Which of the following drugs is an alpha 2 agonist?
What is the mechanism of action of duloxetine?
Treatment of dhatura poisoning is done with:
Mechanism of action of thiazides is by -
Pilocarpine is used in all of the following except:
True about rotavirus vaccine:
Which of the following drugs can cause hypertrophic pyloric stenosis?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 131: 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 132: 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 133: Treatment of dhatura poisoning is done with:
- A. Physostigmine (Correct Answer)
- B. Neostigmine
- C. Naloxone
- D. Pilocarpine
Explanation: ***Physostigmine*** - **Physostigmine** is a **reversible cholinesterase inhibitor** that can cross the **blood-brain barrier**, allowing it to counteract both peripheral and central anticholinergic effects of dhatura poisoning. - It increases the amount of **acetylcholine** at muscarinic and nicotinic receptors, directly competing with the anticholinergic agents. *Neostigmine* - **Neostigmine** is also a **cholinesterase inhibitor**, but it does not cross the **blood-brain barrier** effectively. - Therefore, it is primarily used for its **peripheral effects** and is not suitable for reversing the central nervous system manifestations of dhatura poisoning. *Naloxone* - **Naloxone** is a **pure opioid antagonist** used to reverse the effects of **opioid overdose**. - It has no role in the treatment of **dhatura poisoning**, which involves anticholinergic toxicity. *Pilocarpine* - **Pilocarpine** is a **direct muscarinic agonist** that acts at peripheral muscarinic receptors. - While it could counteract some peripheral anticholinergic effects, it does not cross the **blood-brain barrier** effectively and cannot address the central nervous system manifestations. - It is not the preferred or primary antidote for **anticholinergic toxicity** as it doesn't address both central and peripheral effects like physostigmine does.
Question 134: Mechanism of action of thiazides is by -
- A. Inhibiting Na+K+2Cl- in ascending limb of loop of henle
- B. Inhibiting Na+/Cl- symporter in DCT (Correct Answer)
- C. Inhibiting Na+/Cl- symporter in PCT
- D. Inhibiting Na+K+2Cl- in descending limb of loop of henle
Explanation: **Inhibiting Na+/Cl- symporter in DCT** - Thiazide diuretics primarily act on the **distal convoluted tubule (DCT)** of the nephron [2]. - They inhibit the **Na+/Cl- symporter** (NCC channel) on the apical membrane, preventing reabsorption of sodium and chloride ions [1], [2]. *Inhibiting Na+K+2CI- in descending limb of loop of henle* - The descending limb of the loop of Henle is permeable to water but largely impermeable to solutes; there is no significant Na+K+2Cl- symporter activity here. - This mechanism describes the action of loop diuretics, but they act on the **ascending** limb, not the descending limb. *Inhibiting Na+K+2Cl- in ascending limb of loop of henle* - This mechanism describes the action of **loop diuretics** (e.g., furosemide, bumetanide) [3]. - Loop diuretics inhibit the **Na+K+2Cl- cotransporter (NKCC2)** in the thick ascending limb of the loop of Henle, leading to significant diuresis [3]. *Inhibiting Na+/Cl- symporter in PCT* - The **proximal convoluted tubule (PCT)** is primarily responsible for reabsorbing most of the filtered sodium, chloride, bicarbonate, and other solutes. - While sodium is reabsorbed in the PCT, it's mainly through Na+/H+ exchangers and other mechanisms, not a specific Na+/Cl- symporter that is targeted by thiazides [2].
Question 135: Pilocarpine is used in all of the following except:
- A. Primary, Open Angle Glaucoma
- B. Acute Angle Closure Glaucoma
- C. Malignant Glaucoma (Correct Answer)
- D. Chronic Synechial Angle Closure Glaucoma
Explanation: ***Malignant Glaucoma*** - **Pilocarpine** is contraindicated in **malignant glaucoma** because it can worsen the condition by causing **ciliary body edema** and anterior displacement of the lens-iris diaphragm. - This form of glaucoma requires treatment aimed at posterior displacement of the lens-iris diaphragm, often involving **cycloplegics**, **hyperosmotic agents**, or surgical interventions. *Primary, Open Angle Glaucoma* - **Pilocarpine** is an effective **miotic agent** that increases aqueous humor outflow through the **trabecular meshwork**, thereby lowering intraocular pressure. - It can be used as a treatment for **primary open-angle glaucoma**, although it is less commonly used due to its side effects and the availability of better-tolerated medications. *Acute Angle Closure Glaucoma* - **Pilocarpine** is typically used in the management of **acute angle-closure glaucoma** after the intraocular pressure has been acutely lowered by other agents. - It works by inducing **miosis**, which pulls the iris away from the **trabecular meshwork**, opening the angle and facilitating aqueous outflow. *Chronic Synechial Angle Closure Glaucoma* - In **chronic synechial angle-closure glaucoma**, **pilocarpine** can be used to break or prevent the formation of new **peripheral anterior synechiae** by constricting the pupil. - However, its effectiveness is limited if extensive synechiae have already formed, as these physically block the outflow pathway.
Question 136: True about rotavirus vaccine:
- A. Given orally (Correct Answer)
- B. Killed vaccine
- C. Should be given before 5 years
- D. Given subcutaneous
Explanation: ***Given orally*** - Rotavirus vaccines are **live attenuated vaccines** administered orally to stimulate localized immunity in the gastrointestinal tract. - This oral route is crucial for inducing **mucosal immunity**, which is important for protection against rotavirus infection. *Killed vaccine* - The rotavirus vaccine is an **attenuated live vaccine**, meaning it contains weakened forms of the virus, not killed ones. - Live attenuated vaccines generally provide a **stronger and longer-lasting immune response** compared to killed vaccines. *Should be given before 5 years* - The rotavirus vaccine series is recommended to be completed in **infancy**, typically before 8 months of age, depending on the specific vaccine brand and schedule. - Giving the vaccine at too old an age increases the (still very small) risk of **intussusception** and a lack of efficacy. *Given subcutaneous* - Rotavirus vaccines are administered by the **oral route**, not subcutaneously. - The **subcutaneous route** is used for various other vaccines, but not for rotavirus.
Question 137: Which of the following drugs can cause hypertrophic pyloric stenosis?
- A. Nifedipine
- B. Vancomycin
- C. Phenyl propanolamine
- D. Erythromycin (Correct Answer)
Explanation: ***Erythromycin*** - **Erythromycin** use in infants, particularly during the first few weeks of life, has been associated with an increased risk of developing **hypertrophic pyloric stenosis**. - The mechanism is believed to involve the drug's properties as a **motilin receptor agonist**, which may affect the development or function of the pyloric sphincter. *Nifedipine* - **Nifedipine** is a calcium channel blocker primarily used for cardiovascular conditions like hypertension and angina. - It works by relaxing smooth muscles and is not linked to the development of **pyloric stenosis**. *Vancomycin* - **Vancomycin** is an antibiotic used for severe bacterial infections, particularly against Gram-positive bacteria. - It is not associated with the development of **hypertrophic pyloric stenosis**. *Phenylpropanolamine* - **Phenylpropanolamine** is a sympathomimetic drug previously used as a decongestant and anorectic. - It primarily affects alpha-adrenergic receptors and has no established link to **pyloric stenosis**.