UPSC-CMS 2025 — Pharmacology
28 Previous Year Questions with Answers & Explanations
Which of the following drugs can cause secondary weight gain? I. Insulin II. Propranolol III. Orlistat IV. Thyroxine Select the correct answer using the code given below :
Under which one of the following conditions, the HPA axis suppression is likely to result in crisis due to adrenal insufficiency following withdrawal of glucocorticoids?
Which of the following can be used for the management of severe hyperkalaemia? I. Intravenous calcitonin II. Intravenous sodium bicarbonate III. Oral sodium polystyrene sulphate IV. Intravenous calcium gluconate
Which one of the following is correct regarding arginine vasopressin antagonist Tolvaptan?
A 42-year old man with history of alcohol dependency presents with progressive abdominal distension. Abdominal examination reveals a shifting dullness. Which one of the following is the most appropriate drug to relieve this abdominal distension?
Which one of the following agents used in the treatment of inflammatory Bowel Disease acts by inhibiting the enzyme 'Janus Kinase'?
Which one of the following responses to intravenous adenosine is correctly matched?
Consider the following steps for using a metered dose inhaler (MDI) : I. Incline the head backward to minimize oropharyngeal deposition II. Remove the cap and shake the inhaler III. Breathe out gently and place the mouthpiece into the mouth IV. Hold the breath for 10 seconds V. Simultaneously, begin a slow deep inspiration, depress the canister and continue to inhale Which one of the following is the correct sequence of using MDI?
Treatment of first choice in acute Gout is
Which one of the following is an antidote for Rivaroxaban and Apixaban, when reversal of anticoagulation is needed due to uncontrolled bleeding?
UPSC-CMS 2025 - Pharmacology UPSC-CMS Practice Questions and MCQs
Question 1: Which of the following drugs can cause secondary weight gain? I. Insulin II. Propranolol III. Orlistat IV. Thyroxine Select the correct answer using the code given below :
- A. I and II only (Correct Answer)
- B. I and III
- C. II, III and IV
- D. I, II and IV
Explanation: ***I and II only*** - **Insulin** promotes glucose uptake and storage as glycogen or fat, and its therapeutic use can lead to **weight gain** due to increased fat deposition. - **Propranolol**, a non-selective beta-blocker, can decrease metabolic rate and physical activity tolerance due to slowed heart rate, contributing to **weight gain**. *I and III* - While **Insulin** causes weight gain, **Orlistat** specifically acts as a **lipase inhibitor** to *reduce* fat absorption, thereby *promoting weight loss*, not gain. *II, III and IV* - **Propranolol** can cause weight gain, but **Orlistat** facilitates weight loss. **Thyroxine**, used to treat hypothyroidism, generally *promotes weight loss* by increasing metabolism, not weight gain. *I, II and IV* - **Insulin** and **Propranolol** can cause weight gain. However, **Thyroxine** (levothyroxine) is used to correct hypothyroidism and typically leads to **weight loss** by normalizing metabolic rate, rather than causing weight gain.
Question 2: Under which one of the following conditions, the HPA axis suppression is likely to result in crisis due to adrenal insufficiency following withdrawal of glucocorticoids?
