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M2 Hematology > 7. Hemostasis/Coagulation > Flashcards

7. Hemostasis/Coagulation Flashcards

1
Q

components needed for hemostasis?

A
  • vessel wall/vascular endothelium
  • platelets
  • plasma coag proteins
  • physiologic protease inhibitor
  • endogenous anticoagulants
  • fibrinolytic system
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2
Q

primary hemostasis forms what

A

platelet plug

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3
Q

secondary hemostasis forms what

A

fibrin. coagulation step

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4
Q

overall steps of hemostasis?

A

primary hemostasis, secondary hemostasis, termination of coag reactions, fibrinolysis

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5
Q

what happens when the endothelium is disturbed (by injury, inflammation)?

A

shifts it from an anticoagulant to a procoagulant phenotype.

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6
Q

when not injured, vascular endothelium is procoag or anticoag?

A

anticoag.

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7
Q

besides shifting the endotheluim from anticoag to procoag, what does injury do?

A

exposes subendothelium, which is PROcoag.

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8
Q

what effect does collagen have on coagulation?

A

stimulus for platelet adhesion, activation

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9
Q

what is the very first step of primary hemostasis?

A

vasoconstriction, reduces blood flow to injured area. then formation of platelet plug.

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10
Q

what are the main things required for a platelet plug?

A

von willebrand factor
platelets
fibrinogen

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11
Q

where is vWF synthsized?

A

endothelial cells and megakaryocytes (bone marrow)

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12
Q

where is vWF stored?

A

in endothelial cells: in Weibel Palade bodies

in platelets, in alpha granules

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13
Q

what does ADAMTS-13 do?

A

cleaves vWF into smaller multimers in plasma

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14
Q

3 jobs for vWF?

A

attaches platelets to subendothelium with vascular injury
carries F VIII in blood, prolongs circulating half-life
localizes F VIII at site of injury

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15
Q

where do platelets come from?

A

megakaryocyte (bone marrow). buds from mature megakaryocytes become platelets in circulation

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16
Q

platelets: lifespan in blood?

A

7-10 days

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17
Q

platelet function in blood vessel injury?

A

adhesion
activation/degranulation
aggregation
support coagulation (fibrin)

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18
Q

fibrinogen: synthesized wehre?

A

liver

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19
Q

fibrinogen: role in primary hemostasis?

A

forms bridges between platelets during formation of platelet plug

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20
Q

fibrinogen: role in secondary hemostasis?

A

polymerizes into insoluble mesh around platelets

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21
Q

what receptor connects vWF to platelets?

A

Gp1b

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22
Q

name the elements of a platelet plug from the most internal to the most external

A 
collagen
vWF
Gp1b receptor
platelet
Fibrinogen (GpIIa/IIIb receptors)
PS/PE
coag factors
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23
Q

vWF binds what to what in a platelet plug? using what receptor?

A

collagen to platelet. receptor Gp1b

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24
Q

what prompts the activation/degran of platelets?

A

collagen, soluble agonists (such as epinephrine)

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25
Q

what happens once platelets are activated?

A

-develop pseudopods and degranulate

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26
Q

what 2 types of granules are involved in platelet degranulation?

A

alpha granules

dense granules

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27
Q

what’s in alpha granules?

A 
adhesive proteins (fibronectin, vWF)
coag proteins (fibrinogen, FV)
growth factors
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28
Q

how does Thromboxane A2 enter the picture? where does it come from?

A

secreted by activated platelets

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29
Q

what does Thromboxane 2 do?

A

vasoconstriction, platelet aggregation & activation

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30
Q

when platelets aggregate, what holds them together? what receptor?

A

fibrinogen tethers them together, using receptor GpIIb/IIIa

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31
Q

what agonists stimulate platelets to aggregate?

A

ADP, epinephrine, collagen, thrombin, serotonin, Thromboxane A2

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32
Q

how do platelets support coagulation?

A

exposure of phosphatidyl serine (PS) and PE on platelet surface allows coag factors to bind to surface.

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33
Q

what is the exposure of PS/PE on platelet surface called?

A

platelet factor 3 (PF3) activity.

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34
Q

defect in PF3 is known as what?

A

Scott syndrome

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35
Q

secondary hemostasis is dependent on what ion?

A

calcium!!

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36
Q

what does fibrin look like?

A

spaghetti

37
Q

what is the ultimate goal of the coagulation cascade?

A

conversion of fibrinogen to fibrin

38
Q

where are most coag factors synthesized?

A

liver

39
Q

where is FVIII syntheisized?

A

both liver and vasc endothelium

40
Q

where is vWF synth?

A

megakaryocytes (bone marrow) and vasc endothelial cells

41
Q

which coag factors are dependent on Vit K?

A

2, 7, 9, 10

42
Q

what anticoag factors are dep on Vit K?

A

Protein S, C, Z

43
Q

what happens to monocytes in response to vasc injury?

A

stimulated to produce TF on cell surface

44
Q

what does TF do?

