441-antithrombs only

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jgiantess
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124288
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441-antithrombs only
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2011-12-18 03:38:31
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drugs
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pharmacology
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  1. Acetylsalicylic Acid (Aspirin)
    • antiplatelet: thromboxane A2 inhibitor.
    • Irreversibly inhibits platelet COX1, blocking TXA2 formation (and therefore no platelet shape change, granule release, or aggregation). Overall decreased platelet aggregation (but weakest since blocks only one pathway).
    • Low doses (75-325mg) preferentially inhibits platelet COX over endothelial COX2 (which is important in prostacyclin).
  2. Clopidogrel (Plavix)
    • antiplatelet: ADP-inhibitor. pro-drug.
    • selectively irreversibly blocks ADP binding to P2Y12 platelet receptor, therefore no ADP-induced platelet aggregation because no activation of GPIIb/IIIa receptors. (Also partially prevents aggregation by other agonists since ADP is released from all activated platelets irrespective of agonist.)
    • As save as aspirin.
  3. Ticlopidine (Ticlid)
    • antiplatelet: ADP-inhibitor. pro-drug.
    • interferes with platelet-fibrinogen binding and platelet-platelet int'n, maybe due to inhibition of ADP to P2Y12.
    • Reserved for pts who cannot tolerate ASA.
  4. Prasugrel (effient)
    • antiplatelet: ADP-inhibitor. pro-drug - converted by intestinal and hepatic CYP450.
    • irreversibly binds P2Y12 for lifespan, inhibits platelet activation and aggregation.
    • Can be taken together with ASA.
  5. Abiciximab (ReoPro)
    • antiplatelet: GPIIb/IIIa receptor antagonist.
    • Most potent antiplatelet agents because blocks final common pathway of all stimuli (thrombin, ADP, collagen). Prevents fibrinogen-mediated cross-linkage.
    • monoclonal antiplatelet Ab, prevents binding of fibrinogen and VWF to prevent aggregation.
    • Max inhibition observed when >80% of receptors blocked.
  6. Eptifibatide (Integrilin)
    • antiplatelet: GPIIb/IIIa receptor antagonist.
    • Most potent antiplatelet agents because blocks final common pathway of all stimuli (thrombin, ADP, collagen). Prevents fibrinogen-mediated cross-linkage.
    • small-molecule peptide, resembles fibrinogen RGD recognition sequence.
    • Reversibly inhibits platelet aggreg by preventing binding of fibrinogen and VWF to receptors.
  7. Tirofiban (Aggrastat)
    • antiplatelet: GPIIb/IIIa receptor antagonist.
    • Most potent antiplatelet agents because blocks final common pathway of all stimuli (thrombin, ADP, collagen). Prevents fibrinogen-mediated cross-linkage.
    • non-peptide antagonist of fibrnogen binding to receptor.
    • Reversible. Occupies receptor, therefore inhibits binding of fibrinogen and VWF to receptor.
  8. Dipyridamole
    • antiplatelet: phosphodiesterase inhibitor.
    • reduces platelet adhesiveness by increasing cAMP --> release prostacyclin. Also vasodilator.
  9. Heparin (unfractionated)
    • Anticoagulant: indirect thrombin inhibitor.
    • 5,000-30,000 daltons, injectable. Extracted from porcine mucosa. Strongly anionic due to sulfate and carboxyl groups.
    • Very polar, does not cross membranes easily. Binds to plasma ANTITHROMBIN III via pentasaccharide sequence. Increases affinity of antithrombin to Xa and thrombin (among others), promotes inhibition of Xa
    • Pentasaccharide only (<18 monosac's long, MW<6,000) - only inhibits factor Xa.
    • Longer heps (>18ms, MW>6,000) - have stronger inhibitory capacity against thrombin (heparin must bind to both antithrombin AND thrombin [at exosite 2] to form a ternary complex).
    • Rapid acting - peak after 2-4 hours.
  10. Low Molecular Weight Heparin
    • Anticoagulant: indirect thrombin inhibitor.
    • 4,000-6,000 daltons, injectable. Extracted from porcine mucosa. Strongly anionic due to sulfate and carboxyl groups.
