How do we make blood clots? | Human anatomy and physiology | Health & Medicine | Khan Academy

How do we make blood clots? | Human anatomy and physiology | Health & Medicine | Khan Academy


Let’s look at a blood vessel. A blood vessel is kind of like a tube. I think you’ll agree with me. It’s a tube through which blood travels. So here I’m drawing a tube, and I’m gonna ask you a question which is what makes up the walls of this tube? Now, for a blood vessel, what makes it up, is something called an endothelial cell. So, actually, the walls are
made up of these kind of gooey endothelial cells that
are stuck together tightly and that together form a tube through which the blood will travel. So here I’m drawing a bunch of
cells tightly stuck together. They’re stuck together tightly to prevent blood from
coming out, of course. So this is more or less
what it looks like. Each of these is a
cell, and so, of course, each one has a nucleus, which I’ll just quickly draw like that. Now let’s delete that
and let’s change views to something a little bit easier. So now here is the same blood
vessel in cross section. And so these are the endothelial cells, which we’re seeing in cross section, and maybe here we can draw
the nucleus of this one. Maybe it’s visible right there. So now we have blood moving
through this blood vessel. Here are some red blood cells, and they’re moving along,
providing the body with oxygen. But a very important question
to ask is what happens if this blood vessel gets damaged? So let’s say that those two
cells right there split open, and they break open. What’s gonna happen if we don’t fix this is that all of our blood is
just going to rush out here, and we’re gonna lose blood. So what is your body gonna do about this? Well, it’s going to use a special player that we haven’t talked about
yet, which is the platelet. So I’m drawing a platelet here. And a platelet is basically
a tiny piece of a cell. It doesn’t have a nucleus or anything. It’s a tiny, little piece of a cell that your body uses to
block up holes like this. So you have them floating around
in your blood all the time. Here I’m drawing a bunch. And what happens is when you have a hole in your blood vessel, they’re going to come together. They’re going to stick together, and they’re going to clog up this hole. And so, basically, they’ve
built a little barrier so that we won’t keep
losing all our blood. So are you satisfied? Well, you shouldn’t really be satisfied because there’s a bit
question here which is why are these platelets clumping here, and why aren’t they clumping, you know, for example up here? Why don’t they clump there or maybe even just in circulation? Why don’t they clump up like this? Because if what they do is to clump up, how would they know to
clump up here and not here? What’s telling them? These are things that
we don’t want to happen so I’m gonna put a little X through them. And the solution to
this problem is actually quite simple and beautiful. The point is that the
environment in the blood vessel is different from the environment outside of the blood vessel. So outside, we have some things
that we don’t have inside. And one of those things
I’m going to draw here. I’m drawing it here, and it has a name. It’s called collagen. So I’ll write that down here. It’s called collagen. You don’t have to worry
too much about what it is. Collagen is kind of a structural protein that your body uses to
give structure to things. And so the important thing is you have collagen down here,
and you don’t have it here. You don’t have it here. You don’t have it here. And it turns out that
collagen chemically interacts with the platelets. And maybe we’ll draw a little spark there to show that they’re
chemically interacting. It chemically interacts
them and causes them to stick together and form this plug that we’re talking about. So we can call this, by
the way, a platelet plug because it’s plugging the hole. And by the way, just to be clear, you also have collagen
up here and over here. So it’s basically everywhere
outside the blood vessels. Now it turns out that
this is only step one of the clotting mechanism of your body. So up here we’ll put
number one, platelet plug. And there’s actually two steps, because the platelet plug
itself is not quite as strong as we would like it to be. So there’s a second step which
makes this plug stronger. And that second step involves
something called fibrin. So we’ll write that here, fibrin. And fibrin is not a little
mini cell like platelets are or a fragment of a cell
like platelets are. Fibrin is just a protein, and what fibrin is gonna do is it’s gonna come here, and
it’s gonna try to strengthen this plug by forming this mesh of protein that’s gonna hold all
these platelets together and form a very tight object. Now these fibrin strands, that’s what each of these, you know, little squiggles is. It’s a fibrin strand. These fibrin strands are made
up of little fibrin subunits, which I’ll draw here. And it turns out that
these subunits naturally like to come and stick together. And, I guess, the technical word for this is they polymerize. They form a polymer. Basically, they just stick together and lots of them will
stick together in a line to give you this fibrin
strand we see here. And where does this fibrin come from? Does it come from down here? No, it actually also
circulates in the blood. So let’s draw some little
