FMGE Pharmacology Flashcards

24 sample cards from the Pharmacology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What is the mechanism of digoxin and its therapeutic effect in heart failure?

   Digoxin inhibits the Na+/K+-ATPase, raising intracellular Na+, which reduces Na+/Ca2+ exchange and increases intracellular Ca2+ → positive inotropy. It also increases vagal tone (negative chronotropy), slowing AV conduction (useful in atrial fibrillation).

2. Match each diuretic class to its site of action in the nephron.

   Carbonic anhydrase inhibitors (acetazolamide): proximal tubule. Loop diuretics (furosemide): thick ascending limb (Na-K-2Cl). Thiazides: distal convoluted tubule (Na-Cl). Potassium-sparing (spironolactone/amiloride): collecting duct. Osmotic (mannitol): proximal tubule and descending limb.

3. Why is furosemide called a 'high-ceiling' diuretic and what key electrolyte abnormality does it cause?

   Furosemide acts on the thick ascending limb where ~25% of Na+ is reabsorbed, giving a large maximal diuresis ('high ceiling'). It causes hypokalemia, hypocalcemia, hypomagnesemia, and metabolic alkalosis; ototoxicity is a notable adverse effect.

4. Compare warfarin and heparin: mechanism, route, monitoring, and antidote.

   Warfarin: inhibits vitamin K epoxide reductase (factors II, VII, IX, X); oral; monitor by PT/INR; antidote vitamin K (and FFP). Heparin: activates antithrombin III (inhibits thrombin & Xa); parenteral; monitor by aPTT; antidote protamine sulfate.

5. State the mechanism of aspirin's antiplatelet action and why its effect lasts ~7–10 days.

   Aspirin irreversibly acetylates platelet COX-1, blocking thromboxane A2 synthesis. Because platelets lack a nucleus and cannot regenerate COX, the effect persists for the platelet lifespan (~7–10 days) until new platelets form.

6. Which statin-related adverse effect must be monitored, and what is the statin mechanism?

   Statins inhibit HMG-CoA reductase, the rate-limiting enzyme of cholesterol synthesis, lowering LDL. Key adverse effects to monitor: myopathy/rhabdomyolysis (check CK) and hepatotoxicity (check LFTs); risk rises with fibrate co-administration.

7. Explain the mechanism of metformin and its most serious adverse effect.

   Metformin (a biguanide) activates AMP-kinase, decreasing hepatic gluconeogenesis and increasing peripheral insulin sensitivity; it does not cause hypoglycemia or weight gain. Most serious adverse effect: lactic acidosis (avoid in renal impairment).

8. Compare the onset and duration of rapid-acting versus long-acting insulin analogs.

   Rapid-acting (lispro, aspart, glulisine): onset ~15 min, peak 1 h, duration 3–5 h—taken with meals. Long-acting (glargine, detemir, degludec): peakless, duration ~24 h (degludec >40 h)—provide basal coverage.

9. State the mechanism of sulfonylureas and their main adverse effects.

   Sulfonylureas (glibenclamide, glimepiride) block ATP-sensitive K+ channels on pancreatic beta cells → depolarization → insulin release (require functioning beta cells). Main adverse effects: hypoglycemia and weight gain.

10. Describe the mechanism of carbimazole/methimazole and propylthiouracil in hyperthyroidism.

    Both inhibit thyroid peroxidase, blocking iodination and coupling of tyrosines (thyroid hormone synthesis). Propylthiouracil additionally inhibits peripheral conversion of T4 to T3 and is preferred in the first trimester of pregnancy and thyroid storm.

11. Classify antibiotics by mechanism: name a class for cell wall synthesis, protein synthesis, and DNA/folate inhibition.

    Cell wall synthesis: beta-lactams (penicillins, cephalosporins), vancomycin. Protein synthesis: aminoglycosides, macrolides, tetracyclines, chloramphenicol (50S/30S). DNA/folate: fluoroquinolones (DNA gyrase), sulfonamides + trimethoprim (folate synthesis), rifampicin (RNA polymerase).

12. Which aminoglycoside toxicities must be monitored and what is the mechanism of aminoglycosides?

    Aminoglycosides (gentamicin, amikacin) bind the 30S ribosomal subunit, causing misreading of mRNA (bactericidal). Major toxicities: nephrotoxicity and ototoxicity (vestibular/cochlear); also neuromuscular blockade. They show concentration-dependent killing and a post-antibiotic effect.

