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Pathology > Exam 1: Hemostasis > Flashcards

Exam 1: Hemostasis Flashcards

1
Q

what are the basic events in normal clot formation after initial blood vessel injury

A 
vasoconstriction
platelet adhesion
platelets undergo conformation change
platelet aggregation
clotting (coagulation) pathways activate
formation of fibrin meshwork
resolution of clot formation through fibrinolysis
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2
Q

vasoconstriction occurs from release of _____

A

endothelin by endothelial cells

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3
Q

vasoconstriction decreases ______

A

blood flow (but cant stop blood loss)

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4
Q

vasoconstriction brings _______ to the site of injury

A

platelets and coagulation factors (tissue factor exposure for clotting activation)

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5
Q

what facilitates the binding of platelet (platelet adhesion)

A

exposure of subendothelial collagen following injury

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6
Q

binding is greatly enhanced by

A

von Wellebrand factor (vWF), especially in high flow rate blood vessels

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7
Q

where is vWF stored

A

in endothelial cells and platelets and circulates in blood stream bound to factor VIII

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8
Q

platelets undergo conformation change and release what?

A

stored products in their granules such as Ca, ADP, vWF, thromoxane A2, epinephrine, platelet activating factor

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9
Q

what do these products do

A

activate platelets

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10
Q

the conformation change also exposes ______

A

fibrinogen binding sites

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11
Q

fibrinogen binding sites are important for what

A

platelets to bind to other platelets

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12
Q

in the conformation change, there is a change in platelet membranes that expose

A

specific platelet phospholipids that are important in activation of the clotting cascade

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13
Q

more platelets stick to site of injury by binding to each other via

A

fibrinogen (important in the platelet plug)

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14
Q

clotting activation ocurs quickly after initial vascular injury by exposure of _____ which activates clotting cascade and eventual formation of thrombin

A

tissue factor

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15
Q

thrombin, in turn, cleaves _____ which is vital to the formation of this stabilized clot

A

fibrinogen to fibrin

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16
Q

______ is incorptated into the platelet mass to hold/glue the clot together, forming the ______

A

fibrin; fibrin meshwork

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17
Q

the process of the fibrin meshwork ______ clot formation

A

stabilizes

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18
Q

resolution of clot fomration occurs through

A

fibrinolysis

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19
Q

fibrinolysis is mediated throguh

A

plasmin following activation from plasminogen

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20
Q

must maintain appropriate balance of clot resolution vs. clot retention or will have

A

hemorrhage or thrombosis depending on the imbalance

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21
Q

blood vessel endothelium has what kind of properties

A

anticoagulant and procoagulant properties

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22
Q

what is the lifespan of platelets

A

about 7-10 days

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23
Q

in high shear blood vessels, platelets bind to

A

vWF that has adhered to subendothelial collagen in damaged high shear blood vessels

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24
Q

in low shear blood vessles plateelets bind to

A

directly to collagen or fibronogen that has bound to collagen in the damaged vesssel

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25
Q

after binding to the site of injury, platelets undergo ____

A

conformational changes

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26
Q

what do these confomration changes do?

A

enhance platelet to platelt binding by interaction with fibrinogen
expose membrane phospholipids which initiate clooting factor pathways
releases stored products from granules

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27
Q

thromboxane TxA2 causes what

A

vasoconstriction and platelet aggregation

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28
Q

TxA2 inhibited by

A

aspirin

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29
Q

Ca increased after _____ release

A

TxA2

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30
Q

Ca is essential for

A

clotting factor pathways, contractile elements of platelts

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31
Q

where are the clotting pathways with formation of fibrin and fibrin cross-links essential?

A

after loose plug is formed, it must become stronger with stronger interactions

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32
Q

are factors numbered in order of activation?

A

no

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33
Q

is there a factor VI

A

no

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34
Q

factor I

A

fibrinogen

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35
Q

factor II

A

prothrombin

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36
Q

factor III

A

tissue factor

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37
Q

factor Ia

A

fibrin

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38
Q

factor IIa

A

thrombin

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39
Q

factor IV

A

Ca

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40
Q

factor V through factor

A

XIII

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41
Q

factor XIII

A

fibrin stabilizing factor

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42
Q

what factors require vitamin K for synthesis

A

II, VII, IX, X, protein C and S

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43
Q

where does vitamin K work?

