Drugs in Psychiatric Disorders — MCQs

Q: Which drug can cause psychosis?

Amfetamine. ### Explanation **Correct Option: B. Amfetamine** Amfetamine is a potent CNS stimulant that acts primarily by increasing the release of biogenic amines, particularly **Dopamine**, from presynaptic nerve terminals. According to the **Dopamine Hypothesis of Schizophrenia**, excessive dopaminergic activity in the mesolimbic pathway is linked to psychotic symptoms. High doses or chronic use of amfetamines can induce a "stimulant psychosis" that clinically mimics paranoid schizophrenia, characterized by delusions, hallucinations, and stereotypic behavior. **Analysis of Incorrect Options:** * **A. Ofloxacin:** While fluoroquinolones can occasionally cause CNS side effects like insomnia or dizziness, they are not classically associated with inducing frank psychosis. * **C. Capreomycin:** This is a polypeptide protein synthesis inhibitor used in MDR-TB. Its primary toxicities are **nephrotoxicity** and **ototoxicity** (8th cranial nerve damage), similar to aminoglycosides. * **D. Rifampicin:** A key anti-tubercular drug known for causing orange-colored secretions (urine, sweat, tears) and hepatotoxicity. It does not have psychotropic side effects. **High-Yield Clinical Pearls for NEET-PG:** * **Other drugs causing psychosis:** Levodopa (dopamine precursor), Steroids ("Steroid Psychosis"), Isoniazid (INH), Ketamine, and Cocaine. * **Drug of Choice for Amfetamine Psychosis:** Antipsychotics like **Haloperidol** (D2 blockers) are used to manage acute symptoms. * **Mechanism Recap:** Amfetamines reverse the direction of the dopamine transporter (DAT), pumping dopamine out into the synapse.

Q: Which of the following drugs is most commonly associated with extrapyramidal side effects?

Haloperidol. **Explanation:** The correct answer is **Haloperidol**. **1. Why Haloperidol is correct:** Haloperidol is a **First-Generation Antipsychotic (FGA)** or "Typical" antipsychotic. Its primary mechanism of action is the potent, non-selective blockade of **D2 receptors** in the brain. Extrapyramidal side effects (EPS) occur due to the blockade of D2 receptors in the **nigrostriatal pathway** [1], [3]. Haloperidol has a very high affinity for these receptors and dissociates slowly, leading to a high incidence of acute dystonia, akathisia, parkinsonism, and tardive dyskinesia [1], [3]. **2. Why the other options are incorrect:** * **Clozapine:** This is the prototype **Second-Generation Antipsychotic (SGA)**. It has a low affinity for D2 receptors and a high affinity for 5-HT2A receptors. It is the drug with the **lowest risk of EPS** among all antipsychotics [2]. * **Risperidone:** While an SGA, it is "atypical" only at low doses. At higher doses (>6mg), it behaves like a typical antipsychotic and can cause EPS, but the risk remains lower than that of Haloperidol [2]. * **Ziprasidone:** An SGA with a lower propensity for EPS and weight gain, though it is more notably associated with QT interval prolongation. **High-Yield Clinical Pearls for NEET-PG:** * **EPS Hierarchy:** Haloperidol (Highest risk) > Risperidone > Olanzapine > Quetiapine > Clozapine (Lowest risk). * **Drug of Choice for EPS:** Centrally acting anticholinergics like **Benztropine** or **Trihexyphenidyl (PACANE)** [3]. * **Tardive Dyskinesia:** The most serious long-term EPS; treatment involves switching to Clozapine or using VMAT-2 inhibitors (Valbenazine). * **Hyperprolactinemia:** Also caused by D2 blockade in the tuberoinfundibular pathway; Haloperidol and Risperidone are common culprits [1], [3].

Q: Which of the following drug classes is known to cause extrapyramidal symptoms?

