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SBM > Hemostatsis/Coag Cascade > Flashcards

Hemostatsis/Coag Cascade Flashcards

1
Q

Phases of Hematostatsis

A

Primary Hematostasis
Secondary Hemostatsis- coagulation phase
Termination of coag rxns
fibrinolysis

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2
Q

result of primary hemostatsis

A

platelet plug formation

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3
Q

result of secondary hemostatsis

A

fibrin formation/stabilization

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4
Q

vascular injury exposes

A

subendothelium (procoagulant)

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5
Q

first step of primary hemostasis

A

vasoconstriction

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6
Q

formation of platelet plug requires

A

vWF
platelets
fibrinogen

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7
Q

where is vwf synthesized

A

endothelial cells

megakaryocytes

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8
Q

what is vwf stored as large multimers in

A

weibel-palade bodies in endothelum

alpha granules in plasma cells

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9
Q

lifespan of a platelet

A

7-10 days

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10
Q

where is fibrinogen made

A

liver

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11
Q

3 categories of alpha granules

A

adhesive proteins
coagulant proteins
growth factors, selectins

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12
Q

adhesive proteins

A

fibronectin

vWF

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13
Q

coagulant proteins

A

fibrinogen

factor V

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14
Q

growth factors, selectins

A

PDGF, VEGF

P-selectin

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15
Q

dense

A

adp
atp
serotonin
calcium

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16
Q

Thromboxane A2

A

more vasoconstriction
platelet agg
platelet activation

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17
Q

fibrinogen binds to platelet via

A

GpIIb/IIIa R

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18
Q

platelet factor 3 activity

A

exposure of PS and PE on platelet surface allows coag factors to bind to platelets

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19
Q

secondary hemostasis is required to form

A

thrombus

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20
Q

fibrin

A

forms a mesh around platelets, stabilizes the platelet plus while blood vessel heals

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21
Q

coagulation factors circulate as

A

inactive (zymogen) as well as active forms

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22
Q

which factors are not synthesized by liver

A

Factor VIIII

vWF

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23
Q

what is factor VIII synthesized by

A

liver

vascular endothelium

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24
Q

dep on vit K for fx

A

2,7,9,10,S,C,Z

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25
Q

protein S, C, & Z are

A

endogenous anticoagulant factors

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26
Q

tissue factor

A

monocytes circulate in resting state and are stimulated by vascular injury to produce TF– physiological

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27
Q

TF forms a complex w/ circulating factor VII

A

activation of factor VII to VIIa

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28
Q

factor Ix requires

A

Ca and factor 8 as cofactor to bind to platelet membrane phospholipid
–accelerates activation of factor X to Xa by 100,00 fold

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29
Q

factor 2

A

prothrombin

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30
Q

factor 2a

A

thrombin

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31
Q

prothrombinase complex

A

factor Va anchors factor 10a and prothrombin (2) in close proximity on platelet phospholipid

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32
Q

thrombin burst

A

small amount of thombin feeds back and activates XI to XIa by catalyzing 9-9a and 10-10a, etc

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33
Q

clotting functions of thrombin

A 
hydrolyzes fibrinogen to form fibrin
involved in many feedback activities
activates factor 8 to stabilize fibrin
protects established clot (thrombus) from fibrinolysis
inhibits coag when needed
34
Q

controlling coagulation

A

-hemodillution
hepatic clearance
endogenous anticoags
fibrinolysis (plasmin)

35
Q

Antithrombin

A

produced by liver, endothelial cells

binds and inhibits factor Xa and thrombin

36
Q

heparin

A

increases anticoag activity of AT

37
Q

activated protein C

A

thrombin binds thrombomodulin on endothelial cell surface changing its structure–> can now activate proten C but not others

APC + S–>inactivates factors Va and VIIIa

38
Q

tissue factor pathway inhibitor

A

produced by endothelial cells
binds to and activates factor Xa
inactivates TF/VIIa complex

39
Q

plasminogen

A

synthesized by liver and circulates–> binds to fibrin–>cleaved to plasmin

40
Q

plasmin cleaves

A

fibrin–>D dimers

41
Q

PAI-1

A

stored n platlets; inhibits tPA

42
Q

alpha 2 antiplasmin

A

major inhibitor of plasmin

43
Q

plasma

A

fluid fraction of unclotted, whole blood

contains all soluble components including coag factors, fibrinogen, etc

44
Q

serum

A

fluid remaining after blood has been allowed to clot; contains all soluble components except for coag factors

