Atherosclerosis | Circulatory System and Disease | NCLEX-RN | Khan Academy

Atherosclerosis | Circulatory System and Disease | NCLEX-RN | Khan Academy

September 11, 2019 95 By Kody Olson


– [Voiceover] We know that atherosclerosis is the main contributor to
coronary artery disease, and in the coronary
arteries, atherosclerosis will cause build-up of these fatty cholesterol-filled plaques, like so. You can see me drawing them in here, and they’re occurring all
over the coronary arteries so what they do is they sort of obstruct blood flow down the length
of the coronary arteries and through all the branches
of the coronary arteries because they’re just
these big bulges of fat that are in the way. So how do they develop? What exactly is this
process of atherosclerosis? Well, let me show you what this looks like in a snapshot before we actually look at the mechanisms. I’ll take this piece of
coronary artery here, let’s say this piece right there, and we’ll blow that up. If we look at that … When it’s nice and healthy,
it’s going to look like this. Here’s our healthy blood vessel. Nothing built up inside. You can see blood is going
to flow through this way. This here is a
cross-section of the artery. So as far as we can tell, blood can flow smoothly and nicely
through this blood vessel, no obstruction, everything looks good, but when you start getting
atherosclerosis happening, things can get a little bit different. When you start getting
atherosclerosis happening, your coronary artery might start to look something like this. Immediately, we can see that
there’s a pretty big difference between the first vessel
here, the nice clean one, and the second vessel
here, the atherosclerotic, sort of fatty plaque vessel here. All of this yellow stuff
is some gross fatty plaque that’s been deposited
into the vessel wall. If we look at the cross-section here, we can see that it’s really doing a number on the amount of blood that’s able to flow through this vessel. If we’re blood here in red, we can’t actually get through this vessel quite as much as we could through here. Look how much room we had in this one. Because of all this build-up, this is why we’re going to
get downstream symptoms. How, exactly, does this happen? Well, let’s redraw our own arteries so we can go through it step by step. Here’s our blood vessel there. Now I’m drawing the three layers of the wall of the blood vessels. On the very inside of the blood vessel, as part of this pink layer here, we have a single layer of
cells called the endothelium. Let me just draw out the endothelium here. Although it’s just a single
layer of cells thick, the endothelium has a lot
of really important roles. One of its really important
jobs is to act as a barrier. It acts as a barrier between
stuff that’s in the blood and the rest of the blood vessel wall so stuff can’t just pass through and get into the rest of
the blood vessel wall. This barrier function will become pretty relevant in a minute. You’ll just have to take
my word for it for now. Another really important
job that the endothelium has is to secrete proteins onto its surface that prevent clotting. That keeps blood flowing
nice and smoothly. Those are two of its major jobs. It has a couple more,
but those are the ones that are relevant in atherosclerosis. All right, so you remember that big fatty vessel from before? Well, how do we get from this, our nice clean blood vessel, how do we get from this to that? Let’s take a look. The first thing that has to happen is that there has to be
some irritant present, something in the blood
that’s going to predispose this atherosclerosis to happen. So, what are some irritants? Things like too many lipids, so, specifically, fats and cholesterol, LDL cholesterol, the bad cholesterol. Let’s actually put some
of this cholesterol in the blood vessel so we
can see it really clearly. I’ll just label it LDL, LDL-C, actually, so you know this is cholestero, LDL-C. Another irritant, probably the worst one, is toxins from cigarette smoking. So we’ll put some toxins in the blood from cigarette smoking. We’ll do them in gray here. Another major one is just hypertension, high blood pressure. We’ll try to show that pathologically high blood pressure here by these arrows. High blood pressure. This means high blood pressure. I’ll actually write hypertension here, because I just want to make it clear that it’s the chronic exposure
to high blood pressure, it’s not just high blood
pressure every once-in-a-while. That’s our first step, to
have an irritant present. Our second step is to actually have damage to the endothelium by the irritant. So our barrier, now, is broken down. It’s started to break down. That’s step two. That’s actual damage of the endothelium. In step three, regardless
of whatever damaged the endothelium, I mean, if it was toxins or if it was the cholesterol or if it was the high blood pressure, regardless of what actually
damaged the endothelium, what happens next is that the cholesterol will jump in there and start to collect under the damaged endothelium. Let me actually clear away some of this because we’re going to focus
on the cholesterol now. This is cholesterol and it’s going to sort of settle in here. It’s going to think to itself,
hey, that looks pretty comfy. That looks like a cozy place to be, so I’m going to just jump in there, and, of course, these are
coming from inside the blood. They’re not just sort of multiplying. They’re floating around in the blood and then when they come
across this damaged endothelium, they’re going
to join their friends. When they build up to
this sort of flattened extent here, they’re
known as a fatty streak. One thing that happens to the cholesterol when they get inside the wall
of the blood vessel there is that they start to get oxidized. They sort of change a little bit. When they change, when they get oxidized, that sends a signal to the immune system, to our body’s immune system, and that signal will
bring around these cells of the immune system called monocytes. They’ll sort of show
up, almost like police. Here’s a monocyte here. I’ll draw it in white to remind you that it’s a white blood cell. This monocyte doesn’t really like that the cholesterol
is starting to collect in the blood vessel wall, so the monocyte will actually chase in
after the cholesterol to try to break up the little
party that they’re having. I’ll actually draw what happens next down in this next bit of
the blood vessel down here, just so we can keep in mind
