7.3 Atheriosclerosis

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Okay, next section,

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arteriosclerosis.

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Arterio means arteries,

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and sclerosis means hardening,

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and so in this particular set of disorders,

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what happens is we get hardening of the arterial wall.

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Now, this basically occurs due to thickening of the blood vessel wall,

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and there are three pathologic patterns.

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The first is called atherosclerosis,

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and in atherosclerosis,

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we get a thickening of the intima of the blood vessel wall.

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That's high yield.

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In atherosclerosis,

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it's the intima.

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that becomes thick,

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and this usually occurs in medium and large

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-sized vessels.

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So that's atherosclerosis.

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In arteriolosclerosis,

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the olo tells us that we're dealing with the arterioles,

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so this will occur in small blood vessels,

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and we get thickening of the wall,

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either due to a deposition of protein within the wall

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or an increase in protein within the wall.

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and that's called Heinlein arteriolosclerosis,

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or a hyperplasia of the smooth muscle of the wall,

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which is called hyperplastic arteriolosclerosis,

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but we'll give you some more details as we move forward.

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In Monckeberg medial sclerosis,

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you get calcification of the media of the blood vessel,

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and this is clinically not really significant.

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You'll hear about that at the very end of this lecture.

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So let's start with atherosclerosis.

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Again, remember,

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it's an intimal plaque that obstructs blood flow.

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So here's a blood vessel.

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And of course,

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you've got an intima,

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you've got a media,

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and an adventitia.

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Those are your three layers.

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And this is an intimal plaque in which you get obstruction of

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blood flow.

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Now, important to note that this plaque mostly consists of a necrotic

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lipid core.

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So the key component here would be cholesterol.

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And it has a fibromuscular cap,

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as I've drawn here.

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And often,

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this necrotic lipid core can undergo dystrophic calcification,

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so it's not uncommon for atherosclerosis to be calcified.

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Here's a picture of atherosclerosis.

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This would normally represent the intima with an endothelial layer

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sitting on top of a basement membrane.

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Here is the smooth muscle media.

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You can clearly see that there's expansion of the intima by this necrotic

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lipid core.

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Notice all the cholesterol clefts sitting in the middle of this necrotic

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lipid core.

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And we've got this fibromuscular cap that overlies the necrotic

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lipid core.

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So again,

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intimal plaque.

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that consists of a necrotic lipid core with a fibromuscular cap.

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This involves large and medium -sized arteries,

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as I've already mentioned,

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and the four most common arteries in the body to be involved are the abdominal

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aorta, the coronary arteries,

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the popliteal artery,

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and the internal carotid arteries.

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And the idea here is that when you get involvement in these arteries,

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you're going to develop certain pathology,

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and the pathology is what we're going to discuss both in this section

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and in the cardiac section.

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So the risk factors for atherosclerosis are actually divided into two,

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modifiable and non -modifiable.

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The modifiable risk factors include hypertension.

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That's a very important risk factor for the development of atherosclerosis.

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Hypercholesterolemia,

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for example,

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LDL increases the risk,

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whereas HDL decreases the risk.

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Smoking and diabetes.

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So these are the four key modifiable risk factors that lead to

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atherosclerosis,

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and you need to memorize each of them.

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All right, so you need to know that there's four modifiable key risk factors,

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hypertension, hypercholesterolemia,

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smoking, and diabetes.

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The non -modifiable risk factors include age.

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For example,

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the number and severity of the lesions,

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they increase with age.

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Gender,

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for example,

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there's an increased risk in males and in postmenopausal females.

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Premenopausal females are relatively protected,

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and that's because estrogen is protective.

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And then there are some genetic factors.

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It's basically multifactorial,

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but important to note that family history is highly predictive of risk.

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The pathogenesis of atherosclerosis is debated,

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but one sort of theory is that you've got endothelium here.

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Of course, endothelium is sitting on top of this basement membrane,

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and the idea is that within this intima here,

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you get damage to the endothelium,

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which then results in lipid entering into the intima.

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And as lipid enters into the intima,

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the lipid then gets oxidized.

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And once it gets oxidized,

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it gets taken up by macrophages so that you get collections of macrophages

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with lipid within them.

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That forms the initial lesion of atherosclerosis,

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which is called a fatty streak.

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And where you look at a blood vessel in a very young patient,

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you could see these yellow flat streaks that are running along.

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the large blood vessels,

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and those are called fatty streaks.

