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Surgical biology and methods > Bleeding and hemostasis > Flashcards

Bleeding and hemostasis Flashcards

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1
Q

What are the two stages of hemostasis?

A
  1. Primary hemostasis: formation of initial platelet plug
  2. Secondary hemostasis: proteolytic reactions resulting in generation of fibrin polymers and stable thrombus
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2
Q

Describe the mechanism of primary hemostasis.

A
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3
Q

What are the two different models of secondary hemostasis?

A

Traditional (or cascade model), cell based model

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4
Q

What are the two fundamental paradigms of the cell based model of coagulation?

A
  1. Tissue factor is the primary physiologic initiator of coagulation
  2. Coagulation is localized to, and controlled by, cellular surfaces
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5
Q

Describe the cascade model of coagulation.

A
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6
Q

Describe the cell based model of coagulation.

A
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7
Q

What are the three phases of the cell based model of coagulation?

A

Initiation, amplification, propagation

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8
Q

How does the normal endothelium control platelet reactivity?

A

Through three known inhibitors:
1. Prostacyclin: limits platelet response to TxA
2. ecto-ADPase: metabolizes ADP released from activated platelets
3. Nitric oxide: diffuses into platelets and decreased intracellular Ca2+ flux, reducing the number and affinity of fibrinogen binding sites

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9
Q

What are the three natural anticoagulant pathways?

A
  1. Antithrombin
  2. Activated protein C
  3. Tissue factor pathway inhibitor
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10
Q

Describe the function of the three natural anticoagulant pathways.

A
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11
Q

What are the enzymes primarily responsible for fibrinolysis?

A

Tissue type plasminogen activator, urokinase type plasminogen activator. Both lead to the formation of plasmin which degrades fibrin.

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12
Q

What acts as a cofactor for plasminogen activation?

A

Fibrin, in an autoregulatory manner

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13
Q

What primarily controls/downregulates fibrinolysis?

A
  1. Plasminogen activator inhibitor (produced by platelet alpha granules)
  2. Thrombin activatable fibrinolysis inhibitor
  3. Alpha2-antiplasmin (produced by the liver)
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14
Q

What is the normal BMBT in a dog and cat?

A

Dog: less than 3 minutes
Sedate cat: 34-105 seconds

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15
Q

What does a prolonged BMBT indicate?

A

A defect of primary hemostasis

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16
Q

What are APTT and PT used to assess?

A

Secondary hemostasis

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17
Q

Are APTT and PT predictive of bleeding?

A

No

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18
Q

What pathways in the traditional model do the APTT, PT and ACT test?

A

APTT: Intrinsic and common
PT: Extrinsic and common
ACT: Intrinsic and common - less sensitive than APTT

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19
Q

How decreased does a single factor have to be to cause prolongation of PT/APTT?

A

Decreased to less than 25-30%

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20
Q

Is PT or APTT more sensitive in detecting vitamin K deficiency?

A

PT due to the short half life of factor VII

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21
Q

Is the PT or APTT more sensitive to heparin administration?

A

APTT

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22
Q

What is the difference between fibrin split products and D-dimers?

A

D-dimers are specific fibrin degradation products that indicate both active activation of thrombin and plasmin (FDPs only indicate activation of plasmin). D-dimers are consequently specific for active coagulation and fibrinolysis and are a sensitive indicator of thrombotic conditions such as DIC and thromboembolism.

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23
Q

Is fibrinogen typically elevated or decreased in instances acute inflammation?

A

Increased - it is an acute phase protein

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24
Q

What effect does anemia have on TEG?

A

Causes a relatively hypocoaguable tracing

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25
Q

What can effect ACT results?

A

Thrombocytopenia, thrombopathia, anemia, altered viscosity, incubation temperature

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26
Q

What can cause disorders of primary hemostasis?

A

Thrombocytopenia, thrombopathia or vascular anomaly

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27
Q

What is the definition of acute traumatic coagulopathy?

A

50% prolongation in either PT or APTT. Most common in dogs with increased severity of injury, decreased systolic BP, and increased lactate

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28
Q

What factor is deficient in hemophilia A?

