Haemostasis

• The haemostatic response has three elements:
  • Vasoconstriction
  • Platelet aggregation
  • Clotting cascade

Vasoconstriction

• Occurs as a direct result of vessel injury
• Enhanced by vasoconstricting elements released from platelets
• Pain can also result in reflex sympathetic vasoconstriction

Platelet aggregation

• Platelets are formed in bone marrow from megakaryocytes
• Contain the contractile proteins actin and myosin
• No nucleus but contain endoplasmic reticulum and Golgi apparatus that can produce proteins
• Contain mitochondria that can produce ATP and ADP
• Can also synthesis prostaglandins and thromboxane A₂
• Have a half-life in the blood of 8-12 days
• In response to tissue damage platelets undergo a number of changes
  • Platelet aggregation can result in a 'platelet plug' that can block a small hole
  • Platelets adhere to damaged endothelium (via Von Willebrand factor)
  • Aggregating platelets releases arachadonic acid, converted to thromboxane A2
  • Calcium mediated contraction of actin and myosin results in degranulation
  • Releases ADP which can induces further aggregation and release in a positive feedback fashion

Clotting cascade

• The clotting cascade has two semi-independent pathways
• The intrinsic pathway has all of its components within blood
• The extrinsic pathway is triggered by extravascular tissue damage
• This pathway is activated by exposure to a tissue factor
• Both pathways result in activation of prothrombin (factor II)
• The final common pathway converts fibrinogen to fibrin monomer
• Polymerisation of fibrin results in the formation of long fine strands held together by H-bonds
• These are then converted into covalent bonds with stabilisation of the fibrin polymer
• The intrinsic path ways is relatively slow (2-6 minutes)
• The extrinsic pathways is quite fast (15 seconds)

Bibliography

Dahlback B.  Blood coagulation.  Lancet 2000;  355:  1627-1632

Last updated: 21 April 2009

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