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Flashcards in Thrombosis & DIC Deck (37):
1

What are physiologic coagulation control methods?

blood flow-wash away activated factors
natural anticoagulant processing
-antithrombin inactivates enzymes thrombin & Xa
-protein C digests cofactors V & VIII

2

What makes up Virchow's triad?

endothelial injury *
abnormal blood flow
hypercoagulability

3

Is antithrombin or protein C system vitamin K dependent?

protein C/S system

4

Which type of thrombosis are primary hypercoagulable states associated with?

venous

5

What are the 3 types of primary hypercoagulable states?

deficiency of control proteins (AT, PC, PS)
subtle changes causing control mechanisms (leiden V)
increased coagulation factor levels (prothrombin gene variation G20210A)

6

When does the risk of thrombosis in AT/PC/PS deficiencies increase?

after puberty

7

How do you test for AT, PC/PS deficiencies?

functional AT, PS or PS assay
protein S free antigen

8

What happpens to PTT in a patient with resistance to activated protein C?

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

9

If PTT fails to prolong in response to addition of activated protein C what test do you perform next?

genetic defect of factor V test (gain of function mutation)
(factor V leiden: Arg 506 replaced wtih Gln

10

What are the key features of leidein factor V?

venous throbosis risk factor
causes DVT
common in caucasians

11

What are the key features of prothrombin gene variation?

G20210A mutation, leads to higher levels of transcription
associated with venous events DVT/PE
via elevated thrombin levels
(more freq than def of AT, PC, PS)
risk of venous thrombotic event similar to leiden factor V, weaker than AT/PC/PS

12

What is antiphospholipid antibody syndrome?
Key lab findings?
Symptoms?

venous &/or arterial thrombosis
recurrent fetal wastage/preg loss
evidence of antiphospholipid antibody/lupus like anticoag/positive antiphospholipid serology
may have thrombocytopenia

13

What is the mechanism of antiphospholipid antibody syndrome as understood to date?

auto-antibody to phospholipid-protein complex
-anti-cardiolipin/lupus antigoaculents present
inhibits phospholipid depenant in vitro coag assays
-inhibitor: failure to clot time to correct on 1:1 mix
-phospholipid dependence: clot time corrects with high PL
can cause false positive syphillis serology

14

Features of "lupus-like" anticoagulant

inhibitor of phospholipid dependent in vitro assays of coagulation
-prolonged PL dependent clot time (dRVVT or PTT)
-failture of correction on 1:1 mix study
-correction occurs in lipid rich assay

15

What causes both arterial and venous thrombosis?

homocysteine
apla syndrome

16

What are acquired risk factors of thrombosis?

obstruction to flow (pregnancy)
activation of hemostatic mechanism (spesis, neoplasm, foregin body)
damaged endothelium (infl, atherosclerosis, trauma, etc)

17

What are risk factors for secondary hypercoagulable states?

post op
neoplasm
immobilizaiton

18

What is DIC?

widespread acivation of thrombin nad plasmin mechanisms
-overwhelmed control mechanisms
-consumption of participants in hemostasis
-pay present as bleeding or thrombosis

19

What are syndromes associated with DIC?

intro of extrinsic clot promoting material
intravascular elaboration of procoagulants
vascular injury (ie/sepsis)

20

What is purpura fulminans?

presenting symptom of DIC caused by meningococcal spesis or severe protein C deficiency in a newborn

21

Clinical presentation of DIC?

bleeding from venipunctures and other sites
purpura fulminans

22

What is the screening test for DIC?

D-dimer

23

Lab values for DIC

prolonged PT/PTT
decreased fibrinogen
low platelets
D-dimer elevated

24

What are the consequences fo DIC?

microcirculatory failure leading to multiorgan dysfunction

25

How do you treat DIC?

treat the triggering condition
restore tissue perfusion and acid/base balance
replacement therapy for bleeding

26

What is a D-dimer?

a product from fibrinolysis of cross linked fibrinolysis

27

What disorders are dissociated with increased D dimer?

DIC
DVT
healing (post op/resolving hematoma)
Liver disease
cancer

28

What are lab findings for liver failure?

greatly increased PT
increased PTT
n/c or decreased fibrinogen
n/c or decreased platelets
increased FDP
jaundice

29

What are lab findings for vit K deficiency?

greatly increased PT
increased PTT
n/c in fibrinogen
n/c in platelets
n/c in FDP
malabsorption, liver disease

30

What are lab findings for Lupus anticoagulant?

n/c or increased PT
increased PTT
n/c in fibrinogen
n/c or decrease in platelets
n/c in FDP thrombosis

31

What type of feedback does thrombin exhibit on the clotting cascade?

positive-activates more thrombin
negative: activates Protein C

32

What is accelerated by heparin?

inactivation of thrombin, Xa, IXa, XIa and AT

33

What is the pentad of clinical manifestations of TTP?

microangiopathic hemolytic anemia
thrombocytopenia
CNS/mental status changes
fever
renal insufficiency

34

What does ADAMTS13 do? When is it deficient?

cleaves vWF multimers into monomers
deficient in TTP (acquired or congenital)

35

What causes HIT?

IgG binds to PF-4 heparin complex, activates via FC receptor, leads to generation of procoag rich microparticles

36

Symptoms of HIT?

moderate thrombocytopenia
5-10 days after initial heparin exposure
clots

37

TX for HIT?

stop heparn
do not start LMWH or warfarin
begin alternate anticoag (direct thrombin inhibitor)