Thrombosis

since dr. Mann 3 from Team M Lea's concur now I'm going to discuss about the thrombosis in this video so if you see you know in her body there is an inbuild system so this in bill system will help us to help help the blood in our body to remain in the fluid state or me otherwise the blood if you take outside from our body it will clot okay but inside the body there is an inbuilt system to make the blood to stay in the fluid state it is a normal mechanism in our body and there is a there is a process called as thrombosis and this thrombosis means the formation of a solid mass in the circulation and this solid mass in the circulation fly which is formed from the constant of fluid flowing blood is Corliss a thrombus solid mass is called as a thrombus where this process an entire process is called as a thrombosis so to prevent or to I mean to prevent this thrombosis there are few inbuilt mechanisms in our body and we'll see few factors which are responsible for the thrombosis so if you see here the endothelial injury platelets altered blood flow hypercoagulability state and coagulation system all these factors will have an ecological role in the formation of the thrombus and there are two primary events three primary events which was given by the virtue and the three primary events which predisposed the thrombus formation these are the three events which predispose the thrombus formation which is called as a virtual stride and this includes hyper Kollek cog lability state stresses of the blood and the vessel wall injury so these three muscle wall array and ethereal injury altered blood flow or stasis of blood or a hyper causal ability of blood all these three includes the but just right now we will see the each predisposing factor in detail first we see with the endothelial injury okay actually in fact endothelium has many functions if then in the game is intact so this intact endothelium will protect the flowing blood from the formation of the thrombus and it has the antithrombotic factors antithrombotic factors that which inhibit the thrombosis like heparin like substances which will accelerate the antithrombin 3 thrombomodulin which will convert thrombin into activator of protein c and anticoagulants so this proteins is a Anti Copeland so this thrombomodulin will convert the thrombin into the activator of proteins and inhibitors of platelet aggregation such as a BPA's and PGA Tour cross society and the tissue plasminogen activator which accelerates the fibrin all I take that means it will have a clot lysis activity so these are the important protective mechanisms which prevent the thrombus formation which is seen in the intact endothelium and and there are new few prothrombin factors are also which is released by the pro Coughlin pub properties okay they are thromboplastin one Willebrand factor and platelet activating factor so this thromboplastin will be released from the endothelial cells and one Willebrand factor will cause the apperance of the platelets and platelet activating factor which is activator and aggregator of platelets these are the prothrombin thrombotic factors and in the previous slide we have seen the antithrombotic factors so this diagram defect depicts this thing so usually if the induct end of intact endothelial is there it will prevent the thrombosis formation but if there is any endothelial injury you can see here endothelial injury will expose this sub endothelial matrix to the circulating blood and this an exposure of the sub endothelial matrix to the circulating blood will initiate the three steps that is addition and release an aggregation of platelets and this addition release an aggregation of the platelets okay this is the second step and in the third step there is the activation of the coagulation cascade which results in the fibrin strands and the thrombus formation so these are the steps or the events which occurs if there is an a endothelial injury so that is the first predisposing factor the second thing is your platelet role so we have told you there are three steps in this thing that is platelet addition platelet release action and the platelet aggregation so if you see this platelet addition the important two things are there here to remember one is glycoprotein one P receptor i'm the von Willebrand factor okay this glycoprotein 1b receptor on the platelets it is present on the platelets and it will recognize the site of endothelial injury remember this point this receptor will recognize the site of endothelial injury whereas one Billy Miliband very synthesized by the endothelial cells will bind to this GP 1b receptor and forms the from addition of the platelets these two will leads to the form addition of the platelet so that's why if there is any deficiency of one Willebrand factor which occurs in the von Willebrand disease and or absence of this GP 1b receptor which is seen in but not Sawyer disease remember this thing CP one be receptor is absent in but not solely a disease so if these two things are there it results in the abnormal platelet addition which finally leads to the abnormal bleeding so this is regarding