 The process of lemostasis consists of three steps, mesostasm, platelet plug formation and clot formation. In this video we are going to discuss platelet plug formation. Normally platelets in circulation are disc shaped in resting condition. So this is a resting platelet. These platelets can change their shape and release the contents of the granule when stimulated. The stimulation of this platelet occurs by various mechanisms. And the change in shape of the platelets and release of its granules is known as platelet activation. So activating the platelet spreads out and there are so many pseudopods. This is an activated platelet. From these two changes many other events happen in this process. The stimulus for platelet activation is present at the site of vessel injury. So before going into details we will just see in short what happens at site of vessel. So at site of vessel injury what happens these endothelial cells are injured there is exposure of sub endothelial collagen. At this site this one bilibran factor binds to the sub endothelial collagen. Now circulation is going on platelets are present in circulation. Because of this vessel injury what happens that there is a change in shear force or flow. And these platelets come here and bind with this one bilibran factor. Now on the surface of the platelets there is a protein known as GP1B which has affinity for this one bilibran factor. Now this process binding of GP1B platelet receptor with one bilibran factor is known as platelet addition. So in platelet addition basically platelets are binding to the sub endothelium by means of GP1B and one bilibran factor. Now because of this binding only there is change in shape of the platelets. So they become like this and there is also release of the granules. So the contents of the alpha and dense granules are released to the blood. Now these contents itself the contents of the granules that is ADP, thrombocene A2 these act on the platelets themselves. So these platelets have receptors for ADP, thrombocene A2. Now because of this there is change in affinity of another protein present on the surface of platelet that is GP2B3A. Once our affinity increases it binds to fibrinogen. So these platelets start binding to fibrinogen. There is cross linking between the platelets. So there is this fibrinogen which is bound to GP2B3A receptor of one platelet and also with the other. Then this further binds with fibrinogen of other platelets. So basically you saw that one bilibran factor in GP1B is mediating the binding between platelets and sub endothelium. While GP2B3A receptor is mediating the binding between platelets and other platelets. So this process of platelets binding with other platelets is known as platelet aggregation. So this one is platelet aggregation. So once we understand this process we can also know that what will happen in certain diseases like a decrease in one bilibran factor occurs in inherited disease which is autosomal dominant. Now there is another disease it's a rare disease though that in which there is abnormal GP1B receptor. So that is known as Bernat-Soliers syndrome. Again platelet iteration cannot occur in this. So in this kind of disease number of platelets is normal. There is problem in formation of platelet plug. Similarly there is a disease in which there is abnormal GP2B3A. So that is known as Clansmans from Besthemia. So platelet aggregation problem will be there in this disease. So all these will lead to bleeding disorders because there is abnormal platelet plug formation. Obviously if number of platelets is less that occurs in infections like dengue. There is the idiopathic thrombocytopenic perpura then also there will be problem in platelet plug formation. Now there may be certain diseases in which excessive platelet plugs are formed. In that case by knowing these mechanisms we can innovate this process. And for that there are ADP receptor antagonists present. So one example of such drug is Clopidogrel. Now similarly formation of thrombocytopenic A2 is blocked by aspirin. There is another drug which is used which blocks these receptors GP2B3A receptors. And these are its antagonist. So one example is AppSiximab. So it interferes with platelet aggression. But obviously when you are giving these drugs you have to monitor their dose because otherwise they will cause bleeding. They will block the required necessary platelet plug formation also. But how this platelet plug formation is kept in check normally? Because this process is a positive feedback process. You see that once addition occurs it releases these ADP thrombocytopenic A2 and there is platelet aggression. In turn these also activate further platelets. It is important that this process is kept in check at the site of vascular injury. Otherwise a massive platelet plug will form and keep on enlarging. Now this is done by release of certain chemicals from intact endothelial cells like prostaglandin I2, nitric oxide. Which prevent platelet plug formation then there is ADP's. ADP's leaves extra release ADP which is coming to the other normal site. Also they have a layer of glycocalyx which provides them negative charge. And normal endothelial surface also has a negative charge. So they repel each other. Plus this GP1B normally does not bind with this 1-billion factor. This is also circulating right. But it is not able to bind with it. It is only with change in shear force at the site of the injury that the affinity. There is change in affinity of GP1B towards 1-billion factor. Then only at the site of injury does this binding take place. Now since initial addition of platelets depends on shear force which is more in arteries and artery rewals. Platelets have a major role in hemostasis in arteries and artery rewals. Plus they are so sufficient to plug capillary injuries which occur daily. So that is these capillary injuries occur on a daily basis even without your knowing. Suppose if I clap like this, this sum of my blood vessels, small capillaries have broken. These are all plugged by platelets. Now that is the reason why to prevent or treat arterial thrombosis. Like in coronary arteries and cerebral arteries, anti-platelets are used. And what are anti-platelets? This clopidopril GP2B3 antagonist aspirin. While their sluggish flow is there, that is in veins. If any thrombosis occurs like in deep vein thrombosis, anticoagulants are used. Because fibrin clot formation is more important in veins.