Platelets: Hemostasis - Online Tutor, Practice Problems & Exam Prep

Platelets, or thrombocytes, are crucial for hemostasis, which prevents blood loss after vessel injury. They form a platelet plug through adhesion, activation, and aggregation. Initially inactive, platelets become activated upon injury, changing shape and releasing chemicals like ADP and thromboxane A2. This process is reinforced by blood coagulation, where fibrin stabilizes the plug. Following hemostasis, clot retraction occurs, pulling vessel edges together, and fibrinolysis breaks down the clot once healing is complete, restoring normal blood flow.

Introduction to Platelets

In this video, we're going to begin our introduction to platelets. And so recall from our previous lesson videos that platelets, along with white blood cells, or leukocytes, make up the buffy coat, which recall is one of the 3 main components of blood itself. And also recall that platelets are also known as thrombocytes. Now, these platelets or thrombocytes are unique in that they are not considered complete cells, but instead are considered cell fragments. And functionally, these platelets or thrombocytes are important for plugging holes in damaged blood vessel walls in order to prevent blood loss. Now these platelets or thrombocytes, like erythrocytes or red blood cells, they actually lack a nucleus, and so they do not have a nucleus, and they are considered anucleate. But they do contain cytoplasmic granules that are packed with proteins and other chemicals that are intricately involved in the blood clotting process, which again is going to help to prevent blood loss during injury to the blood vessels. And so what this means is that these platelets or thrombocytes are very critical to the blood clotting process. And again, we'll get to talk more about this blood clotting process as we move forward in our course.

Now these platelets or thrombocytes, which again are cell fragments, actually originate from relatively large cells that are called megakaryocytes. And so these megakaryocytes are going to break apart and fragment to form the platelets themselves, and so we can actually see this in our image down below. Notice on the left-hand side, we have this relatively large cell which is the megakaryocyte, and the megakaryocyte will break apart to form these cell fragments, which are the platelets or the thrombocytes themselves.

Now something that's very important to notice here is that initially, under normal circumstances when there's no injury to our blood vessels, these platelets will be in the blood in their inactive forms, which means that they are not normally going to trigger the blood clotting process, and our blood does not normally clot. And so in order to begin the blood clotting process, these inactive platelets need to first become activated. And so that's exactly what we're showing you over here, is that these are the active platelets.

Now these platelets will become activated under conditions such as damaged blood vessels, and those conditions will activate the platelets. And so upon activation of the platelets, what you'll notice is that these activated platelets will actually change their shape. They have these spiky projections that actually allow them to increase their ability to interact with other platelets, and they also express some negatively charged surface proteins. And you can see that we indicate that by having these negative charges around each of these activated platelets.

Now this negative charge that's associated with these activated platelets is going to be more important as we move forward in our course and talk more details about the blood coagulation process. And so the reason for that is because these negative charges are only just enough to activate some of the blood clotting factors. But these negative charges are not enough to repel these platelets, and the negative charges are not enough to overcome the aggregation mechanisms that cause these platelets to aggregate and clump together upon being activated. And so when these platelets are activated, they are actually going to clump together despite the fact that they have these negatively charged surface proteins.

And so notice over here on the far right, we are actually showing you a blood vessel, and this blood vessel is actually damaged. You can see over here in this region, there's a little bit of damage. And what you'll notice is that these activated platelets are going to aggregate together or clump together to form a plug, a platelet plug. And so this is very important to help prevent blood loss, and it's very important for the blood coagulation or the blood clotting process, which again, we'll get to talk more about as we move forward in our course. And so this here concludes our brief introduction to platelets, and we'll be able to apply these concepts and continue to learn more as we move forward. So I'll see you all in our next video.

Platelets: Hemostasis Example 1

Here we have an example problem that asks, "Which of the following formed elements is not technically considered to be a complete cell?" And we've got these four potential answer options down below. Option A says erythrocytes, which, recall, are red blood cells. Option B says leukocytes, which, recall, are white blood cells. Option C says platelets, which, recall, are also known as thrombocytes. And then Option D says they are all considered to be cells.

Now, of course, recall from our last lesson video that platelets or thrombocytes are not considered complete cells; instead, they are considered cell fragments. And so because they are considered cell fragments, we can go ahead and indicate that Option C here must be the correct answer to this example problem. And, we can eliminate Option D because it says they are all considered to be cells. But again, these platelets are not considered cells; they're considered cell fragments.

Now you might recall from our previous lesson videos that erythrocytes or red blood cells lack a nucleus, and they also lack several organelles. And because of that, they're not technically considered complete cells because they lack many of those common features that are found in many complete cells. However, despite that fact, erythrocytes, or red blood cells, are still considered cells. And so what this means is that Option A here is not going to be the best option for this problem. And the best option for this problem, again, is going to be answer Option C, the platelets, which are definitely cell fragments, not considered cells. And so, because erythrocytes are still considered cells, we can eliminate answer Option A, and then, of course, leukocytes are considered complete cells, so we can eliminate that option. So again, C here is correct. That concludes this problem, and I'll see you all in our next video.

