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of complete
of complete
Laboratory value | Result |
Serum | |
Creatinine | 1.9 mg/dL |
Blood urea nitrogen | 50 mg/dL |
Urine | |
Erythrocytes | 8/hpf |
Leukocytes | 2/hpf |
Protein | 3+ |
Sediment | None |
2024
2023
2022
2021
atherosclerosis in p. 305, 731
atherosclerosis p. 305
atherosclerosis p. 305
abdominal aortic aneurysms and p. 305
aortic aneurysms p. 731
diabetes mellitus and p. 350
familial dyslipidemias p. 92
homocystinuria as cause p. 83
sites of p. 731
stable angina with p. 308
transplant rejection p. 117
atherosclerosis in p. 305, 731
atherosclerosis p. 305
atherosclerosis p. 305
atherosclerosis in p. 305
atherosclerosis in p. 731
atherosclerosis and p. 305
atherosclerosis p. 305
in atherosclerosis p. 305
atherosclerosis and p. 305
atherosclerosis and p. 305
atherosclerosis p. 305
in atherosclerosis p. 305
atherosclerosis p. 305
atherosclerosis in p. 305, 731
atherosclerosis and p. 305
atherosclerosis and p. 305
atherosclerosis p. 305
So these three words look the same: Arteriosclerosis, Atherosclerosis, and Arteriolosclerosis.
Arteriosclerosis is a general umbrella term describing diseases where the wall of the artery becomes thicker, harder, and less elastic than normal.
You can figure that out right from the name: “arterio” which is Greek for artery, and sclerosis which is Greek for “hardening”.
Now the word arteriolosclerosis is any sort of hardening of small arteries in arterioles.
This is also pretty easy to remember since the “olo” in the middle of the word indicates small arterioles.
And then finally, atherosclerosis is the hardening of any artery (even though it’s usually medium- to large-sized arteries) which is caused by the buildup of plaque.
These plaques are called atheromatous plaques and happen in the innermost wall of the blood vessel called the tunica intima or endothelium. Okay now that we’ve differentiated been all three of those words, let’s first take a look at atherosclerosis.
So the blood vessel endothelium is made up of a single layer of cells and does two jobs: First,it protects the rest of the blood vessel wall from the blood, like a coat of varnish on your wood furniture and then, secondly, it secretes proteins on its surface to prevent the blood from clotting, because blood just inherently likes to clot whenever it gets the chance.
Now, Your endothelium can become damaged in lots of different ways. Low density lipoproteins, chemicals from smoking cigarettes, and high blood pressure all wreak havoc on the endothelium because these irritants break down the endothelium.
The damaged endothelium allow low-density lipoproteins to enter the endothelial wall.
The white blood cells called monocyte follow the low-density lipoproteins and break them down through oxidation.
Okay, so you might think macrophages eating the embedded low-density lipoproteins is a good thing, but if there is a lot of low-density lipoprotein, then the macrophage will eat so much cholesterol that it can die. It basically eats itself to death.
After it dies, it deposits itself under the damaged endothelium. So now we have a dead macrophage filled with low density lipoprotein stuck in the damaged endothelium as well.
These dead macrophages are called foam cells and that’s because some guy a while back looked at these things in a microscope and thought they looked like foam on the beach, hence the name.
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