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RUSVM Clinical Pathology > Secondary Hemostasis > Flashcards

Secondary Hemostasis Flashcards

1
Q

Requirements of ACT coagulation test

A

Whole Blood

Contact Activator

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2
Q

Significance of prolonged Thrombin Time

A

Quantitative or qualitative abnormalities of fibrinogen

Inhibitors of fibrin formation

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3
Q

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

A

Tissue Factor

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4
Q

Result of Disseminated Intravascular Coagulation (DIC)

A

Thrombosis of the microvasculature

Depletion of coagulation factors and platelets → bleeding

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5
Q

Significance of prolonged PT

A

Factor VII deficiency

Deficiency or inhibition of common pathway factor

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6
Q

Inhibitor Consumption Tests

A

Antithrombin (AT)

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7
Q

Requirements for PT coagulation test

A

Citrated plasma

Tissue factor

Calcium

Platelet substitute

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8
Q

Cause of Disseminated Intravascular Coagulation (DIC)

A

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

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9
Q

Increased concentration of D-Dimers occurs wtih

A

Increased fibrinolysis

Severe internal hemorrhage with fibrinolysis

Decreased clearance of FDP by liver

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10
Q

Coagulation test for the common pathway

A

Fibrinogen

TT

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11
Q

Tissue Factor Pathway Inhibitor inhibits

A

Generation of Xa

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12
Q

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

A

Fibrin

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13
Q

Thromibin time measures

A

Time for fibrin clot formation in citrated plasma + thrombin

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14
Q

Inhibitors of coagulation

A

Antithrombin

Activated Protein C (APC)

Tissue Factor Pathway Inhibitor (TFPI)

Alpha-2 Macroglobulin

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15
Q

Significance of fibrinogen concentration increase

A

Inflammation

Relative increase with dehydration

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16
Q

Two phases of DIC

A

Hypercoagulabile Phase

Consumptive Phase

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17
Q

Steps of the Common Pathway of the Coagulation Cascade

A
  1. X → Xa
  2. Prothrombin → Thrombin by Xa
  3. Fibrinogen → Fibrin by Thrombin
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18
Q

Vitamin K dependent Factors?

A

II, VII, IX, X

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19
Q

Categories of coagulation tests

A

Procoagulant Tests

Anticoagulat Tests

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20
Q

PIVKA would be increased in

A

Vitamin k antagonism/deficiency

Human hepatocellular carcinomas

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21
Q

Hypercoagulable Phase of DIC

A

Thrombosis

Ischemic necrosis and organ dysfunction

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22
Q

Prothrombin Time (PT) measures

A

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

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23
Q

Clinical signs of DIC

A

Associated with the signs of primary disease

Signs of organ dysfunction secondary to thrombosis

Bleeding

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24
Q

Requirements of aPTT coagulation test

A

Citrated Plasma

Contact activator

Calcium

Platelet substitute

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25
Q

Plasmin degrades fibrin into

A

Fibrin Degradation Products

D- Dimers

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26
Q

Pathogenesis of the hypercoagulable phase of DIC leading to organ dysfuction

A

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

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27
Q

Hemophilia B

A

Factor IX deficiency

Dogs and Cats

Signs and inheritance patterns similar to Hemophilia A

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28
Q

Requirements for Thrombin Time coagulation test

A

Citrated plasma

Thrombin

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29
Q

Mechanism of action of Antithrombin

A
  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
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30
Q

Secondary Hemostasis

A

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

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31
Q

Laboratory findings in Warfarin Toxicity

A

PT - prolonged

aPTT, ACT - prolonged

PIVKA - positive

Platelet count - normal

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32
Q

Three phases of the cell-based model

A

Initiation

Amplification

Propagation

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33
Q

Why does vitamin k antagonism work?

A

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

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34
Q

Hageman’s Disease

A

Factor XII deficiency

Cats and Killer Whales

Deficiency not associated with bleeding - prolonged PTT

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35
Q

Secondary hemostasis occurs on

A

Platelet surface

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36
Q

Fibrin Degradation Products inhibit

A

Platelet function and fibrin polymerization

37
Q

Which of the intrinsic pathway coagulation tests is more sensitive?

A

aPTT

38
Q

Laboratory findings of hemophilia A

A

Platelet Count - Normal

Bleeding Time - Normal

aPTT and ACT - Prolonged

PT- normal

Factor activity - reduced

39
Q

Pathophysiology of Warfarin Toxicity

A

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
Q

Coagulation factors are synthesized in the

A

Liver

41
Q

Treatment of warfarin toxicosis

A

Decontamination

Supplement vitamin K

Plasma and/or blood transfusions

42
Q

Fibrinolytic Activity Tests

A

Fibrin Degradation Products

D-Dimer

43
Q

How is citrated plasma different than blood?

