Which of the following drugs can lead to pemphigus?
Which of the following is a long-acting local anesthetic?
Suxamethonium primarily acts on which type of receptors?
Which of the following is the only clinically available depolarizing muscle relaxant?
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?
Modafinil is primarily used for the treatment of which of the following conditions?
What is the treatment for extrapyramidal side effects induced by Haloperidol?
Which drug is not considered a mood stabilizer?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 121: Which of the following drugs can lead to pemphigus?
- A. Carbamazepine
- B. Penicillamine (Correct Answer)
- C. Isoniazid
- D. Furosemide
Explanation: ***Penicillamine*** - **Penicillamine** is a well-known drug that can induce **pemphigus**, often through mechanisms involving alterations in **desmosome structure** or function. - The drug's sulfhydryl groups are thought to interfere with the integrity of **desmoglein proteins**, leading to blister formation. *Isoniazid* - **Isoniazid** is a first-line antituberculosis drug primarily associated with **hepatotoxicity** and **peripheral neuropathy**. - It is not typically implicated in the development of **pemphigus**. *Carbamazepine* - **Carbamazepine** is an anticonvulsant that can cause various cutaneous reactions, most notably **Stevens-Johnson syndrome (SJS)** and **toxic epidermal necrolysis (TEN)**. - While it can cause severe skin reactions, **pemphigus** is not a common side effect of carbamazepine. *Furosemide* - **Furosemide** is a loop diuretic that can cause **photosensitivity**, rashes, and rarely, severe skin reactions like **erythema multiforme**. - It is not recognized as a drug that induces **pemphigus**.
Question 122: Which of the following is a long-acting local anesthetic?
- A. Dibucaine (Correct Answer)
- B. Prilocaine
- C. Procaine
- D. Lignocaine
Explanation: ***Dibucaine*** - **Dibucaine** is a **long-acting amide local anesthetic** with a duration of action up to 10 hours. - Its high **lipid solubility** contributes to its prolonged effect and greater potency compared to other local anesthetics. *Prilocaine* - **Prilocaine** is considered an **intermediate-duration amide local anesthetic**, with a duration of action typically 1-2 hours. - It carries a risk of **methemoglobinemia** at higher doses, which differentiates it from longer-acting agents. *Procaine* - **Procaine** is a **short-acting ester local anesthetic**, with a duration of action usually less than 1 hour. - It is known for its relatively **high allergenicity** due to its metabolism to para-aminobenzoic acid (PABA). *Lignocaine* - **Lignocaine (Lidocaine)** is an **intermediate-acting amide local anesthetic**, with a duration of action around 1-3 hours. - It is one of the most commonly used local anesthetics, but its duration is not as long as that of dibucaine.
Question 123: Suxamethonium primarily acts on which type of receptors?
- A. Nicotinic acetylcholine receptors (Correct Answer)
- B. Potassium channels
- C. Calcium channels
- D. Chloride channels
Explanation: ***Nicotinic acetylcholine receptors*** - **Suxamethonium** is a depolarizing muscle relaxant that acts as an **agonist at nicotinic acetylcholine receptors** at the neuromuscular junction. - This initial activation leads to muscle fasciculations followed by prolonged depolarization, causing **flaccid paralysis**. *Potassium channels* - While some drugs may affect potassium channels to alter neuronal excitability, suxamethonium's primary mechanism of action is not on these channels. - Blocking potassium channels is characteristic of drugs like **certain antiarrhythmics** or **sulfonylureas**. *Calcium channels* - **Calcium channels** play a role in muscle contraction, but they are not the primary target of suxamethonium. - Drugs like **dihydropyridines** (e.g., nifedipine) target calcium channels for their antihypertensive effects. *Chloride channels* - Chloride channels are involved in maintaining resting membrane potential and inhibitory neurotransmission. - Drugs such as **benzodiazepines** indirectly enhance GABA-mediated chloride influx, which is distinct from suxamethonium's action.
Question 124: 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 125: 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 126: 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 127: 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**.
Question 128: Modafinil is primarily used for the treatment of which of the following conditions?
- A. Narcolepsy (Correct Answer)
- B. Sexual dysfunction
- C. Depression
- D. Anxiety
Explanation: ***Narcolepsy*** - **Modafinil** is a **eugeroic** (wakefulness-promoting agent) specifically approved and widely used for the treatment of excessive daytime sleepiness associated with **narcolepsy**. - Its mechanism involves increasing **dopamine** and **norepinephrine** levels, and modulating **orexin** pathways, promoting alertness without significant psychomotor stimulation. *Sexual dysfunction* - While sometimes explored off-label for certain types of sexual dysfunction, **modafinil** is not a primary or approved treatment for this condition. - Primary treatments for sexual dysfunction often involve specific medications like **PDE5 inhibitors** or hormone therapy, depending on the cause. *Depression* - **Modafinil** is not a primary antidepressant, although it can be used as an **adjunctive therapy** in some cases to combat residual fatigue or hypersomnia associated with depression. - Standard treatment for depression involves **selective serotonin reuptake inhibitors (SSRIs)**, **serotonin-norepinephrine reuptake inhibitors (SNRIs)**, or other classes of antidepressants. *Anxiety* - **Modafinil** is a stimulant-like drug and can sometimes **exacerbate anxiety** in susceptible individuals due to its catecholaminergic effects. - Primary treatments for anxiety disorders include **selective serotonin reuptake inhibitors (SSRIs)**, **benzodiazepines** (for acute relief), and psychotherapy.
Question 129: 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 130: Which drug is not considered a mood stabilizer?
- A. Lithium
- B. Lamotrigine
- C. Imipramine (Correct Answer)
- D. Carbamazepine
Explanation: ***Imipramine*** - Imipramine is a **tricyclic antidepressant (TCA)**, primarily used to treat depression, not to stabilize mood in bipolar disorder. - TCAs can sometimes induce **mania** or hypomania in individuals with bipolar disorder, thus they are generally not used as monotherapy for mood stabilization. *Lithium* - **Lithium** is considered the gold standard and one of the oldest and most effective **mood stabilizers** for bipolar disorder. - It works by modulating **neurotransmitter systems** and second messenger pathways in the brain. *Lamotrigine* - **Lamotrigine** is an **anticonvulsant** medication that is also recognized as an effective **mood stabilizer**, particularly for preventing depressive episodes in bipolar disorder. - Its mechanism involves stabilizing neuronal membranes by blocking **voltage-gated sodium channels**. *Carbamazepine* - **Carbamazepine** is an **anticonvulsant** medication often used as a **mood stabilizer** for the treatment of acute manic and mixed episodes in bipolar disorder. - It works by reducing the excitability of nerve impulses through blocking **voltage-sensitive sodium channels**.