- A. If glucocorticoids have been prescribed repeatedly within the previous year (Correct Answer)
- B. If the dose is less than equivalent of 5 mg prednisolone per day
- C. If glucocorticoids have been given by intravenous route for five days
- D. If glucocorticoids have been administered orally for one week
Explanation: ***Correct: If glucocorticoids have been prescribed repeatedly within the previous year*** - While a **single short course** of glucocorticoids typically does not cause significant HPA axis suppression, **repeated exposure over time** (multiple courses within a year) can lead to **cumulative suppression** of the hypothalamic-pituitary-adrenal axis - This is particularly true if the courses are **frequent, prolonged, or at high doses** without adequate recovery periods between treatments - **Chronic or repeated suppression** impairs the body's ability to produce sufficient endogenous cortisol when exogenous glucocorticoids are withdrawn, increasing the risk of **adrenal insufficiency crisis** - Among the given options, this represents the **highest risk scenario** for HPA axis suppression requiring careful withdrawal management *Incorrect: If the dose is less than equivalent of 5 mg prednisolone per day* - Doses **< 5 mg prednisolone equivalent per day** are considered **physiologic replacement doses** - Such low doses do **NOT suppress** the HPA axis significantly - This represents a **low-risk scenario** for adrenal insufficiency - Standard teaching: HPA suppression risk increases with doses **> 20 mg/day prednisolone equivalent** *Incorrect: If glucocorticoids have been given by intravenous route for five days* - **Short-course therapy (< 7-10 days)**, even at high doses and by IV route, typically does **NOT cause prolonged HPA axis suppression** - The HPA axis usually **recovers rapidly** after brief exposure - Abrupt discontinuation after 5 days **does not typically require tapering** and is unlikely to cause adrenal crisis - The route of administration (IV vs oral) is less important than **duration and total dose** *Incorrect: If glucocorticoids have been administered orally for one week* - Similar to the IV scenario, **one week of oral therapy** is considered a **short course** - Such brief duration typically does not cause significant HPA axis suppression requiring taper - The adrenal glands usually maintain responsiveness after only **7 days** of treatment - **Duration > 3 weeks** at supraphysiologic doses is the traditional threshold for concern about HPA suppression
Question 3: Which of the following can be used for the management of severe hyperkalaemia? I. Intravenous calcitonin II. Intravenous sodium bicarbonate III. Oral sodium polystyrene sulphate IV. Intravenous calcium gluconate
- A. I and II only
- B. I and IV only
- C. I, II and IV
- D. II, III and IV (Correct Answer)
Explanation: ***II, III and IV*** - **Intravenous sodium bicarbonate** helps shift potassium into cells, primarily used in cases of metabolic acidosis. - **Oral sodium polystyrene sulfonate** (Kayexalate) is a cation-exchange resin that binds potassium in the gut, facilitating its excretion. - **Intravenous calcium gluconate** does not lower serum potassium but stabilizes the cardiac membrane, protecting against life-threatening arrhythmias. *I and II only* - **Intravenous calcitonin** is used in hypercalcemia to lower calcium levels and is not indicated for the management of hyperkalemia. - While intravenous sodium bicarbonate is used, relying on it alone with calcitonin would be insufficient and inappropriate. *I and IV only* - **Intravenous calcitonin** is not a treatment for hyperkalemia. - Although intravenous calcium gluconate is crucial for cardiac stabilization, it does not address the underlying hyperkalemia directly, making this option incomplete and incorrect. *'I, II and IV* - **Intravenous calcitonin** has no role in the management of hyperkalemia. - While intravenous sodium bicarbonate and calcium gluconate are important, the inclusion of calcitonin makes this option incorrect.
Question 4: Which one of the following is correct regarding arginine vasopressin antagonist Tolvaptan?
- A. It is useful in hypovolemic hyponatremia
- B. It antagonises the V1 receptor
- C. It is an oral drug (Correct Answer)
- D. It should be used for at least 1 year
Explanation: ***It is an oral drug*** - **Tolvaptan** is an **orally active selective vasopressin V2-receptor antagonist** used in the treatment of hyponatremia. - Its oral bioavailability makes it convenient for long-term management of conditions like **syndrome of inappropriate antidiuretic hormone (SIADH)**. *It is useful in hypovolemic hyponatremia* - **Tolvaptan** is primarily used to treat **euvolemic** and **hypervolemic hyponatremia** by promoting **free water excretion**, which is not ideal in hypovolemic states where fluid status needs to be increased. - In **hypovolemic hyponatremia**, the primary treatment is **fluid resuscitation** with isotonic saline, not free water excretion. *It antagonises the V1 receptor* - **Tolvaptan** is a **selective V2-receptor antagonist**, meaning it specifically blocks the action of vasopressin at the V2 receptors in the renal collecting ducts. - Blocking **V1 receptors** would primarily affect smooth muscle contraction and platelet aggregation, which is not the therapeutic target for tolvaptan in hyponatremia. *It should be used for at least 1 year* - The duration of **Tolvaptan** treatment is variable and depends on the underlying cause of hyponatremia and the patient's response. - There is no standard recommendation for a minimum usage period of at least one year; treatment is typically continued as long as necessary and tolerated.
Question 5: A 42-year old man with history of alcohol dependency presents with progressive abdominal distension. Abdominal examination reveals a shifting dullness. Which one of the following is the most appropriate drug to relieve this abdominal distension?