the platelet addition and the second step is will be of your platelet release action so this activated platelets will undergo release reaction there are two types of platelet granules release year dense bodies there and this dense bodies liberate the ADP that is adenosine diphosphate calcium i'm the serotonin and histamine this dense bodies will liberate whereas this alpha granules will releases the fibrinogen fibronectin and platelet-derived platelet derived growth factor and the finally the platelet aggregation it is follow it will I mean like it follows the release of ADP and this is because of this which and platelet aggregation takes place so this is the role of platelets in the thrombus formation that is plated addition release action and the platelet aggregation is finally dissolved in the formation of a temporary hemostatic plug then the regulation of the coagulation system so this third predisposing factor will be of your coagulation system here there the protein you can see here the protease inhibitors these will act on the coagulation factor so that they will oppose the formation this isn't be in the normal state okay in the normal state this in the coagulation system protease inhibitors are present and this protease inhibitors will oppose the formation of thrombi and the example of this protease inhibitors include antithrombin 3 i'm thus even in activator and alpha 1-antitrypsin antithrombin 3 c 1 in activator and alpha 1-antitrypsin are the examples of this protease inhibitors and if you take the fibrinolytic system here the plasma is a potent classman is a potent fibrinolytic enzyme that means it will realize this it will make the lysis of a clot and here there are two type of plasma notion activators tissue type PA plasminogen activator which are derived from the endothelial cells and the uro kinase like plasma plasminogen activator which is present in the plasma so this is the regulation of correlation system so because of this protease inhibitors and fibrin light exists a thrombus is not formed in the in the blood normally then you can see here in this diagram so in the normally the this is the blood flow you can see the central stream consists of leukocytes and red cells and the platelets whereas the peripheral stream will be of a plus cell free plasma zone that is cells are absent in the peripheral stream and if you take when there is a turbulence or estas is flow this is the normal flow this is turbulence or a staches flow all the Bloods leukocytes that cells and the platelets will be margin ating and pea binding to the peripheries okay margin aiding and preventing the peripheries which will leads to the formation of a thrombus this is in the normal axial flow and this is the turbulence orestes is blood flow then this is the state colons the hypercar Goble state which is very important and this hypercoagulable state is also called as a thrombophilia and there are many reasons for this a hyper coral state and because of this hypercoagulable state there is an increased risk of venous thrombosis okay and this causes includes like an inheritor inherited or hereditary causes and acquired or a secondary causes if you take the inherited causes is deficiency of antithrombin 3 and usually mostly this condition is associated with the venous recurrent episodes of venous thrombosis then deficiency of protein C and the deficiency of protein s okay these are the autosomal dominant disorders and can be mostly associated with the thrombosis of leg veins and the mutation in the factor Phi Laden this is also an autosomal dominant race or disorder here the mutation will replace the original adenine is replaced by glycine at the position 5 0 6 it is very important in the mutation of factor 5 our name is replaced by the glycine at the final 6 position and the most common cause of thrombophilia mutation mutation in the factor v leiden is the most common cause of trauma and the defects in the fibrinolysis like this fibrinogen india and clasp nosing disorders and increased levels of coagulation factors like 2.8 this is due to because of them and genetic mutation and predispose to the thrombosis then coming to the IDE while the secondary factors which leads to the thrombophilia include advanced age prolonged bed rest to long immobilization cigarette smoking and obesity and other predisposing clinical conditions like heart diseases vascular diseases hyper Covell conditions like polycythemia and myeloproliferative disorders dehydration shock tissue damage late pregnancy and certain drugs like anise anesthetic drugs and oral contraceptives and hormonal replacement the replacement area predisposing clinical conditions and if you take this is a antiphospholipid antibody syndrome which is consist of a lupus anticoagulant antibody an anti cardiolipin antibody then these are the examples of their Amalek types of thrombi there is one more thrombi called as a cardio thrombi which can be seen mostly I mean like it can be seen as a vegetative growth on the cardiac and which result in the blood flow mechanical obstruction of the blood flow cardiac thrombi and here comes the arterial