NEET PG 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 concept of MAC (minimum alveolar concentration) in inhalational anaesthesia?

   MAC is the alveolar concentration of an inhaled anaesthetic that prevents movement in 50% of patients in response to a surgical stimulus. Lower MAC = higher potency.

2. List the first-line antihypertensive drug classes (per major guidelines).

   Thiazide diuretics, ACE inhibitors, ARBs, and calcium channel blockers (dihydropyridines). Beta-blockers are no longer first-line unless a compelling indication (e.g., post-MI, heart failure) exists.

3. Why are ACE inhibitors and ARBs preferred in diabetic patients with hypertension?

   They reduce intraglomerular pressure and proteinuria, providing renoprotection in diabetic nephropathy, in addition to lowering blood pressure.

4. What is the characteristic side effect of ACE inhibitors and its mechanism?

   Dry cough (and angioedema), due to accumulation of bradykinin (ACE normally degrades it). ARBs do not cause this because they do not affect bradykinin.

5. How do nitrates relieve angina?

   Nitrates release nitric oxide, increasing cGMP and causing venodilation, which reduces preload (and thus myocardial oxygen demand); they also dilate coronary arteries. Main limitation: tolerance, avoided with a nitrate-free interval.

6. Which drug classes reduce mortality in chronic heart failure with reduced ejection fraction (HFrEF)?

   ACE inhibitors/ARBs (or ARNI sacubitril-valsartan), beta-blockers (carvedilol, bisoprolol, metoprolol succinate), mineralocorticoid antagonists (spironolactone/eplerenone), and SGLT2 inhibitors. Digoxin reduces symptoms but not mortality.

7. State the mechanism and signs of digoxin toxicity.

   Digoxin inhibits Na+/K+-ATPase, raising intracellular Ca2+ (positive inotropy). Toxicity: nausea, visual disturbances (yellow vision), arrhythmias; hypokalemia worsens it. Antidote: digoxin-specific antibody (Fab) fragments.

8. State the Vaughan Williams classification of antiarrhythmic drugs.

   Class I: Na+ channel blockers (Ia quinidine, Ib lidocaine, Ic flecainide). Class II: beta-blockers. Class III: K+ channel blockers (amiodarone, sotalol). Class IV: non-dihydropyridine Ca2+ channel blockers (verapamil, diltiazem).

9. Match diuretic class to site of action: loop, thiazide, potassium-sparing, carbonic anhydrase inhibitor.

   Loop (furosemide): thick ascending limb (Na-K-2Cl). Thiazide: distal convoluted tubule (Na-Cl). Potassium-sparing (spironolactone/amiloride): collecting duct. Carbonic anhydrase inhibitor (acetazolamide): proximal convoluted tubule.

10. Compare the effect of loop diuretics vs thiazides on serum calcium.

    Loop diuretics increase calcium excretion (lower serum Ca, used in hypercalcemia). Thiazides decrease calcium excretion (raise serum Ca, useful in calcium kidney stones/osteoporosis).

11. What is the mechanism of sulfonylureas and their main adverse effect?

    Sulfonylureas (e.g., glimepiride, glipizide) close ATP-sensitive K+ channels on pancreatic beta cells, depolarizing them to stimulate insulin secretion. Main adverse effects: hypoglycemia and weight gain.

12. Why is metformin the first-line drug for type 2 diabetes, and what is its serious adverse effect?

    It reduces hepatic gluconeogenesis (and increases insulin sensitivity) without causing hypoglycemia or weight gain. Serious adverse effect: lactic acidosis (avoid in renal impairment).

13. Classify insulin preparations by onset/duration with one example each.

    Rapid-acting: lispro/aspart (onset ~15 min). Short-acting: regular insulin. Intermediate: NPH. Long-acting: glargine, detemir, degludec (basal, ~24 h, peakless).