A

No RBC, WBC or Platelets

Decreased Calcium

44
Q

Key factor that promotes amplification of secondary hemostasis

A

Thrombin

45
Q

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

A

Blue Top - Citrate Tube

46
Q

Factors involved in the Intrinisc Pathway

A

XII, XI, IX, VIII

47
Q

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

A

IXa

48
Q

Activated Protein C inhibits

A

Va, VIIa

49
Q

Coagulation test for the intrinsic pathway

A

aPTT

ACT

50
Q

aPTT and ACT tests measure

A

Time for fibrin clot formation

51
Q

Factors involved in the Extrinsic Pathway

A

Tissue Factor III

VII

52
Q

Pathways that make up the coagulation cascade

A

Intrinsic pathway - Contact Activation

Extrinsic pathway - Tissue Activation

Common Pathway

53
Q

Clinical features of Warfarin Toxicosis

A

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

Death

54
Q

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

A

Thrombocytopenia

55
Q

Significance in fibrinogen concentration decrease

A

Consumption due to hypercoagulation - excessive conversion of fibrinogen to fibrin

Decreased production by the liver

56
Q

Pathogenesis of hypercoagulable phase of DIC leading to bleeding

A

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

57
Q

Significance of prolonged aPTT and ACT time

A

Deficiency or inhibition of any intrinsic or common pathway factor

Heparin therapy

58
Q

IX is converted to IXa in the Intrinsic Pathway by

A

VIIa

59
Q

Coagulopathy and Liver disease

A

Decreased synthesis of coagulation factors

Production of dysfunctional factors

60
Q

X is converted to Xa by what in the Extrinisic Pathway

A

VIIa

61
Q

Treatment for DIC

A

Identify and eliminate underlying disorder

Fluid therapy

Transfusion therapy

62
Q

Hemophilia A

A

Factor VIII deficiency

X linked recessive inheritance

Causes mild, moderate or severe bleeding

63
Q

Non-Enzymatic factors of the coagulation cascade

A

Tissue Factor (Factor III, Thromboplastin)

Factor VIIIa

Factor Va

Calcium

Platelets

64
Q

Factors affected by amplification

A

XI

VII

VIIIa

Va

65
Q

Coagulation Tests

A

Activated Partial Thromboplastin Time (aPTT, PTT)

Prothrombin Time (PT)

Thrombin Time (TT), Fibrinogen

PIVKA

Special Factor Assay

66
Q

PIVKA

A

Proteins induced by vitamin K antagonism

Indirectly measures abnormal forms of vitamin K dependent factors

67
Q

Increased concentration of fibrin degradation products occus when

A

Increased fibrinolysis

Severe internal hemorrhage with fibrinolysis

Decreased clearance of FDP by liver

68
Q

Antithrombin inhibits

A

Thrombin, IXa, Xa

69
Q

VII is converted to VIIa in the extrinsic pathway by

A

Xa

70
Q

Fibrinogen is an indicator of what in large animals

A

Inflammation

71
Q

Laboratory findings of DIC

A

Thrombocytopenia

PT, aPTT - Prolonged

Fibrinogen - decreased

FDP and D-Dimers - increased

Antithrombin - decreased

Hemorrhagic anemia

Schistocytes

72
Q

aPTT requires ______% deficiency before prolongation is detected

A

70%

73
Q

ACT requires ______% deficiency of factor before prolongation is detected

A

95%

74
Q

Serum biochemistries for DIC depend on

A

Primary Disease

Location of microthrombosis

75
Q

PT requires ______% deficiency of factor before prolongation is detected

A

70%

76
Q

Alpha-2 Macroglobulin inhibits

A

Thrombin

Plasmin

Kallikrein

77
Q

Prothrombin is converted to Thrombin by

A

Xa

78
Q

Enzymatic Factors of the Coagulation Cascade

A

XII, XI, IX, VII, X

Prothrombin

Thrombin

Fibrinogen

Fibrin

79
Q

Pathogenesis of consumptive phase of DIC

A

Depletion of coagulation factors and platelets → bleeding

80
Q

Fibrinogen is converted to Fibrin by

A

Thrombin

81
Q

Activated Clotting Time ACT measures

A

Time for fibrin clot formation in non-anticoagulated whole blood

82
Q

Coagulation test for the extrinsic pathway

A

PT

83
Q

Plasminogen is converted to Plasmin by

A

Tissue Plasminogen Activator (TPA)

84
Q

Inherited Factor Deficiencies

A

Hemophilia A - VIII

Hemophilia B - IX

Hagemans Disease - XII

85
Q

Factors involved in the common pathway

A

X, V

Prothrombin

Fibrinogen

Fibrin

86
Q

Cell Based Model

A

Focuses on the roll of cells involved with coagulation

87
Q

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

A

Because Factor VII has the shortest half life

88
Q

Causes of Warfarin Toxicosis

A

Poisoning with coumarin derivatives

Fat malabsorption

Dietary deficiency

Antibiotics that cause decreased absorption or utilization by liver

89
Q

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

A

Plasma

RUSVM Clinical Pathology (22 decks)

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