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GPAT Pharmacology Flashcards
50 question-and-answer cards covering Pharmacology as it is examined in GPAT. 24 of them are printed below, taken from across the deck — no signup, no paywall on the preview.
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.
What is the mechanism and antidote for organophosphate poisoning?
Organophosphates irreversibly inhibit acetylcholinesterase causing cholinergic crisis. Antidotes: atropine (blocks muscarinic effects) plus pralidoxime (2-PAM, reactivates enzyme if given early before aging).
Name the prototype drugs and mechanism of beta-blockers.
Beta-blockers (e.g., propranolol, atenolol, metoprolol) competitively antagonize β-adrenergic receptors, reducing heart rate, contractility, and renin release; used in hypertension, angina, arrhythmias.
What is the mechanism of action of aspirin?
Aspirin irreversibly acetylates cyclooxygenase (COX-1 and COX-2), inhibiting prostaglandin and thromboxane A2 synthesis; low doses give antiplatelet effect via TXA2 inhibition.
Differentiate non-selective NSAIDs from selective COX-2 inhibitors.
Non-selective NSAIDs inhibit COX-1 and COX-2 (more GI ulceration); selective COX-2 inhibitors (coxibs, e.g., celecoxib) spare COX-1, causing less GI toxicity but higher cardiovascular thrombotic risk.
What is the mechanism of action of paracetamol (acetaminophen) and its antidote in overdose?
It is a weak central COX inhibitor (analgesic, antipyretic, minimal anti-inflammatory). Overdose causes hepatotoxicity via NAPQI; antidote is N-acetylcysteine, which replenishes glutathione.
Classify diuretics by site of action.
Carbonic anhydrase inhibitors (proximal tubule); loop diuretics (thick ascending limb); thiazides (distal convoluted tubule); potassium-sparing (collecting duct); osmotic diuretics (whole nephron).
What is the mechanism of loop diuretics like furosemide?
They inhibit the Na+/K+/2Cl- cotransporter in the thick ascending limb of the loop of Henle, producing potent diuresis.
What is the mechanism and key adverse effect of thiazide diuretics?
They inhibit the Na+/Cl- symporter in the distal convoluted tubule. Key adverse effects: hypokalemia, hyperglycemia, hyperuricemia, hyperlipidemia, and hypercalcemia.
Name the major classes of antihypertensive drugs.
Diuretics, ACE inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers, beta-blockers, alpha-blockers, and centrally acting agents (e.g., clonidine, methyldopa).
What is the mechanism of ACE inhibitors and a characteristic side effect?
They inhibit angiotensin-converting enzyme, reducing angiotensin II and aldosterone (and increasing bradykinin). Characteristic side effect: dry cough; also angioedema and hyperkalemia; contraindicated in pregnancy.
What is the mechanism of action of statins?
Statins competitively inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, lowering LDL cholesterol and upregulating LDL receptors.
What is the mechanism and antidote of warfarin?
Warfarin inhibits vitamin K epoxide reductase, decreasing synthesis of clotting factors II, VII, IX, X (and proteins C, S). Antidote: vitamin K (phytonadione); fresh frozen plasma for urgent reversal.
What is the mechanism and antidote of heparin?
Heparin activates antithrombin III, which inactivates thrombin (IIa) and factor Xa. Antidote: protamine sulfate.
Differentiate bactericidal from bacteriostatic antibiotics with examples.
Bactericidal kill bacteria (penicillins, cephalosporins, aminoglycosides, fluoroquinolones, vancomycin); bacteriostatic inhibit growth (tetracyclines, macrolides, sulfonamides, chloramphenicol).
What is the mechanism of action of beta-lactam antibiotics?
They inhibit bacterial cell wall synthesis by binding penicillin-binding proteins (transpeptidases), preventing peptidoglycan cross-linking, leading to cell lysis.
What is the mechanism of aminoglycosides and their main toxicities?
They bind the 30S ribosomal subunit, causing misreading of mRNA and inhibiting protein synthesis (bactericidal). Main toxicities: nephrotoxicity and ototoxicity.
Which antibiotics inhibit the 30S versus the 50S ribosomal subunit?
30S: aminoglycosides and tetracyclines. 50S: macrolides, chloramphenicol, clindamycin, linezolid.
What is the mechanism of action of fluoroquinolones?
They inhibit bacterial DNA gyrase (topoisomerase II) and topoisomerase IV, preventing DNA replication; bactericidal. Example: ciprofloxacin, levofloxacin.
What is the mechanism of sulfonamides and the basis of synergy with trimethoprim?
Sulfonamides inhibit dihydropteroate synthase (PABA analog); trimethoprim inhibits dihydrofolate reductase. Together they sequentially block folate synthesis, giving synergistic bactericidal action (co-trimoxazole).
What is the mechanism of action of proton pump inhibitors (PPIs)?
PPIs (e.g., omeprazole) irreversibly inhibit the H+/K+-ATPase (proton pump) in gastric parietal cells, suppressing acid secretion.
What is the mechanism of action of insulin?
Insulin binds tyrosine-kinase receptors, promoting cellular glucose uptake (GLUT4 translocation), glycogenesis, lipogenesis, and protein synthesis while inhibiting gluconeogenesis and lipolysis.
What is the mechanism of action of metformin?
Metformin (a biguanide) activates AMP-activated protein kinase, decreasing hepatic gluconeogenesis and increasing peripheral insulin sensitivity/glucose uptake; it does not cause hypoglycemia or weight gain.
What is the mechanism of action of benzodiazepines?
They bind a specific site on the GABA-A receptor and increase the frequency of chloride channel opening, enhancing GABA-mediated inhibition. Antidote: flumazenil.
Differentiate Type A from Type B adverse drug reactions.
Type A (Augmented): dose-dependent, predictable extensions of pharmacological action, common, low mortality. Type B (Bizarre): dose-independent, unpredictable, idiosyncratic/immunologic, rarer but often serious.
What this deck covers
The Pharmacology deck follows the GPAT Pharmacology syllabus — 15 chapters and 0 topics — so questions land on material that is genuinely examinable rather than trivia around it. That works out to roughly 3.3 cards per chapter.
Answers are written to be recallable, not just readable — averaging about 175 characters, which is long enough to carry the reasoning and short enough to say out loud.
A deck like this earns its keep on the second and third pass. Read the syllabus first so you know the shape of the subject, then use the cards to find the specific facts that have not stuck.
Pharmacology flashcards FAQ
How many Pharmacology flashcards are in this GPAT deck?
50 cards. This page previews 24 of them, sampled evenly across the deck so you can judge the difficulty before installing anything.
Are these GPAT flashcards free?
Yes. The preview here is free to read with no signup, and the full 50-card deck is free inside the Examius app.
What do the Pharmacology cards cover?
They follow the GPAT Pharmacology syllabus — 15 chapters and 0 topics — so the questions track what is actually examinable.
How should I use these flashcards?
Read the syllabus first so you know the shape of the subject, then drill the deck. Examius schedules each card with spaced repetition, so cards you keep missing come back sooner and ones you know drift further apart.