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BL Unit 3 > Hemostasis review excel > Flashcards

Hemostasis review excel Flashcards

1
Q

Another name for prothrombin

A

Factor II

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2
Q

Another name for fibrinogen

A

Factor I

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3
Q

Zymogens in the coagulation cascade

A

Factor II, VII, IX, X, XI, XII, XIII ; Not Factor I, V, VIII

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4
Q

Large molecular weight cofactors in the coagulation cascade

A

Factor V, VIII, Tissue factor

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5
Q

Vitamin K dependent factors

A

Factor II, VII, IX, X, Protein C and S

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6
Q

Members of the “tenase” complex

A

Factor VIII, Factor IX, calcium, phospholipid surface. Hint for remembering - tenase activates Factor X

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7
Q

Members of the “prothrombinase” complex

A

Factor V, Factor X, calcium, phospholipid surface. Hint for remembering - prothrombinase activates thrombin

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8
Q

Members of the common pathway

A

Factor I, II, V, X, XIII

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9
Q

Members of the extrinsic pathway

A

Factor VII, tissue factor (aka tissue thromboplastin)

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10
Q

Members of the intrinsic pathway

A

Factor VIII, IX, XI, XII

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11
Q

Physiologic anticoagulants

A

Protein C, S, Tissue factor pathway inhibitor, antithrombin III, thrombomodulin

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12
Q

Factor deficient with hemophilia A

A

Factor VIII

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13
Q

Factor deficient with hemophilia B

A

Factor IX

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14
Q

Factor that acts as a carrier for factor VIII in the plasma

A

Von Willebrand factor

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15
Q

Factor that cleaves and inactivates factors Va and VIIIa

A

Protein C

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16
Q

Cofactor for protein C

A

Protein S

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17
Q

Factors that affect the PT/INR

A

Factor I, II, V, VII, X

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18
Q

Factors that affect the aPTT

A

Factor I, II, V, VIII, IX, X, XI, XII

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19
Q

Factor that crosslinks fibrin to form a “hard clot”

A

Factor XIII

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20
Q

Factor that binds to exposed collagen in a damaged blood vessel, promoting platelet adherence at the site of injury

A

Von Willebrand factor

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21
Q

Key protein in the fibrinolytic pathway

A

Plasmin

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22
Q

Factor exposed after vessel injury that initiates clotting

A

Tissue factor

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23
Q

Factor that when deficient prolongs the aPTT but doesn’t lead to bleeding risk

A

Factor XII

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24
Q

Binds with high affinity to heparin, which increases its activity many fold

A

Antithrombin III

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25
Q

What is the first thing that happens to blood vessels following injury?

A

Vasoconstriction. Result of release of endothelin by endothelial cells and neuro response.

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26
Q

What platelet receptor binds vWF?

A

Gp1b

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27
Q

Where does vWF come from?

A

Endothelial cell Weibel-Palade body and platelet granules, also some circulating in plasma

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28
Q

What receptors do platelets use to adhere to each other?

A

Gp2b/3a

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29
Q

What do platelets release after binding to vWF?

A

ADP and TXA2

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30
Q

What does ADP do for platelets?

A

Upregulates Gp2b/3a

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31
Q

What does TXA2 do for platelets?

A

Promotes aggregation

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32
Q

What drug irreversibly inhibits the production of TXA2?

A

Aspirin

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33
Q

What molecule do platelets use to link their Gp2b/3a receptors?

A

Fibrinogen

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34
Q

What is a primary hemostasis disorder?

A

Disorder of platelet aggregation either due to abnormal platelets or platelet destruction.

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35
Q

What are the typical clinical and lab findings of a primary hemostasis disorder?

A

Mucosal or skin bleeding (epistaxis is most common, intracranial is most serious), petechiae, purpura, ecchymoses, prolonged bleeding time, dec platelet count, increased megakaryocytic

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36
Q

What is the most common cause of thrombocytopenia?

