Secondary hemostasis is the process where the platelet plug initially created in primary hemostasis is reinforced by the conversion of fibrinogen to fibrin. Created by Gricelda Gomez.
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- How can thromboplastin activate the coagulation cascade and how it just simply released into our blood flow if it was at first something that could not come out from our blood vessel(2 votes)
- I didn't understand why the phospholipid bilayer was required for the fibrin mesh, located towards the abrupt ending of the video, where you emphasised on it for just under 5 seconds, could anybody quickly clarify why it is important?(1 vote)
- phospholipid bilayer is important for most part for creation of fibrin mesh as well as most of the secondary hemostasis cascade pathway as it interacts with the calcium ion and helps localize free thrombin (which at this point is cleave to expose negative charge) to the platelets by "chelating" the Ca2+. This results with near by fibrinogen to be cleave to fibrin, and with the help of transglutaminase (FV13) forms a cross linked bridge to get that mesh. I hope this covers your answer.(1 vote)
- What was the purpose of the binding of receptor 2b3a with fibrinogen at the end of the primary hemostasis? Is it related to coagulation cascade or does it help to form the platelet plug?(1 vote)
- Are thromboplastin you mentioned for extrinsic pathway different from thromboxane in the primary homeostasis process?(1 vote)
Voiceover: I want to start with an overview of hemostasis first. Here, we have our blood vessel and it's been damaged. And we want to make sure that we stop any bleeding or minimize it. And the way we do this is through hemostasis. The first part is making this platelet plug. And that happens in primary hemostasis. But it's weak, and we need to make it stronger. And we make it stronger with this fibrin mesh. And that happens during secondary hemostasis. And that's what I'll be focusing on right now. So, let me erase everything. And I'm going to put this blood vessel off to the side in the corner so that you'll remember that we're focusing on secondary hemostasis. Here, we have another blood vessel and it's been damaged. But we've already gone through primary hemostasis. We have our platelet plug, but it's weak. And we need to make it stronger. The way we do this is with fibrin. Fibrin is able to link up and aggregate on top of the platelet plug and stabilize it. Sort of like tying a knot. Fibrin comes in and double knots it and triple knots it so that it's sturdy. But fibrin isn't floating around in our blood as fibrin. It floats around with this extra piece of protein. And when it has this extra piece of protein, it's called fibrinogen. So, we need to wait to get fibrin from fibrinogen. And we get fibrin through the coagulation cascade. In our blood, we have this family of proteins called coagulation factors. And I'm drawing them all as one color right now because they're family of proteins. They're similar, but there are different kinds. But I don't want to go into those details here. And what happens is a coagulation factor will get activated. And then it will activate another and activate another and it will set off this cascade. And ultimately what we end up with is we get fibrin from fibrinogen. And then that fibrin is able to link up on top of that platelet plug and make it stronger. There are two ways that we can activate the coagulation cascade. One way is through a protein called subendothelial collagen. This protein is not normally exposed to the blood. It's underneath the endothelial cells. But when a blood vessel has been injured and the endothelial cells damaged, then that protein is exposed to the blood. Once it's exposed to the blood, then it triggers and activates its set of coagulation factors. That set of coagulation factors is part of the intrinsic pathway of the coagulation cascade. The second way that we can activate the coagulation cascade is through another protein that is secreted by the endothelial cells whenever we have damage to the blood vessels from outside of our bodies. This protein is called tissue factor or it's also called thromboplastin. And when this protein gets released into the blood, it activates its own set of coagulation factors. And these set of coagulation factors are part of the extrinsic pathway of the coagulation cascade. So now that we have fibrin. Before we can make the fibrin mesh and stabilize that platelet plug, we need more two things. One of them is calcium. And the second is a phospholipid surface. And both of these are provided by the platelets. Calcium is released during primary hemostasis when platelets get activated. And the phospholipid surface is provided by the platelet itself. And this is important because it links making the fibrin mesh with the platelet plug. And this is what we call the stable clot.