Haemostasis

Question 1

What is haemostasis?

Answer 1

Cessation (stop) of blood loss from damaged vesicles by a specific sequence of responses

Question 2

What must haemostasis be?

Answer 2

Quick, localised and coordinated by cell-cell communitation

Question 3

What is normal blood volume?

Answer 3

4-6L

Question 4

What is a haemorrhage?

Answer 4

Loss of large amount of blood

Question 5

What are the phases involved in haemostasis?

Answer 5

1) Vascular phase
2) Platelet phase
3) Coagulation (blood clotting) phase

Question 6

What occurs in the vascular phase?

Answer 6

1) Vascular spasm - contraction of smooth muscle leading to vasoconstriction, only in arteries and arterioles

2) Changes in endothelial cells - they contract and expose basal lamina to blood - start releasing chemical factors and local hormones
- ADP (platelet
aggregation)
- Tissue factor (III,
extrinsic)
- Prostacyclin (reduces
spread of aggregation)
- Endothelins (peptide
hormones that stimulate
contraction of SM)
- Endothelial cells become more adhesive

Question 7

Why do endothelial cells become more adhesive in vascular phase?

Answer 7

They stick to the edges of a tear in small arteries/veins, sealing the tear
Can prevent blood flow along damaged capillaries by attaching to opposite sides

Question 8

What are platelets?

Answer 8

Anucleute platelets fragment 
Flattened discs
10 day life span
Production = thrombocytopoesis
Produced in bone marrow

Question 9

What happens in the platelet phase?

Answer 9

1) Platelet adhesion - rapid, stick to damaged part of vessel, required surface mem receptors
2) Platelet activation - change shape by swelling and spike extension, granulolysis releases ADP, serotonin, thromboxane A2, clotting factors (PF3), platelet derived growth factor and Ca2+
3) Platelet aggregation - soluble factors promote formation of platelet plug by +ve feedback loop

Question 10

How is platelet aggregation restricted to site of injury?

Answer 10

• Prostacyclin and NO release from intact endo
• Other compounds released from blood cells
• Aspirin

Question 11

What happens in the coagulation phase?

Answer 11

Starts ~30s after injury
3 pathways:
1) Intrinsic - collagen triggers activation of proenzymes
2) Extrinsic - release of tissue factor from damaged tissue
3) Common pathway - begins with factor X activation - thrombin causes more release of TF and PF3,

Question 12

Which is the fastest pathway of coagulation?

Answer 12

Extrinsic faster than intrinsic

Question 13

How is clotting restricted?

Answer 13

1) Anti-thrombin III in plasma inhibits thrombin
2) Heparin accelerates activation of ant-thrombin III
3) Thrombomodulin converts thrombin to another enzyme
4) Prostacyclin restricts aggregation

Question 14

What is fibrin?

Answer 14

Stabilising factor

Question 15

What is fibrinolysis?

Answer 15

Clot dissolving:

1) Tissue plasminogen activator and thrombin
2) Plasminogen
3) Plasmin
4) Digestion fibrin strands

Question 16

What is deep vein thrombosis caused by?

Answer 16

Inherited

Environmental - prolonged hospitalisation

Question 17

How can liver function be affected by haemostasis?

Answer 17

Synthesises and clears clotting factors etc

- Vitamin K deficiency: needed to synthesis clotting factors

Question 18

What is haemophilia?

What are the types?

Answer 18

Royal disease, abnormal/absent clotting
A: deficiency of factor VIII, X linked recessive
B: deficiency of factor IX, X linked recessive
C: deficiency in factor XI, autosomal recessive
Acquired haemophilia: rare autoimmune

Question 19

What is Von Wilebrand’s disease?

Answer 19

Most common inherited bleeding disorder

• Von Willebrand (vWF) deficiency:
  1) Type 1 - most common, less severe
  2) Type 3 - least common, more severe