What is the primary treatment indication of folic acid?
Which of the following methods can reduce flushing caused by niacin?
A patient undergoing a minor surgical procedure is given lignocaine injection. Assertion: Local anaesthetics act by blocking nerve conduction. Reason: Small fibers and non-myelinated fibers are blocked more easily than large myelinated fibers.
Which of the following drugs is an alpha 2 agonist?
Which of the following is the only clinically available depolarizing muscle relaxant?
What is the treatment for extrapyramidal side effects induced by Haloperidol?
What is the mechanism of action of duloxetine?
Which of the following actions is NOT associated with tricyclic antidepressants?
Which of the following statements about flumazenil is correct?
Which of the following typical antipsychotic drugs is least commonly used in depot form?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 121: What is the primary treatment indication of folic acid?
- A. Prevention of neural tube defects in pregnancy
- B. Treatment of megaloblastic anemia (Correct Answer)
- C. Management of hemoglobinopathies
- D. None of the above
Explanation: ***Treatment of megaloblastic anemia*** - Folic acid is essential for **DNA synthesis** and cell division, and its deficiency leads to impaired red blood cell maturation, causing **megaloblastic anemia**. - Supplementation with folic acid effectively reverses the hematological abnormalities in **folate-deficient megaloblastic anemia**. *Prevention of neural tube defects in pregnancy* - While folic acid is crucial for preventing **neural tube defects** (NTDs), this is a **prophylactic** rather than a primary therapeutic use. - The focus of this question is on the *primary therapeutic* use, implying treatment of an existing condition. *Management of hemoglobinopathies* - Hemoglobinopathies like **sickle cell anemia** or **thalassemia** are genetic disorders affecting hemoglobin structure or production, not primarily due to folic acid deficiency. - Folic acid may be given to these patients to support increased red blood cell turnover, but it does not address the underlying genetic defect. *None of the above* - This option is incorrect because folic acid has a clear primary therapeutic role in treating **megaloblastic anemia**.
Question 122: Which of the following methods can reduce flushing caused by niacin?
- A. All of the options (Correct Answer)
- B. Tachyphylaxis
- C. Laropiprant
- D. Premedication with aspirin
Explanation: ***All of the options*** - **All three methods** (tachyphylaxis, laropiprant, and premedication with aspirin) are effective strategies for reducing niacin-induced flushing. - This demonstrates that multiple pharmacological and physiological approaches can mitigate this common side effect of niacin therapy. **Why each method works:** **Tachyphylaxis:** - Refers to the rapid decrease in response to a drug after repeated administration - With continued niacin use, tolerance develops and flushing intensity decreases over time - This is a natural adaptive response, though not an immediate solution for initial flushing episodes **Laropiprant:** - A selective antagonist of the **prostaglandin D2 receptor 1 (DP1)** - Specifically developed to reduce niacin-induced flushing by blocking prostaglandin D2-mediated vasodilation - Was marketed in combination with niacin (though later withdrawn due to other safety concerns) **Premedication with aspirin:** - **Aspirin** or other NSAIDs taken approximately 30 minutes before niacin administration - Reduces flushing by inhibiting **prostaglandin synthesis**, particularly prostaglandin D2 - Prostaglandins are key mediators of the cutaneous vasodilation that causes flushing
Question 123: A patient undergoing a minor surgical procedure is given lignocaine injection. Assertion: Local anaesthetics act by blocking nerve conduction. Reason: Small fibers and non-myelinated fibers are blocked more easily than large myelinated fibers.
- A. Assertion is false, but Reason is true
- B. Both Assertion and Reason are true, and Reason is not the correct explanation for Assertion (Correct Answer)
- C. Both Assertion and Reason are true, and Reason is the correct explanation for Assertion
- D. Assertion is true, but Reason is false
Explanation: ***Both Assertion and Reason are true, and Reason is NOT the correct explanation for Assertion*** - The **Assertion** is true: Local anesthetics (like lignocaine) block nerve conduction by inhibiting **voltage-gated sodium channels**, preventing the depolarization necessary for action potential propagation - The **Reason** is also true: Small diameter and non-myelinated fibers (like C and Aδ pain fibers) are blocked more easily than large myelinated fibers (like Aα motor fibers), which explains the **differential blockade** pattern seen clinically - However, the **Reason does NOT explain WHY** local anesthetics block nerve conduction—it describes **WHICH** nerve fibers are blocked preferentially. The mechanism of blocking conduction is sodium channel inhibition, not fiber size selectivity - The differential sensitivity is a consequence of fiber characteristics (surface area-to-volume ratio, number of nodes of Ranvier), not the explanation for the blocking mechanism itself *Both Assertion and Reason are true, and Reason is the correct explanation for Assertion* - While both statements are individually true, the Reason does not explain the **mechanism** by which local anesthetics block nerve conduction - The Reason addresses fiber **selectivity**, which is a separate pharmacological property from the **mechanism of action** (sodium channel blockade) *Assertion is true, but Reason is false* - The Assertion is demonstrably true—local anesthetics block nerve conduction - The Reason is also true—this is well-established pharmacology: autonomic (small) > sensory (medium) > motor (large) fiber blockade sequence *Assertion is false, but Reason is true* - The Assertion is fundamentally correct and represents the primary pharmacological action of local anesthetics - Blocking nerve conduction is the therapeutic goal of local anesthetic administration
Question 124: Which of the following drugs is an alpha 2 agonist?
