PGIMER Entrance 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 serotonin syndrome and which drug combinations cause it?

   A potentially fatal syndrome of neuromuscular excitation (clonus, hyperreflexia), autonomic instability, and altered mental status from excess serotonin, e.g. SSRI + MAOI, SSRI + tramadol/triptans/linezolid.

2. What dietary/drug precaution is essential with MAO inhibitors?

   Avoid tyramine-rich foods (aged cheese, wine, cured meats) which can cause a hypertensive crisis (cheese reaction), and avoid sympathomimetics and serotonergic drugs.

3. Name the three classes of opioid receptors and the predominant effects of mu-receptor activation.

   Mu, kappa, and delta. Mu activation produces analgesia, euphoria, respiratory depression, miosis, constipation, and physical dependence.

4. What is the opioid overdose triad and its antidote?

   Triad: respiratory depression, pinpoint pupils (miosis), and coma/CNS depression. Antidote is naloxone, a pure opioid antagonist (short-acting, may need repeat dosing).

5. Which IV anesthetic is preferred in hypovolemic/shock patients and why?

   Ketamine, because it produces dissociative anesthesia with sympathetic stimulation that maintains blood pressure, heart rate, and bronchodilation; it also provides analgesia.

6. What determines the speed of induction with an inhalational anesthetic?

   The blood:gas partition coefficient - a low coefficient (e.g. nitrous oxide, desflurane) means low solubility, faster rise in alveolar/brain partial pressure, and faster induction and recovery.

7. List the major classes of antihypertensive drugs.

   Diuretics, ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, alpha-blockers, central sympatholytics, and direct vasodilators.

8. What is the characteristic adverse effect of ACE inhibitors and its cause?

   Dry cough (and angioedema) due to accumulation of bradykinin (and substance P) because ACE/kininase II normally degrades bradykinin. ARBs avoid this.

9. How does nitroglycerin relieve angina?

   It releases nitric oxide, increasing cGMP and causing venodilation that reduces preload (and at higher doses, coronary/arterial dilation), thereby lowering myocardial oxygen demand.

10. Why are dihydropyridine calcium channel blockers (e.g. amlodipine) and non-dihydropyridines (e.g. verapamil) used differently?

    Dihydropyridines act mainly on vascular smooth muscle (vasodilation, antihypertensive). Non-dihydropyridines (verapamil, diltiazem) act on the heart (negative chronotropic/inotropic), useful in arrhythmias and angina.

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

    Carbonic anhydrase inhibitors - proximal tubule; loop diuretics - thick ascending limb (Na-K-2Cl); thiazides - distal convoluted tubule (Na-Cl); potassium-sparing - collecting duct.

12. Which diuretics are potassium-sparing and how do they act?

    Spironolactone/eplerenone (aldosterone receptor antagonists) and amiloride/triamterene (epithelial Na channel blockers) in the collecting duct; they retain potassium while promoting sodium loss.

13. Which four drug classes improve survival (mortality) in chronic heart failure with reduced ejection fraction?

    ACE inhibitors/ARBs (or ARNI), beta-blockers (carvedilol, bisoprolol, metoprolol succinate), mineralocorticoid receptor antagonists (spironolactone), and SGLT2 inhibitors.

14. What is the mechanism of digoxin in heart failure?

    Digoxin inhibits the Na+/K+-ATPase, raising intracellular Na+ and thus intracellular Ca2+ via Na/Ca exchange, increasing cardiac contractility (positive inotropy); it also increases vagal tone, slowing AV conduction.

15. Classify antimicrobials by whether they inhibit cell wall synthesis.

    Cell wall synthesis inhibitors include beta-lactams (penicillins, cephalosporins, carbapenems, monobactams), glycopeptides (vancomycin), and bacitracin.

16. Which antibiotic classes inhibit bacterial protein synthesis and at which ribosomal subunit?

    30S: aminoglycosides and tetracyclines. 50S: macrolides, clindamycin, chloramphenicol, linezolid, and streptogramins.

17. What is the mechanism and key toxicity of aminoglycosides?

    Aminoglycosides bind the 30S subunit causing misreading of mRNA (bactericidal, concentration-dependent). Key toxicities are nephrotoxicity and ototoxicity (vestibular/auditory).

18. What is the mechanism of fluoroquinolones and a notable adverse effect?

    They inhibit DNA gyrase (topoisomerase II) and topoisomerase IV, blocking DNA replication. Notable adverse effects include tendinitis/tendon rupture, QT prolongation, and cartilage damage (avoid in children/pregnancy).

19. What is the cell cycle specificity concept in cancer chemotherapy? Give an example of a cell-cycle-specific drug.

    Cell-cycle-specific (CCS) drugs act on cells in a particular phase (e.g. methotrexate and 5-FU act in S phase; vinca alkaloids in M phase). Cell-cycle-nonspecific drugs (e.g. alkylating agents) act on cells in any phase.

20. What toxicity is associated with doxorubicin and how is it reduced?

    Doxorubicin (anthracycline) causes dose-dependent cardiotoxicity (cardiomyopathy/heart failure) via free radical generation; dexrazoxane (an iron chelator) is used to reduce it.

21. Name two calcineurin-inhibitor immunosuppressants and their main toxicity.

    Cyclosporine and tacrolimus inhibit calcineurin, blocking IL-2 production and T-cell activation; both are notably nephrotoxic (tacrolimus also more neurotoxic/diabetogenic).

22. Differentiate sulfonylureas from biguanides in mechanism for type 2 diabetes.

    Sulfonylureas (e.g. glibenclamide) close pancreatic beta-cell K-ATP channels to stimulate insulin secretion (risk of hypoglycemia/weight gain). Biguanides (metformin) decrease hepatic gluconeogenesis and improve insulin sensitivity (no hypoglycemia, weight neutral).

23. What is the mechanism of action of insulin on its target cells?

    Insulin binds a receptor tyrosine kinase, triggering autophosphorylation and signaling that recruits GLUT4 transporters to the membrane, increasing glucose uptake into muscle and fat, and promoting glycogen, protein, and fat synthesis.

24. Compare the effects of thyroid hormone replacement (levothyroxine) with antithyroid drugs (carbimazole/propylthiouracil).

    Levothyroxine (T4) replaces deficient hormone in hypothyroidism. Carbimazole/PTU inhibit thyroid peroxidase to reduce hormone synthesis in hyperthyroidism; PTU additionally blocks peripheral T4-to-T3 conversion and is preferred in first-trimester pregnancy.

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