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Anti-Platelets
Anticoagulants, Plt Inhibitors, Fibrinolytics
| Question | Answer |
|---|---|
| virshow's triad leads to a thrombus (vessel occlusion) | endothelial injury, hypercoagulability, abnormal blood flow |
| defects in formation of plt plug | von willebrand disease |
| defects in clotting mechanism | hemophilia |
| antiplatelet agents (prevent plt aggregation; prevent plts from forming) | asa, Plavix-clopidogrel, dipyridamole, cilostazol, ticlopidine, prasugrel |
| anticoagulant agents (prevent clots from forming; interfere with clotting cascade) | heparin, warfarin-Coumadin, direct thrombin inhibitors, factor 10a inhibitors |
| fibrinolytics(lyse clots already formed) | tPA |
| blocks GP2b/3a | abciximab, triofiban, eptifibatide |
| endothelial injury causes | damage blood vessel, diabetes, HTN, atherosclerosis; exposes collagen, clotting cascade, vWf occurs |
| hypercoagulability causes | excess clotting factors: post sx, post-partum |
| abnormal blood flow causes | stasis, sluggish blood flow: bedrest, shock, CHF |
| fibrinogen | soluble, attach to GP2a/3b to anchor other plts |
| GP1b | glycoprotein, attach to vWf to allow plt to attach |
| GP2b/3a | glycoprotein, allows plts to anchor to one another with the use of fibrinogen |
| 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 |
| von willebrand factor (vWf) | produced by endothelial cells, protein attaches to exposed collagen after blood vessel injury; plt now activated |
| thrombin | potent plt activator |
| fibrin | insoluble |
| activation of plts occurs through? | thromboxane (TXA2) and ADP (breakdown of ATP) |
| 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; |
| APD (breakdown of ATP) | secreted from plts, plt activator, inducer of plt aggregation |
| 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 |
| COX1 | express plts only |
| COX2 | express inflammation only |
| Arachidonic acid blocked by what meds? | corticosteroid meds |
| cyclooxygenase pathway is blocked by what meds? | ASA and NSAIDS |
| cyclooxygenase pathway produce what? | thromboxane, prostaglandins |
| ASA | inhibit plt aggregation (COX1), anti-inflammatory (COX2), used for MI, stroke, atherosclerosis, given at low dose 81 mg; irreversible, antipyretic |
| selective COX2 inhibitors | anti-inflammatory, antipyretic, analgesic; no plt effect b/c it does not block COX1; meds: celecoxib, meloxicam |
| 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) |
| 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 |
| 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 |
| ADP decrease cAMP causing what? | energy to stimulate plt aggregation and activate plts |
| Ticlopidine ADP-Receptor inhibitors antiplatelet agents) | irreversible, N/V/D, hemorrhage, leukopenia |
| 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 |
| Prasugrel ADP-Receptor inhibitors (antiplatelet agents) | irreversible, rapid (1 step activation-advantage), potent/consistent blockade of ADP receptor than clopidogrel, better therapeutic effect |
| 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) |
| 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 |
| Eptifibatide GP2a/3b inhibitors (antiplatelet agents) | fibrinogen analog, highly efficacious inhibitor of plt aggregation, blocks binding of fibrinogen to receptor |
| Abciximab GP2a/3b inhibitors (antiplatelet agents) | monoclonal AB against GP2a/3b; irreversible, 18-24 hr dissociation |
| Tirofiban GP2a/3b inhibitors (antiplatelet agents) | tyrosine analog, reversibly antagonizes binding of plts to fibrinogen |
| If thromboxane is blocked how are plts activated? | ADP will activate plts |
| If ADP is blocked how are the plts activated? | thromboxane will activate plts |
| If GP2a/3b is blocked what happens to plts? | no plt aggregation |
| True/False Thromboxane is the primary plt-activating agent produced by plts | True |
Created by:
cburrows
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