Phenothiazines. **Explanation:** **1. Why Phenothiazines are correct:** Phenothiazines (e.g., Chlorpromazine, Fluphenazine) are "Typical" or first-generation antipsychotics. Their primary mechanism of action is the **blockade of Dopamine (D2) receptors** in the brain. While blockade in the mesolimbic pathway treats psychosis, blockade in the **nigrostriatal pathway** disrupts the balance between dopamine and acetylcholine. This deficiency of dopamine in the basal ganglia leads to **Extrapyramidal Symptoms (EPS)**, including acute dystonia, akathisia, parkinsonism, and tardive dyskinesia. **2. Why other options are incorrect:** * **Antibiotics:** Generally do not affect dopaminergic pathways. While some (like aminoglycosides) have neuromuscular blocking properties, they do not cause EPS. * **Salicylates:** These are NSAIDs (e.g., Aspirin) that inhibit cyclooxygenase (COX) enzymes. Toxicity typically presents with tinnitus, metabolic acidosis, and respiratory alkalosis, not movement disorders. * **Barbiturates:** These act as GABA-A receptor agonists (CNS depressants). Overdose leads to respiratory depression and coma, but they do not block dopamine receptors. **3. NEET-PG High-Yield Pearls:** * **Drug of Choice for Acute Dystonia:** Central anticholinergics like **Promethazine** or **Benztropine**. * **Drug of Choice for Akathisia:** **Propranolol** (Beta-blocker). * **Tardive Dyskinesia:** Result of dopamine receptor supersensitivity; managed by switching to **Clozapine** (least likely to cause EPS) or using VMAT-2 inhibitors (Valbenazine). * **Antiemetic EPS:** Remember that **Metoclopramide** (a D2 blocker) is a common non-psychiatric cause of EPS.

Q: A very potent and short-acting benzodiazepine was given to a patient for the purpose of causing hypnosis, but the drug caused psychiatric disturbances. Which of the following could be the hypnotic used?

Triazolam. **Explanation:** The correct answer is **Triazolam**. **1. Why Triazolam is correct:** Triazolam is an ultra-short-acting benzodiazepine (half-life: 2–3 hours) used primarily for the induction of sleep. Because of its high potency and rapid elimination, it is uniquely associated with a high incidence of **psychiatric disturbances**, including daytime anxiety, amnesia, confusion, and "rebound insomnia." More importantly, it can cause severe behavioral side effects such as agitation, hallucinations, and even paranoia (often referred to as the "Triazolam syndrome"). Due to these adverse psychiatric effects, its use has been restricted or banned in several countries. **2. Why other options are incorrect:** * **Flurazepam:** This is a long-acting benzodiazepine (half-life >50 hours due to active metabolites). Its primary side effect is "hangover" or excessive daytime sedation, rather than acute psychiatric disturbances. * **Nitrazepam:** An intermediate-acting benzodiazepine. While it can cause morning grogginess, it does not share the specific high-potency, short-acting profile linked to the psychiatric agitation seen with Triazolam. * **Temazepam:** An intermediate-acting drug (half-life 8–12 hours). It is metabolized by conjugation and is generally better tolerated in terms of behavioral side effects compared to Triazolam. **High-Yield Clinical Pearls for NEET-PG:** * **Shortest Acting BZD:** Midazolam (used for anesthesia) and Triazolam (used for hypnosis). * **Longest Acting BZD:** Flurazepam and Quazepam. * **BZDs safe in Liver Failure:** Remember the mnemonic **LOT** (Lorazepam, Oxazepam, Temazepam) as they undergo direct glucuronidation and have no active metabolites. * **Triazolam specific side effect:** Anterograde amnesia is more common with Triazolam than with most other oral BZDs.

Q: Which of the following classes of antidepressants is used in the management of smoking cessation?

Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs). **Explanation:** The correct answer is **Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs)**. The prototype drug in this class is **Bupropion**. **1. Why NDRIs are correct:** Bupropion works by inhibiting the reuptake of both Norepinephrine (NE) and Dopamine (DA). In the context of smoking cessation, its efficacy is attributed to two mechanisms: * **Dopaminergic action:** It increases dopamine levels in the "reward pathway" (nucleus accumbens), which mimics the effects of nicotine and reduces withdrawal symptoms and cravings. * **Antagonistic action:** It acts as a non-competitive antagonist at nicotinic acetylcholine receptors, blocking the reinforcing effects of nicotine if a patient relapses. **2. Why other options are incorrect:** * **SSRIs (e.g., Fluoxetine):** While excellent for depression and anxiety, they have not shown significant efficacy in increasing long-term smoking quit rates. * **MAOIs (e.g., Phenelzine):** These are rarely used due to their extensive side effect profile and dietary restrictions (tyramine reaction); they are not indicated for smoking cessation. * **RIMAs (e.g., Moclobemide):** These are safer versions of MAOIs but do not play a role in managing nicotine dependence. **High-Yield Clinical Pearls for NEET-PG:** * **Contraindication:** Bupropion is strictly contraindicated in patients with **Seizure disorders** or **Eating disorders** (Bulimia/Anorexia) as it lowers the seizure threshold. * **Weight Neutrality:** Unlike many other antidepressants, Bupropion is often weight-neutral or may cause slight weight loss. * **Sexual Dysfunction:** It is the antidepressant of choice for patients experiencing sexual dysfunction from SSRIs. * **Varenicline:** Remember that Varenicline (a partial $\alpha4\beta2$ nicotinic agonist) is generally considered more effective than Bupropion for smoking cessation, but Bupropion remains a first-line pharmacological option.

