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CV Perf Tech II > Overview of Coagulation- Exam 1 > Flashcards

Overview of Coagulation- Exam 1 Flashcards

1
Q

What is the purpose of blood circulation “checks and balances”?

A

Preserve blood fluidity
Seal off site of bleeding
Balance anticoagulant/procoagulant factors

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2
Q

Anticoagulant Factors

A

Released by endothelial cells

Ex. prostacyclin, vascular plasminogen activator

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3
Q

Procoagulant Factors

A

Platelets
Plasma proteins- inactive state (zymogen)
release of lining when vascular hose gets disrupted

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4
Q

Zymogen

A

Inactivate state of plasma proteins

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5
Q

When does the intrinsic pathway come into play?

A 
In vitro (not in vivo)
Ex. in the ECC
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6
Q

3 Phases of Cell-Based Coag Model

A

Initiation
Amplification
Propagation

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7
Q

What is the most significant event to initiate coagulation?

A

FVIIa/TF complex activity (Initiation Phase)

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8
Q

What is TF?

A

Tissue factor, a membrane-bound protein exposed to plasma during vascular damage

Receptor and cofactor for FVII

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9
Q

What happens when FVII (zymogen) is bound to TF?

A

TF converts FVII to FVIIa to create FVIIa/TF complex

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10
Q

Where is FXa formed in the initiation phase?

A

ON the cell; remains on cell surface

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11
Q

What zymogens does FVIIa/TF complex activate?

A

FX and FIX

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12
Q

What happens with TF-bearing cells in the absence of injury?

A

TF-bearing cells bind FVIIa, low level FIXa, low level FXa

*BUT separated from amplification components by normally intact blood vessel wall

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13
Q

What is the purpose of the small amt of thrombin generated on the TF-bearing cell?

A

Serves as the “signal” for Phase II: Amplification to begin

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14
Q

FIIa

A

Thrombin

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15
Q

FII

A

Prothrombin

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16
Q

What happens when sufficient thrombin (FIIa) is generated on or adjacent to TF-bearing cells?

A

Platelets are activated

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17
Q

What does the small amt of TF-bearing cell-generated thrombin do?

A
  1. Activates Platelets
  2. Activates FVa from FV
  3. Activates FVIIIa and dissociates it from vWF
  4. Activates FXIa from XI
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18
Q

What is the first step in phase III: propagation?

A

Production of vast amounts of thrombin on the surface of activated platelets

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19
Q

What happens when vascular injury occurs?

A
  1. Platelets leave blood vessel
  2. Platelets bind to collagen/vWF/vessell wall receptors
  3. Platelets activated by factors and priming thrombin
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20
Q

What is the first step in the formation of the platelet “plug” necessary for primary hemostasis?

A

The adherence of platelets to the damaged tissue

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21
Q

What factors form the the platelet tenase complex?

A

FVIIIa and FIXa

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22
Q

When is most of the thrombin produced generated?

A

AFTER the initial fibrin clot is formed

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23
Q

What does the exposive amt of thrombin produced do?

A

Continues to activate FXIII and other factors

Helps to keep constructing the platelet/thrombin clot

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24
Q

Arterial circulaton

A

requires rapid response system to seal bleeding sites

platelets take leading role followed by fibrin formation

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25
Q

What agents are used to prevent coronary thrombosis in arterial circulation?

A

Antiplatelet agents

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26
Q

Venous circulation

A

slower response acceptable

rate of thrombin generated takes leading role

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27
Q

What agents are used to prevent DVT in venous circulation?

A

Antithrombin agents

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28
Q

What happens when an arterial blood vessel is damaged?

A

Vascular constriction
Platelet adhesion/activation (platelet plug)
Activation of cell-based coagulation cascade–> fibrin clot
Clot retraction
Activation of fibrinolytic cascade
Vessel repair/regeneration

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29
Q

What happens when the blood vessel itself is injured?

A

Persistent constriction of smooth muscles

Most prominent following severe crushing type injuries

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30
Q

Describe the layers in an artery.

A

Most have 2 layers (except uterine artery)
Inner-circular
Outer-longitudinal

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31
Q

Shear stress for larger arteries

A

500/sec

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32
Q

shear stress for arterioles

A

5,000/sec

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33
Q

Shear stress is __________ related to flow velocity.

A

Inversely

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34
Q

Why does shear stress make platelet adhesion a problem?

A

Opposes any tendency of flowing blood to clot
Limits time available for procoagulant reactions to occur
Displaces cells or proteins not tightly bound to the vessel wall

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35
Q

Coaxial migration

A

Platelets pushed to the vessel perimeter by larger erythrocytes and leukocytes- which are in the center

Flow is slower along the edges and faster in the center

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36
Q

What binding sites does “capture” of platelet adhesion depend on?