14. What is the mechanism of the antithyroid drugs propylthiouracil and carbimazole/methimazole?

    Both inhibit thyroid peroxidase, blocking iodine organification and coupling of iodotyrosines. PTU additionally inhibits peripheral conversion of T4 to T3 (preferred in thyroid storm and first-trimester pregnancy).

15. Classify antibiotics by mechanism: give the cell-wall, protein-synthesis (30S vs 50S), DNA, and folate inhibitors.

    Cell wall: beta-lactams (penicillins, cephalosporins), vancomycin. Protein synthesis 30S: aminoglycosides, tetracyclines; 50S: macrolides, chloramphenicol, clindamycin, linezolid. DNA: fluoroquinolones (gyrase), metronidazole. Folate: sulfonamides, trimethoprim. RNA: rifampicin.

16. List the major mechanisms of bacterial antibiotic resistance.

    1) Enzymatic inactivation (e.g., beta-lactamases); 2) Target modification (e.g., altered PBPs in MRSA, ribosomal methylation); 3) Reduced uptake/decreased permeability; 4) Increased efflux pumps; 5) Bypass/overproduction of target pathway.

17. Match antimalarial drug to use: chloroquine, primaquine, artemisinin.

    Chloroquine: blood schizonticide for sensitive P. vivax/ovale/malariae. Primaquine: kills hypnozoites (liver) to prevent relapse (radical cure) and gametocytes; risk of hemolysis in G6PD deficiency. Artemisinin (ACT): first-line for P. falciparum, rapid blood schizonticide.

18. Name a representative antiviral and antifungal with mechanism: acyclovir and amphotericin B.

    Acyclovir: a guanosine analog activated by viral thymidine kinase, then inhibits viral DNA polymerase (herpes viruses). Amphotericin B: binds ergosterol in the fungal membrane, forming pores; key toxicity is nephrotoxicity.

19. Give one example each of an alkylating agent, antimetabolite, and a phase-specific cell-cycle anticancer drug.

    Alkylating agent: cyclophosphamide (cross-links DNA; toxicity: hemorrhagic cystitis, prevented by mesna). Antimetabolite: methotrexate (dihydrofolate reductase inhibitor; rescue with leucovorin). Phase-specific: vincristine (M phase, blocks microtubule assembly).

20. Name commonly used immunosuppressants and the key mechanism of calcineurin inhibitors.

    Calcineurin inhibitors: cyclosporine (binds cyclophilin) and tacrolimus (binds FKBP) inhibit calcineurin, blocking IL-2 transcription and T-cell activation. Others: mycophenolate, azathioprine, sirolimus (mTOR inhibitor), corticosteroids.

21. Differentiate the action of H1 vs H2 antihistamines.

    H1 antagonists (e.g., cetirizine, diphenhydramine) treat allergy, urticaria, and motion sickness (first-gen cause sedation). H2 antagonists (e.g., ranitidine, famotidine) block gastric acid secretion (peptic ulcer, GERD).

22. Explain the mechanism of NSAIDs and the advantage and risk of selective COX-2 inhibitors.

    NSAIDs inhibit cyclooxygenase (COX), reducing prostaglandin synthesis (anti-inflammatory, analgesic, antipyretic). Non-selective agents cause GI ulcers (COX-1 inhibition). Selective COX-2 inhibitors (e.g., celecoxib) spare the gastric mucosa but increase cardiovascular thrombotic risk.

23. Why is aspirin used in low doses for cardioprotection?

    Low-dose aspirin irreversibly acetylates COX-1 in platelets, blocking thromboxane A2 synthesis. Because platelets lack a nucleus and cannot resynthesize COX, the antiplatelet effect lasts the platelet lifespan (~7-10 days).

24. List the key pharmacological effects of corticosteroids and a major adverse effect of long-term use.

    Effects: anti-inflammatory, immunosuppressive, glucose elevation, sodium/water retention. Long-term adverse effects: Cushingoid features, osteoporosis, hyperglycemia, immunosuppression, and HPA-axis suppression (must taper, never stop abruptly).

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