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
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