3Rd Year - Hemo - Hemostasis

Front 1

What are the 4 steps to primary hemostasis?

Back 1

1 - initiated by vascular injury
2 - platelet adhesion to damaged endothelium
3- platelet aggregation --> activation of intrinsic clotting
4 - platelet thrombus

Front 2

What is the goal of secondary hemostasis?

Back 2

stabilizes the platelet thrombus by formation of a fibrin network
-extrinsitc, intrinsic, common pathways

Front 3

What pathway is the most important?

Back 3

extrinsic (factor 7)

Front 4

What is factor 7 activated by?

Back 4

tissue thromboplastin (factor)

-this is released from damaged vascular cells

Front 5

What does activated factor 7 do?

Back 5

activates factor 10 of the common pathway

Front 6

What are factors 12, 11, 9, 8 activated by?

Back 6

collagen (exposed by vascular damage) phospholipid, and other substances

Front 7

What does factor 8 do once activated?

Back 7

activated factor 10

Front 8

Which factors convert prothrombin to thrombin?

Back 8

10 and 5

Front 9

What is the final step of secondary hemostasis?

Back 9

conversion of fibrinogen to fibrin using factor 2

Front 10

What are the inhibitors of coagulation?

Back 10

protein C,
antithrombin III,
tissue factor pathway inhibitor - 1,
protein S,
plasmin

Front 11

What must he platelet count be to cause hemorrhage?

Back 11

50,000 or below

Front 12

What are the pirmary coagulopathies?

Back 12

thrombocytopenia, thrombocytopathic
endothelial disease

Front 13

What are petechia most often associated with?

ecchymosis?

Back 13

abnormal primary hemostasis

abnormal secondary hemostasis (coagulopathy)

Front 14

What is epistaxis most commonly associated with?

Back 14

primary hemostasis

Front 15

What does Buccal mucosal bleeding time measure?

Back 15

platelet and endothelial function --> prolonged by any one of the problems that cause primary coagulopathies

Front 16

What does prothrombin time test?

Back 16

extrinsic and common pathways

Front 17

WIth Vitamin K def., what increases first?

What about with heparin?

Back 17

PT before PTT

PTT before PT

Front 18

What is ACT?

Back 18

time for visible clot to form
-tests intrinsic and common pathways

Front 19

Why might fibrinogen be decreased?

increased?

Back 19

-decreased production by liver or increased consuption (DIC)

inflammation

Front 20

What are FDPs formed by?

Back 20

break down of fibriongen and fibrin (fibrinolysis)

Front 21

What do elevated FDPs infer?

Back 21

excessive coagulation with subsequent fibrionlysis as in DIC

Front 22

What do D-dimers measure?

Back 22

fibrin degradation products

Front 23

When is AT III decreased?

Back 23

in DIC, neprhotic syndrome

Front 24

What are the 4 main causes of thrombocytopenia?

Back 24

1 - destruction
2 - consumption
3 - sequestration
4 - decreaed production

Front 25

What are 2 reasons why platelets may be destroyed?

Back 25

1 - immune-mediated (primary or secondary (to neoplasia, infection, drugs)
2 - infectious

Front 26

What are 3 reasons why platelets may be consumed?

Back 26

1 - DIC
2 - vasculitis (rickettsial infections, FIP, immune-mediated)
3 - severe acute hemorrhage

Front 27

Why would platelets be sequestered?

Back 27

hyperspenism

Front 28

What are 7 reasons why platelets would stop being produced?

Back 28

1 - marrow neoplasia
2 - immune-mediated
3 - infection (Ehrlichia, FeLV)
4 - drugs
5 - estrogen
6 - myelofibrosis
7 - myelodysplasia

Front 29

What test would you want to perform if you have thrombocytopenia and have already done a PE, CBC, chemistry, and UA?

Back 29

serological tests for: Babesia, RMSF,
Ehrlichia, FeLV, FIV

-rads

-antinuclear antibodies (for immune-mediated disease)

Front 30

What things (3) may cause secondary IMTP?

Back 30

- infection: Ehrlichia and RMSF
-vaccination (3-10 days post)
- drugs (sulfonamides)

Front 31

What is seen on a CBC with IMTP?

Back 31

-severe thrombocytopenia (<40,000 and often less than 10,000)
-anemia (due to bleeding)
- neutrophilia

Front 32

What is Evan's Syndrome?

Back 32

Concurrent IMTP and immune-mediated hemolytic anemia

Front 33

What concurrent diseases should you look for with IMTP?

Back 33

neoplasia
infection (RMSF, Ehrilichia, HW, sepsis, viral
DIC
Drugs/vaccinnation history

Front 34

What is the treatment for IMTP?

Back 34

1 - cage rest
2 - platelet transfusion
3 - Immunosuppression (gluococorticoids)

Front 35

How should you taper the prednisone dose when treating IMTP?

Back 35

- taper by 25-33% every 2-4 weeks after platelet count goes back to normal

Front 36

What are common clinical findings in animals with von Willebrands Disease?

Back 36

- hemorrhage following trauma or surgery
-mucosal bleeding - epistaxis or urogenital

Front 37

How do you diagnose von Willebrand's disease?

Back 37

- vWf:ag
-buccal mucosal bleeding time
- genetic test

Front 38

What is the most effective treatment for von Willebrand's disease?

Back 38

cryoprecipitate

-desmopressin causes release of vWF from endothelium

Front 39

What is the difference between warfarin and second gen vit. K antagonists such as brodifacoum, dipheacinon?

Back 39

duration of action

warfarin - short acting with duration 10-14 d

sec gen - duration of action 3-4 weeks

Front 40

What are the vit k dep. coagulation factors?

Back 40

2,7,9,10

Front 41

Why is PT increased before PTT with vit. K antagonists?

Back 41

factor 7 has the shortest half-life (6 hours)

Front 42

What is the treatment for vit. k antagonists?

Back 42

Vitamin K1
-oral initially if not showing CS
-SQ initial if showing CS followed by oral

- with plasma or whole blood

-RBC
-IV fluids
-thoracocentisis

Front 43

What are 4 acquired coagulation factor def?

Back 43

1 - vitamin K antagonist
2 - liver disease
3 - neoplasia
4 - DIC

Front 44

What are the results of hepatic failure?

- must be severe

Back 44

1 - factor def. (coag)
2 - def. of vitamin K (due to cholestasis with anorexia)

Front 45

What is very important in perpetuating DIC?

Back 45

antithrombin III deficiency

Front 46

What are the CS associated with chronic compensated DIC?

Back 46

none

Front 47

What are CS associated with acute decompensated DIC?

Back 47

- hemorrhage
-shock (hemorrhage due to using up coagulation factors and hypotension)
- organ failure
-thrombosis of any organ

Front 48

What are common this used to diagnose DIC?

Back 48

1 - prolonged PT and PTT
2 - thrombocytopenia
3 -increased FDP and D-dimer
4 - decreased fibrinogen - due to fibrinolysis
5 -decreased AT - III
6 -schistocytes

Front 49

What is the best treatment for DIC?

Back 49

resolution of the primary problem

-also IV fluids
-oxygen
-plasma transfusion
-anticoagulant treatment - heparin (low doses)

Front 50

What does low dose heparin do for DIC patients?

Back 50

- activates AT III, making it more potent
-acts on AT III to inactivate factor Xa