 remains the essential target. **High-Yield Clinical Pearls for NEET-PG:** 1. **Nigrostriatal Pathway:** Blockade of D2 receptors here leads to **Extrapyramidal Side Effects (EPS)**. 2. **Tuberoinfundibular Pathway:** D2 blockade here causes **Hyperprolactinemia** (galactorrhea, gynecomastia). 3. **Threshold:** Antipsychotic effects typically require **60-80%** D2 receptor occupancy; exceeding 80% significantly increases the risk of EPS.

Q: Which of the following is a non-sedating antidepressant?

Fluoxetine. Fluoxetine is a **Selective Serotonin Reuptake Inhibitor (SSRI)**. Unlike older antidepressants, SSRIs have minimal affinity for histamine ($H_1$), atarget="_blank" href="https://www.ncbi.nlm.nih.gov/books/NBK538466/" alpha-adrenergic, and muscarinic receptors. The lack of $H_1$ receptor blockade makes SSRIs generally non-sedating. In fact, Fluoxetine is often described as **"activating"** or CNS-stimulating [1], which can cause insomnia or agitation in some patients. For this reason, it is typically administered in the morning. **Analysis of Incorrect Options:** * **B. Mianserine:** An atypical antidepressant (Tetracyclic) that is highly sedating due to its potent **$H_1$ receptor antagonism**. It is often used in depressed patients with significant insomnia. * **C. Amoxapine:** A tetracyclic antidepressant (a metabolite of the antipsychotic loxapine) that possesses significant sedative properties and potential extrapyramidal side effects due to $D_2$ blockade [2]. * **D. Imipramine:** A classic **Tricyclic Antidepressant (TCA)**. TCAs cause significant sedation because they block $H_1$ histamine receptors and $\alpha_1$-adrenergic receptors. **NEET-PG High-Yield Pearls:** * **Fluoxetine** has the longest half-life among SSRIs (due to its active metabolite, **norfluoxetine**), requiring a 5-week washout period before starting an MAO inhibitor to avoid **Serotonin Syndrome**. * **Drug of Choice (DOC):** SSRIs are the first-line treatment for Depression, OCD, Panic Disorder, Social Phobia, and Bulimia Nervosa (specifically Fluoxetine) [2]. * **Side Effects:** While non-sedating, SSRIs are frequently associated with **sexual dysfunction** (most common long-term side effect) and GI upset. * **Weight Neutrality:** Fluoxetine is generally weight-neutral compared to TCAs or Mirtazapine, which cause weight gain.

Q: Which of the following is a true statement regarding lithium toxicity?

Toxicity is increased by decreased serum sodium levels.. **Explanation:** The correct answer is **B: Toxicity is increased by decreased serum sodium levels.** **Mechanism of Action:** Lithium is a monovalent cation that is handled by the kidneys in a manner very similar to sodium. It is filtered by the glomerulus and approximately 80% is reabsorbed in the **proximal convoluted tubule (PCT)**. Lithium and sodium compete for the same transport mechanisms. When serum sodium levels are low (hyponatremia), the body attempts to conserve sodium by increasing its reabsorption in the PCT. Consequently, the kidneys inadvertently increase the reabsorption of lithium as well, leading to toxic serum levels. **Analysis of Incorrect Options:** * **Option A:** Increased serum sodium levels (hypernatremia) or high salt intake actually promote lithium excretion, thereby *decreasing* lithium levels. * **Option C:** While renal failure affects lithium clearance, the question specifically asks for a "true statement regarding lithium toxicity" in the context of physiological triggers. While ATN reduces clearance, the relationship with sodium (Option B) is a more fundamental pharmacological principle frequently tested in NEET-PG. * **Option D:** Lithium has a **narrow therapeutic index** (0.6–1.2 mEq/L). Toxicity does not require "triple" the dose; clinical signs of toxicity can appear at levels as low as 1.5 mEq/L, and severe toxicity occurs above 2.0 mEq/L. **High-Yield Clinical Pearls for NEET-PG:** * **Drugs that increase Lithium levels:** Thiazide diuretics (most common trigger), NSAIDs (except Aspirin/Sulindac), and ACE inhibitors. * **Early signs of toxicity:** Coarse tremors (fine tremors are a side effect), nausea, vomiting, and diarrhea. * **Late signs:** Ataxia, dysarthria, seizures, and coma. * **Management:** Hemodialysis is the treatment of choice for severe toxicity (levels >3.5 mEq/L or >2.5 mEq/L with symptoms).

Q: Which of the following is not a Serotonin-Norepinephrine Reuptake Inhibitor (SNRI)?

