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13 Cards in this Set

  • Front
  • Back
indirect thrombin inhibitors
HEF
heparin (UFH)
enoxaparin (SC)- low molecular wt heparins
fondaparinux (SC)-long half life synthetic pentasaccharide analog of heparin
Unfractionated heparin vs low molecular wt heparin
UFH-accelerates interaction w/ both thrombin and factor Xa
LMWH-accelerates interaction w/ factor Xa only
ITI side effects
hemorrhage
osteoporosis
heparin-induced thrombocytopenia (HIT)-monitor platelet count; discontinue heparin and use direct thrombin inhibitor
Direct thrombin inhibitors
LBAD
lepirudin (IV)-derivative of hirudin
bivalirudin (IV)-synthetic 20aa analog of lepirudin
argatroban (IV)-derivative of L-arginine
dabigatran (oral)-synthetic non-peptide analog
DTI MOA
prevent thrombosis-inhibit thrombin and prolong aPPT
therapy monitored by aPTT
blood tests not required for dabigatran because its given orally
DTI side effects
hemorrhage-doesn't cause thrombocytopenia
oral anticoagulants
warfarin-inhibits Vit K epoxide reductase-->inhibits synthesis of Vit K dependent clotting factors II, VII, IX and X
site of genetic resistance
Rx interactions
antagonize coumarin action-barbituates
potentiate coumarin action action-cimetidine, grapefruit juice
displacement from protein-binding sites-sulfonamides
aspirin
antiplatelet agent
decreases TXA2 (accelerates platelet clotting) and PGL2 (maintains fluidity of blood in contact w/ endothelium
side effects-GI discomfort, bleeding
ADP inhibitors
1. clopidogrel
2. prasugrel
MOA-irreversibly ihibits ADP binding to platelet on receptor-->decreases platelet aggregation and increases bleeding time
lifetime effect
alternative to ASA to prevent MI or stroke
GP IIb/IIIa receptor blockers
1. Abciximab
2. Eptifibatide
MOA-inhibit ligand binding to IIb/IIIa receptor, decreasing platelet aggregation
thrombolytic (fibrinolytic) drugs
tissue-type plasminogen activator (alteplase)-recombinant form of thrombolytic enzyme
reteplase-derivative of tissue plasminogen activator
streptokinase-obtained from beta-hemolytic streptococci
thrombolytic drugs MOA
converts plasminogen to plasmin-->degrades fibrin and fibrinogen and increases clot dissolution