- A. Lactulose
- B. Spironolactone (Correct Answer)
- C. Propranolol
- D. Octreotide
Explanation: **Spironolactone** - **Spironolactone** is an **aldosterone antagonist**, which is the **first-line diuretic** used in the management of **ascites** due to **cirrhosis**, often developing secondary to alcohol dependency. - It works by blocking aldosterone receptors in the **renal collecting duct**, leading to increased sodium and water excretion while conserving potassium, effectively reducing fluid accumulation. *Lactulose* - **Lactulose** is a non-absorbable disaccharide primarily used to treat and prevent **hepatic encephalopathy** by reducing ammonia levels. - It does not directly relieve abdominal distension caused by ascites, and its use is unrelated to fluid overload. *Propranolol* - **Propranolol** is a **non-selective beta-blocker** used to reduce **portal pressure** and prevent **variceal bleeding** in patients with cirrhosis. - While it addresses a complication of chronic liver disease, it does not directly manage or relieve ascites. *Octreotide* - **Octreotide** is a **somatostatin analog** used to treat complications like **acute variceal bleeding** or **hepatic encephalopathy** by reducing splanchnic blood inflow. - It is not indicated for the management of ascites or relief of abdominal distension caused by fluid accumulation.
Question 6: Which one of the following agents used in the treatment of inflammatory Bowel Disease acts by inhibiting the enzyme 'Janus Kinase'?
- A. Adalimumab
- B. Vedolizumab
- C. Tofacitinib (Correct Answer)
- D. Infliximab
Explanation: ***Tofacitinib*** - **Tofacitinib** is an oral medication that functions as a small molecule **Janus Kinase (JAK) inhibitor**, primarily targeting JAK1 and JAK3. - By inhibiting JAK enzymes, tofacitinib disrupts the signaling pathways of several **cytokines** involved in inflammation, including those implicated in **inflammatory bowel disease (IBD)**. *Adalimumab* - **Adalimumab** is a monoclonal antibody that targets and neutralizes **tumor necrosis factor-alpha (TNF-α)**, a key inflammatory cytokine. - It is not a JAK inhibitor but rather works by blocking the interaction of TNF-α with its receptors on cell surfaces. *Vedolizumab* - **Vedolizumab** is an anti-integrin monoclonal antibody that selectively blocks the α4β7 integrin on lymphocytes. - This action prevents lymphocytes from migrating into the gastrointestinal tract, thereby reducing inflammation in IBD. *Infliximab* - **Infliximab** is a chimeric monoclonal antibody that, like adalimumab, targets and neutralizes **tumor necrosis factor-alpha (TNF-α)**. - It works by binding to soluble and transmembrane forms of TNF-α, preventing its pro-inflammatory effects.
Question 7: Which one of the following responses to intravenous adenosine is correctly matched?
- A. Atrial flutter - Termination and complete recovery
- B. Atrio-ventricular nodal reentrant tachycardia - Termination and complete recovery (Correct Answer)
- C. Ventricular tachycardia - Termination and complete recovery
- D. Atrial fibrillation - Termination
Explanation: ***Atrio-ventricular nodal reentrant tachycardia - Termination and complete recovery*** - Adenosine acts on **adenosine A1 receptors** in the AV node, causing **transient AV nodal block** and interrupting the reentrant circuit in **AVNRT**, leading to abrupt termination and recovery of normal sinus rhythm. - This characteristic response makes adenosine a primary diagnostic and therapeutic agent for **AVNRT**. *Atrial flutter - Termination and complete recovery* - Adenosine can transiently increase **AV block** in atrial flutter, making the flutter waves more apparent and aiding diagnosis, but it **rarely terminates atrial flutter** itself. - The underlying reentrant circuit for atrial flutter is typically in the **atria**, outside the AV node. *Ventricular tachycardia - Termination and complete recovery* - Adenosine is **generally ineffective** in terminating **most forms of ventricular tachycardia (VT)** because VT originates below the AV node. - While it can be helpful diagnostically by excluding supraventricular tachycardias or unmasking broad complex SVT, adenosine **does not usually terminate VT**. *Atrial fibrillation - Termination* - Adenosine **does not terminate atrial fibrillation**; instead, it can temporarily **slow the ventricular rate** by increasing the AV nodal block. - The rapid and chaotic atrial activity in atrial fibrillation is largely **unaffected by adenosine**, as the drug primarily acts on the AV node.
Question 8: Consider the following steps for using a metered dose inhaler (MDI) : I. Incline the head backward to minimize oropharyngeal deposition II. Remove the cap and shake the inhaler III. Breathe out gently and place the mouthpiece into the mouth IV. Hold the breath for 10 seconds V. Simultaneously, begin a slow deep inspiration, depress the canister and continue to inhale Which one of the following is the correct sequence of using MDI?