Platelets are similar to erythrocytes in that both structures do not contain a _________________. Platelets are similar to leukocytes in that both their primary functions involve ________________ the body.

• A. Plasma membrane; nourishing.
• B. Plasma membrane; protecting.
• C. Nucleus; nourishing.
• D. Nucleus; protecting.

Overview of Hemostasis

In this video, we're going to begin our overview of hemostasis. Now although the terms are related, the term hemostasis is not to be confused with the term homeostasis, which, recall, applies to any process that maintains stable conditions. Whereas the term hemostasis refers specifically to the fast, local, and controlled process to prevent and control bleeding after an injury. And so the end result of hemostasis is the formation of a blood clot, which can effectively help to prevent blood loss after an injury. Now, it's very important to note that under normal circumstances, when there is no injury to the blood vessel, the blood does not clot. And the reason for this is because the clotting factors that are involved in forming the blood clot are going to circulate in the blood in their inactive forms. And these inactive clotting factors must first become activated before the blood clotting process can begin. And the activation of these clotting factors happens after an injury to the blood vessel. And so upon blood vessel injury, hemostasis is actually going to consist of three steps that we will overview below in this video. But moving forward in separate videos, we're going to dive into more detail for each of these steps. And so again, this process of hemostasis occurs after injury to the blood vessels. And so notice that we're highlighting an injury here to this person's hand when they cut themselves while cutting some carrots. And so notice that the very first step of hemostasis is vascular spasm, and vascular spasm refers to when the blood vessels will constrict or contract immediately after blood vessel injury. And so you can see that the contraction of this blood vessel is being highlighted here by these arrows that you see here. And the contraction is going to decrease the diameter of the blood vessel, and that is ultimately going to decrease the blood flow. And so notice that we're indicating decreased blood flow with a down arrow, and the decreased blood flow is going to help to prevent blood loss and to help buy some time for the rest of the hemostasis steps to occur. And so the second step of hemostasis is platelet plug formation, and as its name implies, this is when the platelets are going to become activated and form a platelet plug. And so notice here in this image that the platelets are aggregating and plugging the hole in the damaged blood vessel wall. And so, the platelets are going to aggregate to plug that hole, and this is going to be an unstable fix. So it is going to help prevent blood loss, but this platelet plug needs to be reinforced to make it more effective at preventing blood loss. And so that's exactly what this third and final step is all about. That is coagulation or blood clotting. And so in this third and final step, coagulation, or blood clotting, that platelet plug that was formed in step number two is going to be reinforced with a protein called fibrin. And that fibrin protein is going to create a stable and more effective blood clot that helps to prevent blood loss. And once step three here is complete, then the hemostasis process is complete. However, it is important to note that after hemostasis is complete, there are two other steps that help complete the healing process, and those two steps are going to be clot retraction and fibrinolysis. And so we'll talk about these two steps after we talk about the three steps of hemostasis in more detail. And so this here concludes our brief overview of hemostasis, and we'll be able to apply these concepts and learn more as we move forward. So I'll see you all in our next video.

Platelets: Hemostasis Example 2

So here we have an example problem that says, when someone gets a wound, it is advised to compress and tightly wrap the wound. And then it asks, why? And we've got these four potential answer options down below. Now option a says it causes the clotting factors to become inactive. But recall from our last lesson video that it's actually the activation of these clotting factors that allows the blood clot to form. And the blood clot is a good thing because it can help to prevent blood loss. And so if it were the case that compression and tightly wrapping the wound actually did cause clotting factors to become inactive, then that would be something that would not be advised to do. And so because it is something that is advised to do, we know that answer option a must not be the correct answer, and we can cross it off. Now option b says that it decreases the oxygen content in the blood that is being lost. But again, if this were the case, this would be something that is not advised to do

Which physiological response causes a reduction in blood flow immediately after a blood vessel injury?

• A. Migration of leukocytes to the site of the injury.
• B. Platelet plug formation.
• C. Vascular spasm.
• D. Release of tissue plasminogen activator.

Vascular Spasm

This video, we're going to talk about vascular spasm, which is the first step of hemostasis, the process that helps to prevent and control bleeding after an injury. Vascular spasm refers to the immediate contraction, or the immediate vasoconstriction of damaged blood vessels to reduce the diameter of those damaged blood vessels, which helps to reduce the amount of blood flow to the damaged site, and that ultimately helps to reduce the amount of blood that is lost. Vascular spasm, or this contraction or vasoconstriction of the damaged blood vessel, is the result of the contraction of smooth muscle cells that are present in the walls of most blood vessels.

