Drugs in Psychiatric Disorders Practice Questions

Q: Buspirone as compared to benzodiazepines:

Does not interfere with GABAergic transmission. **Explanation:** **Mechanism of Action (The Core Concept):** Buspirone is a non-benzodiazepine anxiolytic that acts as a **selective partial agonist at 5-HT1A receptors** [1], [2]. Unlike Benzodiazepines (BZDs), which act as positive allosteric modulators of the GABA-A receptor complex to enhance GABAergic inhibition [2], Buspirone has **no affinity for GABA receptors** [1]. Therefore, it does not interfere with GABAergic transmission, making Option B the correct answer. **Analysis of Incorrect Options:** * **Option A:** Buspirone lacks anticonvulsant and muscle relaxant properties [1]. BZDs are the drugs of choice for acute seizures (e.g., Diazepam, Lorazepam). * **Option C:** Buspirone has a slow onset of action (taking 2–4 weeks for effect) [1], [2]. It is ineffective in acute anxiety or panic attacks [1], where BZDs or SSRIs are preferred [3]. It is primarily used for Generalized Anxiety Disorder (GAD) [1], [2]. * **Option D:** One of the primary clinical advantages of Buspirone is that it **lacks sedative, hypnotic, and cognitive-impairing effects** [1], [2]. It does not cause psychomotor impairment or "hangover" effects common with BZDs [1], [2]. **High-Yield Clinical Pearls for NEET-PG:** * **No Interaction with Alcohol:** Unlike BZDs, Buspirone does not potentiate the effects of CNS depressants like alcohol [2]. * **No Dependence:** It has no abuse potential and does not cause withdrawal symptoms or rebound anxiety upon discontinuation [1]. * **Driving Safety:** It is preferred for patients whose occupations require high mental alertness (e.g., pilots, drivers). * **Metabolism:** It is metabolized by **CYP3A4**; its levels can increase significantly if taken with grapefruit juice or erythromycin.

Q: Which of the following is/are not a side effect of lithium?

Hyporeflexia. **Explanation:** Lithium is a gold-standard mood stabilizer with a narrow therapeutic index (0.6–1.2 mEq/L). Understanding its side effects is crucial for NEET-PG, as toxicity often manifests through neurological and renal symptoms. **Why Hyporeflexia is the Correct Answer:** Lithium toxicity characteristically causes **Hyperreflexia**, not hyporeflexia. As lithium levels rise, patients develop neuromuscular irritability, leading to tremors, ataxia, myoclonus, and brisk deep tendon reflexes (hyperreflexia). Hyporeflexia is more commonly associated with magnesium toxicity or certain sedative-hypnotic overdoses. **Analysis of Incorrect Options:** * **Seizure (A):** Lithium lowers the seizure threshold. In cases of severe toxicity (>2.5 mEq/L), neurological complications like seizures, encephalopathy, and coma are common. * **Nephrogenic Diabetes Insipidus (C):** This is the most common renal side effect. Lithium accumulates in the collecting ducts and interferes with ADH (Vasopressin) action, leading to polyuria and polydipsia. * **Alopecia (D):** Dermatological side effects of Lithium include thinning of hair (alopecia), acneiform eruptions, and the exacerbation of psoriasis. **High-Yield Clinical Pearls for NEET-PG:** * **L-I-T-H-I-U-M Mnemonic for Side Effects:** **L**eukocytosis, **I**nsipidus (NDI), **T**remors/Teratogenicity (Ebstein’s Anomaly), **H**ypothyroidism, **I**ncreased Weight, **U**nderactive Heart (Bradycardia/T-wave flattening), **M**uscle twitching/Hyperreflexia. * **Drug Interactions:** Thiazides, NSAIDs, and ACE inhibitors increase Lithium levels (decreasing clearance), while Caffeine and Theophylline decrease levels. * **Monitoring:** Thyroid Function Tests (TFT) and Renal Function Tests (RFT) must be performed before and during treatment.

Q: Administration of which of the following drugs requires monitoring?

