Essay on atherosclerotic plates
The development of atherosclerotic plates begins during breastfeeding. Initial deposits are fatty stretch marks formed by lipids, smooth and macrophage muscle cells containing lipids. These lesions appear and disappear in the early stages of life. Later, intimate alterations consist of fibrous plates that contain lipids. Conjunctive tissue, smooth muscle cells, cholesterol crystals and calcium deposits. These plates do not disappear (although some recent data indicate that they can return) and can remain stable or progress towards the formation of intimate hemorrhages and intimate calcification.
There are several theories about the pathogenesis of the development of atherosclerotic plaque. All try to identify the factors responsible for the proliferation of smooth muscle, conjunctive tissue formation, lipid deposit and foam cell accumulation. The current pathogenesis theory of atherosclerosis is called the hypothesis of the response to the lesion. States that atherosclerosis lesions begin in response to some form of arterial endothelium injury. Endothelial cell lesion increases arterial wall permeability to plasma components, including lipids. Platelets and monocytes are attracted to the damaged area. As these cells adhere to places of injury, they penetrate the intimate layer of the artery and begin a series of physical and biochemical alterations. Monocytes are transformed into macrophages, which in turn accumulate lipids and become foamy cells. Platelets and monocytes release several growth factors that stimulate the migration of smooth muscle cells from the average artery to the interior of the intimate. Smooth muscle cells proliferate and synthesize collagen and proteoglycans, two components of the extracellular matrix that contribute to the increase in atherome size.
Tobacco is involved in atherosclerosis theories in several ways. The theory of the lesion is reinforced by the fact that the act of smoking produces hypoxia of the wall of the vessels and a myintimal thickening caused by the lesion. The transient hypertension that occurs when this process is smoked. The hypoxia of the vessel wall increases the permeability of the wall to the lipoproteins and facilitates the deposit of the plate. Tobacco indirectly influences arterial occlusive disease, decreasing the synthesis of prostaciclin, a natural inhibitor of platelet aggregation, which increases the tendency to formation of clots in the already stenned arterial lights.
Once the plate formation has begun, it can be extended to the mean, which produces ulceration and hemorrhage. The roughness of the surface facilitates the new platelet tank and causes a thrombus. In addition, plate growth results in progressive blood flow obstruction. The magnitude of narrowing (stenosis) that produces the decrease in flow is called critical stenosis. The stenned arteries are also less elastic because of the calcium deposit. The combination of stenosis and loss of elasticity translates into an inability of the arterial system to respond to the highest demand for hystic perfusion. The final result is the ischemia of the tissues irrigated by the affected arteries.
Chronic arterial occlusions (which are developed over time) give rise to the development of collateral circulation, which consists of an increase in the size of the smallest vessels in order to reach sufficient amount of blood to the tissues affected by the stenosis. Collateral circulation may or may not be adequate to maintain tissue viability. On the contrary, acute (or abrupt) arterial occlusion does not allow the development of collateral circulation and tissue ischemia is more pronounced and more dangerous for its viability.
The areas where arteriosclerotic plates are developed are the main arterial bifurcations. It seems that turbulence and perpendicular tensions that occur in these locations can facilitate the formation of plates. In addition to the main bifurcations, other frequently affected areas are the aorta and the superficial femoral artery in the Hunter channel.
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