13. Name the first-line antitubercular drugs and the characteristic toxicity of each.

    Isoniazid: peripheral neuropathy (give pyridoxine), hepatitis. Rifampicin: hepatitis, orange body fluids, enzyme induction. Pyrazinamide: hyperuricemia, hepatotoxicity. Ethambutol: optic neuritis (red-green color blindness). Streptomycin: ototoxicity/nephrotoxicity.

14. Compare amphotericin B and azoles in antifungal mechanism.

    Amphotericin B binds ergosterol in the fungal membrane forming pores (fungicidal; nephrotoxic, infusion reactions). Azoles (fluconazole, itraconazole) inhibit CYP450-dependent 14-alpha-demethylase, blocking ergosterol synthesis (fungistatic; inhibit human CYPs causing interactions).

15. State the mechanism of acyclovir and why it is selective for infected cells.

    Acyclovir is a guanosine analog activated by viral thymidine kinase to acyclovir monophosphate (then triphosphate), which inhibits viral DNA polymerase and causes chain termination. Selectivity arises because only HSV/VZV-infected cells contain the activating viral thymidine kinase.

16. Which antimalarial is used for radical cure of P. vivax/ovale and what enzyme deficiency must be screened first?

    Primaquine is used for radical cure (kills hypnozoites in the liver). Screen for G6PD deficiency first, as primaquine causes hemolysis in G6PD-deficient patients.

17. Name the drug of choice for most tissue/intestinal nematodes and its mechanism.

    Albendazole/mebendazole (benzimidazoles) inhibit microtubule polymerization by binding beta-tubulin, impairing glucose uptake in helminths. Used for ascariasis, hookworm, enterobiasis, etc. For tissue filariasis/strongyloides, ivermectin (glutamate-gated Cl channels) is used.

18. Describe the cell-cycle specificity concept in anticancer chemotherapy with one example of each type.

    Cell-cycle-specific drugs act on dividing cells in a particular phase (e.g. methotrexate/5-FU in S phase, vinca alkaloids in M phase). Cell-cycle-nonspecific drugs act on cells in any phase including resting (e.g. alkylating agents like cyclophosphamide, cisplatin).

19. State the mechanism and a key toxicity of methotrexate, plus its rescue agent.

    Methotrexate inhibits dihydrofolate reductase, blocking tetrahydrofolate and thus DNA synthesis. Key toxicities: myelosuppression and mucositis (also hepatotoxicity, nephrotoxicity). Rescue with leucovorin (folinic acid) to spare normal cells.

20. Differentiate the mechanism of action of NSAIDs from paracetamol (acetaminophen).

    NSAIDs inhibit cyclooxygenase (COX-1 and COX-2) peripherally and centrally, giving anti-inflammatory, analgesic, antipyretic, and antiplatelet effects. Paracetamol acts mainly centrally with weak peripheral COX inhibition—analgesic and antipyretic but minimal anti-inflammatory/antiplatelet action.

21. What is the antidote for paracetamol overdose and how does it work?

    N-acetylcysteine (NAC) replenishes hepatic glutathione, which detoxifies the reactive metabolite NAPQI. It is most effective when given within 8–10 hours of overdose.

22. Compare H1 first-generation and second-generation antihistamines.

    First-generation (chlorpheniramine, diphenhydramine): cross the BBB causing sedation, plus anticholinergic effects. Second-generation (cetirizine, loratadine, fexofenadine): poorly cross BBB, minimal sedation and anticholinergic effects—preferred for allergic rhinitis/urticaria.

23. Classify drugs used in peptic ulcer disease and acid suppression with the most potent class.

    H2 blockers (ranitidine, famotidine) block histamine-stimulated acid; proton pump inhibitors (omeprazole) irreversibly inhibit the H+/K+-ATPase and are the most potent acid suppressants; antacids neutralize acid; mucosal protectives (sucralfate, misoprostol); and anti-H. pylori triple therapy.

24. Name the bronchodilator drug classes used in asthma and give an example of each.

    Short-acting beta-2 agonists (salbutamol) for acute relief; long-acting beta-2 agonists (salmeterol, formoterol); muscarinic antagonists (ipratropium, tiotropium); methylxanthines (theophylline). Anti-inflammatory controllers include inhaled corticosteroids and leukotriene antagonists (montelukast).

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