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They arise early in life,

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and actually they're seen in most teenagers.

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That's how early atherosclerosis begins.

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Now eventually you get inflammation and healing and increased deposition

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of this lipid within the intima,

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and that's going to result in a thickening of this lipid layer with a

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necrotic lipid core and the formation of a fibromuscular cap.

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Now that fibromuscular cap is due to the inflammation and healing,

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which leads to deposition of extracellular matrix.

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and proliferation of smooth muscle.

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And so in the end,

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what's going to happen is that this is going to be the blood vessel,

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and you're obviously

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going to have this atherosclerotic plaque that will occlude the blood flow or

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that will decrease the blood flow

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Complications of atherosclerosis account for more than half of disease in the Western world,

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and let's walk our way through some of these now.

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The first is stenosis of medium -sized vessels,

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and here's the idea.

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If this is a blood vessel and it's going into an organ,

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you know that the medium -sized blood vessels are those vessels that feed the major organs.

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So let's say that this is the artery and this is the vein and this is the organ.

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If we get atherosclerosis here,

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then that atherosclerosis is going to cause stenosis of the blood vessel.

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i .e.,

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you've decreased the luminal caliber of that blood vessel.

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And of course,

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that can result in various signs and symptoms.

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So this can occur,

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for example, in the popliteal artery,

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resulting in peripheral vascular disease.

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It can also occur in the coronary artery,

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which would give you episodic chest pain or angina.

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And then it can also occur in the mesenteric arteries,

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which could give ischemic bowel disease.

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So that's complication number one.

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It's important to note that you usually don't get symptoms until you have greater than 70

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% stenosis.

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That's high yield.

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Greater than 70 % stenosis before you actually get complications.

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Complication number two is plaque rupture with thrombosis,

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and the idea here is you've got this blood vessel,

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and obviously this blood vessel's feeding the organ.

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Let's pretend that you've got atherosclerosis here.

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Now,

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one of the complications of atherosclerosis is that at the neck,

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this is the place where it usually ruptures,

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at the neck,

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you can get rupture,

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which would then expose all that necrotic lipid core.

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And if the necrotic lipid core and the tissue underneath it is exposed,

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that's going to result in activation of the coagulation cascade.

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And so you'd rapidly develop a thrombus here,

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which could then occlude the vessel,

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creating an infarction in this organ.

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And actually,

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that's the way by which a myocardial infarction occurs.

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It's usually due to plaque rupture with thrombosis.

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So the examples would be if this occurred in the coronary artery,

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the patient would develop a myocardial infarction.

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If this occurred,

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for example, in the middle cerebral artery,

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the patient could develop a stroke.

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So that's a second complication of atherosclerosis.

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The third complication of atherosclerosis is plaque rupture with embolization.

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Now here's the idea.

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You've got this atherosclerotic plaque.

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It's possible for this plaque to break off,

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and then part of that plaque could embolize and go through the blood supply and then lodge

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in a distant site,

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and that's called embolization.

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Now that results in something called an atherosclerotic embolus,

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and remember that the hallmark of atherosclerotic emboli are the presence of

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cholesterol clefts.

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Now here's a picture of that.

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This is a blood vessel.

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This blood vessel contains an atherosclerotic embolus,

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and the way by which you know that it's an atherosclerotic embolus is because you see these

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cholesterol clefts.

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The fourth complication is weakening of the vessel wall,

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and the idea here is that,

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remember the vessel wall contains an intima,

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it contains a media,

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and it contains an adventitia.

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And of course,

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this is where the blood would be present.

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Now remember that the blood vessel wall,

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i .e.

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the intima, media,

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and the adventitia,

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these are all alive,

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and they require oxygen in order to maintain themselves and

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to be healthy.

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Now normally,

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what's nice about the blood vessel is that the blood

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carries oxygen and the oxygen from the blood actually feeds the entire vessel

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wall however if a patient gets atherosclerosis so that this intima becomes

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thick it creates a diffusion barrier so that oxygen can't feed this wall

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so this wall will become weak and will become atrophic now as the

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wall weakens what's going to happen is you're going to increase the risk of ballooning of that wall

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because now there's a weak wall with a lot of stress and so the complication of

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that would be that you would develop

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something called an aneurysm,

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which is a balloon -like dilatation of the blood vessel wall.

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This is a fourth complication of atherosclerosis,

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and it's going to be very important as we move forward in this particular chapter.