A

x

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44
Q

most clotting factors are produced by the

A

liver

45
Q

what factors are the only ones without enzymatic like activity

A

V and VIII and IV

46
Q

what does this mean for these factors that have enzymatic activity

A

not necessarily consumed in the reaction ot activate the clotting pathway

47
Q

so factors V and VIII are

A

consumed and have a risk of depletion if the liver cant keep up production levels

48
Q

what are the two classical methods of clotting pathways

A

classical (in-vitro) or Y model

Cell-based or in-vivo model

49
Q

in secondary hemostasis, what is needed for all stages?

A

calcium

50
Q
  1. after injury to vascular endothelium, the exposure of ____ on cells beneath the endothelium initiates the hemostatic reaction
A

tissue factor

51
Q

what is the only relevant activator of hemostatic pathwayss in real life

A

tissue factor

52
Q

tissue factor is expressed on what membranes

A

subendothelial fibroblasts, smooth muscle cells, other stromal cells and monocytes

53
Q

______ then binds to tissue factor on the membrane of one or more of these cells to allow the formation of the extrinsic tenase complex

A

factor VIIia

54
Q

what is the only factor that circulates in the blood in active form

A

factor VIIa (although only 1% is in active form)

55
Q

what does the activated factorVIIa/TF complex do

A

activates more factor VII and VIIa, which will bind more TF and form more extrinsic tenase complexes

56
Q

extrinsic tenase complexes now promotes _____

A

circulating factor X to bind and become activated to factor Xa

57
Q

circulating factor V can now bind to the complex and become

A

factor Va by factor Xa

58
Q

this activation is very ______ at this point

A

slow and inefficient

59
Q

V to Va is much more dependent on _____ for activation

A

thrombin

60
Q

small amounts of circulating _______ can also bind to the complex and become activated to _____

A

factor IX, IXa

61
Q

this complex is now composed of

A

tissue factor, Ca, factors VIIa, Xa, Va, IXa

62
Q

this complex with these factors is now called

A

1st prothrombinase complex

63
Q

1st prothrombinase complex main purpose is to

A

allow binding and activation of prothrombin to thrombin

64
Q

thrombin at this point will begin to perform its multitude of functions to include

A

activating platelets, cleaving circulating factor VIII from vWF that in turn allows activation of factor VII, activataing circulating factor V, activating circulating factor XI and cleaving fibrinogen to fibrin

65
Q

only a small amount of prothrombin is activated to thrombin at this point, and if the reaction does not proceed to amplification stage of hemostasis, what will happen to the clot

A

will not form properly

66
Q

what is the key to amplification step of secondary hemostasis

A

dissociation of some factor IXa from the 1st prothrombinase complex

67
Q

why does this dissociation occur?

A

because some factors are not tightly bound to the copmplex and can dissociate

68
Q

factor xa usually stays associated with the 1st prothrombin complex, but if it dissociates _____ or ______ can quickly break it down

A

antithrombin or tissue factor pathway inhibitor (TFPI)

69
Q

once factor ixa dissociates from the 1st prothrombin complex, it is free to bind to

A

adjacent platelet membrane phospholipid

70
Q

factor ixa is subject to degradation by

A

minimally by antithrombin

71
Q

factor ixa is now available to bind with factor viiia on the surface of

A

platelet membrane

72
Q

foactor viia becomes activated when

A

thrombin that was generated from 1st prothrombinase coplex cleaves circulating ffactor vii from vwf at the site of injury

73
Q

the combination of factor viia, ixa, ca and platelet membrane is called

A

intrinsic tenase complex

74
Q

intrinsic tenase complex is responsible for

A

binding and accelerating the formation of factor x to xa on the surface of platelets which previously was limited to the tissue factor/viia site

