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Immunity > Hemostasis I > Flashcards

Hemostasis I Flashcards

1
Q

What are the active pro-coagulant enzymes?

A

Serine proteases

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2
Q

What are the following co-factors that favor coagulation, i.e. the accelerants

  1. ) Soluble
  2. ) Cell-bound
A
  1. ) V and VIII

2. ) Tissue factor

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3
Q

Another accelerant co-factor is

A

Von Willebrand Factor

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4
Q

What are three anti-coagulant factors?

A

Thrombomodulin, Protein C, and Protein S

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5
Q

What is step one of hemostasis?

A

Local Vasoconstriction

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6
Q

The local vasoconstriction is caused by the release of the powerful vasoconstrictor

A

Endothelin

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7
Q

Step 2 of primary hemostasis is formation of the

A

Platelet plug

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8
Q

Hemostasis depends on

A

Platelet function

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9
Q

Platelets originate from the

A

Hematopoetic stem cells

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10
Q

Thrombopoiesis is regulated by the

A

Megakaryocyte

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11
Q

The platelet massis regulated by

A

Thrombopoietin

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12
Q

We see decreased platelet and megakaryocyte mass with increased

A

TPO

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13
Q

DNA replicates without nuclear or cell division

A

Endomitosis

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14
Q

A megakaryocyte nucleus MUST be polypoid to produce

A

Platelets

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15
Q

Platelets are formed in the bone marrow from

A

Megakaryocytes

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16
Q

What is a normal platelet count

A

150K to 350K

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17
Q

Characterized by too few platelets

A

Thrombocytopenia

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18
Q

Characterized by too many platelets

A

Thrombocytosis

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19
Q

Platelet size correlates with reactivity i.e. larger platelets are typically younger and are

A

Prothrombotic

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20
Q

Normal endothelial monolayer is

A

Anti-thrombogenic

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21
Q

Important for platelet adhesion when the endothelial monolayer is injured

A

von Willebrand Factor

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22
Q

A large circulating multimer, synthesized in endothelial cells and megakaryocytes

A

von Willebrand Factor

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23
Q

von Willebrand factor is stored in

A

Weibel-Pallade bodies

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24
Q

Plays an important role in both primary and secondary hemostasis

A

von Willebrand Factor (vWF)

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25
Q

At the side of injury, vWF adheres to exposed

A

Collagen

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26
Q

Facilitates platelet tethering to subendothelial BM

A

vWF

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27
Q

With injury, vWF adheres to the vessel

A

Subendothelial matrix

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28
Q

With shear, vWF multimers uncoil, causing the adherence and activation of

A

Platelets

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29
Q

Activated platelets expose phosphatodyl serine and bind

-to facilitate clotting

A

FVIII

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30
Q

Bleeding ceases by platelet-fibrin plug, sealing vascular injury and is followed by

A

Thrombolysis and tissue repair

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31
Q

Deficiency of GpIIb-IIIa complex causes

A

Glanzmann thrombasthenia

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32
Q

Deficiency of GpIb causes

A

Bernard-Soulier syndrome

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33
Q

Deficiency of vWF causes

A

von Willebrand disease

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34
Q

Activatedby adhesion and soluble mediators

A

Platelets

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35
Q

Resting platelets are smooth and disc shaped, while activated platelets have an

A

Irregular shape

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36
Q

Platelet aggregation occurs through binding of two

A

GPIIb/IIIa’s

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37
Q

Primary hemostasis can be summarized as

A

Adhesion, Activation, and Aggregation

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38
Q

Adhesion is primarily through

A

vWF

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39
Q

Activation occurs primarily through

A

Collagen and ADP

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40
Q

Aggregation occurs primarily through

A

Fibrinogen, GPIIb/IIIa, and aIIbb3

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41
Q

What are three drugs that target platelet function improve outcome in patients with unstable angina

A

Aspirin, Thienopyridines, Glycoprotein IIb/IIIainhibitors

42
Q

Blocks TXA2 production

A

Aspirin

43
Q

Block ADP receptors (P2Y12)

A

Thienopyridines

44
Q

Block platelet adhesion to fibrinogen/fibrin and vWF

A

Glycoprotein IIb/IIIainhibitors

45
Q

Not normally active in circulation

A

Platelets

46
Q

LOW platelet counts (<10 to 20K) result in

A

Petechiae

47
Q

Reddish purple discolorations on the skin that do not blanche on applying pressure

A

Petechiae

48
Q

Release trophic factors which maintain cell-cell contacts

A

Platelets

49
Q

The initial platelet plug is not very

A

Strong

50
Q

Thus, the platelet plug requires a strong

A

Sealant

51
Q

An essential component of hemostasis is the formation of

A

Cross-linked fibrin

52
Q

The process by which cross-linked fibrin is formed

A

Secondary hemostasis

53
Q

The clotting cascade results in the formation of fibrinfrom

A

Fibrinogen

54
Q

What are the three major classes of pro-coagultion players?

