Anticoags Flashcards
coag factors are ___
enzymes
each step of the cascade amplifies the ___
initial signal
coag factors are made in the ___
liver
“Final pathway” results in:
conversion of prothrombin (II) to thrombin
which catalyzes the conversion of fibrinogen to fibrin
fibrin activates the ____
fibrinolytic system (plasmin, tissue plasminogen activator (tPA))
Homeostasis of the cascade is maintained by balance of
procoagulants (coag factors) endogenous anticoagulants (proteins C & S, antithrombin III)
proteins C and S are important for ___
warfarin dosing
antithrombin III is important for ___
heparin dosing
purpose of fibrinolytic system
degrades fibrin
fibrinolytic system results in:
fibrin split products (FSP) AKA fibrin degredation products (FDPs) Fibrin dimers (d-dimers)
increased fibrin degradation product or d dimer levels suggest presence of ___
thrombi
consequence of inappropriate thrombosis:
venous thrombi
arterial thrombi
venous thrombi:
DVT
Red thrombus AKA venous stasis thrombi
VTE (venous thromboembolism)
arterial thrombi are __ driven
platelet driven
complication of venous thrombi
pulmonary embolism
arterial thrombi
white thrombus
complication of arterial thrombi
strokes, myocardial infarction
thrombosis risk factors
surgery cancer immobility varicose veins pregnancy
potential complication of anticoagulant agents
BLEEDING
complications of anticoagulation agents are NOT an ___. it is an extension of their ___
allergy; MOA
heparin binds to ___
antithrombin III
heparin binding requires specific _____
pentasaccharide sequence
Heparin’s limitations
heparin activates platelets directly
Heparin can dinduce immune response in the form of HIT/HITTs
Heparin exhibits nonlinear dose response
Heparin increases affinity of thrombin for fibrin
unfractionated heparin is a :
heterogenous mix of sulfated glycosaminoglycans
only ___ of UFH molecules have the pentasaccharide
~1/3
UFH antithrombin complex is approx ______ x > anticoagulant than antithrombin alone
100-1000x
UFH is only effective on ____ fibrin
soluble (non clot-bound fibrin)
UFH prevents the ____ of the thrombus
growth/propagation
UFH allows the patient’s fibrinolytic system to ___
degrade the clot
UFH is measured by the ______
activated partial thromboplastin time aPTT)
DVT prophylaxis – subQ heparin
UFH
5,000 units SubQ q12h or q8h
Risk of HIT is that of ___ UFH
IV (increased risk)
Advantages of UFH
immediate anticoag measured by aptt effects reversed by protamine prevents propagation of a clot may be given subQ for prophylaxis usually done by Pharmacy Dosing Service
disadvantages of UFH
non-linear kinetics frequent lab tests required increased risk of bleeding potential for life-threatening immune-mediated thrombocytopenia "HIT) minimal effect on interior of the clot
___ is used to reverse UFH heparins
protamine sulfate
MOA of protamine sulfate
combines with strongly acidic heparin
2 types of HIT
HIT 1 (non-immune) 10% HIT II (immune) VERY BAD <3% of patients
HIT I is transient due to ___
clumping of platelets (actually an artifact)
HIT-I happens ___
immediately
HIT II is seen after ___ of heparin
5-10 days
in HIT II, platelet count falls by ____ from baseline
> 50%
HIT II is immune mediated by ____
anti-platelet factor 4
test for PF4
LMWH have a more favorable ___
benefit/risk ration
LMWH have predictable ____
dose response ratio
LMWH ahs ___ dosing
weight base
LMWH has less risk fo ___
HIT (if started initially)
LMWH (fractionated) has ___ administration
subQ
Available LMWH agent
enoxaprin (lovenox)
indications for LMWH
ACS treatment
DVT
PE
VTE prophylaxis in high risk populations