75
Q

once intrinsic tenase complexs are adequately functioning on the surface of platelets, what happens to the extrinsic tenase complex

A

become relatively insignificant and are shutdown primarily by TFPI

76
Q

at this point the reaction is ready to proceed to the second phase of amplification process with the formation of the

A

2nd prothrombinase complex

77
Q

once factor xa has been generated, factor _____ must be incorporated into the complex in order for factor xa to optimally function

A

va

78
Q

factor va has arlready been generated from

A

thrombin that was produced by the end product of the 1st prothrombinase complex

79
Q

incorporation of factor Va, platelet membranes, Ca, factor IXa, factor VIIIa, and factor Xa make up the

A

2nd prothrombinase complex

80
Q

this complex is now ready to activate ____ into _____

A

thrombin into prothrombin

81
Q

which prothrombinase complex is higher for thrombin generation

A

2nd

82
Q

during the course of this entire process, circulating _____ has been incorporated into the platelet mass; as well as

A

fibrinogen; binding platelets to platelets

83
Q

high thrombin gneration is now responsible for

A

cleaving fibrinogen to fibrin and surrounding the clot

84
Q

to stabilize the clot, thrombin activates what

A

circulating factor XIII to XIIIa

85
Q

XIIIa does what

A

cross-links fibrin within the clot to strengthen it

86
Q

at this point, thrombin is being generated by 2nd and will continue to be produced until

A

the reaction is shut down

87
Q

thrombin strongly activates platelets, causing them to do what

A

release granules and alter their outer phospholipid membranes to expose phosphatidylserine (PS)

88
Q

how does thrombin generate VIIIa and free vWF

A

activates factor V to Va and cleaves the circulating bound proteins factor VIII/vWF

89
Q

thrombin activates

A

factor XIII to XIIIa

90
Q

thrombin is a _____ for leukocytes

A

chemo-attractant

91
Q

after the clot has formed, what must be done

A

clotting pathways must be inactivated

92
Q

inactivation of the pathays occurs by what methods

A

tissue factor pathway inhibitor
antithrombin
thrombomodulin

93
Q

TFPI is produced and stored in

A

endothelial cells (also stored in plateles)

94
Q

TFPI primarily does what

A

inactivates factor VIIa and factor Xa, thrombin to a lesser degree

95
Q

antithrombin does what

A

inativates factor IIa and Xa, But also prefers

96
Q

thrombomodulin

A

small molecule produced on the endothelial surface combines with thrombin to perform actions

97
Q

heparin sulfate molecules and exogenous heparin do wha

A

amplify antithrombin to maximize degradation of actor IIa and factor Xa

98
Q

thrombomodulin and trhombin active ______ then in conjunctive with proein S. inactivates ncativation factor Va, and VIIIa

A

exogenous hyperia

99
Q

lastly, what happens to the clot

A

it must be broken down to prevent thrombosis and without causing hemorrhage (fibrinolysis)

100
Q

diruing initial clot formation, endothelial cells release

A

plasminogen activator inhibitor

PIa-1

101
Q

PAI-1 does wht

A

prevents the activation of plasminogen to plasmin

102
Q

as the clot stablizies and endothelial cells being healing, the endothelium releases

A

tiue plasminogen activator (t-pa)

103
Q

t-PA does what

A

converts plasminogen to plasmin

104
Q

what is plasminogen

A

a protein produced by the liver that circulates in the plasma and becomes incorporated with the clot but doesnt have any fibrinolytic activity until activated to plasmin

105
Q

t-pa does not convert plasminogen to plasmin unless ______ is also present

A

fibrin or cross-linked fibrin (generally does not occur until clot has stabilized)

106
Q

certain drugs or compounds can convert plasminogen to plasmin such as

A

urokinase or streptokinases

107
Q

if plasmin is released into the plasma

A

alpha2-anthiplasmin (antip-plasmin) will inactivate it unless the system is overwhelemed

108
Q

____ cells eventually move into and remove much of the material from the clot and normal resolution, the blood vessel heals normally and restores blood flow

A

phagocytic cells

Pathology (17 decks)

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