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Small Animal Medicine > Hematology - Hemostasis 2 > Flashcards

Hematology - Hemostasis 2 Flashcards

1
Q

______ is needed for medium/large vessels.

A

Fibrin

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2
Q

What cells are key players for secondary hemostasis?

A

Platelets and fibroblasts

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3
Q

What proteases are involved in secondary hemostasis?

A

FXIa, FIXa, Fxa, FIIa, and FVIIa

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4
Q

What cofactors are involved in secondary hemostasis?

A

Tissue factor (FIII), FVa, and FVIIIa

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5
Q

What crosslinkers are involved in secondary hemostasis?

A

FXIIIa

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6
Q

What activators are involved in secondary hemostasis?

A

Vitamin K

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7
Q

What inhibitors are involved in secondary hemostasis?

A

Antithrombin, protein C, and protein S

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8
Q

What is the end result of secondary hemostasis?

A

Generation of thrombin which forms a crosslinked fibrin clot

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9
Q

Secondary hemostasis is a series of enzymatic reactions involving what three main things?

A

Coagulation factors, calcium, and Phosphatidylserine on platelets

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10
Q

What does thrombin (FIIa) do?

A

It cleaves fibrinogen (FI) into fibrin

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11
Q

How does fibrin form the fibrin clot?

A

It is cross-linked to form the fibrin clot by FXIIIa

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12
Q

What is the extrinsic pathway composed of?

A

Tissue factor (TF), FVII, and calcium

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13
Q

What is the intrinsic pathway composed of?

A

FXII, FXI, and FIX, FVIII, calcium, and phosphatidylserine

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14
Q

What is the end result of the intrinsic pathway?

A

FIXa and cofactor FVIIIa to activate X into Xa

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15
Q

What factors are involved in the common pathway?

A

Fxa, prothrombin (FII), FXIII (crosslinker), FV, calcium, and phosphatidylserine

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16
Q

What tests assess the functionality of both the intrinsic and common pathways?

A

Activated partial thromboplastin time (aPTT) and activated coagulation time (ACT)

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17
Q

What test assesses the functionality of the common pathway alone?

A

Thrombin clot time (TCT)

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18
Q

What tests assess the functionality of both the extrinsic and common pathways?

A

Prothrombin time (PT) and PIVKA

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19
Q

What is involved in the initiation phase of the cell-based model?

A

Extrinsic pathway, tissue factor, and the cell surface of fibroblasts

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20
Q

What is involved in the amplification phase of the cell-based model?

A

Intrinsic factor, thrombin, and the cell surface of the platelet

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21
Q

What cell surface is associated with the propagation phase of the cell-based model?

A

the platelet

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22
Q

What are the functions of thrombin?

A

Activation of the intrinsic patway (FXI, FVIII, and FV to make more thrombin), activation of FXIII to crosslink fibrin, cleaves fibrinogen into soluble fibrin, and activation of platelets for more surface for the intrinsic pathway

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23
Q

Which model of secondary hemostasis explains what goes on in the body better?

A

the cell based model

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24
Q

What can go wrong with secondary hemostasis?

A

Too few or too many coagulation factors and antagonized or inactive vitamin K

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25
Q

What are the inherited coagulation disorders?

A

Hemophilia A and B

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26
Q

What coagulation factor is deficient in hemophilia A?

A

FVIII (8) deficiency

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27
Q

What coagulation factor is deficient in hemophilia B?

A

FIX (9) deficiency

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28
Q

What are the acquired causes of coagulation disorders?

A

Anticoagulant rodenticide, DIC, and Liver disease

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29
Q

How does DIC result in a coagulation disorder?

A

it consumes clotting factors

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30
Q

How does liver disease result in a coagulation disorder?

A

There is not enough production of clotting factors

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31
Q

How do rodenticides lead to coagulation deficiency?

A

they antagonize vitamin K - specifically epoxide-reductase enzyme which turns Vitamin K epoxide into Vitamin K quinone

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32
Q

What factors are dependent on vitamin K?

A

Factors, II, VII, IX, and X

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33
Q

What clinical signs are associated with secondary hemostasis?

A

Bleeding into body cavities (hemoabdomen and hemothorax), Large bruises/hematomas, joint bleeds (hemarthroses), and prolonged bleeding after surgery and trauma

34
Q

What screening coagulation assays can be done for secondary hemostasis?

A

PT, aPTT, +/- TCT/fibrinogen

35
Q

What in-house test can be done to asses secondary hemostasis?

A

activated coagulation time

36
Q

If there is a long PT only, what factor is deficient and what pathway is that associated with?

A

FVII - extrinsic pathway

37
Q

If there is a long aPTT only, what factor(s) are deficient and what pathways are associated with that?

A

FXII, FXI, FIX, and FVIII - Intrinsic pathway

38
Q

If both PT and aPTT are long, what factor could be deficient, what pathway is that associated with, and could something else be going on?