Lithium. **Explanation:** **Lithium** is the correct answer because it is a drug with a **narrow therapeutic index**, meaning the difference between a therapeutic dose and a toxic dose is very small. Regular **Therapeutic Drug Monitoring (TDM)** is mandatory to ensure efficacy and prevent toxicity. The therapeutic range for Lithium is typically **0.6 to 1.2 mEq/L**. Levels above 1.5 mEq/L are considered toxic, and levels above 2.0 mEq/L constitute a medical emergency. **Incorrect Options:** * **Haloperidol:** A typical antipsychotic. While it requires monitoring for extrapyramidal side effects (EPS), it does not require routine blood level monitoring. * **Diazepam:** A benzodiazepine used for anxiety and seizures. It has a wide therapeutic window; monitoring is clinical (respiratory rate/sedation) rather than through blood levels. * **Acetazolamide:** A carbonic anhydrase inhibitor used in glaucoma and altitude sickness. It requires monitoring of electrolytes (potassium/bicarbonate) in specific cases, but not routine drug level monitoring. **High-Yield Clinical Pearls for NEET-PG:** * **Sample Timing:** Lithium levels should be checked **12 hours after the last dose** (Trough level). * **Steady State:** It takes about **5 days** (5 half-lives) to reach a steady state before the first level should be checked. * **Toxicity Triggers:** Dehydration, low-sodium diets, and drugs like **NSAIDs, Thiazides, and ACE inhibitors** can increase Lithium levels, leading to toxicity. * **Side Effects:** Look for "LITH" mnemonic: **L**eukocytosis, **I**nsipidus (Diabetes Insipidus), **T**remors/Teratogenicity (Ebstein's Anomaly), **H**ypothyroidism.

Q: Which renal lesion is associated with the chronic use of lithium?

Chronic interstitial nephritis. **Explanation:** **Correct Answer: C. Chronic interstitial nephritis** Lithium is a narrow therapeutic index drug primarily excreted by the kidneys. While the most common renal side effect of lithium is **Nephrogenic Diabetes Insipidus (NDI)** (due to interference with ADH action in the collecting ducts) [1], long-term chronic use is associated with **Chronic Interstitial Nephritis** [2]. Pathologically, this manifests as tubulointerstitial fibrosis and atrophy, which can slowly progress to chronic kidney disease (CKD) over decades of therapy [2]. **Analysis of Incorrect Options:** * **A. Acute tubular necrosis (ATN):** Typically caused by acute ischemia or nephrotoxins like aminoglycosides and cisplatin. While acute lithium toxicity can cause functional impairment, it does not characteristically present as ATN. * **B. Membranous glomerulopathy:** This is a nephrotic syndrome pattern associated with drugs like NSAIDs, gold salts, and penicillamine, but not typically lithium. Lithium is more rarely associated with Minimal Change Disease. * **D. Crystal formation:** This is characteristic of drugs like **Acyclovir, Sulfonamides, and Methotrexate**, which precipitate in the renal tubules, leading to obstructive uropathy. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of NDI:** Lithium enters the principal cells of the collecting duct through **ENaC channels** and inhibits adenylate cyclase, making cells unresponsive to ADH [1]. * **Treatment of Lithium-induced NDI:** **Amiloride** is the drug of choice as it blocks ENaC channels, preventing lithium entry into the tubular cells [1]. * **Monitoring:** Renal function (Serum Creatinine/GFR) must be monitored regularly in patients on long-term Lithium [3]. * **Drug Interactions:** Thiazides, NSAIDs, and ACE inhibitors increase lithium levels by reducing its renal clearance [1].

Q: What is the most common receptor for typical antipsychotics?

