Haemostasis Flashcards

1
Q

What is the vessel wall lined with and what are it’s characteristics?

A
  • Epithelium
  • “Non-stick surface teflon”
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2
Q

Which substances do we have to encourage flow?

A
  • heparans, anticoagulants – TFPI, prostacyclin, nitric oxide
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3
Q

What happens when you are cut? What systems are at play?

A
  • You bleed at the site of the injury
  • For how long? 3-4 mins
  • Stops – you form a clot Platelets, vWF, Coagulation Factors
  • The clot remains confined to the site of injury Natural Anticoagulants
  • 1 week later the clot has vanished Fibrinolytic System
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4
Q

What states are platelets and coagulation factors generally in the blood?

A
  • Platelets and coag factors remain in resting state until activated – localised signals, production at area of damage of physiological activators cause activation
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5
Q

What causes platelets to adhere to site of damage?

A
  • Platelets are seeing something not used to – subendothelial collagen, as soon as they see this they stick to it and become sitcky/activated.
  • Vwfactor binds and allows us to start clotting. Just at area of damage there is physiological activator (tissue factor)
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6
Q

What exist on the surface of platelets and their roles?

A
  • Receptors – normally for things created in context of trauma
  • Glycoprotein receptors – capable of binding to ligands, relevant to blood coagulation
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7
Q

How do platelets work?

A
  • Bind to collagen
  • Bind to von willebrand factor
  • Bind to fibrinogen
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8
Q

What are platelets role in haemostatis?

A
  • Adhere
  • Activate
  • Aggregrate
  • Provide phospholipid surface for coagulation
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9
Q

Which parts of the platelet are responsible for adherence?

A
  • GP 1b
  • GP1a (x2)
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10
Q

How do platelets activate?

A
  • ADP pathway (P2Y12)
  • Activation of cyclooxygenase pathway
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11
Q

What allows the aggregration of platelets?

A
  • Thromboxane allows platelets to stick to each other
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12
Q

What allows proteins to attach to platelets?

A

Externalised phospholipids

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13
Q

What is the PRIMARY platelet plug?

A
  • Platelets have adhered, activated and bound fibrinogen = PRIMARY haemostatic plug
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14
Q

What stabilises the primary platelet plug?

A
  • Fibrin clot formation
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15
Q

How can we make a fibrin clot?

A
  • Primary aim is to cleave fibrinogen..

So:

  • There is a clotting cascade of proteins, much like a row of dominoes, they must all ‘fall over’ to finally cleave fibrinogen creating the fibrin clot
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16
Q

What happens if one of the coagulation factors is missing?

A
  • Process is flawed, cascade doesn’t complete, continue bleeding
  • Anticoagulants work by stopping the dominoes falling over!
17
Q

What is the protein cascade pathway?

A
  • 7a binds to 10, activates it,
  • 10a with 5a activated thrombin – makes fibrin
18
Q

What is the role of natural anticoagulants?

A
  • To confine the clot to the area of damage
19
Q

What are the three main natural anticoagulants?

A
  • antithrombin
  • activated protein C and S
  • TFPI
20
Q

How does TFPI function?

A
  • TFPI inactivated activated form of tissue activator 7a and 10a – reduces amount of thrombin
21
Q

How does protein C and S function?

A
  • A5 and A8 – switches them off, reduces thrombin
22
Q

How does antithrombin work?

A
  • Inhibits 10a and thrombin, switching the process off
23
Q

What is the process of fibrinolysis?

A
  • Endothelial cells – produces activators of plasminogen.
  • t-PA cleaves the bridge creating active plasmin (protease), starts to break fibrin clot down.
  • Produces degradation products:
    • D-dimer: piece of fibrin that has been broken down
24
Q

What is the mechanism of antiplatelets?

A
  • Aspirin prevents platelet from being sticky by preventing arachadonic acid forming thromboxane
  • Clopidogrel/Ticagrelor – preventing platelet from sticking
  • Other drugs normally used in coronary cath lab.
25
Q

How do anticoagulants function?

A

Warfarin

  • Prevent dominoes from falling over – 2,7,9,10 – vit k dependent factors: inhibits vitamin K.

DOACs

  • Stop 10a working