The contraction of those smooth muscle cells is initiated by chemicals that are released by either damaged endothelial cells that are present in the walls of all blood vessels, or those chemicals can actually be released by damaged smooth muscle cells themselves, or the contraction can be initiated by chemicals that are released by activated platelets. Now, vascular spasm, this contraction or vasoconstriction, is something that can occur continuously over a relatively large period of time. Several minutes, such as 20 to 30 minutes, up to several hours in some cases. This reduction or this contraction and the reduction of the size of the diameter reduces blood flow, reduces blood loss. That reduced blood loss for that extended period of time helps to buy sufficient amount of time for the next two steps of hemostasis to occur, which are platelet plug formation and blood coagulation, or blood clotting.

Notice, on the left-hand side down below, we're focusing in on the blood vessel before the injury, and so you can see this is how it might look. And then on the right side, we're focusing in on what the blood vessel looks like immediately after injury. Notice that here we have some damage to the blood vessel wall, and notice that some blood is actually escaping, and this person would actually be bleeding. Immediately after the injury, vascular spasm would occur. Vascular spasm is going to be contraction or the vasoconstriction of the damaged blood vessel. Notice here the arrows represent the constriction of the blood vessel walls. And, notice that the diameter is actually narrowing down, and that reduces the blood flow to the damaged site, which reduces how much blood is actually lost from the damaged site.

Again, vascular spasm can occur for long periods of time, and that helps to buy enough time for the next two steps of hemostasis to occur. This here concludes our brief lesson on vascular spasm. In our next video, we'll be able to talk more about the second step of hemostasis, which is platelet plug formation. So I'll see you all there.

Platelets: Hemostasis Example 3

So here we have a pretty straightforward example problem that tells us that damaged endothelial cells release peptide hormones called endothelins, which help to initiate vascular spasm. Considering this, what is the primary effect of endothelins? And we've got these 4 potential answer options down below. Now although we did not talk about endothelins directly in our last lesson video, we can use the information in this problem to solve it. And so we need to highlight the fact that endothelins are going to help initiate vascular spasm, and so whatever the primary effect of endothelin is, it must help initiate vascular spasm. We know from our last lesson video that vascular spasm has to do with the contraction or vasoconstriction of damaged blood vessels. And so notice option B says vasoconstriction, and that is actually going to be the correct answer to this example problem, so we can indicate B is correct.

Now, option A says vasodilation, which is the exact opposite of vasoconstriction, where the blood vessels are going to enlarge their diameter. But that is not going to be the case for vascular spasm, and that's why we can eliminate answer option A. Option C says platelet aggregation, but platelet aggregation is going to be something that occurs in step 2 of hemostasis, which is the platelet plug formation. It is not necessarily something that is going to occur with vascular spasm, and so for that reason, we can eliminate answer option C. And option D says increased blood pressure, and although increased blood pressure may be an indirect result of vasoconstriction, the function of vascular spasm is not necessarily to increase blood pressure, but it is to vasoconstrict. And so for that reason, the primary effect of endothelin is not going to be to increase blood pressure. It is to vasoconstrict. And so option B is the correct answer to this problem, and I'll see you all in our next video.

Which of the following statements about vascular spasms is false?

• A. It occurs when smooth muscle cells surrounding the blood vessel relax, increasing the vessel's diameter.
• B. It can help reduce blood flow immediately after a blood vessel is damaged, thereby reducing blood loss.
• C. It is the first step of hemostasis, directly preceding platelet plug formation.
• D. It is initiated by chemicals released by damaged endothelial cells, smooth muscle, & activated platelets.