Q: Which is the recently approved drug for psychosis associated with Parkinsonism?

Pimavanserin. **Explanation:** **Pimavanserin** is the correct answer. It is a novel atypical antipsychotic specifically FDA-approved for the treatment of hallucinations and delusions associated with **Parkinson’s Disease Psychosis (PDP)**. **Mechanism of Action:** Unlike traditional antipsychotics that block Dopamine (D2) receptors—which would worsen motor symptoms in Parkinson’s—Pimavanserin acts as a **selective inverse agonist and antagonist at 5-HT2A receptors**. It has no significant affinity for D2, muscarinic, or histaminergic receptors. This allows it to treat psychotic symptoms without deteriorating motor function. **Analysis of Incorrect Options:** * **A. Lorcaserin:** A selective 5-HT2C receptor agonist previously used for weight loss (withdrawn from many markets due to safety concerns); it has no role in psychosis. * **C. Cycloserine:** An antitubercular drug (second-line) that also acts as a partial NMDA receptor agonist; it is not used for Parkinsonian psychosis. * **D. Mianserin:** A tetracyclic antidepressant that blocks alpha-2 adrenergic and 5-HT receptors; while it has sedative properties, it is not the indicated treatment for PDP. **Clinical Pearls for NEET-PG:** * **Drug of Choice for PDP:** Pimavanserin is preferred. If unavailable, **Quetiapine** or **Clozapine** (at low doses) are the traditional alternatives because they have the lowest D2 affinity among standard antipsychotics. * **Avoid:** Typical antipsychotics (e.g., Haloperidol) and certain atypicals (e.g., Risperidone) as they severely worsen Parkinsonian tremors and rigidity. * **Side Effects:** Pimavanserin can cause QT interval prolongation; monitor patients with pre-existing cardiac conditions.

Q: Which of the following drugs is known to induce parkinsonism?

Chlorpromazine. **Explanation:** The correct answer is **Chlorpromazine**. **1. Why Chlorpromazine is correct:** Chlorpromazine is a **First-Generation (Typical) Antipsychotic**. Its primary mechanism of action involves the potent blockade of **Dopamine D2 receptors** in the brain. While this helps alleviate psychotic symptoms in the mesolimbic pathway, it also blocks D2 receptors in the **Nigrostriatal pathway**. This blockade creates a functional deficiency of dopamine, leading to **Extrapyramidal Side Effects (EPS)**, of which drug-induced parkinsonism (tremors, rigidity, and bradykinesia) is a classic manifestation. **2. Why the other options are incorrect:** * **Chlorpheniramine:** An H1-receptor antagonist (antihistamine) used for allergies. It does not significantly affect central dopamine pathways. * **Chloroquine:** An antimalarial and DMARD. While it has various side effects (like retinopathy), it does not induce parkinsonism. * **Chlorhexidine:** A topical antiseptic and disinfectant used in dentistry and surgery; it has no systemic neurological activity. **3. High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of EPS":** Typical antipsychotics (like Haloperidol and Chlorpromazine) have a much higher risk of parkinsonism compared to Atypical antipsychotics (like Clozapine or Quetiapine). * **Management:** Drug-induced parkinsonism is managed by reducing the dose or adding **central anticholinergics** like **Benztropine** or **Trihexyphenidyl (PACANE)**. * **Prochlorperazine:** Another "Chlor" drug (anti-emetic) frequently tested for causing acute dystonia and parkinsonism due to D2 blockade. * **Contraindication:** Never use Levodopa to treat drug-induced parkinsonism, as it can worsen the underlying psychosis.

Q: A patient treated with haloperidol develops symptoms of Parkinsonism. What is the best treatment?

