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Anticoagulation and thrombolysis | Health & Medicine | Khan Academy



okay so here we have a blood vessel and it's been injured so right now I want to do an overview of hemostasis first we want to make sure when a blood vessels been injured that the blood that's flowing through that blood vessel continues to flow through the blood vessel and we try to minimize as much as possible the amount of blood that leaks out of the blood vessel at that side of an injury and the way we do that is through hemostasis and the first part of hemostasis is making that platelet plug and this happens during primary hemostasis but it's still kind of weak so we need to make it stronger and the way we make it stronger is during secondary hemostasis and what we do is we get this protein called fibrin and we link it up together and we create this fibrin mesh over the platelet plug and this fibrin mesh over the platelet plug is what we call a clot now what were to happen if hemostasis were to continue and nothing were to stop it so we just get clot after clot after clot after clot so you can see that that's a problem now the blood that should be flowing flowing through is getting backed up behind this clot and not getting to where it needs to go so even though hemostasis is good if we have too much clotting then that can be bad so our bodies need a way to make sure we don't get many clots so let me get rid of these clots and the way that our bodies do this is through two processes called anticoagulation and thrombolysis anticoagulation is the process that prevents any clots from forming and thrombolysis is the process that breaks down clots after they've been formed and these two processes are what I'm going to focus on today and this tug-of-war between two competing processes happens a lot in our body our bodies like to maintain a certain equilibrium a middle ground a set point we have a normal in on a day to day basis our bodies need ways to get back to normal let's take body temperature for example our body's like to stay at 98.6 degrees Fahrenheit which is about 37 degrees Celsius so that's normal that's where we'd like to be at of course it's a range so it can be a little bit higher a little bit lower but nothing too drastic but sometimes we can get lower than that and it can be too cold say it's snowing outside and you don't have a sweater and so what our bodies do in order to get our temperature back up is we shiver our muscles create create heat to get our bodies back up to the temperature that we like or sometimes our bodies can get too hot say we have a fever we're sick or or maybe we're running on a hot day and what our bodies do in order to cool ourselves off and get a temperature back down is we start sweating and that calls us off and that lets off the extra heat that we have in our body and that gets us back to normal so let me erase this now and let me show you how this is similar to what's going on in our blood vessels so our set point our middle ground let's say good but good blood flow and this is important because if we have good blood flow then all our tissues are getting what they need they're getting oxygen and nutrients that's carried in our blood but sometimes we can have some injury to that blood vessel and then we'll start bleeding and that goes away from what we want which is good blood flow and so what we do in response to that to get us to get us back to having good blood flow as we go through hemostasis and that allows us to make a clot stop the bleeding at that injured blood vessel and get us back to having good blood flow but if we have to mention well stasis or any other any other process that causes us to clot we have too much clotting then as we saw before the clots can block the blood flow going through that blood vessel and so the way that we take care of that is through anticoagulation and thrombolysis and with these men with anticoagulation and thrombolysis will break down any cloud or prevent more clots from happening and make sure that we have good blood flow in your blood vessel so this is the balance between hemostasis and anticoagulation and thrombolysis let's go over exactly what our bodies do in order to prevent any clots or breakdown clots so let's talk about anticoagulation first in anticoagulation we want to prevent any clots from forming so we want to prevent hemostasis and in hemostasis we can prevent the platelet plug or we can prevent making the fibrin mesh so let's talk about making the platelet plug first and how we prevent primary hemostasis so here we have our platelets then are floating around in our blood so we don't we want to make sure we prevent clots from happening there's no injured endothelial cells so we don't need we don't need hemostasis to happen we don't need platelets to get there so our healthy endothelial cells will secrete 2 2 molecules they both do the same thing the first thing ly that they do is that they prevent platelets from getting to the endothelial cells I'm sticking to them so they kind of block the platelets from getting close and the other thing that they do is they act on the smooth muscle the smooth muscle cells of the blood vessel and