A

initiates the coag cascade with F VIIa

45
Q

draw the coag cascade…

A

on paper!

46
Q

two ways in which TF/VIIa initiates coag?

A

direct: X to Xa
indirect: IX to IXa, then X to Xa in presence of VIIIa and Ca2+

47
Q

Extrinsic pw: starts with what?

A

X to Xa

48
Q

intrinsic pw: starts with what?

A

IX to IXa

49
Q

intrinsic pw v extrinsic pw: which is more efficient?

A

INTRINSIC. by 100,000x

50
Q

overall, why do people with hemophilia bleed?

A

deficient in VIII or IX, can’t run intrinsic pw.

51
Q

what is it about the intrinsic pw that makes it more efficient?

A

uses VIIIa and Ca2+ as cofactors.

52
Q

where does F V come from, what does it do?

A

released from platelets. cofactor (with Ca2+) for prothrombin to thrombin.

53
Q

what’s the prothrombinase complex? what does it do?

A

Xa, Va, Ca2+

bindns to platelet surface, activates prothrombin –> thrombin

54
Q

where is secondary hemostasis occuring?

A

on surface of platelets

55
Q

what catalyzes fibrinogen to fibrin?

A

thrombin

56
Q

where does fibrinogen come from?

A

platelets

57
Q

what’s the Thrombin Burst?

A

thrombin activates FXI -> XIa; very efficient way to run the intrinsic pathway

58
Q

what does thrombin activate?

A

platelets, V, VIII, IX, XIII

59
Q

what factor stabilizes fibrin?

A

XIII (thirteen)

60
Q

can thrombin protect clot from fibrinolysis?

A

yes!

61
Q

can thrombin inhibit coag when needed?

A

yes!

62
Q

how does thrombin work to form/stabilize fibrin?

A

Converts fibrinogen to a monomer (fibrin) by cleaving off peptides A and B. Monomer then self-associates/polymerizes into spaghetti formation.

63
Q

4 ways that coagulation is controlled?

A
  • hemodilution
  • hepatic clearance
  • endogenous anticoagulants
  • fibrinolysis
64
Q

what is hemodilution?

A

activated coag factors are diluted by systemic circulation

65
Q

hepatic clearance in regards to control of coagulation?

A

activated coag factors are cleared by the liver

66
Q

what are 4 endogenous anticoagulants?

A

activated protein C/protein S
antithrombin
tissue factor pathway inhibitor (TFPI)
protein Z

67
Q

what does protein Z do?

A

inactivates factor Xa

68
Q

if there is much less circulation than usual, how can that effect control of coagulation?

A

may form a big clot due to absence of hemodilution.

69
Q

what are the MAJOR control points of coagulation?

A

Xa and thrombin: both controlled by anti-thrombin.

70
Q

what does anti-thrombin do (AT)?

A

inhibits Xa and thrombin.

71
Q

what does TFPI do?

A

tissue factor pathway inhibitor: inhibits VIIa and Xa

72
Q

what does APC/S do?

A

inhibits V and VIII

73
Q

where is antithrombin produced?

A

liver, endothelial cells

74
Q

what drug increases the activity of antithrombin?

A

heparin

75
Q

how does thrombin inhibit coagulation?

A

binds thrombomodulin on endothelial cells. now thrombomodulin can activate Protein C. APC and its cofactor (S) can INACTIVATE factors Va and VIIIa.

76
Q

what does APC/S do?

A

inactivates factors Va and VIIIa, thus slowing coagulation

77
Q

where is TFPI produced?

A

endothelial cells

78
Q

what does TFPI do?

A

binds/inactivates Xa. then the TFPI/Xa complex inactivates the TF/VIIa complex.

79
Q

overall process of fibrinolysis?

A

plasminogen converted to plasmin by TPA/UPA. Plasmin is the scissors that cleaves fibrin to degradation products

80
Q

what can cause deficiency in things that STOP the fibrinolytic agents? what is the state that this causes?

A

result in bleeding disorders. deficiency in PAI-1 (stops TPA), alpha-2-antiplasmin (stops Plasmin).

81
Q

plasma: definition

A

fluid fraction of unclotted whole blood. contains coag factors.

82
Q

serum: def

A

fluid remaining after blood has been allowed to clot. does NOT contain coag factors

83
Q

coag studies performed with plasma or serum?

A

PLASMA

84
Q

what does a blue top tube contain? how does that help? how are the labs performed?

A

contains citrate, which binds calcium and makes it unavailable for coag reactions. in lab, Ca is added back to make coag reactions go

85
Q

electrolytes tested in plasma or serum?

A

plasma, with heparin

86
Q

antibodies, other proteins assayed in plasma or serum?

A

serum.

87
Q

cells assayed in what form of blood? how does EDTA help?

A

whole blood. EDTA preserves morphology of cells

88
Q

what is thrombocytopenia?

A

decr platelet count

89
Q

what is associated with thrombocytopenia?

A

spontaneous bleeding, if count is lower than 10k/uL

M2 Hematology (15 decks)

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