    • Better bioavailability (less binding to endothelium and plasma proteins).
    • Longer t1/2...predictable anticoagulant response.
    • e.g. dalteparin, enoxaparin, nadroparin, tinzaparin.
  11. Lepirudin
    • Anticoagulant: direct thrombin inhibitor.
    • recombinant Hirudin
    • Bivalent irreversible binding to thrombin catalytic site and exosite 1.
    • inhibits free and bound thrombin.
    • No HIT.
  12. Bivalirudin
    • Anticoagulant: direct thrombin inhibitor.
    • short synthetic peptide, resembles Hirudin.
    • Bivalent reversible binding to thrombin catalytic site and exosite 1.
    • inhibits free and bound thrombin.
    • No HIT.
  13. Argatroban.
    • Anticoagulant: direct thrombin inhibitor.
    • small molecule, binds only to catalytic site -> monovalent.
    • Reversible, inhibits free and bound thrombin.
    • No HIT.
  14. Dabigatran
    • Anticoagulant: direct thrombin inhibitor.
    • first oral direct monovalent thrombin (factor IIa) inhibitor.
    • Is a prodrug that is converted by esterases in blood.
    • Reversible, inhibits free and bound thrombin.
    • No HIT.
  15. Fondaparinux
    • Anticoagulant: factor Xa inhibitor, indirect (binds to antithrombin to enhance affinity 300x).
    • synthetic pentasaccharide with the sequence of heparin. Parenteral.
    • Long t1/2. Lower risk of HIT.
  16. Rivaroxaban
    • Anticoagulant: factor Xa inhibitor, DIRECT and oral.
    • Competitively, selectively, directly inhibits factor Xa...10,000x greater.
    • Prolongs clotting times in human plasma.
  17. Warfarin, Nicoumalone
    • Anticoagulant: vitamin K antagonist
    • Structure similar to Vitamin K, therefore competitively inhibits and interferes with hepatic synthesis of Vit K-dependent clotting factors - II, VII, IX, X, anticoagulant protein C. (decreases availability of hydroquinone).
    • Substrate of CYP450. No effect on previously synthesized factors...first anticoag effect at 8-12 hours.
    • Effective anticoag at least 1 week - due to half-lives of clotting factors.
  18. Heparan sulfate-Danaparoid
    • Anticoagulant: alternative
    • mixture of non-heparin low MW sulfated glycosaminoglycuronans...some affinity to antithrombin...ahtithrombotic.
    • Choice for pts with HIT.
  19. Xigris - recombinant human protein C - drotrecogin alfa.
    • Anticoagulant: alternative
    • Protein C, with co-factor protein S, degrades factors Va and VIIIa --> natural anticoag by inhibiting activation of prothrombin and factor X.
  20. Aminocaproic acid
    plasmin inhibitor, used as necessary to counteract effects of thrombolytic drugs.
  21. Streptokinase
    • Thrombolytic: 1st gen
    • purified from beta-hemolytic streptococci
    • forms active complex with plasminogen to convert uncomplexed plasminogen to active plasmin.
    • Non-selective between circulating and fibrin-bound plasminogen.
    • Non-fibrin selective: also catalyzes degradation of fibrinogen and factors V and VII.
    • Given by infusion...need loading dose to over come antibodies.
  22. t-PA (tissue plasminogen activator)
    • Thrombolytic: 2nd gen
    • mostly from recombinant DNA, is also a naturally occurring intrinsic compound.
    • Low affinity for plasminogen, but rapidly activates plasminogen bound to fibrin in a thrombus or hemostatic plug (specific to stuff at fibrin surface x00 times more than in circulation).
    • Fibrin-selective - esp at low doses (no fibrinogen)
    • short half-life - administered as initial bolus then infusion.
  23. r-PA
    • Thrombolytic: 3rd gen
    • recombinant PA.
    • less expensive to make but less fibrin-specific
  24. tenecteplase
    • Thrombolytic: 3rd gen
    • more fibrin specific than t-PA, made by introducing aa modifications to t-PA. longer half-life.

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