heparin
heparin structure
MOA
negatively charged, CHO containing glucuronic acids
heparin inhibits thrombin
dervives its antioagulant effect by activating antithrombin III
unfractionated and low molecular weight
Coumadin MOA
interferes with hepatic synthesis of vitamin K dependent coagulation factors II, VII, IX< X
MOA of fibrinolytics
convert plasminogen into plasmin, which cleaves fibring causing clot dissolution
what is DIC
systemic coagulation system activation leading to thrombus formation and exhaustion of platelets and coagulation factors
Factor V
normal protein for clotting
*when enoguh fibrin has been made, Substance C inactivates factor V - helping the clot from growing any larger
if the patient has antithrombin III deficiency is the heparin more or less effective
heparin doesnt work - give FFP
onset of vitamin K - warfarin's reversal
6-8 hours for correction
diluted in 100 mL bag over 30 minutes
examples of fibrinolytics
tissue plasmiogen activator (tPA), streptokinase (SK), and urokinase (UK)
causes of DIC (5)
trauma, amniotic fluid, malginancy, sepsis, or incompatible blood transfusions
factor V Leiden
mutation in genes for Factor V
abnormal version of Factor V is resistant to the action of activated Protein C
*cannot stop factor V ledin from makig more fibrin
heparin's rapid reversal
protamine
fast reversal of coumadin
prothrombin complex concentrates (PCC)
reccombinant factor VIIa and FFP
examples of antifibrinolytcs
tranexemic acid
aminocapropic acid
aprotinin
*inhibits the conversion of plasmingen to plasmin
labs durig DIC
reduced platelet
prolonged PT/PTT/TT (thombin time)
elevated concnetrations of soluble fibrin degradation products
anesthetic risks with factor V Leiden
increased risk of developing DVT with ot without PE
*patients are on anticoagulants
labs to montior on Heparin
PTT and ACT
T/f platelets are needed for emergent surgery for a patient receiveing antiplatlet medication
true - platelets are irreversibly damaged
* DC drugs on time
fondaprinaux
used to treat VTE
synthetic Xa inhibitor
typically PF4 and heparin immune complexes clear from the circulation within 3 months
management and treatment of DIC
allevilate the udnerlying conditions
treatment with blood component transfusions to replete coag factors and platelets consumed
first presentiation of factor V leiden
DVT
repeated missed abortions and reccurent late fetal losses
*prophalytic anticoagulation may be indicated to prevent venous or placental thrombosis bc improved placental blood flow
commonly on warfarin, unfractionated heparin, LMWH
LMWH
effective for VTE prophylaxis
predictable - fewer effects on platelet function, and reduced risk of HIT
monitoring not frequently preformed
diagnosis and treatment of HIT
diagnosis if person experiencing thrombocytopneia or thrombosis after heparin administration
Dc heparin STAT
alternetive non-heparin anticoagulation myst be administered concurrently
*direct thrombin inhbitor (bivalirudin, lepirudan, argatroban)
what is HIT mediated by
immune complexes (IgG antibody, platelet factor 4 (PFR) and heparin)
increase likelihood of thrombosis 5-14 days later
absolute risk 30-75%
what is contraindicated with DIC
antifibrinolytics - potential for catashtrophic thrombotic complications
HIT (heparin inducted thrombocytopenia)
onset
causes
hallmark sign
autoimmune mediated drug reaction 5% of patietns with exposure to unfractionated heparin or LWMH (rare)
thrombocytopenia occuring 5-14 days after intial therapy
hallmark pet < 100,000
HIT results in platlet activation and the potential for arterial and venous thrombosis