NEET-PG 2019 - Pharmacology Practice Questions

Q: Mechanism of action of teduglutide in short bowel syndrome:

GLP-2 analog that inhibits apoptosis. ***GLP-2 analog that inhibits apoptosis*** - **Teduglutide** is a synthetic analog of **glucagon-like peptide-2 (GLP-2)**, which is a naturally occurring human hormone [1]. - Its primary mechanism in **short bowel syndrome** involves promoting mucosal growth and inhibiting epithelial cell apoptosis, thereby enhancing nutrient absorption and gut adaptation. *GLP-1 analogs that inhibits apoptosis* - **GLP-1 analogs** like exenatide or liraglutide are primarily used for **type 2 diabetes mellitus** to stimulate insulin secretion and suppress glucagon [2]. - While they can have some effects on gut motility, their main role is not in promoting mucosal growth or inhibiting apoptosis in the context of short bowel syndrome. *HT1A inhibitor* - **HT1A inhibitors** (5-HT1A receptor antagonists) are typically involved in modulating serotonin pathways, often with applications in conditions like **anxiety** or **depression**. - There is no known direct link between HT1A inhibition and the treatment of short bowel syndrome. *C-peptide analogs* - **C-peptide** is a byproduct of insulin production and has been studied for potential roles in preventing diabetes complications, particularly in relation to **microvascular complications** [3], [4]. - It does not play a direct role as a therapeutic agent for promoting intestinal adaptation or inhibiting apoptosis in short bowel syndrome.

Q: Mannitol is used in the management of:-

Acute angle-closure glaucoma. ***Acute angle-closure glaucoma*** - **Mannitol** is an osmotic diuretic [1] used to rapidly reduce **intraocular pressure** in conditions like acute angle-closure glaucoma [2]. - It works by creating an **osmotic gradient** that draws fluid from the vitreous humor into the bloodstream [2]. - This is a well-established **emergency indication** for mannitol [2]. *Acute renal failure* - While mannitol may be used in **prevention** of acute kidney injury (e.g., in rhabdomyolysis, cardiovascular surgery) [2], its use in established acute renal failure is generally **contraindicated** if the patient is **anuric**, as it can exacerbate fluid overload [2]. - It is **not a primary management** for acute renal failure among the given options. *Pulmonary edema* - **Mannitol** is generally **contraindicated** in pulmonary edema because its initial effect is to increase **intravascular volume** [2], which can worsen fluid accumulation in the lungs. - Loop diuretics like **furosemide** are preferred for their rapid onset and profound diuretic effect in pulmonary edema. *Congestive cardiac failure* - **Mannitol** is typically **contraindicated** in congestive cardiac failure as it can cause a **transient increase in plasma volume**, potentially worsening cardiac workload and leading to decompensation [2]. - Diuretics commonly used in heart failure, such as **loop diuretics** (e.g., furosemide) or **thiazide diuretics**, are preferred to reduce fluid overload.

Q: Drug of choice for Digoxin induced Ventricular Tachycardia:

Lignocaine. ***Lignocaine*** - **Lignocaine** (also known as lidocaine) is the drug of choice for digoxin-induced ventricular tachycardia due to its ability to suppress ventricular arrhythmias without further compromising cardiac contractility [1]. - It works by blocking **sodium channels** in the myocardium, reducing automaticity and stabilizing the cardiac membrane [1]. *Diltiazem* - **Diltiazem** is a calcium channel blocker primarily used for supraventricular tachycardias and angina [1]. - It is contraindicated in digoxin toxicity as it can worsen myocardial depression and AV nodal blockade [1]. *Propranolol* - **Propranolol** is a beta-blocker that can suppress some arrhythmias but is generally not the first-line treatment for digoxin-induced ventricular tachycardia [1]. - Beta-blockers can worsen **bradycardia** and **AV block** often seen in digoxin toxicity [1]. *Verapamil* - **Verapamil** is a calcium channel blocker similar to diltiazem and can exacerbate digoxin toxicity [1]. - It is known to increase serum **digoxin levels** and can worsen the underlying cardiotoxic effects.