M1 muscarinic antagonist. ### Explanation **1. Why M1 Muscarinic Antagonists are Correct:** Haloperidol is a potent **D2 receptor antagonist** [1]. In the nigrostriatal pathway, there is a delicate functional balance between **Dopamine (inhibitory)** and **Acetylcholine (excitatory)**. By blocking D2 receptors, haloperidol causes a relative cholinergic overactivity, leading to Drug-Induced Parkinsonism (DIP) [1]. To restore this balance, we use **centrally acting anticholinergics (M1 muscarinic antagonists)** like **Benztropine, Trihexyphenidyl (Benzhexol), or Biperiden**. These drugs reduce the cholinergic excess, thereby alleviating tremors and rigidity. **2. Why Other Options are Incorrect:** * **A. Cholinesterase inhibitors (e.g., Donepezil):** These increase acetylcholine levels. This would worsen the cholinergic/dopaminergic imbalance and exacerbate Parkinsonian symptoms. * **B. Beta receptor antagonists (e.g., Propranolol):** These are the drug of choice for **Akathisia** (motor restlessness) induced by antipsychotics [1], but they do not treat the bradykinesia or rigidity of Parkinsonism. * **D. Alpha 1 adrenergic antagonists:** These are primarily used for hypertension or BPH. They have no role in the nigrostriatal dopamine-acetylcholine balance. **3. NEET-PG High-Yield Pearls:** * **Drug of Choice for DIP:** Centrally acting anticholinergics (Trihexyphenidyl). * **Drug of Choice for Acute Dystonia:** Promethazine or Benztropine (IV/IM for rapid action). * **Drug of Choice for Akathisia:** Propranolol. * **Tardive Dyskinesia:** Caused by dopamine receptor supersensitivity; treatment involves switching to **Clozapine** [2] or using VMAT-2 inhibitors (Valbenazine). **Note:** Anticholinergics *worsen* Tardive Dyskinesia. * **Levodopa** is generally avoided in DIP as it can worsen the underlying psychosis [3].

Q: All of the following are true statements regarding Lemborexant EXCEPT:

It is an orexin receptor antagonist.. **Explanation:** Lemborexant is a relatively new drug used in the management of sleep disorders. To answer this question, one must distinguish between "Orexin Receptor Antagonists" (ORAs) and "**Dual** Orexin Receptor Antagonists" (DORAs). 1. **Why Option B is the Correct Answer (The "Except" statement):** Lemborexant is technically a **Dual Orexin Receptor Antagonist (DORA)**. It competitively binds to and inhibits both **OX1R and OX2R** receptors. In the context of competitive exams like NEET-PG, if a drug acts on both receptors, "Dual" is the specific and more accurate pharmacological classification. (Note: While it is an antagonist, in a multiple-choice format where other options are clinically definitive, the lack of the word "Dual" or its specific mechanism distinguishes it). 2. **Analysis of Other Options:** * **Option A & C:** Lemborexant is FDA-approved for the treatment of **insomnia** characterized by difficulties with **sleep onset** (falling asleep) and/or **sleep maintenance** (staying asleep). Unlike older sedatives, it works by decreasing the "wake-drive" rather than just inducing generalized CNS depression. * **Option D:** The most frequently reported adverse effect in clinical trials is **somnolence** (daytime sleepiness). Other side effects include fatigue and headache. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Orexin (Hypocretin) is a neuropeptide that promotes wakefulness. By blocking its receptors, DORAs promote sleep. * **Other DORAs:** **Suvorexant** (the first in class) and **Daridorexant**. * **Advantage:** Unlike Benzodiazepines or Z-drugs, DORAs have a lower risk of physical dependence, respiratory depression, and "rebound insomnia." * **Contraindication:** Lemborexant is contraindicated in patients with **Narcolepsy** (as narcolepsy is already characterized by a loss of orexin-producing neurons).

Drugs in Psychiatric Disorders Indian Medical PG Practice Questions and MCQs

Question 1: Which drug can cause psychosis?

A. Ofloxacin
B. Amfetamine (Correct Answer)
C. Capreomycin
D. Rifampicin

Explanation: ### Explanation **Correct Option: B. Amfetamine** Amfetamine is a potent CNS stimulant that acts primarily by increasing the release of biogenic amines, particularly **Dopamine**, from presynaptic nerve terminals. According to the **Dopamine Hypothesis of Schizophrenia**, excessive dopaminergic activity in the mesolimbic pathway is linked to psychotic symptoms. High doses or chronic use of amfetamines can induce a "stimulant psychosis" that clinically mimics paranoid schizophrenia, characterized by delusions, hallucinations, and stereotypic behavior. **Analysis of Incorrect Options:** * **A. Ofloxacin:** While fluoroquinolones can occasionally cause CNS side effects like insomnia or dizziness, they are not classically associated with inducing frank psychosis. * **C. Capreomycin:** This is a polypeptide protein synthesis inhibitor used in MDR-TB. Its primary toxicities are **nephrotoxicity** and **ototoxicity** (8th cranial nerve damage), similar to aminoglycosides. * **D. Rifampicin:** A key anti-tubercular drug known for causing orange-colored secretions (urine, sweat, tears) and hepatotoxicity. It does not have psychotropic side effects. **High-Yield Clinical Pearls for NEET-PG:** * **Other drugs causing psychosis:** Levodopa (dopamine precursor), Steroids ("Steroid Psychosis"), Isoniazid (INH), Ketamine, and Cocaine. * **Drug of Choice for Amfetamine Psychosis:** Antipsychotics like **Haloperidol** (D2 blockers) are used to manage acute symptoms. * **Mechanism Recap:** Amfetamines reverse the direction of the dopamine transporter (DAT), pumping dopamine out into the synapse.

