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This deck focuses on Pharmacology, giving you a quick way to review the definitions, rules, and examples that matter most for NAPLEX.
Study Pharmacology in NAPLEX with focused flashcards that help you recognize the idea, recall the key rule, and apply it in practice-style prompts.
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What is the primary mechanism of action of amphotericin B?
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Binds ergosterol to form membrane pores causing cell leakage. Amphotericin B creates channels in fungal membranes, allowing leakage of cellular contents and leading to cell death.
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This deck focuses on Pharmacology, giving you a quick way to review the definitions, rules, and examples that matter most for NAPLEX.
Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.
Answer: Binds ergosterol to form membrane pores causing cell leakage. Amphotericin B creates channels in fungal membranes, allowing leakage of cellular contents and leading to cell death.
Answer: Aldosterone receptor antagonist in collecting duct (potassium-sparing). Spironolactone blocks mineralocorticoid effects, reducing sodium reabsorption while preserving potassium in the distal nephron.
Answer: Potentiates antithrombin to inhibit thrombin (IIa) and factor Xa. Heparin enhances the activity of a natural anticoagulant, rapidly inactivating key clotting factors to prevent thrombus formation.
Answer: Inhibits VKORC1, decreasing factors II, VII, IX, X and proteins C, S. Warfarin blocks vitamin K recycling, depleting gamma-carboxylated clotting factors necessary for blood coagulation.
Answer: Irreversibly blocks P2Y12 (ADP) receptor to inhibit platelet aggregation. Clopidogrel prevents ADP-mediated activation of glycoprotein IIb/IIIa, crucial for platelet cross-linking and clot formation.
Answer: Inhibit Na-K-2Cl cotransporter in thick ascending limb. Loop diuretics cause potent natriuresis by inhibiting salt transport in the loop of Henle, decreasing extracellular fluid volume.
Answer: Binds D-Ala-D-Ala to inhibit peptidoglycan cell wall synthesis. Vancomycin targets the terminal dipeptide in peptidoglycan precursors, halting cell wall assembly in Gram-positive bacteria.
Answer: Bind 50S ribosome to inhibit translocation and protein synthesis. Macrolides prevent the movement of the peptidyl-tRNA from the A site to the P site during translation elongation.
Answer: Irreversibly bind 30S ribosome causing misreading and bactericidal effect. Aminoglycosides disrupt protein synthesis by interfering with mRNA reading on the ribosome, resulting in faulty proteins and bacterial death.
Answer: Inhibit HMG-CoA reductase to decrease hepatic cholesterol synthesis. Statins lower LDL cholesterol by blocking the rate-limiting step in the mevalonate pathway, upregulating LDL receptors.
Answer: Neuraminidase inhibitor that blocks influenza virion release. Oseltamivir prevents sialic acid cleavage, trapping new influenza viruses on the host cell surface and limiting spread.
Answer: Close pancreatic KATP channels to increase insulin release. Sulfonylureas stimulate beta cells by blocking potassium efflux, depolarizing the membrane and triggering insulin secretion.
Answer: Protamine sulfate. Protamine neutralizes heparin's anticoagulant effect by forming a stable complex, restoring normal clotting.
Answer: Decreases hepatic gluconeogenesis and increases insulin sensitivity. Metformin improves glycemic control by suppressing liver glucose output and enhancing peripheral glucose uptake.
Answer: Four-factor PCC plus vitamin K (phytonadione). This combination rapidly replenishes vitamin K-dependent factors and supports long-term correction of coagulopathy.
Answer: Inhibit 14-α-demethylase to reduce ergosterol synthesis. Azoles disrupt fungal membrane integrity by inhibiting a key enzyme in the ergosterol biosynthetic pathway.
Answer: Inhibit NaCl cotransporter in distal convoluted tubule. Thiazides promote diuresis by blocking sodium reabsorption in the distal nephron, reducing blood volume and pressure.
Answer: Competitive opioid receptor antagonist (highest affinity for μ). Naloxone reverses opioid effects by competitively displacing agonists from receptors, particularly the mu subtype involved in analgesia and respiratory depression.
Answer: Block angiotensin II type 1 (AT1) receptors. ARBs prevent angiotensin II from binding its receptor, mitigating vasoconstriction and aldosterone release without affecting bradykinin.
Answer: Inhibit PBPs (transpeptidases) to block bacterial cell wall cross-linking. Beta-lactams weaken bacterial cell walls by preventing the final cross-linking step in peptidoglycan synthesis, leading to cell lysis.
Answer: Sequential folate synthesis inhibition (DHPS then DHFR). The combination synergistically blocks tetrahydrofolate production, essential for bacterial nucleotide synthesis and growth.
Answer: Inhibit ACE, decreasing angiotensin II and increasing bradykinin. ACE inhibitors reduce vasoconstriction and sodium retention while potentiating a vasodilatory peptide, lowering blood pressure.
Answer: Irreversibly inhibits COX-1, decreasing thromboxane A2. Aspirin suppresses platelet activation by reducing a pro-aggregatory eicosanoid, providing antithrombotic effects.
Answer: Guanosine analog; inhibits viral DNA polymerase after phosphorylation. Acyclovir mimics a nucleoside and, once activated by viral thymidine kinase, terminates DNA chain elongation in herpes viruses.
Answer: Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV. Fluoroquinolones interfere with bacterial DNA replication and repair by targeting enzymes essential for supercoiling and decatenation.