all of the past events. You may have noticed
that I drew this white blood cell to look like
a Pac-Man sort of thing, eating up this cholesterol because that’s essentially what it does. Once it gets into the endothelium, it converts into something
called the macrophage, macro meaning big and
phage meaning to eat. So it’s really this big eater. It’s job here is to devour
that LDL cholesterol that’s collected in the endothelium. Unfortunately, things don’t go as planned for our macrophage, because
what ends up happening is it starts to gorge itself. The macrophage eats so much cholesterol that it just sort of becomes too full of these yellow cholesterol drops and it sort of dies off, but it’s full of cholesterol. Someone a long time ago looked down a microscope and thought that these dead macrophages filled with cholesterol looked like foam, like sea
foam that you see at the beach, so these dead macrophages
filled with cholesterol are now called foam cells. Let’s catch our list up. Remember, these foam cells were actually white blood cells, so
when they die they release these signals that sort
of call in reinforcements. I’m going to use that to remind you that atherosclerosis is primarily an inflammatory disease, it’s
an inflammatory condition. When these foam cells
release their cytokines, their signals, they
call in reinforcements, and the whole process sort of proceeds in this viscous cycle, as you’ll see. Don’t forget that LDL is
also still being deposited into the wall from the blood stream. As part of this
inflammation, more and more endothelial cells get
damaged, so I’ll move our drawing down even
further so we can look at the next sort of development. You can see this mountain of cholesterol and foam cells, dead macrophages that are filled with cholesterol. You can see this mountain
just keep on building, and keep on building, and bulging out into the middle of the blood vessel. By now, things are just
way out of control. These guys in here, this is the smooth muscle part
of the artery, by the way, so this is the smooth muscle layer, these guys start to take notice, these smooth muscle cells. What ends up happening
is that you get smooth muscle cells that sort of migrate out of the smooth muscle layer, and they sort of migrate. I hope you can see this. I’ll draw them a little bit thicker. They start to migrate out
of the smooth muscle layer and into the fatty plaque here, because they can sort of sense that something’s not quite right. What they start to do is
they really want the plaque covered up, because they
don’t want the thrombogenic — Remember thrombogenic means clot-forming. They don’t want the thrombogenic plaque to be exposed to the blood, so what they start to do is they start to secrete a fibrous cap. They sort of spit out
this collagen and elastin protein cap that covers up, I’m drawing it in purple, that covers up this plaque and shields it from the blood stream. That’s called a fibrous cap. They also do something else. These smooth muscle
also do something else. You remember these foam
cells that died in here. When they release their
signals after they die, they induce the smooth
muscle into depositing calcium into the plaque. I’ll draw that in. I’ll draw in these little
calcium crystals now, so you can see, it’s just starting to look like a mess in here. There’s just all sorts of stuff going on. Again, this is really not something you want to have happening in your body. Just by looking at this, what can we say is happening
to the blood vessel? Well, we can see this huge bulge. We can see that the plaque is obviously bulging into the blood vessel, and it’s probably going to restrict the flow of blood that
can get through here. That’s one thing that
atherosclerosis is doing. It’s occluding, it’s
blocking off, the arteries. The second thing is look at this calcium. If there’s one thing that
we know about calcium is that it’s really
tough, it’s really hard. By the smooth muscle laying down calcium, that’s one of the ways
that atherosclerosis makes your arteries really hard, and that’s actually part of the name. Atherosclerosis actually means hardening of your arteries. But I think in terms of
coronary artery disease, the biggest reason that
atherosclerosis is bad is because it can cause
complete blockage of the artery, and that blockage of the artery can happen because sometimes this
plaque, this fatty plaque, it can rupture. When it ruptures, all
this thrombogenic plaque material gets exposed to the blood. When it gets exposed to the blood, it starts to form this
really big blood clot in the middle of your artery, in the middle of one of
your coronary arteries. Let’s just draw that in here. Let’s just draw this big blood clot. Pretend that this has been ruptured, and this yellow thrombogenic
material has been exposed, and this big blood clot’s going to form. By the way, I’m originally from Jamaica and blood clot is a bad word in Jamaica, so I apologize to any of my Jamaicans who are watching this. So this big clot could form, and it could totally block
off the blood vessel. When that happens, no blood
can get through, right? So this is really the biggest reason that we don’t want atherosclerosis to be happening in our coronary arteries, because you can see that we’ve blocked off the blood flow, and if blood isn’t allowed to get passed this clot
and get to the piece of the heart that it’s
supposed to be serving within about 20 minutes, then you get irreversible damage and death
of that piece of heart muscle. For example, what we
drew is this little piece of artery here, in blue. So if an atherosclerotic plaque and a clot developed right there, as
it has in our vessel here, then that would be really,
really, really bad, because all the blood for
this whole part of the heart is coming from this upstream vessel. So without getting blood
flow through this vessel for about 20 minutes,
if this clot persists for about 20 minutes,
all of this heart muscle would start to die off. That would be a massive heart attack. Actually, let me just clarify. We say heart attack,
but in medicine we refer to a heart attack as a myocardial infarct, or an MI. Myocardial just refers to heart muscle, cardia for heart, and myo for muscle, so heart muscle. And infarct means death of tissue due to lack of oxygen from lack of blood. So a myocardial infarct
is death of heart muscle due to lack of oxygen. Here we’ve had a myocardial infarct due to this big plaque
that developed here.