FMGE 2025 — Pharmacology

Q: Which anti-epileptic drug is commonly associated with gum hypertrophy and dizziness as side effects?

Phenytoin. ***Phenytoin*** - It is classically associated with **gingival hyperplasia** (gum hypertrophy) due to increased stimulation of **fibroblast activity** and **collagen synthesis** in the gingiva, which is a major distinction from other AEDs. - Dose-dependent **dizziness** and **ataxia** are very common CNS side effects, reflecting its non-linear kinetics and narrow therapeutic index. *Carbamazepine* - Its most characteristic serious side effects include **aplastic anemia** and agranulocytosis, requiring baseline and periodic complete blood counts (CBCs). - It is a potent inducer of **CYP450 enzymes** and frequently causes **hyponatremia** (via Syndrome of Inappropriate Antidiuretic Hormone secretion, SIADH). *Levetiracetam* - This drug is generally well-tolerated but is notably associated with significant **behavioral side effects** such as irritability, aggression, and mood instability. - It does not cause **gum hypertrophy** or significant liver enzyme induction, unlike Phenytoin or Carbamazepine. *Topiramate* - Commonly causes side effects related to cognition, often called **"Dopamax"**, leading to cognitive slowing, difficulty concentrating, and language problems. - Other unique side effects include **weight loss** and the formation of **kidney stones** (nephrolithiasis) due to inhibition of carbonic anhydrase. [Practice more Pharmacology PYQs on OnCourse]

Q: Which anti-tubercular drug is associated with mutations in the katG gene?

Isoniazid. ***Isoniazid*** - It is a **prodrug** that requires activation by the **catalase-peroxidase enzyme** complex, which is encoded by the **katG gene** in *Mycobacterium tuberculosis*. - Mutations or deletions in the **katG gene** are the most common cause of high-level Isoniazid resistance, preventing the drug from converting into its active form (isonicotinic acyl radical). *Rifampicin* - Resistance is predominantly caused by mutations in the **rpoB gene**, which encodes the **beta-subunit of RNA polymerase**. - Mutations in **rpoB** prevent Rifampicin from binding to the RNA polymerase, thereby inhibiting its primary mechanism of blocking transcription. *Moxifloxacin* - This drug belongs to the fluoroquinolone class and targets **DNA gyrase** (encoded by *gyrA* and *gyrB*) and **topoisomerase IV**. - Resistance is typically mediated by point mutations within the **Quinolone Resistance Determining Regions (QRDRs)** of these target genes. *Ethambutol* - Resistance to Ethambutol is most frequently associated with mutations in the **embB gene**. - The **embB gene** encodes the **arabinosyl transferase** enzyme, which is crucial for synthesizing the **arabinogalactan layer** of the mycobacterial cell wall. [Practice more Pharmacology PYQs on OnCourse]

Q: Which of the following conditions is not reversed with the administration of atropine?

Muscle weakness due to neuromuscular blockade. ***Muscle weakness due to neuromuscular blockade*** - Atropine is a **muscarinic receptor antagonist** and therefore has no direct effect on the **nicotinic receptors** responsible for neuromuscular transmission and muscle strength. - The reversal of **non-depolarizing neuromuscular blockade** requires increasing acetylcholine via a **cholinesterase inhibitor** (e.g., neostigmine), which acts at the **neuromuscular junction**. *Bradycardia* - Atropine blocks **M2 receptors** on the heart's sinoatrial (SA) node, inhibiting **vagal tone** and increasing the heart rate, thereby reversing bradycardia. - It is the primary drug used to treat hemodynamically significant **bradyarrhythmias**. *Excessive salivation* - Atropine is an anticholinergic agent that blocks **M3 receptors** on exocrine glands, effectively reducing all secretions, including **saliva**. - This is why it is often used as a pre-anesthetic agent to dry secretions and reduce the risk of **aspiration**. *Bronchoconstriction* - Atropine blocks **M3 receptors** in the bronchial smooth muscle, leading to relaxation and **bronchodilation**. - While effective, related synthetic compounds like **ipratropium** are often preferred for treating bronchoconstriction due to fewer systemic anticholinergic side effects. [Practice more Pharmacology PYQs on OnCourse]

Q: Which adverse effect of Bleomycin is exacerbated by radiation exposure?

