Hemostasis is the process which stops bleeding after an injury. Blood vessels are repaired by the creation of a platelet plug during primary hemostasis, and the platelet plug is further reinforced by the conversion of fibrinogen to fibrin during secondary hemostasis. Created by Gricelda Gomez.
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- I Watched this video on youtube about the circulatory system and I wondered that since astronauts have a weaker circulatory system than people on earth are they more prone to arterial bleeding resulting in death in 0G since the blood is now floating in the body instead of being pumped at high pressure from the heart?
Here is the video just in case you are curious as to what I watched:
- Would an example of primary hemostasis (at3:48) be the soft, film like covering over the cut, and an example of secondary hemostasis (at4:38) be the hard, firm scab that shows up after a day or two of the cut? Or what would an example of each be?(3 votes)
- Primary and secondary hemostasis happen relatively quickly (all done in a minute or two), and help to create that soft covering you mention. The hard scab is the dried-out remains that hang around while the skin cells are regenerating underneath.(4 votes)
- In my book it shows that the fibrin and activated platelets form a tangled net contained RBCs to stop blood flow. Is this true, or do fibrin and platelets work on their own?(2 votes)
- Your book is correct. Blood clots have red blood cells and white blood cells in them as well as platelets and fibrin. Hope this helps!(6 votes)
- At4:40- When does fibrin "know" when to strengthen the platelet plug? Also how does the platelet plug "know" when to stop forming and building?(2 votes)
- Actually as she said - Not going into details, she was briefing about the hemostasis. Fibrin is actually in an inactivated state called fibrinogen which gets activated by thrombin which in turn was in an inactive form called prothrombin. So the sequence of formation of prothrombin largely depends on prothrombin activator. Hence, its formation is what has 2 mechanisms - Intrinsic and Extrinsic via which PA is formed - via the help of clotting/coagulation factors that are released at the time of platelet activation prior to aggregation. (Remember 3 A's - Firstly adhesion, activation, aggregation). Remember that prothrombin and fibrinogen are in plasma and are part of clotting factors. Clotting factors are NOT synthesised by platelets - they just store few factors essential to initiate aforesaid mechanisms/cascade process in the presence of plasma clotting factors.(5 votes)
- So I have learned that platelets tend to change shape when they bind to the collagen and each other. They get these arm-like extensions. What causes them to change shape and is there some kind of advantage that it gives them to make them more efficient?(2 votes)
- Platelets are like little balloons that float around our blood, filled with clotting factors. When they attach to the clotting scaffold, a protein reaction causes them to turn themselves inside out, exposing the damaged environment to their pro-clotting materials. This shape change allows them to have a targeted response, so that they don't just cause clotting everywhere. (Which happens in some disease states.)(4 votes)
- Great video, but I think it might be worth noting the differences between a "clot" and a "thrombus." They are often used interchangeably, but there are actually several differences. A thrombus is a clump of platelets and fibrin -- as described in this video -- formed in response to endothelial injury. Thrombus formation is an ACTIVE process, unlike clotting. Clotting is a PASSIVE process that does not involve platelet plug formation. Blood will clot anywhere -- in a vial, in the blood vessels of a cadaver, in the body following internal bleeding -- but a thrombus only forms in the blood vessels of a living organism.(3 votes)
- I know this question might sound stupid to some, but is there any way the clot/thrombus can break off when the skin's healed, causing a clot to form somewhere else?(2 votes)
- In a normal healthy person the clot from a small wound gets broken down by other enzymes in the blood. Even if some of the clot broke off, it would still soon get dissolved before it caused any problems. In larger wounds such as broken bones it is possible for large thrombi to form, which can detach and get stuck in small blood vessels, which is called embolism, but doesn't cause clotting at the new site.(2 votes)