A

Subendothelial molecules of vWF and collagen

Platelet surface receptor Glycoprotein Ib (GPIb)

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37
Q

Glycoprotein Ib

A

Platelet surface receptor
Makes cells “sticky”
Low-affinity interaction with vWF, binds easily

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38
Q

What holds vWF in place?

A

vWF binding to subendothelial collagen

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39
Q

What happens when platelet GPIb interacts with vWF?

A

Transmembrane Signaling; which coupled with high shear stress results in activation of the platelet.

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40
Q

What happens when a platelet is activated?

A

Platelet loses normal discoid shape
Plt receptor GPIIb/IIIa undergoes calcium-dependent conformational change
GPIIb/IIIa binds with vWF (high-affinity)/or fibrinogen
Collagen binds w. plt receptor GPIa/IIa
Collagen binds w. plt receptor GPIV –> activation

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41
Q

What kind of bond is GPIb and vWF?

A

Low affinity interaction

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42
Q

What kind of bond is GPIIb/IIIa and vWF?

A

High affinity bond

43
Q

Subendothelial collagen bond with GPIa/IIa

A

at medium shear stress strong enough to bind platelet to subendothelium

44
Q

What are the goals of platelet activation?

A

Recruit of additional platelets
Vasoconstriction of smaller arteries
Local release of ligands needed for stable platelet-platelet matrix
Localization and acceleration of platelet-associated fibrin formation
Protection of clot from fibrinolysis

45
Q

What do activated platelets release?

A

Thromboxane
Serotonin
ADP

46
Q

Thromboxane A2 (TXA2) and where is it formed?

A

Platelet agonist and vasconstrictor
Formed in cytosol following cyclooxygenase cleavasge of arachidonic acid (cyclooxygenase activity irreversibly inhibited by aspirin-no TXA2 formation)

47
Q

What will irreversibly inhibit cyclooxygenase activity?

A

Aspirin

48
Q

Serotonin

A

release from platelet granules

platelet agonist and vasoconstrictor

49
Q

Adenosine Diphosphate (ADP)

A

release from platelet granules; platelet agonist no known vasoactive role

Strong recruiter and activator of platelets

50
Q

Why should you not use platelet gel on coronary arteries?

A

Induce profound arterial constriction

Grafts will shut down, st segements go up and induce a heart attack

51
Q

Where are fibrinogen and vWF stored?

A

Alpha-granules within platelet

Release following activation

52
Q

What creates a tight matrix between the platelets?

A

Fibrinogen and vWF bonds form between platelets

53
Q

How many GPIIb/IIIa receptors are present on the platelet surface?

A

More than 50,000

Additional receptor molecules are available within cytoplasm

54
Q

What are some additional clotting factors?

A 
Prekallikein
High molecular weight kininogen
AT; ATIII
Lipoprotein-associated coag inhibitor (extrinsic pathway inhibitor)
Antiplasmin
Plasminogen activator inhibitor
Alpha2-Macroglobulin
Protein C
Protein S
55
Q

What is an extrinsic pathway inhibitor example?

A

Lipoprotein-associated coagulation inhibitor

56
Q

When is the termination system initiated to disrupt the clotting process and the clot itself?

A

As the fibrin clot is being formed

57
Q

4 autologous anticoagulants that help control the spread of coagulation activation

A 
Tissue Factor Pathway Inhibitor (TFPI)
Protein C (PC)
Protein S (PS)
Antithrombin III (AT or ATIII)
58
Q

What does TFPI do?

A

Forms a quarternary complex called TF/FVIIa/FXa/TFPI which inactivates various factors and limits coagulation

59
Q

What do proteins C and S do?

A

Proteins C and S inactivate FVa and FVIIIa cofactors

S is a helper; makes C work better

60
Q

Protein C

A

Vitamin K-dependent plasma glycoprotein which helps break down FVa and FVIIIa

61
Q

How is Protein C activated?

A

Thrombin (negative feedback loop?) and its activity is increased by PS (which is also vitamin K-dependent)

62
Q

What does AT do?

A

Inhibits thrombin and the Serine Proteases such as FIXa, FXa, FXIa, and FXIIa

63
Q

Examples of Serine Proteases

A

FIXa, FXa, FXIa, and FXIIa

64
Q

What signals the fibrinolytic phase of coagulation?

A

The production of plasmin

65
Q

How is plasmin produced?

A

Produced from zymogen plasminogen by the urokinase-type activator (uPA) and tissue-type plasminogen activator (tPA)

66
Q

How are uPA and tPA regulated?

A

Regulated by plasminogen activator inhibitors 1 and 2 (PAI-1 and PAI-2)

67
Q

What activates tPA?