Platelet Plug Formation

This video, we're going to talk about the second step of hemostasis, which is platelet plug formation. As its name implies, platelet plug formation is when platelets aggregate or clump together to plug a hole in a damaged blood vessel wall to help reduce blood loss. This platelet plug formation process actually occurs in 3 steps that we have numbered down below in our text as steps 2a, 2b, and 2c. Each of these steps in the text corresponds with the steps that you can see down below in the image as well. Before we continue talking about these steps of platelet plug formation, it's important to reiterate from our previous lesson videos that this process of hemostasis occurs after injury and damage to blood vessels. When blood vessels are damaged, the walls are typically going to be damaged in a way where they expose components that are not typically exposed under normal circumstances, such as collagen embedded in the walls of the blood vessel, for example. When these components, such as collagen, are exposed in the damaged blood vessel walls, it will typically serve to mark the site of damage within the blood vessel for these hemostasis components. That being said, let's dive into these steps of hemostasis so that we can get a better understanding of this. The very first step of platelet plug formation, step 2a, is adhesion of the platelets to the damaged site in the blood vessel wall. The adhesion of the platelets to the damaged site involves a plasma protein called von Willebrand factor, which is commonly abbreviated as VWF. This von Willebrand factor or VWF plasma protein is a protein that is dissolved in the plasma of the blood and circulates in the blood, and what it does is it will bind to exposed collagen at the damaged site in the blood vessel wall. When the VWF binds to this exposed collagen, it will help to serve as a bridge to anchor the platelets to the damaged site. If we take a look at this image down below of step 2a, adhesion of the platelet to the damaged site, you'll notice a damaged blood vessel, and notice that you can see the damage to the wall right here in this region. If we zoom into this damaged site, as you see here in the circle, you'll notice that within the wall of the damaged blood vessel, we are labeling the exposed collagen right here in this region. The yellow diamond right here is actually representing this Von Willebrand factor or VWF protein. We can go ahead and label it as so. This Von Willebrand factor protein is a plasma protein circulating in the blood, and it will bind to the exposed collagen on the damaged site. When it binds to this exposed collagen, it will also simultaneously serve as a bridge to anchor nearby platelets to the damaged site. Notice that the platelet here is binding to the VWF, which is bound to the exposed collagen. This allows for the adhesion of the platelet to the damaged site. Now, one thing I also want to point out is that the platelets have cytoplasmic granules that are filled with chemicals, and these chemicals are going to be important for the formation of the platelet plug. After step 2a, adhesion of the platelet to the damaged site, we have the next step of platelet plug formation, step 2b, which is the activation and degranulation of the platelet. We already know from our previous lesson videos that initially, the platelets are going to circulate in the blood in their inactive forms, and these inactive platelets need to first become activated before they can form the platelet plug. Recall that the activation of these platelets will involve physical changes to the platelets, such as them extending spiky projections, which if you take a look at the image down below for step 2b, you'll notice that this platelet is activated because its physical characteristics are changing in such a way where it extends these spiky projections, and those extended spiky projections allow the platelet to better interact with nearby platelets. Recall from our previous lesson videos that activated platelets will express some negatively charged surface proteins that are not enough to repel these aggregating platelets, but it is just enough to activate some blood clotting factors, and we'll talk more about this idea as we move forward and talk about the 3rd step of hemostasis and blood coagulation or blood clotting. Also, the activation of the platelet will also cause the degranulation of the platelet, which is really just a fancy way of saying that it is going to release the chemical-filled granules that it contains, in order to continue this process of platelet plug formation. Some of the chemicals that can be found in these granules include ADP, serotonin, and thromboxane A2, which can serve as aggregating agents to help recruit platelets to the damaged site. If we take a look at the image down below, notice that the cytoplasmic granules are degranulating, and the chemical contents, these aggregating agents, are being released, and they can go on to help recruit other nearby platelets to the damaged site. As more and more platelets aggregate to the area and are recruited to the area, they will again bind to the damaged site, and they will become activated themselves. There's this positive feedback loop between the aggregation of the platelets and the activation of the platelets. This leads us right into the 3rd and final step of platelet plug formation, which is step 2c, aggregation. In this step, we're going to see more and more platelets being recruited to this damaged site in the blood vessel wall. You can actually see some of that happening here progressively in this image. Notice that initially upon adhesion, there are very few platelets bound, but over time, as we go from left to right in our image, you'll notice that more and more platelets are slowly becoming aggregated until we get to this final step over here, 2c aggregation, where we see lots and lots of platelets aggregating into the area to create that platelet plug. Now the platelet plug has been formed. It can be effective to help reduce blood loss, and we can indicate that right here, that it can help to reduce blood loss. However, something that's very important to note is that this initial platelet plug that is formed over here is usually going to be a relatively unstable platelet plug. Although it can be effective to help reduce blood loss, because it is unstable, it's very important that this unstable platelet plug is reinforced to stabilize it further so that it can more effectively help prevent blood loss. The reinforcement of this unstable platelet plug is what happens in the 3rd and final step of hemostasis, which is blood coagulation or blood clotting, which we'll talk about in our next lesson video. The very last thing that I'll leave you with is that the formation of the platelet plug is going to be very effective at reducing blood loss, specifically when the hole in the damaged blood vessel wall is quite small, and it's even more effective at repairing, or it's even more effective at plugging holes in small blood vessels. However, if the hole is very large in the damaged blood vessel wall, then usually medical intervention is going to be required. This platelet plug formation process will only work effectively to a certain extent depending on how big the hole is in the damaged vessel wall. It's more effective the smaller the hole is. The larger the hole is, the less effective it is, and the greater the likelihood that medical intervention is required. That being said, this concludes our brief lesson on platelet plug formation, and as we move forward in our course, we'll be able to apply these concepts and learn more. I'll see you all in our next video.

