FMGE 2013 — Pharmacology

Q: All of the following diuretics increase K+ excretion EXCEPT:

Triamterene. ***Triamterene*** - **Triamterene** is a **potassium-sparing diuretic** that blocks epithelial sodium channels (ENaC) in the collecting duct, thereby reducing sodium reabsorption and potassium secretion. - Unlike most other diuretics, it causes **decreased K+ excretion** and can lead to hyperkalemia. *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** that acts in the proximal tubule, inhibiting bicarbonate reabsorption. - This leads to increased delivery of sodium and bicarbonate to the collecting duct, which enhances **potassium secretion** and increases K+ excretion. *Thiazide* - **Thiazide diuretics** (e.g., hydrochlorothiazide) act by inhibiting the Na+/Cl- cotransporter in the **distal convoluted tubule**. - This increases the delivery of sodium to the collecting duct, which stimulates the exchange of sodium for **potassium**, leading to increased K+ excretion and hypokalemia. *Furosemide* - **Furosemide** is a **loop diuretic** that inhibits the Na+/K+/2Cl- cotransporter in the **thick ascending limb of the loop of Henle**. - This prevents the reabsorption of these ions, leading to increased delivery of sodium to the collecting duct, which promotes **potassium secretion** and increased K+ excretion. [Practice more Pharmacology PYQs on OnCourse]

Q: All are features of organophosphorus poisoning, except:

Mydriasis. ***Mydriasis*** - Organophosphorus poisoning leads to excessive **acetylcholine** activity, causing **miosis** (pinpoint pupils), not mydriasis. - Mydriasis would indicate **anticholinergic** effects, which are opposite to the symptoms of organophosphorus poisoning. *Lacrimation* - Excess **acetylcholine** stimulates **muscarinic receptors** in lacrimal glands, leading to excessive tear production. - This is a classic "SLUDGE" symptom (Salivation, Lacrimation, Urination, Defecation, Gastric upset, Emesis). *Bradycardia* - Increased **acetylcholine** activity at cardiac muscarinic receptors (M2 receptors) slows the heart rate, causing **bradycardia**. - This is a common and potentially dangerous cardiovascular effect of organophosphorus poisoning. *Sweating* - **Acetylcholine** acts on muscarinic receptors in secretory glands, including sweat glands, causing profuse **sweating**. - This is another characteristic cholinergic symptom due to widespread autonomic overstimulation. [Practice more Pharmacology PYQs on OnCourse]

Q: Antidote for benzodiazepine poisoning: FMGE 10, 13; NEET 14

Flumazenil. ***Flumazenil*** - **Flumazenil** is a competitive **benzodiazepine receptor antagonist** that can reverse the sedative and other central nervous system effects of benzodiazepines. - It works by blocking benzodiazepines from binding to their receptor sites on the **GABA-A receptor complex**. *Naloxone* - **Naloxone** is a competitive **opioid receptor antagonist** used to reverse opioid overdose. - It has no effect on **benzodiazepine toxicity** as it targets different receptor systems. *Atropine* - **Atropine** is an **anticholinergic drug** used to reverse the effects of **cholinergic poisoning** (e.g., from organophosphates, carbamates) or symptomatic bradycardia. - It works on muscarinic acetylcholine receptors and is not involved in benzodiazepine metabolism or action. *N-acetyl-cysteine* - **N-acetyl-cysteine (NAC)** is primarily used as an antidote for **acetaminophen (paracetamol) poisoning**, where it replenishes glutathione. - It is also used in some cases of mucolysis but has no role in reversing benzodiazepine toxicity. [Practice more Pharmacology PYQs on OnCourse]

3 Previous Year Questions with Answers & Explanations

Questions

All Subjects Anatomy (1)Forensic Medicine (1)Microbiology (1)Pharmacology (3)Surgery (2)

All of the following diuretics increase K+ excretion EXCEPT:

All are features of organophosphorus poisoning, except:

