Transcription
It's Medical Perfectionelis, where medicine makes perfect sense. We have talked about procoagulation and anticoagulation factors before today. Let's compare between the two, and let's get started and continue our series on bleeding and coagulation. Here is my playlist, and we have talked about all of this nice stuff before, so make sure to subscribe.
Anti-clotting versus pro-clotting: anti-clotting. Let's start with the smooth endothelium. It's smooth. Okay, if it's smooth, the platelet is going to adhere, so a clot cannot occur. Next, it vasodilates; it secretes nitric oxide, which vasodilates and inhibits platelet aggregation. It produces heparin-like molecules such as heparan sulfate, which stimulates antithrombin three, which inactivates the serine proteases. What are the serine proteases? Prothrombin, seven, nine, ten, eleven, twelve. Next is the prostaglandin I2, the prostacyclin, which keeps the blood cycling. What do you mean vasodilation and inhibits platelet aggregation? Thrombomodulin modulates the thrombin from being procoagulation to being anticoagulation; the TPA, which converts plasminogen into the active plasmin causing fibrinolysis. Heparin, heparin. Do we have heparin in our bodies? Yes, right now all of you have heparin in your body, no exception. It stimulates antithrombin three, which inactivates the serine proteases again: prothrombin, seven, nine, ten, eleven, twelve. Then heparin-like molecules. We've talked about this. It's the heparin sulfate protein.
CNS, the breaks of coagulation. They are vitamin K dependent. Those were the anti-clotting.
Pro-clotting: you told us that the smooth endothelium is anti-clotting. Yes, but the activated endothelium, the injured endothelium, is procoagulation, and it secretes the endothelin to help with the platelet blood coagulation, and it adheres to platelets thanks to GP1b and the great von Willebrand factor. Okay.
From boxane A2, it has three major jobs: vasoconstriction, increased platelet aggregation, and bronchoconstriction. What does bronchoconstriction have to do with this coagulation? Nothing. Tissue factor, also an s tissue thromboplastin, which activates the extrinsic pathway by activating factor seven into the active form of factor seven. The subendothelial causing which helps with primary hemostasis by helping platelets to adhere and then by helping secondary hemostasis, especially the intrinsic pathway by activating factor 12. The von Willebrand factor. Yep, adhesion. Who synthesized the von Willebrand factor? The answer is the endothelium, specifically that Weibel-Palade bodies. Who stores this von Willebrand factor? The endothelium and the platelets, because it's part of the alpha granules in the platelets. Platelets are procoagulation big time, or pro-clotting, the activated endothelium and the coagulation factors, which are beta globulins secreted by the liver.
Quick review of the arachidonic acid pathway by the cyclooxygenase. We have the prostaglandins, depending on the tissue. We have thromboxane A2 by the platelets and prostaglandin I2 by the endothelium; this promotes coagulation; this inhibits coagulation. Boom. That's it. Get all of my notes by going to patreon.com/medicosis. Thanks for watching. Don't forget to subscribe. This is Medicosis Perfectionales. As always, be safe, stay happy, and study hard. See you next time.