Pulmonary toxicity. ***Pulmonary toxicity*** - Bleomycin is well-known for causing dose-dependent **pulmonary fibrosis**. It damages **type I pneumocytes**, leading to inflammation, proliferation of **type II pneumocytes**, and eventual fibrosis, impairing gas exchange. - The risk of pulmonary toxicity is significantly increased by concurrent or prior **chest radiation therapy** and administration of high concentrations of supplemental **oxygen**, as both are also injurious to lung tissue. *Gastric toxicity* - Bleomycin is not typically associated with significant gastric toxicity. Common side effects are milder and include **mucositis** and **stomatitis** rather than severe gastric damage. - There is no evidence of a synergistic toxic effect on the gastric mucosa when Bleomycin is combined with radiation therapy. *Neural toxicity* - Neurotoxicity is not a characteristic side effect of Bleomycin. Chemotherapeutic agents like **vincristine** and **cisplatin** are more commonly associated with peripheral neuropathy. - While radiation can cause nerve damage, this is not a known interaction that is specifically exacerbated by Bleomycin administration. *Hepatotoxicity* - Severe liver damage (**hepatotoxicity**) is a rare side effect of Bleomycin. Mild and transient elevations of liver enzymes may occur but are not clinically significant. - Unlike the lungs, the liver is not a primary site for synergistic toxicity between Bleomycin and radiation therapy. [Practice more Pharmacology PYQs on OnCourse]

31 Previous Year Questions with Answers & Explanations

Questions

Which anti-epileptic drug is commonly associated with gum hypertrophy and dizziness as side effects?

Which anti-tubercular drug is associated with mutations in the katG gene?

Which of the following conditions is not reversed with the administration of atropine?

Which adverse effect of Bleomycin is exacerbated by radiation exposure?

What is the key difference between Cisplatin and Carboplatin?

A 25-year-old woman presents to the emergency department 6 hours after ingesting a large quantity of paracetamol tablets. What is the most likely progression of paracetamol poisoning in this case?

A patient with rheumatoid arthritis is taking indomethacin and an ACE inhibitor for hypertension. What potential side effect is likely to be seen?

A patient with penicillin allergy presents with fever, burning micturition, and hearing problems accompanied by dizziness. Which drug is the most appropriate for the management?

A 35-year-old male experiences headache, nausea, and shortness of breath while trekking. The physician prescribes a drug to alleviate his symptoms. The drug administered primarily acts on which part of the nephron?

Q10

Which of the following drug dosages is incorrect for the treatment of leprosy in adults?

FMGE 2025 - Pharmacology FMGE Practice Questions and MCQs

Question 1: Which anti-epileptic drug is commonly associated with gum hypertrophy and dizziness as side effects?

A. Carbamazepine
B. Topiramate
C. Phenytoin (Correct Answer)
D. Levetiracetam

Explanation: ***Phenytoin*** - It is classically associated with **gingival hyperplasia** (gum hypertrophy) due to increased stimulation of **fibroblast activity** and **collagen synthesis** in the gingiva, which is a major distinction from other AEDs. - Dose-dependent **dizziness** and **ataxia** are very common CNS side effects, reflecting its non-linear kinetics and narrow therapeutic index. *Carbamazepine* - Its most characteristic serious side effects include **aplastic anemia** and agranulocytosis, requiring baseline and periodic complete blood counts (CBCs). - It is a potent inducer of **CYP450 enzymes** and frequently causes **hyponatremia** (via Syndrome of Inappropriate Antidiuretic Hormone secretion, SIADH). *Levetiracetam* - This drug is generally well-tolerated but is notably associated with significant **behavioral side effects** such as irritability, aggression, and mood instability. - It does not cause **gum hypertrophy** or significant liver enzyme induction, unlike Phenytoin or Carbamazepine. *Topiramate* - Commonly causes side effects related to cognition, often called **"Dopamax"**, leading to cognitive slowing, difficulty concentrating, and language problems. - Other unique side effects include **weight loss** and the formation of **kidney stones** (nephrolithiasis) due to inhibition of carbonic anhydrase.

Question 2: Which anti-tubercular drug is associated with mutations in the katG gene?

A. Moxifloxacin
B. Isoniazid (Correct Answer)
C. Ethambutol
D. Rifampicin

Explanation: ***Isoniazid*** - It is a **prodrug** that requires activation by the **catalase-peroxidase enzyme** complex, which is encoded by the **katG gene** in *Mycobacterium tuberculosis*. - Mutations or deletions in the **katG gene** are the most common cause of high-level Isoniazid resistance, preventing the drug from converting into its active form (isonicotinic acyl radical). *Rifampicin* - Resistance is predominantly caused by mutations in the **rpoB gene**, which encodes the **beta-subunit of RNA polymerase**. - Mutations in **rpoB** prevent Rifampicin from binding to the RNA polymerase, thereby inhibiting its primary mechanism of blocking transcription. *Moxifloxacin* - This drug belongs to the fluoroquinolone class and targets **DNA gyrase** (encoded by *gyrA* and *gyrB*) and **topoisomerase IV**. - Resistance is typically mediated by point mutations within the **Quinolone Resistance Determining Regions (QRDRs)** of these target genes. *Ethambutol* - Resistance to Ethambutol is most frequently associated with mutations in the **embB gene**. - The **embB gene** encodes the **arabinosyl transferase** enzyme, which is crucial for synthesizing the **arabinogalactan layer** of the mycobacterial cell wall.