Antidote for benzodiazepine poisoning: FMGE 10, 13; NEET 14

FMGE 2013 - Pharmacology FMGE Practice Questions and MCQs

Question 1: All of the following diuretics increase K+ excretion EXCEPT:

A. Acetazolamide
B. Triamterene (Correct Answer)
C. Thiazide
D. Furosemide

Explanation: ***Triamterene*** - **Triamterene** is a **potassium-sparing diuretic** that blocks epithelial sodium channels (ENaC) in the collecting duct, thereby reducing sodium reabsorption and potassium secretion. - Unlike most other diuretics, it causes **decreased K+ excretion** and can lead to hyperkalemia. *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** that acts in the proximal tubule, inhibiting bicarbonate reabsorption. - This leads to increased delivery of sodium and bicarbonate to the collecting duct, which enhances **potassium secretion** and increases K+ excretion. *Thiazide* - **Thiazide diuretics** (e.g., hydrochlorothiazide) act by inhibiting the Na+/Cl- cotransporter in the **distal convoluted tubule**. - This increases the delivery of sodium to the collecting duct, which stimulates the exchange of sodium for **potassium**, leading to increased K+ excretion and hypokalemia. *Furosemide* - **Furosemide** is a **loop diuretic** that inhibits the Na+/K+/2Cl- cotransporter in the **thick ascending limb of the loop of Henle**. - This prevents the reabsorption of these ions, leading to increased delivery of sodium to the collecting duct, which promotes **potassium secretion** and increased K+ excretion.

Question 2: All are features of organophosphorus poisoning, except:

A. Lacrimation
B. Bradycardia
C. Sweating
D. Mydriasis (Correct Answer)

Explanation: ***Mydriasis*** - Organophosphorus poisoning leads to excessive **acetylcholine** activity, causing **miosis** (pinpoint pupils), not mydriasis. - Mydriasis would indicate **anticholinergic** effects, which are opposite to the symptoms of organophosphorus poisoning. *Lacrimation* - Excess **acetylcholine** stimulates **muscarinic receptors** in lacrimal glands, leading to excessive tear production. - This is a classic "SLUDGE" symptom (Salivation, Lacrimation, Urination, Defecation, Gastric upset, Emesis). *Bradycardia* - Increased **acetylcholine** activity at cardiac muscarinic receptors (M2 receptors) slows the heart rate, causing **bradycardia**. - This is a common and potentially dangerous cardiovascular effect of organophosphorus poisoning. *Sweating* - **Acetylcholine** acts on muscarinic receptors in secretory glands, including sweat glands, causing profuse **sweating**. - This is another characteristic cholinergic symptom due to widespread autonomic overstimulation.

Question 3: Antidote for benzodiazepine poisoning: FMGE 10, 13; NEET 14

A. Flumazenil (Correct Answer)
B. Naloxone
C. Atropine
D. N-acetyl-cysteine

Explanation: ***Flumazenil*** - **Flumazenil** is a competitive **benzodiazepine receptor antagonist** that can reverse the sedative and other central nervous system effects of benzodiazepines. - It works by blocking benzodiazepines from binding to their receptor sites on the **GABA-A receptor complex**. *Naloxone* - **Naloxone** is a competitive **opioid receptor antagonist** used to reverse opioid overdose. - It has no effect on **benzodiazepine toxicity** as it targets different receptor systems. *Atropine* - **Atropine** is an **anticholinergic drug** used to reverse the effects of **cholinergic poisoning** (e.g., from organophosphates, carbamates) or symptomatic bradycardia. - It works on muscarinic acetylcholine receptors and is not involved in benzodiazepine metabolism or action. *N-acetyl-cysteine* - **N-acetyl-cysteine (NAC)** is primarily used as an antidote for **acetaminophen (paracetamol) poisoning**, where it replenishes glutathione. - It is also used in some cases of mucolysis but has no role in reversing benzodiazepine toxicity.