Q: Drug inhibiting granulocyte migration is:-

Colchicine. ***Colchicine*** - **Colchicine** inhibits **granulocyte migration** by binding to tubulin, thereby disrupting microtubule assembly and function [2]. - This action is crucial in its use for conditions like **gout**, where it reduces the inflammatory response by preventing neutrophil chemotaxis to crystal deposits [1], [2]. *Montelukast* - **Montelukast** is a **leukotriene receptor antagonist** that primarily reduces bronchoconstriction and inflammation. - While it affects inflammatory pathways, its direct action is not inhibiting granulocyte migration but rather blocking the effects of leukotrienes. *Cromoglycate* - **Cromoglycate** (e.g., cromolyn sodium) is a **mast cell stabilizer** that prevents the release of inflammatory mediators. - Its main mechanism involves preventing mast cell degranulation, not directly inhibiting granulocyte migration. *Felbamate* - **Felbamate** is an **antiepileptic drug** used in the treatment of seizures. - Its mechanism of action involves blocking NMDA receptors and modulating GABAergic transmission; it has no known role in inhibiting granulocyte migration.

Q: Cilastatin is given in combination with Imipenem because:-

Cilastatin prevents degradation of Imipenem in kidney. ***Cilastatin prevents degradation of Imipenem in kidney*** - **Imipenem** is extensively metabolized in the renal tubules by the enzyme **dihydropeptidase-I**, leading to its inactivation and potential nephrotoxicity. - **Cilastatin** is a **dihydropeptidase-I inhibitor** that prevents this enzymatic breakdown, increasing the bioavailability and efficacy of imipenem and reducing the risk of renal damage. *Inhibits the enzymes that digest Imipenem in stomach* - **Imipenem** is a parenteral antibiotic and is not administered orally; therefore, degradation in the stomach is not a relevant concern. - Its combination with cilastatin is specifically to address renal metabolism, not gastric degradation. *Cilastatin increase absorption of Imipenem* - **Cilastatin** does not enhance the absorption of imipenem; its role is primarily to inhibit renal metabolism. - Imipenem is administered intravenously, bypassing the need for gastrointestinal absorption. *Reduces side effects of Imipenem* - While cilastatin does prevent the formation of nephrotoxic metabolites of imipenem, its primary role is to **maintain therapeutic levels** and prevent drug inactivation. - The reduction in **nephrotoxicity** is a consequence of preventing degradation, rather than a direct mitigation of general side effects.

Q: Which of the following is a contraindication to the use of Beta Blockers:

Severe asthma with bronchospasm. ***Severe asthma with bronchospasm*** - Beta-blockers, especially **non-selective ones**, can block beta-2 receptors in the lungs, leading to **bronchoconstriction** and worsening asthma symptoms. - This can precipitate a severe **asthma attack** and respiratory distress, making it an **absolute contraindication**. - Even cardioselective beta-blockers should be avoided in severe asthma. *Thyroid storm* - Beta-blockers are often used in **thyroid storm** to manage hyperadrenergic symptoms like **tachycardia** and **tremors**. - Propranolol also has the added benefit of inhibiting peripheral conversion of T4 to T3. - They are not contraindicated but rather an important part of treatment. *Glaucoma* - Topical beta-blockers (e.g., timolol) are commonly used to treat **glaucoma** by **reducing aqueous humor production**, thereby lowering intraocular pressure. - Oral beta-blockers also have this effect and are not contraindicated in glaucoma. *AV nodal reentrant tachycardia (AVNRT)* - Beta-blockers are frequently used in the management of **AVNRT** by slowing AV nodal conduction. - They are effective in both acute termination and prophylaxis of AVNRT episodes. - **Note:** Beta-blockers ARE contraindicated in **atrial fibrillation with Wolff-Parkinson-White syndrome** (pre-excited AF), as blocking the AV node can preferentially conduct through the accessory pathway, potentially causing ventricular fibrillation.

