 Damage, stop the bleeding. Now, at any, we already, the damage has already happened. We've started vasoconstriction and we've started activating our platelets to form the platelet plug. That isn't the clot formation. Clot formation is fast. Now, take a minute to think about this. Vasoconstriction, platelet plug, stimulates. Those things help stimulate the formation of a clot. And the faster a clot can form in damaged tissue, like the better off you're going to be. Those who can form clots faster are more likely to stop the bleeding. But if you form clots too fast, it's likely to be a done deal, dead doggy on the ground because your blood will clot all the way up. How? What? At any given time, you have procoagulants in your blood. These are proteins that prevent clot formation. And you have, excuse me, I said that totally backwards. You have procoagulants, pro-positive, go for clot formation. They're trying to make a clot form. And you have who? Anti-coagulants. And the anti-coagulants are saying, dude, we do not need to clot. Now, who's winning in undamaged tissue? Both of them are present. There are proteins that are found in the blood plasma. Both of them are present in the blood at all times, but anti-coagulants are present if they're in a greater amount if there is no clotting that has happened. Upon damage, the procoagulants, the concentration of procoagulants in your blood increases. Why? The damaged vessel creates chemicals that the activated platelets create chemicals that increase the number of procoagulants in the system. Watch this amazingness. The procoagulants, there's like a jillion of them. Okay, maybe not that many. There's a whole bunch of them, and it's this crazy complex, like what? Multiple pathways that we can end up with, but they all end up doing the same thing ultimately. It's like a cascade of chemical reactions. One procoagulant feeds into the next one, which feeds into the next one, which feeds into the next one, until we ultimately end up with a substance called pro-thrombin activator, pro-thrombin activator. And I could totally show you a picture, and we could memorize all the procoagulants that are involved in all the different pathways and how you know you're going to go one pathway or the other pathway, but the end game is that we get pro-thrombin activator. Pro-thrombin activator, what do you think it does? Dudes, it activates pro-thrombin. Watch, pro-thrombin, that says pro-thrombin. Pro-thrombin is this chilling plasma protein. It's not doing jack doodly. It's just floating around in your blood. And when it comes in contact with pro-thrombin activator, this is awesome, pro before pro-thrombin becomes thrombin. Now, pro-thrombin is produced in the liver. So let's just make a little star next to that, indicating that this guy is made in the liver. A lot of plasma proteins are, and I want to say something else to you. Vitamin K is involved in pro-thrombin production. So if you have low vitamin K, you're not going to be able to produce as much pro-thrombin. This is interesting. So if everything's normal, you have normal amounts of vitamin K, not all this pro-thrombin floating in your plasma. Thank you, liver. Now we've had damage. We get a pro-quaggulant crazy cascade. And now we have pro-thrombin activator, which turns pro-thrombin into thrombin. Guess what thrombin does? Thrombin is not the end game. There is another plasma protein floating around in your blood, produced also by the liver, and it is fibrinogen. Fibrinogen, fibrinogen also produced in the liver. Let's make our little star there so that you remember that this is just another plasma protein. Garbage, just producing osmotic pressure. Awesome. Just hang out there. Do nothing until it comes in contact with thrombin. And then guess what happens to fibrinogen? It's got to be orange, dog pounds got to be orange. It turns into a substance. Thrombin makes contact with fibrinogen, causes a chemical reaction and turns fibrinogen into fibrin. And guess what a blood clot is made out of? Fibrin fibers, in fact, look and be amazed. This is a red blood cell and these are fibrin fibers. Fibrin is just a protein, fiber that is sticky and grabs blood cells, it grabs anything in the vicinity and it makes this net of total madness. And the fibrin is actually the bulk of a clot. Over time, the clot itself, the fibrin equals the clot. Like it's this sticky net that creates an actual blood clot. Fibrin, when it, over time after the clot has formed, it actually retracts platelets, play a role in that. Platelets have, you know, they get all puffy and activated. They also have calcium in their endoplasmic reticulums because remember they have some cell parts, those platelets do. They release calcium into their cytoplasms and then they have these contractile proteins inside them like muscles and that actually causes them to constrict, to tighten down and your clot like squeezes down and becomes tighter and smaller. And fluid is squeezed out of your clot and that's like that clear, fluid-y stuff that can come out of a damaged wound. That's the process of the shrinking, like I imagine it, like you're ringing out the blood clot, you're making it take up less space and there's fluid that comes out of that clot that you just formed and as it gets contracted, it has an actual name, retraction. Clot retraction just means it's like tightening down, it's becoming more dense. It becomes a layering or a covering that's super tough, like scabs are not messing around. It's a scab. You just made a scab through the process of retraction. There's something else that I really wanted to tell you about. Oh, so, oh no, I already told you that, that the healthy cells are producing like undamaged cells are producing the anticoagulants that prevent clot formation in the first place. Okay, how do you feel? Oh, no, this was the really cool thing. Okay, I knew there was something really cool that I wanted to remember at the end. The clot forms and it's also a, like you can imagine, if you take too long to clot, it's not going to be very effective. So the clot, as it forms, it covers up the damaged endothelium. You've got this whole positive feedback thing that's happening, but eventually the clot covers the damage which prevents the stimulus that creates all these procoagulants and ultimately you have a negative feedback. That prevents clotting from all the way all over the place. So the, the healthy tissue surrounding the damage, the healthy tissue goes back to producing its anticoagulants, to producing things that are going to keep your blood vessels happy and open and not clotting. And it's because the clot covers over the damage. Once that damage stimulus is removed, then the clot formation stops. How do you feel? I have to just say one more thing? No, I won't. Okay, now let's talk about some mechanisms that might work, some mechanisms by which anticoagulants might function.