Platelets: Hemostasis Example 4

So here we have a pretty straightforward example problem that asks, which molecule acts as the glue between exposed collagen and damaged endothelial cells and platelets, initiating platelet plug formation? And we've got these 4 potential answer options down below. Now, of course, recall from our last lesson video that it is the Von Willebrand factor plasma protein, or VWF protein, that is going to serve as the bridge that anchors platelets to the exposed collagen at the damaged site in the blood vessel. And so we can go ahead and indicate that option a, von Willebrand factor, is the correct answer to this problem. Now recall that ADP, serotonin, and thromboxane A₂ are going to serve as aggregating agents that are released through the activation and degranulation of the platelets after adhesion of the platelet to the damaged site. And so, for that reason, we can eliminate these options. And again, a, here is the correct answer, and I'll see you all in our next video.

Prostacyclin is a hormone that is normally active in the blood but becomes inactive when a blood vessel ruptures and hemostasis begins. Considering this, which of the following is the most likely function of prostacyclin?

• A. Causes platelets to aggregate.
• B. Prevents platelets from aggregating.
• C. Activates vWF.
• D. Initiates coagulation.

Coagulation (Blood Clotting)

Hi, everyone. Behind me is our lesson on blood coagulation or blood clotting, which is the third and final step of hemostasis, the process that helps to prevent and control bleeding after an injury. Now, there is a lot of information here in this lesson, so we're going to break it down and approach it one step at a time starting with this top section that you can see boxed in red. So let's zoom in and get started. Now, recall from our last lesson video that the second step of hemostasis resulted in the formation of a relatively unstable platelet plug. And so, in this third step of hemostasis, blood coagulation or blood clotting, it actually reinforces that unstable platelet plug from step number 2 to make it more stable and more effective at preventing and controlling blood loss. And it does this reinforcement by using a protein called fibrin as a molecular glue to stabilize that platelet plug. And so, it's really important to remember moving forward that really the main goal of blood coagulation is to generate this fibrin protein. Now it turns out that fibrin forms via a very complex enzyme cascade, as you can see by this complex diagram behind me. In fact, there are over 30 chemical reactions and over a dozen clotting factors. And many of these clotting or coagulation factors involved are numbered with Roman numerals in terms of the order of their discovery, not necessarily the order that they're involved in the pathway. Now that is just super complex. But the good thing is that this is really the medical school level of detail, and this process can be simplified into just 3 phases that focus on some of the most important coagulation factors, just like what you can see here. Now that is just so much better. And note that we've strategically implemented these interactive blanks for the first letters of many of these coagulation factors. And that's because we're going to utilize them in memory tools in our next lesson video.

So stay tuned for that. So let's shrink this image down, so I can show you the text in our lesson for each phase. Phase 1, phase 2, and phase 3. So we're going to cover each of these 3 phases 1 by 1, starting with phase number 1. So let's re-enlarge this image and push phase number 1 up to the top. And there's still quite a lot of information being shown here. So let's wipe this slate clean, so we can take this step by step. So phase 1 of blood coagulation can occur via 1 of 2 different pathways, and those are the extrinsic pathway and the intrinsic pathway. And as you can see in this diagram down below, regardless of how phase 1 is initiated, both of these pathways will ultimately lead to the formation of prothrombin activator, which is an enzyme that's also sometimes referred to as prothrombinase. And so down below in our image, we can fill in the interactive blank for the first letter of prothrombin activator. And again, although both of these pathways ultimately lead to the formation of prothrombin activator, we can see in this diagram that technically these two pathways meet at an earlier step here at this intersecting point, which is factor 10 activation. And so the Roman numeral 10 is represented as the letter X, and so we can remember this detail by remembering that X marks the spot where these two pathways technically meet. Now the extrinsic pathway, as its name implies, is initiated by factors that are extrinsic to or that are outside of the blood itself. And so these factors are not a component of the blood. And more specifically, the extrinsic pathway is initiated by a protein called tissue factor or factor 3, which is a protein that is expressed on damaged tissues. And so down below in our image, we can fill in the interactive blank for the first letter of tissue factor here. And notice that in this image on the left, we're showing you some tissue immediately outside of the blood vessel, and notice that it is damaged right here in this region. And this damaged tissue is expressing some tissue factor, which are these blue little dots. And so when the damaged blood vessel releases blood and when the blood comes into contact with that tissue factor, it will actually initiate the extrinsic pathway, which again will ultimately lead to the formation of prothrombin activator.