Dopamine receptor 2 (D2). ### Explanation **Correct Option: B. Dopamine receptor 2 (D2)** The therapeutic efficacy of **typical (first-generation) antipsychotics** (e.g., Haloperidol, Chlorpromazine) is primarily attributed to their potent antagonism of **D2 receptors** in the **mesolimbic pathway**. According to the Dopamine Hypothesis of Schizophrenia, positive symptoms (hallucinations and delusions) result from overactivity in this pathway. Clinical studies show that for an antipsychotic to be effective, it must typically block approximately **60–80% of D2 receptors** in the brain. **Why other options are incorrect:** * **D1 Receptors:** While some antipsychotics (like Phenothiazines) have a mild affinity for D1, it is not the primary target for clinical efficacy in treating psychosis. * **D3 Receptors:** These are primarily located in the limbic system. While some newer atypical agents (like Cariprazine) target D3, typical antipsychotics do not primarily act here. * **D4 Receptors:** This receptor gained fame due to **Clozapine’s** high affinity for it. However, typical antipsychotics have a much higher affinity for D2 than D4. **High-Yield NEET-PG Clinical Pearls:** 1. **The "D2 Paradox":** While D2 blockade in the *mesolimbic* pathway treats psychosis, blockade in the *nigrostriatal* pathway leads to **Extrapyramidal Side Effects (EPS)**, and blockade in the *tuberoinfundibular* pathway causes **Hyperprolactinemia**. 2. **Potency:** The clinical potency of a typical antipsychotic is directly proportional to its D2 receptor binding affinity (e.g., Haloperidol is high-potency; Chlorpromazine is low-potency). 3. **Atypical Antipsychotics:** Unlike typicals, atypical antipsychotics (SGAs) are defined by a high **5-HT2A to D2 receptor blockade ratio**, which reduces the risk of EPS.

Q: Which drug possesses both antidepressant and antipsychotic properties?

Amoxapine. **Explanation:** **Amoxapine** is a tetracyclic antidepressant (TeCA) and is a metabolite of the antipsychotic drug loxapine. It is unique because it possesses a dual mechanism of action: 1. **Antidepressant property:** It inhibits the reuptake of norepinephrine (and to a lesser extent, serotonin), similar to tricyclic antidepressants. 2. **Antipsychotic property:** Unlike other antidepressants, it significantly blocks **Dopamine D2 receptors**. Due to this dual action, Amoxapine is the drug of choice for **Psychotic Depression** (Major Depressive Disorder with psychotic features). **Analysis of Incorrect Options:** * **Buspirone (A):** An anxiolytic that acts as a partial agonist at 5-HT1A receptors. It lacks D2 blocking (antipsychotic) properties. * **Trazodone (C):** A Serotonin Antagonist and Reuptake Inhibitor (SARI). It is primarily used as an antidepressant and for its sedative properties in insomnia; it does not have antipsychotic efficacy. * **Mianserin (D):** A tetracyclic antidepressant that blocks alpha-2 adrenergic receptors. While it shares a chemical class with Amoxapine, it does not possess significant D2 receptor antagonism. **High-Yield Clinical Pearls for NEET-PG:** * **Side Effects:** Because of its D2 blocking activity, Amoxapine can cause **Extrapyramidal Side Effects (EPS)**, such as parkinsonism or akathisia, and hyperprolactinemia—side effects not typically seen with other antidepressants. * **Metabolism:** Remember that Amoxapine is the N-demethylated metabolite of **Loxapine**. * **Clinical Use:** Always consider Amoxapine or a combination of an SSRI + Antipsychotic for patients presenting with "delusional depression."

Q: Akathisia is treated by which of the following medications, except?

Haloperidol. **Explanation:** **Akathisia** is a common and distressing Extrapyramidal Side Effect (EPS) characterized by subjective feelings of inner restlessness and an objective inability to sit still. It is most commonly caused by **Dopamine (D2) receptor antagonists**, such as typical antipsychotics. **Why Haloperidol is the correct answer:** Haloperidol is a high-potency typical antipsychotic and a potent D2 receptor blocker. It is a **primary cause** of akathisia, not a treatment for it. Administering haloperidol to a patient with akathisia would exacerbate the condition. **Analysis of other options:** * **Protolol (Beta-blockers):** Centrally acting lipophilic beta-blockers like Propranolol are considered the **first-line treatment** for akathisia. They help reduce the subjective feeling of restlessness. * **Trihexyphenidyl (Anticholinergics):** Centrally acting anticholinergics are effective in treating various EPS, including acute dystonia and parkinsonism. While less effective for akathisia than beta-blockers, they are still used as second-line agents. * **Promethazine:** This is an antihistamine with significant anticholinergic properties. It is frequently used in clinical practice to manage acute EPS. **High-Yield Clinical Pearls for NEET-PG:** 1. **Drug of Choice (DOC):** For Akathisia is **Propranolol**. 2. **Acute Dystonia:** The earliest EPS to appear (within hours); treated with intravenous/intramuscular anticholinergics (e.g., Benztropine, Promethazine). 3. **Tardive Dyskinesia:** Occurs after long-term use; characterized by choreoathetoid movements. Treatment involves switching to Clozapine or using VMAT-2 inhibitors (Valbenazine). 4. **Benzodiazepines:** Can also be used as an adjunct treatment for akathisia to reduce anxiety and motor restlessness.

