Uncover the body's strategy for blood clotting to halt excessive blood loss. Learn about the crucial roles of endothelial cells, platelets, and fibrin in creating a platelet plug. Understand the chemical interactions between collagen and platelets, and the conversion of fibrinogen into fibrin, facilitated by tissue factor. Get a clearer picture of this essential process through the coagulation cascade. Created by Patrick van Nieuwenhuizen.
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- What medications can people take to reduce the chance of clots?(14 votes)
- There are a large number of medications that work in various different ways. Some affect the platelets like aspirin and clopidogrel. Others interrupt parts of the clotting cascade such as warfarin and heparin.
- What causes blood clots to happen where they aren't supposed to? When there isn't a break in the vessel.(13 votes)
- Clots can form for a number of reasons. Stating it simply, the introduction of any factor in the coagulation cascade will result in a clot in a fully functional coagulation system in the human body. These factors can be the result of medications, injuries, sickness, or introduction of foreign materials or compounds to the body. When we talk about a broken vessel most people think in terms of cuts and scraps, but blood vessels can break from impacts to the skin whether it results in a visible bruise of not, cell death and sloughing of the endothelial cells, or blood pressure causing ruptures.(14 votes)
- After the plug is made, what happen to the blood vessels? do the wall of the blood vessel grow around the platelet plug? how is the plug get rid of?
in general are the blood vessel cells regularly been replaced? how are they replaced? does the blood vessels cells divide and grow from the existing cells? are they constrained by the collagen? or can they grow out of their existing structure?(12 votes)
- At1:20, I believe there is a mistake. RBCs do not contain a nucleus.(3 votes)
- That is not a RBC and you're correct, they shed their nuclei before they enter circulation. What he is drawing is endothelial cells lining the blood vessel.
Hope this helped! :)(13 votes)
- At8:13he mentions tissue factor exactly what is that?(3 votes)
- Tissue factor is part of the coagulation cascade. It's a molecule in the tissue that, onece exposed, acts as a catalyst on a clotting factor, that ultimately leads to the formation of the fibrin clot.(4 votes)
- Due to the cut wouldn't the collagen and tissue factor enter the blood stream and later cause platelets and fibrinogen to collect together ??(4 votes)
- I believe the effect tissue factor has is localized to the injury, and once the clot is formed tissue factor will no longer "leak" into the blood. The interaction of blood components (fibrinogen) with tissue components (tissue factor) start this cascade - once they are no longer interacting (injury is plugged) there should no potential for a later clot to form within the blood.
Collagen is an extracellular matrix protein and shouldn't diffuse into the blood stream. Theoretically, there is probably a chance for a piece of collagen molecule to enter, but I strongly doubt enough to create a clot cascade. Additionally, I believe tissue factor is released during the injury by the tissue itself, not the collagen support protein/ecm. Thus, the theoretical entry of collagen into blood may not (I really dont think it will) even trigger such a cascade.(1 vote)
- When we knock our arm or leg on something we bruise ourselves and you notice that you have a mauve mark that eventually turns green and disappears. my question is Why do specialists warn about against flying a long distance too often because of D.V.T Does anyone know about this and what happens to someone who gets diagnosed with this complaint(2 votes)
- DVT is deep vein thrombosis, it is a blood clot in a vessel in your leg and has nothing to do with bruising. Doctors warn against too many long distance flights because you are sitting statically for too long without walking and getting your blood flowing. Sitting statically for too long too often can cause DVT.(4 votes)
- Is there any disease where people can't make clots? If so, for what reason it doesn't make them?(1 vote)
- The disease you are referring to is Hemophilia. There is a mutation in F8 or F9 gene leading to the production of an abnormal version of coagulation factor (reduce the amount of one of these proteins). These genes are passed on through X-linked recessive pattern. So if you are a female, both of your X-linked genes need to be recessive to get hemophilia. If you are male and the X-linked is the recessive for hemophilia, you will have this disease.(5 votes)
- So if the purple cells clog the hole where the vessel is broken will that kill you or will it save your life. Because it seems like it would save your life. So please someone answer me :)?(2 votes)
- is there a treatment to prevent blood clots?(2 votes)
- Yes… Anticoagulant (clot-busting) drugs like Heparin, Dalteparin sodium, Argatroban, Bivalirudin, Lepirudin, Heparin Sodium, etc. Also called blood thinners.(2 votes)
