08-19-2018, 04:36 PM
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
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.
Mönckeberg arteriosclerosis is benign and does not obstruct arterial flow since the intima is not involved.
Mönckeberg arteriosclerosis is classically described to have a "pipestem" appearance on X-ray.
Arteriolosclerosis is a form of arteriosclerosis affecting the small arteries and arterioles, associated with hypertension and diabetes mellitus.
Hyaline arteriolosclerosis is seen in chronic hypertension and/or diabetes mellitus. The renal vasculature is especially prone.
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.
Atherosclerosis: endothelial cell damage/dysfunction of muscular and elastic arteries, characterized by a fibrous cap and an atheromatous core within the tunica intima.
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
The risk factors for developing atherosclerosis include:
Modifiable Non-modifiable
• Smoking
• Hypertension
• Hyperlipidemia
• Diabetes
• Increased age
• Sex (more common in men & postmenopausal women)
• Family history
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 forma
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
Complications of atherosclerosis are due to emboli and infarction and include:
• Myocardial infarction, angina
• Stroke
• Ischemic bowel disease
• Abdominal aneurysm (recall: no vasa vasorum below the renal arteries)
• Peripheral vascular disease