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Topic 1 Flashcards

1
Q

Homeostasis

A

Normal blood circulation is maintained by a system of checks and balances

  • preservation of blood fluidity
  • ability to seal off any site of bleeding
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2
Q

Anticoagulant factors are released by

A

Endothelial cells
(prostacyclin, vascular plasminogen activator)
-These tend to be released from the lining of the vascular garden hose

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3
Q

Procoagulant factors include

A

platelets and plasma proteins – inactive state (zymogen)

-These tend to be released when the lining of that vascular garden hose gets disrupted

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4
Q

Three Phase Model includes

A

Initiation
Amplification
Propagation

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5
Q

Phase I: Initiation- In vivo

A

The activity of the FVIIa/TF (Tissue Factor) complex is THE most significant event to initiate coagulation

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6
Q

Phase I: Initiation-

Activation of FVII

A

Vascular damage exposes TF (a membrane-bound protein) to plasma. TF is both a receptor and cofactor for FVII. When the zymogen FVII binds TF it converts to FVIIa and forms the FVIIa/TF complex.

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7
Q

Phase I: Initiation-

After the FVIIa/TF complex activates the FIX and FX zymogens…. then…

A

FXa formed on the TF-bearing cell interacts with cofactor Va to form a prothrombinase complex and generates a very small amount of “priming” thrombin on the surface of TF-bearing cells. FXa remains on the cell surface

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8
Q

Phase I: Initiation-

When does FIXa not interact further with the TF-bearing cell and is no longer involved in Phase I: Initiation

A

After the priming thrombin is formed.
However, if tissue injury occurrs and activates near by platelets, FIXa will diffuse to those platelets, bind to their surface, and (in conjunction with cofactor VIIIa) activate zymogen FX to FXa

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9
Q

Phase I: Initiation-

TF-bearing cells appear to bind to

A

FVIIa and low levels of FIXa and FXa even in the absence of injury but are separated from the Phase II: Amplification components by the normally intact blood vessel wall.

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10
Q

Whats the signal for Phase II: Amplification

A

The thrombin generated on the TF-bearing cell serves as the “signal” for Phase II: Amplification to begin

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11
Q

Phase II: Amplification-

When sufficient thrombin (FIIa) is generated on or adjacent to TF-bearing cells…then…

A

platelets are activated

NOTE: At this point there is not nearly a sufficient amount of thrombin to cause formation of a clot

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12
Q

Phase II: Amplification-

The small amount of TF-bearing cell-generated thrombin activates…

A

Activates platelets
Activates FVa from FV
Activates FVIIIa and dissociates it from vWF
Activates XIa from XI

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13
Q

Phase III: Propagation-

First step is…

A

The production of vast amounts of thrombin on the surface of activated platelets

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14
Q

Phase III: Propagation-

When vascular injury occurs, platelets leave the blood vessel…then…

A

bind to collagen/vWF/blood vessel wall receptors and are activated by a combination of those factors and the “priming” dose of thrombin
-This adherence of platelets to the damaged tissue is the first step in the formation of the platelet “plug” necessary for primary hemostasis

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15
Q

Phase III: Propagation-

The newly-activated platelets bind to…

A

FVa and FVIIIa

FIXa is freshly-liberated by the FVIIa/TF complex

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16
Q

Phase III: Propagation-

Freshly-generated XIa binds to…

A

the freshly-activated platelet (effectively bypassing the need for FXIIa). Membrane-bound FXIa keeps on activating FIX to FIXa

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17
Q

Phase III: Propagation-

FVIIIa and co-factor FIXa form

A

platelet tenase complex (PTC)

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18
Q

Phase III: Propagation-

The PTC activates even more…

A

FX to FXa.

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19
Q

Phase III: Propagation-

FXa combines with FVa to form

A

Prothrombinase complex

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20
Q

Phase III: Propagation-

The XaVa “Prothrombinase” complex causes…

A

the EXPLOSIVE burst of thrombin that helps produce a stable fibrin clot

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21
Q

Arterial circulation requires

A

rapid response system to seal off any bleeding sites.

-platelets take leading role followed by fibrin formation

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22
Q

Venous circulation has a

A

slower response.