they cause vasodilation and that's important because we want to make sure that our blood vessels stay open and blood blood is able to flow through smoothly these two molecules are called one of them is called process like prostacyclin this is a peptide and the other one is a chemical called nitric oxide so now let's talk about secondary hemostasis and how we prevent that in secondary hemostasis let me scroll over we make the fibrin mesh to make that platelet plug stronger which again in this case we don't need because there's no entry and so we don't need to make a clot and the way we make that fibrin mesh is we activate the coagulation cascade so here we have our clotting factors a family of the family protein and ultimately what when we activate the coagulation cascade what we'll end up with is getting thrombin and fibrin the fibrin linking up on top of the platelet plug is what creates a vibrant mesh and makes the platelet plug stronger so the way that our bodies our blood vessels prevent making prevent secondary hemostasis is through two different molecules that endothelial cells so these the same cells that are lining the inner inner wall of the blood vessels and these are the same cells that are making prostacyclin and nitric oxide we just talked about it makes two molecules one of them is called it's called heparin like molecule and this molecule is on the surface of the endothelial cell communicating with the blood and what this molecule does is it interacts with another protein that's already floating around in our blood this protein is called antithrombin 3 so you can see in hemostasis we have thrombin and we want to make a clot and now in anticoagulation we have antithrombin 3 and we want to prevent a clot so what will happen is antithrombin 3 will interact with this Hepburn like molecule and when antithrombin 3 interacts with heparin like molecule what it'll do is it'll inactivate thrombin so it'll prevent thrombin from making fibrin from fibrinogen and it will also inactivate a coagulation factor coagulation factor 10 and the second molecule that our endothelial cells have on the surface of their cells that's communicating with the blood is a protein called rumba module n' thrombo again means clot and module n' is module 8 so to change or alter so we said ramen is what gets fibrin from fibrinogen but what thrombomodulin wood will do is if there's thrombin floating around in our blood and we want to make sure that we don't clot too much is it'll get thrombin and it'll change what thrombin actually normally does which is make a clot so that it at is actually working in anticoagulation but it's not just thrombin and thrombomodulin that works in anticoagulation when we have thrombin and thrombomodulin working together in interacting with each other then now protein C with the help of protein s will get activated and once it's activated it will interact with the thrombin thrombomodulin complex those three things help with anticoagulation the way that it helps with anticoagulation is that it inactivates to specific calculation factors coagulation factor 5 and inhibits coagulation factor 8 so now that we covered anticoagulation let's talk a little bit more now about drum Bowl Isis so like I said in turn Bowl Isis we're breaking down the club that we already mean so the way that we're able to break down that clot is with this protein called plasmon I like to think of it as like a little shark floating around waiting to break down this clot so I'm going to draw it like this like a little saw and this protein is called plasma and what plasma will do is it will break down fibrin and fibrinogen but plasmon isn't floating around in our blood all the time or also we wouldn't be able to clot at all because plasma would be breaking down fibrin and fibrinogen all the time so we want to make sure that we can have plasma whenever we whenever we need it and we need plasmon whenever we don't want to make a clot and whenever we don't need to make the clot and so we get plasmin from plasminogen and just like fibrinogen plasminogen is made with just an extra piece of protein and the way we get plasmin from plasminogen is there are healthy endothelial cells again our endothelial cells will release and secrete plasminogen activator and this tissue plasminogen activator will take off that extra piece of protein from plasminogen and make plasmon so now let's zoom out and take a look at the entire picture of how anticoagulation and thrombolysis works

42 thoughts on “Anticoagulation and thrombolysis | Health & Medicine | Khan Academy

  1. Good effort and helpful. I think it could be made even better with different narration. Sal Khan and Rishi Desai had this way of expressing their own interest in the subject, infusing their narrations with their fascination. It's a real trick to be able to do that, and when it's achieved, it makes a video or talk more interesting and, consequently, easier to grasp. But nice job in any case.

  2. Great video! Thanks a lot!

    I would just add that the alpha-granules (from activated platelet degranulation) contains Thromboglobuline, which works as a plasminogen activator too!

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