Haemostasis

Haemostasis occurs as a result of three processes, vascular spasm, platelet plugging and the coagulation cascade

Vascular Spasm

Smooth muscle of vessel constricts after damage or cuts

Platelet Plugging

Activated platelets become sticky and adhere to the injury to form a temporary plug - sufficient to block small wounds and capillary bleeding

Damaged epithelium causes a "release reaction" in platelets during which their inert contents are activated

Coagulation Cascade

Blood clotting

Necessary factors for clotting

Factors I - XII

I fibrinogen

II prothrombin

III thromboplastin (released on tissue or platelet injury)

IV calcium ions

VIII antihaemophilic globulin (antihaemophilic factor A)

IX Christmas factor (antihaemophilic factor B)

Fibrin + blood cells forms a clot

The clot later shrinks as healing progresses

Stages in clot formation

A clot may be initiated when collagen from damaged vessel walls comes into contact with factor XII (Hageman factor) casing it to be activated. Alternatively thromboplastin is released from damaged tissue and platelets.

platelet breakdown collagen + factor XII

thromboplastin

tissue damage activated factor XII

calcium ions

prothrombin ---------------- thrombin

fibrinogen ------------------ fibrin + cells + plasma = clot

Factors influencing clotting

• Vitamin K is necessary for the formation of prothrombin, obtained orally/im and synthesised by bacterial flora in large bowel

• Heparin prevents conversion of prothrombin to thrombin

• Bile is necessary for all fat soluble vitamins (K) absorption

• Rough surface in a diseased vessels may lead to formation of thromboplastin and on to a thrombosis

• Sodium citrate de-ionises calcium in blood and is used in transfusion blood

• Streptokianase is thrombolytic

Causes of bleeding

• local causes eg. failure to secure wound after surgery

• tissue damage - contusions

• thrombocytopenia

• liver disease

• anti-coagulant drugs

• massive blood transfusion

• genetic blood disorders

• viper venom

Fibrinolysis

Plasminogen (a plasma protein) is trapped in the clot.

Damaged tissues and vascular endothelium release a substance called tissue plasminogen activator.

Over the course of a few days this will progressively convert the trapped plasminogen into plasmin.

Plasmin acts as a protein digesting, (proteolytic) enzyme which breaks down the fibrin (Plasmin is also sometimes called fibrinolysin).

Tissue plasminogen activator

plasminogen -------- plasmin

insoluble fibrin --------- soluble products