- A. III, II, I, V, IV
- B. II, I, IV, III, V
- C. II, III, I, V, IV (Correct Answer)
- D. III, I, II, IV, V
Explanation: ***II, III, I, V, IV*** - The correct sequence for using an MDI starts with **preparing the inhaler** (shaking it and removing the cap), followed by **proper positioning** and **breathing technique** to maximize drug delivery. - After preparing and positioning, the patient should inhale deeply while actuating the device, then **hold their breath** to allow for drug deposition. - **Note:** In standard MDI technique, the head should be in a **neutral or slightly upright position**, not inclined backward. Inclining the head backward would actually **increase** oropharyngeal deposition, contrary to what step I suggests. However, given the options provided in this question, this is the correct sequence. *III, II, I, V, IV* - This sequence incorrectly places **removing the cap and shaking the inhaler** (II) after beginning to breathe out and placing the mouthpiece (III), which means the inhaler isn't properly prepared before use. - The MDI needs to be shaken well before each use to ensure the medication is evenly distributed and delivered at the correct dose. *II, I, IV, III, V* - This sequence incorrectly places **holding the breath for 10 seconds** (IV) before placing the mouthpiece into the mouth and inhaling (III and V). - The breath hold should occur *after* inhalation to maximize drug deposition in the lungs. *III, I, II, IV, V* - This sequence places **removing the cap and shaking the inhaler** (II) very late, after preparing to breathe and inclining the head, which is incorrect. - The inhaler must be properly shaken *before* it is placed in the mouth and activated to ensure proper medication delivery.
Question 9: Treatment of first choice in acute Gout is
- A. Oral Methotrexate
- B. Sulfasalazine
- C. Allopurinol
- D. Oral Colchicine (Correct Answer)
Explanation: ***Oral Colchicine*** - **Colchicine** is highly effective in treating **acute gout attacks** by reducing inflammation caused by uric acid crystal deposition. - It works best when initiated within **24-36 hours** of symptom onset. - Considered a **first-line option** for acute gout, particularly in patients with contraindications to NSAIDs or corticosteroids. - **Mechanism:** Inhibits microtubule polymerization, thereby reducing neutrophil migration and phagocytosis of urate crystals. *Oral Methotrexate* - **Methotrexate** is an **immunosuppressant** primarily used for chronic inflammatory conditions, such as **rheumatoid arthritis** or **psoriasis**. - It is not a first-line treatment for the rapid relief of acute gout symptoms. *Sulfasalazine* - **Sulfasalazine** is an anti-inflammatory and immunomodulatory drug, commonly used in **inflammatory bowel disease** and **rheumatoid arthritis**. - It has no role in the immediate treatment of an acute gout flare. *Allopurinol* - **Allopurinol** is a **xanthine oxidase inhibitor** used for the **long-term prevention** of gout by lowering uric acid levels. - It is generally *not initiated* during an acute attack, as it can potentially worsen the flare by mobilizing urate crystals. - Used for **prophylaxis** in patients with recurrent gout attacks or chronic tophaceous gout.
Question 10: Which one of the following is an antidote for Rivaroxaban and Apixaban, when reversal of anticoagulation is needed due to uncontrolled bleeding?
- A. Hydroxocobalamin
- B. Glucarpidase
- C. Andexanet Alfa (Correct Answer)
- D. Idarucizumab
Explanation: ***Andexanet Alfa*** - **Andexanet Alfa** is a **modified recombinant factor Xa molecule** that acts as a decoy to bind and sequester direct factor Xa inhibitors like rivaroxaban and apixaban. - It is specifically indicated for the reversal of anticoagulation in patients treated with **rivaroxaban** or **apixaban** experiencing life-threatening or uncontrolled bleeding [1]. *Hydroxocobalamin* - **Hydroxocobalamin** is an antidote for **cyanide poisoning**, not for anticoagulant reversal. - It works by binding to cyanide to form cyanocobalamin, which can be excreted, thereby detoxifying the patient. *Glucarpidase* - **Glucarpidase** is used to rapidly lower **methotrexate concentrations** in patients with delayed methotrexate elimination and associated toxicity. - It is an enzyme that hydrolyzes methotrexate into inactive metabolites, facilitating its clearance. *Idarucizumab* - **Idarucizumab** is a specific reversal agent for **dabigatran**, a direct thrombin inhibitor. - It is a monoclonal antibody fragment that binds to dabigatran with high affinity, neutralizing its anticoagulant effect.