Q: Which of the following is a selective serotonin and norepinephrine reuptake inhibitor?

Venlafaxine. **Explanation:** **Venlafaxine** is the correct answer because it belongs to the class of **Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)** [1], [2]. These drugs work by inhibiting the transporters for both serotonin (5-HT) and norepinephrine (NE), thereby increasing the synaptic concentration of both neurotransmitters [1], [3]. At lower doses, venlafaxine primarily inhibits serotonin reuptake, while at higher doses, its effect on norepinephrine becomes more pronounced [2], [3]. **Analysis of Incorrect Options:** * **A. Fluoxetine:** This is a **Selective Serotonin Reuptake Inhibitor (SSRI)** [1], [3]. It selectively inhibits the reuptake of serotonin with minimal effect on norepinephrine or dopamine. * **C. Selegiline:** This is a **MAO-B inhibitor** (Monoamine Oxidase-B inhibitor). It is primarily used in Parkinson’s disease to prevent the breakdown of dopamine. At higher doses, it can act as a non-selective MAO inhibitor used for depression. * **D. Aripiprazole:** This is an **Atypical Antipsychotic**. It acts as a partial agonist at $D_2$ and $5-HT_{1A}$ receptors and an antagonist at $5-HT_{2A}$ receptors. **High-Yield Clinical Pearls for NEET-PG:** * **SNRIs include:** Venlafaxine, Desvenlafaxine, Duloxetine, and Milnacipran [1], [2]. * **Duloxetine** is specifically preferred in patients with comorbid **neuropathic pain** or fibromyalgia [3]. * **Side Effect Profile:** Because SNRIs increase norepinephrine, they can cause a dose-dependent **increase in blood pressure** (hypertension) and heart rate. * **Venlafaxine** has a short half-life; abrupt discontinuation often leads to a significant **withdrawal syndrome** (dizziness, electric shock-like sensations).

Q: Which of the following is a tricyclic antidepressant (TCA)?

Amoxapine. ### Explanation **Correct Option: A. Amoxapine** Amoxapine is a **Tricyclic Antidepressant (TCA)** belonging to the dibenzoxazepine subclass. While it acts by inhibiting the reuptake of norepinephrine and serotonin, it is unique among TCAs because its metabolite (7-hydroxyamoxapine) possesses **dopamine (D2) receptor blocking activity**. This gives it mild antipsychotic properties but also increases the risk of extrapyramidal side effects (EPS). **Incorrect Options:** * **B. Citalopram:** This is a **Selective Serotonin Reuptake Inhibitor (SSRI)**. SSRIs are currently the first-line treatment for depression due to their better safety profile and lower side-effect burden compared to TCAs. * **C. Venlafaxine:** This is a **Serotonin-Norepinephrine Reuptake Inhibitor (SNRI)**. It inhibits the reuptake of both neurotransmitters but lacks the significant antihistaminic and anticholinergic effects seen with TCAs. * **D. Bupropion:** This is an **Atypical Antidepressant** that acts as a Norepinephrine-Dopamine Reuptake Inhibitor (NDRI). It is notably used for smoking cessation and has a lower risk of causing sexual dysfunction or weight gain. **High-Yield Clinical Pearls for NEET-PG:** * **Classification Tip:** TCAs are divided into Tertiary amines (Amitriptyline, Imipramine, Clomipramine) and Secondary amines (Nortriptyline, Desipramine). * **Amoxapine Unique Fact:** It is the TCA most likely to cause **Extrapyramidal Symptoms (EPS)** and tardive dyskinesia due to D2 blockade. * **TCA Toxicity:** The "3 Cs" of TCA overdose are **C**oma, **C**onvulsions, and **C**ardiotoxicity (arrhythmias due to Na+ channel blockade). The antidote for cardiotoxicity is Sodium Bicarbonate. * **Clomipramine:** The most serotonin-selective TCA; it is the drug of choice for Obsessive-Compulsive Disorder (OCD) among TCAs.

