Hemostasis: drives from the Greek meaning “The stoppage of blood flow”. a process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel. It is the first stage of wound healing. Hemostasis can be divided into two stages: Primary and Secondary. 1- Primary hemostasis includes the platelet and vascular response to vessel injury. 2- Secondary hemostasis includes the coagulation factors response to such injury.
Together, platelets, vessels, and coagulation factors combine to stop bleeding and allow for vessel repair through formation of a stable fibrin-platelet plug at the site of injury. Primary Means, it is individual there is no dependence, But Secondary will always depends on Primary, primary first should complete, There is no precondition to primary, but for Secondary Primary is the Precondition, first there should do primary, then only it would able to do secondary. * Primary hemostasis is characterized by vascular contraction, platelet adhesion and formation of a soft aggregate plug. It begins immediately after endothelial disruption. Injury causes temporary local contraction of vascular smooth muscle. Vasoconstriction slows blood flow, enhancing platelet adhesion and activation. Secondary hemostasis
Responsible for stabilizing the soft clot and maintaining vasoconstriction. Vasoconstriction is maintained by platelet secretion of serotonin, prostaglandin and thromboxane. The soft plug is solidified through a complex interaction between platelet membrane, enzymes, and coagulation factors. Coagulation factors are produced by the liver and circulate in an inactive form until the coagulation cascade is initiated. The cascade occurs in steps. The completion of each step activates another coagulation factor in a chain reaction which leads to the conversion of fibrinogen to fibrin The clotting cascade is made up of a number of protein factors which ultimately generates fibrin. There are 2 pathways by which these factors may be activated, the extrinsic and intrinsic pathway. The clotting cascade
is the made up of a number of protein factors which ultimately generates fibrin, the protein basis of a clot (a) form is the activated form. I.e. thrombin (IIa) is the activated form of prothrombin (II). Most clotting factors are produced in the liver and circulate in the plasma in their inactive forms. There are 2 pathways by which these factors may be activated, the extrinsic and intrinsic pathway. Many of these factors (II, VII, IX and X) require vitamin K for synthesis. It is a fat soluble vitamin produced by enteric bacteria and is required for the gamma-carboxylation of glutamic acid residues. A dietary deficiency, impaired absorption or warfarin administration will lead to a decrease in these factors. Consequentially, a decrease in these factors will lead to increased incidence of bleeding. Warfarin is a vitamin K antagonist and its administration will mimic a dietary deficiency of vitamin K. As a final note, the cascade has a number of steps and is advantageous in 2 ways. First, it provides an amplification mechanism so that a small stimulus may initiate a larger response. Second, many steps allows for many foci of regulation, both positive and negative. Extrinsic:
Clotting, via the extrinsic pathway, is initiated when collagen within the tissue becomes exposed due to an injury. What is exposed is Factor III (tissue factor). Factor III combines w/ Factor VII that is floating around in the serum to become VIIa. VIIa, along with more Factor III, cleaves or cuts Factor X to become Xa. Xa, plus some Va, converts Factor II (prothrombin) to Iia (thrombin). The activation of thrombin happens on the surface of the platelets and causes the platelets to become further activated and release more chemicals that result in the platelets sticking to the wound site. While the platelets begin to stick to tissue, thrombin continues to work by turning fibrinogen to fibrin. The...