Now the intrinsic pathway, on the other hand, is initiated by factors that are intrinsic to the blood, or that are inside of the blood itself. And so these factors are a component of the blood or the blood plasma. And more specifically, the intrinsic pathway is initiated by a plasma protein called Hagemann factor or factor 12. And so down below in our image, we can fill in the interactive blank for the first letter of Hagemann factor here, and notice that inside of the blood vessel in the image in the bottom left, we are abbreviating Hageman Factor as HF. And so it's important to note that Hageman Factor must first become activated before it can initiate the intrinsic pathway. And so Hageman factor is activated by negatively charged surfaces, which is why we have this negatively charged symbol here inside of the blood vessel. And so this negatively charged surface could, for example, be the negatively charged surface of activated platelets, as we discussed in some of our previous lesson videos, or it could be the negatively charged surface of the glass in a test tube, which is why our blood clots inside of a test tube. Now it's also important to note that the extrinsic pathway is a relatively fast pathway that will form a prothrombin activator and ultimately lead to a blood clot in a matter of seconds. Whereas the intrinsic pathway is a relatively slow pathway that will typically take several minutes to activate prothrombin act

Platelets: Hemostasis Example 5

So here we have a pretty straightforward example problem that asks, which phase 1 pathway of coagulation can be initiated by components that are not present in the blood, and we've got these 4 potential answer options down below. Now, of course, recall from our last lesson video that phase 1 of blood coagulation can actually occur via one of two different pathways, and those are the extrinsic pathway and the intrinsic pathway. And as its name implies, the extrinsic pathway is going to be initiated by factors that are extrinsic to the blood or that lie outside of the blood and are not a part of the blood itself. And again, that's exactly what our problem is asking about. So we can indicate that answer option A is going to be the correct answer to this example problem. Now option B says the intrinsic pathway, which is the other pathway, and recall that that is going to be initiated by factors that are intrinsic to the blood or that lie inside of the blood and are considered part of the blood. So for that reason, we can eliminate option B. And then option C says neither extrinsic nor intrinsic pathways, so that will not be correct. And then option D says both extrinsic and intrinsic pathways, but again that's not going to be correct as well. A, here is the correct answer, so I'll see you all in our next video.

Which of the following is the most likely outcome if platelets could not release aggregating agents?

• A. Platelets would not be able to bind to collagen within damaged endothelial cells.
• B. Too many platelets would aggregate at the site of the injury, causing blood clots that are too large.
• C. Not enough platelets would aggregate at the site of the injury and an effective clot may not form.
• D. There would be no effect.

How To Remember Important Coagulation Components

In this video, we're going to talk about 2 different memory tools to help us remember the important coagulation components. And so the first memory tool is over here on the left-hand side, and the second memory tool is over here on the right-hand side. Now with the first memory tool, notice that we've got this old fellow right here, and he is actually an ex track and field star that is actually in the hall of fame. And believe it or not, he only retired 3 years ago with a total of 12 gold medals. Now, notice that the bolded and underlined letters that you see here can help us remember that the extrinsic pathway of blood coagulation is triggered by tissue factor, and tissue factor is also known as factor number 3. And then the end hall of fame, again the bolded and underlined letters can help us remember that the intrinsic pathway of blood coagulation is triggered by Hageman Factor, and Hageman Factor is also known as factor number 12. And so hopefully, just by remembering ex track and field star in the hall of fame, that will help you remember some of these important details. Now over here on the right-hand side, we've got another memory tool that is more specific to remembering the details about the important coagulation factors and the order that they are involved in the pathway. And so this memory tool is just platelets packed tightly for fibrin. And so notice in the image up above here, what we have are some really tightly packed platelets that don't seem to be too happy about that. And over here on the right, what we have is the platelet plug that is reinforced with fibrin, and so it's forming this blood clot. And we know that fibrin is the end result and the main goal of blood coagulation, so that that fibrin can serve as the glue that reinforces and stabilizes the platelet plug. And so just by remembering platelets packed tightly for fibrin, that can really help with putting these important coagulation components in the correct order. And so the P in platelets is for the P in prothrombin activator, and the P in PAC is for the P in prothrombin. Now because they both start with p, of course, it's the activator, the prothrombin activator, that must come first because the prothrombin activator must activate prothrombin. And so, that can hopefully be helpful there. Platelets pack, And then tightly is going to be for thrombin. The t in tightly is for the t in thrombin. The f, in 4 is for the F in fibrinogen, and the F in fibrin is for the F in fibrin. Now, we know that the end result of blood coagulation is to produce the fibrin, and so fibrin is going to be last, but fibrinogen is going to come just before. And so, again, just by remembering platelets packed tightly for fibrin, that can be very helpful and effective in remembering these important coagulation factors in the correct order. And so this here concludes our brief lesson on how to remember the important coagulation components, and I'll see you all in our next video.

Which option correctly arranges/orders the components of the coagulation pathway?

• A. Prothrombin Activator → Thrombin → Prothrombin → Fibrinogen → Fibrin.
• B. Prothrombin Activator → Prothrombin → Thrombin → Fibrinogen → Fibrin.
• C. Prothrombin → Prothrombin Activator → Thrombin → Fibrinogen → Fibrin.
• D. Prothrombin Activator → Prothrombin → Thrombin → Fibrin → Fibrinogen.