Bupropion. **Explanation:** The correct answer is **D. Bupropion**. **1. Why Bupropion is the correct answer:** Bupropion is classified as a **Norepinephrine-Dopamine Reuptake Inhibitor (NDRI)**. Unlike SNRIs, it does not significantly inhibit the reuptake of Serotonin. Its primary mechanism involves increasing the synaptic concentration of Dopamine and Norepinephrine. Clinically, this unique profile makes it useful for treating depression without the common serotonergic side effects like sexual dysfunction or weight gain. **2. Why the other options are incorrect:** * **Venlafaxine (Option A):** A prototypical SNRI. At low doses, it primarily acts on serotonin; at higher doses (>150 mg), it significantly inhibits norepinephrine reuptake. * **Duloxetine (Option B):** A potent SNRI used not only for depression but also for chronic pain conditions like diabetic neuropathy and fibromyalgia. * **Milnacipran (Option C):** An SNRI with a higher selectivity for norepinephrine reuptake compared to serotonin. It is frequently used in the management of fibromyalgia. **3. High-Yield NEET-PG Clinical Pearls:** * **Bupropion & Seizures:** Bupropion is strictly contraindicated in patients with **epilepsy** or eating disorders (bulimia/anorexia) as it lowers the seizure threshold. * **Smoking Cessation:** Bupropion is a first-line pharmacological aid for smoking cessation. * **SNRI Indications:** SNRIs are preferred over SSRIs in patients where depression is accompanied by chronic pain (e.g., Duloxetine). * **Desvenlafaxine:** This is the active metabolite of Venlafaxine and is also a common SNRI.

Q: Floppy baby syndrome occurs due to fetal exposure to which of the following?

Lithium. **Explanation:** **Floppy Baby Syndrome** (neonatal hypotonia) occurs due to fetal exposure to **Lithium** during pregnancy. Lithium is a mood stabilizer used for bipolar disorder that crosses the placenta. When taken near term, it can cause neonatal lithium toxicity, characterized by lethargy, poor suck reflex, cyanosis, and marked hypotonia (the "floppy" appearance). Additionally, first-trimester exposure to Lithium is classically associated with **Ebstein’s anomaly** (tricuspid valve displacement). **Analysis of Incorrect Options:** * **Warfarin (A):** Exposure leads to **Fetal Warfarin Syndrome**, characterized by nasal hypoplasia, stippled epiphyses (chondrodysplasia punctata), and CNS defects. It does not typically present as acute neonatal floppiness. * **Valproate (B):** Primarily associated with **Neural Tube Defects** (e.g., spina bifida) due to interference with folate metabolism, as well as "Fetal Valproate Syndrome" (craniofacial dysmorphism). * **Phenytoin (C):** Causes **Fetal Hydantoin Syndrome**, presenting with midface hypoplasia, cleft lip/palate, and digital hypoplasia (hypoplastic nails/phalanges). **NEET-PG High-Yield Pearls:** * **Lithium Toxicity:** Apart from floppiness, it can cause neonatal diabetes insipidus and thyroid dysfunction. * **Management:** Most cases of Lithium-induced floppiness are self-limiting as the drug is cleared by the neonate’s kidneys; however, hydration is key. * **Other causes of Floppy Baby:** Must be differentiated from Down Syndrome (most common chromosomal cause), Spinal Muscular Atrophy (SMA Type 1), and Prader-Willi Syndrome. * **Drug of choice for Bipolar in Pregnancy:** Lamotrigine is often preferred over Lithium/Valproate due to a lower teratogenic profile.

Question 1

Which drug possesses antidepressant and antipsychotic properties?

Accepted Answer

Amoxapine

Answer

Buspirone

Answer

Trazodone

Answer

Mianserine

Question 2

Which of the following is a non-selective MAO inhibitor?

Accepted Answer

Isocarboxazid

Answer

Moclobemide

Answer

Rasagiline

Answer

Selegiline

Question 3

Akathisia is most commonly seen with the use of which of the following medications?

Accepted Answer

Haloperidol

Answer

Clozapine

Answer

Propranolol

Answer

Benztropine

Question 4

Which of the following effects is unlikely to occur during treatment with imipramine?

Accepted Answer

Elevation of seizure threshold

Answer

Mydriasis

Answer

Sedation

Answer

Urinary retention

Question 5

Antipsychotic drugs primarily act through blockade of which of the following receptors?

Accepted Answer

Dopamine D2 receptor

Answer

Dopamine D1 receptor

Answer

Dopamine D3 receptor

Answer

Dopamine D4 receptor

Question 6

Which of the following statements regarding Lithium is false?

Accepted Answer

There is no individual variation in the rate of excretion.

Answer

Maximum plasma concentration is avoided due to its low therapeutic index.

Answer

It is contraindicated in pregnancy.

Answer

80% is reabsorbed in the proximal convoluted tubule.

Question 7

Which of the following is a non-sedating antidepressant?

Accepted Answer

Fluoxetine

Answer

Mianserine

Answer

Amoxapine

Answer

Imipramine

Question 8

Which of the following is a true statement regarding lithium toxicity?

Accepted Answer

Toxicity is increased by decreased serum sodium levels.

Answer

Toxicity is increased by increased serum sodium levels.

Answer

Toxicity is increased in acute tubular necrosis.

Answer

Toxicity appears when the serum levels become triple the dose of therapeutic levels.

Question 9

Which of the following is not a Serotonin-Norepinephrine Reuptake Inhibitor (SNRI)?

Accepted Answer

Bupropion

Answer

Venlafaxine

Answer

Duloxetine

Answer

Milnacipram

Question 10

Floppy baby syndrome occurs due to fetal exposure to which of the following?

Accepted Answer

Lithium

Answer

Warfarin

Answer

Valproate

Answer

Phenytoin

Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders — MCQs

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