Voiceover: Hi everyone. I want to start off by talking about Mary. Mary likes to play soccer, and she was at one of her games, and she was running really fast. She scored a goal, and then she tripped and fell, and scrapped her knee, and then she started to bleed. Now, normally our bodies want to make sure that our blood, which flows through our blood vessels stays in our body. If we have an injury that allows blood to leak out of the blood vessel and out of our body, we want to make sure we can stop that. We do that through a process called hemostasis. It's through hemostasis that we create this clot. This clot allows the bleeding to stop. It stabilizes the injury in the blood vessel, and it gives the blood vessel time to heal. Now, let's take a look at exactly what's going on in Mary's knee, and exactly how we make this clot. So, here we have a blood vessel, and in our blood vessel we have our blood. In our blood, we have many different types of cells. One of the most important ones is our red blood cell that carries oxygen all over to all our tissues in our body. In this blood vessel, we make sure that blood is flowing smoothly in one direction. Did you know that if we were to line up all of our blood vessels, the total length of our blood vessels would come out to about 150 thousand kilometers? Which, is about 93 thousand miles. This is the same distance as if you were to travel around the Earth a little bit less than four times. So, you can see our blood vessels have a lot of work to do. One of the cells that helps with this are the cells that line the inner wall of the blood vessel. The cells that communicate with the blood. These cells are called endothelial cells. It's these cells that allow the blood to flow smoothly, and these are the cells that communicate with the blood whenever there's been a injury, and hemostatisis needs to begin. Now, let's take a look at Mary's knee. She scrapped her knee, so, let's cause a break in her skin. Let's say this is her skin. She also caused damage to the blood vessel underneath. So, let me erase this. Let me cause some damage to the blood vessel. You can see blood that should be flowing in this direction now can come out of the blood vessel, and out of the skin in this direction. We want to stop this. The way we stop this is through hemostasis. There are two stages to hemostasis. The first stage is primary hemostasis. This begins immediately after there's been an injury. What happens is the endothelial cells, at that sight of injury, begin to secrete proteins. This sends signals to the blood that there's been an injury. In our blood we have platelets, these platelets are made in the bone marrow just like red blood cells, and their purpose is to respond to injured blood vessels. I drew them as squares, but their actually about this small compared to red blood cell. The reason I drew squares is I want to make a note of what they carry inside of them. They carry these sacs or granules that carry molecules and proteins that are necessary for hemostasis. So, they store them, and they're ready for use whenever needed. What happens is, the endothelial cells secrete these proteins and send a signal to the platelets to come to that sight of injury. Then, a sequence of events happens with the platelets. I won't go into details here, but it allows the platelets to stick to that sight of injury. They get activated. They change shape. They release what they have inside, and then they start clumping together and call more platelets, and cause more platelets to clump there as well. What we end up with is what we call a platelet plug. This is the first step of stopping any bleeding. This is still kind of weak, and we need to make this stronger. That's where secondary hemostasis comes into play. In secondary hemostasis, we make this platelet plug stronger with a protein called fibrin. What fibrin does is it lays over and links up on top of this platelet plug, and makes it tighter and sturdier. It's like tying a knot. In order to prevent it from getting loose, you double-knot it or triple-knot it. This is exactly what fibrin is doing. Fibrin doesn't flow in our blood as fibrin, it carries around an extra piece of protein, and when it has this extra piece of protein, it's called fibrinogen. So, we need a way of getting fibrin from fibrinogen. The way we do that is with this family of proteins called coagulation factors. I'm drawing them all in one color, but there are several different types of coagulation factors. The injured blood vessel will send signals to these coagulation factors to get activated, and once when one gets activated, it will activate another, and activate another, and activate another, and then ultimately, that extra protein on fibrinogen will get cut off. That will allow fibrin to link up on the platelet plug and make it stronger. This sequence of activation of coagulation factors is what we call the coagulation cascade. I won't go into the details here either. It's just key to remember that in secondary hemostasis, we make this platelet plug stronger by getting fibrin from fibrinogen through the coagulation cascade, and it's with this fibrin mesh over the platelet plug, that we create this clot. It's this clot that stops bleeding, allows blood flow to continue through the blood vessel, and allows the blood vessel to heal.