Patogenesis Aterosklerosis - The risk of progression of atherosclerosis in part genetically determined. Incidence and clinical consequences of atherosclerosis such as ischemic disease increases with age, especially after 40 years. Atherosclerosis is much more common in men than women, this difference is likely to occur due to the protective effects of estrogen, and progressively disappear after menopause. Important risk factor predisposing to atherosclerosis covers cigarettes, hypertension, diabetes, and high serum cholesterol.
The hypothesis regarding the pathogenesis of atherosclerosis, the most widely accepted is that atherosclerosis is initiated by injury or endothelial dysfunction. Cinderung plaque formed on areas that have a variety of stress-strain hemodynamic (eg in arterial branching or bifurcation). Endothelial particularly vulnerable to damage to the site, as evidenced by an increase in turnover (turnover) and endothelial cell permeability. Stimulate monocyte adhesion of endothelial dysfunction, white blood cells that accumulate in the bottom layer of endothelial manolayer, and become macrophages.
Macrophages normally play an important role during inflammation and is the body's response to injury and infection. Macrophages perform that role by working as a cell carrier (scavenger cells) to transport a dead cell or a foreign object, and also release cytokines and growth factors to stimulate healing. However, macrophages in the arterial wall can be abnormally activated, causing a type of inflammatory reaction is slow, resulting in harmful plaque and clinical information
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