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Y3 immunology and haematology > haemostasis > Flashcards

haemostasis Flashcards

1
Q

how does the blood maintain flow normally

A

red cells, white cells and platelets flowing through vessel

endothelium produces natural heparins, tissue factor pathway inhibitor, thrombomodulin which are all anti-coagulants

constant secretion of NO and prostacyclin from endothelium also prevent cells sticking to vessel wall

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2
Q

what substances are involved in clot formation

A

platelets

vWF

coagulation factors

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3
Q

how does a clot remain confined to the site of injury

A

natural anticoagulants

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4
Q

how does the clot disappear over time after the injury has occurred

A

fibrinolytic system

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5
Q

what signals result in platelets and coagulation factors being activated

A

abnormal surface

physiological activator

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6
Q

how does platelet adhesion occur

A

platelets in the area become activated and sticky

platelet recognises exposed collagen as abnormal and binds to it to plug the hole

von willebrand factor in the circulation sticks the platelets to the abnormal surface

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7
Q

what does physiological activator do

A

sets in place a variety of things including the coagulation cascade to form a definitive clot

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8
Q

components of a clot

A

platelet

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9
Q

surface of a platelet

A

ADP is released into circulation when there is cell/tissue damage

epinephrine is also released into the circulation and you generate thrombin

all these things are produced as a result of trauma and the platelet needs to be able to recognise them to be able to go on and make a clot

platelet glycoproteins bind lots of things:

  • vWF
  • fibrinogen
  • collagen
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10
Q

what happens inside a platelet

A

cell surface receptors

energy sources

tubule system - open canalicular system

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11
Q

what is important about the open canalicular system inside platelets

A

allows the content of the platelets (which is held in granules - alpha, dense, lysosomes) to be secreted onto the surface of the platelets and make them sticky

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12
Q

what do dense granules in platelets produce

A

ADP

calcium

serotonin

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13
Q

what do alpha granules in platelets contain

A

thrombin

vWF

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14
Q

process of clot formation

A
  1. platelet travels to break in vessel wall
  2. binds to collagen, vWF and to other platelets –> 1y platelet clot
  3. platelet has also changed its confirmation to allow it to bind fibrinogen
  4. once fibrinopeptides A and B are cleaved off it forms the fibrin clot –> definitive fibrin clot
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15
Q

what is the role of platelets in haemostasis (3A +P)

A

adhere
activation
aggregation

provide phospholipid surface for coagulation

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16
Q

process of platelet adherence

A
  1. adheres to collagen (glycoprotein Ia)
  2. adheres to vWF (glycoprotein Ib)
  3. activation of platelets
17
Q

process of platelet activation and how can different pathways be targeted

A
  1. ADP: P2Y12 pathway - targeted to prevent platelet becoming sticky (prasugrel, ticagrelor, clopidogrel)
  2. cycloxygenase pathway - arachidonic acid –> thromboxane A2 (aspirin inhibits this pathway)
18
Q

process of platelet aggregation

A

thromboxane A2 causes platelets to aggregate

19
Q

process of platelet coagulation

A

scramblase acts on the internal membrane of the platelet and allows the phospholipid to be expressed on the external surface

20
Q

in what form is vWF produced

A

made as a molecule then dimerises and multimerises into a multimodal form

21
Q

what does vWF bind to

A

factor VIII - required for clot formation

glycoprotein Ib

glycoprotein IIb-IIIa

collagen surface

22
Q

von willebrand disease - variants

A

different variants depend on which site the mutation occurred in

e.g. D1 domain abnormality - prevents you forming high weight multimer (type IIA vWD)

D domain mutation - corresponds to factor VIII binding site (type IIA)

23
Q

fibrin formation

  • just need to know that all the factors are there and working properly to be able make a solid fibrin clot
A

normal clotting sequence: factor XII, XI, IX, VIII, X, prothrombin, fibrinogen –> fibrin

  1. tissue factor binds VII and activates it
  2. activated VII activates X
  3. X and V activates prothrombin –> thrombin
  4. thrombin cleaves fibrinogen that’s sat on top of the platelets into fibrin - secures the clot

intrinsic pathway is then fed by thrombin:

  1. cleave XI into XIa which then cleaves IX into IXa
  2. IXa and VIIIa then cleaves X into Xa which produces a big burst of thrombin –> stable fibrin clot
24
Q

what factor is deficient in haemophilia A

A

facto VIII

25
Q

what factor is deficient in haemophilia B

A

IX

26
Q

what is the result of abnormalities in the clotting pathway

A

fibrinogen isn’t cleaved into fibrin and bleeding continues

27
Q

how does the clot remain in place where it formed

A
  1. tissue factor pathway inhibitor (TFPI) - binds to and inhibits activated factor VII and X, stop making thrombin - stop making clot
  2. activated protein C system: binds to co-factor (protein S) and together they switch off activated factor VIII and V
  3. antithrombin: protease inhibitor, binds to and inactivates activated factor X and binds to and inactivates thrombin
28
Q

how is the clot removed and remodelled

A
  1. fibrinolysis
29
Q

fibrinolysis process

A
  1. endothelial cells respond to formed clot by secreting activators of plasminogen tissue plasminogen activator (t-PA) and urokinase PA
  2. t-PA and u-PA cleave plasminogen to make plasmin
  3. plasmin is the serine protease and attacks the clot and breaks it down
  4. fibrin degradation products are released (e.g. d-dimer)
30
Q

inhibitors of plasminogen

A

phi I - prevents plasminogen activator from degradation so no plasmin is produced
phi II

31
Q

examples of P2Y12 pathway/ADP receptor inhibitors and when are they used

A

clopidogrel, prasugrel, ticagrelor

STEMI, PCI pts

32
Q

mechanism of action of aspirin

when is it used

A

inibits cycloxygenase (prevents production of thrombin and therefore prevents aggregation)

used in combination w/ P2Y12 inhibitors

33
Q

GP IIb/IIIa inhibitors

examples and how do they work

when are they used

A

abciximab, tirofiban, eptifibatide

prevent binding of fibrinogen to GP IIb/IIIa

PCI patient - looks like they’re continuing to thrombose their stent despite dual antiplatelet therapy

34
Q

how does warfarin work

A

vitamin K antagonist

vit K is required for the pro-translational modification of factors II, VII, IX and X

35
Q

how can you reverse warfarin action

A

vit K administration (oral/IV)

OR

infusion of coagulation factor concentrate (II, VII, IX, X) - prothrombin complex concentrate

36
Q

how does low-molecular weight heparin differ from unfractionated heparins

A

LMWH is the same molecule but w/ cytokines cleaved off

changes it’s characteristics

dosing, 1/2 life, bioavailability and metabolism

relevant for individuals w/ abnormal renal function

37
Q

how do heparins work

A

bind to antithrombin - allows antithrombin to cleave thrombin and activating factor X more quickly

38
Q

new anticoagulants - examples and how do they work

A

rivaroxaban, edoxaban, apixaban

inhibit serine proteases

small molecules, sit on active site of activated factor X and prevent it cleaving prothrombin to thrombin

no fibrin formation

39
Q

direct thrombin inhibitors

how do they work

examples

A

dabigatran, bivalirudin/argatroban

directly stick to the thrombin and prevent it performing it’s function

Y3 immunology and haematology (20 decks)

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