Haemostasis

Question 1

Define haemostasis

Answer 1

Stopping of haemorrhage/prevent further bleeding

Question 2

3 main steps of haemostasis

Answer 2

1) Clot initiation
2) Clot formation and control
3) Fibrinolysis

Question 3

How are platelets activated?

Answer 3

1) binding to collagen
2) ADP (from activated platelets and injured RBCs)
3) Thromboxane A2 (activated platelets)
4) Thrombin

Question 4

Describe what platelets do when activated

Answer 4

1) Stick to subendothelium (collagen) through vWF
2) Aggregate with other platelets (fibrinogen mesh)
3) Swell and change shape into sticky and spiny spheres
4) Secrete factors to help grow platelet plug and aid clotting

Question 5

How does Aspirin decrease platelet aggregation?

Answer 5

It irreversibly inactivated cyclooxygenase (enzyme for producing thromboxane A2)

Question 6

Describe the clotting cascade

Answer 6

-amplification system activation of precursor proteins to generate Thrombin 2A

Question 7

What does Thrombin 2A do?

Answer 7

Converts soluble Fibrinogen to soluble Fibrin

Question 8

What does Fibrin do?

Answer 8

Enmeshed platelet plug to stabilise it

Question 9

What do vascular walls do during haemostasis?

Answer 9

• Vasoconstrict = decrease pressure downstream
• promote clotting = produce more vWF and collagen exposure
• decrease clotting = secrete plasminogen activator and thrombomodulin (activate protein C which is an anticoagulant)

Question 10

How is haemostasis/clot formation regulated?

Answer 10

1) Natural anticoagulants = stops further coagulation by inhibiting further activation of thrombin 2A e.g. protein C, protein S, anti-thrombin
2) Fibrinolysis

Question 11

Describe Fibrinolysis

Answer 11

Dissolving of a blood clot

-plasminogen activator converts plasminogen to plasmin (enzyme that destroy fibrin clot)

Question 12

How is coagulation measured clinically?

Answer 12

Measure factors in clotting cascade to see which pathway is malfunctioning (intrinsic or extrinsic)
PT (prothrombin time) = extrinsic; requires endothelial injury
APTT (activated partial thromboplastin time) = intrinsic; can happen without endothelial injury

Question 13

Describe Haemophilia A

What it is, presentation and treatment

Answer 13

• X-linked recessive
• deficiency of factor 8
• present with easy bruising, haemorrhage after trauma, spontaneous haemorrhage from minor trauma
• normal platelet count, bleeding time and PT BUT longer APTT
• treat with recombinant factor 8 and DDAVP (increase release of factor 8)

Question 14

Describe Haemophilia B

What it is, presentation and treatment

Answer 14

• X-linked recessive
• deficiency in factor 9
• present with easy bruising, haemorrhage after trauma and spontaneous haemorrhage after minor trauma
• treat with recombinant factor 9

Question 15

Describe Von Willebrand’s disease

What it is, presentation and treatment

Answer 15

• (usually) autosomal dominant
• deficiency/abnormality in vWF = abnormal platelet adhesion and reduced f8 activity
• present with skin and mucous membrane bleeding (e.g. epistaxis) and prolonged bleeding after trauma
• longer bleeding time and APTT
• no cure but can be managed

Question 16

Describe thrombocytopenia

What it is, presentation and treatment

Answer 16

• severely lowered platelet count than normal range
• prolonged bleeding time but normal PT and APTT
• present with spontaneous bleeding from small vessels such as in GI
• causes: decreased platelet production, decreased platelet survival, sequestration and dilution
• treat with blood transfusions

Question 17

Describe disseminated intravascular coagulopathy

What it is, presentation and treatment

Answer 17

• clotting activators in blood causing microthrombi formation throughout circulation (consuming platelet, fibrin and coagulation factors)
• usually a complication of a different disease e.g. sepsis
• occasional treatment of heparin (anticoagulant)

Question 18

Describe thrombophilia

Answer 18

A group of inherited or acquired defects in haemostasis leading to a predisposition to thrombosis e.g. abnormal factor 5, anticoagulant deficiency