Anticoagulants, Plt Inhibitors, Fibrinolytics
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| virshow's triad leads to a thrombus (vessel occlusion) | endothelial injury, hypercoagulability, abnormal blood flow
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| defects in formation of plt plug | von willebrand disease
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| defects in clotting mechanism | hemophilia
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| antiplatelet agents (prevent plt aggregation; prevent plts from forming) | asa, Plavix-clopidogrel, dipyridamole, cilostazol, ticlopidine, prasugrel
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| anticoagulant agents (prevent clots from forming; interfere with clotting cascade) | heparin, warfarin-Coumadin, direct thrombin inhibitors, factor 10a inhibitors
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| fibrinolytics(lyse clots already formed) | tPA
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| blocks GP2b/3a | abciximab, triofiban, eptifibatide
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| endothelial injury causes | damage blood vessel, diabetes, HTN, atherosclerosis; exposes collagen, clotting cascade, vWf occurs
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| hypercoagulability causes | excess clotting factors: post sx, post-partum
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| abnormal blood flow causes | stasis, sluggish blood flow: bedrest, shock, CHF
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| fibrinogen | soluble, attach to GP2a/3b to anchor other plts
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| GP1b | glycoprotein, attach to vWf to allow plt to attach
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| GP2b/3a | glycoprotein, allows plts to anchor to one another with the use of fibrinogen
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| why do plts change shape from round to square? | results in change of shape in GP2a/3b receptor so it can bind to fibrinogen = plt aggregation = formation of plt plug; to adhere (stick) to both GP1b and GP2b/3a
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| von willebrand factor (vWf) | produced by endothelial cells, protein attaches to exposed collagen after blood vessel injury; plt now activated
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| thrombin | potent plt activator
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| fibrin | insoluble
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| activation of plts occurs through? | thromboxane (TXA2) and ADP (breakdown of ATP)
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| Thromboxane (TXA2) | activates plts and GP2a/3b to bind to fibrinogen to allow binding of other plts, potent vasoconstrictor, secreted within plts from arachidonic acid; blocked by ASA and NSAIDS;
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| APD (breakdown of ATP) | secreted from plts, plt activator, inducer of plt aggregation
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| cyclooxygenase inhibitors | irreversibly (ASA) inhibit COX1; cannot make plts b/c COX1 is blocked; blocks the formation of cyclooxygenase pathway which is necessary for plt aggregation
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| COX1 | express plts only
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| COX2 | express inflammation only
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| Arachidonic acid blocked by what meds? | corticosteroid meds
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| cyclooxygenase pathway is blocked by what meds? | ASA and NSAIDS
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| cyclooxygenase pathway produce what? | thromboxane, prostaglandins
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| ASA | inhibit plt aggregation (COX1), anti-inflammatory (COX2), used for MI, stroke, atherosclerosis, given at low dose 81 mg; irreversible, antipyretic
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| selective COX2 inhibitors | anti-inflammatory, antipyretic, analgesic; no plt effect b/c it does not block COX1; meds: celecoxib, meloxicam
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| phosphodiesterase inhibitors (antiplatelet agents) | phosphodiesterase is a enzyme that breaks down cAMP which causes it to cAMP to rise = increase cellular cAMP = decreased plt agg.
dipyridamole (older), cilostazol (newer), viagra (vasodilator)
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| dipyridamole (older) phosphodiesterase inhibitors (antiplatelet agents), | vasodilator can induce coronary steal, used in combo w/ASA 25mg for CV ischemia or warfarin, weak effects if used alone
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| ADP-Receptor inhibitors (antiplatelet agents) | clopidogrel (Plavix), ticlopidine, prasugrel; inhibit ADP-pathway of plt activation& agg, competitive inhibitors, irreversible, prodrug that form covalent (it sticks and stays = irreversible)S-S bonds with the receptor ADP
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| ADP decrease cAMP causing what? | energy to stimulate plt aggregation and activate plts
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| Ticlopidine ADP-Receptor inhibitors antiplatelet agents) | irreversible, N/V/D, hemorrhage, leukopenia
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| Clopidogrel (Plavix) ADP-Receptor inhibitors (antiplatelet agents) | Drawbacks: irreversible, prodrug (requires 2 activation reactions-2 liver conversions), slow onset which it takes a while to get to active compound
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| Prasugrel ADP-Receptor inhibitors (antiplatelet agents) | irreversible, rapid (1 step activation-advantage), potent/consistent blockade of ADP receptor than clopidogrel, better therapeutic effect
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| Ticagrelor ADP-Receptor inhibitors (antiplatelet agents) | reversible = less unwanted bleeding, PO, given in active form, no activation, more consistent response, faster onset, no liver conversion (CYP metabolism)
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| GP2a/3b inhibitors (antiplatelet agents) | eptifibatide, abciximab, tirofiban; given IV only-cons and pros-can regulate dose given; great potency = increase risk of bleeding, increase side effects; all work at the last step of pathway = plts will not stick at all; used for: unstable angina, PCI
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| Eptifibatide GP2a/3b inhibitors (antiplatelet agents) | fibrinogen analog, highly efficacious inhibitor of plt aggregation, blocks binding of fibrinogen to receptor
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| Abciximab GP2a/3b inhibitors (antiplatelet agents) | monoclonal AB against GP2a/3b; irreversible,
18-24 hr dissociation
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| Tirofiban GP2a/3b inhibitors (antiplatelet agents) | tyrosine analog, reversibly antagonizes binding of plts to fibrinogen
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| If thromboxane is blocked how are plts activated? | ADP will activate plts
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| If ADP is blocked how are the plts activated? | thromboxane will activate plts
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| If GP2a/3b is blocked what happens to plts? | no plt aggregation
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| True/False Thromboxane is the primary plt-activating agent produced by plts | True
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