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Pathology II > Hemodynamics Part I: hemostasis > Flashcards

Hemodynamics Part I: hemostasis Flashcards

1
Q

hemostasis occurs as the result of …

A

well regulated and balanced process of maintaining blood in a fluid state while allowing for controlled and focused clotting to prevent blood loss

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2
Q

3 general components that contribute to hemostasis

A

endothelium/vascular wall

platelts

coagulation cascade

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3
Q

sequence of clot formation (5)

A
  1. brief vasoconstriction
  2. endothelial damage exposes subendothelium casuing platelts to become activated and adhere.
  3. TF is released and activates the coagulation cascade forming fibrin
  4. platelet activation furthers coagulation
  5. fibrin and platelets form a clot thereby plugging the defect to prevent blood loss
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4
Q

factors which activate endothelium and shift the function to the procoagulant state include (4)

A

infectious agents
hemodynamic forces
cytokines
plasma mediators

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5
Q

antithrombotic mechanisms of the endothelium

A
  • acts as barrier to suendothelium
  • prostacyclin PGI2 and NO inhibit platelet aggregation (thrombin and several cytokines stimulate PGI2 and NO synthesis)
  • adenosine diphosphatase degrades ADP thereby inhibiting platelet aggregation
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6
Q

anticoagulant activites of endothelium

A
  • heparin-like molecules are cofactors to antithrombin
  • thrombomodlin converts thrombin to an anticoagulant
  • fibrinolytic (endothelial cells make tPA)
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7
Q

prothrombotic mechanisms of the endothelium

A
  • endothelial cells synthesize von Willebrand factor, which serves to firmly bind platelets to the subendothelium
  • endotoxin and some cytokines induce enothelial cells to make tissue factor
  • endothelial cells secrete plasminogen activator inhibitor
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8
Q

under normal conditions, endothelial cells inhibit platelet adherence and blood clotting

A

injury or activation of endothelial cells results in procoagulant state

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9
Q

from what do platelet cells derive?

A

magakaryocytes

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10
Q

platelet adhesion: vWF links the subenothellium to _________ on platelets

A

glycoprotein Ib receptors

this mediates firma dherence of platelets to vessel wall

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11
Q

_____- activates the platelets causing the release of their granules

A

adhesion

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12
Q

platelet granule contents

A

calcium
ADP
platelet factor 4
serotonin

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13
Q

function of calcium

A

critical coagulation cascade

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14
Q

function of ADP

A

mediates platelet aggregation which drives increasing platelet aggregation at the site (along with thromboxane)

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15
Q

function of platelet factor 4

A

binding of heparin by platelet factor 4 results in its inactivation

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16
Q

function of serotonin

A

induces vasoconstriction

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17
Q

fibrinogen links platelets via _____

A

GpIIb-IIIa

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18
Q

GpIIb - IIIa inhibitors are used to ——-

A

inhibit thrombosis

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19
Q

where does thrombin bind

A

platelet surface

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20
Q

platelet activation causes expression of __________ on surface of platelets

A

phospholipid complexes on suface of platelts which act as surfaces to bind coagulation factors and calcium –> promotes coagulation

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21
Q

actions of thrombin

A

thrombin converts fibrinogen to fibrin monomer but also effects local vasculature, inflammation and fibrinolysis

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22
Q

forms glue for platelet plug

A

fibrin crosslinks

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23
Q

when is tissue factor released?

A

when tissue is injured

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24
Q

where do the intrinsic and extrinsic pathways converge?

A

factors IX and X

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25
Q

what surface is best for maximum coagulation factor activity?

A

phospholipid surface

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26
Q

warfarin (Coumadin)

A

prolongs prothrombin time PT (extrinsic)

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27
Q

heparin

A

prolongs partial thromboplastin time PTT (intrinsic )

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28
Q

TENET XV

A

intrinsic longer pathway PTT

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29
Q

fibrinogen –> fibrin

A

via thrombin

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30
Q

3 anticoagulants

A

antithrombin III

protein C

Plasmin

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31
Q

action of antithrombin III

A

directly inactivates serine proteases thrombin and Xa (also IXa, XIa and XIIa)

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32
Q

what potentiates the action of antithrombin III

A

heparin

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33
Q

cleaves the cofactors Va and VIIIa

A

protein C

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34
Q

breaks down fibrin

A

plasmin

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35
Q

enhances the activity of protein C

A

protein S

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36
Q

activates protein C

A

thrombomodulin

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37
Q

activated by thrombin

A

thrombomodulin

binds to thrombin to alter its conformation

38
Q

inhibits VIIa tissue factor complex (extrinsic arm)

A

tissue pathway factor inhibitor

39
Q

where is plasmin activity optimized?

A

at sites of fibrin deposition

40
Q

how is free plasmin inactivated

A

by circulating alpha2 antiplasmin

41
Q

what inactivates tPA

A

PAI plasminogen activator inhibitor

42
Q

how do endothelial cells modulate coagulation/anticoagulation balance?

A

by releasing PAI

43
Q

what increases PAI?

A

thrombin and various cytokines

44
Q

what breaks down fibrin?

