Arteriosclerosis by rockingdevang

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Blood Vessels

Arteriosclerosis is a general term also called hardening of the arteries is a chronic disease characterized by abnormal thickening and hardening of the walls of arteries, with a resulting loss of elasticity.
The major form of arteriosclerosis is atherosclerosis, in which plaques of fatty deposits, or atheromas, form on the inner walls of the arteries. Morphologic entities under arteriosclerosis includes: a) Senile Arteriosclerosis

b) Hypertensive Arteriosclerosis
c) Monckeberg’s Arteriosclerosis d) Atherosclerosis

a) Senile Arteriosclerosis Senile arteriosclerosis is the thickening of media and intima of the arteries seen due to aging. -Affect most of the arteries

-Induced by stress
-Intima and media are thickened due to increase in elastic and collagen tissue -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

b) Hypertensive Arteriosclerosis Progressive increase in muscle and elastic tissue of arterial walls, resulting from hypertension. -in longstanding hypertension, elastic tissue forms numerous concentric layers in the intima and there is replacement of muscle by collagen fibres and thickening of the intima of arterioles. -It is of three type: -Hyaline Arteriosclerosis -Hyperplastic Arteriosclerosis -Necrotising Arteriosclerosis

Hyaline Arteriosclerosis
-Common arteriolar lesion that may be seen due to aging -Visceral arterioles are involved -Thickening of vascular walls with narrowed or obligated lamina

-Lesion result most probably from leakage of components of plasma across the vascular endothelium
-Permeability of vessel wall is increased due to heamodynamic stress in hypertension and metabolic stress in diabetes



Hyperplastic Arteriosclerosis
-characteristic lesion of malignant hypertension -Morphologic changes affect mainly the intima, especially of the interlobular arteries in the kidney -Severe intimal sclerosis results in narrowed or obliterated lumen -Probable pathology: changes result following endothelial injury from systemic hypertension, hypoxia or immunological damage



Nacrotising Arteriosclerosis In case of severe hypertension and malignant hypertension, parts of small arterioles show necrosis, or necrosis may be superimposed on hyaline sclerosis. Pathological changes: fibrinoid necrosis of vessel wall, acute inflammatory infiltrate of neutrophils in the adventitia (outermost connective tissue covering of any organ, vessel, or other structure ) Pathogenesis: direct physical injury to the vessel wall due to sudden and greater elevation of pressure



c) Monckeberg’s Arteriosclerosis -Monckeberg’s arteriosclerosis is calcification of the media of large and medium sized muscular arteries -involving the peripheral arteries, especially of the legs of older people, with deposition of calcium in the medial coat (pipestem arteries) but with little or no encroachment on the lumen. -occurs as an age related degenerative process -Pathological changes: deposition of calcium salts in the media produces pipestem like rigid tubes

d) Atherosclerosis
Atherosclerosis is patchy intimal plaques (atheromas) in medium and large arteries; the plaques contain lipids, inflammatory cells, smooth muscle cells, and connective tissue.

-can affect all large and mediumsized arteries, including the coronary, carotid, and cerebral arteries, the aorta, its branches, and major arteries of the extremities.

Risk Factors in Atherosclerosis:

I. Major risk factor a) Constitutional (non modifiable): Age Sex Genetic factor Familial and racial factor b) Acquired (controllable) Hyperlipidemia Hypertension Diabetes mellitus Smoking

II. Minor risk factor Environmental influences Obesity Hormones Physical inactivity Stressful life Infections

Pathogenesis of atherosclerosis:
- not caused by a single etiologic factor but is a multifactorial disease

Major components of plaque

• Cells (SMC, macrophages and other WBC) • ECM (collagen, elastin, and PGs) • Lipid = Cholesterol (Intra/extracellular) • (Often calcification)

Two theories of pathogenesis:

Response to injury Hypothesis

Monoclonal Hypothesis

Response to injury hypothesis

– * Injury to the endothelium – * Chronic imflammatory response – * Migration of SMC from media to intima – * Proliferation of SMC in intima – Excess production of ECM – Enhanced lipid accumulation

Normal Artery

Response to Injury

Endothelial Dysfunction

Initiation of Fatty Streak

Fatty Streak

Fibro-fatty Atheroma

Response to injury hypothesis
1. Chronic EC injury – EC dysfunction – Increased permeability – Leukocyte adhesion

2. 3. 4. 5. 6.

Accumulation of LDL (cholesterol) Oxidation of lesional LDL Adhesion & migration of blood monocytes; transformation into macrophages and foam cells Adhesion of platelets Release of factors from platelets, macrophages and ECs

7. 8. 9. 10.

Migration of SMC from media to intima Proliferation of SMC ECM production by SMC Enhanced lipid accumulation Intracellular (SMC and macrophages) Extracellular

Monoclonal Hypothesis
This hypothesis is based on the postulate that proliferation of smooth muscle cell is the primary event and that this proliferation is monoclonal in origin similar to cellular proliferation in neoplasm. This proliferation may be initiated by mutation caused by exogenous chemicals

endogenous metabolites
or viruses like herpesvirus

Consequences of Atherosclerosis

Altered Vessel Function


Vessel change – Plaque narrows lumen – Wall weakened – Thrombosis – Breaking loose of plaque – Loss of elasticity


Consequence – Ischemia, turbulence – Aneurysms, vessel rupture – Narrowing, ischemia, embolization – Athero-embolization – Increase systolic blood pressure

Late Changes
• • • Calcification – An example of dystrophic calcification Cracking, ulceration, rupture – Usually occurs at edge of plaque Thrombus formation – Caused by endothelial injury,ulceration, turbulence – Organization of thrombus – More thrombus Encroachment – Weakens vessel wall Bleeding – Ulceration, cracking and angiogenesis

• •

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