Platelets and Haemostasis

  • Platelets are fragments of megakaryocyte cells from the bone marrow, containing mostly cytoplasm which, crucial to platelet function, contains (alpha-) granules
    • Production is thought to be stimulated by thrombopoeitin which is released from the liver and kidney.  They have a lifespan of around 10 days.
    • Alpha granules contain substances such as von Willebrand factor, fibrinogen and platelet factors important in haemostasis


Has 3 major components

  • Vascular spasm
    • A damaged vessel immediately goes into vasospasm.  This is thought to be secondary to the effects of mediators such as serotonin released from platelets
  • Platelet plug formation
    • Platelet adhesion
      • von Willebrand factor present in the blood adheres to exposed collagen from the damaged vessel.  This can then bind to receptors on the platelets
    • Platelet activation
      • The collagen then activates the platelets and causes them to change their morphology to make them, essentially, more ‘sticky’ to other platelets.  They also release mediators, such as ADP, to aid this process by binding to other platelets
        • ADP, however, is also important in the suppression of clot overgrowth as it stimulates the release of nitrous oxide and prostaglandins from adjacent normal vessel wall.  These are powerful inhibitors of plug formation.
      • The whole process takes minutes.  The platelets contract and strengthen the plug to allow clot formation to occur.
    • Clot formation
      • Essentially the conversion of fibrinogen (factor I) (disorganised/soluble molecule released by the liver and present in the blood) to fibrin (insoluble, thread like molecule)
        • Catalysed mainly by thrombin.  Thrombin (factor IIa) also activates clotting factor XIII, important in stabilising fibrin.
          • Thrombin is not normally present in the blood (otherwise clotting would occur continuously), so it needs an activating system- the clotting cascade.
      • The clotting cascade



        • The intrinsic pathway is activated in tissue damage or blood exposed to an external environment i.e. all the components present in blood
          • Initiator is factor XII (Hagemen) activation (by exposure e.g. to collagen, glass etc)
        • The extrinsic pathway is activated by tissue thromboplastin (factor III) and factor VII.  Factor III is not found in blood but in damaged tissues.
  • Clot breakdown
    • Main mediator is plasmin.  Again not normally present in the blood- requires plasminogen to be converted (this is done by several factors including Hageman’s factor)

Preventing inappropriate clot formation

  • Plasmin can also be activated by tissue plasminogen activator (tPA) which is released from many tissues (especially lung)
    • This activates plasmin to breakdown any ‘accidental’ clot formation

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