A

plasmin (from plasminogen)

45
Q

what 3 substance activate plasminogen?

A

urokinase

tPA

streptokinase

46
Q

prevent clot formation and extension

A

anticoagulants

47
Q

interfere with platelet activty

A

antiplatelet drugs

48
Q

dissolve existing thrombi

A

thrombolytic agents

49
Q

blood clot that forms abnormally within a blood vessel

A

thrombus

50
Q

a dislodged blood clot which travels through the bloodstream

A

embolus

51
Q

naturally occurring anticoagulant produced by basophils and mast cells to prevent formation and extension of blood clots

A

heparin

52
Q

does heparin disintegrate clots that have already formed?

A

NO

53
Q

how is heparin given?

A

intravenously or by subcutaneous injection

54
Q

how does heparin work?

A

binds and activates antithrombin III (inhibits thrombin, factor IXa, factor Xa)

55
Q

how is warfarin administered?

A

oral medication

56
Q

how does warfarin decrease blood coagulation?

A

by interfering with vitamin K metabolism

57
Q

what are the vitamin K dependent clotting factors>

A

VII
IX
X
II

58
Q

what clotting factors does heparin attack?

A

9a
10a
2

59
Q

what clotting factors does coumadin attack?

A

9
7
10
2

60
Q

dabigatran

A

direct thrombin inhibitor

61
Q

rivaroxaban

A

direct factor Xa inhibitor

62
Q

apixaban

A

direct factor Xa inhibitor

63
Q

TFPI tissue factor pathway inhibitor

A

new anticoagulation drug

64
Q

extrinsic assessment of coagulation

A

prothrombin time PT

65
Q

what drug increased the prothrombin time

A

warfarin (coumadin)

66
Q

which factors require vitamin K for synthesis

A

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

67
Q

describe the international normalized ratio INR

A

compares patient PT to the normal PT which compensates for differences in tissue factor

68
Q

intrinsic assessment of coagulation

A

partial thromboplastin time PTT

69
Q

what prolongs the PTT

A

heparin
hemophilia
antiphospholipid antibody

70
Q

what are the only factors not included in PTT

A

factors VII and XIII

71
Q

how would you distinguish between an inhibitor and factor deficiency

A

mixing pt sample with normal plasma:

if inhibitor: no clotting
if deficiency: clotting

72
Q

low dose heparin PT and PTT

A

PT normal

PTT prolonged

73
Q

high dose heparin PT and PTT

A

PT prolonged

PTT prolonged

74
Q

low dose warfarin PT adn PTT

A

PT prolonged

PTT normal

75
Q

high dose warfarin PT and PTT

A

PT prolonged

PTT prolonged

76
Q

what is warfarin necrosis?

A

thighs, breasts, and buttocks multiple or single lesion, with localized pain and erythema that develops into a painful necrotic eschar

low levels of protein C –> transient hypercoagulable state causing local thrombosis of dermal vessels

77
Q

describe heparin induced thrombocytopenia

A

platelet factor 4 is released by plateltes and bidns heparin thus blocking its action and pormoting coagulation

antibodies to heparin bind heparin/platelet factor 4 complex —-> endothelila injury and platelet activation (prothombotic state)

78
Q

bernard-soulier diesease

A

platelet abnormality

defect of platelet adhesion

autosomal recessive

lacking glycoprotein Ib

79
Q

glanzmann’s thrombasthenia

A

platelet abnormality: defect of platelet aggregation

autosomal recessive

lacking glycoprotein IIb/IIIA

80
Q

TTP thrombotic thrombocytopenic Purpura

A

platelet abnormality: antibodies direct against the von Willebrand factor cleaving protease, ADAMTS-13

81
Q

Idiopathic thrombocytopenic purpura ITP

A

platelet abnormality

antibodies directly agianst platelets

82
Q

aplastic anemia/ pancytopenia

A

platelet abnormality

all the cell lines are gone- marrow destroyed

83
Q

von Willerbrand’s disease

A

coagulopathy

deficiency of von Willebrand’s antigen

easily bruised, nosebleed, etc.

most common bleeding disorder

84
Q

factor VIII deficiency

A

hemophilia A

x-linked recessive most common hemophilia

85
Q

factor IX deficiency

A

hemophilia B

x-linked recessive coagulopathy

86
Q

factor XI deficiency

A

hemophila C

mildest hemophilia associated with the EJws

87
Q

factor XII deficiency

A

not clinically important

neither is the presence of lupus anticoagulant

88
Q

purpura petechia and ecchymoses are most likely

A

platelet deficiency

89
Q

trouble stopping blleding most likely

A

coagulation factor deficiency

90
Q

DIC

A

NOT a specific diagnosis

widespread activation of the caogulation system (thrombin) that from tiny thrombi throughout body leading to thrombocytopenia and consumptive coagulopathy (organ failure and bleeding)

91
Q

peripheral blood smear of DIC

A

observe sheared RBC

92
Q

what do D-DIMER assays measure

A

plasmin-cleaved insoluble cross-linked fibrin (indirect measure of thrombin which is required for fibrin formation)

used in diagnosis of DIC

Pathology II (14 decks)

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