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Flashcards in Secondary Hemostasis Deck (89):
1

Requirements of ACT coagulation test

Whole Blood

Contact Activator

2

Significance of prolonged Thrombin Time

Quantitative or qualitative abnormalities of fibrinogen

Inhibitors of fibrin formation

3

_______________ is required for the initation of secondary hemostasis when initiated by wounds

Tissue Factor

4

Result of Disseminated Intravascular Coagulation (DIC)

Thrombosis of the microvasculature

Depletion of coagulation factors and platelets → bleeding

5

Significance of prolonged PT

Factor VII deficiency

Deficiency or inhibition of common pathway factor

6

Inhibitor Consumption Tests

Antithrombin (AT)

7

Requirements for PT coagulation test

Citrated plasma

Tissue factor

Calcium

Platelet substitute 

8

Cause of Disseminated Intravascular Coagulation (DIC)

Continued activation of coagulation and fibrinolysis

Induction or exposure of tissue factor or other activators of coagulation

Endothelial damage exposing collagen

Proteolytic enzymes

Stagnant blood flow

9

Increased concentration of D-Dimers occurs wtih

Increased fibrinolysis

Severe internal hemorrhage with fibrinolysis

Decreased clearance of FDP by liver

10

Coagulation test for the common pathway

Fibrinogen

TT

11

Tissue Factor Pathway Inhibitor inhibits

Generation of Xa

12

Loads of thrombin generated on the platelet surface drives the formation of

Fibrin

13

Thromibin time measures

Time for fibrin clot formation in citrated plasma + thrombin

14

Inhibitors of coagulation

Antithrombin

Activated Protein C (APC)

Tissue Factor Pathway Inhibitor (TFPI)

Alpha-2 Macroglobulin

15

Significance of fibrinogen concentration increase

Inflammation

Relative increase with dehydration

16

Two phases of DIC

Hypercoagulabile Phase

Consumptive Phase

17

Steps of the Common Pathway of the Coagulation Cascade

  1. X → Xa
  2. Prothrombin → Thrombin by Xa
  3. Fibrinogen → Fibrin by Thrombin

18

Vitamin K dependent Factors?

II, VII, IX, X

19

Categories of coagulation tests

Procoagulant Tests

Anticoagulat Tests

20

PIVKA would be increased in

Vitamin k antagonism/deficiency

Human hepatocellular carcinomas

21

Hypercoagulable Phase of DIC

Thrombosis

Ischemic necrosis and organ dysfunction

22

Prothrombin Time (PT) measures

Time for fibrin clot formation in citrated plasma + tissue factor + calcium + platelet phospholipid substitute 

23

Clinical signs of DIC

Associated with the signs of primary disease

Signs of organ dysfunction secondary to thrombosis

Bleeding

24

Requirements of aPTT coagulation test

Citrated Plasma

Contact activator

Calcium

Platelet substitute

25

Plasmin degrades fibrin into

Fibrin Degradation Products

D- Dimers

26

Pathogenesis of the hypercoagulable phase of DIC leading to organ dysfuction

Thrombus formation → blockage of the microvasculature → Ischemic necosis → Organ dysfunction

27

Hemophilia B

Factor IX deficiency

Dogs and Cats

Signs and inheritance patterns similar to Hemophilia A

28

Requirements for Thrombin Time coagulation test

Citrated plasma

Thrombin

29

Mechanism of action of Antithrombin

 

  1. Heparin binds to antithrombin
  2. Heparin causes conformational change and exposes the thrombin binding site
  3. Thrombin binds to AT = TAT complex and heparin floats away
  4. Tat Comples is cleared by the phagocytic system

30

Secondary Hemostasis

Stabilization of the platelet plug via fibrin meshwork - used in large defects

31

Laboratory findings in Warfarin Toxicity

PT  - prolonged

aPTT, ACT - prolonged

PIVKA - positive

Platelet count - normal

32

Three phases of the cell-based model

Initiation

Amplification

Propagation

33

Why does vitamin k antagonism work?

Vitamin K dependent factors los their negative charge and are not recruited to sites of injury

34

Hageman's Disease

 

Factor XII deficiency

Cats and Killer Whales

Deficiency not associated with bleeding - prolonged PTT

35

Secondary hemostasis occurs on

Platelet surface

36

Fibrin Degradation Products inhibit

Platelet function and fibrin polymerization

37

Which of the intrinsic pathway coagulation tests is more sensitive?

aPTT

38

Laboratory findings of hemophilia A

Platelet Count - Normal

Bleeding Time - Normal

aPTT and ACT - Prolonged

PT- normal

Factor activity - reduced

39

Pathophysiology of Warfarin Toxicity

Coumarins block enzymes required to reduce vitamin K

Negative charge not transferred to coagulation factors

Platelet surface charge remains positive

Factors X and II unable to bind to platelet

40

Coagulation factors are synthesized in the 

Liver

41

Treatment of warfarin toxicosis

Decontamination

Supplement vitamin K

Plasma and/or blood transfusions

42

Fibrinolytic Activity Tests

Fibrin Degradation Products

D-Dimer

43

How is citrated plasma different than blood?