A

FX could be deficient so that would mean thecommon pathway is involved. There could also be multiple defects going on

39
Q

True or False: Hemophilia A only affects males.

A

True - it is X linked

40
Q

How are bleeds managed in hemophilia A cases?

A

transfusions

41
Q

What physiologic mechanisms are present to keep the extrinsic pathway in check?

A

Tissue factor pathway inhibitor (TFPI)

42
Q

What physiologic mechanisms are present to keep factors II and X in the intrinsic and common pathways in check?

A

Antithrombin

43
Q

What physiologic mechanisms are present to keep vitamin K in check in the intrinsic and common pathways?

A

Protein C and S

44
Q

What therapeutic methods can be used to keep secondary hemostasis in check?

A

Heparin and warfarin

45
Q

What toxic methods keep secondary hemostasis in check?

A

Warfarin-based anticoagulant rodenticides

46
Q

What does TFPI act on?

A

TF-FVIIa-Fxa

47
Q

What does activated protein C, protein S, and thrombomodulin act on?

A

FVIIIa and Fva

48
Q

What activates APC and TM?

A

thrombin

49
Q

What does antithrombin act on?

A

thrombin

50
Q

What does heparin do?

A

It binds to antithrombin, allowing it to inhibit FII and FXa

51
Q

What can go wrong with inhibitors?

A

They are too active, too few, or there are acquired problems with consumption, loss, and decreased production

52
Q

What is the cause of too active inhibitors?

A

you are the cause - they are iatrogenic

53
Q

What can cause consumption of inhibitors?

A

Sepsis and DIC

54
Q

What generally can cause loss of inhibitors?

A

protein-losing disorders

55
Q

What protein-losing disorders can cause loss of inhibitors?

A

protein losing enteropathies and protein losing nephropathies

56
Q

What can cause decreased production of inhibitors?

A

liver disease

57
Q

What is tertiary hemostasis?

A

fibrinolysis to re-establish blood flow through the vessels

58
Q

What are the cellular players of fibrinolysis?

A

endothelial cells

59
Q

What substrate proteins are involved in fibrinolysis?

A

fibrin

60
Q

What protease proteins are involved in fibrinolysis?

A

Tissue plasminogen activator and plasmin

61
Q

What activator proteins are involved in fibrinolysis?

A

Activated factor XIIa, bradykinin, and kallikrein

62
Q

What inhibitor priteins are involved in fibrinolysis?

A

Thrombin activatable fibrinolysis inhibitor (TAFI), antiplasmin, and plasminogen activator inhibitor (PAI)

63
Q

What is fibrinolysis?

A

fibrin clot breakdown by plasmin

64
Q

What activates plasmin?

A

tPA

65
Q

What is the end point of fibrinolysis?

A

Release of degradation products - D-dimers and fibrinogen degredation product (FDPs)

66
Q

What are D dimers released from?

A

cross-linked fibrin

67
Q

What are the physiologic inhibitors of fibrinolysis?

A

antiplasmin, plasminogen activator inhibitor, and thrombin activatable fibrinolysis inhibitor

68
Q

What does antiplasmin do?

A

inhibits plasmin

69
Q

What does plasminogen activator inhibitor do?

A

inhibits tPA

70
Q

What does thrombin activatable fibrinolysis inhibitor do?

A

prevents fibrinolysis

71
Q

What are some therapeutic inhibitors of fibrinolysis?

A

e-aminocaproic acid and tranexamic acid

72
Q

What are e-aminocaproic acid and tranexamic acid used to do?

A

stabalize clots

73
Q

What can go wrong with fibrinolysis?

A

excessive activation or inhibition, or acquired defect

74
Q

What acquired condition can disturb fibrinolysis?

A

DIC

75
Q

What is DIC initiated by?

A

Severe underlying disease - sepsis, severe inflamatory disease, and metastatic cancer

76
Q

What severe inflammatory diseases can cause DIC?

A

heat stroke, pancreatitis, and immune-mediated disease like IMHA

77
Q

What are the two main mechanisms of DIC?

A

Excessive activation of hemostasis leading to too much thrombin and excessive clotting AND loss of control and restriction of hemostasis

78
Q

Excessive activation of hemostases leads to consumption of what?

A

platelets, coagulation factors, and inhibitors

79
Q

What does loss of control/restriction of hemostasis result in?

A

Decreased inhibitors and expression of TF by cells that don’t normally express TF all independent of vessel injury

80
Q

What diagnostic results should tell you that DIC may be going on?

A

Low platelets, prolonged goagulation time, low to normal fibrinogen, high D-dimer or FDP, and low AT

81
Q

What should you treat first if you can in DIC patients?

A

the underlying disease

82
Q

If you cannot treat the underlying disease in DIC patients, what should you give?

A

Plasma for the hemorrhagic phase and heparin for the thrombotic phase

Small Animal Medicine (100 decks)

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