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Pathology > 4.9 Clotting Cascade > Flashcards

4.9 Clotting Cascade Flashcards

1
Q

what is the last thing platelets do

A

secrete PL layer which is important to localize the lesion

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2
Q

what else helps localize where you’re going to clot

A

collagen and binding of vonWB

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3
Q

how many clotting factors are there

A

13

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4
Q

goal of clotting factors

A

generate thrombin

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5
Q

action of thrombin

A

cleaves fibrinogen to make fibrin

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6
Q

Componets needed for clotting

A

enzyme, substrate, cofactor (like Ca), and PL surface

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7
Q

1

A

fibrinogen

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8
Q

1a

A

fibrin

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9
Q

2

A

protrhombin

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10
Q

2a

A

thrombin

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11
Q

3

A

tissue factor

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12
Q

4

A

Ca ion

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13
Q

5

A

prothrombin accelerator

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14
Q

6

A

doesn’t really exist, is actually just 5a

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15
Q

7

A

proconvertin,

co-thromboplasmin

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16
Q

8

A

antihemophillic factor

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17
Q

9

A

christmas factor

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18
Q

10

A

prothrombinase, stuart prower fac

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19
Q

11

A

thromboplasmin antecedent

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20
Q

12

A

hageman factor

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21
Q

13

A

fibrinase,

fibrin stabilizing factor

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22
Q

Intrinsic

A

12 11 9 –>10 2 1 8

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23
Q

Extrinsic

A

3 7 –> 10 2 1 8

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24
Q

Crosstalk areas

A

7 also to 9, 10 also to 7

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25
Q

Extrinsic path begins with

A

endothlial ijury releaseing 3

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26
Q

3 is a cofactor that

A

complexes with 7 forming 3/7a

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27
Q

3/7a activates

A

10 to 10a (in the same ways as 9a)

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28
Q

at the 3/7a step a burst of

A

thrombin is produced_this is needed early on to form the secondary plug

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29
Q

Intrinsic path begins with

A 
exposure of collagen causing a complex of 
prekallikrein, 
HMW kininogen, 
factor 9, and 
factor 7 to from
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30
Q

Prekallikrein is converted to

A

kallikrein

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31
Q

Kallikrein activates

A

12 to 12a

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32
Q

12a activates

A

11 to 11a and cleaves more prekallikrein to more kallikrein

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33
Q

11a activates

A

9 to 9a

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34
Q

9a activates

A

10 to 10a on surface of platelets

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35
Q

10 can only be activate by 9 a if

A

the tenase complex is fromed on the PL layer of the platelet plug

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36
Q

tenase complex

A

8a, 9a, 10, Ca

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37
Q

8 is activated by

A

early fromed thrombin from extrinsic pathway

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38
Q

8a is the

A

receptor for 9a and 10 (cofactor for cleavage of 10 by 9a)

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39
Q

2 –> 2a (prothrombin –> thrombin)

A

10a, 5a, 2, and Ca complex on PL to allow 2 to be cleaved into 2a

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40
Q

5a is a cofactor in the formation of 2a similar to

A

8a in the formation of 10a

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41
Q

thrombin activates

A

8 to 8a

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42
Q

function of 8a

A

a transglutimase that crosslinks fibrinmaing it more stable

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43
Q

thrombin activates factors

A

11, 8, 5, and plays a major role in early platelet activation

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44
Q

thrombin also activates

A

protein C

45
Q

Protein C

A

in the presence of protein S and PL degrades 5a and 8a –> INHIBITORY PATH

46
Q

antithrombin 3 inhibits

A

thormbin (major) and 9a, 10a, 11a, 12a

47
Q

heparin enhances

A

antithrombin 3 activity 1000 fold

48
Q

warfarin/comadin

A

anticoagulation factor

49
Q

vit K

A

cofactor in clotting and warfarin inhibits the thing that Vit k binds?

50
Q

Ca is needed for clevage of

A

11 by 12a, 9 by 11a, 10 by 9a, 2 by 10a

51
Q

5a is needed for

A

clevage of 2 by 10a

52
Q

PL layer needed to gererate

A

10a and 2a(thrombin)

53
Q

slide 45

A

picture of this

54
Q

from which factor onward is there an amplification and crossover of intrinsic and extrinsic paths

A

9a

55
Q

severe deficiences in which factors do NOT result in serious bleeding

A

12 and 11

56
Q

Thrombosis

A

pathological coagulation of blood, number 1 cause of mortality and morbidity in USA

57
Q

Virchow’s Triad

A

endothelial injury,
stasis/turbulence,
hypercoagulability

58
Q

endothelial injury

A

even just stress and not complete death of endothelial cells can cause change to the phenotype

59
Q

Stasis/turbulence

A

understand moving stasis - formation of eties

60
Q

hypercoagulability is determined by

A

genetic and environmental factors

61
Q

Endothelial injury can be due to

A 
trauma, 
ischemia (MI), 
atherosclerosis, 
endotoxins, 
cigarette smoke, 
autoimmunity
62
Q

Common pathway

A

exposure of subendothelial connective tissue to plasma and/or phenotypic changes in endothelial cells

