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haem > haemostasis > Flashcards

haemostasis Flashcards

1
Q

What 3 processes take part in haemostasis

A

vasoconstriction, primary haemostasis, secondary haemostasis (coagulation)

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2
Q

describe primary haemostasis

A

Formation of a platelet plug:
platelet adhesion, platelet release reaction, platelet aggregation

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3
Q

what are platelets

A

non-nucleated, granule-containing cells formed from the fragmentation of megakaryocyte cytoplasm

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4
Q

mechanism of adhesion

A

injury to vessel walls –> platelets stick to damaged endothelium- on collagen, the GPIb receptor or indirectly through VWF which then binds to GPIb receptor

adhesion changes platelet shape from a disc to rounded with spicules

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5
Q

What happens to platelets after platelet adhesion?

A

they get activated
contents of alpha and dense granules released
through invaginated membrane

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6
Q

components of alpha and dense granules in platelets?

A

ADP, fibrinogen, von Willebrand factor

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7
Q

What is thromboxane A2?

A

vasoconstrictor

involved in platelet aggregation

prostaglandin

derived from arachidonic acid in cell membrane

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8
Q

what happens after granular release in primary haemostasis?

A

platelet activation causes conformational change in GPIIb/IIIa receptor on endothelial cells to allow for fibrinogen binding

fibrinogen has a key role in linking platelets to form the platelet plug

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9
Q

how are the effects of primary haemostasis counterbalanced?

A

active flow of blood and the release of prostacyclin PGI2 from endothelial cells

prostacyclin is a powerful vasodilator and suppresses platelet activation

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10
Q

name anti platelet drugs

A

aspirin, clopidgrel

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11
Q

how does aspirin work?

A

irreversibly binds to platelets, inhibiting them (single dose aspirin effects persist for around 7 days)

aspirin binds specifically to cycle-oxygenase COX

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12
Q

how does clopidogrel work

A

irreversible blocking of ADP receptor on platelet cell membranes (effects also last for 7 days)

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13
Q

what is the VWF?

A

glycoprotein synthesised by endothelial cells and megakaryoctes

mediates adhesion of platelets to sites of injury, promotes platelet-platelet aggregation

also specific carrier for factor 8

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14
Q

What’s secondary haemostasis?

A

coagulation - formation of a stable fibrin clot

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15
Q

where are most clotting factors synthesised?

A

the liver

factor VIII and VWF are made by endothelial cells

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16
Q

Which factors are dependent on vitamin K for function, and therefore effected by warfarin?

A

factors II, VII, IX and X
2 5 7 10

vit K needed for carboxylation of glutamic acid residues on them

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17
Q

What does calcium do in coagulation?

A

plays an important role in the binding of activated clotting factors to the phospholipid surfaces of platelets

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18
Q

What is the trigger to initiate coagulation?

A

Tissue factor (TF)

found only in tissue so does not come into contact with blood until vascular injury occurs

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19
Q

What is the initiation phase in coagulation?

A

TF binds to VIIa, triggering factor X and IX to be activated- this leads to the activation of factor II (prothrombin) being activate to form small amounts of thrombin (factor IIa)

20
Q

What is the amplification phase in coagulation?

A

small amount of thrombin mediates activation of factors V and VIII (co-factors) and the zymogen factor X11 (11) and platelets.

Factor XI activates factor IX to IXa, which, with factor VIIIa, amplifies the conversion of factor X to Xa

21
Q

What is the propagation phase in coagulation?

