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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
Prevalence is 0.1 to 0.5% in the general population, the vast majority remain symptom free.
Inherited autosomal disease | Heterozygous Protein C deficiency
26
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.
acquired thrombogenic stimulus
27
Protein C is activated upon
the production of thrombin.
28
Thrombin generation promotes clot formation by
cleaving fibrinogen into fibrin | and also activates the protein C system.
29
Activated protein C subsequently suppresses further thrombin generation and enhances what?
fibrinolytic potential
30
Activated protein C, along with protein S, act to inhibit the intrinsic coagulation pathway by inactivating what factors?
factors Va and XIIa
31
Activated PC also neutralizes
Plasminogen Activator Inhibitor, which enhances fibrinolysis
32
Is Protein C Deficiency a problem for Perfusionists?
Kinda bu not really, Patients’ should still achieve anticoagulation with heparin
33
“Protein C deficiency is associated with what, following open heart surgery"?
massive cerebral thrombosis
34
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 ?
subsequent morbidity associated with thrombotic complications
35
How do you restore normal levels Protein C Pre-CPB ?
Prime- As per protocol with the addition of one unit of FFP to normalize Protein C levels
36
What is the concentration of Protein C in FFP ?
87 ±15 U/dL
37
As a general rule- 2 units of PC per kg. of body weight will give what ?
1% rise in Protein C levels
38
What are 2 Other Protein C Sources ?
Cryoprecipitate | Protein C Concentrates
39
Why is the long term use of FFP or Protein C concentrates not a reasonable alternative ?
1/2 life of Protein C is ~ 8 hrs
40
Suspected Protein C Deficiency CPB Management & Action
Pre-CPB Restore normal levels - FFP - Cryoprecipitate Slow, conservative heparin reversal
41
Activated Protein C Resistance is present in what percentage of the population ?
3 - 7 %
42
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.
glycine for arginine
43
A Factor V Leiden abnormality results in a ?
prothrombotic state
44
Protein S, a cofactor | Enhances the effect of activated protein C by a factor of ?
10
45
Protein S Is down regulated by compliment regulatory protein ?
(C4bBP)
46
Protein S Deficiency Type I =
Quantitative
47
Protein S Deficiency Type II =
Qualitative
48
Dysfunctional Thrombomodulin | can result from ?
structural or conformational changes that alter the expression or function of the molecule.
49
Quantitative Fibrinolytic Disorder ?
Hypoplasminogenemia
50
Qualitative Fibrinolytic Disorder ?
Dysplasminogenemia
51
Name 2 Fibrinolytic Disorders AKA Plasminogen activator deficiency ?
- Decreased TPA | - Increased plasminogen activator inhibitor
52
Hypercoagulable States such as Dysfibrinogenemias which is a qualitative abnormality of fibrinogen, can be detected by what ?
``` - Prolongation of thrombin time. - Prolongation of Reptilase time. - Disproportionately lower levels of fibrinogen ```
53
What does Fibren degradation products (FDP) tell us?
If were clotting or breaking down clots.
54
Dysfibrinogenemia with a defective thrombin binding to the abnormal fibrinogen would lead to what ?
increased circulating thrombin which would be a prothrombotic stimulus for processes such as platelet aggregation.
55
Resistant lysis of the abnormal fibrin, is possibly the result of ?
defective binding of t-PA or plasminogen to the abnormal fibrin
56
By itself, is not associated with clinical bleeding. | It is associated with a predisposition to thrombosis
Lupus-like Anticoagulant Antibody to phospholipid which causes an increased APTT
57
APL antibodies often interfere with in vitro tests of hemostasis by ?
impeding the anchoring of coagulation proteins to phospholipid surfaces
58
An autoimmune disorder associated with lupus ?
erythematosus
59
Antiphospholipid antibody Syndrome =
inhibits the protein C system
60
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.
Secondary Hypercoagulable States
61
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 ?
TEG
62
Vasculitis and homocystinuria describes what ?
Abnormalities of the blood vessel wall
63
Oral contraceptives, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria, and hyperlipidemia describes what ?
Abnormalities of blood composition.

CVPR 330 Blood (25 decks)

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