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CVPR 330 Blood > Hypercoagulable States and CPB / Test 3/3 > Flashcards

Hypercoagulable States and CPB / Test 3/3 Flashcards

1
Q

“Hypercoagulability” can be broadly defined as a risk of ______1_______ in circumstances that would not cause thrombosis in a normal subject.
It can be either ____2____ or ___3_____.

A
  1. ) Thrombosis
  2. ) Inherited
  3. ) Acquired
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2
Q

A hereditary tendency to thrombosis, irrespective of its cause has been referred to as ?

A

Thrombophilia

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3
Q

2 factors that accelerate clot formation ?

A

Factor VIII & Factor V

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4
Q

3 factors that Inhibit clot formation ?

A

Protein C, Protein S, Thrombomodulin

Antithrombin III

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5
Q

What inhibits thrombin and other serine proteases ?

A

Natural Anticoagulant Antithrombin III

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6
Q

What inhibits Factor V and VIII ?

A

Natural Anticoagulant

Protein C

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7
Q

Cofactor for protein C ?

A

Natural Anticoagulant

Protein S

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8
Q

What does the (Natural Anticoagulant) Tissue Factor Pathway Inhibitor bind to ?

A

binds factor Xa and VII-tissue complex

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9
Q

True hypercoaguable states can only be determined after RULING OUT other causes…

A

Pregnancy
Recent surgery Immobilization (stasis)
Obesity
Malignancy

Fracture

Heart failure
Oral contraceptive use

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10
Q

CRITERIA for True hypercoaguable state ?

A
  • Recurrent thrombosis
  • thrombosis in Unusual sites (cerebral veins, hepatic veins, renal veins, IVC, mesenteric veins)
  • First time thrombosis at age
  • Family history of thrombosis
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11
Q

What can make a patient PRONE to coagulability ?

A
  • Protein C deficiency
  • AT III deficiency
  • Protein S deficiency
  • Activated Protein C (APC) resistance
  • Mutation of factor V that makes it resistant
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12
Q

Quantitative or Qualitative abnormalities of individual, specific coagulation factors that directly produce a pro-thrombotic state describes what state of hypercoagulability ?

A

Primary Hypercoagulable State

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13
Q

Represents a diverse group of clinical disorders that are associated with a thrombotic tendency

A

Secondary Hypercoagulable State

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14
Q

Mutations of one of the physiological antithrombotic factors which leads to a quantitative deficiency or loss of function?

A

Inherited

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15
Q

Hypercoagulable States

that are sometimes inherited, but are more commonly ACQUIRED ?

A

Acquired:

Cancer
Liver Problems
Birth Control Pills > PE

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16
Q

Antithrombin/Heparin Disorder ?

A

Antithrombin deficiency

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17
Q

Protein C/Protein S Disorders

?

A

Protein C deficiency
Protein S deficiency
Resistance to activated protein C

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18
Q

Fibrinolytic Disorders

A

Hypoplasminogenemia
or
Dysplasminogenemia

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19
Q

Prevalence of deficiencies of hemostatic factors responsible for hereditary thrombotic disease.

AT III
Protein C
Protein S
APC Resistance

A

AT III 1%
Protein C 8%
Protein S 10%
APC Resistance 17%

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20
Q

Characterized by proportionate reductions in activity and antigen levels, each to about 50% of normal in heterozygous individuals, indicating synthetic abnormality of a functionally normal molecule describes what deficiency ?

A

Antithrombin III Deficiency Type 1

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21
Q 
Normal or near normal antigen levels are accompanied by low activity levels, indicating a functionally defective molecule.
- Affecting heparin binding
- impaired reactive site function
- multiple abnormalities 
  causing both abnormal 
  heparin binding and 
  abnormal protease inhibition
A

Antithrombin III Deficiency

Type 2

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22
Q

Suspected ATIII DefieciencyCPB Management & Action.

ACT

A 
Repeat Bolus
ACT still low
- Give 2 units FFP … or
- Give Thrombate
Recheck ACT
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23
Q

A naturally occurring anticoagulant which preserves blood fluidity and limits clot formation to the sites of vascular injury.

A

Protein C

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24
Q

Rare but fatal hereditary condition (Inherited autosomal disease) manifested by massive disseminated intravascular coagulaopathy and purpura fulminans in the neonatal period?

A

Homozygous Protein C deficiency

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25
Q

Prevalence is 0.1 to 0.5% in the general population, the vast majority remain symptom free.

A

Inherited autosomal disease

Heterozygous Protein C deficiency

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26
Q

Patients with heterozygous PC deficiency are at lifelong risk for thrombosis, but the episodic nature of clinical thrombosis suggests that an _____ ______ _____ may be necessary to trigger a clinically significant thrombotic event.

A

acquired thrombogenic stimulus

27
Q

Protein C is activated upon

A

the production of thrombin.

28
Q

Thrombin generation promotes clot formation by

A

cleaving fibrinogen into fibrin

and also activates the protein C system.

