Changes in blood cells or plasma components can affect normal function of Hemostasis a complex process which causes the bleeding process (hemorrhaging) to stop. Often this includes the changing of blood from a fluid to a solid state. Both bleeding and thrombosis, the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system, needs to be highly regulated.
Intact blood vessels and the proper interactions between endothelial cells, and blood cells (platelets, red blood cells and white cells) are central to moderating hemostasis. The endothelial cells of intact vessels prevent blood coagulation by secretion of heparin-like molecules and thrombomodulin and prevent platelet aggregation by the secretion of nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells cease secretion of coagulation and aggregation inhibitors. Instead compounds such as von Willebrand factor and Tissue Factor, a protein present in subendothelial tissue, platelets, and leukocytes appear in the circulation, initiating vasoconstriction, temporary blockage of a break by a platelet plug, and blood coagulation, that seals the damaged region until tissues are repaired. In pathology, several factors can imbalance hemostasis, including PS exposing red blood cells, that act like activated platelets. In addition to alterations in markers of endothelial activation such as soluble VCAM 1 (sVCAM-1), a dysregulation of hemostasis can be identified by the activation of hemostatic pathways, and can be measured by altered levels of Fragment 1+2 (F1.2), D-dimer, or the thrombin-antithrombin complex (TAT).