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Course: Health and medicine > Unit 3
Lesson 2: Atherosclerosis, arteriosclerosis, and arteriolosclerosisArteriolosclerosis - part 2
See how hyperplastic arteriolosclerosis (Protein in the arterial wall) makes it difficult for blood to go through blood vessels. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.
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- How Inverse relation between plasma HDL levels and atherosclerosis(3 votes)
- Rishi talks about looking at these under a microscope. How are these blood vessels checked in patients?(2 votes)
- Sometimes, especially if a patient is seen by a vascular surgeon, a vessel biopsy can be performed, where the amount of occlusion can be seen. Most of the time, we can do doppler studies. If you were to dissect out an artery from a cadaver, you could do histological studies on segments to see the pathogenesis and stages of atherosclerosis.(2 votes)
- When Rishi drew the straight-lined endothelial cells, is that because they're filled with glucose or are they just the same as the first picture?(1 vote)
- Why/how does malignant hypertension cause hyperplastic changes? It seems like hyperplastic changes usually arise from chronic hypertension, rather than a rapid increase in blood pressure.(1 vote)
- hypertension would hypertrophy the atrial walls, meaning they grow to attempt to handle the additional force of the blood running through them. I think it's more of an effect seen over time, because these changes don't just appear, they evolve.(0 votes)
- is this a disease or an infection(0 votes)
- It isn't a disease caused by bacteria or viruses, etc. It is a result of conditions in your body about proteins, hypertension, and the process he describes is how all this happens from specific conditions in your body.(1 vote)
Video transcript
OK, so we left off talking
about arteriolosclerosis, and specifically hyaline
arteriolosclerosis, which is where you see pink, glassy
material in the tunica media. And we talked about the
two major ways or diseases where you see it getting there. So there's another term
now I want to introduce, and that's called hyperplastic
arteriolosclerosis. It's kind of a mouthful. And here I think
of it as what would happen if the process of hyaline
arteriolosclerosis kept going. What would happen? So just keep
imagining this vessel. And let's say that the
situation continues. And now you've got years
and years of protein buildup in that space, in the
tunica media space. Well what would happen next? Well you can start by imagining
the same vessel, like that. This is the external
layer, the tunica externa. And then right on the inside
of that is the tunica media. And this tunica media, we know--
I drew a little bulge there by accident-- but we
know this tunica media is full of smooth muscle cells. And when these smooth muscle
cells are around protein-- and they're not supposed to be
around serum proteins, right? When they're around
protein for a long time and they keep getting
exposed to it, they react. And what they do when they
react is they start multiplying. So you get more and more of
these smooth muscle cells. More and more of them. In fact, so many of them that it
completely fills up the space. So the smooth muscle cells
keep dominating all the space. Right? And they keep crowding
out all the other layers. So in response to
the proteins-- I haven't even drawn
in the proteins yet, but let me show you
some proteins that made their way into this space. In response to these
proteins, these serum proteins that went across the
basement membrane, either because they got pushed
out because of hypertension or maybe they got there because
the base membrane became leaky. Either way, these
proteins are now here. And the smooth muscle cells
start dividing over time. They start dividing a lot. And as a result, what
happens is that you get kind of this
inner layer of-- this is now the basement membrane
and let me show that here. And this basement membrane
has on the other side of it the endothelial cells. So we've got the same
layers as before. But the main difference, the
main thing I want you to see, is that the tunica
media is thick. It is thick. And it's thick
specifically because of all of the smooth muscle
cells dividing. Now I've drawn in
the endothelial cells and I've drawn in a little,
tiny lumen, a small lumen. Now compare that to
what it used to look like-- enormous lumen
now has become very tiny. And so because it's
so tiny it makes it really hard for blood
flow through there. And under a microscope the
way that people describe this if they see this is they say,
well this looks like an onion. So they call this
onion skinning. And meaning that the onion
has many layers to it. Right? And this actually looks like the
many, many layers of an onion. That proliferated smooth
muscle layer, the tunica media, is now very thick. And that's why it gets that
name, the thick tunica media. And the other issue
is that usually you see this in cases of
high blood pressure. So we talked about the fact that
if your process of hypertension goes on a long time or if
diabetes goes on a long time you might get this. The classic situation
where you see this is malignant hypertension. That's usually the
one where you'll hear about this the most. And malignant hypertension,
just to remind you, is when you have a rapid
rise in blood pressure. And it can go as
high as, let's say, 240 over 120, so
really, really high. And usually these
people have symptoms. So generally speaking, people
with the malignant hypertension have some sort of symptoms. So-- oh, extra hump on my m. So if you have
malignant hypertension and you look in the blood
vessels of these folks, there is a good chance you might
see a very thick tunica media. And we would call
that hyperplastic arteriolosclerosis.