3.

Arteriosclerosis & Atherosclerosis

1.

A: Arteriosclerosis is the hardening of blood vessels with thickening and loss of elasticity of vessel walls.
The three types of arteriosclerosis are:

 Mönckeberg arteriosclerosis (medial calcific sclerosis)

 Arteriolosclerosis
 Atherosclerosis
c

2.

A: Mönckeberg arteriosclerosis (medial calcific sclerosis): form of arteriosclerosis involving dystrophic

calcification of the media of small- to medium-sized muscular arteries, typically the radial and ulnar
arteries.
c

3.

A: Mönckeberg arteriosclerosis is benign and does not obstruct arterial flow since the intima is not
involved.
c

4.

A: Mönckeberg arteriosclerosis is classically described to have a "pipestem" appearance on X-ray.

c

5.
A: Arteriolosclerosis is a form of arteriosclerosis affecting the small arteries and arterioles, associated
with hypertension and diabetes mellitus.
c

6.

A: Hyaline arteriolosclerosis is seen in chronic hypertension and/or diabetes mellitus. The renal
vasculature is especially prone.
c

7.

A: Hyperplastic arteriolosclerosis is seen in malignant hypertension. It appears as concentric,

hyperplastic “onion skinning” of the walls of small arteries and arterioles, associated with fibrinoid
deposition and vessel wall necrosis.
c

8.

A: Atherosclerosis: endothelial cell damage/dysfunction of muscular and elastic arteries, characterized by

a fibrous cap and an atheromatous core within the tunica intima.
c

9.

A: Vessels commonly affected by atherosclerosis, in order of decreasing frequency:

1. Abdominal aorta
Rationale: no vasa vasorum below the renal arteries (L2 vertebral level) ∴ the infrarenal abdominal
aortic wall is more susceptible to ischemic damage than the thoracic aorta)
2. Coronary arteries
3. Popliteal artery
4. Carotid artery
 c

10.

A: The risk factors for developing atherosclerosis include:

Modifiable Non-modifiable

 Smoking  Increased age

 Hypertension  Sex (more common in men &
 Hyperlipidemia postmenopausal women)
 Diabetes  Family history
c

11.

A: The pathogenesis of atherosclerosis involves:

1. Fatty streak*: endothelial cell damage/dysfunction → LDL entry into intima → macrophages
recruited and phagocytose the oxidized LDL → foam cell (lipid laden-macrophages) formation
2. Plaque progression: smooth muscle cell migration to tunica intima due to PDGF → altered matrix
synthesis and degradation
3. Plaque disruption: hemodynamic stress and degradation of extracellular matrix → fibrous plaque
rupture → thrombus formation

*Link to fatty streak image

c

12.

A: Histopathologic features:
 Necrotic central core: cholesterol, cholesterol esters, foam cells (lipid laden-
macrophages), and debris

 Fibrous cap (plaque): covers the central lipid core and is made of a dense collagen-rich extracellular
matrix with occasional smooth muscle cells, macrophages and T cells
c

13.

A: Complications of atherosclerosis are due to emboli and infarction and include: MIS-PA
 Myocardial infarction, angina

 Stroke
 Ischemic bowel disease
 Abdominal aneurysm (recall: no vasa vasorum below the renal arteries)
 Peripheral vascular disease
c