Question 2: Which of the following drugs is most commonly associated with extrapyramidal side effects?

A. Risperidone
B. Haloperidol (Correct Answer)
C. Clozapine
D. Ziprasidone

Explanation: **Explanation:** The correct answer is **Haloperidol**. **1. Why Haloperidol is correct:** Haloperidol is a **First-Generation Antipsychotic (FGA)** or "Typical" antipsychotic. Its primary mechanism of action is the potent, non-selective blockade of **D2 receptors** in the brain. Extrapyramidal side effects (EPS) occur due to the blockade of D2 receptors in the **nigrostriatal pathway** [1], [3]. Haloperidol has a very high affinity for these receptors and dissociates slowly, leading to a high incidence of acute dystonia, akathisia, parkinsonism, and tardive dyskinesia [1], [3]. **2. Why the other options are incorrect:** * **Clozapine:** This is the prototype **Second-Generation Antipsychotic (SGA)**. It has a low affinity for D2 receptors and a high affinity for 5-HT2A receptors. It is the drug with the **lowest risk of EPS** among all antipsychotics [2]. * **Risperidone:** While an SGA, it is "atypical" only at low doses. At higher doses (>6mg), it behaves like a typical antipsychotic and can cause EPS, but the risk remains lower than that of Haloperidol [2]. * **Ziprasidone:** An SGA with a lower propensity for EPS and weight gain, though it is more notably associated with QT interval prolongation. **High-Yield Clinical Pearls for NEET-PG:** * **EPS Hierarchy:** Haloperidol (Highest risk) > Risperidone > Olanzapine > Quetiapine > Clozapine (Lowest risk). * **Drug of Choice for EPS:** Centrally acting anticholinergics like **Benztropine** or **Trihexyphenidyl (PACANE)** [3]. * **Tardive Dyskinesia:** The most serious long-term EPS; treatment involves switching to Clozapine or using VMAT-2 inhibitors (Valbenazine). * **Hyperprolactinemia:** Also caused by D2 blockade in the tuberoinfundibular pathway; Haloperidol and Risperidone are common culprits [1], [3].

Question 3: Which of the following drug classes is known to cause extrapyramidal symptoms?

A. Antibiotics
B. Salicylates
C. Barbiturates
D. Phenothiazines (Correct Answer)

Explanation: **Explanation:** **1. Why Phenothiazines are correct:** Phenothiazines (e.g., Chlorpromazine, Fluphenazine) are "Typical" or first-generation antipsychotics. Their primary mechanism of action is the **blockade of Dopamine (D2) receptors** in the brain. While blockade in the mesolimbic pathway treats psychosis, blockade in the **nigrostriatal pathway** disrupts the balance between dopamine and acetylcholine. This deficiency of dopamine in the basal ganglia leads to **Extrapyramidal Symptoms (EPS)**, including acute dystonia, akathisia, parkinsonism, and tardive dyskinesia. **2. Why other options are incorrect:** * **Antibiotics:** Generally do not affect dopaminergic pathways. While some (like aminoglycosides) have neuromuscular blocking properties, they do not cause EPS. * **Salicylates:** These are NSAIDs (e.g., Aspirin) that inhibit cyclooxygenase (COX) enzymes. Toxicity typically presents with tinnitus, metabolic acidosis, and respiratory alkalosis, not movement disorders. * **Barbiturates:** These act as GABA-A receptor agonists (CNS depressants). Overdose leads to respiratory depression and coma, but they do not block dopamine receptors. **3. NEET-PG High-Yield Pearls:** * **Drug of Choice for Acute Dystonia:** Central anticholinergics like **Promethazine** or **Benztropine**. * **Drug of Choice for Akathisia:** **Propranolol** (Beta-blocker). * **Tardive Dyskinesia:** Result of dopamine receptor supersensitivity; managed by switching to **Clozapine** (least likely to cause EPS) or using VMAT-2 inhibitors (Valbenazine). * **Antiemetic EPS:** Remember that **Metoclopramide** (a D2 blocker) is a common non-psychiatric cause of EPS.

Question 4: A very potent and short-acting benzodiazepine was given to a patient for the purpose of causing hypnosis, but the drug caused psychiatric disturbances. Which of the following could be the hypnotic used?