Q: 5-HT1A partial agonists are used as which class of drugs?

Anti-anxiety drugs. **Explanation:** The correct answer is **Anti-anxiety drugs**. **Buspirone**, along with its derivatives Gepirone and Ipsapirone, acts as a **selective 5-HT1A receptor partial agonist**. By binding to these presynaptic and postsynaptic receptors in the raphe nuclei and hippocampus, these drugs modulate serotonin neurotransmission to produce anxiolytic effects. Unlike benzodiazepines, they do not interact with GABA receptors, meaning they lack sedative, hypnotic, anticonvulsant, or muscle-relaxant properties. **Why other options are incorrect:** * **Antipsychotic drugs:** These primarily target Dopamine (D2) receptors and 5-HT2A receptors (in the case of atypicals). While some atypicals have 5-HT1A activity, it is not their defining mechanism. * **Anti-reflux medications:** These typically involve Proton Pump Inhibitors (PPIs) or H2 blockers. However, **Mosapride** (a prokinetic) is a 5-HT4 agonist, not a 5-HT1A agonist. * **Anti-emetic drugs:** These are typically **5-HT3 antagonists** (e.g., Ondansetron) or D2 antagonists (e.g., Metoclopramide). **High-Yield Clinical Pearls for NEET-PG:** * **Latency of Action:** Buspirone has a slow onset of action (taking **1–2 weeks**) and is therefore not useful for acute anxiety or panic attacks. * **Safety Profile:** It has **no potential for abuse or addiction**, does not cause rebound anxiety upon withdrawal, and does not potentiate the effects of alcohol. * **DOC:** It is a preferred choice for Generalized Anxiety Disorder (GAD) in patients where sedation must be avoided (e.g., elderly or heavy machinery operators).

Question 1

Buspirone as compared to benzodiazepines:

Accepted Answer

Does not interfere with GABAergic transmission

Answer

Is a more potent anticonvulsant

Answer

Is more effective in severe anxiety with panic attacks

Answer

Produces significantly more sedation

Question 2

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

Accepted Answer

Hyporeflexia

Answer

Seizure

Answer

Nephrogenic diabetes insipidus

Answer

Alopecia

Question 3

Administration of which of the following drugs requires monitoring?

Accepted Answer

Lithium

Answer

Haloperidol

Answer

Diazepam

Answer

Acetazolamide

Question 4

Which renal lesion is associated with the chronic use of lithium?

Accepted Answer

Chronic interstitial nephritis

Answer

Acute tubular necrosis

Answer

Membranous glomerulopathy

Answer

Crystal formation

Question 5

What is the most common receptor for typical antipsychotics?

Accepted Answer

Dopamine receptor 2 (D2)

Answer

Dopamine receptor 1 (D1)

Answer

Dopamine receptor 3 (D3)

Answer

Dopamine receptor 4 (D4)

Question 6

Which drug possesses both antidepressant and antipsychotic properties?

Accepted Answer

Amoxapine

Answer

Buspirone

Answer

Trazodone

Answer

Minaserine

Question 7

Akathisia is treated by which of the following medications, except?

Accepted Answer

Haloperidol

Answer

Trihexyphenidyl

Answer

Propanolol

Answer

Promethazine

Question 8

Which of the following is a selective serotonin and norepinephrine reuptake inhibitor?

Accepted Answer

Venlafaxine

Answer

Fluoxetine

Answer

Selegiline

Answer

Aripiprazole

Question 9

Which of the following is a tricyclic antidepressant (TCA)?

Accepted Answer

Amoxapine

Answer

Citalopram

Answer

Venlafaxine

Answer

Bupropion

Question 10

5-HT1A partial agonists are used as which class of drugs?

Accepted Answer

Anti-anxiety drugs

Answer

Antipsychotic drugs

Answer

Anti-reflux medications

Answer

Anti-emetic drugs

Drugs in Psychiatric Disorders — MCQs

Drugs in Psychiatric Disorders — MCQs

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