Anticoagulation and thrombolysis | Health & Medicine | Khan Academy
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Anticoagulation and thrombolysis | Health & Medicine | Khan Academy

Voiceover: Okay, so here we have a blood vessel and it’s been injured. So right now I want to do an
overview of hemostasis first. We want to make sure when an
blood vessel’s been injured, that the blood that’s flowing
through that blood vessel continues to flow through
the blood vessel, and we try to minimize as much as
possible, the amount of blood that leaks out of the blood
vessel at that site of an injury. And the way we do that
is through hemostasis. And the first part of hemostasis is making that platelet plug. And this happens during
primary hemostasis. But it’s still kind of weak,
so we need to make it stronger. And the way we make it stronger is through secondary hemostasis. And what we do is we get
this protein called fibrin. And we link it up together and we create this fibrin mesh over the platelet plug. And this fibrin mesh over the platelet plug is what we call a clot. Now, what were to happen
if hemostasis were to continue and nothing were to stop it? So we’d just get clot after
clot after clot after clot. So you can see that that’s a problem. Now the blood that
should be flowing through is getting backed up behind this clot and not getting to where it needs to go. So even though hemostasis
is good, if we have too much clotting, then that can be bad. So our bodies need a way to make sure we don’t get many clots. So let me get rid of these clots. And the way that our
bodies do this is through two processes, called
anticoagulation, and thrombolysis. Anticoagulation is the process that prevents any clots from forming. And thrombolysis is the process that breaks down clots after
they’ve been formed. And these two processes are
what I’m gonna focus on today. And this tug-of-war between two competing processes happens a lot in our body. Our bodies like to maintain
a certain equilibrium. A middle ground, a set
point, we have a normal. On a day to day basis, our bodies need ways to get back to normal. Let’s take body temperature, for example. Our bodies like to stay at
98.6 degrees Fahrenheit, which is about 37 degrees Celsius. So that’s normal, that’s
where we like to be at. Of course it’s a range, so it
can be a little bit higher, a little bit lower, but
nothing too drastic. But sometimes we can get lower than that and we can be too cold. Say it’s snowing outside and
you don’t have a sweater. And so what our bodies
do in order to get our temperature back up, is we shiver. Our muscles create heat to get our bodies back up to the temperature that we like. Or sometimes our bodies can get too hot. Say we have a fever, or sick, or or maybe we’re running on a hot day. And what our bodies do in
order to cool ourselves off and get our temperature back
down, is we start sweating. And that cools us off, and
that lets off the extra heat that we have in our body, and
that gets us back to normal. So let me erase this now. And let me show you how this is similar to what’s going on in our blood vessels. So our sub-point, our middle ground, let’s say good blood flow. And this is important because
if we have good blood flow, then all our tissues are
getting what they need. They’re getting oxygen and nutrients that’s carried in our blood. But sometimes we can have some
injury to that blood vessel, and then we’ll start bleeding. And that goes away from what we want, which is good blood flow. And so what we do in response
to that to get us back to having good blood flow,
is we go through hemostasis. And that allows us to
make a clot, stop the bleeding at that injured blood vessel, and get us back to having good blood flow. But if we have too much
hemostasis or any other process that causes us to clot,
we have too much clotting, then as we saw before, the clots can block the blood flow going
through that blood vessel. So the way that we take care of that is through anticoagulation and thrombolysis. And with anticoagulation
and thrombolysis, we’ll break down any clot and prevent
more clots from happening, and make sure that we have good blood flow in our blood vessel. So this is the balance between hemostasis and anticoagulation and thrombolysis. Let’s go over exactly what
our bodies do in order to prevent any clots or break down clots. So let’s talk about anticoagulation first. In anticoagulation we want to prevent any clots from forming. So we want to prevent hemostasis. And in hemostasis we can
prevent the platelet plug, or we can prevent making the fibrin mesh. So let’s talk about making
the platelet plug first, and how we prevent primary hemostasis. So here we have our platelets that are floating around in our blood. So we want to make sure we
prevent clots from happening. There’s no injured endothelial
cells, so we don’t need hemostasis to happen, we don’t
need platelets to get there. So our healthy endothelial cells
will secrete two molecules. They both do the same thing. The first thing that
they do is that they do prevent platelets from getting to the endothelial cells, from sticking to them. So they kind of block the
platelets from getting close. And the other thing
that they do is they act on the smooth muscle cells of the blood vessel, and they cause vasodilation. And that’s important
because we want to make sure that our blood vessels stay open and blood is able to flow through smoothly. These two molecules are
called, one of them is called prostacyclin,
and this is a peptide. And the other one is a
chemical called nitric oxide. So now let’s talk about secondary hemostasis and how we prevent that. In secondary hemostasis,
let me scroll over, we make the fibrin mesh to make
that platelet plug stronger. Which again, in this case we
don’t need because there’s no injury, and so we don’t
need to make the clot. And the way we make that fibrin mesh is we activate the coagulation cascade. So here we have our clotting factors, the family of proteins. And ultimately when we activate
the coagulation cascade, what we’ll end up with
is getting thrombin. The fibrin linking up
on top of the platelet plug is what creates that fibrin mesh and makes the platelet plug stronger. So the way that our
bodies, our blood vessels prevent secondary hemostasis
is through two different molecules so that endothelial cells, the same cells that are
lining the inner wall of the blood vessels, and these are
the same cells that are making prostacyclin and nitric oxide,
what we just talked about. It makes two molecules. One of them is called
heparin-like molecule. And this molecule is on the
surface of the endothelial cell, communicating with the blood. And what this molecule
does is, it interacts with another protein that’s already
floating around in our blood. This protein is called anti-thrombin III. So you can see, in hemostasis we have thrombin and we want to make a clot. And now in anticoagulation, we have anti-thrombin III, and we
want to prevent a clot. So what will happen is anti-thrombin III will interact with this
heparin-like molecule. And when anti-thrombin III interacts with heparin-like molecule, what it’ll do is it’ll inactivate thrombin. So it’ll prevent thrombin
from making fibrin from fibrinogen, and
it will also inactivate a coagulation factor,
coagulation factor X. And the second molecule
that our endothelial cells have on the surface of their
cells that’s communicating with the blood, is a protein
called thrombomodulin. “Thrombo,” again, means clot,
and “modulin” is modulate. So, to change or alter. So we said thrombin is what
gets fibrin from fibrinogen. But what thrombomodulin will
do is if there’s thrombin floating around in our blood
and we want to make sure that we don’t clot too much,
is it’ll get thrombin and it’ll change what thrombin actually normally does, which is make a clot. So that it is actually
working in anticoagulation. But it’s not just thrombin
and thrombomodulin that works in anticoagulation. When we have thrombin and thrombomodulin working together and interacting
with each other, then now protein C, with the help of
protein S will get activated. And once it’s activated,
It’ll interact with the thrombin/thrombomodulin complex. Those three things help
with anticoagulation. The way that it helps with
anticoagulation is that it inactivates two specific
coagulation factors. Coagulation factor V, and
inhibits coagulation factor VIII. So now that we’ve covered anticoagulation, let’s talk a little more
now about thrombolysis. So like I said in thrombolysis we’re breaking down the clot
that we already made. So the way that we’re able
to break down that clot is with this protein called plasmin. I like to think of it
as, like a little shark floating around waiting
to break down those clots. So I’m gonna draw it like
this, like a little saw. And this protein is called plasmin. And what plasmin will do is it will break down fibrin and fibrinogen. But plasmin isn’t floating
around in our blood all the time, or else we wouldn’t be able to
clot at all, because plasmin would be breaking down fibrin
and fibrinogen all the time. So we want to make sure that we can have plasmin whenever we need it. And we need plasmin whenever
we don’t want to make a clot or whenever we don’t need to make a clot. And so we get plasmin from plasminogen. And just like fibrinogen, plasminogen is made with just an extra piece of protein. And the way we get plasmin
from plasminogen is through our healthy
endothelial cells again. Our endothelial cells will release and secrete plasminogen activator. And this tissue plasminogen activator will take off that extra piece of protein from plasminogen and make plasmin. So now let’s zoom out and take
a look at the entire picture of how anticoagulation
and thrombolysis works.

