NEET-PG 2025 — Pharmacology
10 Previous Year Questions with Answers & Explanations
Benralizumab acts on which receptor?
A patient with tumor lysis syndrome has elevated uric acid levels. What is the mechanism of action of pegloticase?
A woman diagnosed with migraine has a family history of coronary artery disease. What is the drug of choice for migraine prophylaxis?
A patient is started on hydrochlorothiazide for hypertension and later develops renal stones. Which metabolic effect of hydrochlorothiazide is most likely responsible?
A patient with paroxysmal supraventricular tachycardia (PSVT) requires treatment for prophylaxis. Which drug is appropriate?
A patient presents with GERD. Which drug helps in contraction of LES and increases gastric emptying?
By what primary mechanism does hydrochlorothiazide help prevent the formation of calcium stones?
Patient came with fever headache and nuchal rigidity. LP shows gram-negative diplococci in gram stain. Which of the following will be used for chemoprophylaxis in close contacts of a patient with meningococcal meningitis?
A patient with recurrent episodes of PSVT (Paroxysmal Supraventricular Tachycardia) is being considered for long-term prophylactic therapy to prevent future episodes. Which of the following is the most appropriate preventive treatment?
A patient on hydrochlorothiazide develops renal stones. What explains this adverse effect?
NEET-PG 2025 - Pharmacology NEET-PG Practice Questions and MCQs
Question 1: Benralizumab acts on which receptor?
- A. IL1
- B. IL4
- C. TNF alpha
- D. IL 5 (Correct Answer)
Explanation: ***IL 5***- Benralizumab is a monoclonal antibody that specifically targets the **alpha subunit (IL-5Rα) of the Interleukin-5 Receptor** [1].- By blocking this receptor, it facilitates the depletion of **eosinophils** via **antibody-dependent cell-mediated cytotoxicity (ADCC)**, crucial for treating severe eosinophilic asthma [1].*IL4*- IL-4 is a key mediator of **Type 2 inflammation** often targeted by drugs like **Dupilumab**, which inhibits both IL-4 and **IL-13 signaling**.- Targeting IL-4 is generally aimed at reducing IgE production and overall Th2 response, a different mechanism than the eosinophil depletion mechanism of Benralizumab.*IL1*- IL-1 is a potent **pro-inflammatory cytokine** primarily associated with **autoinflammatory diseases** and targeted by agents like **Anakinra** (IL-1 receptor antagonist).- It is not the primary or specific therapeutic target in severe eosinophilic asthma, which involves Th2 mechanisms and eosinophil recruitment.*TNF alpha*- **TNF-alpha** is a major systemic inflammatory cytokine targeted by biological agents like **Infliximab** and **Etanercept** used in conditions such as **Rheumatoid Arthritis** and **Crohn’s disease**.- While inflammation is involved in asthma, TNF-alpha antagonists are not the standard specific treatment for severe eosinophilic asthma.
Question 2: A patient with tumor lysis syndrome has elevated uric acid levels. What is the mechanism of action of pegloticase?
- A. Urat-1 receptor inhibition
- B. Oxidises uric acid (Correct Answer)
- C. Xanthine oxidase inhibition
- D. Excretion of uric acid
Explanation: ***Oxidises uric acid*** - Pegloticase is a recombinant pegylated uricase enzyme that directly catalyzes the conversion of highly insoluble **uric acid**. - It oxidizes uric acid into **allantoin**, which is a highly soluble compound easily excreted by the kidneys, effectively lowering serum uric acid levels. *Xanthine oxidase inhibition* - This is the mechanism of action for drugs like **allopurinol** and **febuxostat**, used to prevent the formation of uric acid. - These agents act upstream by inhibiting the enzyme responsible for synthesizing uric acid from xanthine and hypoxanthine. *URAT1 receptor inhibition* - URAT1 inhibitors (**lesinurad**) prevent the reabsorption of native uric acid from the renal tubules back into the bloodstream. - This mechanism is characteristic of **uricosuric agents**, which increase the renal clearance of uric acid. *Excretion of uric acid* - While pegloticase ultimately facilitates excretion (as allantoin), this option is too broad; its primary action is **enzymatic conversion**. - Direct excretion of native uric acid is increased by **uricosuric drugs** (e.g., probenecid), not by pegloticase's oxidative action.