A

a rapid burst in thrombin generation

cleaves circulating fibrinogen to form insoluble fibrin (the clot)

22
Q

inhibitory mechanism ensuring coagulation is confined to site of injury? (anticoagulation pathway)

A

antithrombin inhibits thrombin and factor Xa

protein C activated by binding of thrombin thrombodulin on endothelial cell surfaces to form APC

APC inactivates factors Va and VIIIa in the presence of co-factor protein S

23
Q

anticoagulant drugs

A

heparin, warfarin, direct oral anticoagulants

24
Q

heparin

A

mixture of glycosaminylglycan chains extracted from porcine mucosa

works indirectly- potentiates action of antithrombi, leading to inactivation of factors Xa and IIa (thrombin)

administered intravenously/subcutaneous injection

25
Q

warfarin

A

vit K antagonist- reduces synthesis of factors II, VII, IX and X by liver

oral tablet, effect must be regularly monitored

takes several days for effect

26
Q

Direct oral anticoagulants (DOACs)

A

Orally available drugs that directly inhibit either thrombin or factor Xa (i.e. without the involvement of antithrombin)

​These do not usually require monitoring

27
Q

what’s fibrinolysis?

A

breakdown of fibrin to generate fibrin-degradation produces (FDPs)

28
Q

what is the principal fibrinolytic enzyme?

A

plasmin (zymogen form plasminogen) activation of plasmin is mediated by tissue plasminogen activator, t-PA

29
Q

how do thrombolytic agents work?

A

e.g. recombinant t-PA

generate plasmin to lyse clots- administered intravenously to patients w ischaemic stroke

high risk of bleeding

30
Q

what does tranexamic acid do?

A

binds to plasminogen (it is similar to lysine) competitively

prevents activation of plasminogen to plasmin

less fibrinolysis

31
Q

when is tranexamic acid used mainly

A

to treat bleeding in trauma and surgical patients, and patients with inherited blood disorders

32
Q

what’s the intrinsic pathway

A

where all the factors are found inside the blood-

XII-> XI -> VIII and IX

then common

common is V X –> II –> fibrinogen to fibrin

33
Q

what’s the extrinsic pathway

A

kicked off by TF, then common

34
Q

what’s prothrombin time(PT)?

A

measures integrity of extrinsic pathway

35
Q

mechanism of the PT test?

A

blood collected in bottle with sodium citrate
stops blood from clotting by chelating calcium in sample
sample spun to produce platelet poor plasma
TF and phospholipid added to the citrated plasma with calcium to start the reaction
time taken for clotting is measured

36
Q

when is PT prolonged?

A

when there is a reduction in factors VII, X, V, II
or fibrinogen

37
Q

how are results expressed when PT is used to monitor via K antagonist anticoagulant therapy (eg warfarin)?

A

INR - international normalised ratio

involves correction for diff thromboplastin reagents sued by diff labs around the world- so all labs have the same INR result for a given sample

38
Q

what does Activated partial thromboplastin time (APTT) measure?

A

integrity of intrinsic pathway

39
Q

mechanism of APTT?

A

performed by contact activation of factor XIIa by a surface like glass, or using a contact activator like silica or kaolin
contact activator and phospholipid added to citrated plasma followed by calcium
time for clotting measured

40
Q

when is APTT prolonged?

A

where there is a reduction in a single or multiple clotting factors- in the latter there could be a prolonged PT as well

isolated prolonged APTT is seen in patients w haemophilia A, B and factor XI deficiency (sometimes also by factorXII deficiency which doesn’t result in bleeding)

41
Q

what can bleeding be caused by?

A

reduction in platelet number or function
reduction in coagulation factors
increased fibrinolysis

42
Q

what is haemophilia a

A

deficiency of factor VIII (x linked)

43
Q

what is haemophilia B

A

factor IX deficiency, x linked

44
Q

acquired causes of reduced coagulation factors?

A

liver disease
anticoagulant drugs
disseminated intravascular coagulation

45
Q

what Is thrombosis

A

term used to describe formation of a blood clot where it is not needed

46
Q

3 contributory factors to thrombosis?

A

blood, vessel wall, blood flow

47
Q

which factors increase the risk of venous thrombosis?

A
  1. reduced levels of anticoagulant proteins
    - -reduced fibrinolytic activity
  2. increased levels of clotting factors/ platelets
  3. hyperviscosity (e.g. due to polycythaemia)

haem (4 decks)

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