A

Factor VIII

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29
Q

What are the three hypotheses to explain acute traumatic coagulopathy?

A
  1. DIC with a fibrinolytic phenotype
  2. Enhanced expression of the thrombomodulin thrombin protein C pathway
  3. Catecholamine induced endothelial damage
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30
Q

What are the six factors that have been identified in the development of acute traumatic coagulatopathy?

A
  1. Tissue injury
  2. Hypoperfusion
    These are the initiating causes.
  3. Acidosis
  4. Hemodilution
  5. Hypothermia
    These result in traumatic induced coagulopathy (TIC) which propagates ATC.
  6. Systemic inflammation
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31
Q

What is the lethal triad?

A

Coagulopathy, acidosis, hypothermia

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32
Q

What effect does acidemia have on fXa-Va complex activity?

A

fXa-Va complex activity is decreased by 50% at a pH of 7.2, 70% at pH 7.0, and 90% at pH 6.8

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33
Q

What is the definition of massive transfusion?

A

Replacement of blood components that is greater than a patients blood volume within 24 hours, or half blood volume over 3-hours

34
Q

What clotting factor is most affected by hemodilution?

A

Fibrinogen (due to limited synthesis). At fibrinogen levels less than 50 mg/dL no clot is formed

35
Q

What prolongation of PT/APTT represents a clinical bleeding risk?

A

1.5 times

36
Q

Will TEG detect thrombopathies related to von Willebrands disease?

A

No

37
Q

What factor deficiencies can variations in PT/APTT diagnose?

A
38
Q

What physical signs of bleeding are typically associated with primary hemostatic deficits?

A

Ecchymoses and spontaneous bleeding from mucosal surfaces. Petechiae are more common with thrombocytopenia rather than thrombopathia

39
Q

What physical signs of bleeding are typically associated with secondary hemostatic deficits?

A

Large hematomas and by bleeding into the subcutaneous tissues, body cavities, muscles and joints

40
Q

What are the best tests to detect hyperfibrinolysis?

A

TEG is the best. Markedly elevated D-dimers or low fibrinogen concentrations may also be suggestive

41
Q

What is damage control resuscitation?

A

Aggressive correction of coagulopathies while reducing hypoperfusion, hemodilution and hypothermia. Transfusion of platelets and plasma help to prevent dilutional coagulopathy

42
Q

What are the targets of damage control resuscitation?

A

Maintain the PT and APTT within 1.5 times normal, and the platelet count over 50,000/uL

43
Q

What ratio of PRBCs, platelets and plasma is advocated in damage control resuscitation?

A

1:1:1

44
Q

What are contraindications for hypotensive resuscitative strategies?

A

Traumatic brain or spinal cord injury as mean arterial pressure is closely correlated to central nervous system perfusion

45
Q

What is the lifespan of platelets in the dog and cat?

A

6-8 days

46
Q

Describe the various plasma component transfusions and their indications.

A
47
Q

Describe the various options for platelet transfusions and their advantages/disadvantages.

A
48
Q

When should antithrombotic drugs be discontinued prior to surgery?

A
49
Q

What is the mechanism of action of desmopressin?

A

Vasopressin analogue that acts at V2 receptors to release subendothelial stores of vWF. Onset of action is 30 minutes, and DOA is 2 hours.

50
Q

What is the mechanism of action of tranexamic acid and epsilon aminocaproic acid?

A

Lysine analogues that block the binding and activation of plasminogen (antifibrinolytics)

51
Q

How much more likely were greyhounds to have clinically hemorrhage following amputation without the administration of E-aminocaproic acid in one study?

A

5.7 times

52
Q

What are the primary causes of thrombocytopenia?

A

Decreased production, increased destruction, increased consumption, sequestration

53
Q

What are the three types of von Willebrands disease?

A

Type 1: presence but decrease of all multimers
Type 2: loss of high molecular weight multimers (Shorthaired pointers)
Type 3: almost complete absence of vWF (<0.1%) (chesapeke bay retriever, shetland sheepdog, scottish terriers)

54
Q

What vWF ELISA result indicates deficiency?

