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Haematology and Transfusion Science > HS2 - Haemostasis 2 > Flashcards

HS2 - Haemostasis 2 Flashcards

0
Q

Where do larger denser red and white cells tend to travel inside a blood vessel?

A

Centre of the lumen

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1
Q

Inside a blood vessel, where is the flow rate at its greatest?

A

Centre of the lumen

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2
Q

Where do platelets tend to travel inside a blood vessel?

A

Near to the vessel walls

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3
Q

Why do platelet travel near the walls of blood vessels?

A

Slower blood flow, platelets light so forced to the outside edge.

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4
Q

Endothelium plays an anti-haemostatic role by inhibiting platelet adhesion, how does it do this?

A

Electrostatic repulsion:

Endothelium: Proteoglycans -ve charge
Platelets : Sialic acid, surface glycoproteins -ve charge

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5
Q

Why is blood flow slowest nearest to the vessel walls?

A

Friction between vessel walls and adjacent layer of blood causes a drag effect, slowing blood down.

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6
Q

Name 3 endothelium derived platelet inhibitors.

A
  • Nitric oxide (NO)
  • Prostacyclin (PGI2)
  • ecto-ADPase
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7
Q

The endothelium derived platelet inhibitor nitric oxide is formed by the action of which enzyme on L-Arg

A

Nitric oxide synthase (NOS)

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8
Q

The endothelium derived platelet inhibitor Prostacyclin is formed by the action of which enzyme on arichidonic acid?

A

COX-1

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9
Q

What is the function of ecto-ADPase found on surface of endothelial cells?

A

De-phosphorylates ADP released by platelets to form adenosine (a platelet inhibitor)

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10
Q

What is the effect of the basal release of prostacyclin on blood vessels?

A

Maintains vascular tone

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11
Q

What factors stimulate the release of prostacyclin?

A
  • Shear stress
  • Thrombin
  • Cytokines
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12
Q

What is the plasma half-life of prostacyclin!

A

3 minutes

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13
Q

What occurs when prostacyclin binds to a prostacyclin receptor?

A
  • Activation of adenylate cyclase
  • ATP converted to cAMP
  • activates protein kinase
  • decreases cytosolic calcium
  • platelet inhibition, smooth muscle relaxation
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14
Q

How does NO act as a platelet inhibitor?

A
  • Diffuses through membrane of endothelial cell
  • Activates guanylate cyclase
  • GTP converted to cGMP
  • protein kinase activation
  • decreased cytosolic calcium
  • platelet inhibition, smooth muscle relaxation
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15
Q

Name 4 natural inhibitors of coagulation.

A
  • Antithrombin (AT)
  • Protein C
  • TFPI (Tissue factor pathway inhibitor)
  • TAFI (Thrombin activated fibrinolysis inhibitor)
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16
Q

Antithrombin is a member of which family of molecules?

A

Serpin (serine protease inhibitors)

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17
Q

What is the mechanism of action of antithrombin?

A
  • forms stable complexes with thrombin, FXa, and FIXa (serine proteases)
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18
Q

What two substances greatly potentiate the action of antithrombin?

A
  • proteoglycans (on endothelial surfaces)

- heparin (released by mast cells, and administered as an anticoagulant)

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19
Q

Protein C is a plasma protein which circulates in an inactive form, what substance causes it’s activation?

A

Thrombomodulin (protein bound to endothelial surfaces)

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20
Q

What cofactor is required by protein C ?

A

Protein S

21
Q

Protein C forms a complex with what to inactivate factors Va and VIIIa?

A
  • phospholipid
  • Calcium ions
  • Protein S
22
Q

Which activated clotting factors does Protein C inactivate?

A
  • Va

- VIIIa

23
Q

How is protein C activated?

A

Activated by thrombin complexed to thrombomodulin

24
Q

What does TFPI stand for?

A

Tissue factor pathway inhibitor

25
Q

TFPI is a serine protease inhibitor, what cells release this factor?

A
  • Platelets

- Endothelial cells

26
Q

What is the function of TPFI?

A

It controls excessive activation of coagulation.

27
Q

What is the mechanism of action of TPFI?

A
  • Forms an inhibitory complex with FXa

- FXa-TFPI complex binds with TF-FVIIa complex inactivating it.

28
Q

What protein increases the affinity of TFPI for FXa?

A

Protein S

29
Q

What is the effect on individuals who have a deficiency of either Protein S, Protein C or antithrombin?

A

They have an increased risk if thrombosis.

30
Q

What is the function of plasmin?

A

It cleaves fibrin and fibrinogen in a controlled manner.

31
Q

What enzyme breaks down clots once they have formed?

A

Plasmin

32
Q

Plasmin circulates in the plasma in an inactive form, what is this called?

A

Plasminogen

33
Q

What is the primary activator of plasminogen to plasmin?

A

tPA (Tissue plasminogen activator)

34
Q

What is the name of a secondary activator of plasminogen to plasmin?

A

uPA (Urokinase type plasminogen activator)

35
Q

What substance inhibits the conversion of plasminogen to plasmin?

A

PAI-1 (Plasminogen activator inhibitor 1)

36
Q

What substance binds any inappropriately activated plasmin to inactivate it?

A

α2-antiplasmin

37
Q

What 2 circulating inhibitors limit plasmin activation?

A
  • PAI-1

- α2-antiplasmin

38
Q

How is plasmin generation localised to the clot surface?

A
  • tPA and plasminogen form a complex on the lysine residues on the fibrin where they are protected from the inactivators PAI-1 and α2-antiplasmin.
39
Q

What is the structure of fibrinogen?

A
  • dimer 3 polypeptide chains linked at central E domain
  • 3 polypeptide chains (α, β and γ)
  • Fibrinopeptide A and Fibrinopeptide B at ends of α and β chains (by E domain)
  • Aα and Bβ fragments (by D domain)
40
Q

Which peptides are found at the N-terminal ends of the α and β chains in the fibrin dimer?

A

Fibrinopeptides A and B

41
Q

Which peptides are found at the C-terminal ends of the α and β chains in the fibrin dimer?

A

Aα and Bβ fragments

42
Q

What action does Thrombin have on fibrin?

A

Chops off Fibrinopeptides A and B leaving a fibrin monomer which can cross link.

43
Q

What is the action of Plasmin on fibrinogen?

A
  • chops off Aα and B fragments

- cleaves the chains ultimately forming 2 D and 1 E fragments

44
Q

What is the action of plasmin on fibrin?

A
  • Cleaves the joints between D and E fragments forming D-dimers
45
Q

What would a positive D-dimer test indicate?

A
  • patient has a DVT
46
Q

How is fibrinolysis regulated?

A
  • plasminogen and tPA form complex on lysine res.
  • complex protected from PAI-1 and
    α2-antiplasmin.
  • Annexin II on endothelium also bind tPA and plasminogen at sites of tissue damage
  • Free plasmin inactivated by α2-antiplasmin
47
Q

What cells release tPA?

A
  • Damaged endothelial cells
48
Q

What does TAFI stand for?

A

thrombin-activatable fibrinolysis inhibitor

49
Q

What activates TAFI?

A

Thrombin complexed with thrombomodulin

50
Q

How does TAFI inhibit fibrinolysis?

A

Removes lysine binding site so tPA and plasminogen cannot bind to fibrin

Haematology and Transfusion Science (10 decks)

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