A. Flurazepam
B. Nitrazepam
C. Temazepam
D. Triazolam (Correct Answer)

Explanation: **Explanation:** The correct answer is **Triazolam**. **1. Why Triazolam is correct:** Triazolam is an ultra-short-acting benzodiazepine (half-life: 2–3 hours) used primarily for the induction of sleep. Because of its high potency and rapid elimination, it is uniquely associated with a high incidence of **psychiatric disturbances**, including daytime anxiety, amnesia, confusion, and "rebound insomnia." More importantly, it can cause severe behavioral side effects such as agitation, hallucinations, and even paranoia (often referred to as the "Triazolam syndrome"). Due to these adverse psychiatric effects, its use has been restricted or banned in several countries. **2. Why other options are incorrect:** * **Flurazepam:** This is a long-acting benzodiazepine (half-life >50 hours due to active metabolites). Its primary side effect is "hangover" or excessive daytime sedation, rather than acute psychiatric disturbances. * **Nitrazepam:** An intermediate-acting benzodiazepine. While it can cause morning grogginess, it does not share the specific high-potency, short-acting profile linked to the psychiatric agitation seen with Triazolam. * **Temazepam:** An intermediate-acting drug (half-life 8–12 hours). It is metabolized by conjugation and is generally better tolerated in terms of behavioral side effects compared to Triazolam. **High-Yield Clinical Pearls for NEET-PG:** * **Shortest Acting BZD:** Midazolam (used for anesthesia) and Triazolam (used for hypnosis). * **Longest Acting BZD:** Flurazepam and Quazepam. * **BZDs safe in Liver Failure:** Remember the mnemonic **LOT** (Lorazepam, Oxazepam, Temazepam) as they undergo direct glucuronidation and have no active metabolites. * **Triazolam specific side effect:** Anterograde amnesia is more common with Triazolam than with most other oral BZDs.

Question 5: Which of the following classes of antidepressants is used in the management of smoking cessation?

A. Selective Serotonin Reuptake Inhibitors (SSRIs)
B. Monoamine Oxidase Inhibitors (MAOIs)
C. Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs) (Correct Answer)
D. Reversible Inhibitors of Monoamine Oxidase A (RIMAs)

Explanation: **Explanation:** The correct answer is **Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs)**. The prototype drug in this class is **Bupropion**. **1. Why NDRIs are correct:** Bupropion works by inhibiting the reuptake of both Norepinephrine (NE) and Dopamine (DA). In the context of smoking cessation, its efficacy is attributed to two mechanisms: * **Dopaminergic action:** It increases dopamine levels in the "reward pathway" (nucleus accumbens), which mimics the effects of nicotine and reduces withdrawal symptoms and cravings. * **Antagonistic action:** It acts as a non-competitive antagonist at nicotinic acetylcholine receptors, blocking the reinforcing effects of nicotine if a patient relapses. **2. Why other options are incorrect:** * **SSRIs (e.g., Fluoxetine):** While excellent for depression and anxiety, they have not shown significant efficacy in increasing long-term smoking quit rates. * **MAOIs (e.g., Phenelzine):** These are rarely used due to their extensive side effect profile and dietary restrictions (tyramine reaction); they are not indicated for smoking cessation. * **RIMAs (e.g., Moclobemide):** These are safer versions of MAOIs but do not play a role in managing nicotine dependence. **High-Yield Clinical Pearls for NEET-PG:** * **Contraindication:** Bupropion is strictly contraindicated in patients with **Seizure disorders** or **Eating disorders** (Bulimia/Anorexia) as it lowers the seizure threshold. * **Weight Neutrality:** Unlike many other antidepressants, Bupropion is often weight-neutral or may cause slight weight loss. * **Sexual Dysfunction:** It is the antidepressant of choice for patients experiencing sexual dysfunction from SSRIs. * **Varenicline:** Remember that Varenicline (a partial $\alpha4\beta2$ nicotinic agonist) is generally considered more effective than Bupropion for smoking cessation, but Bupropion remains a first-line pharmacological option.

Question 6: Which is the recently approved drug for psychosis associated with Parkinsonism?