A

Serine proteases, cell-associated cofactors, and soluble cofactors

55
Q

Serine proteases circulate as

A

Zymogens

56
Q

An example of a cell-associated cofactor is

A

Tissue factor

57
Q

Which three pro-coagulation players are NOT made in the liver?

A

Tissue factor, VIII, and vWF

58
Q

Most coagulation factors are serine proteases that circulate as

A

Zymogens

59
Q

When activated, coagulation factors are written with an

A

“a” i.e. X –> Xa

60
Q

What are the two components of the Extrinsic hemostasis pathway?

A

Factor VII and tissue factor

61
Q

What are the three components of the Intrinsic hemostasis pathway?

A

Factors IX, XI, and XII

62
Q

What are the two components of the common hemostasis pathway?

A

Factor X and Factor II (prothrombin)

63
Q

In the extrinsic pathway, vessel wall injury increases

A

Tissue factor expression

64
Q

A transmembrane protein that is not normally accessible

A

Tissue Factor

65
Q

Synthesized and expressed by endothelial cell AND monocytes

A

Transmembrane protein

66
Q

Step 2 of the extrinsic pathway is tissue factor is bound by

A

Factor VII

67
Q

Circulating Factor VII binds Tissue Factor (TF) and is activated, thus it becomes

A

Factor VIIa

68
Q

Tissue Factor activates

A

Factor VII

69
Q

Then Factor IX (9) is recruited to the complex and

A

Activated

70
Q

Then, TF:FVIIa:FIXacomplex activates

A

Factor X

71
Q

Then, FXaactivates Prothrombin (FII/2) to

A

Thrombin

72
Q

Thrombin then cleaves fibrinogen to form

A

Fibrin

73
Q

Step 4 is called

A

Amplification #1

74
Q

During amplification #1, thrombin activated more

A

Factor IX and VIII

75
Q

Anti-hemophilic factor activated by thrombin

A

Factor VIII

76
Q

Factor VIII circulated in the plasma in a complex with

A

vWF

77
Q

Links platelets to subendothelial BM

A

vWF

78
Q

Binds to and stabilizes Factor VIII, extending half-life from 8 minutes to 8 hours

A

vWF

79
Q

The most common inherited bleeding disorder

A

von Willebrand disease

80
Q

Characterized by easy bruising, skin bleeding, and prolonged bleeding from mucosal surfaces

A

Von Willebrand Disease

81
Q

A soluble co-factor with no enzymatic activity

A

Factor VIII

82
Q

Factor VIIIa functions as an accelerant/catalyst for

A

Factor IXa

83
Q

What is the clinical significance of the Factor VIII/IX complex?

A

Hemophilia A (VII) and Hemophilia B (IX)

84
Q

Another soluble co-factor with no enzymatic activity that functions as an accelerant/catalyst for Factor Xa

A

Factor V

85
Q

Factor IXa-VIIIacomplex generates LARGE amounts of activated

A

Factor X

86
Q

Converts prothrombinto thrombin 300,000X faster than FREE factor Xa

A

Factor Xa-Va complex

87
Q

What are the three pro-coagulant complexes that are essential to coagulation?

A
  1. ) Tissue Factor::Factor VIIa::IXa≈ Factor X
  2. ) Factor IXa::VIIIa≈ Factor X
  3. ) Factor Xa::Va ≈ Factor II (Prothrombin)
88
Q

Which pro-coagulant factors are dependent on Vitamin K?

A

Prothrombin (II) and Factors VII, IX,

89
Q

Which anticoagulants are dependent on Vitamin K?

A

Proteins, C, S, and Z

90
Q

Dependent on Vitamin K

A

Serine proteases

91
Q

Vitamin K dependent factors have glutamate rich

A

N-terminus

92
Q

Carboxylation of the GLU residues is required for

A

Activation

93
Q

Carboxylation is dependent on

A

Vitamin K

94
Q

The basis for anticoagulant action of sodium citrate

A

Blocking Ca2+

95
Q

VitK2 is synthesized by colonic flora which can be disturbed by antibiotics leading to relative

A

Vitamin K deficiency

96
Q

What are the two important forms of Vitamin K

A

Phylloquinone(K1) and Menaquinones(K2)

97
Q

A drug that targets Vitamin K,was initially developed as a rodenticide

A

Warfarin

98
Q

Action of warfarin is to block VitK dependent

A

Reductases

99
Q

How is the intrinsic pathway activated?

A

Contact activation

100
Q

Contact activation is independent of

A

Tissue Factor

Immunity (33 decks)

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