Haemostasis Process Overview

Haemostasis

• Haemostasis is the process that stops blood loss from the body when a blood vessel is cut or broken
• The sequence of events in haemostasis after injury to a blood vessel are:
  • Vascular spasm
  • Formation of a platelet plug
  • Formation of a blood clot and clot retraction
  • Growth of fibrous tissue into the clot to form a permanent seal at the point of vessel damage
  • Removal of excess fibrous tissue (fibrinolysis)
  • Repair of blood vessel endothelium

Vascular Spasm

• This is a process in which the injured blood vessel contracts to narrow its lumen, reducing blood loss
• The contraction is due to the response of the smooth muscle of the blood vessel to direct stimulation from the injury and nervous reflexes from pain impulses from the injured area or nearby tissues
• Vascular spasm lasts approximately 20-30 minutes

Formation of Platelet Plug

• There are approximately 200,000 to 400,000 platelets per mm of blood
• Platelets move freely along the lumen of blood vessels due to the smooth endothelial lining
• When a blood vessel is cut, the endothelium lining is breached, and platelets contact the underlying collagen fibres
• Contact with collagen or damaged endothelium causes platelets to become sticky and aggregate
• Platelets release ADP and enzymes (thromboxane A) that cause further aggregation leading to the formation of a platelet plug that seals the injured site

Formation of Blood Clot and Clot Retraction

• Blood coagulation occurs at the site of injury
• After the fibrin mesh is formed, the clot begins to contract or retract, pulling the wound edges together and reducing the size of the injured area, aiding tissue repair
• Fibrous tissue invades the clot, leading to dense fibrous tissue formation, which seals the cut in the blood vessel

Fibrinolysis

• Once the blood vessel is healed, fibrinolysis removes the clot to restore normal blood flow
• Plasminogen, trapped in the clot, is activated to plasmin which dissolves fibrin and breaks down the clot

Repair of Blood Vessel Endothelium

• The damaged endothelium is replaced by the formation of a new lining, marking the final stage of haemostasis

Blood Clotting

• Clotting factors are involved in forming a blood clot
• Blood clotting is caused by a series of complex mechanisms involved in converting prothrombin to thrombin, and fibrinogen to fibrin
  • Formation of thromboplastin (or prothrombin activator)
  • Conversion of prothrombin to thrombin
  • Conversion of fibrinogen to fibrin

Extrinsic Pathway

• Triggered by trauma to the vascular wall or surrounding extravascular tissues
• Involves release of tissue factor (Factor III) by traumatised tissue, which is composed of phospholipids and a lipoprotein complex that acts as a proteolytic enzyme
• Activation of Factor X
• Formation of prothrombin activator

Intrinsic Pathway

• Triggered by trauma to the blood or exposure of the blood to collagen from a traumatized blood vessel
• Involves contact of blood with collagen or a foreign surface to activate Factor XII, a proteolytic enzyme, damaging the platelets
• Activation of Factors XI and IX
• Activation of Factor X to create the prothrombin activator

Conversion of Prothrombin to Thrombin

• Prothrombin is formed in the liver with vitamin K required in its formation
• Prothrombin is converted to thrombin by the prothrombin activator in the presence of calcium ions

Conversion of Fibrinogen to Fibrin

• Fibrinogen is formed in the liver
• Thrombin converts fibrinogen to fibrin monomers, which aggregate to form fibrin threads
• Fibrin threads form a meshwork trapping blood cells, platelets, and plasma

Clot Retraction

• The final step in the clotting process
• Clot contracts a few minutes after clot formation, squeezing out most of the fluid (serum)
• Platelets facilitate clot retraction
• Myosin and actin in platelets are important for retraction
• Excess fibrin is removed (fibrinolysis) and damaged endothelium is replaced by new one

Clinical Correlates

• Vitamin K deficiency: Vitamin K is essential for clotting factor production in the liver. Deficiency leads to excessive bleeding.
• Liver disease: Liver diseases can cause clotting defects and bleeding.
• Haemophilia: A bleeding disorder caused by deficiencies in clotting factor VIII. Factor VIII has a large and a small component. Deficiency of the smaller component causes classic haemophilia. Deficiency of the larger component causes Von Willebrand's disease.
• Thrombocytopenia: Very low platelet count, resulting in bleeding.
• Thrombi and emboli: A clot that develops in a blood vessel is called a thrombus. A freely flowing clot is an embolus.

Anticoagulants

• Heparin and coumarins are used clinically to block important clotting stages or inhibit clotting factors
• Substances that bind to ionic calcium are also anticoagulants, as calcium is needed for clotting factor conversion

Mechanism of Assessment

• Bleeding time: Measures how long it takes for a small cut to stop bleeding, assesses platelet function
• Clotting time: Measures the time it takes for blood to form a clot
• Prothrombin time: Measures the time between the addition of procoagulants and the occurrence of clotting, inversely related to prothrombin concentration.

This quiz covers the essential steps and components involved in the haemostasis process, which is critical for stopping blood loss. You will learn about vascular spasms, platelet plug formation, and how the body repairs damaged blood vessels. Test your knowledge of these vital physiological responses.