- A. Apraclonidine (Correct Answer)
- B. Timolol
- C. PG analogues
- D. Verapamil
Explanation: ***Apraclonidine*** - **Apraclonidine** is a synthetic **alpha-2 adrenergic agonist** that reduces aqueous humor production and increases uveoscleral outflow, thereby lowering intraocular pressure. - It is primarily used for the short-term treatment of **open-angle glaucoma** or ocular hypertension. *Timolol* - **Timolol** is a **non-selective beta-adrenergic blocker** that reduces aqueous humor production, leading to a decrease in intraocular pressure. - It does not act on alpha-2 receptors, distinguishing it from apraclonidine. *PG analogues* - **Prostaglandin analogues** (PG analogues) such as latanoprost, bimatoprost, and travoprost are primarily used to treat glaucoma by **increasing uveoscleral outflow** of aqueous humor. - They act on **prostaglandin F2α receptors**, not alpha-2 adrenergic receptors. *Verapamil* - **Verapamil** is a **calcium channel blocker** primarily used to treat hypertension, angina, and arrhythmias. - It acts by blocking calcium channels in vascular smooth muscle and the heart, and does not have significant alpha-2 adrenergic agonist activity.
Question 125: Which of the following is the only clinically available depolarizing muscle relaxant?
- A. Decamethonium
- B. Suxamethonium (Correct Answer)
- C. Mivacurium
- D. None of the options
Explanation: ***Suxamethonium*** - **Suxamethonium** (also known as succinylcholine) is currently the **only depolarizing neuromuscular blocker** available for clinical use. - It works by mimicking acetylcholine, binding to and activating nicotinic acetylcholine receptors at the **neuromuscular junction**, causing initial muscle fasciculations followed by relaxation. *Decamethonium* - **Decamethonium** is a depolarizing neuromuscular blocker but is **no longer clinically available** due to its prolonged action and side effects. - It also acts by opening nicotinic acetylcholine receptor channels, leading to depolarization and muscle paralysis. *Mivacurium* - **Mivacurium** is a **nondepolarizing neuromuscular blocker**, meaning it acts as a competitive antagonist at the acetylcholine receptor. - It is known for its **short duration of action** due to rapid hydrolysis by plasma cholinesterases but is not depolarizing. *None of the options* - This option is incorrect because suxamethonium is indeed a clinically available depolarizing muscle relaxant. - The question specifically asks for the *only* clinically available one, which suxamethonium fulfills.
Question 126: What is the treatment for extrapyramidal side effects induced by Haloperidol?
- A. Barbiturates
- B. SSRIs
- C. Benzodiazepines
- D. Anticholinergic drugs (Correct Answer)
Explanation: ***Anticholinergic drugs (effective treatment)*** - **Anticholinergic medications**, such as **benztropine** or **diphenhydramine**, are the primary treatment for **acute extrapyramidal symptoms (EPS)** like dystonia and parkinsonism induced by antipsychotics like haloperidol. - They work by **blocking muscarinic acetylcholine receptors**, helping to restore the balance between dopamine and acetylcholine in the basal ganglia. *Benzodiazepines (used for anxiety and muscle relaxation)* - While benzodiazepines can offer some relief for **akathisia** (a form of EPS characterized by restlessness) due to their sedative and muscle relaxant properties, they are **not the first-line treatment for other acute EPS** such as dystonia or parkinsonism. - They primarily enhance **GABAergic transmission** and are effective for anxiety and seizure control rather than direct antagonism of EPS mechanisms. *Barbiturates (used as sedative-hypnotic drugs)* - **Barbiturates** are strong central nervous system depressants used for sedation, anesthesia, and seizure control, but are **not indicated for the treatment of EPS**. - Their significant **sedative and addictive potential**, along with a narrow therapeutic index, makes them unsuitable for this purpose. *SSRIs (used for depression and anxiety)* - **SSRIs (Selective Serotonin Reuptake Inhibitors)** are antidepressants that work by increasing serotonin levels in the brain and are used to treat depression, anxiety, and obsessive-compulsive disorder. - They **do not have a direct role** in ameliorating dopamine-acetylcholine imbalance responsible for haloperidol-induced EPS.
Question 127: What is the mechanism of action of duloxetine?
