Anti-Thrombotic Therapy Flashcards
Thrombosis
a,d,d
under path conditions, a thrombus can form into otherwise norm vessles
obstruct flow
obliterate valves
AMI,DVT,DE
DIC
prim condition such as
primary condition such as septicemia/trauma/burns
ischemia/multiple infarctions/excessive bleeding thrombocytopenia
organ failure
Pathophysiology of DIC
acute episode?
what happens?
acute epidose overwhelming stim of coagulation
bleeding and clotting
Clinical Sympt of DIC
oozing, bleeding from mult sites due to consumpt of clotting factors
often evidence of organ damage from fibrin deposition
Antithrombotics
limit or prevent clotting by supressing synth or funct of hemostasis
goal to prevent thrombosis w out causing hemorrhage
Anti-Plts
inhibit aggregation
Anti Coag
inhibit cascade
Thrombolytics
dissolve clot
Warfarin
cooumadin
oral anticoag short half llife
Arrestsv VIT K in its storage form/unavailable, adds a second carboxly group to produce complete vit K dependent factors
(2,7,9,10)
Warfarin monitoring
what monthy tests…
TR
caution?
by PT and INR monthly
theraputic range 2-3
caution: food rich in cit K interfere
Heparin vs warfarin
pts with what condition
what treatment
pts w venous thrombosis = unfract heparin acutely followed by long term anti coags
Heparin (UFH/STD)
causes?
increases?
causes confromational change in the AT molecule, increases inhibition effect
Antithrombin forms an irre…
heparin not consumed?
what complex
neutralizes?
when not consumed what happens?
irreversable complex w IIa Xa to slowly neutralize heparin,
heparin not consumed in process can be a cofactor for AT molecule
Heparin Sulfate
by what cells?
does what to levels
Predisposes pt to what? due to what?
heparin like sulfate by EC, decrease levels
AT predispose pts to recurrent thrombosis if stopped early before oral coag effective
Protamine sulfate reverses?
what effects?
may cause?
Therapy monitored by?
anticoag effects
may cause HIT, therapy monitored by aPTT/Anti Xa assay