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Now the second type of arteriosclerosis,

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remember arteriosclerosis is the global term that refers to these three

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mechanisms by which we can create thickening of the blood vessel wall.

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So the second type of arteriosclerosis is arteriolosclerosis,

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implying that we're dealing with the small blood vessels.

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Now what happens here is you get thickening of the wall of the small blood vessels,

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which then narrows those small blood vessels and then creates complications

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downstream.

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Arteriolosclerosis comes in two flavors.

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Number one,

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highline arteriolosclerosis,

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and number two,

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hyperplastic.

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In highline arteriolosclerosis,

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you get proteins leaking into the vessel wall.

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This produces vascular thickening,

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and you see it on microscopy as pink highline within the blood vessel.

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So here's what it looks like.

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This is obviously a blood vessel here,

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and you can see that the wall of this blood vessel is relatively thick,

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and what's thickening it here is the presence of this pink Heinlein

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material.

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And so this is an example of Heinlein arteriolosclerosis.

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Very important to note that it arises due to two things.

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You have to know this.

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This is super high yield.

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It's going to be something that we're going to hear about regularly as we move through pelvic

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floor.

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pathology.

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Number one,

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benign hypertension.

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Patients who have long -standing benign hypertension,

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they get highline arteriolosclerosis.

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And the idea here is that the high blood pressure forces protein into the

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wall, giving us this change.

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And number two,

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we see it in diabetics.

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So patients who have diabetes,

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they get non -enzymatic glycosylation of the basement membrane,

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which then makes this blood vessel wall leaky,

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and then protein begins to leak in,

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giving us highline

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I cannot emphasize this enough.

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It's so high yield.

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It will come up over and over again in our discussions of pathology.

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Highline arteriolosclerosis is a consequence of

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two things.

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Number one,

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benign hypertension.

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Number two,

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diabetes.

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Now, the consequence of highline arteriolosclerosis is that you're going to get a reduced

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vessel caliber,

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which is then going to result in end organ ischemia.

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This can occur throughout the body,

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but it classically occurs within the kidney,

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producing glomerular scarring.

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And here's the idea.

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It's very high yield to be aware of.

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You've got this glomerulus here,

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okay?

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and there's an afferent arteriole here,

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and there's an efferent arteriole here.

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Imagine if you get highline arteriolosclerosis so that you get thickening

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of the blood vessel wall.

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As you thicken the blood vessel wall,

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slowly over time,

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you're slowly going to decrease the amount of blood that's actually supplying this glomerulus.

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This glomerulus will then scar.

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and you'll get something called glomerular scarring.

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So this is a key consequence of highline arteriolosclerosis.

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And in fact, this is the reason why patients with diabetes and patients with high blood

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pressure, they get chronic renal failure because over time,

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they develop this glomerular scarring due to the highline

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arteriolosclerosis.

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And that's what I've stated here in your text where I say that it classically produces

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glomerular scarring.

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Now when it produces glomerular scarring,

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we call that arteriolo.

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nephrosclerosis, arteriolo,

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small arterioles.

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Nephro,

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kidney, sclerosis,

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you get sclerosis of both the glomeruli as well as those small

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blood vessels.

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And of course,

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this is how we get to chronic renal failure in patients with long -standing

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hypertension and in patients with diabetes.

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Now,

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of course, as you get this...

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glomerular scarring,

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you're going to shrink the kidney,

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so the kidney will become shrunken.

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And on top of that,

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you'll see the scarring on the surface of the kidney.

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Now, when you look at the outside of the kidney,

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you're really getting a look at the cortex.

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So the outside represents the cortex.

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The surface of the kidney is really up against the cortex,

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basically.

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And so this is a classic example of arteriolonephrosclerosis.

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The other type of arteriolosclerosis is called hyperplastic arteriolosclerosis.

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And again, this is going to involve the small blood vessels,

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and we're gonna get thickening of the small blood vessels.

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However, instead of the thickening being due to this protein

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that's leaking into the vessel wall,

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we get hyperplasia of the smooth muscle that results in that thickening,

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which then gives something called an onion skin appearance.

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So here's the classic image,

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and this is again a small blood vessel or an arteriole.

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and we've got thickening of the arterial,

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and you can see that there's too many muscular cell layers

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here, and that's producing layer after layer of smooth muscle,

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which then is called onion skinning because each layer looks like the skin of

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an onion.

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Now, this reduces the luminal caliber,

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which then decreases the blood flow going to the end

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organ.

