ARTERIOSCLEROSIS

LEARNING OUTCOMES

• At the end of the lesson the learner should be able to: -

1. Define atheroma and atherosclerosis

2. Outline the causes of atheroma

3. Describe the risk and predisposing factors of atheroma

4. Describe the pathogenesis and pathology of atheroma

5. Outline the effects and complications of atheroma

Arteriosclerosis is a general term used to include all conditions with thickening and hardening of the
arterial walls.

Arteriosclerosis affects both arteries and arterioles.

 Arteriosclerosis differs from atherosclerosis in that there is no intimal lipid deposition with

 resultant inflammation.

 CAUSES

 It is due to gradual replacement of vascular smooth muscle cells by collagen and deposition of
plasma proteins in the smooth muscle to produce hyaline change.

 This process is accelerated by age, hypertension, and diabetes mellitus.

 Arteriosclerosis:

 Lowers the compliance of the arterial tree.

 Contributes to the age-related increase in systolic blood pressure and pulse pressures.

 Alters circulatory stability and tissue auto-regulation.

 The beneficial effect is decreased susceptibility of elderly and chronically hypertensive

 hypotension accounts for the increased mortality of shock in elderly and hypertensive patients.

CLASSIFICATION

• The following morphological entities are included under arteriosclerosis:

1. Senile arteriosclerosis.

2. Hypertensive arteriolosclerosis.

3. Mönckeberg’s arteriosclerosis (Medial calcific sclerosis).

4. Atherosclerosis.

1
 The last-named, atherosclerosis is the most common and most important form of arteriosclerosis.

If not specified, the two terms are used interchangeably with each other.

SENILE ARTERIOSCLEROSIS

 This is the thickening of media and intima of the arteries seen due to aging.

 The changes are non-selective and affect most of the arteries.

 These are possibly induced by stress and strain on vessel wall during life.

Pathologic Changes

1. Fibroelastosis - The intima and media are thickened due to increase in elastic and collagen
tissue.

2. Elastic reduplication - The internal elastic lamina is split or reduplicated so that two wavy layers
are seen. Eventually, the fibrotic changes result in age-related elevation of systolic blood
pressure.

HYPERTENSIVE ARTERIOLOSCLEROSIS

• Arteriolosclerosis is the term used to describe three morphologic forms of vascular disease
affecting arterioles and small muscular arteries. These are:

1. Hyaline arteriolosclerosis.

2. Hyperplastic arteriolosclerosis.

3. Necrotising arteriolitis.

All the three types are common in hypertension but may occur due to other causes as well.

Hyaline Arteriolosclerosis

 Hyaline sclerosis is a common arteriolar lesion that may be seen physiologically due to aging, or
may occur pathologically in hypertensives and in diabetics.

 The lesions are more severe in patients with hypertension, especially in the kidneys.

Pathologic Changes

 The visceral arterioles are particularly involved.

 The vascular walls are thickened and the lumina narrowed or even obliterated.

 Microscopically, the thickened vessel wall shows structureless, eosinophilic, hyaline material in
the intima and media.

Hyperplastic Arteriolosclerosis

 Hyperplastic changes are seen, particularly in the temporal artery of elderly patients.

1. Malignant hypertension – a characteristic lesion.

2
2. Haemolytic-uraemic syndrome.

3. Scleroderma.

4. Toxaemia of pregnancy.

Pathologic Changes

• The morphologic changes affect mainly the intima, especially of the interlobular arteries in the
kidneys. Three types of intimal thickening may occur:

1. Onion-skin lesion consists of loosely-placed concentric layers of hyperplastic intimal smooth

2. Mucinous intimal thickening is the deposition of amorphous ground substance.

3. Fibrous intimal thickening is less common and consists of bundles of collagen, elastic fibres and
hyaline deposits in the intima.

4. Severe intimal sclerosis results in narrowed or obliterated lumen.

5. With time, the lesions become more and more fibrotic.

Necrotising Arteriolitis

 In cases of severe and malignant hypertension, parts of small arteries and arterioles show
changes of hyaline sclerosis and parts of these show necrosis, or necrosis may be superimposed
on hyaline sclerosis.

 However, hyaline sclerosis may not be always present in the vessel wall.

Pathologic Changes

• Besides the changes of hyaline sclerosis, the changes of necrotising arteriolitis include:

 Fibrinoid necrosis of vessel wall.

 Acute inflammatory infiltrate of neutrophils in the adventitia.

 Oedema and haemorrhages often surround the affected vessels.

Pathogenesis

• Since necrotising arteriolitis occurs in vessels in which there is sudden and great elevation of
pressure, the changes are said to result from direct physical injury to the vessel wall.

MÖNCKEBERG’S ARTERIOSCLEROSIS (MEDIAL CALCIFIC SCLEROSIS

• This is calcification of the media of large and medium-sized muscular arteries, especially of the
extremities and of the genital tract.

3
• The condition occurs as an age-related degenerative process, and therefore, an example of
dystrophic calcification, commonly seen in the elderly individuals and has little or no clinical
significance.

• However, medial calcification also occurs in some pathological states like pseudoxanthoma
elasticum and in idiopathic arterial calcification of infancy.

Pathologic Changes

 Medial calcification is often an incidental finding in X-rays of the affected sites.

 The deposition of calcium salts in the media produces pipestem-like rigid tubes without
causing narrowing of the lumen
 Microscopically, Mönckeberg’s arteriosclerosis is characterised by deposits of calcium salts in
the media without associated inflammatory reaction while the intima and adventitia are spared.

 Often, the coexistent changes of atherosclerosis are present altering the histologic appearance.

Pathogenesis

 It is common and occurs independently of atherosclerosis.

 It is more frequent in people aged > 50 years and in people with diabetes.

 In advanced cases, vessels may become rigid and lose their distensibility.

 Extensive calcification occurs within atherosclerotic plaques.