- A. Selective serotonin reuptake inhibition
- B. Selective norepinephrine reuptake inhibition
- C. Inhibition of both serotonin and norepinephrine reuptake (Correct Answer)
- D. No effect on neurotransmitter reuptake
Explanation: ***Inhibition of both serotonin and norepinephrine reuptake*** - **Duloxetine** is a **serotonin-norepinephrine reuptake inhibitor (SNRI)**, meaning it blocks the reuptake of both neurotransmitters, increasing their concentrations in the synaptic cleft [2]. - This dual action contributes to its efficacy in treating **depression**, **anxiety disorders**, and **neuropathic pain** [2], [3]. *Selective serotonin reuptake inhibition* - This describes the mechanism of **SSRIs (Selective Serotonin Reuptake Inhibitors)**, such as fluoxetine or sertraline, which primarily target serotonin [1]. - Duloxetine's mechanism is broader, affecting both serotonin and norepinephrine [2]. *Selective norepinephrine reuptake inhibition* - This mechanism is characteristic of medications like **atomoxetine**, used for ADHD, which primarily targets norepinephrine. - Duloxetine has a dual action, not selective to norepinephrine alone. *No effect on neurotransmitter reuptake* - Medications with no effect on neurotransmitter reuptake would not typically be effective as antidepressants or treatments for neuropathic pain. - Duloxetine's therapeutic effects are directly linked to its inhibition of reuptake for both serotonin and norepinephrine [2], [4].
Question 128: Which of the following actions is NOT associated with tricyclic antidepressants?
- A. Block 5-HT or NE reuptake
- B. Anticholinergic action
- C. MAO inhibition (Correct Answer)
- D. Causes sedation
Explanation: ***MAO inhibition*** - Tricyclic antidepressants (TCAs) primarily exert their effects by inhibiting the reuptake of **norepinephrine** and **serotonin**, not by inhibiting monoamine oxidase (MAO). - **MAO inhibitors** are a distinct class of antidepressants with a different mechanism of action and side effect profile. *Anticholinergic action* - Many TCAs have significant **anticholinergic effects**, blocking muscarinic receptors and leading to side effects like dry mouth, constipation, and blurred vision. - These effects contribute to the **adverse event profile** of TCAs, especially in elderly patients. *Block 5-HT or NE reuptake* - The primary mechanism of action of TCAs involves the **inhibition of serotonin (5-HT)** and **norepinephrine (NE) reuptake** into presynaptic neurons. - This action increases the concentration of these neurotransmitters in the **synaptic cleft**, thereby potentiating their effects. *Causes sedation* - TCAs frequently cause **sedation**, particularly the more histaminergic ones (e.g., amitriptyline, doxepin), due to their **histamine H1 receptor antagonism**. - This side effect can be beneficial for patients with insomnia but can be problematic for daytime functioning.
Question 129: Which of the following statements about flumazenil is correct?
- A. Can be used in barbiturate poisoning
- B. Specific antidote for opiate overdose
- C. Can be used in benzodiazepine overdose (Correct Answer)
- D. None of the options
Explanation: ***Can be used in benzodiazepine overdose*** - **Flumazenil** is a **competitive antagonist** at the **GABA-A receptor**, specifically designed to reverse the effects of **benzodiazepines**. - It binds to the same receptor site as benzodiazepines, effectively blocking their sedative and anxiolytic actions, making it useful in emergent overdose situations. *Can be used in barbiturate poisoning* - **Flumazenil** is **ineffective** in **barbiturate overdose** because barbiturates bind to a different site on the GABA-A receptor than benzodiazepines. - Barbiturates enhance **GABAergic activity** through a distinct mechanism, which flumazenil does not antagonize. *Specific antidote for opiate overdose* - The **specific antidote for opiate overdose** is **naloxone**, which acts as an opioid receptor antagonist. - **Flumazenil** has **no affinity** for opioid receptors and thus no role in reversing opiate toxicity. *None of the options* - This option is incorrect because **flumazenil** is indeed used for **benzodiazepine overdose**, as described above. - Its specific mechanism of action targets benzodiazepine-induced central nervous system depression.
Question 130: Which of the following typical antipsychotic drugs is least commonly used in depot form?
- A. Haloperidol
- B. Fluphenazine
- C. Chlorpromazine (Correct Answer)
- D. Trifluoperazine
Explanation: ***Chlorpromazine*** - Chlorpromazine is a **typical antipsychotic** that is **NOT available in depot form** for clinical use. - It is available only in **oral** and **short-acting injectable** formulations, making it the **least commonly used in depot form** among the options listed. - Its high sedative properties, orthostatic hypotension risk, and pharmacokinetic profile make it unsuitable for long-acting depot formulation. *Haloperidol* - **Haloperidol decanoate** is one of the **most widely used depot formulations** of typical antipsychotics. - Administered intramuscularly every **3-4 weeks**, it is highly effective for **long-term maintenance treatment** in schizophrenia. - Its favorable pharmacokinetic profile makes it ideal for depot preparation. *Fluphenazine* - **Fluphenazine decanoate** and **fluphenazine enanthate** are **well-established depot preparations** with decades of clinical use. - These formulations allow for dosing every **2-4 weeks**, significantly improving **medication adherence** in chronic psychotic disorders. - Fluphenazine depot is a first-line option for long-acting injectable antipsychotic therapy. *Trifluoperazine* - Trifluoperazine is primarily available and used as an **oral medication** for maintenance therapy. - While some limited depot formulations have been reported in older literature, they are **not commonly used in clinical practice**. - However, it is still more available in depot form than chlorpromazine, which has essentially **no depot use**.