121514 hypercoagulable actual thrombosis and DIC part Flashcards

1
Q

what are coagulation control mechanisms?

A

blood flow-washes away activated factors

natural anticoagulant processing (antithrombin inactivating 2a and 10a, protein C system digesting cofactors 5 and 8)

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2
Q

protein C is activated by

A

thrombin, which binds to thrombomodulin

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3
Q

protein C does what?

A

degrades 8a and 5a

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4
Q

primary hypercoagulable state

A

associated with venous thromboembolism

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5
Q

primary hypercoagulable states–ex of conditions

A

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)

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6
Q

what percentage of familial thromboses are due to AT, proteinC, protein S deficiencies?

A

5-15%

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7
Q

what tests can you order if you suspect AT, proteinC, or protein S deficiency?

A

functional AT, PC or PS assay

protein S free antigen

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8
Q

what would you see for a disease with resistance to activated protein C on a PTT assay?

A

failure of PTT to prolong in response to addition of activated protein C

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9
Q

factor V Leiden

A

arg 506 replaced by Gln

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10
Q

factor V leiden is venous or arterial thrombotic risk factor?

A

venous

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11
Q

prothrombin gene variation

A

RNA for prothrombin is more stable

associated with venous events (DVT, PE)

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12
Q

antiphospholipid antibody syndrome

A

auto-Ig against phospholipid binding proteins (a lot of coagulation cascade proteins are phospholipid binding proteins)

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13
Q

what symptoms do you see for antiphospholipid antibody syndrome?

A

venous and/or arterial thrombosis

recurrent fetal wastage

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14
Q

lab signs for antiphospholipid antibody syndrome

A

evidence of antiphospholipid antibody:
lupus-like anticoagulant
positive antiphosphlipid serology

may have thrombocytopenia

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15
Q

what is interesting about antiphospholipid antibody syndrome?

A

inhibits phosphlipid dependent in-VITRO coagulation assays

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16
Q

sites of thrombosis-both arterial and venous-what would cause this?

A

antiphosphlipid syndrome

homocysteine

17
Q

syndromes associated with DIC

A

introduction of extrinsic clot promoting material

intravascular elaboration of procoagulants (heparin associated thrombocytopenia)

vascular injury (bacterial viral sepsis)

18
Q

DIC is not a disease: true or false

A

true–DIC is a manifestation of another disease

19
Q

purpura fulminans may be the presenting symptoms of

A

meningococcal sepsis
severe protein C deficiency in a newborn

can be associated with DIC

20
Q

clinical presentation of DIC

A
bleeding from venipunctures and other sites
purpura fulminans (microthrombosis in skin and elsewhere)
21
Q

D dimer

A

when plasmin cuts up clot, cuts up D dimers

22
Q

how is diagnosis of DIC made?

A

largely on clinical suspicion and appropriate clinical setting

23
Q

lab studies supportive of DIC

A

PT, PTT prolonged
fibrinogen reduced
platelets reduced
D-dimer elevated (not specific to DIC)

24
Q

differential diagnosis of DIC

A

DIC
liver failure
vit K deficiency
lupus anticoagulant