121514 hypercoagulable actual thrombosis and DIC part Flashcards
what are coagulation control mechanisms?
blood flow-washes away activated factors
natural anticoagulant processing (antithrombin inactivating 2a and 10a, protein C system digesting cofactors 5 and 8)
protein C is activated by
thrombin, which binds to thrombomodulin
protein C does what?
degrades 8a and 5a
primary hypercoagulable state
associated with venous thromboembolism
primary hypercoagulable states–ex of conditions
deficiency of control proteins (antithrombin, protein C or protein S)
subtle changes causing control mechanisms (factor V Leiden-resistance to aPC)
increased coagulation factor levels (prothrombin gene variation G20210A)
what percentage of familial thromboses are due to AT, proteinC, protein S deficiencies?
5-15%
what tests can you order if you suspect AT, proteinC, or protein S deficiency?
functional AT, PC or PS assay
protein S free antigen
what would you see for a disease with resistance to activated protein C on a PTT assay?
failure of PTT to prolong in response to addition of activated protein C
factor V Leiden
arg 506 replaced by Gln
factor V leiden is venous or arterial thrombotic risk factor?
venous
prothrombin gene variation
RNA for prothrombin is more stable
associated with venous events (DVT, PE)
antiphospholipid antibody syndrome
auto-Ig against phospholipid binding proteins (a lot of coagulation cascade proteins are phospholipid binding proteins)
what symptoms do you see for antiphospholipid antibody syndrome?
venous and/or arterial thrombosis
recurrent fetal wastage
lab signs for antiphospholipid antibody syndrome
evidence of antiphospholipid antibody:
lupus-like anticoagulant
positive antiphosphlipid serology
may have thrombocytopenia
what is interesting about antiphospholipid antibody syndrome?
inhibits phosphlipid dependent in-VITRO coagulation assays
sites of thrombosis-both arterial and venous-what would cause this?
antiphosphlipid syndrome
homocysteine
syndromes associated with DIC
introduction of extrinsic clot promoting material
intravascular elaboration of procoagulants (heparin associated thrombocytopenia)
vascular injury (bacterial viral sepsis)
DIC is not a disease: true or false
true–DIC is a manifestation of another disease
purpura fulminans may be the presenting symptoms of
meningococcal sepsis
severe protein C deficiency in a newborn
can be associated with DIC
clinical presentation of DIC
bleeding from venipunctures and other sites purpura fulminans (microthrombosis in skin and elsewhere)
D dimer
when plasmin cuts up clot, cuts up D dimers
how is diagnosis of DIC made?
largely on clinical suspicion and appropriate clinical setting
lab studies supportive of DIC
PT, PTT prolonged
fibrinogen reduced
platelets reduced
D-dimer elevated (not specific to DIC)
differential diagnosis of DIC
DIC
liver failure
vit K deficiency
lupus anticoagulant
