so virtous Triad describes the three primary abnormalities that lead to the formation of a thrombus and a thrombus is basically just a blood clot and before we go into the three factors that make up verow Triad um I think it'd be helpful to quickly delineate the difference between what a thrombus is and what an embolis is because I remember being somewhat confused with what the difference was between these two terms so a thrombus is as I said just a blood clot but an embolis is any detached intravascular solid liquid or gaseous mass that is carried by the blood to a sight distance from its origin so basically an emis can be anything as long as it has just traveled from where it was formed or where it came from to the site that it is currently found in and a thrombus can become an embolis or a thrombo embolis if a piece of the blood clot breaks off and then lodges into a different part of the vasculature elsewhere in the body so it would be called a thrombus in the original site of clotting but it would be called an embolis in the site where it had traveled to so hopefully that helps clear things up a little bit so now on to what virchow's Triad is virchow's Triad is as I said made up of three factors and some would argue the most important factor is endothelial injury or basically injury to the blood vessel's inner wall that's what the endothelium is the second factor that makes up ver child's Triad is either turbulence or stasis of blood flow that is the second factor that makes up virtous Triad for thrombus formation and then the final third factor is hypercoagulability which is an increased propensity to clot so all three of these factors describe ver child's Triad which leads to the formation of a thrombus so thrombi can form anywhere within the cardiovascular system in the chambers of the heart on the valves between the four chambers of the heart they can form in the arteries that feed the heart the coronary arteries or other arteries and veins in the system so now let's go back to the concept of endothelial injury or injury to the blood vessel's inner wall this can be caused caused by a wide variety of insults including say hypertension uh or high blood pressure infection toxins any sort of metabolic disturbances like hyper lipidemia or high cholesterol and what happens is essentially there is loss of endothelium that can lead to exposure of the subendothelial extracellular Matrix and this initiates a clotting Cascade which leads to the adhesion of platelets release of tissue factor and eventually the formation of a fibron clot it's important to remember though that it's not always necessary to have an overt exposure of the endothelium for formation of a thrombus any disruption in the sort of dynamic balance of either prothrombotic or anti-thrombotic factors in endothelium can influence the local clotting environment of that vessel so now let's talk a little bit more about how turbulence or stasis plays a role in for child's Triad turbulence is just a fancy term for abnormal flow of any fluid in this case blood so if normal blood flow is smooth and organized or laminer like this then turbulent blood flow looks a little bit more disorganized like this you have little pockets of swirling blood that kind of has chaotic movement to it and turbulent blood flow can not only be caused by endothelial injury but it can also lead to further endothelial injury so it's kind of like a catch 22 and so these little local pockets of turbulence lead to stasis which is basically just slow flowing or stagnant blood and the disruption in laminer flow also brings platelets into contact with the endothelium so the actual slowing of the blood and the increased contact time that platelets and the blood have with the wall of the vessel leads to activation of these platelets to start the clotting Cascade and now back to hypercoagulability basically any alteration in the coagulation Pathways will predispose to thrombus formation and these causes can be divided into either primary or innate causes so in essence any sort of genetic mutations and plotting factors or proen genes one of the most common examples is Factor five lien mutation which you'll learn about in hology and then the second category of causes would be secondary or acquired causes such as the development of a heart arhythmia like atrial fibrillation so what is the fate of a thrombus once it has been formed well one of four things can happen so the first thing can be the thrombus just dissolves basically so dissolution and this occurs through the process of fibrinolysis or basically breaking up of the Little Fibers that make up the clot and the younger the clot the easier it is to dissolve with thrombotic agents such as tissue plasminogen activator explains why one of the indications for using this medication is that the claw is less than 4 and 1/2 hours old the second thing that can happen to to a thrombus is propagation so basically the thrombus just keeps growing and gets bigger by accumulating more platelets and fibrin the third thing that can happen is the thrombus reorganizes and re canalizes so recanalization which basically just involves the in growth of smooth muscle cells fiberblast and the endothelium into a fiber enrich thrombus and if this process proceeds it can provide capillary SES channels through the thrombus for continuity blood flow through the entire thrombus but this doesn't necessarily mean that sufficient blood flow for the metabolic needs of the downstream tissue has been met and then the fourth fate of a thrombus possibly the most dreaded fate is embolization which is as I said basically a part of the blood clot breaks off and then propagates further Downstream in the vessel or vasculature to another side in the body so what are the clinical consequences of thrombi well for Venus thrombi you often worry about the DVT PE one two punch so what is a DVT PE basically a DVT describes a deep Venus thrombosis which tends to happen in the lower extremity so somewhere in one of the deep veins of the leg legs and what happens is a piece of this D vain thrombosis or thrombus can break off and then propagate because of the way the vasculature is the anatomy of the vasculature it will break off and propagate to the pulmonary vasculature creating a pulmonary EMAs which is what a PE is and this can lead to extreme respiratory distress and even death so that is one important clinical consequence of the formation of a thrombus and that's usually for Venus thrombi so for arterial thrombi we worry about occlusion of important arteries such as coronary arteries that profuse her heart and cerebral arteries that profuse her brain so if you have the occlusion of any of these arteries they can lead to a heart attack and a stroke respectively so an MI which is a myocardial infarction or B basically heart attack and then stroke are probably the most key clinical consequences for arterial thrombi and then one dreaded complication is called disseminated intravascular coagulation or diic in DIC there's basically widespread fibrin thrombi in the microcirculation for any number of reasons which can cause diffus circulatory insufficiency in several organs and then because of all the consumption of the clotting f factors this actually leads to a concurrent widespread bleeding that occurs throughout the body so DIC is another disease entity to be aware of and now briefly just to go over the concept of an emis again there can be many types of emilii so there's of course a thrombo embolis like we talked about with the DVT PE combo where a piece of the thrombus from a deep vein breaks off becoming an embolis in the lungs uh you can also have fat embolis which usually occurs in major trauma where you have large broken bones and fat droplets from the marrow of the bones enters a circulation and can become lodged in uh any part of the vasculature you worry about the pulmonary vasculature causing respiratory distress and the same thing kind of goes with an amniotic fluid embolism which again occurs if there's some sort of trauma to the womb and some amniotic fluid were to accidentally enter the mother's vascul and embolize somewhere so just like in real estate for an embolis it's all about location location location and it's all about location because of the way our anatomy is linked together so for an arterial Source um it will usually propagate to any of the uh abdominal organs or the brain or any of the extremities whereas if you have a Venus Source it usually is likely to get caught somewhere in the pulmonary vasculature and very rarely you can have uh Venus EMAs that can propagate through a defect in the heart called a Paton Fame inov Valley and and Lodge into a cereal artery causing a stroke so there you have it now you know the difference between a thrombus and an embolis and you also know about the three factors that make up for a child's Triad