29
Q

Activated protein C subsequently suppresses further thrombin generation and enhances what?

A

fibrinolytic potential

30
Q

Activated protein C, along with protein S, act to inhibit the intrinsic coagulation pathway by inactivating what factors?

A

factors Va and XIIa

31
Q

Activated PC also neutralizes

A

Plasminogen Activator Inhibitor, which enhances fibrinolysis

32
Q

Is Protein C Deficiency a problem for Perfusionists?

A

Kinda bu not really, Patients’ should still achieve anticoagulation with heparin

33
Q

“Protein C deficiency is associated with what, following open heart surgery”?

A

massive cerebral thrombosis

34
Q

The possibility of an abnormally low anticoagulant potential at the time when the patient is separated from bypass and heparinization is reversed may be an important factor in what ?

A

subsequent morbidity associated with thrombotic complications

35
Q

How do you restore normal levels Protein C Pre-CPB ?

A

Prime- As per protocol with the addition of one unit of FFP to normalize Protein C levels

36
Q

What is the concentration of Protein C in FFP ?

A

87 ±15 U/dL

37
Q

As a general rule- 2 units of PC per kg. of body weight will give what ?

A

1% rise in Protein C levels

38
Q

What are 2 Other Protein C Sources ?

A

Cryoprecipitate

Protein C Concentrates

39
Q

Why is the long term use of FFP or Protein C concentrates not a reasonable alternative ?

A

1/2 life of Protein C is ~ 8 hrs

40
Q

Suspected Protein C DeficiencyCPB Management & Action

A

Pre-CPB
Restore normal levels
- FFP
- Cryoprecipitate

Slow, conservative heparin reversal

41
Q

Activated Protein C Resistance is present in what percentage of the population ?

A

3 - 7 %

42
Q

Factor V Leiden is produced by a single point mutation at position 1691 with a substitution of ___ _ ___, which eliminates the protein C cleavage site on activated or functional factor V.

A

glycine for arginine

43
Q

A Factor V Leiden abnormality results in a ?

A

prothrombotic state

44
Q

Protein S, a cofactor

Enhances the effect of activated protein C by a factor of ?

A

10

45
Q

Protein S Is down regulated by compliment regulatory protein ?

A

(C4bBP)

46
Q

Protein S Deficiency Type I =

A

Quantitative

47
Q

Protein S Deficiency Type II =

A

Qualitative

48
Q

Dysfunctional Thrombomodulin

can result from ?

A

structural or conformational changes that alter the expression or function of the molecule.

49
Q

Quantitative Fibrinolytic Disorder ?

A

Hypoplasminogenemia

50
Q

Qualitative Fibrinolytic Disorder ?

A

Dysplasminogenemia

51
Q

Name 2 Fibrinolytic Disorders
AKA
Plasminogen activator deficiency ?

A
  • Decreased TPA

- Increased plasminogen activator inhibitor

52
Q

Hypercoagulable States such as
Dysfibrinogenemias
which is a qualitative abnormality of fibrinogen, can be detected by what ?

A 
- Prolongation of thrombin 
  time.
- Prolongation of Reptilase 
  time.
- Disproportionately lower 
  levels of fibrinogen
53
Q

What does Fibren degradation products (FDP) tell us?

A

If were clotting or breaking down clots.

54
Q

Dysfibrinogenemia with a defective thrombin binding to the abnormal fibrinogen would lead to what ?

A

increased circulating thrombin which would be a prothrombotic stimulus for processes such as platelet aggregation.

55
Q

Resistant lysis of the abnormal fibrin, is possibly the result of ?

A

defective binding of t-PA or plasminogen to the abnormal fibrin

56
Q

By itself, is not associated with clinical bleeding.

It is associated with a predisposition to thrombosis

A

Lupus-like Anticoagulant

Antibody to phospholipid which causes an increased APTT

57
Q

APL antibodies often interfere with in vitro tests of hemostasis by ?

A

impeding the anchoring of coagulation proteins to phospholipid surfaces

58
Q

An autoimmune disorder associated with lupus ?

A

erythematosus

59
Q

Antiphospholipid antibody Syndrome =

A

inhibits the protein C system

60
Q

Thrombosis-prone due to multiple and often complex abnormalities of the hemostatic system.

  • Abnormalities of blood flow.
  • Abnormalities of blood composition.
  • Abnormalities of the vessel wall.
A

Secondary Hypercoagulable States

61
Q

In patients with a diagnosed hypercoagulable state undergoing CPB, normalize with the deficient product if possible.
Monitor closely during heparin reversal and into the post-operative period. The use of the following is suggested ?

A

TEG

62
Q

Vasculitis and homocystinuria describes what ?

A

Abnormalities of the blood vessel wall

63
Q

Oral contraceptives, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria, and hyperlipidemia describes what ?

A

Abnormalities of blood composition.

CVPR 330 Blood (25 decks)

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