Hemostatsis/Coag Cascade Flashcards Preview

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Flashcards in Hemostatsis/Coag Cascade Deck (81):
1

Phases of Hematostatsis

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

2

result of primary hemostatsis

platelet plug formation

3

result of secondary hemostatsis

fibrin formation/stabilization

4

vascular injury exposes

subendothelium (procoagulant)

5

first step of primary hemostasis

vasoconstriction

6

formation of platelet plug requires

vWF
platelets
fibrinogen

7

where is vwf synthesized

endothelial cells
megakaryocytes

8

what is vwf stored as large multimers in

weibel-palade bodies in endothelum
alpha granules in plasma cells

9

lifespan of a platelet

7-10 days

10

where is fibrinogen made

liver

11

3 categories of alpha granules

adhesive proteins
coagulant proteins
growth factors, selectins

12

adhesive proteins

fibronectin
vWF

13

coagulant proteins

fibrinogen
factor V

14

growth factors, selectins

PDGF, VEGF
P-selectin

15

dense

adp
atp
serotonin
calcium

16

Thromboxane A2

more vasoconstriction
platelet agg
platelet activation

17

fibrinogen binds to platelet via

GpIIb/IIIa R

18

platelet factor 3 activity

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

19

secondary hemostasis is required to form

thrombus

20

fibrin

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

21

coagulation factors circulate as

inactive (zymogen) as well as active forms

22

which factors are not synthesized by liver

Factor VIIII
vWF

23

what is factor VIII synthesized by

liver
vascular endothelium

24

dep on vit K for fx

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

25

protein S, C, & Z are

endogenous anticoagulant factors

26

tissue factor

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

27

TF forms a complex w/ circulating factor VII

activation of factor VII to VIIa

28

factor Ix requires

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

29

factor 2

prothrombin

30

factor 2a

thrombin

31

prothrombinase complex

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

32

thrombin burst

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

33

clotting functions of thrombin

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

controlling coagulation

-hemodillution
hepatic clearance
endogenous anticoags
fibrinolysis (plasmin)

35

Antithrombin

produced by liver, endothelial cells
binds and inhibits factor Xa and thrombin

36

heparin

increases anticoag activity of AT

37

activated protein C

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

tissue factor pathway inhibitor

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

39

plasminogen

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

40

plasmin cleaves

fibrin-->D dimers

41

PAI-1

stored n platlets; inhibits tPA

42

alpha 2 antiplasmin

major inhibitor of plasmin

43

plasma

fluid fraction of unclotted, whole blood
contains all soluble components including coag factors, fibrinogen, etc

44

serum

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

45

coag factors are performed with

plasma

46

citrate

anticoag for coagulation tests
binds Ca making ti unavailable for coagulation reactions

47

bleeding time

measures primary hemostasis

48

PFA-100

measures how long it takes for platelets to clot

49

PT

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

measures extrinsic

50

PT normal time

12.2-14.8

51

INR

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

52

aPTT

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

contact activators

glass
kaolin
celiate
ellagic acid

54

aPTT is prolonged with

issues in the common and intrinsic pathways

55

prolonged PT could mean

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

56

prolonged aPTT could mean

hemostatic factor dysfunction (hemophilia)
vWF disease
heparin

57

prolonged PT and PTT

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

58

therapeutic warfarin inhibits factors

2,7,9,10

59

mixing studies and inhibitor

doesnt fix clotting

60

mixing study and factor def

fixes clotting

61

how does thrombin clotting time test work

exogenous thrombin + patient plasma

62

thrombin time prolonged in

hypofibrinogenemia
dysfibrinogenemia
heparin, thombin inhibitors

63

what does thrombin clotting time detect

fibrinogen abnormalities

64

D-dimer is a maker of

clot formation/breakdown

65

three ways to get a quantitative thrombocytopenia

increased destruction
sequestration in spleen
decreased production

66

what does heparin do to platelets?

low platelets, but no bleeding-- paradoxical state of hypercoagulation

67

8 ways to get destruction/consumption of platelets

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

68

enlarged spleen can hold up to

90% of platlets

69

enlarged spleen vs normal spleen and platelets

normal spleen- can hold 30%
enlarged spleen- 90%

70

come causes of splenmegaly and platelet sequestration

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

71

decrease in production of platelets (6)

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

6 categories of hereditary qualitative disorders

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

73

berniar soluier disease

defect in GP1B R

74

Glanzzmann Thrombasthenia

defect in GPIIb/IIIa R

75

storage disorders

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

76

delta granule disorders

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

77

scott syndrome

defect in assembly on platlet surface

78

8 ways to get aquired qualitative platelet disorders

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

79

aspirin

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

80

GPIIb/IIIA inhibitor

abciximab

81

ADP R inhibiors

clopidogrel
prasurgel