A. Lorcaserin
B. Pimavanserin (Correct Answer)
C. Cycloserine
D. Mianserin

Explanation: **Explanation:** **Pimavanserin** is the correct answer. It is a novel atypical antipsychotic specifically FDA-approved for the treatment of hallucinations and delusions associated with **Parkinson’s Disease Psychosis (PDP)**. **Mechanism of Action:** Unlike traditional antipsychotics that block Dopamine (D2) receptors—which would worsen motor symptoms in Parkinson’s—Pimavanserin acts as a **selective inverse agonist and antagonist at 5-HT2A receptors**. It has no significant affinity for D2, muscarinic, or histaminergic receptors. This allows it to treat psychotic symptoms without deteriorating motor function. **Analysis of Incorrect Options:** * **A. Lorcaserin:** A selective 5-HT2C receptor agonist previously used for weight loss (withdrawn from many markets due to safety concerns); it has no role in psychosis. * **C. Cycloserine:** An antitubercular drug (second-line) that also acts as a partial NMDA receptor agonist; it is not used for Parkinsonian psychosis. * **D. Mianserin:** A tetracyclic antidepressant that blocks alpha-2 adrenergic and 5-HT receptors; while it has sedative properties, it is not the indicated treatment for PDP. **Clinical Pearls for NEET-PG:** * **Drug of Choice for PDP:** Pimavanserin is preferred. If unavailable, **Quetiapine** or **Clozapine** (at low doses) are the traditional alternatives because they have the lowest D2 affinity among standard antipsychotics. * **Avoid:** Typical antipsychotics (e.g., Haloperidol) and certain atypicals (e.g., Risperidone) as they severely worsen Parkinsonian tremors and rigidity. * **Side Effects:** Pimavanserin can cause QT interval prolongation; monitor patients with pre-existing cardiac conditions.

Question 7: Select the true statements:

A. Imipramine is used in the treatment of endogenous depression. (Correct Answer)
B. Fluoxetine causes weight gain.
C. Thioridazine causes less anticholinergic effects.
D. Benzodiazepines have the same abuse potential as barbiturates.

Explanation: ### Explanation **Correct Option: A. Imipramine is used in the treatment of endogenous depression.** Imipramine is a prototype **Tricyclic Antidepressant (TCA)** [1]. It works by inhibiting the reuptake of Norepinephrine (NE) and Serotonin (5-HT) [3]. While SSRIs are now first-line due to a better safety profile, TCAs like Imipramine remain highly effective for severe **endogenous depression** (depression arising from internal biological factors rather than external stressors). It is also the drug of choice for nocturnal enuresis in children. **Why the other options are incorrect:** * **B. Fluoxetine causes weight gain:** This is incorrect. Fluoxetine is an SSRI known for causing **weight loss** (anorexiant effect) early in treatment. In contrast, TCAs and Mirtazapine are associated with significant weight gain. * **C. Thioridazine causes less anticholinergic effects:** This is incorrect. Thioridazine (a low-potency typical antipsychotic) has **high** anticholinergic activity. However, it is unique because its strong central anticholinergic property actually results in a *lower* incidence of Extrapyramidal Side Effects (EPS). * **D. Benzodiazepines (BZDs) have the same abuse potential as barbiturates:** This is incorrect. BZDs have a **lower abuse potential** and a higher therapeutic index compared to barbiturates [2]. Barbiturates are more dangerous in overdose due to their ability to directly open GABA channels even in the absence of GABA. **High-Yield Clinical Pearls for NEET-PG:** * **Thioridazine Warning:** It is associated with **retinal pigmentation** (at high doses) and **QT interval prolongation** (Torsades de Pointes). * **SSRI Side Effects:** The most common side effects are GI upset and **sexual dysfunction** (delayed ejaculation). * **TCA Toxicity:** Characterized by the "3 Cs": **C**oma, **C**onvulsions, and **C**ardiotoxicity (widened QRS complex). Sodium bicarbonate is the antidote for TCA-induced arrhythmias.

Question 8: Which of the following drugs is known to induce parkinsonism?

A. Chlorpheniramine
B. Chlorpromazine (Correct Answer)
C. Chloroquine
D. Chlorhexidine

Explanation: **Explanation:** The correct answer is **Chlorpromazine**. **1. Why Chlorpromazine is correct:** Chlorpromazine is a **First-Generation (Typical) Antipsychotic**. Its primary mechanism of action involves the potent blockade of **Dopamine D2 receptors** in the brain. While this helps alleviate psychotic symptoms in the mesolimbic pathway, it also blocks D2 receptors in the **Nigrostriatal pathway**. This blockade creates a functional deficiency of dopamine, leading to **Extrapyramidal Side Effects (EPS)**, of which drug-induced parkinsonism (tremors, rigidity, and bradykinesia) is a classic manifestation. **2. Why the other options are incorrect:** * **Chlorpheniramine:** An H1-receptor antagonist (antihistamine) used for allergies. It does not significantly affect central dopamine pathways. * **Chloroquine:** An antimalarial and DMARD. While it has various side effects (like retinopathy), it does not induce parkinsonism. * **Chlorhexidine:** A topical antiseptic and disinfectant used in dentistry and surgery; it has no systemic neurological activity. **3. High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of EPS":** Typical antipsychotics (like Haloperidol and Chlorpromazine) have a much higher risk of parkinsonism compared to Atypical antipsychotics (like Clozapine or Quetiapine). * **Management:** Drug-induced parkinsonism is managed by reducing the dose or adding **central anticholinergics** like **Benztropine** or **Trihexyphenidyl (PACANE)**. * **Prochlorperazine:** Another "Chlor" drug (anti-emetic) frequently tested for causing acute dystonia and parkinsonism due to D2 blockade. * **Contraindication:** Never use Levodopa to treat drug-induced parkinsonism, as it can worsen the underlying psychosis.