Clot Retraction & Fibrinolysis

So now that we've covered the three steps of hemostasis in our previous lesson videos, in this video, we're going to talk about clot retraction and fibrinolysis. And so recall from our previous lesson videos that after hemostasis is complete and the blood clot has been formed, there are still two more steps that help complete the healing process. And again, these two steps are clot retraction and fibrinolysis. Now, clot retraction is actually a platelet-induced process that helps to further stabilize the blood clot, and it helps to promote the overall healing process in order to allow the damaged blood vessels and the damaged tissues to regenerate and resume back to their normal states. Now, in this process of clot retraction, the coagulated platelets that are in the blood clot will actually contract. In fact, these coagulated platelets contain actin and myosin protein filaments, and so their contraction is similar to the contraction of smooth muscles, which we covered in previous lesson videos. And so in this process of clot retraction, the coagulated platelets, when they actually contract, the entire blood clot will retract, and that will actually squeeze out fluids from the blood clot, and that will stabilize the blood clot. And also, as the blood clot retracts, it's also going to pull the ruptured edges of the blood vessel closer together, which is going to promote the overall healing process. Now, in addition to this, during the process of clot retraction, the platelets are also going to secrete a hormone called platelet-derived growth factor, which can be abbreviated as PDGF. And so this platelet-derived growth factor or PDGF is actually going to help to promote the overall healing process by triggering mitosis of cells to allow for the regeneration of the damaged tissues. And so if we take a look at our image down below, notice on the left-hand side, we're focusing in on clot retraction. And so notice that we have our damaged blood vessel down below, and you can see that hemostasis has successfully produced a blood clot that is reinforced with fibrin. And again, after hemostasis is complete and the blood clot has formed, clot retraction is going to occur. And clot retraction entails the platelets actually contracting, which causes the overall blood clot to retract in this fashion. And that again, that's going to squeeze out fluids from the blood clot to stabilize the blood clot, and again, it's going to pull the edges, the ruptured edges of the damaged blood vessels closer together, which is going to promote the healing process. And what you'll notice is that zooming into these platelets, you can see that they contain these actin and myosin protein filaments, and so again, their contraction is similar to the contraction of smooth muscles. Now, fibrinolysis is a process that occurs after clot retraction is complete and after the blood vessel healing process is complete as well. And so if we take a closer look at the roots within the word fibrinolysis, you'll notice that it has the word fibrin embedded in it, and it also has the root lysis embedded in it. And that root lysis means to break down or break apart. And so in this process of fibrinolysis, the fibrin protein that is serving as the molecular glue to stabilize the blood clot is actually going to be broken down. And through the breakdown of fibrin, it's also going to dissolve and remove the entire blood clot. And so in this process of fibrinolysis, again, it is going to break down the fibrin protein in order to remove the now unneeded blood clot. And the reason that the blood clot is now unneeded is because, again, the blood vessel healing process has already been completed, and so removing that blood clot is going to help to resume the normal blood flow through that blood vessel. Now the fibrinolysis process is going to involve an inactive plasma protein called plasminogen, which circulates through the blood in its inactive form. And this plasminogen inactive plasma protein is actually going to be incorporated into the blood clot as the blood clot is forming. And so during this process of fibrinolysis, the plasminogen inactive plasma protein is going to be converted into plasmin, which is an active enzyme, specifically a fibrin-digesting enzyme, and so its role is to break down fibrin, Again, that molecular glue that stabilizes the blood clot, and so breaking down the fibrin is going to help to remove the unneeded blood clot. So let's take a look at our image down below over here on the right-hand side for fibrinolysis, and what you'll notice is that the blood vessel that was initially damaged has now completed the healing process. And so notice that the walls of the blood vessel are no longer ruptured, and, the healing process is complete. And so what this means is that the blood clot that was formed is now unneeded. It's no longer needed, and so it actually needs to be broken down and removed so that the normal blood flow can resume through this blood vessel. And so this is going to involve taking this plasminogen protein, this inactive protein, and converting it into its active form that we call plasmin. And plasmin is going to be an active fibrin-digesting enzyme. And so notice in this image, you can actually see that plasminogen is a plasma protein that is dissolved in the plasma and circulates in the blood in its inactive form. And, again, it will be incorporated into the blood clot as the blood clot is forming. And during fibrinolysis, the plasminogen that's incorporated into the blood clot is gonna be converted into plasmin. So you can now see that the plasmin is active inside of the blood clot, and it is digesting the fibrin protein in order to, again, break down the blood clot, dissolve it, and remove it. And so after that, the entire healing process has been completed. And so this here concludes our lesson on clot retraction and fibrinolysis. Moving forward, we'll be able to apply these concepts and learn more. So I'll see you all in our next video.