thrombosis I original origin iota there may be of aneurysms and arthritis if the origin is in coronary arteries you can see atherosclerosis misandric artery arteries of the limbs which includes a kilo sclerosis Bugis disease rain or diseases which are discussed and renal artery will also cause and cerebral or origin of the arterial thrombosis the origin of the venous thrombi the lower leg popliteal and iliac veins pulmonary veins hepatic and portal veins superior vena cava inferior vena cava misandric lines and renal veins all these are the origin of the venous and there are also called as capillary thrombi me there this is the very minut thrombi which composed mainly of a pack the red cells and these are formed in the capillaries in acute inflammatory lesions vasculitis and the disseminated intravascular coagulation and this vasculitis mostly feeling there are German disorders so those are the origin of the thrombi and here you can see the differences between the arterial and venous throw me in for tintin arterial thrombosis venous drama sites is more common in iota in the cerebral iliac femur renal and mesenteric arteries if you see the venous thrombosis or common in superficial varicose veins or a deep leg veins or a popliteal means and the thrombo genesis formed following the endothelial injury example of this arterial thrombosis three doses and please relate all these things here arterial and venous disorders are in the general surgery okay and this formed in the venous testing after following the venous tasks and example include abdominal operations and the childbirth and development usually mural and not excluding the human completely whereas this will be of usually occlusive in microscopy it will have a white frea bill with lines of John and surface this is very important whereas this is red blue with fibrin strands and John lines of Jan and this in microscopy also there is a distinct lines of Jan and here also lines of John with more abundant red blood cells are seen whereas here this distinct lines of xan consist of platelets fibrin and entangled with red and white blood cell so the difference you can see here the composition of this lines okay this is very important and finally it leads to the ischemia effect where it leads to thromboembolism edema ulcers and poor own healing this is the difference between ante-mortem trauma and the post-mortem thrombi in the grass picture you this anti Mottram bottom trauma will be of dry granular whereas this postmortem clots will be of gelatinous soft if it is other end to the vessel wall and this post-mortem clots are weakly attached to the vessel wall shape may or may not fit their vascular contours but here this postmortem clots will take the shape of the vessel and the microscope it contains apparent lines of zein whereas this is very very important the post-mortem clots will have will surface is a chicken fat alone covering the underlying red currant jelly okay the second fat alone and kuren jelly two words are very important these are seen on the microscopic picture and it is related to the postmortem clots then finally fate of thrombus want promise will defeat the outcome of thrombi can be like it will be like resolution resolution that means thrombus activates the thrombus will activate the fibrinolytic system by itself and which it releases the plasma okay the thrombus after activating the fibrinolytic system then a plasma is released so that this plasma will resolve the complete thrombus so this is the resolution one feet and the other fate is organization that means the thrombus will exclude from the vascular lumen and it becomes the part of the vessel wall the thrombus will become the part of the vessel wall and it will develop the new blood vessels and new recanalization blood flow it will develops the new things okay that is call as an organization that means it will organize its own blood flow and recanalization example includes the phlebology here in organization then the propagation that means that thrombus will enlarge in the size due to more and more deposition of the constant and finally it caused the obstruction of the important muscle and finally the thromboembolism thromboembolism means the thrombin early stage and the infected thrombi or quite I mean like they are very fragile and they will get int attached from the original site and they'll go in detached from the vessel one and result in the partial or a complete obstruction of blood stream such as Mbali in ends it is called as a thromboembolism okay in this the thrombus thrombus will get detached okay so this is the fate of thrombus that is resolution organization propagation and a thromboembolism so that's is that is the thrombus formation and here you have to remember about the differences between the post-mortem lot and antemortem thrombus and the the path I mean like predisposing factors of the thrombus formation okay remember one thing there is no elevator to success for every anything okay you have to take the stage that means you have to go hard for anything and along with your hard working just add a smart work also so that you'll succeed