A

ITP (autoantibody typically to Gp2b/3a)

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37
Q

T or F: You will see increase PT or PTT in ITP?

A

FALSE

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38
Q

How can you treat someone with ITP?

A

Given them IVIG. Distracts the splenic macrophages into eating IVIG rather than IG coated platelets.

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39
Q

What causes thrombotic thrombocytopenia purpura?

A

Decreased ADAMTS13 which normally cleaves vWF multimers into monomers. Usually due to an acquired antibody to ADAMTS13.

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40
Q

What causes hemolytic uremic syndrome?

A

infection with E. coli O157:H7 which damages endothelial cells

41
Q

What are a classic smear finding of TTP and HUS?

A

Shistocytes (helmet cells)

42
Q

In which disorder to you classically see enlarged platelets?

A

Bernard-Soulier syndrome. Due to Gp1b deficiency.

43
Q

What is Glanzmann thrombasthenia?

A

Decreased platelet aggregation due to Gp2b/3a deficiency.

44
Q

What is a secondary hemostasis disorder?

A

A problem with the coagulation cascade

45
Q

Where are coagulation cascade factors produced?

A

The liver

46
Q

What activates the extrinsic pathway?

A

Tissue thromboplastin which activates Factor VII

47
Q

What activates the intrinsic pathway?

A

Subendothelial collagen which activates factor XII

48
Q

T or F: Calcium is necessary for the coagulation cascade?

A

TRUE

49
Q

T or F: Phospholipid surface is necessary for the coagulation cascade?

A

True. It is the surface of the platelet

50
Q

PT tests for deficiency in which pathway(s)?

A

Extrinsic (and common)

51
Q

PTT tests for deficiency in which pathway(s)?

A

Intrinsic (and common)

52
Q

T or F: PT will be elevated in hemophilia A.

A

False. PTT will be elevated

53
Q

T or F: PTT will be elevated in von Willebrand Disease.

A

True. vWF stabilizes factor VIII

54
Q

How do you test for vW Disease?

A

Ristocetin test - ristocetin induces vWF to bind to platelets and promote aggregation, but if the patient has dec vWF or abn vWF, then platelet aggregation will be decreased.

55
Q

How do you treat for vW Disease?

A

Give desmopressin (arginine vassopressin, a type of ADH analog) which releases vWF from Weibel-Palade bodies.

56
Q

What does Vit K do in the coagulation cascade?

A

In the liver, gamma carboxylates factors II, VII, IX, X, protein C and S. Gamma carboxylation is the carboxylation of a glutamate residue which is important for calcium and platelet binding.

57
Q

Where does vitamin K come from?

A

Produced by gut flora

58
Q

What are the most common causes of vit K deficiency?

A

Malabsorption, disruption of gut flora (long-term antibiotic therapy), newborns who are not yet colonized.

59
Q

What is the most common cause of loss of coagulation factors?

A

Liver failure and large volume transfusion (dilutes blood)

60
Q

Which side of the coagulation pathway does heparin inhibit?

A

Intrinsic

61
Q

T or F: Your body can develop antibodies to heparin?

A

True.

62
Q

What is DIC?

A

Pathologic activation of the coagulation cascade. This results in clotting which uses up coag factors, resulting in bleeding other places.

63
Q

What are the most common causes of DIC?

A

Obstetric complications, adenocarcinoma, sepsis, APL, exercise induced heat stroke, rattlesnake bite

64
Q

What lab tests can done to find DIC?

A

Platelet count (dec), PT/PTT (inc), fibrinogen (inc), smear (shistocytes), fibrin split products/D-dimers (inc)

65
Q

How is DIC treated?

A

Find the underlying cause and give cryoprecipitate

66
Q

What is the final goal of the coagulation cascade?

A

Activation of thrombin (factor IIa)

67
Q

What does thrombin do? (4)

A

1.) convert fibrinogen to fibrin 2.) promote platelet aggregation 3.) activates FV and VIII 4.) activates fibrinolytic factors and protein C 5.) activates Factor XIII

68
Q

Which factor generates thrombin?

