 So at all times in your body right now there is a balance between substances that are anticoagulants and substances that are pro-coagulants, cragulants. And it's constant. There's a constant production of anticoagulants, but there's also a constant like, no, we might need to clot. We don't want to lose blood, so there's this push-pull that is constantly happening. Pro-coagulants are produced by damaged tissue, pro-coagulants result here and initiate clot formation. Anticoagulants are constantly saying, hey, dude, it's just a little issue. Let's settle down, platelets. You don't need to be doing your thing. Anticoagulants are produced by healthy endothelial cells, so they just chill and produce anticoagulants, which is how you don't end up with a crazy clot that gets rolling over here in clot formation land and basically clots your entire blood supply, as all that stuff starts happening and all of a sudden your whole system is clotted, because the healthy endothelium away from the damage is saying, it's great over here. Anticoagulant action, like no need to be clotting right now. Let's look at some mechanisms for how anticoagulants work. You can imagine. We have a whole process here. We have a bunch of molecular events. We have a mechanism by which we're getting clot formation. If you block any one of these steps at any part in here, you are going to function as an anticoagulant. An example of an anticoagulant is aspirin. Aspirin is a blood thinner. It's actually recommended for people to take a baby aspirin a day if you have heart disease, because thinner blood means fewer clots. Fewer clots means less of a chance that a little blood clot will get caught in your heart if you cause a heart attack or lodged in your brain and cause a stroke. That's a good thing. Let's avoid that. Aspirin is a cox inhibitor. You know what that is, right? Inhibit, inhibitor. No, you don't know what that means. Cox is an enzyme that produces thromboxane A2. If you inhibit the enzyme that's making thromboxane A2, you're going to inhibit vasoconstriction. You're going to inhibit activation of platelets and the platelet plug formation and all the chemical craziness that happens when platelets get activated. In that way, aspirin acts as an anticoagulant. There's an anticoagulant called cumidin or warfarin. I don't know which one is warfarin. I don't know which one is the term that's the most... One of them is like a generic term and one of them is a name brand term. I got nothing. This guy, it impacts potassium levels. I got to make sure that I got this right. Oh, no, no, no. I knew there was a K involved, but potassium sounded weird. Vitamin K, it blocks vitamin K. Now, you might be thinking, of course you're thinking, like, dude, vitamin K, what does vitamin K have to do with anything? Vitamin K is required to produce pro-thrombin in the liver. So if you don't have vitamin K, you're not going to make pro-thrombin. If you don't make pro-thrombin, you're not going to be able to have it activated by pro-thrombin activator and turned into thrombin, but you're not going to do fibrin. So anything that reduces vitamin K functionality is going to reduce your ability to form a blood clot. And I have one more for you. This one is called citrate. I mean, citrate is just a chemical name, like it's just a substance, but citrate actually comes in and combines with calcium and it renders calcium inactive. And you might be like, but calcium, like why do we care if calcium is inactive? I'll tell you why. Calcium is required for almost every single one of these steps over here, except for like three. All the rest of the chemical cascade crazy madness requires calcium in order to take place. So if you take calcium out of the scene, like if you render it inactive, then you can't form a clot. Citrate is apparently what they use when they hook you up to that aphoresis machine when you decide to donate platelets because you're a rock star. Calcium prevents clotting from happening. Holy moly, how's that? That makes perfect sense. You should know the mechanisms for those different anticoagulants and be able to relate them to the processes that are happening under normal circumstances during clot formation. All right, we just hemostaced and now we're going to look at the last, like little bit of blood function and that's the immune system. Now take a deep breath because for the most part it should be pretty straightforward but we're going to spend another two entire lectures talking about the immune system. So nothing, nothing in physio is ever straightforward. All right, I'll be right back.