Let's look at a blood vessel. A blood vessel is kind of like a tube. I think you'll agree with me. It's a tube through which blood travels. So here I'm drawing a tube, and I'm gonna ask you a question which is what makes up the walls of this tube? Now, for a blood vessel, what makes it up, is something called an endothelial cell. So, actually, the walls are made up of these kind of gooey endothelial cells that are stuck together tightly and that together form a tube through which the blood will travel. So here I'm drawing a bunch of cells tightly stuck together. They're stuck together tightly to prevent blood from coming out, of course. So this is more or less what it looks like. Each of these is a cell, and so, of course, each one has a nucleus, which I'll just quickly draw like that. Now let's delete that and let's change views to something a little bit easier. So now here is the same blood vessel in cross section. And so these are the endothelial cells, which we're seeing in cross section, and maybe here we can draw the nucleus of this one. Maybe it's visible right there. So now we have blood moving through this blood vessel. Here are some red blood cells, and they're moving along, providing the body with oxygen. But a very important question to ask is what happens if this blood vessel gets damaged? So let's say that those two cells right there split open, and they break open. What's gonna happen if we don’t fix this is that all of our blood is just going to rush out here, and we're gonna lose blood. So what is your body gonna do about this? Well, it's going to use a special player that we haven't talked about yet, which is the platelet. So I'm drawing a platelet here. And a platelet is basically a tiny piece of a cell. It doesn't have a nucleus or anything. It's a tiny, little piece of a cell that your body uses to block up holes like this. So you have them floating around in your blood all the time. Here I'm drawing a bunch. And what happens is when you have a hole in your blood vessel, they're going to come together. They're going to stick together, and they're going to clog up this hole. And so, basically, they've built a little barrier so that we won't keep losing all our blood. So are you satisfied? Well, you shouldn’t really be satisfied because there's a bit question here which is why are these platelets clumping here, and why aren't they clumping, you know, for example up here? Why don’t they clump there or maybe even just in circulation? Why don’t they clump up like this? Because if what they do is to clump up, how would they know to clump up here and not here? What's telling them? These are things that we don’t want to happen so I'm gonna put a little X through them. And the solution to this problem is actually quite simple and beautiful. The point is that the environment in the blood vessel is different from the environment outside of the blood vessel. So outside, we have some things that we don’t have inside. And one of those things I'm going to draw here. I'm drawing it here, and it has a name. It's called collagen. So I'll write that down here. It's called collagen. You don’t have to worry too much about what it is. Collagen is kind of a structural protein that your body uses to give structure to things. And so the important thing is you have collagen down here, and you don’t have it here. You don’t have it here. You don’t have it here. And it turns out that collagen chemically interacts with the platelets. And maybe we'll draw a little spark there to show that they're chemically interacting. It chemically interacts them and causes them to stick together and form this plug that we're talking about. So we can call this, by the way, a platelet plug because it's plugging the hole. And by the way, just to be clear, you also have collagen up here and over here. So it's basically everywhere outside the blood vessels. Now it turns out that this is only step one of the clotting mechanism of your body. So up here we'll put number one, platelet plug. And there's actually two steps, because the platelet plug itself is not quite as strong as we would like it to be. So there's a second step which makes this plug stronger. And that second step involves something called fibrin. So we'll write that here, fibrin. And fibrin is not a little mini cell like platelets are or a fragment of a cell like platelets are. Fibrin is just a protein, and what fibrin is gonna do is it's gonna come here, and it's gonna try to strengthen this plug by forming this mesh of protein that's gonna hold all these platelets together and form a very tight object. Now these fibrin strands, that's what each of these, you know, little squiggles is. It's a fibrin strand. These fibrin strands are made up of little fibrin subunits, which I'll draw here. And it turns out that these subunits naturally like to come and stick together. And, I guess, the technical word for this is they polymerize. They form a polymer. Basically, they just stick together and lots of them will stick together in a line to give you this fibrin strand we see here. And where does this fibrin come from? Does it come from down here? No, it actually also circulates in the blood. So let's draw some little fibrin molecules up here. So they're circulating in the blood. Is this right? Well, this actually can't be exactly right, 'cause I just told you that these