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haematology > haemostasis > Flashcards

haemostasis Flashcards

1
Q

how do platelets and coagulation factors know when to become activate

A
  • platelets see abnormal surface: rough collagen and bind to receptors
  • when blood vessel damaged, small amount of physiological activator is released in circulation
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2
Q

platelet adhesion

A
  • blood vessel broken
  • platelets are activated and become sticky
  • VWF sticks to platelets and abnormal surface
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3
Q

components of clot: platelet surface receptors

A

ADP receptor, epinephrine receptor, thrombin receptor

ADP, epinephrine released and thrombin produced when injury sustained to vessel. They bind to receptors and allow platelets to form clot

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4
Q

components of clot: platelet surface glycoproteins

A

bind to important and relative ligands

binding site for fibrinogen, WbF, collagen

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5
Q

inside platelet

A
  • tubular system
  • open canalicular system - allows content of platelet held in alpha, dense and lysosomal granules to be secreted out onto surface
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6
Q

inside platelet: what do dense granules produce

A

ADP/ATP
calcium
serotin

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7
Q

inside platelet: what do alpha granules produce

A

thrombin

VWF

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8
Q

contents of inner platelet granules squished onto surface by…

A

actin and myosin when platelet activated to make it sticky

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9
Q

collagen sticks to platelet via …

A

glycoprotein 1A and glycoprotein 6

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10
Q

how does VWF stick to platelet

A

glycoprotein 1B59

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11
Q

how does platelet bind to fibrinogen

A

glycoprotein 2B3A changes confirmation allowing it to bind fibrinogen

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12
Q

platelet role in haemostasis: ahere

A

to abnormal surface - collagen

VWF

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13
Q

platelet role in haemostasis: activation

A

ADP pathway

COX pathway - arachidonic acid converted to thromboxane A2

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14
Q

platelet role in haemostasis: aggregation

A

to form clump - platelet plug

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15
Q

platelet role in haemostasis: provide phospholipid surface for coagulation

A
  • phospholipid surface on internal surface flips over to allow coagulation on top of platelet surface
  • need phospholipid for some of coagulation reaction
  • sramblase allows phospholipid membrane to be expressed on external surface
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16
Q

P2Y12 pathway inhibitors

A 
ADP pathway (platelets)
e.g. clopidogrel
17
Q

what does aspirin inhibit

A

cyclo-oxygenase pathway - arachindonic acid conversion to thromboxane

18
Q

von willebrand factor

A

made as promolecule/pro-peptide then dimerises and multimerises into a multi-meric form

lots of binding sites

19
Q

what does VWF bind o

A

factor VIII
platelet
collagen

20
Q

VWF disease: abnormality of D1 domain

A

prevents formation of high-weight multimers

classical of type 2A VWF disease

21
Q

primary haemostatic platelet plug

A

30s-1min after trauma
platelets activated and stuck to eachother, VWF and collagen
changes confirmation to bind to fibrinogen

22
Q

what allows fibrinogen to form fibrin

A

fibrinogen bound to platelets must be cleaved by thrombin which allows it to form fibrin

23
Q

what makes the platelet plug secure

A

the formation of fibrin - bleeding will stop

24
Q

extrinsic pathway

A

small reaction/burst to produce small amount fibrin
tissue factor binds to FVII and activates it
FVII activates FX which then activates prothrombin to thrombin
thrombin cleaves fibronogen

25
Q

intrinsic pathway

A

fed by thrombin
thrombin cleaves FXI to FXIa which then cleaves FIX to FIXa
FIXa and FVIIIa cleave Fx to FXa which produces big burst of thrombin

26
Q

natural anticoagulants

A

confine clot to area of injury

tissue factor pathway inhibitor
activated protein C
anti-thrombin

27
Q

tissue factor pathway inhibitor

A

able to bind to and inhibit FVII and FX

prevents thrombin being made and so clot formation

28
Q

activated protein C

A

binds to cofactor: protein S
these molecules switch off FVIII and FV
reduce thrombin production

29
Q

anti-thrombin

A

most powerful natural anticoagulant

binds to and inactivates lots of activated coag factors, incl FX and thrombin

30
Q

fibrinolysis

A

when form clot, endothelial cells respond by secreting tissue plasminogen activator and urokinase

these cleave plasminogen into plasmin which attacks clot and breaks it down

31
Q

fibrin degredation products

A

produced when breaking down a clot

e.g. D dimer

32
Q

inhibitors of plasminogen

A

PA1-1

PA1-2

33
Q

how does PA1 inhibit plasminogen

A

prevents plasminogen activator from degradation

prevents cleaving of plasminogen stops plasmin being formes

34
Q

mechanism of clopidogrel and tricagrelor

A

P2Y12 pathway/ADP receptor pathway

35
Q

mechanism of aspirin

A

cyclo-oxygenase pathway

prevent production of thromboxane and so aggregation

36
Q

mechanism of abciximab, tirofiban, eptifibatide

A

GP2B/3A receptor (for binding fibrinogen)

37
Q

warfarin

A

vitamin K antagonist

vitamin K needed for F2, 7, 9 and 10

38
Q

low molecular weight heparins

A

same as heparin but with side chain cleaved off

bind to anti-thrombin which cleaves thrombin and activated F10

haematology (32 decks)

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