A

Thrombin and venous occlusion (negative feedbackloop)

Released by endothelial cells

68
Q

Fibrin Degradation Products

A

Cleaved fibrin result
FDPS; Fibrin split products
Measured to determine DIC, amt of fibrinolysis occurring

69
Q

What activates Plasminogen to turn into Plasmin?

A

Extrinsic: tPA, uPA
Intrinsic: FXIIa, HMWK, kallikrein
Exogenous: streptokinase

70
Q

Endothelial Cells as Endogenous Anticoagulant

A

Negative charge repels platelets
Release NO and prostacyclin (PGI2) which inhibit platelet adhesion and aggregation
Release ADPase

71
Q

Nitric Oxide

A

Endothelium- derived relaxant factor

72
Q

ADPase

A

inactivates platelet released ADP limiting ability to recruit other platelets

73
Q

Effects of coag on CPB

A

Bleeding
Circuit Integrity
Inflammation
Disease state of patient

74
Q

Bleeding on CPB

A

Bad outcome; increased cost; increase exposure to blood products; increased chance of infection

75
Q

Circuit integrity on CPB

A

large foreign surface stimulates coagulation cascade; concerned with coagulation monitoring, treatment of circuit surface/protocols

76
Q

Inflammation on CPB

A

coagulation cascade will stimulate inflammation activities

77
Q

what patient conditions will affect coagulation status?

A

Diabetes; liver disease, DIC, obesity, sepsis

78
Q

Effects of CPB on Coagulation

A

Activates intrinsic and extrinsic coagulation pathways
Activates neutrophils and monocytes–>leukocytes
Expose subendothelium–> coagulation
Platelet activation
Vascular endothelial cell activation

79
Q

Coronary Suction on Bypass

A

introduces TF form damanged cells

Activates extrinsic pathway

80
Q

Negatively Charged Surface affect on Bypass

A

Activates intrinsic pathway

Activates fibrinolysis–> complement system

81
Q

What causes bleeding?

A 
Mechanical
Insufficient fibrin formation
Insufficient clot integrity
Insufficient clot adhesion
Fibrinolysis
82
Q

Antiplatelet agent

A

Aspirin (treats stroke/thrombosis)

83
Q

Antithrombin agent

A

heparin, warfarin (treats DVT)

84
Q

Gold standard for measuring soluble coagulation

A

PT (guide warfarin dosing) and aPTT (guide heparin dosing)

85
Q

How much of total thrombin generated during clotting process occurs in the propagation phase?

A

96%

86
Q

Most common lab test of soluble coagulation measure kinectics of what phase only?

A

Initiation Phase; even though most thrombin is generated in the propagation phase

87
Q

In PT and aPTT, the appearance of fibrin gel indicates what percent completion of the total reaction?

A

<5%

88
Q

Intrinsic Tenase Complex composed of what factors

A

FVIIIa/IXa complex

89
Q

Hemophilia A

A

Lacks FVIII

90
Q

Hemophilia B

A

Lacks FIX

91
Q

Extrinsic Tenase Complex composed of what factors

A

TF/VIIa complex

92
Q

Extrinsic Tenase vs Intrinsic Tenase Efficacy

A

Intrinsic Tenase shows 50-fold increase in efficacy than extrinsic tenase generation

93
Q

Rxn on platelet membrane vs free proteases

A

Assembly of entire rxn on platelet confers 13-million fold increase in catalytic efficiency over proteases free in solution

94
Q

Prothrombinase promotes prothrombin activation rate enhancement ________fold > free FXa on prothrombin

A

300,000 fold

95
Q

What is the rate-limiting reagent in prothrombin cleavage? (Forming thrombin)

A

Platelet Bound FXa

96
Q

In vitro, platelets must drop how much before prolongation in time of clot formation?

A

< 10,000/uL

97
Q

In surgery, thrombocytopenia can produce arterial bleeding at higher platelet counts of how much?

A

~50,000/uL

98
Q

Shear rates at ateriosclerotic plaques of 50% stenosis reach ….?

A

3,000 to 10,000/sec

99
Q

Platelets circulate for how many days?

A

7 to 10 days

100
Q

Bernard-Soulier Syndrome

A

deficient in platelet receptor GPIb, 50% receptor density

101
Q

What is the major adhesive ligand participating in matrix formation in venous clots?

A

Fibrinogen

102
Q

_____% of fibrin stabilizing activity in blood resides in platelets released at sites of bleeding.

A

50%

103
Q

disintegrins

A

compete with fibrinogen and vWF for binding sites on platelet GPIIb/IIIa receptors; platelet anesthetic

CV Perf Tech II (17 decks)

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