fibrin molecules naturally stick together. And so if we had these fibrin molecules circulating in the blood like this, what would happen? Well, they would actually stick together in the blood, and they would form these long strands in the blood that we didn’t want, because we only want the strands here at the platelet plug. So let me remove those strands. So it turns out that we don’t have fibrin circulating in the blood. What we have is something slightly different. We have fibrinogen. Fibrinogen. And so I'll draw a fibrinogen down here. Of course, keep in mind, these are all my little cartoons and probably it doesn't look like this. So these guys, we said, were fibrin. Fibrin. But now this molecule is a fibrinogen. And you'll notice it's the same as a fibrin, except it has an added, little piece to it, and that little piece, as you can tell, is gonna keep it from sticking to itself. These fibrinogen are not gonna be able to stick together the way that these fibrin are. So what to do we need to do then? Well, of course, we need to turn this fibrinogen into fibrin, but where are we gonna do that? Only at the site where we want fibrin strands to gather. So only here, where we have that damage. And so, again, we face the same question that we faced with the platelets, which was, how do they know, how do the platelets know to aggregate here? Well, likewise, we wanna know how do the fibrinogen know to turn into fibrin here so that they can then stick together and form the strands? And the answer, basically, is, luckily, the same. And so we have some chemicals down here. Now we're not talking about collagen anymore. We're talking about something else. And if you really want to know what it is, I'll write the name here but it's not really the name that's important. It's the principle here. So the principle is you have these little proteins down here called tissue factor. And they're normally not in the blood. They're only down here outside of the endothelial cells lining the blood vessel, and so these little proteins, tissue factors, are going to be right here in this little wound and around the wound, and there they'll cause these fibrinogen to become little fibrin protein molecules, and then those fibrin will be able to stick together, and they also stick to the platelets by the way. I hope I was clear about that. And form the mesh that we see there. Now if we want to get really fancy, we can ask how this tissue factor turned fibrinogen into fibrin. And you can ask, is tissue factor kind of like a little knife? And by knife I really mean enzyme. Is it a little knife or enzyme that causes this piece to break off of the fibrin so that we're left with just fibrin? And actually, unfortunately, the story is much more complicated than that. And there's actually a good reason for it. Because let me propose to you a situation. Let's say you have to turn a million fibrinogen into fibrin. Because each of these fibrinogen is a very small protein, so we need about a million of them to make up this clot here. And let's say that you are tissue factor. So you are tissue factor, and you want to turn a million fibrinogen into fibrin. Is the best way to do it for you to actually sit down and chop off this piece off of all these fibrinogen, one by one? That would take you a long time. Is that better, or is it better for you, as tissue factor, to call up five friends and have each of those call up five friends, and have each of those friends call up five friends, and keep doing that until you have a huge number of people there ready to help you? And now get all of those people to help you convert fibrinogen to fibrin. So, obviously, that latter scenario is a more efficient mechanism. And so that's what your body does, and that's what tissue factor does. So tissue factor, and by the way, I know this getting convoluted but try to stick with me. Tissue factor is going to turn another protein that we haven'the talked about, into its active form. And then that other active form of that protein that we haven't talked about, is going to activate another protein that we haven't talked about into its active form. And then that one is gonna do the same. And then that one is gonna do the same. And so, basically, every time you introduce a new protein there, you're ramping up the total number of activated proteins of that type. And so, finally, by the time you get to the one that's going to break the fibrinogen apart and create fibrin, and by the way, I'll draw him. And he has a special name called thrombin. Again, I don’t think thrombin is necessarily a word you need to know, but just in case. So by the time you get to thrombin, you have a lot more activated thrombin than you had tissue factor in the beginning. But the tissue factor here is the spark, and that's the guy that really got us going. So that's basically it. This is how your body plugs holes in blood vessels and keeps you from losing too much blood. And if you want to know more about that kind of complicated stuff I said at the end about, you know, all these different levels of activated proteins, you can look it up. It's called the coagulation cascade. And it's called the cascade because you're cascading through all these different levels of proteins.