Blood Vessel Diseases
Atherosclerosis - Part 1 See how Atherosclerosis (Fat in the blood vessel wall) hardens the arterial wall and makes it harder for blood to flow through. Rishi is a pediatric infectious disease physician and works at Khan Academy.
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- so I want to talk to you a little bit about {atherosclerosis},
- and I have already cheated a little bit, and I started drawing,
- I already make a slightly nice drawing, because I want to make sure that
- the important thing is we can actually see them, and that is --it's pretty clear.
- So, in the top left, I have a small vessel,
- and it have the three layers, and in the middle is the lumen,
- and on the outside is the --the outside.
- So, this little white box I've drawn, I've tried to blow it up for you a little bit here,
- so again, over on this side we have the lumen, just to orient you again,
- and this is the outside of a blood vessel.
- So, we know that a blood vessel have three layers and this particular blood vessel is--
- actually, let me lable it, is a middle or large arteries.
- so I'm specifically talking about {large and middle size arteries} here.
- And the reasons that this makes the differece, I'll point out specifically again,
- but there're these green little coils I've drawn here, these little green squigglies,
- and this is a little protein called the {elastin},
- and I specifically want to talk about these arteries, because
- these large and middle arteries that have --in them, in the walls-- elastin,
- are very very susceptible to atherosclerosis, this process.
- And so, I've thought that it makes sense to point out just for you to know exactly
- which vessels are being affected by this process.
- So let's go through and --quckly refresh ourselves, and talk about three layers of the vessel,
- we have the intima, the {tunica intima}.
- And I was writing 'T' for tunica.
- And then --that's the innermost layer.
- The middle layer right here, in red, is the {tunica media},
- and remember that, because it's the middle layer, so media, middle.
- And on the outside right here is the {tunica externa}. Externa, kind of the external layer.
- And sometimes you see that as {adventitia}, another word for it.
- So these are the three layers, we know this.
- And the way that atherosclerosis happens, now this is a process in --it's a,
- it's a process that affects millions and millions of people.
- The way this happens is that it usually affects these large vessels --large or middle arteries,
- and actually these vessels just --to give you a little bit an orientation,
- I'm talking about 1 mm size of vessels all the way about 25 mm in diameter.
- So kind of a --kind of biggest vessels, that you could actually see with your naked eye,
- this could be like the artery, that maybe-- maybe the aorta, the largest artery,
- or could be an artery that goes up to my arm, the brachial artery.
- So in here these large or middle size arteries fit in this category,
- and they're affected by atherosclerosis.
- So the first step in atherosclerosis, let's just jump and do it,
- it's that you have an irritant, some irritant.
- And that could be --I'm not talking about, maybe someone's annoying little brother or sister, annoying neighbour,
- but some irritant like, let's say you have --here I'll draw in red-- a toxin from cigarrette smoke.
- So let say you've got some toxin that's swimming through your blood vessels, and that could be an irritant.
- Another irritant could be --so I'll put smoking up here for that--
- another irritant could be, maybe having too much lipids, so maybe hyperlipidemia.
- Hyperlipidemia.
- And when I say lipid, I mean specifically fats and cholesterols.
- So, you could have little droplets --it's showed a little yellow droplets, 'cuz I think yellow as fat,
- of LDL, this is a protein. LDL stands for --actually I'll write that out--
- Low Density --that's what the L dan D are--
- Low Density Lipoprotein.
- So this is basically something that carries fat and cholesterol around your blood.
- So you could have too much of it. You could have too much LDL in your blood,
- in the blood vessels, in the arteries.
- And that could be an irritant.
- Or it could be --maybe I'll use a dark-- maybe a white colour here,
- maybe could be high blood pressure,
- high blood pressure pushing out on these vessels, could be an irritant.
- So any of these things could be an irritant, hyperlipidemia, smoking, or hypertension or high blood pressure.
- Could be an irritant.
- And what is being irritated?
- What is the thing that is being irritated?
- That's number two.
- It's the layer of cells right here, these inner layer cells in the tunica intima.
- and that layer itself we know as the endothelial layer. {endothelial cells}
- So that's the layer that's being offended somehow, so it's being upset or angry.
- It's getting upset at these irritants, so I'm going to show some unhappy faces here,
- maybe some unhappy faces down here from the LDL,
- maybe some unhappiness from that high blood pressure.
- And right behind it, --just to orient you-- is the basement membrane,
- but really again it's the endothelial cells that're being irritated.
- Right, so that would be step two, is endothelial --actually leaving the same colour--
- {endothelial disfunction}. This stop working the way they like to work,
- in all, try to be a little bit more specific,
- endothelial cells are basically a barrier, right?
- they're creating a barrier between what is flowing through the blood and the wall itself,
- right, they're the first thing that molecules and cells in the blood are gonna see.
- And so, if you have endothelial disfunction, what you get is
- that this barrier starts breaking down.
- And so this barrier --let me erase some of this stuffs now, just to make some space,
- we know that LDL is Low Density Lipoprotein, I'll erase that.
