DNB CET 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. Explain the role of blood-gas partition coefficient in the speed of induction with inhaled anesthetics.

   A low blood-gas partition coefficient (e.g. nitrous oxide, desflurane, sevoflurane) means the agent is poorly soluble in blood, so alveolar partial pressure rises quickly, giving rapid induction and recovery. A high coefficient (e.g. halothane, ether) means more drug dissolves in blood before partial pressure rises, causing slow induction and recovery.

2. Name the main drug classes used in Parkinson disease and their mechanisms.

   Levodopa + carbidopa (dopamine precursor + peripheral dopa-decarboxylase inhibitor; most effective). Dopamine agonists (pramipexole, ropinirole, bromocriptine). MAO-B inhibitors (selegiline, rasagiline). COMT inhibitors (entacapone, tolcapone) prolong levodopa. Anticholinergics (trihexyphenidyl) for tremor. Amantadine (NMDA antagonist, releases dopamine) for dyskinesia.

3. Why is levodopa combined with carbidopa, and what is the 'on-off' phenomenon?

   Carbidopa is a peripheral dopa-decarboxylase inhibitor that does not cross the blood-brain barrier; it prevents peripheral conversion of levodopa to dopamine, reducing nausea and cardiovascular effects and allowing more levodopa to reach the brain (lower dose needed). The 'on-off' phenomenon is unpredictable fluctuation between mobility (on) and sudden immobility (off) seen with long-term levodopa use.

4. Classify antihypertensive drug classes with one prototype each.

   Diuretics (hydrochlorothiazide, furosemide); ACE inhibitors (enalapril); ARBs (losartan); calcium channel blockers (amlodipine, verapamil); beta-blockers (metoprolol); alpha-1 blockers (prazosin); central sympatholytics (clonidine, methyldopa); direct vasodilators (hydralazine, minoxidil); direct renin inhibitor (aliskiren).

5. What distinguishes the adverse effects of ACE inhibitors from ARBs?

   ACE inhibitors block angiotensin II formation and degradation of bradykinin, so they commonly cause dry cough and angioedema (bradykinin-mediated) plus hyperkalemia and first-dose hypotension; contraindicated in pregnancy and bilateral renal artery stenosis. ARBs block the AT1 receptor without affecting bradykinin, so they cause far less cough/angioedema while retaining hyperkalemia and pregnancy contraindication.

6. Compare the three mechanisms by which antianginal drugs relieve angina.

   Nitrates (glyceryl trinitrate) release NO, causing venodilation that reduces preload and myocardial oxygen demand (also coronary dilation). Beta-blockers reduce heart rate, contractility, and oxygen demand. Calcium channel blockers cause coronary/peripheral vasodilation reducing afterload and (verapamil/diltiazem) reduce heart rate. All improve the supply-demand balance.

7. State the Vaughan-Williams classification of antiarrhythmic drugs.

   Class I: sodium channel blockers - Ia (quinidine, procainamide), Ib (lignocaine, mexiletine), Ic (flecainide, propafenone). Class II: beta-blockers (propranolol, esmolol). Class III: potassium channel blockers prolonging repolarization (amiodarone, sotalol, ibutilide). Class IV: calcium channel blockers (verapamil, diltiazem). Plus adenosine, digoxin, magnesium (unclassified).

8. What are the major toxicities of amiodarone?

   Amiodarone (class III) causes pulmonary fibrosis, thyroid dysfunction (hypo- and hyperthyroidism due to iodine content), corneal microdeposits, blue-grey skin discoloration, hepatotoxicity, photosensitivity, and peripheral neuropathy. It has a very long half-life (weeks) and many drug interactions (raises digoxin and warfarin levels).

9. Which drug classes reduce mortality in chronic heart failure with reduced ejection fraction?

   Mortality-reducing classes: ACE inhibitors/ARBs (or ARNI sacubitril-valsartan), beta-blockers (carvedilol, bisoprolol, metoprolol succinate), mineralocorticoid receptor antagonists (spironolactone, eplerenone), and SGLT2 inhibitors (dapagliflozin). Digoxin and loop diuretics relieve symptoms but do not reduce mortality.

10. Explain the mechanism and toxic features of digoxin.

    Digoxin inhibits the Na+/K+-ATPase, raising intracellular sodium and then calcium (via Na/Ca exchanger), giving positive inotropy; it also increases vagal tone, slowing AV conduction. Toxicity (narrow TI, worsened by hypokalemia): nausea, vomiting, yellow-green vision (xanthopsia), confusion, and arrhythmias. Treated with digoxin-specific antibody (Fab) fragments.

11. Classify oral antidiabetic drug groups with their mechanisms.

    Biguanides (metformin): decrease hepatic gluconeogenesis, increase insulin sensitivity (first-line). Sulfonylureas (glibenclamide, glimepiride): stimulate insulin release (risk hypoglycemia, weight gain). Thiazolidinediones (pioglitazone): PPAR-gamma agonist increasing sensitivity. DPP-4 inhibitors (sitagliptin) and GLP-1 agonists (liraglutide): incretin-based. SGLT2 inhibitors (empagliflozin): block renal glucose reabsorption. Alpha-glucosidase inhibitors (acarbose): slow carbohydrate absorption.

12. Compare the onset and duration of insulin preparations.

    Rapid-acting (lispro, aspart, glulisine): onset 5-15 min, duration 3-5 h, given at meals. Short-acting/regular: onset 30 min, duration 6-8 h. Intermediate (NPH): onset 1-2 h, duration 12-18 h. Long-acting (glargine, detemir, degludec): onset 1-2 h, peakless, duration up to 24 h or longer for basal coverage.

