haemostasis and fibrinolysis Flashcards

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
Q

A2AP

A

inhibits plasmin

26
Q

TAFI

A

deleys plasmin generation and fibrin degradation

27
Q

thrombin

A

converts protein C into APC

28
Q

bernard soulier syndrome

A

autosomal recessive disease in which GPib can not bind to VWF

29
Q

glanzmann thromasthenia

A

GPIIb/IIIa does not function properly and VWF can no longer be liked between platelets, you can not form a plug

30
Q

storage pool disease

A

defects in release reaction

31
Q

kidney failure

A

due to kidney failure you can have uremia

32
Q

liver cirrhosis

A

due to liver cirrhosis you will bleed more

33
Q

what does aspirin and NSAID (reversible) do

A

it inhibits COX and thus you will have less TxA2. thus you will have less platelet aggregation

34
Q

what doe clopidogrel, prasugrel and ticagrelor do

A

inhibit the ADP receptor

35
Q

what does abciximab do

A

inhibits GPIIb/IIIa

36
Q

type 1 VWF

A

partial deficiency of VWF due to reduced synthesis of normal VWF or intracellular retention of VWF

37
Q

type 2A VWF

A

due to lack of high molecular weight multimers smaller vWF

38
Q

type 2B VWF

A

increased affinity for GPIb which causes spontaneous binding to the receptor without subendothelial collagen exposed

39
Q

type 2M VWF

A

mutation in the protein where it cna not interact with the receptor anymore; reduced binding affinity for the platelets

40
Q

type 2N VWF

A

factor VIII has a reduced affinity and thus there is reduced secondary haemostasis

41
Q

type 3 VWF

A

complete deficiency of VWF