Arterial disease

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Arterial disease

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Questions

USMLE® Step 1 style questions USMLE

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A 75-year-old man is brought to the emergency department due to sudden-onset confusion and headaches accompanied by nausea and vomiting. The patient has a history of poorly controlled hypertension and hyperlipidemia due to noncompliance with medications. The patient has smoked a pack of cigarettes daily for 40 years. The patient’s temperature is 37.0°C (98.6°F), pulse is 100/min, and blood pressure is 205/140 mmHg. On physical examination, the patient is dyspneic. Fundoscopic examination reveals bilateral papilledema. Laboratory results are obtained and shown below:  
 
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 
Which of the following histologic findings would likely be seen if this patient’s renal artery was biopsied?  

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Abdominal aorta p. 370

atherosclerosis in p. 305, 731

Aneurysms p. 529

atherosclerosis p. 305

Angina

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

Carotid artery

atherosclerosis in p. 305, 731

Cholesterol

atherosclerosis p. 305

Claudication

atherosclerosis p. 305

Coronary arteries

atherosclerosis in p. 305

Coronary artery

atherosclerosis in p. 731

Diabetes mellitus p. 350-358

atherosclerosis and p. 305

Emboli

atherosclerosis p. 305

Fibrous plaque in atherosclerosis p. 305

Foam cells

in atherosclerosis p. 305

Hyperlipidemia p. 307

atherosclerosis and p. 305

Hypertension p. 304

atherosclerosis and p. 305

Infarcts

atherosclerosis p. 305

Inflammation

in atherosclerosis p. 305

Ischemia p. 206, 685

atherosclerosis p. 305

Popliteal artery p. 458

atherosclerosis in p. 305, 731

Smoking

atherosclerosis and p. 305

Smooth muscle (vascular)

atherosclerosis and p. 305

Thrombi

atherosclerosis p. 305

Transcript

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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.

Sources

  1. "The pathogenesis of atherosclerosis: a perspective for the 1990s" Nature (1993)
  2. "Atherosclerosis — An Inflammatory Disease" New England Journal of Medicine (1999)
  3. "Robbins Basic Pathology" Elsevier (2017)
  4. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  5. "What Are the Signs and Symptoms of Atherosclerosis? - NHLBI, NIH" NHLBI, NIH (22 June 2016)
  6. "Atherosclerosis" Harvard Health Publications Harvard Health Publications (2011)
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