haemostasis and fibrinolysis Flashcards

(41 cards)

1
Q

FI

A

fibrinogen, for coagulation

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2
Q

FII

A

thrombin, converts fibrinogen into fibrin, coagulation

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3
Q

FIII

A

TF, together with coagulation factor VIIa does it bring FX to an active form

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4
Q

FIV

A

calcium ion

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5
Q

FV

A

will help speed up the reaction of II to IIa

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6
Q

FVII

A

together with FVIIa able to bring coagulation factor X to an active form

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7
Q

FVIII

A

binds to VWF, when let go it will interact with IX in order to stimulate FX

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8
Q

FIX

A

together with Ca2+ and VIII it converts X to active form

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9
Q

FX

A

able to bring II to active form

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10
Q

FXI

A

activates factor IX

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11
Q

FXII

A

converts XI and PL into active form

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12
Q

FXIII

A

makes crosslinks between the D domains of fibrin monomers

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13
Q

HMWK

A

participates in the initation of blood coagulation, helps activating XII and XI

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14
Q

PK

A

ihelps HWMK with activating XII

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15
Q

protein C

A

converst Va and VIIIa into inactive form

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16
Q

protein S

A

cofactor to protein C in the inactivation of factors Va and VIIIa

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17
Q

plasmin

A

a protease that is able to degrade the fibrin in order to make it soluble again

18
Q

thrombomodulin

A

needed to activate protein C

19
Q

TFPI

A

inhibits Xa by generating a Xa-TFPI complex

20
Q

antithrombin III

A

inhibits thrombin, IIa, IXa and XIa

21
Q

fibrin

A

costimulator to converts plasminogen to plasmin

22
Q

tPA

A

together with fibrin converts plasminogen to plasmin

23
Q

uPA

A

can convert plasminogen to plasmin

24
Q

PAI-1

A

inhibits tPA and uPA

25
A2AP
inhibits plasmin
26
TAFI
deleys plasmin generation and fibrin degradation
27
thrombin
converts protein C into APC
28
bernard soulier syndrome
autosomal recessive disease in which GPib can not bind to VWF
29
glanzmann thromasthenia
GPIIb/IIIa does not function properly and VWF can no longer be liked between platelets, you can not form a plug
30
storage pool disease
defects in release reaction
31
kidney failure
due to kidney failure you can have uremia
32
liver cirrhosis
due to liver cirrhosis you will bleed more
33
what does aspirin and NSAID (reversible) do
it inhibits COX and thus you will have less TxA2. thus you will have less platelet aggregation
34
what doe clopidogrel, prasugrel and ticagrelor do
inhibit the ADP receptor
35
what does abciximab do
inhibits GPIIb/IIIa
36
type 1 VWF
partial deficiency of VWF due to reduced synthesis of normal VWF or intracellular retention of VWF
37
type 2A VWF
due to lack of high molecular weight multimers smaller vWF
38
type 2B VWF
increased affinity for GPIb which causes spontaneous binding to the receptor without subendothelial collagen exposed
39
type 2M VWF
mutation in the protein where it cna not interact with the receptor anymore; reduced binding affinity for the platelets
40
type 2N VWF
factor VIII has a reduced affinity and thus there is reduced secondary haemostasis
41
type 3 VWF
complete deficiency of VWF