Platelets: Hemostasis Example 6

So here we have an example problem that asks, which of the following issues might arise if fibrinolysis did not occur? And we've got these 4 potential answer options down below. Now, of course, if we analyze the roots within the word fibrinolysis, it will be very helpful to reveal what this process entails. And so, again, notice that it has the word fibrin embedded in it, and it also has the root lysis in it as well. And the root lysis means to break down, and what's being broken down is the fibrin protein, and recall that the fibrin protein serves as the molecular glue that stabilizes blood clots. And so if fibrin is broken down, then so is the molecular glue that holds together the blood clot, and that is going to cause the blood clot to dissolve, break apart, and be removed. However, if fibrinolysis did not occur, then that means that those blood clots would not break down, and there would be a buildup of blood clots throughout the vascular system. And so notice option d says buildup of blood clots, and so we can indicate that option d is the correct answer to this problem. And for options a, b, and c, they are not correct because the fibrinolysis process does not directly affect blood pressure, platelet count, or the hematocrit. And so again, d here is correct. That concludes this problem, and I'll see you all in our next video.

What would happen if plasminogen was activated before clot retraction?

• A. Clot retraction would be completed even faster.
• B. Fibrinolysis would occur too early & the healing process could be interrupted.
• C. There would be no significant effect.

Here’s what students ask on this topic:

What are platelets and what role do they play in hemostasis?

Platelets, also known as thrombocytes, are small cell fragments derived from megakaryocytes. They are crucial for hemostasis, the process that prevents blood loss following vessel injury. Platelets circulate in the blood in an inactive form and become activated upon encountering damaged blood vessel walls. Once activated, they change shape, develop spiky projections, and release chemicals like ADP and thromboxane A2. These changes facilitate the adhesion, activation, and aggregation of more platelets to form a platelet plug. This plug temporarily seals the injury site. The process is further reinforced by blood coagulation, where fibrin stabilizes the platelet plug, forming a more durable blood clot. This sequence of events effectively prevents excessive blood loss and initiates the healing process.

What are the three steps of hemostasis?

Hemostasis involves three primary steps: vascular spasm, platelet plug formation, and blood coagulation. The first step, vascular spasm, is the immediate constriction of the blood vessel to reduce blood flow and minimize blood loss. The second step, platelet plug formation, involves the adhesion, activation, and aggregation of platelets at the injury site to form a temporary plug. This process is facilitated by chemicals like ADP and thromboxane A2 released from activated platelets. The third step, blood coagulation, reinforces the platelet plug with fibrin, a protein that acts as molecular glue, stabilizing the clot and making it more effective at preventing blood loss. These steps collectively ensure rapid and controlled cessation of bleeding following vessel injury.

How do platelets become activated during hemostasis?

Platelets become activated during hemostasis when they encounter damaged blood vessel walls. The exposure of subendothelial components like collagen triggers the activation process. A plasma protein called von Willebrand factor (VWF) binds to the exposed collagen and serves as a bridge for platelets to adhere to the damaged site. Upon adhesion, platelets undergo a shape change, developing spiky projections that enhance their ability to interact with other platelets. They also release chemical-filled granules containing ADP, serotonin, and thromboxane A2, which further recruit and activate additional platelets. This positive feedback loop ensures a rapid and effective formation of the platelet plug to prevent blood loss.

What is the role of fibrin in blood coagulation?

Fibrin plays a crucial role in blood coagulation by stabilizing the platelet plug formed during hemostasis. The main goal of blood coagulation is to generate fibrin, which acts as a molecular glue. Fibrin is produced through a complex enzyme cascade involving multiple clotting factors. In the final phase of coagulation, the enzyme thrombin converts the soluble plasma protein fibrinogen into insoluble fibrin strands. These fibrin strands interweave and cross-link to form a stable mesh that reinforces the platelet plug, creating a more durable blood clot. This stabilized clot effectively prevents further blood loss and allows the damaged vessel to heal properly.

What happens during clot retraction and fibrinolysis?

Clot retraction and fibrinolysis are processes that occur after the initial hemostasis to complete the healing process. Clot retraction is a platelet-induced process where the coagulated platelets contract, pulling the edges of the damaged blood vessel closer together. This contraction stabilizes the blood clot and promotes tissue regeneration. Platelets also release platelet-derived growth factor (PDGF), which stimulates cell division and tissue repair. Fibrinolysis occurs after the vessel has healed, involving the breakdown of the fibrin mesh that stabilized the clot. The inactive plasma protein plasminogen, incorporated into the clot, is converted into the active enzyme plasmin. Plasmin digests fibrin, dissolving the clot and restoring normal blood flow.