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Arteriolosclerosis - part 1

See how hyaline arteriolosclerosis (Protein in the arterial wall) causes hardening of the blood vessels. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.

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Video transcript

Let's talk about arteriolosclerosis. I'm going to first point out a couple of important big picture ideas. Why it is arteriolosclerosis matter? Well, we know that it's basically soft, flexible kind of vessels like this that are very elastic and can expand, becoming very rigid, firm like pipes. And this is basically the big picture on why it matters. You lose compliance. In fact, let me write that in a different color-- lose compliance. And this is the big picture, right? You want to make sure you don't lose compliance. And that's exactly what's happening with arteriolosclerosis. And we also know where it's happening because we have a little clue. We know based on the fact that we have an O-L-O here, this is different than arteriosclerosis. And that this process is happening in the small arteries and arterioles. And just to get a sense of size, I wanted to quickly put up here this is usually around 0.01 millimeters to about 1 millimeter. So pretty tiny and really kind of hard to see with your eyes. So I have drawn an example of what a cut vessel might look like if you were to look at it under a microscope. And inside of this vessel of course you've got your blood cells here. And you've got let's say little platelets here. But you also have something very, very important that we don't always talk about or think about, and that is you've got little proteins here. So you've got protein hanging out in the blood vessel. And these are serum proteins. Serum, S-E-R-U-M, proteins. And all that means is that it's in the blood or the serum. And that protein usually should stay in the middle of the vessel. It shouldn't be making its way into the blood vessel. But in arteriolosclerosis, the main problem, the core problem, is that this protein goes into this space, this tunica media space. So this is the second, the tunica media, and usually has just smooth muscle cells. But if the serum proteins go and settle in there, let's say they're able to make it through this barrier. This is the key barrier. This is the basement membrane. If they can make it through the basement membrane and settle into the tunica media, then you've got a problem. In fact, let me draw a few proteins here. If these proteins can kind of make their way out here, then you've got a problem. In fact, that is exactly how arteriolosclerosis happens. This is the process. So really if you look under a microscopic and you start seeing pink protein in the tunica media, you can be fairly certain that you have arteriolosclerosis happening. In fact, they even call it hyaline-- you might see this word hyaline-- arteriolosclerosis. And hyaline refers to the fact that under a microscope this vessel is going to look like it's got some pink glassy stuff in the tunica media that doesn't belong there. And that pink glassy stuff is the serum protein. And I put glassy in quotes because I don't think that it looks very glassy. And I was always a little surprised that that's what it means. But somebody at some point certainly thought it did. So the term hyaline is really just descriptive and arteriolosclerosis is the process. So now think about this for a second. Think about the fact that if you have a protein moving from the lumen of the blood vessel into the tunica media, there's got to be a couple different ways, or processes, that can happen logically, right? So one logical way could be that maybe it's being forced out. Maybe the serum protein is being forced out of the lumen and has so much force that it's actually driving it through the basement membrane. And that's actually exactly what happens in people that have hypertension. So if you have hypertension, or high blood pressure, you have so much blood pressure, or so much force in the actual middle of the blood vessel, pushing out on the walls of the blood vessel-- and I'll erase all this for a second-- that it literally forces these proteins outside. So that could be one way, right? Force the proteins out. And that's what happens in hypertension. Now, in diabetes, which is the other disease that you often hear about with hyaline arteriolosclerosis-- in diabetes, a different thing is happening. So let's talk about how it happens in diabetes. Again, the key is you've got to figure out how did protein end up in the tunica media. So protein-- and I'll put serum protein-- in tunica media. Because that's kind of a summary of what's happening, right? This is the key thing that's happening. So in diabetes the way that happens is actually the basement membrane becomes leaky. So it's not that you're actually forcing the proteins out. You're actually making it easier for them to get into the tunica media because the basement membrane-- basement membrane, I'll just put BM-- becomes leaky. And how it becomes leaky is actually kind of an interesting story. And you'll learn as I go through it step by step a couple of interesting facts. So fact number one, we know that there's a lot of glucose in the blood vessels. So lots of glucose in the blood vessels of someone with diabetes. So let's draw in some glucose. This purple stuff, these little dots, are going to be glucose. Fair enough. So lots of glucose in the blood vessel. And step number two is that that glucose is going into these endothelial cells. So I'm just going to draw a few of them here. So a few of these cells got a lot of this purple glucose in them. I know you're thinking why in the world would these endothelial cells have glucose in them? I thought that glucose only gets in with insulin. And the whole problem with diabetes is that you don't have insulin allowing that glucose in or having some other difficulty getting that glucose in. So how is that glucose getting into those cells? And here is kind of fact number one, and that is that glucose can get into the endothelial cells without the help of insulin. So endothelial cells take in glucose without-- there's the big catch-- without insulin. So they don't need insulin to take in the glucose. There have other ways of getting the glucose in there. So now you can see that if you have a lot of glucose in the blood vessels-- because every other cell in the body seems to need insulin to get it in and so it's unable to get in. It's kind of hanging out in the middle of the blood vessels. If it's just hanging out there and the endothelial cells don't need insulin to get the glucose in, then they're going to be loaded with glucose, right? So these endothelial cells become loaded with glucose. Let me scroll up a little bit so we have some space. So they become loaded with glucose. And let's draw that here. I'm going to draw that out so that you can see it. These endothelial cells and below them we've got the basement membrane here. This is the basement membrane. And these endothelial cells have a lot of glucose in them, right? So this is all that glucose that they've picked up. And they, of course, have proteins themselves. So they have proteins doing all sorts of interesting jobs. And so let's draw some proteins in here. Maybe this protein here and this protein here, maybe another protein here. So these proteins are hanging out doing their usual job in the cell, and all of a sudden you've got lots of glucose in there. So what happens is that this glucose starts to stick onto, or bind onto, these proteins. And these proteins all of a sudden have tons of glucose on them that they don't usually have. So these proteins are considered glycosylated. In fact, another longer term for it is that they turn into what they call advanced-- let me write it out here-- advanced glycosylation-- that's kind of a fancy word-- glycosylation end product. So all that's happened is that a normal protein, normal protein or enzyme, that was doing its job-- in fact, let me stay consistent here with the colors. So normal protein that was doing its job in the cell, in these endothelial cells, becomes what we call an AGE, advanced glycosylation end product. So these AGEs are basically the same protein, but now with glucose on them. They actually don't do as good a job as they're supposed to. That's kind of the bottom line. They aren't working the way they should. And one of their jobs is to make sure that that basement membrane is doing a good job of forming a barrier. And that basement membrane becomes very leaky. So the basement membrane actually becomes thicker-- which is counterintuitive, right-- becomes thicker. Because you think if it's thicker it's doing a better job being a barrier, but actually it's a worse job being a barrier-- and leaky. And this is really the important issue. Because that leakiness is what's allowing all the serum proteins to come across and settle into the tunica media. So let's stop there and we'll pick up.