 Whenever injury to blood vessels happens certain mechanisms get activated to minimize and stop blood loss from blood vessels. Now question arises why all these processes start only after vessel injury and why clot does not form without it. This is because of crucial balance which is maintained by anticoagulant and procoagulant activities. Now procoagulants we have already dealt with that is the factors which are causing activation of platelets and clotting factors. But what are the anticoagulant mechanisms? One is the presence of smooth endothelium itself. Then there is negative charge on endothelium which repels the platelets. Then the endothelium releases certain substances like rostocycline, nitric oxide, adpases which all keep platelet activation in check. So these are all basically preventing platelet plug formation. The ones which act on clotting mechanisms are different. There is thrombomodulin it's a transmembrane protein present on the surface of endothelial cells. Now this thrombomodulin actually binds with thrombin and this complex can in turn activate protein C to activated protein C. Activated protein C has directly anticoagulant activity because in combination with the protein S it inhibits factor 10. There is another protein known as antithrombin 3. So this was thrombomodulin. Now this is antithrombin 3. Now this antithrombin has the ability to bind with thrombin and inactivate it. Plus in presence of heparin the ability of antithrombin 3 to bind with thrombin increases many folds. Also this heparin antithrombin 3 complex has the ability to inactivate some other clotting factors that is 9, 10, 11 and 12. These mechanisms also keep the clot localized to the site of injury because the proagulant factors would become dominant only at the site of the injury because these endothelial factors all these factors even thrombomodulin is attached to the endothelium they will become ineffective at the site of the injury. Now if there is a problem with these anticoagulant mechanisms it would lead to formation of thrombus. Thrombus is nothing but inappropriate clot formation or excessive clot formation. These are dangerous since they can block blood vessels and thus decreases blood supply to the tissues. Now by knowing this we can reasonably predict when thrombus formation may occur obviously one when there is excessive endothelial injury. Second we also know that the stool is for platelet addition is the high shear stress. So in cases where there is high shear stress it leads to platelet blood formation so second will be high shear stress. Not only high shear stress stasis of blood so third is stasis of blood also leads to thrombus formation because it prevents wash out of platelets and coagulation factors from that particular site. Normally they are in circulation and will are constantly removed and they are not allowed to accumulate at one particular site. So wherever vessels are dilated like in case of aneurysms or if there is a blockage of say atrial outflow as in a mitral valve stenosis it leads to atrial dilatation that is also causing stasis of blood. If there is slow movement of blood due to high resistance to flow occurs in polycythemia. So there is high resistance to blood flow blood starts moving slowly that also predisposes to thrombus formation and obviously third one if there is inherent problem with clotting factors or there is deficiency of any of these anticoagulant mechanisms.