-rate of thrombin generation takes leading role

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23
Q

Arterial circulation uses what to prevent coronary thrombosis

A

antiplatelet agents

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24
Q

Venous circulation uses what to prevent deep venous thrombosis

A

antithrombin agents

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25
Q

What Happens When An Arterial Blood Vessel Is Damaged? (7)

A
  1. Vascular constriction
  2. Platelet adhesion
  3. Platelet activation- formation of the platelet plug
  4. Activation of cell-based coagulation cascade- formation of fibrin clot
  5. Clot retraction
  6. Activation of fibrinolytic cascade
  7. Vessel repair / regeneration
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26
Q

Vascular Constriction is seen when

A

blood vessel itself is injured

-persistent constriction of the smooth muscles

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27
Q

Vascular Constriction is most prominent following

A

severe crushing type injuries

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28
Q

Describe the smooth muscle layers typically found in blood vessels

A
  1. Tunica Intima -contains the endothelium
  2. Tunica Media- circularly arranged smooth muscle cells and sheets of elastin. Maintains blood pressure and continuous blood circulation
  3. Tunica Externa- loosely woven collagen fibers
    protect and reinforce the vessel, and anchor it to surrounding structures
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29
Q

Main Platelet Adhesion - PROBLEM

A

Shear stress along vessel wall

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30
Q

Shear stress inversely related to

A

flow velocity

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31
Q

Shear stress values at vessel wall for large arteries

A

500/sec

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32
Q

Shear stress values at vessel wall for arterioles

A

5,000/sec

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33
Q

Shear stress opposes any tendency of flowing blood to clot because it

A
  1. limits time available for procoagulant reactions to occur

2. displaces cells or proteins not tightly bound to the vessel wall

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34
Q

Platelets are able to adhere to cell walls despite shear stress because

A

platelets are pushed to vessel perimeter by larger erythrocytes & leukocytes (coaxial migration)

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35
Q

Platelet Adhesion-

Adhesion must occur very

A

rapidly – i.e. instantaneously

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36
Q

Platelet Adhesion-

“Capture” depends on several binding sites:

A
  • subendothelial molecules of vWf and collagen

- platelet surface receptor: Glycoprotein Ib (GPIb)

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37
Q

Platelet Adhesion-

vWf is held in place by binding to

A

subendothelial collagen

38
Q

Platelet Adhesion-

GPIb binds easily with

A

vWf, but it is a low-affinity interaction

- - Slows, but does not stop the platelet – tumbles slowly over endothelium

39
Q

Platelet Adhesion-

Interaction between platelet GPIb and the vWf molecule causes

A

transmembrane signaling

40
Q

Platelet Adhesion-

Transmembrane signaling coupled with high shear stress results in

A

activation of the platelet

41
Q

After platelet activation, the platelet loses

A

normal discoid shape

42
Q

Platelet activation-

Platelet receptor GPIIb/IIIa undergoes

A

conformational change

43
Q

Platelet activation-

GPIIb/IIIa now able to bind to another binding site on…

A

vWf

  • high-affinity bond that secures activated platelet to subendothelium
  • (GPIIb/IIIa site of action of newer antiplatelet agents)
44
Q

Platelet activation-

Subendothelial collagen binds with…

A
  1. platelet receptor GPIa/IIa-at medium shear stress strong enough to bind platelet to subendothelium
  2. platelet receptor GPIV which causes activation of the platelet
45
Q

Platelet Activation - Goals (5)

A
  1. Recruitment of additional platelets
  2. Vasoconstriction of smaller arteries
  3. Local release of ligands needed for stable platelet-platelet matrix
  4. Localization and acceleration of platelet-associated fibrin formation
  5. Protection of clot from fibrinolysis
46
Q

Activated platelets release

A

platelet agonists

47
Q

3 platelet agonists

A 
Thromboxane A2 (TXA2)
Serotonin
Adenosine diphosphate (ADP)
48
Q

Thromboxane A2 (TXA2)

A

platelet agonist and vasoconstrictor

  • formed in cytosol following cyclooxygenase cleavage of arachidonic acid
  • cyclooxygenase activity irreversibly inhibited by aspirin= no TXA2 formation
49
Q

Serotonin

A

released from platelet granules - platelet agonist and vasoconstrictor

50
Q

Adenosine diphosphate (ADP)