About James Carlton

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43 thoughts on “Anticoagulation and thrombolysis | Health & Medicine | Khan Academy

  1. Small correction at 5:30– Prostacyclin (aka Prostaglandin I2) is a LIPID (derived from arachidonic acid, a fatty acid), NOT A PEPTIDE.
    This is an excellent series of videos, thank you for making them!

  2. Wondering why you feel a little ‘off’ or below par all the time after you have been taking Warfarin for months and more?
    I was fitted with an artificial heart valve 15 years ago, so I'm on warfarin for the rest of my life. For the first 10 years that was me feeling 'off' all the time, and was the source of my questions, constantly to doctors. Not one doctor gave me the true answer. Then I figured it out for myself, Its the subtle acid effect that warfarin has on your body that puts you out of balance and causes a variety of minor side effects, any or all of which make you feel ‘off’. To find out how to rebalance yourself and fix this, read my book. Get your E copy or hard copy on the net at;- Enjoy! and you will be amazed how much better you feel in a few weeks, Plus how the answer gets you away from most if not all those other pills they prescribe for your ‘off’ issues, while you still taking your warfarin. Once you get settled with this rebalance answer, you will come to see and feel that most of the bad things you hear and learn about warfarin are all the direct result of you not being told all the facts as to how to keep your body in tune while taking warfarin. Plus you will find that your INR tests become more consistent and so can be spaced further apart in time.

  3. Although how you explained is great, there was too much stammering. That was kinda distracting. But you are genius.

  4. Great video! Thanks a lot!

    I would just add that the alpha-granules (from activated platelet degranulation) contains Thromboglobuline, which works as a plasminogen activator too!

  5. I wish they can replace this video with someone speaks louder. this one good example of bad teacher and good narrator.

  6. Good effort and helpful. I think it could be made even better with different narration. Sal Khan and Rishi Desai had this way of expressing their own interest in the subject, infusing their narrations with their fascination. It's a real trick to be able to do that, and when it's achieved, it makes a video or talk more interesting and, consequently, easier to grasp. But nice job in any case.

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