Question 3: Which of the following conditions is not reversed with the administration of atropine?

A. Bradycardia
B. Bronchoconstriction
C. Excessive salivation
D. Muscle weakness due to neuromuscular blockade (Correct Answer)

Explanation: ***Muscle weakness due to neuromuscular blockade*** - Atropine is a **muscarinic receptor antagonist** and therefore has no direct effect on the **nicotinic receptors** responsible for neuromuscular transmission and muscle strength. - The reversal of **non-depolarizing neuromuscular blockade** requires increasing acetylcholine via a **cholinesterase inhibitor** (e.g., neostigmine), which acts at the **neuromuscular junction**. *Bradycardia* - Atropine blocks **M2 receptors** on the heart's sinoatrial (SA) node, inhibiting **vagal tone** and increasing the heart rate, thereby reversing bradycardia. - It is the primary drug used to treat hemodynamically significant **bradyarrhythmias**. *Excessive salivation* - Atropine is an anticholinergic agent that blocks **M3 receptors** on exocrine glands, effectively reducing all secretions, including **saliva**. - This is why it is often used as a pre-anesthetic agent to dry secretions and reduce the risk of **aspiration**. *Bronchoconstriction* - Atropine blocks **M3 receptors** in the bronchial smooth muscle, leading to relaxation and **bronchodilation**. - While effective, related synthetic compounds like **ipratropium** are often preferred for treating bronchoconstriction due to fewer systemic anticholinergic side effects.

Question 4: Which adverse effect of Bleomycin is exacerbated by radiation exposure?

A. Neural toxicity
B. Hepatotoxicity
C. Gastric toxicity
D. Pulmonary toxicity (Correct Answer)

Explanation: ***Pulmonary toxicity*** - Bleomycin is well-known for causing dose-dependent **pulmonary fibrosis**. It damages **type I pneumocytes**, leading to inflammation, proliferation of **type II pneumocytes**, and eventual fibrosis, impairing gas exchange. - The risk of pulmonary toxicity is significantly increased by concurrent or prior **chest radiation therapy** and administration of high concentrations of supplemental **oxygen**, as both are also injurious to lung tissue. *Gastric toxicity* - Bleomycin is not typically associated with significant gastric toxicity. Common side effects are milder and include **mucositis** and **stomatitis** rather than severe gastric damage. - There is no evidence of a synergistic toxic effect on the gastric mucosa when Bleomycin is combined with radiation therapy. *Neural toxicity* - Neurotoxicity is not a characteristic side effect of Bleomycin. Chemotherapeutic agents like **vincristine** and **cisplatin** are more commonly associated with peripheral neuropathy. - While radiation can cause nerve damage, this is not a known interaction that is specifically exacerbated by Bleomycin administration. *Hepatotoxicity* - Severe liver damage (**hepatotoxicity**) is a rare side effect of Bleomycin. Mild and transient elevations of liver enzymes may occur but are not clinically significant. - Unlike the lungs, the liver is not a primary site for synergistic toxicity between Bleomycin and radiation therapy.

Question 5: What is the key difference between Cisplatin and Carboplatin?

A. Cisplatin has more nephrotoxic side effects compared to Carboplatin (Correct Answer)
B. Cisplatin is less neurotoxic than Carboplatin
C. Carboplatin is more neurotoxic than Cisplatin
D. Cisplatin causes fewer gastric issues compared to Carboplatin

