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Anti-Platelets

Anticoagulants, Plt Inhibitors, Fibrinolytics

QuestionAnswer
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