63
Q

on a smear of a heavy smoker

A

you see weird looking cells that are killed endothelial cells

64
Q

left ventricle thrombus

A

get into carotids leading to stroke

65
Q

right ventricle thrombus

A

getin into capilaries of lungs

66
Q

septal defects and thrombi

A

normally if there is a septal defect the pressure on the right is more than the left so flow occurs nromally, but if the valsalva maneuver occurs then there can be a reversal of flow causing problems

67
Q

stasis/turbulents disrupts

A

laminar flow

68
Q

stasis/turbulence stresses

A

endothelium

69
Q

stasis/turbulence diminishes

A

anticoagulants

70
Q

stasis/turbulents concentrates

A

procoagulants

71
Q

does moving stasis disturb flow

A

no

72
Q

stasis/turbulence excludes

A

inhibitors

73
Q

during stasis/turbulence

A

more activate clotting factors, and potential for clotting is reduced, along with inhition of clotting

74
Q

where is the most common place for thrombotic events

A

deep veins

75
Q

why is the most common place for thrombotic events the deep veins

A

bc under the valves of deep veins there are eties of turbulence

76
Q

hypercoagulability can occur due to

A 
inherited deficiencies in anticoagulants, 
heparin induced thrombocytopenia, 
antiphospholipid antibodies, 
medications/prostheses, 
sickle cell disease
77
Q

how does heparin induce thrombocytopenia

A

when a large MW heparin is givin,
Ab forms agains it that cross react with platelets.
So the next time you give the heparin there is a huge rise in Ab that bind the platelets and use them up

78
Q

what disease is associated with antiPL antibodies

A

lupus, seen in young wooen - these tend to coressreact with platelets too

79
Q

hypercoag - leiden mutation for factor 5( replacing glut for arg) makes factor 5 resistant to ceavage by

A

protein C - seen in 2 - 15% of caucasians

80
Q

hypercoag - mutation in prothrombin causing

A

prothrombin to inc - seein in 1-2% of population

81
Q

homocysteinemia is correlated with_..and can be treated with_..

A

cardiovascular disease__.vitamins

82
Q

deficiencies in Protein S and C

A

hypercoaguable bc no cleavage of factor 5

83
Q

who should be suspected for inherited hypercoaguable states?

A

patients under 50 who thrombose with no underlying cause

84
Q

hypercoag - fibrolytic activity

A

this is an inhibition of coagulation bc it eats up the ealy nascent clots - loss of this ability makes you more hypercoaguable

85
Q

effects of aniPL

A

recurrent arterial/venous thromboses,
miscarriages,
cardiac valve vegetations,
thrombocytopenia

86
Q

post mortem clots

A

chicken fat and currant jelly due to gravity

87
Q

antemortem clots

A

Lines of Zahn - blood is moving so it looks like its stirred with a stick

88
Q

Mural thrombi

A

walled - in the walls of the heart

89
Q

Fate of Thrombi

A

Propogation,
Dissolution,
organization and recanalization,
embolization

90
Q

what does heparin do

A

helps to prevent propagation, it DOES NOT dissolve clots

91
Q

Emboli

A

detached intravascular solid, liquid, or gas that is cared by blood to a distant site

92
Q

99% of emboli are

A

are thromboemboli

93
Q

other emboli

A

nitrogen,
air,
fat,
artherosclerotic plaque

94
Q

Pulmonary thromboembolism

A

clinically important event and frequent cause of sudden death,
may or maynot cause infarction,
majority from deep leg veins

95
Q

organs least prone to infarction after thromboembolism

A

lung and
liver

due to collateral blood supply

96
Q

so probability of infarction goes up as you go more

A

distal

97
Q

in pulmonary thromboembolism sudden death is due to more

A

proximal events —- tend to be bigger and kill you

98
Q

in pulmonary thromboembolism, infarction is more likely to occur

A

in more peripheral (distal?) tissue due to capillary drop off

99
Q

if a clot formd after death

A

it would fall away from the walls

100
Q

if the lung tissue still looks healthy when you see a pulmonary thromboembolism

A

this means the person died suddenly with no time to develop disease and destroy tissue

101
Q

difference btw infarct and hemmoragic thromboembolism

A

infarct is rock hard bc tissue is dead and surrounding blood is pumping into dead tissue, but hemmoragic would be squishy

102
Q

when you start to see organization there are

A

fibroblasts - tells you that the clot happened a long time ago

103
Q

Fat emboli

A

occurs after crush injuries to bone where small liquid blobules of fat shower curgulation

104
Q

what does fat do to platelets

A

activates platelets and injures endothelium leading to thrombosis

105
Q

Amniotic fluid embolism

A

rare but dangerous bc of the biochemical effects of the amniotic fluid in the mother’s blood, and squamous cells and lanugo hair lodge in the mother’s pulmonary vessels, sends mother into shock, massive DIC

106
Q

Gas embolisme most frequently occurs as

A

decompression sickness seen in divers and casson workers

107
Q

to see symptoms of gas embolism need

A

more than 100cc gas

108
Q

orthepedic surgery and gas emolism

A

since bone breaks are prone to vessels being exposed to air, air can be sucked into the patient bc the vessels in the bone are held wide open - if enough air comes in it can kill the patient

109
Q

Arterial emboli arise from

A

most arise from mural thrombi in heart, other form
aneurysms,
artherosclerotic plaques, or
valves

Pathology (26 decks)

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