A

released from platelet granules - platelet agonist no known vasoactive role

51
Q

Formation of Platelet Plug-

Surface receptor GPIIb/IIIa undergoes

A

calcium dependent conformational change

-able to bind with fibrinogen or vWf

52
Q

Formation of Platelet Plug-

Fibrinogen and vWf stored in…

A

alpha-granules within platelet – released following activation

53
Q

Formation of Platelet Plug-

Fibrinogen and vWf bonds form between

A

platelets binding them together in a tight matrix

54
Q

Formation of Platelet Plug-

More than ______ GPIIb/IIIa receptors present on platelet surface

A

50,000

– additional receptor molecules available within cytoplasm

55
Q

Clotting Factor I

A

Fibrinogen

56
Q

Clotting Factor II

A

Prothrombin

57
Q

Clotting Factor III

A

Tissue thromboplastin

58
Q

Clotting Factor IV

59
Q

Clotting Factor V

A

Proaccelerin

Labile factor

60
Q

Clotting Factor VII

A

Proconvertin

Stable factor

61
Q

Clotting Factor VIII

A

Antihemophilic factor A

62
Q

Clotting Factor IX

A

Plasma thromboplastin component
Antihemophilic factor B
Christmas factor

63
Q

Clotting Factor X

A

Stuart factor

Stuart-Prower

64
Q

Clotting Factor XI

A

Plasma thromboplastin antecedent

Antihemophilic factor C

65
Q

Clotting Factor XII

A

Hageman factor

Antihemophilic factor D

66
Q

Clotting Factor XIII

A

Fibrin stabilizing factor

Laki-Lorand factor

67
Q

Additional Clotting Factors (9)

A
  1. Prekallikrein
  2. High-molecular-weight kininogen
  3. Antithrombin; Antithrombin III
  4. Lipoprotein-associated coagulation inhibitor (extrinsic pathway inhibitor)
  5. Antiplasmin
  6. Plasminogen activator inhibitor
  7. alpha2-Macroglobulin
  8. Protein C
  9. Protein S
68
Q

Phase IV: Termination-

4 autologous anticoagulants help control the spread of coagulation activation

A
  1. Tissue Factor Pathway Inhibitor (TFPI)
  2. Protein C (PC)
  3. Protein S (PS)
  4. Antithrombin III (AT or AT-III)
69
Q

Phase IV: Termination-

TFPI forms a quarternary complex called the

A

TF/FVIIa/FXa/TFPI which inactivates various factors and limits coagulation

70
Q

Phase IV: Termination-

Proteins C and S inactivate

A

FVa and FVIIIa cofactors

71
Q

Phase IV: Termination-

PC is a

A

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

72
Q

Phase IV: Termination-

PC is activated by

A

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

73
Q

Phase IV: Termination-

AT inhibits thrombin and the

A

“Serine Proteases”-such as FIXa, FXa, FXIa, and FXIIa

74
Q

Fibrinolysis-

What signals the Fibrinolytic phase of coagulation

A

The production of plasmin

75
Q

Fibrinolysis-

Plasmin is produced from the zymogen plasminogen by the action of

A

urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA)

76
Q

Fibrinolysis-

uPA & tPA are regulated by

A

Plasminogen Activator Inhibitors 1 & 2 (PAI-1 & PAI-2)

77
Q

Fibrinolysis-

tPA is released by

A

endothelial cells and activated by thrombin (negative feedback loop) and venous occlusion

78
Q

Fibrinolysis-

tPA and plasminogen bind to the

A

growing fibrin polymer as fibrinogen (FI) is converted into fibrin (Fia)

79
Q

Fibrinolysis-

plasminogen is activated to

A

plasmin which cleaves fibrin strands

80
Q

Fibrinolysis-

Cleaved fibrin produces

A

Fibrin Degradation Products (FDPs or Fibrin Split Products)

81
Q

Fibrinolysis-

FDPs are measured to help determine the

A

amount of fibrinolysis occurring

82
Q

Endogenous Anticoagulants

A

Prevent clotting – keep blood liquid

Require intact endothelial cell barrier

83
Q

endothelial cells negative charge repels

84
Q

endothelial release of _______ – inhibit platelet adhesion and aggregation

A

nitric oxide (endothelium-derived relaxant factor) & prostacyclin (PGI2)

85
Q

endothelial release of ______ – inactivates platelet released ADP limiting ability to recruit other platelets

86
Q

Effect of Bypass/Surgery on Coagulation:

Activates what pathways

A

intrinsic and extrinsic coagulation pathways

  1. large negatively charged surface activates intrinsic pathway (which also activates fibrinolysis which activates complement)
  2. coronary suction introduces tissue factor from damaged cells which activates the extrinsic pathway
87
Q

Effect of Bypass/Surgery on Coagulation:

Activates what cells

A

neutrophils and monocytes

-activation of complement cascade results in leukocyte activation

88
Q

Effect of Bypass/Surgery on Coagulation:

Surgery will expose the

A

Subendothelium

-stimulates coagulation

89
Q

Effect of Bypass/Surgery on Coagulation:

Platelet activation

A

contact with foreign surface of the circuit

activation of intrinsic and extrinsic pathways

90
Q

Effect of Bypass/Surgery on Coagulation:

_______ cell activation

A

Vascular endothelial

Perf Tech (8 decks)

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