A

<50% vWF concentration as compared to the pooled control sample

55
Q

What factor deficiency causes hemophilia A and B?

A

Factor VIII and IX (sex linked in males)

56
Q

What factor deficiency can cause a marked increase in APTT without clinical hemorrhagic tendency?

A

Factor XII

57
Q

What coagulation factors require vitamin K for activation?

A

II, VII, IX, X

58
Q

What can cause vitamin K deficiency?

A

Dietary insufficiency, decreased intestinal absorption, vitamin K antagonism (warfarin)

59
Q

What is the MOA of warfarin?

A

Antagonizes vitamin K epoxide reductase which is the enzyme responsible for vitamin K recycling

60
Q

With vitamin K deficiency is APTT/PT prolonged?

A

Both, but PT is prolonged first due to the short half life of fVII

61
Q

What level of functional hepatic mass has to be lost for decreased coagulation factor synthesis to occur?

A

> 70%

62
Q

What constitutes Virchow’s triad?

A

Endothelial injury, vascular stasis, hypercoagulability

63
Q

What are the characteristics of a hypercoaguable TEG tracing?

A

Increased G-value, decreased R and K values, increased MA and alpha values

64
Q

What tests can be used to assess for evidence of hypercoaguability?

A

TEG is best. Can also consider antithrombin levels, fibrinogen levels, and D-dimers

65
Q

What diagnostics should be considered in instances of suspected pulmonary thromboembolism?

A

Thoracic radiographs, arterial blood gas analysis, echocardiography, D-dimer concentration, CT angiography

66
Q

What are the most common arterial blood gas abnormalities in instances of pulmonary thromboembolism?

A

Increased A-a ratio, hypoxemia, hypocapnia, decreased oxygen responsiveness

67
Q

What thoracic radiograph findings are suggestive of PTE?

A

Alveolar infiltrates (particularly right and caudal lobes), Westermark sign

68
Q

Are anti-platelet drugs typically used for arterial or venous thromobprophylaxis?

A

Arterial

69
Q

Are anticoagulants drugs typically used for arterial or venous thromobprophylaxis?

A

Venous

70
Q

What is the mechanism of action of unfractionated heparin?

A

Potentiation of antithrombin activity leading to inactivation of thrombin and factor fXa

71
Q

What is the goal of unfractionated heparin therapy?

A

Prolongation of APTT by 1.5 to 2 times normal

72
Q

What is the mechanism of action of low molecular weight heparin?

A

Smaller molecule than unfractionated heparin (4000-6500 Daltons, compared to 5000-30,000). This leads to far greater inhibition of fXa than thrombin and much more predictable results with dosing

73
Q

How is the action of low molecular weight heparin monitored?

A

Anti-fXa activity, although TEG may be superior

74
Q

Why should heparin therapy overlap warfarin therapy for the first 2 days of therapy?

A

Because warfarin therapy takes 24-48 hours to exert an effect (only coagulation proteins with short half lives fVII and protein C are initially impacted).

75
Q

What is the goal of warfarin therapy?

A

A PT that is 1.25 to 1.5 times baseline

76
Q

What is the antithrombotic MOA of aspirin?

A

Inhibits COX-1 which suppresses the synthesis of TxA2. May also suppress prostacyclin release from endothelial cells, although this is also mediated by COX-2. Therefore suggested to use low doses of aspirin that block platelet COX-1 while sparing endothelial COX-1 and 2

77
Q

What is the onset of action of aspirin?

A

Immediate and lasts for the length of the lifespan of the platelet

78
Q

What is the MOA of clopidogrel?

A

This is a thienopyridine that requires hepatic metabolism for active metabolite. It blocks ADP binding on the platelet.

79
Q

What is the onset of action of clopidogrel?

A

2 days, and reaches steady state after 5-7 days.

80
Q

What markers can be used for the diagnosis of DIC?

A

The presence of an underlying condition that could trigger DIC with three or more of the following: thrombocytopenia, elevated PT and/or APTT, elevated fibrin split products or D-dimers, hypofibrinogenemia, reduced antithrombin activity, and/or red blood cell fragmentation

Surgical biology and methods (11 decks)

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