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Antithrombotic Pharm


primary hemostasis platelet plug formation
secondary hemostasis fibrin formation
drugs that infere with thrombus formation antithrombotics
drugs that promote degradatio of existing thrombi thrombolytics/fibrinolytics
thrombi that form in arteries white thrombi
thrombi w/more platelets and less fibrin white thrombi
thrombi that form in veins red thrombi
thrombi w/more fibrin and less platelets red thrombi
types of antithrombotic drugs antiplatelets and anticoagulants
drugs that interfere w/platelet plug formation antiplatelets
test(s) used to measure antiplatelet effectiveness bleeding time
drugs that interfere w/fibrin formation anticoagulants
test(s) used to measure anticoagulant effectiveness PT, INR, and PTT
site of von Willebrand factor binding glycoprotein Ib receptors
1st step of platelet plug formation platelet adhesion
2nd step of platelet plug formation platelet activation/secretion
3rd step of platelet plug formation platelet aggregation
needed to anchor platelets to BV wall von Willebrand factor
5HT, ADP, and PDGR are secreted via platelet cytoplasmic granules
TXA2 is secreted via de novo synthesis/secretion
undergoes conformation change during platelet activation glycoprotein IIb/IIIa receptors
platelet activation allows this to bind fibrinogen molecules
instrinc and extrinsic pathways converge here factor X
measures integrity of extrinsic and common pathways PT
measures integrity of intrinsic and common pathways PTT
usually ordered w/PT INR
test(s) ordered to check warfarin's efficacy PT & INR
test(s) ordered to check unfractionated heparin's efficacy PTT
test(s) ordered to check LMW heparin's efficacy factor Xa inhibition assay
MOA = irreversibly acetylates COOX, inhibiting production of TXA2 ASA
cardioprotective dose of ASA 75-325 mg/day
avoid in pts w/asthma and nasal polyps ASA
tinnitus may indicate ASA toxicity
AE = GI sx, hemorrhagic strokes ASA
MOA = inhibit ADP-mediated platelet activation by irreversibly binding to ADP receptors thienopyridines
ticlopidine thienopyridines
clopidogrel thienopyridines
prasugrel thienopyridines
AE = dyspepsia, diarrhea, neutropenia thienopyridines
AE = thombotic thrombocytopenic purpura, severe neutropenia ticlopidine
dosing = twice daily ticlopidine, ticagrelor
used w/ASA following coronary stenting and for acute corony syndromes clopidogrel
dosing = once daily clopidogrel
metabolized by CYP-2C19 clopidogrel
30% are "poor responders" clopidogrel
used w/ASA following PCI prasugrel
CI= elderly, TIA/CVA hx, small frame prasugrel
MOA = reversibly binds to platelet ADP receptors ticagrelor
used w/ASA for acute coronary syndromes ticagrelor
most effective antiplatelet drugs GP IIb/IIIa inhibitors
MOA = prevent fibrinogen-mediated platelet aggregation GP IIb/IIIa inhibitors
MOA = monoclonal AB against GPIIb/IIIa receptors abciximab
MOA = peptide antagonist eptifibatide
MOA = nonpeptide antagonist tirofiban
MOA = inc cAMP in platelets, decreasing cystolic Ca++ and inhibiting platelet aggregation dipyridamole
AE = thrombocytopenia abciximab
not usually given alone, but may enhance effect of other antithrombotics dipyridamole
needs at least 18 saccharide residues to produce effect heparin
selectively inhibits factor Xa LMW heparin
has equal inhibitory activity against factor Xa and thrombin UF heparin
AE = bleeding, thrombocytopenia, osteoporosis, skin necrosis, alopecia, hypoaldosteronism heparin
lower incidence of heparin-induced thrombocytopenia LMW heparin
given when severe bleeding complications occur w/heparin protamine sulfate
most common type of HIT non-immune mediated
life-and-limb threatening thrombosis can occur with this immune-mediated HIT
IgG + heparin + PF4 = platelet activation/aggregation
given when immune-mediated HIT occurs direct thrombin inhibitors
MOA= inhibit thrombin activity independent of antithrombin III direct thrombin inhibitors
lepirudin direct thrombin inhibitors
bivalirudin direct thrombin inhibitors
argatroban direct thrombin inhibitors
AE = BLEEDING direct thrombin inhibitors
MOA = synthetic heparin analog, bind to antithrombin III fondaparinux
inhibits factor Xa without causing HIT fondaparinux
dosing = subQ injection once daily fondaparinux
used for DVT prophylaxis in ortho surgery, and to treat DVT/PE fondaparinux
MOA = inhibits formation of reduced Vit K warfarin
necessary for activation of coagulation factors II, VII, IX, and X Vit K
delayed onset of anticoagulation warfarin
Vit K protein w/shortest half life Protein C
avoid large loading doses warfarin
given to avoid transient paradoxical hypercoagulable state warfarin and heparin together
AE = bleeding, teratogenic, skin necrosis warfarin
associated w/protein C or S deficiency & warfarin use skin necrosis
given when bleeding complications occur with warfarin vit K or fresh frozen plasma transfusion
used for DVT, atrial fib, mechanical heart valve, and STEMI warfarin
used for unstable angina/NSTEMI, STEMI, DVT, and PCI UF heparin
used for unstable angina/NSTEMI, STEMI, and DVT LMW heparin
used for PIC and HIT direct thrombin inhibitors
used for chronic angina, unstable angina/NSTEMI, STEMI, and PCI ASA
used for unstable angina/NSTEMI and STEMI thienopyridines
used for PCI and unstable angina/NSTEMI GP IIb/IIIa inhibitors
given if pt is unable to take warfarin for mechanical heart valve or a fib UF heparin
Created by: drhermy