Question 3: A woman diagnosed with migraine has a family history of coronary artery disease. What is the drug of choice for migraine prophylaxis?
- A. Topiramate
- B. Ergotamine
- C. Amitriptyline
- D. Propranolol (Correct Answer)
Explanation: ***Propranolol*** - **Propranolol** is a first-line drug for migraine prophylaxis, particularly favored in patients with co-existing conditions like hypertension, anxiety, or, as in this case, risk factors for **Coronary Artery Disease (CAD)**. - As a non-selective beta-blocker, it provides effective migraine prevention while potentially offering **cardioprotective benefits**, making it the safest and best choice here. *Topiramate* - **Topiramate** is also a first-line prophylactic agent, but it is often preferred when patients need to avoid weight gain or have co-existing seizure disorders. - It has no particular advantage over propranolol in lowering cardiac risk and is associated with common side effects such as cognitive impairment (**'fogginess'**) and **nephrolithiasis**. *Ergotamine* - **Ergotamine preparations** are severe vasoconstrictors and are used primarily for the **acute termination** of migraine attacks, not for long-term prophylaxis. - They are absolutely **contraindicated** in patients with established or high risk of **Coronary Artery Disease** (CAD) due to the risk of **myocardial infarction** and stroke. *Amitriptyline* - **Amitriptyline** (a TCA) is used for prophylaxis, especially in patients with co-existing **insomnia** or chronic **tension headaches**. - While effective, TCAs can have potential **cardiac side effects** (e.g., QTc prolongation, orthostatic hypotension) which makes **propranolol** a medically safer choice for patients with a family history of CAD.
Question 4: A patient is started on hydrochlorothiazide for hypertension and later develops renal stones. Which metabolic effect of hydrochlorothiazide is most likely responsible?
- A. Hypocitraturia
- B. Hypocalciuria
- C. Hypomagnesemia
- D. Hyperuricemia (Correct Answer)
Explanation: ***Hyperuricemia*** * Hydrochlorothiazide causes **hyperuricemia** by competing with uric acid for secretion in the proximal tubule, leading to decreased uric acid excretion. * Elevated serum uric acid levels increase the risk of **uric acid stone formation**, which is a well-recognized adverse effect of thiazide diuretics. * This is why thiazides can precipitate gout attacks and increase uric acid stone risk. *Hypocalciuria* * HCTZ causes **decreased urinary calcium excretion** (hypocalciuria) by enhancing calcium reabsorption in the DCT. * This effect is **stone-PROTECTIVE**, not causative - thiazides are actually used therapeutically to prevent recurrent calcium stones. * This would NOT explain stone formation in this patient. *Hypomagnesemia* * While HCTZ can cause magnesium loss, hypomagnesemia is not a primary mechanism for stone formation with thiazide use. * Magnesium is actually a stone inhibitor, so low levels could theoretically contribute, but this is not the main mechanism. *Hypocitraturia* * HCTZ does not typically cause significant citrate wasting or hypocitraturia. * Hypocitraturia is more characteristic of **carbonic anhydrase inhibitors** and chronic metabolic acidosis, not thiazide diuretics.
Question 5: A patient with paroxysmal supraventricular tachycardia (PSVT) requires treatment for prophylaxis. Which drug is appropriate?
- A. IV esmolol
- B. Oral phenytoin
- C. Oral verapamil (Correct Answer)
- D. IV adenosine
Explanation: ***Verapamil*** - It is an oral **non-dihydropyridine calcium channel blocker** commonly used for long-term **prophylaxis** of recurrent PSVT (AVNRT/AVRT) by slowing conduction through the AV node [1], [2]. - It is effective for reducing the frequency of episodes and achieving chronic **rate and rhythm control** in stable patients [1]. *IV adenosine* - Adenosine is the drug of choice for the **acute termination** of PSVT due to its rapid onset and extremely short half-life, making it unsuitable for chronic long-term **prophylaxis** [2]. - It works by transiently blocking the **AV node** conduction [2]. *IV esmolol* - Esmolol is an ultra-short-acting **beta-blocker** administered intravenously, primarily used for **acute control** of heart rate or rhythm in emergency settings [3]. - Since the requirement is for prophylaxis, an oral formulation (e.g., oral metoprolol) would be preferred over an **intravenous agent** [3]. *Oral phenytoin* - Phenytoin is mainly an anti-epileptic and is historically reserved for the treatment of **digitalis-induced ventricular arrhythmias**. - It is **not a standard or primary agent** recommended by current guidelines for the long-term prophylactic management of typical non-digitalis-induced PSVT.