Q: Reason for preferring Cisatracurium over Atracurium is:-

Lesser provocation of histamine release. ***Lesser provocation of histamine release*** - **Cisatracurium** is preferred over atracurium primarily due to its significantly **lower potential to induce histamine release**, leading to fewer cardiovascular side effects like hypotension and tachycardia. - This property makes cisatracurium a **safer option** for patients prone to hemodynamic instability or allergic reactions. *Faster acting than Atracurium* - Both atracurium and cisatracurium are **intermediate-acting** neuromuscular blockers, and their onset times are quite similar, with cisatracurium sometimes having a slightly *slower* onset. - The difference in onset time is **not clinically significant** enough to be a primary reason for preference. *Shorter action than Atracurium* - **Cisatracurium** has a slightly **longer duration of action** compared to atracurium, although both are considered intermediate-acting drugs. - Therefore, a shorter duration of action is **not a reason for its preference**; instead, it might even be a slight disadvantage in certain clinical scenarios requiring rapid reversal. *Does not undergo Hoffman elimination* - Both atracurium and cisatracurium undergo **Hoffman elimination** (non-enzymatic degradation) and ester hydrolysis, which allows for their use in patients with renal or hepatic dysfunction. - This is a shared characteristic, not a distinguishing factor that makes cisatracurium superior, and cisatracurium actually relies *more* heavily on Hoffman elimination.

Q: Which of the following drugs is used for smoking cessation?

Varenicline. ***Varenicline*** - **Varenicline** is a **partial agonist** at the **α4β2 nicotinic acetylcholine receptor**, reducing cravings and withdrawal symptoms while decreasing the rewarding effects of nicotine [2]. - It is a first-line pharmacotherapy for **smoking cessation**, often initiated a week before the target quit date. *Gabapentin* - **Gabapentin** is primarily an **anticonvulsant** and is also used to treat **neuropathic pain**. - It is not indicated for **smoking cessation** and acts by modulating **GABAergic neurotransmission**, unrelated to nicotine dependence. *Acamprosate* - **Acamprosate** is used to maintain **abstinence from alcohol** in patients with alcohol dependence. - Its mechanism involves restoring the balance between **excitation and inhibition** in the brain, which is not directly applicable to nicotine dependence. *Nalmefene* - **Nalmefene** is an **opioid system modulator** used for reducing **alcohol consumption** in adults with alcohol dependence [1]. - It acts as an **opioid receptor antagonist**, a mechanism distinct from the neurotransmitter systems involved in nicotine addiction [1].

Q: Hypertension and pulmonary edema associated with scorpion sting is managed by :-

Prazosin. ***Prazosin*** - **Prazosin** is an **alpha-1 adrenergic receptor blocker** that causes vasodilation, reducing both preload and afterload, which is crucial in managing scorpion sting-induced **hypertension** and **pulmonary edema** [1]. - It effectively counteracts the massive catecholamine release triggered by scorpion venom, which leads to widespread vasoconstriction and increased cardiac workload [1]. *Phentolamine* - **Phentolamine** is a non-selective alpha-adrenergic blocker, but it has a shorter duration of action and is typically used for managing **hypertensive crises** during pheochromocytoma surgery. - While it can lower blood pressure, its rapid onset and short half-life make it less suitable for sustained management of scorpion sting complications compared to prazosin. *Spironolactone* - **Spironolactone** is an **aldosterone antagonist** and a potassium-sparing diuretic, primarily used in conditions like heart failure, cirrhosis, and primary hyperaldosteronism. - It is not an acute treatment for hypertension or pulmonary edema caused by scorpion venom, as its mechanism of action is too slow and indirect to counteract the immediate effects of catecholamine surge. *Carvedilol* - **Carvedilol** is a non-selective beta-blocker with alpha-1 blocking activity, commonly used in chronic heart failure and hypertension [2]. - While it has some alpha-blocking properties, its dominant **beta-blocking effects** can exacerbate pulmonary edema in an acute setting and may worsen cardiac output if bradycardia or myocardial depression occurs [2].

