Hemostasis: Stages, Steps & Clinical Applications

Haemostasis is the mechanism that prevents the bleeding. The integrity of the blood vessel is necessary to carry blood to the tissues. The damage to the blood vessels is repaired by the process named as haemostasis , which involves the formation of clot at the site of the vessel injury. There are two stages of the haemostasis : Primary and Secondary. During the blood vessel injury, firstly there is transient vasoconstriction ( facilitated by serotonin) and then the primary haemostasis platelet plug formation occurs. Then secondary haemostasis occurs which stabilizes the platelet drug and is mediated by the coagulation cascade.

Primary Hemostasis

There are three stages - Adhesion, Activation and Aggregation.

Steps of Adhesion

• After an injury to the blood vessel wall, the collagen get exposed and VWF ( from Weibel- Palade bodies of endothelial cells and a-granules of platelets) binds to it.
• Platelets in the blood comes and bind to the VWF using the GP1b receptor.

                                     Steps of Adhesion

Steps of Activation

• Adhesion induces activation of a cascade effect and that will cause change in shape of the platelet called as Degranulation. 
• Platelets will release ADP which will expose the GpIIb/IIIa receptors on the platelets.
• Thromboxin A2 will be produced that will promote the next step that is called as Platelet aggregation.

                                      Steps of Activation

Steps of Aggregation

• Platelets will start binding each other at the injury site via GPIIb/IIIa using fibrinogen as a linking molecule. This results in the formation of platelet plug.
• This completes the Primary Hemostasis but the platelet plug is still weak therefore secondary hemostasis will play its role now to strengthen this plug.

                                     Steps of Aggregation

Also Read: Membrane Potentials & Resting Membrane Potential

Secondary Haemostasis

• There will activation of secondary pathway also called as coagulation pathway on the surface of the platelet that will strengthen the plug.
• Here Coagulation cascade will form thrombin which further tranforms fibrinogen in the platelet plug to fibrin.
• It has two ways- Intrinsic pathway and extrinsic pathway. Intrinsic pathway is initiated if blood is in the test tube.
• In Extrinsic pathway, Tissue factor combines with factor VII and activates the factor IX and X.
• The activated factor X is called as Xa and it will convert prothrombin into thrombin which further generates fibrin from fibrinogen. Thrombin will generate a positive feedback system that activates the factors on its own.

                                             Secondary Haemostasis

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Haemostasis/Coagulation pathways investigations

• PT ( Prothrombin time) and a PTT ( activated partial thromboplastin) testing are done.
• Prolongation of PT means there is a deficiency of any factor in the extrinsic pathway whereas prolongation of aPTT signifies the factor deficiency in the intrinsic pathway.
• Prolonged Bleeding time suggests the Primary haemostasis disorder.

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Haemostasis clinical applications

Vitamin K deficiency causes 2,7,9,10 factor deficiency but the factor 7 has the shortest life therefore during early Vitamin K deficiency only PT is prolonged but in the chronic stage , both PT and aPTT are prolonged.

Also Read: Hematopoiesis And Blood Cells

Disorders of Primary Haemostasis

• Immune Thrombocytopenic purpura ( Autoantibodies production against platelet antigens)
• Microangiopathic Hemolytic anemia
• Hemolytic uremic syndrome
• Bernard- Soulier syndrome ( gpIb deficiency leads to impairment of platelet adhesion)
• Glanzmann thrombasthenia ( gpIIb/IIIa deficiency leads to impairment of platelet aggregation)

Also Read: Types of Signaling in the Body / Endocrine System

Disorders of Secondary Haemostasis

• Hemophilia A
• Von Willebrand Factor disease ( disrupts primary pathway also)
• Vitamin K deficiency
• Liver failure

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