fibrin molecules up here. So they’re circulating in the blood. Is this right? Well, this actually
can’t be exactly right, ’cause I just told you
that these fibrin molecules naturally stick together. And so if we had these
fibrin molecules circulating in the blood like this, what would happen? Well, they would actually
stick together in the blood, and they would form these
long strands in the blood that we didn’t want, because
we only want the strands here at the platelet plug. So let me remove those strands. So it turns out that we
don’t have fibrin circulating in the blood. What we have is something
slightly different. We have fibrinogen. Fibrinogen. And so I’ll draw a fibrinogen down here. Of course, keep in mind, these
are all my little cartoons and probably it doesn’t look like this. So these guys, we said, were fibrin. Fibrin. But now this molecule is a fibrinogen. And you’ll notice it’s
the same as a fibrin, except it has an added,
little piece to it, and that little piece, as you can tell, is gonna keep it from sticking to itself. These fibrinogen are not gonna
be able to stick together the way that these fibrin are. So what to do we need to do then? Well, of course, we need
to turn this fibrinogen into fibrin, but where
are we gonna do that? Only at the site where we
want fibrin strands to gather. So only here, where we have that damage. And so, again, we face the same question that we faced with the
platelets, which was, how do they know, how
do the platelets know to aggregate here? Well, likewise, we wanna know how do the fibrinogen know
to turn into fibrin here so that they can then stick
together and form the strands? And the answer, basically,
is, luckily, the same. And so we have some chemicals down here. Now we’re not talking
about collagen anymore. We’re talking about something else. And if you really want to know what it is, I’ll write the name here but it’s not really the name that’s important. It’s the principle here. So the principle is you have these little proteins down
here called tissue factor. And they’re normally not in the blood. They’re only down here outside
of the endothelial cells lining the blood vessel, and so these little
proteins, tissue factors, are going to be right
here in this little wound and around the wound, and there they’ll cause these fibrinogen to become little fibrin protein molecules, and then those fibrin will
be able to stick together, and they also stick to
the platelets by the way. I hope I was clear about that. And form the mesh that we see there. Now if we want to get really fancy, we can ask how this tissue
factor turned fibrinogen into fibrin. And you can ask, is tissue factor kind
of like a little knife? And by knife I really mean enzyme. Is it a little knife or
enzyme that causes this piece to break off of the fibrin so that we’re left with just fibrin? And actually, unfortunately, the story is much more
complicated than that. And there’s actually a good reason for it. Because let me propose to you a situation. Let’s say you have to
turn a million fibrinogen into fibrin. Because each of these fibrinogen
is a very small protein, so we need about a million of them to make up this clot here. And let’s say that you are tissue factor. So you are tissue factor, and you want to turn a million
fibrinogen into fibrin. Is the best way to do it
for you to actually sit down and chop off this piece off
of all these fibrinogen, one by one? That would take you a long time. Is that better, or is it better
for you, as tissue factor, to call up five friends and have each of those
call up five friends, and have each of those
friends call up five friends, and keep doing that until
you have a huge number of people there ready to help you? And now get all of those people to help you convert fibrinogen to fibrin. So, obviously, that latter scenario is a more efficient mechanism. And so that’s what your body does, and that’s what tissue factor does. So tissue factor, and by the way, I know this getting convoluted
but try to stick with me. Tissue factor is going
to turn another protein that we haven’the talked about, into its active form. And then that other active
form of that protein that we haven’t talked about, is going to activate another protein that we haven’t talked
about into its active form. And then that one is gonna do the same. And then that one is gonna do the same. And so, basically,
every time you introduce a new protein there, you’re ramping up the total
number of activated proteins of that type. And so, finally, by the time you get to the one that’s going to
break the fibrinogen apart and create fibrin, and by
the way, I’ll draw him. And he has a special name called thrombin. Again, I don’t think
thrombin is necessarily a word you need to know, but just in case. So by the time you get to thrombin, you have a lot more activated thrombin than you had tissue
factor in the beginning. But the tissue factor here is the spark, and that’s the guy that
really got us going. So that’s basically it. This is how your body plugs
holes in blood vessels and keeps you from losing too much blood. And if you want to know
more about that kind of complicated stuff I said at the end about, you know, all these different
levels of activated proteins, you can look it up. It’s called the coagulation cascade. And it’s called the cascade because you’re cascading through all these different levels of proteins.