- And I'll erase this white areas for the hypertension.
- And I'll even erase that ciggarette smoke, the toxin.
- and I'll leave the LDL for a second, you'll see why.
- But please let me show you that these cells start getting unhappy,
- and they start breaking down, and --I guess I'll erase a lot of it and I'll draw some of it back.
- And what you get is something like this.
- We've --We have, now, a breach. A breach.
- So you have these cells here, but now they're letting stuff through.
- And the stuff they get through, primarily --and this is of importance to us, is the LDL.
- So even if something else was the irritant,
- let's say cigarrete smoke was the major irritant here,
- and you got endothelial disfunction from that,
- the next step in atherosclerosis, step three, is LDL goes into --I'll just write--
- into T. or tunica intima.
- This is kind of the next major step, is that LDL decides that it wants to go inside,
- it likes to be inside of this layer.
- And so you got LDL hanging out over here --I'll just write LDL here, so you'll know what we're talking about.
- So all this little molecule of LDL, which again, you bring with them a lot of fat and cholesterol,
- and they're all now in this tunica intima layer.
- So they're all within this tunica intima layer --let me try make that very clear,
- all within this layer tunica intima.
- So they're not usually there. And that's step three.
- Now step four, really really interesting,
- this is where things get really kind of wild,
- is you have cells in your immune system that are right here, called {macrophages}
- Macrophages.
- and these macrophages, they have huge mouth,
- and they're --actually macrophages really means 'big eater'.
- So, macro-big, and 'phage' meaning to eat.
- Macrophages actually swim through the blood, and they're patroling the blood,
- almost like police officers,
- and they sense that, "hey, something is not right with this wall, there's LDL in there"
- and they go in pursuit --they go after that LDL.
- And now they go into the wall.
- So now you got LDL on the wall, you got macrophages on the wall,
- and so I'm gonna draw these macrophages, it's not to scale, just again they're bigger than this.
- But they're now in the wall, they're hanging out in this area, right.
- And they start devouring, again they're big eaters.
- So they start devouring, gobbling up all that fat.
- So this is gonna get a little bit tricky, but let me try to sketch it out again up here for you.
- These're gobbling up fat, and they get loaded with this little fat,
- these little particles of LDL.
- So this is now LDL that's inside of the macrophages, right?
- and if you look through microscope, what this may look like?
- is --you have to use your imaginaton here, but is seafoam.
- So if you actually look --go out to the sea, you know, let's say you go to Mediteranean Sea.
- And you look at seafoam, that's actually what it would look like, potentially.
- That 's someone's thought anyway.
- And so they called these cells, these macrophages that've gobbled up LDL,
- and actually died, so these cells has now died.
- I'll draw a little Xs, because it is so much have died.
- These cells they called them {foam cells}.
- Foam cells. I'll just write a little arrow here,
- so you know which one I'm talking about. Foam cells.
- So if you look in the tunica intima again, that's for all the action is, right?
- this is --this is the important part here --I'll draw box around it.
- That's kind of the central stage.
- The LDL, the macrophages that chase down, now the dead foam cells,
- are all sitting in here, in this lake of fat.
- So now you got macrophages in step four --let me just make sure I catch up with our picture.
- Macrophages and plus foam cells.
- foam cells.
- into tunica intima, right.
- So now we're on the same page.
- And this --this intima now, really, starts looking a lot like this.
- Let me erase this, clean this up a little bit,
- because it's getting quite a mess here, then you'd --you'd agree it needs a little cleaning up.
- So let me erase all this stuff on the outside.
- We know that LDL was in the blood, but it went into the intima, we know that.
- So --so now you have, basically, this LDL, all of these molecules (...) is start merging,
- into literally a lake. Think about it like a lake of fat.
- and how disgusing about is that, right? Like a lake of lard, here, or fat, here.
- It's your fat, or this person's fat.
- And it's all, in this layer, called the tunica intima.
- In fact, let me even draw another dead macrophage.
- It's another foam cell, I'm making a foam cell out of this.
- Looks like seafoam, maybe.
- And so you have here a lake of LDL.
- You have foam cells, and it's all sitting in the tunica intima.
- And if you're actually to, let's say you're to fillet this cell open,
- or this blood vessel open --let me to try to show what I mean.
- If you're --let's say you have this blood vessel.
- I'm drawing you very simply now, you know that that there're three layers,
- it's not the one that I'm drawing there,
- but let's imagine that you took a knife and you slice through it.
- So now, you basically are looking at kind of just the inside of it.
- Right, it's the inside of it.
- What you would see is basically this giant streak of fat.
- And this is kind of that lake, that I just showed you, right.
- Now, looking at it lengthwise.
- So this lake of fat is called the {fatty streak}.
- So if you open up a blood vessel, and look at it,
- if this process has been going on, you might start seeing fatty streaks.
- and so that's basically the first half of atherosclerosis.
- So let's pick up there in the next video.
- ~o0o~
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At 5:31, how is the moon large enough to block the sun? Isn't the sun way larger?
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