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Hemostatsis/Coag Cascade Flashcards

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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
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

SBM (18 decks)

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