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Anticoagulants, Plt Inhibitors, Fibrinolytics

Anticoagulants inhibit blood clotting cascade, prevent clot formation, toxicity = bleeding
Heparin, Warfarin (Coumadin), Factor 10a Inhibitors, Direct thrombin inhibitors anticoagulants
clotting factors circulating inactive protein produced by liver
factor 10 inactive in clotting cascade
factor 10a active in clotting cascade, where intrinsic and extrinsic pathways meet, prothrombin (circulating PRO) to thrombin to fibrinogen to fibrin (final product)
Fibrin insoluble, binds to plt plug wraps around it to form blood clot
blood vessel and tissue injury activates what? clotting cascade
Can you have blood vessel injury w/o tissue injury? Yes, HTN, DM, smoking, atherosclerosis
clotting cascade need previous factor to activate next factor (if not cascade stops)
Why is calcium important for clotting? play a role in clotting cascade, co-factor for prothrombin to thrombin
EDTA in tube for labs binds to calcium in that tube to prevent clotting (traps calcium), keeps blood from clotting
Heparin anticoagulant given IV, sulfated mucopolysaccharide, natural made, negatively charged, acidic, found in mast cells, heterogeneous, comes in different sizes and risks with same MOA, potent, used prophylaxis of thrombus, used in combo w/anti-plt for ACS & unstable angina
Unfractionated heparin (HMW-large polymer) anticoagulant made by bovine lung and porcine gut, high affinity for antithrombin 3 1000x; speeds up (cofactor) inactivation of factor 10a and thrombin = greater risk of bleeding
LMW Heparin (enoxaparin-Lovenox)and Rivaroxban-Xarelto anticoagulant made by gel filtration, selectively inhibit factor 10a, poorly inactivate thrombin = less risk and bleeding; wt. based; thrombin still active; greater therapeutic index
Fondaparinux (Arixtra) anticoagulant made by synthetic pentasaccharide (5 sugar), no effect on thrombin, selectively inactivate factor 10 only; wt. based; thrombin still active
Heparin anticoagulant act as a co-factor which enhance the actions of protease anti-thrombin 3, well-tolerated, immediate effects b/c its a co-factor of AT3 stimulating inactivation of clotting factors
Anti-thrombin 3 (AT3) function? inactivate thrombin and factor 10a; inhibit clotting factors 2a, 9a, 10a (thrombin); inactivate factor 10a to factor 10 = shutting clotting cascade pathway down
Treatment for heparin toxicity - bleeding? protamine sulfate - heparin antagonist, basic, + charged protamine binds with - charged heparin
HIT (heparin-induced thrombocytopenia) pts on HMW for 7 days, autoimmune activation & destruction of plts = thrombotic disorder; hypercoagulable state
Whose at risk for HIT? surgical, elderly pts, venous thrombosis increase w/ indwelling catheter, renal failure
Treatment of HIT? d/c heparin, protamine sulfate, direct thrombin inhibitor, anticoagulant
Etiology of HIT heparin binds to plt (hapten) which attracts IgG then IgG binds to plts activating the complement system to destroy (splenic macrophages) plts (thrombocytopenia); plt activation, plt release, plt aggregation = thrombosis
Which form of heparin is NOT reversed by protamine? Warfarin (Coumadin) and Fondaparinux (Arixtra): LMW
Warfarin (PO) anticoagulant oral anticoagulant, inhibits the regeneration of vit.K, inhibits liver vit.k reductase: cannot bring oxidized vit.k to reduced vit.k, prevents synthesis of 4 clotting factors: 2, 7, 9, 10
Vitamin K essential co-factor for synthesis of clotting factors in the liver
Vitamin K reductase takes oxidized form of vit.K and reduce it to make vit.k active
vitamins made by the body serve as what? co-factors which are recycled
Oxidized vitamin K cannot be used as a co-factor for clotting synthesis/factors
Warfarin (PO) anticoagulant delays-cons: not seen for 18-24 hrs b/c there is clotting factors still in circulation; clotting factors already made need to be used up first which takes about 24 hrs; long half-life and given orally (PO); pros: 100% absorbed, 99% plasma PRO bound
warfarin Bound to plasma protein inactive
warfarin displaced from plasma protein active
y-glutamylcarboxylase requires the presence of reduced vit.k
Warfarin anticoagulant metabolized by liver CYP450, activated by liver CYP2C9, half-life 36 hrs, interact through plasma PRO displacement or CYP450 effects; do not during pregnancy (cross placenta bleeding in fetus)
Drugs that decrease warfarin effects cholestyramine, barbs, rifampin, reduced vit.k, phenytoin, carbamazepine
Drugs that enhance warfarin effects chloral hydrate, amiodarone, Plavix, ethanol, fluconazole, fluoxetine, metronidazole, sulfamethoxazole (TMP-SMX), broad-spectrum ABX (cephalosporins), anabolic steroids
what would reverse the effects of warfarin most quickly? activated vitamin K (replaced the vit.k being blocked) and whole plasma b/c active clotting factors
Factor 10a inhibitors anticoagulants Rivaroxban (Xarelto) LMW
Rivaroxban (Xarelto) anticoagulant, LMW factor 10a inhibitor, PO, used for prevention of venous thrombosis following hip/knee replacement, a.fib, stroke, given as a fixed dose-no monitoring, more rapid onset, shorter half-life (10h) than warfarin
Direct thrombin Inhibitors anticoagulants given IV; bind and block the active site of thrombin; hirudin (lepirudin), bivalirudin, argatroban, melagatran, ximelagatran, dabigatran
Hirudin (lepirudin) Direct thrombin Inhibitors anticoagulants from leech saliva (recombinant lepirudin) bind to both catalytic and active site of thrombin
Bivalirudin Direct thrombin Inhibitors anticoagulants approved for coronary angioplasty, bind to both catalytic and active site of thrombin
Argatroban, Melagatran Direct thrombin Inhibitors anticoagulants used for HIT and angioplasty; bind only to thrombin active site
Ximelagatran Direct thrombin Inhibitors anticoagulants first oral agent, removed from market r/t liver toxicity; pros: reversible, no effect on 10a
Dabigatran (PO) Direct thrombin Inhibitors anticoagulants no antidote, pros: reversible, no effect on 10a
True/False Warfarin is the preferred anticoagulant in pregnant women false-cross placenta leading to bleeding in the fetus
Created by: cburrows



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