Anticoagulants Flashcards
heparin MOA
antithrombin III activation, decreases IIa and Xa function`
heparin antidote
protamine sulfate (very positive to sequester the heparin)
what are the low molecular weight heparins
Enoxaparin, dalteparin: subQ, no lab. monitoring, not easily reversible
heparin induced thrombocytopenia cause
IgG against heparin bound to platelet factor 4 (PF4) leads to activated platelets and thromobosis/thrombocytopenia
Argatroban and bivalirudin
Derivatives of hirudin from leeches; inhibits thrombin directly. Use for patients with HIT
warfarin MOA
interferes with normal synthesis and gamma-carboxylation of II, VII, IX, X, C, and S.
warfarin metabolism
metabolized by P-450 pathway
warfarin toxicity
teratogenic, skin tissue necrosis, drug/drug interactions
apixaban and rivaroxaban
direct factor Xa inhibitors
direct Xa inhibitors use
tx and ppx of dvt and PE (rivaroxaban), stroke ppx in a.fib. no coagulation monitoring. non reversible
thrombolytics antidote
aminocaproic acid, fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies
do thrombolytics destroy clotting factors?
???
What is tPA, rPA, and TNK-tPA
tissue Plasminogen activator, recominant plasminogenic activator, and tenecteplase tPA
aspirin MOA
covalent acetylation of COX-1 and 2, platelets can’t produce more
aspirin labs
inc. bleeding time, dec. TXA2 and prostaglandins, no effect on PT or PTT
aspirin toxicity
CN VIII tinnitus, acute renal failure, interstitial nephritis.
what does cox inhibition by ASA actually do?
prevents formation of TXA2, which facilitates platelet aggregation via gpIIb/IIIa. It also causes vasoconstriction in Prinzmetal’s
clopidogrel, ticlopidine
ADP receptor inhibitors
ADP receptor inhibitors MOA
prevent gpIIb/IIIa from entering platelets plasma membrane
ticlopidine toxicity
neutropenia.
ADP receptor inhibitor toxicity
TTP/HUS may be seen
Cilostazol, dipyridamole MOA
Phosphodiesterase III inhibitor; inc. cAMP in plaelets, inhibiting platelet aggregation; vasodilators
what does inc. cAMP in platelets actually do?
it increases Protein Kinase A which decreases aggregation, in smooth muscle: it prevents activation of myosin light chain kinase to allow for relaxation
GPIIb/IIIa inhibitors
abciximab, eptifibatide, tirofiban