Explanation: ***Cisplatin has more nephrotoxic side effects compared to Carboplatin*** - This is the **KEY clinical difference** between these platinum-based chemotherapy agents - Cisplatin causes **severe nephrotoxicity** requiring aggressive hydration and electrolyte monitoring - Carboplatin has **minimal renal toxicity**, making it safer in patients with renal impairment - This difference is why Carboplatin is often preferred when nephrotoxicity is a concern *Cisplatin is less neurotoxic than Carboplatin* - This is INCORRECT - the reverse is true - Cisplatin causes MORE neurotoxicity (peripheral neuropathy, ototoxicity) - Carboplatin has significantly less neurotoxicity *Carboplatin is more neurotoxic than Cisplatin* - This is INCORRECT - Carboplatin is actually LESS neurotoxic than Cisplatin - Neurotoxicity (including ototoxicity) is a major dose-limiting toxicity of Cisplatin, not Carboplatin *Cisplatin causes fewer gastric issues compared to Carboplatin* - This is INCORRECT - Cisplatin is one of the MOST emetogenic chemotherapy agents - Carboplatin causes significantly less nausea and vomiting than Cisplatin - The primary toxicity of Carboplatin is **myelosuppression (thrombocytopenia)**, not GI effects **Summary of Key Differences:** - **Cisplatin:** More nephrotoxic, more neurotoxic, more emetogenic - **Carboplatin:** Less nephrotoxic, less neurotoxic, less emetogenic, MORE myelosuppressive

Question 6: A 25-year-old woman presents to the emergency department 6 hours after ingesting a large quantity of paracetamol tablets. What is the most likely progression of paracetamol poisoning in this case?

A. Recovery within 72 hours
B. Paracetamol achieves peak concentration within 4 hours
C. Liver failure within 24 hours
D. Increase in liver enzymes starting around 24 hours (Correct Answer)

Explanation: ***Increase in liver enzymes starting around 24 hours*** - Phase 2 of paracetamol toxicity, occurring **24–72 hours post-ingestion**, is characterized by the onset of **hepatotoxicity**, marked by rising **AST** and **ALT** levels. - The patient is currently 6 hours post-ingestion (late Phase 1), so the most likely progression is entering Phase 2, where biochemical evidence of liver damage begins around 24 hours and continues to rise. *Liver failure within 24 hours* - **Acute liver failure** (manifested by coagulopathy, jaundice, and encephalopathy) typically develops around 3 to 4 days (72–96 hours) post-ingestion (Phase 3). - Within the first 24 hours, symptoms are usually mild or absent (Phase 1: nausea, vomiting, or asymptomatic). *Paracetamol achieves peak concentration within 4 hours* - While **peak plasma concentration** for standard paracetamol typically occurs around 4 hours post-ingestion, this pharmacokinetic event has already occurred since the patient presents at 6 hours. - The question asks for the subsequent toxicological *progression* (clinical course), not a past pharmacokinetic event. *Recovery within 72 hours* - Recovery (Phase 4) typically occurs after the peak injury period (around 4 days or later), especially with effective antidote treatment (**N-acetylcysteine**). - Given the ingestion of a **large quantity**, the patient is expected to progress through Phase 2 (**hepatotoxicity** at 24-72 hours) and possibly Phase 3 (peak toxicity at 72-96 hours), not recover within 72 hours.

Question 7: A patient with rheumatoid arthritis is taking indomethacin and an ACE inhibitor for hypertension. What potential side effect is likely to be seen?

A. Hyperkalemia (Correct Answer)
B. Hypercalcemia
C. Hypernatremia
D. Hyperphosphatemia

Explanation: ***Hyperkalemia*** - The co-administration of an **ACE inhibitor** and an **NSAID (indomethacin)** significantly increases the risk of **hyperkalemia** due to synergistic effects on renal potassium balance. - **ACE inhibitors** directly block aldosterone synthesis (leading to reduced potassium excretion), while **NSAIDs** reduce prostaglandin synthesis, impairing renin release, which also suppresses aldosterone effect. *Hypercalcemia* - This scenario is not associated with hypercalcemia; drugs notorious for causing hypercalcemia include **thiazide diuretics**, or conditions like **primary hyperparathyroidism**. - Neither ACE inhibitors nor NSAIDs directly impair calcium homeostasis leading to clinically significant increases. *Hypernatremia* - **ACE inhibitors** decrease aldosterone levels, which promotes sodium excretion, typically resulting in **hyponatremia** or normonatremia, not hypernatremia. - Although NSAIDs can cause fluid retention, this is largely due to increased water reabsorption leading to expansion of extracellular fluid, not an increase in serum sodium concentration. *Hyperphosphatemia* - **Hyperphosphatemia** is primarily seen in end-stage **chronic kidney disease (CKD)** because the kidneys cannot excrete phosphate effectively. - The combination of indomethacin and an ACE inhibitor does not directly impair phosphate excretion via the mechanisms needed to cause clinically significant hyperphosphatemia.

Question 8: A patient with penicillin allergy presents with fever, burning micturition, and hearing problems accompanied by dizziness. Which drug is the most appropriate for the management?