Q: Which of the following is the first line drug for mastitis?

Cloxacillin. ***Cloxacillin*** - **Cloxacillin** is a penicillinase-resistant penicillin, making it effective against **Staphylococcus aureus**, the most common causative organism of mastitis. - It is the **first-line oral antibiotic** for treating mastitis in patients without penicillin allergy. - As a penicillin derivative, it should be **avoided in penicillin-allergic patients**, who may be treated with cephalosporins (if no cross-reactivity) or macrolides instead. *Cefazolin* - **Cefazolin** is a first-generation cephalosporin, typically administered intravenously. While effective against methicillin-sensitive *S. aureus*, it is not the first-line oral treatment for mastitis. - It is usually reserved for hospitalized patients or those needing parenteral therapy, not for initial outpatient management. *Ampicillin* - **Ampicillin** is a penicillin antibiotic that is susceptible to degradation by beta-lactamases produced by many *Staphylococcus aureus* strains. - It is generally **not effective** against beta-lactamase-producing *S. aureus*, which is the predominant pathogen in mastitis. *Metronidazole* - **Metronidazole** is an antibiotic primarily effective against **anaerobic bacteria** and certain **parasites**. - It has **no significant activity** against aerobic bacteria like *Staphylococcus aureus*, making it inappropriate for treating typical bacterial mastitis.

Question 1

Mechanism of action of teduglutide in short bowel syndrome:

Accepted Answer

GLP-2 analog that inhibits apoptosis

Answer

HT1A inhibitor

Answer

C-peptide analog

Answer

GLP-1 analog that inhibits apoptosis

Question 2

Mannitol is used in the management of:-

Accepted Answer

Acute angle-closure glaucoma

Answer

Acute renal failure

Answer

Pulmonary edema

Answer

Congestive cardiac failure

Question 3

Drug of choice for Digoxin induced Ventricular Tachycardia:

Accepted Answer

Lignocaine

Answer

Diltiazem

Answer

Propranolol

Answer

Verapamil

Question 4

Drug inhibiting granulocyte migration is:-

Accepted Answer

Colchicine

Answer

Montelukast

Answer

Cromoglycate

Answer

Felbamate

Question 5

Cilastatin is given in combination with Imipenem because:-

Accepted Answer

Cilastatin prevents degradation of Imipenem in kidney

Answer

Inhibits the enzymes that digest Imipenem in stomach

Answer

Reduces side effects of Imipenem

Answer

Cilastatin increases absorption of Imipenem

Question 6

Which of the following is a contraindication to the use of Beta Blockers:

Accepted Answer

Severe asthma with bronchospasm

Answer

Thyroid storm

Answer

Glaucoma

Answer

AV nodal reentrant tachycardia (AVNRT)

Question 7

Reason for preferring Cisatracurium over Atracurium is:-

Accepted Answer

Lesser provocation of histamine release

Answer

Faster acting than Atracurium

Answer

Shorter action than Atracurium

Answer

Does not undergo Hoffman elimination

Question 8

Which of the following drugs is used for smoking cessation?

Accepted Answer

Varenicline

Answer

Gabapentin

Answer

Acamprosate

Answer

Nalmefene

Question 9

Hypertension and pulmonary edema associated with scorpion sting is managed by :-

Accepted Answer

Prazosin

Answer

Phentolamine

Answer

Spironolactone

Answer

Carvedilol

Question 10

Which of the following is the first line drug for mastitis?

Accepted Answer

Cloxacillin

Answer

Cefazolin

Answer

Ampicillin

Answer

Metronidazole

NEET-PG 2019 — Pharmacology