Haemostasis Flashcards

1
Q

What is haemostasis?

A

The body’s reaction to injury or bleeding, formations of blood clots to prevent blood loss

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2
Q

What are the stages of haemostasis?

A
  1. Contraction of the blood vessel
  2. Unstable platelet plug formation (primary)
  3. Stabilisation of unstable platelet plug (secondary)
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3
Q

What 2 glycoproteins does platelet plasma membrane contain?

A

GP1a and GP1b

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4
Q

How do GP1a and GP1b work in forming a platelet plug?

A

When a vessel is damaged the GP1a can bind to the wall directly
GP1b binds to circulating von Willebrand factor which then binds to the wall of the damaged vessel

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5
Q

What physical change occurs when platelets use their glycoproteins to bind to the vessel wall or VWF and why?

A

They change from a disc shape to a more spherical shape with spicules, which help the platelets clump and form an unstable platelet plug
They also release the contents of their storage granules

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6
Q

What granules are present in platelets?

A

Alpha-granules and dense-granules

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7
Q

What is contained in the granules within platelets?

A

ADP, fibrinogen and VWF

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8
Q

How do the granules get released?

A

The platelet membrane invaginates, forming a passage to the surface of the cell

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9
Q

How does vasoconstriction occur in the first stage of haemostasis?

A

Arachidonic acid fromt eh membrane of the platelets is used to produce thromboxane A2, a vasoconstrictor

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10
Q

What does the release of ADP and thromboxane cause?

A

It causes a positive feedback loop, alongside thromboxane A2, which stimulates platelet activation and aggregation
The ADP binds to P2Y12 and thromboxane A2 to the thromboxane A2 receptor which causes the GP2b/3a receptor to change shape and become capable of binding to fibrinogen

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11
Q

What happens when fibrinogen binds to the activated GP2b/3a?

A

This further causes platelets to link together due to them binding to fibrinogen (primary haemostasis)

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12
Q

What does prostacyclin do?

A

It causes vasodilation and suppresses platelet activation, stopping them from aggregating when the blood doesnt need to clot

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13
Q

What does aspirin do?

A

Irreversibly inhibits the cyclo-oxegenase(COX) enzyme required for the production of thromboxane A2, therefore prevents platelet aggregation

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14
Q

Which factor does VWF carry?

A

Factor VIII

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15
Q

How is a unstable platelet plug stabilised?

A
  1. Blood coagulation produces thrombin

2. Thrombin cleaves fibrinogen to form a fibrin clot, stabilising the platelet plug

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16
Q

What clotting factors arent produced by the liver?

A

Factor VIII and VWF

17
Q

Which clotting factors require vitamin K to become activated?

A

Factors II, VII, IX, X

18
Q

Where do clotting factors work?

A

On the phospholipid membrane of platelets

19
Q

How does Heparin work?

A

It indirectly helps antithrombin work better so antithrombin can inactivate factors Xa and IIa(thrombin) quicker. Can be given intravenously or subcutaneously

20
Q

How does Warfarin work?

A

It is a vitamin K antagonist so stops factors II, VII, IX, X from becoming functional. Taken orally, taken in emergency as no need to monitor

21
Q

How do direct oral anticoagulants work?

A

They directly inhibit IIa or Xa

22
Q

How does flibrinolysis occur?

A

Tissue plasminogen activator(t-PA) and plasminogen come together on the clot by binding to fibrin, then plasminogen is converted to plasmin which breaks down fibrin to form Fibrin-degradation products

23
Q

What does tranexamic acid do?

A

Binds to plasminogen preventing it from binding to fibrin so it cannot convert into plasmin = no fibrinolysis

24
Q

What is thrombosis?

A

The formation of a clot in a stable vessel

25
Q

What factors contribute to thrombosis?

A
  • Something wrong with the components of blood
  • Something wrong with the vessel wall
  • How blood is flowing