A. Ciprofloxacin (Correct Answer)
B. Ampicillin-Clavulanic acid
C. Amikacin
D. Azithromycin

Explanation: ***Ciprofloxacin***- Ciprofloxacin is a **fluoroquinolone** that provides excellent coverage against common **uropathogens** (like *E. coli*) and is the preferred choice for managing complicated UTIs in patients with a **penicillin allergy**.- It is the most appropriate choice because, unlike aminoglycosides, it does not carry a high risk of **ototoxicity** or **vestibulotoxicity**, which is crucial as the patient already presents with hearing problems and dizziness.*Azithromycin*- Azithromycin is a **macrolide** that is generally not the first-line empirical antibiotic for typical urinary tract infections (UTIs) due to higher resistance rates among common uropathogens.- While safe in penicillin allergy, its primary spectrum targets atypical pathogens, making it less suitable than Ciprofloxacin for suspected UTIs complicated by fever.*Amikacin*- Amikacin is an **aminoglycoside** known to cause significant **ototoxicity** (leading to hearing loss) and **vestibulotoxicity** (causing dizziness and imbalance).- Given the patient already presents with hearing problems and dizziness, administering Amikacin is **absolutely contraindicated** as it would severely worsen these existing neurotoxic symptoms.*Ampicillin-Clavulanic acid*- This combination includes **Ampicillin**, which belongs to the **penicillin** class of antibiotics.- It is strictly contraindicated because the patient has a confirmed history of **penicillin allergy**, risking a potentially severe, life-threatening hypersensitivity reaction.

Question 9: A 35-year-old male experiences headache, nausea, and shortness of breath while trekking. The physician prescribes a drug to alleviate his symptoms. The drug administered primarily acts on which part of the nephron?

A. Loop of Henle
B. Collecting duct (CD)
C. Proximal convoluted tubule (PCT) (Correct Answer)
D. Distal convoluted tubule (DCT)

Explanation: ***Proximal convoluted tubule (PCT)***- The clinical presentation (headache, nausea, shortness of breath while trekking) is consistent with **Acute Mountain Sickness (AMS)**, which is typically prevented or treated with **Acetazolamide**.- **Acetazolamide** is a **carbonic anhydrase inhibitor** that acts primarily in the PCT, reducing bicarbonate reabsorption and inducing metabolic acidosis, which stimulates ventilation to counteract altitude-induced respiratory alkalosis.*Loop of Henle*- This segment is the primary site for **Loop Diuretics** (e.g., **Furosemide**), which inhibit the **Na+-K+-2Cl- cotransporter** in the thick ascending limb.- Loop diuretics promote powerful diuresis but are not the standard pharmacological choice for treating or preventing the symptoms of AMS.*Distal convoluted tubule (DCT)*- The DCT is the target site for **Thiazide Diuretics** (e.g., **Hydrochlorothiazide**), which block the **Na+-Cl- cotransporter**.- Thiazides primarily manage hypertension and edema and lack the necessary mechanism (carbonic anhydrase inhibition) to directly increase ventilation required for AMS treatment.*Collecting duct (CD)*- The collecting duct is where **Potassium-sparing diuretics** and **Aldosterone antagonists** (e.g., **Spironolactone**) exert their effects by controlling final sodium and potassium balance.- While these drugs can influence fluid balance, their primary actions are far removed from the need to induce metabolic acidosis to stimulate central respiratory drives in high-altitude illness.

Question 10: Which of the following drug dosages is incorrect for the treatment of leprosy in adults?

A. Clofazimine 50 mg
B. Dapsone 100 mg
C. Rifampicin 450 mg (Correct Answer)
D. Clofazimine 300 mg

Explanation: ***Rifampicin 450 mg*** - The standard dose of Rifampicin for leprosy treatment in adults is **600 mg once monthly** (supervised dose) as per WHO MDT regimen - 450 mg is an incorrect dosage and not part of the recommended treatment protocol - This makes it the correct answer to this negation question *Clofazimine 50 mg* - This is the correct **daily self-administered dose** of Clofazimine in Multibacillary (MB) leprosy - Used as part of the WHO MDT-MB regimen *Dapsone 100 mg* - This is the correct **daily dose** of Dapsone for both Paucibacillary (PB) and Multibacillary (MB) leprosy - Standard component of WHO MDT regimen *Clofazimine 300 mg* - This is the correct **monthly supervised dose** of Clofazimine in Multibacillary (MB) leprosy - Given once a month under supervision as part of WHO MDT-MB regimen