Question 6: A patient presents with GERD. Which drug helps in contraction of LES and increases gastric emptying?
- A. Vonoprazan
- B. Ranitidine
- C. Pantoprazole
- D. Metoclopramide (Correct Answer)
Explanation: ***Metoclopramide*** - It is a **prokinetic agent** that acts as a D2 dopamine receptor antagonist, which increases esophageal tone, enhances peristalsis, and facilitates **gastric emptying**. - It specifically increases the pressure of the **Lower Esophageal Sphincter (LES)**, reducing reflux associated with GERD. *Pantoprazole* - This is a **Proton Pump Inhibitor (PPI)** that reduces acid production by irreversible inhibition of the H+/K+-ATPase pump in parietal cells [1], [2]. - It does not have any significant effect on **LES contraction** or **gastric motility**. *Vonoprazan* - This is a **Potassium-Competitive Acid Blocker (P-CAB)**, which directly and reversibly inhibits the H+/K+-ATPase pump. - Like other acid suppressants, it decreases acid secretion but does not improve **LES function** or **gastric emptying**. *Ranitidine* - This is an **H2 receptor antagonist** that blocks histamine receptors on parietal cells, leading to decreased acid secretion [3]. - It treats GERD by reducing acidity but has no direct action on **LES tone** or stomach **motility**.
Question 7: By what primary mechanism does hydrochlorothiazide help prevent the formation of calcium stones?
- A. It directly dissolves existing calcium stones by altering urinary pH and increasing their solubility.
- B. It increases the urinary excretion of citrate, which acts as a chelating agent.
- C. It increases calcium reabsorption in the distal convoluted tubule, leading to a decrease in urinary calcium excretion. (Correct Answer)
- D. It increases the filtration of calcium at the glomerulus, thereby reducing serum calcium levels.
Explanation: ***It increases calcium reabsorption in the distal convoluted tubule, leading to a decrease in urinary calcium excretion.*** - By inhibiting the **sodium-chloride cotransporter (NCC)** in the **distal convoluted tubule (DCT)**, thiazides indirectly enhance calcium reabsorption via the basolateral Na+/Ca2+ exchanger. - This pharmacological effect causes **hypocalciuria**, which reduces the supersaturation of calcium oxalate/phosphate in the urine, thereby preventing stone formation. *It increases the urinary excretion of citrate, which acts as a chelating agent.* - While citrate is a powerful inhibitor of stones, thiazides are **not** primarily known to substantially increase urinary citrate excretion. - Other measures, such as oral **potassium citrate**, are used specifically to increase urinary citrate levels in stone formers. *It increases the filtration of calcium at the glomerulus, thereby reducing serum calcium levels.* - Thiazides actually tend to cause a slight **increase** in serum calcium (due to enhanced reabsorption in the DCT and bone effects), a condition known as thiazide-induced hypercalcemia. - Their mechanism of stone prevention is focused on reducing **urinary** calcium, not primarily filtering more calcium. *It directly dissolves existing calcium stones by altering urinary pH and increasing their solubility.* - Thiazides are primarily **preventative** medications for stone formation; they do not have a role in directly dissolving existing calcium stones. - The dissolution of some stones (like uric acid stones) is usually achieved by urinary alkalinization (e.g., using **potassium citrate**), which is not the main action of HCTZ.
Question 8: Patient came with fever headache and nuchal rigidity. LP shows gram-negative diplococci in gram stain. Which of the following will be used for chemoprophylaxis in close contacts of a patient with meningococcal meningitis?