No RBC, WBC or Platelets

Decreased Calcium

44

Key factor that promotes amplification of secondary hemostasis

Thrombin

45

For collection of blood for coagulation tests, what tube should be used?

Blue Top - Citrate Tube

46

Factors involved in the Intrinisc Pathway

XII, XI, IX, VIII

47

X is converted to Xa by what in the Intrinisc Pathway?

IXa

48

Activated Protein C inhibits

Va, VIIa

49

Coagulation test for the intrinsic pathway

aPTT

ACT

50

aPTT and ACT tests measure

Time for fibrin clot formation

51

Factors involved in the Extrinsic Pathway

Tissue Factor III

VII

52

Pathways that make up the coagulation cascade

Intrinsic pathway - Contact Activation

Extrinsic pathway - Tissue Activation

Common Pathway

53

Clinical features of Warfarin Toxicosis

Bleeding - Anemia, weakness, pallor, hypovolemia, shock, dyspnea, lameness, neurologic signs

Death

54

What is the cardinal bloodwork finding for a patient in consuptive phase of DIC?

Thrombocytopenia

55

Significance in fibrinogen concentration decrease

Consumption due to hypercoagulation - excessive conversion of fibrinogen to fibrin

Decreased production by the liver

56

Pathogenesis of hypercoagulable phase of DIC leading to bleeding

Thrombus formation → fibrinolysis → increased FDPs → decreased platelet function → bleeding

57

Significance of prolonged aPTT and ACT time

Deficiency or inhibition of any intrinsic or common pathway factor

Heparin therapy

58

IX is converted to IXa in the Intrinsic Pathway by

VIIa

59

Coagulopathy and Liver disease

Decreased synthesis of coagulation factors

Production of dysfunctional factors

60

X is converted to Xa by what in the Extrinisic Pathway

VIIa

61

Treatment for DIC

Identify and eliminate underlying disorder

Fluid therapy

Transfusion therapy

62

Hemophilia A

Factor VIII deficiency

X linked recessive inheritance

Causes mild, moderate or severe bleeding

63

Non-Enzymatic factors of the coagulation cascade

Tissue Factor (Factor III, Thromboplastin)

Factor VIIIa

Factor Va

Calcium

Platelets

64

Factors affected by amplification

XI

VII

VIIIa

Va

65

Coagulation Tests

Activated Partial Thromboplastin Time (aPTT, PTT)

Prothrombin Time (PT)

Thrombin Time (TT), Fibrinogen

PIVKA

Special Factor Assay

66

PIVKA

Proteins induced by vitamin K antagonism

Indirectly measures abnormal forms of vitamin K dependent factors

67

Increased concentration of fibrin degradation products occus when

Increased fibrinolysis

Severe internal hemorrhage with fibrinolysis

Decreased clearance of FDP by liver

68

Antithrombin inhibits

Thrombin, IXa, Xa

69

VII is converted to VIIa in the extrinsic pathway by

Xa

70

Fibrinogen is an indicator of what in large animals

Inflammation

71

Laboratory findings of DIC

Thrombocytopenia

PT, aPTT - Prolonged

Fibrinogen - decreased

FDP and D-Dimers - increased

Antithrombin - decreased

Hemorrhagic anemia

Schistocytes

72

aPTT requires ______% deficiency before prolongation is detected

70%

73

ACT requires ______% deficiency of factor before prolongation is detected

 

95%

74

Serum biochemistries for DIC depend on

Primary Disease

Location of microthrombosis

75

PT requires ______% deficiency of factor before prolongation is detected

70%

76

Alpha-2 Macroglobulin inhibits

Thrombin

Plasmin

Kallikrein

77

Prothrombin is converted to Thrombin by

Xa

78

Enzymatic Factors of the Coagulation Cascade

XII, XI, IX, VII, X

Prothrombin

Thrombin

Fibrinogen

Fibrin

79

Pathogenesis of consumptive phase of DIC

Depletion of coagulation factors and platelets → bleeding

80

Fibrinogen is converted to Fibrin by

Thrombin

81

Activated Clotting Time ACT measures

Time for fibrin clot formation in non-anticoagulated whole blood

82

Coagulation test for the extrinsic pathway

PT

83

Plasminogen is converted to Plasmin by

Tissue Plasminogen Activator (TPA)

84

Inherited Factor Deficiencies

Hemophilia A - VIII

Hemophilia B - IX

Hagemans Disease - XII

85

Factors involved in the common pathway

X, V

Prothrombin 

Fibrinogen

Fibrin

86

Cell Based Model

Focuses on the roll of cells involved with coagulation

87

Why is PT a good choice in test for screening for Vitamin K deficiency?

Because Factor VII has the shortest half life

88

Causes of Warfarin Toxicosis

Poisoning with coumarin derivatives

Fat malabsorption

Dietary deficiency

Antibiotics that cause decreased absorption or utilization by liver

89

It is good practice to supplement a patient with prolonged aPTT with what before surgery?

Plasma