45
Q

coag factors are performed with

A

plasma

46
Q

citrate

A

anticoag for coagulation tests

binds Ca making ti unavailable for coagulation reactions

47
Q

bleeding time

A

measures primary hemostasis

48
Q

PFA-100

A

measures how long it takes for platelets to clot

49
Q

PT

A

time required to form fibrin clot when citrated patient plasma is added to thromboplastin Ca mixture

measures extrinsic

50
Q

PT normal time

A

12.2-14.8

51
Q

INR

A

standardizes PT
=patient PT/mean PT
normal=1
anticoag=2-3

52
Q

aPTT

A

activated partial thromboplastin time; not natural- lab driven

time required to form fibrin clot when citrated patient plasma is added to PHOSPHOLIPID+ Ca+ contact activator

53
Q

contact activators

A

glass
kaolin
celiate
ellagic acid

54
Q

aPTT is prolonged with

A

issues in the common and intrinsic pathways

55
Q

prolonged PT could mean

A

mild liver disease
early vitamin K def
early warfarin
factor 7 issue

56
Q

prolonged aPTT could mean

A

hemostatic factor dysfunction (hemophilia)
vWF disease
heparin

57
Q

prolonged PT and PTT

A 
severe liver disease
consumptive coagulopathy
hemodilution
severe vitamin K def
therapeutic warfarin
hypofibrinogenemia/dysfibrinogenemia
direct thrombin inhibitors
58
Q

therapeutic warfarin inhibits factors

A

2,7,9,10

59
Q

mixing studies and inhibitor

A

doesnt fix clotting

60
Q

mixing study and factor def

A

fixes clotting

61
Q

how does thrombin clotting time test work

A

exogenous thrombin + patient plasma

62
Q

thrombin time prolonged in

A

hypofibrinogenemia
dysfibrinogenemia
heparin, thombin inhibitors

63
Q

what does thrombin clotting time detect

A

fibrinogen abnormalities

64
Q

D-dimer is a maker of

A

clot formation/breakdown

65
Q

three ways to get a quantitative thrombocytopenia

A

increased destruction
sequestration in spleen
decreased production

66
Q

what does heparin do to platelets?

A

low platelets, but no bleeding– paradoxical state of hypercoagulation

67
Q

8 ways to get destruction/consumption of platelets

A 
autoimmune mediated processes
medications
DIC
TTP
HELLP syndrome in pregnancy
HUS
severe bleeding
vWF, type 2b
68
Q

enlarged spleen can hold up to

A

90% of platlets

69
Q

enlarged spleen vs normal spleen and platelets

A

normal spleen- can hold 30%

enlarged spleen- 90%

70
Q

come causes of splenmegaly and platelet sequestration

A 
portal htn (hepatic cirrhosis, thrombosis of portal or hepatic vein)
myeloproliferative diseases
71
Q

decrease in production of platelets (6)

A 
primary bone marrow disorders (leukemia, aplastic anemia, etc)
bone marrow infiltrative process
viral infections (hep, hiv)
toxic exposures to megakaryocytes
nutritional deficiencies
hereditary disorders
72
Q

6 categories of hereditary qualitative disorders

A 
bernard-soulier
glanzmann thromboasthenia
storage disorders
delta granule disorders
signal transduction disorders (decrease in release of granules)
scott syndrome
73
Q

berniar soluier disease

A

defect in GP1B R

74
Q

Glanzzmann Thrombasthenia

A

defect in GPIIb/IIIa R

75
Q

storage disorders

A

gray platelet syndrome (absent alpha granules)

quebec platelet syndrome (inc uPa in alpha granules so they are degraded)

76
Q

delta granule disorders

A

decrease in release of ADP due to hermansky pudak, chediak-higashi syndrome

77
Q

scott syndrome

A

defect in assembly on platlet surface

78
Q

8 ways to get aquired qualitative platelet disorders

A 
aspirin
nsaid
gpIIb/IIIa inhibitors
ADP R inhibitors
SSRI
Herbal
uremia
myeloproflierative disorders
79
Q

aspirin

A

irreversibly acetylates cyclooxygenase–>results in inhibition of thromboxane A2 production

80
Q

GPIIb/IIIA inhibitor

A

abciximab

81
Q

ADP R inhibiors

A

clopidogrel

prasurgel

SBM (18 decks)

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