- A. Amoxicillin
- B. Rifampicin (Correct Answer)
- C. Doxycycline
- D. Ethambutol
Explanation: ***Rifampicin*** - **Rifampicin** is one of the preferred agents for chemoprophylaxis against meningococcal meningitis in close contacts because it effectively eliminates **Neisseria meningitidis** colonization from the nasopharynx. - The other common options for prophylaxis include **Ceftriaxone** (single IM dose, safe in pregnancy) or **Ciprofloxacin** (single oral dose). *Amoxicillin* - Amoxicillin is commonly used for **otitis media** and **sinusitis** but is ineffective for reliable elimination of nasopharyngeal colonization by **Neisseria meningitidis**. - It is not a recommended prophylactic agent for **meningococcal disease** in close contacts. *Doxycycline* - While a broad-spectrum antibiotic, **Doxycycline** is not the standard or preferred drug for routine **meningococcal prophylaxis**. - It is often used for atypical pneumonias or tick-borne diseases like **Rocky Mountain spotted fever**. *Ethambutol* - **Ethambutol** is a primary anti-mycobacterial drug, used exclusively in the treatment regimen for **Tuberculosis (TB)**. - It has no role or efficacy in the prophylaxis or treatment of **bacterial meningitis** caused by **Neisseria meningitidis**.
Question 9: A patient with recurrent episodes of PSVT (Paroxysmal Supraventricular Tachycardia) is being considered for long-term prophylactic therapy to prevent future episodes. Which of the following is the most appropriate preventive treatment?
- A. IV Adenosine
- B. Oral Nifedipine
- C. Oral Verapamil (Correct Answer)
- D. IV lignocaine
Explanation: ***Oral Verapamil*** - This is a non-dihydropyridine **Calcium Channel Blocker** that effectively slows conduction and increases refractoriness in the **AV node**. - It is a standard oral medication used for the **long-term prevention (prophylaxis)** of recurrent PSVT, especially in cases of AVNRT or AVRT. *IV lignocaine* - Lignocaine (Lidocaine) is a **Class IB antiarrhythmic** primarily used to treat and prevent **ventricular arrhythmias** (premature ventricular contractions, VT). - It is generally ineffective for chronic prophylaxis of supraventricular tachycardias like PSVT. *IV Adenosine* - **Adenosine** is the preferred drug for the **acute termination** of PSVT due to its potent, transient block of the AV node (half-life of <10 seconds). - It has an extremely short half-life, making it unsuitable for a chronic, **oral preventive regimen**. *Oral Nifedipine* - Nifedipine is a **dihydropyridine Calcium Channel Blocker** primarily acting as a **peripheral vasodilator**. - It has minimal effects on the **AV nodal conduction** properties required for PSVT prophylaxis and is therefore not used for this purpose.
Question 10: A patient on hydrochlorothiazide develops renal stones. What explains this adverse effect?
- A. Decreased urinary citrate (Correct Answer)
- B. Increased urinary citrate
- C. Decrease urinary calcium
- D. Increase urinary calcium
Explanation: ***Decreased urinary citrate*** - **Hydrochlorothiazide** (HCTZ) can cause hypokalemia associated with **metabolic alkalosis** - Metabolic alkalosis leads to **decreased urinary citrate** excretion (hypocitraturia) - **Citrate is a key inhibitor** of calcium oxalate and calcium phosphate stone formation by complexing with urinary calcium - Hypocitraturia theoretically increases stone formation risk by reducing this protective effect - **Clinical Note:** Despite this mechanism, thiazides are actually used to **prevent** recurrent calcium stones due to their dominant effect of reducing urinary calcium excretion *Increased urinary calcium* - This would promote stone formation, but thiazides actually **decrease** urinary calcium excretion (hypocalciuria) - The calcium-lowering effect is why thiazides are used therapeutically for **preventing** calcium nephrolithiasis - In this question, the mechanism relates to altered citrate, not calcium excretion *Decreased urinary calcium* - Thiazides do decrease urinary calcium, which is **protective** against stones, not causative - This is the primary beneficial effect that makes thiazides useful in preventing recurrent calcium nephrolithiasis - The stone formation in the question stem relates to the **citrate** mechanism, not calcium *Increased urinary citrate* - Increased citrate would be **protective** against stone formation by binding urinary calcium - Thiazides cause the opposite effect: **hypocitraturia** (decreased citrate) due to associated metabolic alkalosis - Higher urinary citrate is actually a therapeutic goal in stone prevention