A

Factor X

69
Q

Which factors generate Factor X?

A

Factors VIII and IX or Factor VII and tissue factor (aka tissue thromboplastin)

70
Q

What does Factor XIII do?

A

Crosslinks fibrin and hardens the fibrin clot

71
Q

How does Factor X generate thrombin?

A

It binds to cofactor V and converts prothrombin to thrombin

72
Q

What is the Propagation Phase of coagulation?

A

The formation of the tenase/prothrombinase complexes which leads to the generation of thrombin

73
Q

What is the Acceleration Phase of coagulation?

A

When thrombin enhances the activity of cofactors V and VIII greatly enhancing the activity of the tenase/prothrombinase complexes.

74
Q

Which factors has no known function and does not affect bleeding?

A

Factors XII

75
Q

What does Antithrombin III do?

A

1.) Inactivates thrombin 2.) inactivates Factors XII, XI, IX, and X

76
Q

What does protein C do?

A

Cleaves Va and VIIIa (decreasing coagulation)

77
Q

What does tissue factor pathway inhibitor do?

A

Inhibits Factor Xa and the VIIa-TF complex

78
Q

What does tissue plasminogen activator do?

A

Activates plasminogen to plasmin

79
Q

What does plasmin do?

A

Degrades fibrin => forming fibrin split products and D-dimer

80
Q

What does alpha 2-antiplasmin do?

A

inhibits plasmin

81
Q

What does Warfarin do?

A

Interferes with Vit K modification of cofactors (II, VII, IX, X)

82
Q

What does plasminogen activator inhibitor-1 do?

A

Inhibits tissue plasminogen activator

83
Q

What is normal bleeding time?

A

2-9 minutes

84
Q

What is normal thrombin time (TT)?

A

12-18 seconds

85
Q

What is thrombin time?

A

Measure the procoagulant activity of fibrinogen

86
Q

What is normal activated thromboplastin time (aPTT)?

A

25-32 seconds

87
Q

What is normal protime (PT)?

A

9-12 seconds

88
Q

What is INR?

A

International normalized ratio - normal value 1.0. Allows the reporting of PT as ratio for controls in order to control for potency of thromboplastin used in the lab to start the reaction.

89
Q

What is the inheritance patterns of hemophilia A and B?

A

both are X-linked recessive

90
Q

When are minor hemophilia problems typically diagnosed?

A

After trauma or surgery which fails to heal well.

91
Q

What is the inheritance pattern for Factor XI and Factor VII deficiency?

A

both autosomal recessive

92
Q

What are the types of vW Disease?

A

Type 1 - partial vWF deficiency. Type 2 - abnormal vWF. Type 3 - total vWF deficiency

93
Q

What is the most common acquired factor inhibitor disorder?

A

Autoantibodies to Factor VIII

94
Q

How are acquired factor inhibitor disorders treated?

A

Immunosuppressants

95
Q

What is the differential for prolonged PT > prolonged PTT?

A

Liver disease, Vit K deficiency, warfarin. Why? because liver disease affect the vit K modification of factors II, VII, X to a very high degree

96
Q

What is the differential for prolonged PTT > prolonged PT?

A

DIC

97
Q

What is the differential for prolonged PTT but not PT?

A

Heparin, Hemophilia A or B, Factor IX deficiency, Factor XII deficiency, Acquired hemophilia, von Willebrand Disease, Lupus anticoagulant

98
Q

What is the lupus anticoagulant?

A

An IgG which reacts in the platelet membrane or endothelial cells. This results in prolonged PTT by binding up the phospholipid used to test PTT.

99
Q

What are the most common causes of inherited hypercoaguable state?

A

Deficiencies of antithrombin III, protein C, protein S, or mutant Factor V which is not deactivated by protein C.

BL Unit 3 (9 decks)

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