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LSS 1: CVS > 13 - Haemostasis 1 > Flashcards

13 - Haemostasis 1 Flashcards

1
Q

What are coagulation factors?

A
  • help to form clots

- proteins denoted by roman numerals

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2
Q

What are regulatory factors?

A
  • stop premature firing of coagulation factors

- proteins

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3
Q

What is the vWF and its features?

A
  • von willebrand factor
  • giant adhesive plasma protein
  • several binding sites (for platelets, collagen and F8)
  • monomers joined together
  • bundles up in blood (binding sites hidden)
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4
Q

What happens to vWF when it’s bound to collagen?

A
  • low of blood pushes it along
  • it stretches
  • becomes long, thin molecule
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5
Q

What are some features of platelets?

A
  • no nucleus
  • half life of ~10 days
  • fragments of megakaryocytes from bone marrow
  • granules full of ADP, fibrinogen and vWF
  • stimulatory receptors at top (where ADP and thromboxane bind)
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6
Q

What happens to activated platelets?

A
  • change shape
  • expose phospholipids: change in membrane composition due to autocrine and paracrine effects of ADP make platelets more sticky
  • present new/activated proteins on surface (membrane changes): expression of GlpIIb/IIIa due to TXA2 allows fibrinogen binding
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7
Q

What are the synthesis sites for coagulation factors and what do they produce?

A
  • liver: I, V, VII and X
  • endothelial cells: VIII and vWF
  • megakaryocytes: V and vWF (stored inside α granules)
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8
Q

What does primary haemostasis require?

A
  • collagen
  • platelets
  • vWF
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9
Q

What does secondary haemostasis require?

A
  • plasma membrane
  • clotting factors
  • calcium
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10
Q

What is the process of primary haemostasis (platelet plug)?

A
  • vWF binds to collagen and gets stretched
  • lots of binding sites exposed to platelets
  • platelets bind to collagen via GlpIa when slowed down by vWF (binding via GlpIb)
  • collagen signals into platelet and activates it (thrombin binding triggers activation)
  • ADP, prostaglandin, fibrinogen and vWF released (arachidonic acid liberated)
  • phospholipid taken from platelet surface and thromboxane made
  • positive feedback event
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11
Q

What is tissue factor (TF)?

A
  • cofactor for VIIa
  • physiological initiator
  • regulates coagulation cascade
  • released from vessel wall injury site
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12
Q

What is the intrinsic clotting cascade?

A
  • XII activated
  • XIIa activates XI
  • XIa activates IX
  • IXa activates X
  • damping mechanism: tissue factor pathway inhibitor binds Xa, TF and VIIa in sequested form to turn off mechanism
  • coagulation activation almost immediately gets turned off
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13
Q

What is the extrinsic clotting cascade?

A
  • TF-VIIa complex is trigger for cascade
  • IX and X are activated
  • IXa also activates X
  • Xa makes thrombinogen (II) which is converted to thrombin (IIa)
  • IIa activates cofactors V and VIII
  • VIIIa forms complex with IXa
  • Va forms complex with Xa
  • IIa cleaves fibrinogen to fibrin
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14
Q

What is the thrombin burst?

A
  • stronger, denser clot generated (resistant to fibrinolysis)
    VIII and V cross link fibrin, inhibiting fibrinolysis
  • thrombin activates TAFI (fibrinolysis inhibitor)
  • blood clots rapidly, minimising blood loss
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15
Q

What happens to haemostasis at rest?

A
  • ADPs released from platelets degraded by ADPase’s found on endothelial cells
  • PGI2 and NO stop platelet activation
  • endothelial cells are anti-coagulants
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16
Q

What is the indirect inhibition of coagulation?

A
  • antithrombin inhibits thrombin and other clotting factors (IIa, IXa, Xa, XIa) in initiation phase
  • heparin accelerates action of antithrombin (used for immediate coagulation in venous thrombosis and pulmonary embolism)
17
Q

What is the direct inhibition of coagulation?

A
  • inhibition of thrombin generation by protein C anticoagulant pathway
  • thrombomodulin binds free thrombin and redirects it
  • cleaves and activates protein c
  • breaks down Va, VIIIa with cofactor protein
18
Q

What is fibrinolysis (clot breakdown)?

A
  • tPA (tissue plasminogen activator) in active form activates plasminogen to plasmin
  • tPA and Pgn brought together by fibrin (Ia), forms enzyme-substrate complex
  • tPA and Pgn circulate in blood but don’t react until fibrin created
  • plasmin breaks down fibrin (Ia) to complete wound healing
  • anti-plasmin stops plasmin circulating in blood and degrading things (breaks down plasmin)
19
Q

What is thrombomodulin?

A
  • extrinsic protein of endothelial cells
  • creates enzyme-substrate complex to breakdown co-factors V and VIII
  • paired to protein c
  • binding of thrombin to thrombomodulin allows protein s in blood to bind to protein c and activate it
  • activated protein c/protein s complex acts as enzyme

LSS 1: CVS (17 decks)

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