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A 75-year-old woman is brought to the emergency department because of sudden loss of the upper half of vision in her left eye that lasted 2 minutes. The episode occurred 5 hours ago and is not associated with pain or loss of consciousness. Medical history is significant for hypertension and hyperlipidemia. Fundoscopic examination of the left eye shows Hollenhorst plaques, lodged in a retinal artery with restored distal blood flow. Visual acuity testing shows 20/20 vision in both eyes and there are no visual field deficits by confrontation. Which of the following is the most appropriate next step in management?
Content Reviewers:Rishi Desai, MD, MPH
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.
Also, when the macrophage dies, it releases cytokines, which calls over more monocytes which come over and eat low-density lipoprotein, inevitably dying while doing so, and thus this vicious cycle of gross overeating and massive fatalities has begun.
As more and more of these foam cells build up, they form a lesion we call a fatty-streak.
Now the fatty streak is thrombogenic meaning that blood can clot on it.
Now normally smooth muscle cells are supposed to stay within the middle layer of the blood vessel, the tunica media.
The release of platelet-derived growth factor draws the media smooth muscle cells to the tunica intima where they multiply.
The growing smooth muscle secretes collagen, proteoglycans, and elastin fibrous cells that help form a wall around the fatty streak, preventing blood clotting.We call this extracellular matrix wall a fibrous cap, and together both the fatty streak and the surrounding fibrous cap is called plaque.
The presence of fatty streaks cause the underlying smooth muscle in the blood vessel wall to also start depositing calcium into the plaque, creating crystals.
Normally calcium is deposited into the vessel wall by low-density-lipoproteins and is then removed by high-density lipoproteins.
The accumulation of plaque in the vessel messes up the ability of high-density lipoproteins to remove calcium from the vessel, so a buildup of calcium occurs in the vessel wall and it crystallizes.
Now remember calcium makes stuff hard, which is why your bones are full of calcium, right? So this deposit of calcium into the plaque is what stiffens the walls of the arteries.
Now remember the word that describes the immune system getting involved with something is called inflammation, so atherosclerosis is an inflammatory disease.
Now as another aside, the protein called C-reactive protein increases in the blood during an infection or when inflammation is occurring somewhere in the body.
While an elevated C-reactive protein isn’t specific enough to diagnose atherosclerosis, it can act as a red flag that atherosclerosis might be occurring, especially if someone has atherosclerosis symptoms or other risk factors.
From time-to-time that fibrous cap can crack and expose the underlying thrombogenic foam cells to blood.
And, this can happen randomly, and when it does, within moments you can see a blood clot start form within the already partially occluded artery, quickly leading to even less blood being able to flow by.
After about 70% of a blood vessel is occluded from the plaque and the new overlying blood clot, cell injury and death begin in the areas that were relying on the blood flow.
Seriously occluded internal carotid and middle cerebral arteries lead to strokes and cerebral atrophy, an occluded superior mesenteric artery affects the small intestine, and an occluded popliteal artery can cause peripheral vascular ischemia, like gangrene or claudication, which is frequent leg cramping during exercise.
But the complications of atherosclerosis don’t stop there! If we move on to the kidneys, plaque build up in the renal arteries reduces blood flow to the kidney, and tricks the kidney into thinking blood pressure is low.
Occasionally, some of the plaque can also break off from the main plaque deposit and become an embolism, floating around in the blood stream until it gets stuck in a smaller blood vessel or another artery with significant atherosclerotic plaque build up.
And you can totally see this in a tissue biopsy, as the affected blood vessel will have cholesterol clefts, these big white entities in the middle of the blood vessel.
So, moral of the story, atherosclerosis isn’t great. There are a few things you can do to prevent it though.
- "The pathogenesis of atherosclerosis: a perspective for the 1990s" Nature (1993)
- "Atherosclerosis — An Inflammatory Disease" New England Journal of Medicine (1999)
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "What Are the Signs and Symptoms of Atherosclerosis? - NHLBI, NIH" NHLBI, NIH (22 June 2016)
- "Atherosclerosis" Harvard Health Publications Harvard Health Publications (2011)