Atherosclerosis pathology
The pathological changes of Atherosclerosis is involving the circulatory system large elastic artery (aorta) and medium-sized muscular artery elasticity, minimal involvement of pulmonary arterial circulation. Distribution of more than a number of disease tissues and organs involved at the same time, but sometimes can also be concentrated in a particular organ of the artery, while other arteries were normal. First multi-site lesions in the aortic wall and blood vessels, such as intercostal artery branch openings; and high blood pressure in these areas, wall to bear a greater impact of blood flow, which is also more obvious lesions.
Normal artery wall is composed of inner wall, middle membrane and outer membrane. Intima is composed of the monolayer of endothelial cells, connective tissue and the inner-hole stretch panels. Smooth muscle cells in childhood is extremely rare, with age the growth of endometrial stromal cells and smooth muscle components of the gradual build-up. Stretch in the muscle-type arteries, medial oblique, almost all from the smooth muscle cells and the number of uncertain collagen, elastic fibers and glycoproteins, such as around the smooth muscle cells, and its form generally does not change with age. Adventitia contains fibroblasts, in addition there are collagen, glycoprotein, and a mixture of smooth muscle cells. Between outer membrane and the membrane was also separated by a discontinuous outer layer of elastic plates. Occurrence of atherosclerosis, pathological changes is that lipid stripes appear in the artery wall, fiber plaque lesions and composite lesions.
1. lipid stripe disease: the disease early, commonly found in young people, limited to arterial intima, a few mm in size or length of the yellow fat of up to a few centimeters of fat yellow stripes. Characterized by intimal macrophages and smooth muscle cells showed a small number of focal accumulation of lipid and outside cells. Lipid composition of mainly cholesterol and cholesterol ester, and phospholipid and triglyceride, etc.; as a result of lipid stripes are flat or only slightly higher in the endometrial lesions, there is no involvement of the arterial obstruction so that does not cause clinical symptoms, its importance lies in its potential for the plaque.
2. fiber plaque lesions: for atherosclerosis of the most characteristic lesions, the general was light yellow, slightly bulge into the arteries and blood vessels surrounding the cavity or opening branches, causing luminal stenosis. Such lesions of intimal hyperplasia by connective tissue and smooth muscle cells containing lipid, composed of macrophages. Lipid is cholesterol and cholesterol esters, lipids from peripheral cells, collagen and elastic fibers and around glycoprotein. Desmoplastic lesions Department formed a fibrous membrane, covering a large number of lipid in the deep on top of sediments mixed with lipid cell debris and cholesterol crystallization. Patch size increases, the expansion of the membrane wall, the wall can damage muscle fibers and elastic fibers and replaced by new connective tissue and capillary proliferation. More lipid, its central base at the bottom of malnutrition due to degeneration and necrosis and collapse, the collapse of the formation of complexes with mixed-lipid atherosclerosis material is atherosclerotic plaque or aneurysm.
3. composite lesions: occurrence of fibrous plaque hemorrhage, necrosis, ulceration, calcification of the quarter will be the formation of mural thrombus. Intimal surface of atherosclerotic plaque can rupture and the formation of the so-called atherosclerotic ulcer; atherosclerosis after rupture the material into the blood to become emboli, can cause rupture Department bleeding ulcer surface roughness easily thrombosis, mural thrombosis and increase the lumen to the occlusion or stenosis. Gradually in the blood vessel occlusion, it also emerged from the vicinity of blood vessels and collateral circulation, thrombosis of machine and then be able to pass, so that the restoration of blood flow to part of. Composite membrane lesions are characterized by calcification. Artery involvement reduced flexibility, increased brittleness, easy to break down, gradually narrowing its lumen or total occlusion, but also the formation of aneurysm expansion.
Atherosclerosis can lead to systemic circulatory system or individual organ dysfunction:
1. Due to atherosclerosis, Aorta cause lower wall elasticity, when the heart contraction, it is part of a temporary expansion and retention of blood from the heart of the role that reduced systolic blood pressure to rise and widened pulse pressure. Aortic formed atherosclerotic aneurysms, the wall is replaced by fibrous tissue, not only the loss of tension and bulge outward. these are enough to affect the regulation of systemic blood flow, but also increase the burden on the heart.
2. Organs or limbs arterial stenosis or occlusion of the lumen, the right side of the cycle in the case can not be compensated, so that organs and tissues of blood supply of the obstacles, resulting in ischemia, fibrosis or necrosis. Such as coronary atherosclerosis can cause angina, myocardial infarction, or myocardial fibrosis; brain caused by atherosclerosis of brain atrophy; renal artery atherosclerosis caused by high blood pressure or kidney atrophy; lower limbs caused by atherosclerosis of lower limb intermittent claudication or gangrene.
3. Artery wall and the muscular layer of the elastic layer is damaged, so that the fragile wall, in the case of fluctuations in blood pressure is easy bleeding. Ruptured cerebral arteries often cause death.