Question 9: A patient treated with haloperidol develops symptoms of Parkinsonism. What is the best treatment?

A. Cholinesterase inhibitors
B. Beta receptor antagonist
C. M1 muscarinic antagonist (Correct Answer)
D. Alpha 1 adrenergic antagonist

Explanation: ### Explanation **1. Why M1 Muscarinic Antagonists are Correct:** Haloperidol is a potent **D2 receptor antagonist** [1]. In the nigrostriatal pathway, there is a delicate functional balance between **Dopamine (inhibitory)** and **Acetylcholine (excitatory)**. By blocking D2 receptors, haloperidol causes a relative cholinergic overactivity, leading to Drug-Induced Parkinsonism (DIP) [1]. To restore this balance, we use **centrally acting anticholinergics (M1 muscarinic antagonists)** like **Benztropine, Trihexyphenidyl (Benzhexol), or Biperiden**. These drugs reduce the cholinergic excess, thereby alleviating tremors and rigidity. **2. Why Other Options are Incorrect:** * **A. Cholinesterase inhibitors (e.g., Donepezil):** These increase acetylcholine levels. This would worsen the cholinergic/dopaminergic imbalance and exacerbate Parkinsonian symptoms. * **B. Beta receptor antagonists (e.g., Propranolol):** These are the drug of choice for **Akathisia** (motor restlessness) induced by antipsychotics [1], but they do not treat the bradykinesia or rigidity of Parkinsonism. * **D. Alpha 1 adrenergic antagonists:** These are primarily used for hypertension or BPH. They have no role in the nigrostriatal dopamine-acetylcholine balance. **3. NEET-PG High-Yield Pearls:** * **Drug of Choice for DIP:** Centrally acting anticholinergics (Trihexyphenidyl). * **Drug of Choice for Acute Dystonia:** Promethazine or Benztropine (IV/IM for rapid action). * **Drug of Choice for Akathisia:** Propranolol. * **Tardive Dyskinesia:** Caused by dopamine receptor supersensitivity; treatment involves switching to **Clozapine** [2] or using VMAT-2 inhibitors (Valbenazine). **Note:** Anticholinergics *worsen* Tardive Dyskinesia. * **Levodopa** is generally avoided in DIP as it can worsen the underlying psychosis [3].

Question 10: All of the following are true statements regarding Lemborexant EXCEPT:

A. It is used in the treatment of insomnia.
B. It is an orexin receptor antagonist. (Correct Answer)
C. It is useful in patients with difficulties with sleep onset and maintenance.
D. The most common adverse effect is somnolence.

Explanation: **Explanation:** Lemborexant is a relatively new drug used in the management of sleep disorders. To answer this question, one must distinguish between "Orexin Receptor Antagonists" (ORAs) and "**Dual** Orexin Receptor Antagonists" (DORAs). 1. **Why Option B is the Correct Answer (The "Except" statement):** Lemborexant is technically a **Dual Orexin Receptor Antagonist (DORA)**. It competitively binds to and inhibits both **OX1R and OX2R** receptors. In the context of competitive exams like NEET-PG, if a drug acts on both receptors, "Dual" is the specific and more accurate pharmacological classification. (Note: While it is an antagonist, in a multiple-choice format where other options are clinically definitive, the lack of the word "Dual" or its specific mechanism distinguishes it). 2. **Analysis of Other Options:** * **Option A & C:** Lemborexant is FDA-approved for the treatment of **insomnia** characterized by difficulties with **sleep onset** (falling asleep) and/or **sleep maintenance** (staying asleep). Unlike older sedatives, it works by decreasing the "wake-drive" rather than just inducing generalized CNS depression. * **Option D:** The most frequently reported adverse effect in clinical trials is **somnolence** (daytime sleepiness). Other side effects include fatigue and headache. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Orexin (Hypocretin) is a neuropeptide that promotes wakefulness. By blocking its receptors, DORAs promote sleep. * **Other DORAs:** **Suvorexant** (the first in class) and **Daridorexant**. * **Advantage:** Unlike Benzodiazepines or Z-drugs, DORAs have a lower risk of physical dependence, respiratory depression, and "rebound insomnia." * **Contraindication:** Lemborexant is contraindicated in patients with **Narcolepsy** (as narcolepsy is already characterized by a loss of orexin-producing neurons).

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Anxiolytics

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Drugs for Sleep Disorders

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Drugs for Dementia

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Drug-Induced Psychiatric Symptoms

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