Anticoag's Flashcards
take home points for coag cascade 1
coag factors are enzymes
each step amplifies the initial signal
made in the liver
take home points for coag cascade 2
final pathway results in prothrombin –> thrombin which catalyzes the conversion of fibrinogen –> fibrin
fibrin activates the fibrinolytic system (plasmin and t-PA)
vitamin K dependent factors
II, VII, IX and X
homeostasis is maintained by the balance of:
procoagulants endogenous anticoags (protein C&S important for warfarin dosing and antithrombin III important for heparin dosing)
fibrinolytic system
degrades fibrin
fibrinolytic system results in:
fibrin split pdts (FSP), fibrin depredation pdts (FDPs), fibrin Dimers (D-Dimer)
inc levels suggest presence of thrombin (think DVT!)
venous thrombi
DVT "red thrombus" AKA: venous stasis thrombi VTE complications: PE
arterial thrombi
platelet driven
“white thrombus”
complications: stroke, MI
thrombi RF’s
sx, CA, immobility, varicose veins and preg
potential complication of anticoag’s
BLEEDING, not an allergy!! extension of MOA
Heparin MOA
binds to antithrombin III
binding requires specific pentasaccharide sequence
Heparin limitations
directly activates platelets –>
HIT (true allergy!)
inc dose does not cause linear response
can only bind thrombin that is free in circulation (so doesn’t tx initial clot, prevents further clots)
Unfractionated Heparin
heterogeneous mix of sulfated glycosaminoglycans
only ~1/3 of molecules have the pentasaccharide
only effective on soluble fibrin (not clot-bound fibrin)
prevents the grow/propagation of the thrombus
Unfractionated Heparin cont
UFH-antithrombin complex is 100-1000 x > anticoagulant than antithrombin alone
allows the pt’s fibrinolytic system to degrade the clot
measured by aPTT
`Adv of UFH
immediate anticoag
effects reversed by protamine
may be given subQ for prophylaxis
usually done by PDS