13. Differentiate the drug treatment of hyperthyroidism and hypothyroidism.

    Hyperthyroidism: thioamides (carbimazole/methimazole, propylthiouracil) inhibit thyroid peroxidase blocking hormone synthesis (PTU also blocks peripheral T4 to T3); plus beta-blockers for symptoms, radioactive iodine, or surgery. Hypothyroidism: levothyroxine (T4) replacement, taken on an empty stomach, titrated to TSH.

14. Compare H1 and H2 antihistamines in their uses.

    H1 antagonists treat allergic conditions: first-generation (chlorpheniramine, diphenhydramine, promethazine) are sedating, cross the blood-brain barrier, and have antimuscarinic/antiemetic effects; second-generation (cetirizine, loratadine, fexofenadine) are non-sedating. H2 antagonists (ranitidine, famotidine) block gastric acid secretion and are used for peptic ulcer/GERD.

15. Explain the difference between non-selective NSAIDs and selective COX-2 inhibitors.

    Non-selective NSAIDs (ibuprofen, naproxen, diclofenac) inhibit both COX-1 (gastroprotective prostaglandins, platelet thromboxane) and COX-2 (inflammatory prostaglandins), causing analgesia/anti-inflammation but GI ulceration and antiplatelet effect. Selective COX-2 inhibitors (celecoxib, etoricoxib) spare COX-1, reducing GI bleeding but increasing cardiovascular/thrombotic risk.

16. Why is aspirin's antiplatelet effect irreversible and clinically useful at low doses?

    Aspirin irreversibly acetylates COX-1 in platelets, blocking thromboxane A2 synthesis for the platelet's entire lifespan (7-10 days) since platelets cannot synthesize new enzyme. Low doses (75-150 mg) selectively inhibit platelet COX-1 while sparing endothelial prostacyclin, giving antithrombotic protection in coronary and cerebrovascular disease.

17. Classify beta-lactam antibiotics and state their common mechanism.

    Beta-lactams (penicillins, cephalosporins, carbapenems, monobactams) inhibit bacterial cell wall synthesis by binding penicillin-binding proteins (transpeptidases), blocking peptidoglycan cross-linking; they are bactericidal. Resistance is mainly via beta-lactamase enzymes (countered by clavulanate, sulbactam, tazobactam) or altered PBPs (e.g. MRSA).

18. Compare the mechanism and key toxicity of macrolides versus aminoglycosides.

    Macrolides (erythromycin, azithromycin) bind the 50S ribosomal subunit, are bacteriostatic, and cause GI upset, QT prolongation, and CYP3A4 inhibition. Aminoglycosides (gentamicin, amikacin) bind the 30S subunit, are bactericidal and concentration-dependent (need oxygen for uptake, so ineffective against anaerobes), and cause nephrotoxicity and ototoxicity.

19. List the first-line antitubercular drugs with their characteristic toxicities.

    Isoniazid (H): peripheral neuropathy (give pyridoxine), hepatotoxicity. Rifampicin (R): hepatotoxicity, orange body fluids, potent CYP inducer. Pyrazinamide (Z): hepatotoxicity, hyperuricemia. Ethambutol (E): optic neuritis (red-green color vision loss). Standard regimen: 2 months HRZE then 4 months HR.

20. Name the major classes of antiretroviral drugs (HAART) with a prototype of each.

    NRTIs (zidovudine, tenofovir, lamivudine) - inhibit reverse transcriptase as chain terminators. NNRTIs (efavirenz, nevirapine) - non-nucleoside RT inhibition. Protease inhibitors (ritonavir, lopinavir) - block viral maturation. Integrase inhibitors (dolutegravir, raltegravir). Entry/fusion inhibitors (maraviroc CCR5, enfuvirtide). HAART combines 3 drugs from at least 2 classes.

21. Compare the main classes of antifungal drugs by mechanism.

    Azoles (fluconazole, itraconazole, voriconazole) inhibit ergosterol synthesis (14-alpha-demethylase). Polyenes (amphotericin B, nystatin) bind ergosterol forming membrane pores (amphotericin causes nephrotoxicity and infusion fever). Echinocandins (caspofungin) inhibit beta-1,3-glucan cell wall synthesis. Allylamines (terbinafine) inhibit squalene epoxidase. Flucytosine inhibits DNA/RNA synthesis.

22. Differentiate the antimalarials used for chloroquine-resistant falciparum and for radical cure of vivax.

    Chloroquine-resistant P. falciparum: artemisinin-based combination therapy (ACT, e.g. artemether-lumefantrine) is first-line; alternatives are quinine plus doxycycline. Radical cure of P. vivax/ovale requires primaquine (or tafenoquine) to kill the hypnozoite liver stages - test for G6PD deficiency first to avoid hemolysis.

23. State the mechanism of action and indications of the major anthelmintics.

    Benzimidazoles (albendazole, mebendazole) inhibit microtubule polymerization (bind beta-tubulin), used for most intestinal nematodes. Pyrantel pamoate is a depolarizing neuromuscular blocker (spastic paralysis). Praziquantel increases calcium permeability causing paralysis - drug of choice for cestodes and schistosomes. Ivermectin opens glutamate-gated chloride channels - used for filariasis/onchocerciasis and strongyloides.

24. Classify the major cell-cycle-specific and cell-cycle-nonspecific anticancer drug groups and explain a key mechanism of resistance.

    Cell-cycle nonspecific: alkylating agents (cyclophosphamide) and platinum (cisplatin) cross-link DNA. Cell-cycle specific: antimetabolites (methotrexate-S phase, 5-FU), vinca alkaloids (M phase, block microtubule assembly), taxanes (M phase, stabilize microtubules). A major resistance mechanism is overexpression of the MDR1/P-glycoprotein efflux pump that pumps drugs out of the cell; others include increased DNA repair and target gene amplification.

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