NEET-PG 2019 - Pharmacology Practice Questions

Q: What is the primary mechanism by which colchicine exerts its anti-inflammatory effects in acute gout?

Acts by inhibiting neutrophil migration. ***Acts by inhibiting neutrophil migration*** - Colchicine primarily functions by **disrupting microtubule formation** in neutrophils, which impairs their chemotaxis and migration to sites of inflammation. - This inhibition of neutrophil activity is crucial in dampening the **inflammatory response** triggered by uric acid crystals in acute gout. *Acts primarily as a uricosuric agent* - While other medications like **probenecid** are uricosuric and increase uric acid excretion, colchicine does not have this primary mechanism of action. - Its main anti-inflammatory effect is independent of uric acid metabolism or excretion. *Is the first-line treatment for chronic gout management* - Colchicine is effective for **acute gout attacks** and as a prophylactic against attacks during initiation of urate-lowering therapy. - However, **allopurinol** and **febuxostat** are the first-line treatments for chronic gout because they reduce uric acid production. *Has no effect on microtubule function* - This statement is incorrect; colchicine's entire mechanism of action is dependent on its ability to **bind to tubulin** and inhibit microtubule polymerization. - This disruption of microtubules is responsible for its anti-inflammatory effects and also its common side effects.

Q: MOA of Teduglutide in short bowel syndrome?

GLP-2 analog. ***GLP-2 analog*** - Teduglutide is a **glucagon-like peptide-2 (GLP-2) analog** that binds to and activates GLP-2 receptors. - This activation promotes **intestinal adaptation** by enhancing mucosal growth, increasing nutrient absorption, and improving fluid balance in patients with short bowel syndrome. *5-HT1A receptor antagonist* - 5-HT1A receptor antagonists are primarily used in conditions related to **serotonin pathways**, such as anxiety or depression. - They do not have a direct mechanism to address the **malabsorption** issues seen in short bowel syndrome. *GLP-1 receptor agonist* - GLP-1 receptor agonists are primarily used in the management of **type 2 diabetes** to enhance insulin secretion and reduce glucagon levels. - While GLP-1 and GLP-2 are related, GLP-1 does not have the same direct **trophic and restorative effects** on the intestinal mucosa as GLP-2. *C-peptide analog* - C-peptide is a byproduct of **insulin production** and its analogs have been studied for potential effects on diabetic neuropathy or nephropathy, but not for intestinal adaptation. - It does not play a direct role in regulating **intestinal growth** or nutrient absorption in the context of short bowel syndrome.

Q: What is the recommended dose of diphtheria antitoxin for adults?

20000 to 50000 IU. ***20000 to 50000 IU*** - For adults with **diphtheria**, the recommended dose of **diphtheria antitoxin (DAT)** in the range of 20,000 to 50,000 IU is appropriate for **pharyngeal or laryngeal diphtheria** of moderate severity (typically disease present for 48-72 hours). - This dosage aims to neutralize the **diphtheria toxin** circulating in the bloodstream and prevent further tissue damage. - **Note:** More severe or extensive disease (>3 days duration or with bull neck) may require higher doses (80,000-120,000 IU). *1000 to 2000 IU* - This dosage is **too low** for therapeutic treatment of diphtheria in adults. - Such a low dose would be insufficient to neutralize the substantial amount of **toxin** produced during an active infection, regardless of disease severity. *10000 to 20000 IU* - This dose is **suboptimal** for most forms of diphtheria in adults. - Even for **mild cutaneous diphtheria**, doses typically start at 20,000 IU or higher. - For respiratory diphtheria, this range would be inadequate to effectively counteract the toxin. *None of the options* - This is incorrect because **20,000 to 50,000 IU** is a recognized and recommended range for diphtheria antitoxin in adult treatment of moderate pharyngeal/laryngeal disease. - Diphtheria antitoxin is a crucial and **specific treatment** for diphtheria, and evidence-based dosage ranges exist based on disease severity and location.

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.

Question 1

What is the primary mechanism by which colchicine exerts its anti-inflammatory effects in acute gout?

Accepted Answer

Acts by inhibiting neutrophil migration

Answer

Acts primarily as a uricosuric agent

Answer

Is the first-line treatment for chronic gout management

Answer

Has no effect on microtubule function

Question 2

MOA of Teduglutide in short bowel syndrome?

Accepted Answer

GLP-2 analog

Answer

5-HT1A receptor antagonist

Answer

GLP-1 receptor agonist

Answer

C-peptide analog

Question 3

What is the recommended dose of diphtheria antitoxin for adults?

Accepted Answer

20000 to 50000 IU

Answer

1000 to 2000 IU

Answer

10000 to 20000 IU

Answer

None of the options

Question 4

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 5

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 6

Drug of choice for Digoxin induced Ventricular Tachycardia:

Accepted Answer

Lignocaine

Answer

Diltiazem

Answer

Propranolol

Answer

Verapamil

Question 7

Drug inhibiting granulocyte migration is:-

Accepted Answer

Colchicine

Answer

Montelukast

Answer

Cromoglycate

Answer

Felbamate

Question 8

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 9

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 10

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

NEET-PG 2019 — Pharmacology