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All right,

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once you've understood the histology,

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then the next question is,

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what does this process do to?

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And it's very important to note that this process is a consequence of malignant

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hypertension.

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Malignant hypertension.

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And so the idea here is that when you get super high blood pressure,

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sort of the smooth muscle begins to respond by hyperplasing,

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almost trying to contain that high blood pressure.

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And so that's called hyperplastic arteriolosclerosis.

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Now, of course,

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the luminal narrowing that's going to occur here is going to result in

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reduced vessel caliber,

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and so we'll get end -organ ischemia.

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Now that high blood pressure can also result in fibrinoid necrosis.

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Remember from chapter one when we talked about necrosis,

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we said that when you get death of the blood vessel wall,

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that's called fibrinoid necrosis,

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and we see that in two circumstances.

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We see that in malignant hypertension,

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and we see that in vasculitis.

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So this is an example of where we might get fibrinoid necrosis of the blood vessel

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wall.

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Now the classic finding is also present within the kidney when patients

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have

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highline arteriolosclerosis,

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and that is that they get acute renal failure with something called a flea bitten

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appearance to the kidney.

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The acute renal failure,

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again, is because you're getting acute damage due to the very high blood pressure to the

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kidney, and at the same time,

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you get this flea bitten appearance because on the surface of the kidney,

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you have these little pinpoint hemorrhages where you've had,

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you know,

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blowing out of the blood vessels,

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for example,

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which then results in hemorrhage.

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So this is a very high yield principle to be aware of.

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Now let me just summarize this because this is,

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the entire discussion is so central to so much of pathology.

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So basically what we've said so far in these few slides that we've covered are

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that you can get thickening of the blood vessel wall,

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and when you have thickening of the blood vessel wall,

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that's called arteriosclerosis.

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If you get thickening of the large or medium -sized blood vessels with

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an intimal plaque,

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that's called atherosclerosis,

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and that will have four complications,

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which we've already discussed.

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And then the other possibility is that you can get thickening of the small arterioles,

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and that's called arteriolosclerosis.

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Arteriolosclerosis can be divided into two types,

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hyperplastic and highline.

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In highline arteriolosclerosis,

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you get leaking of protein across the blood vessel wall,

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which thickens the blood vessel wall,

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giving it a pink appearance.

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And of course,

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the two ways by which you can get highline arteriolosclerosis are hypertension,

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which squeezes protein across that blood vessel wall,

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and diabetes,

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in which you get non -enzymatic glycosylation of the basement membrane of

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the vessel wall,

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which then allows protein to leak in.

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So Heinlein arteriolosclerosis,

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benign hypertension,

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and diabetes.

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The other way by which you can get arteriolosclerosis of a small blood vessel

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wall would be hyperplastic arteriolosclerosis.

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This is where you get thickening of the blood vessel wall due to hyperplasia of the smooth muscle,

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and it's classically seen with malignant hypertension.

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You've got to have all that summary very well established in your minds

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to be able to understand the discussions that we're going to have as we move forward.

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Now the third way by which you can have arteriosclerosis

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would be a disease or a disorder called Monckeberg's medial calcific sclerosis.

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And the idea here is that you get calcification of the media.

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That's why it's called media,

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and that's why it's called calcific,

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calcification of the media.

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This is non -obstructive,

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and therefore it's not clinically significant.

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And it's seen as an incidental finding on x -ray or mammography.

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This is what the histology looks like.

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You see a blood vessel wall.

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This layer here represents the intima.

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You can see the intima is right up against the

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smooth muscle media as it should be.

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And then within the media,

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you can see that you've got this area of calcification.

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So this is Monckeberg's medial calcific sclerosis.

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Again, it does not alter the luminal caliber,

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and therefore it does not affect blood flow,

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and therefore it is not clinically significant.

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The only reason you need to know about it is because it can show up on x -ray,

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in particular on mammography.

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Now, you know that on mammograms,

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you're classically looking for calcification as a sign of cancer.

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Remember,

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that's one of the things that we screen for is the presence of calcifications.

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And so it's important to note that you can also get calcifications of the blood

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vessel wall.

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And so this is an example of a calcification that's running in a vascular

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pattern.

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And so this is called Monckeberg's medial calcific sclerosis.

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It's important to note that that would then result in

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incidental calcifications on for example a mammogram and

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that closes off this particular section

7.3 Atheriosclerosis

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