Q. Pathophysiology of Chronic wasting disease?
We all know that heart attack i.e. myocardial infarction is not the beginning but a last stage representing acute clinical manifestation of CHD. Several clinical trials and autopsy studies have indicated that the process of developing atherosclerotic lesions can begin as early as during infancy and that it may take several decades for the lesions to develop into fatty streaks and fibrous plaques that ultimately cause stenos is.(Complete blockage) of the arteries. Diffuse intima thickening during infancy which is considered to be a normal physiological and not a pathological process can result in the initialization of early clinical manifestations which may appear in the smooth muscle cell layer between the endothelium and the internal elastic lamina. These lesions may progress and develop into fatty streaks to reach their maximum extent in the aortas over a period of two decades among individuals having elevated cholesterol and/or triglyceride levels. There is also focal proliferation of smooth muscle cells which are termed as gelatinous lesions because they have a low lipid but high water content. Some f these lesions may become large and develop a grayish opaque center which remaining soft and translucent around the edges. These are referred to as the transitional lesions. These lesions at times develop a fibrous cap with atheromatous lipids in the center and are known as fibrous plaques. Such fibrous plaques may coalesce together resulting in blockage of the arteries and hence reduced flow of blood to the tissues. The irritating presence of plaques may cause injury to the intima of the arteries which may result in thrombosis. Myocardial infarction/cerebral stroke is the ultimate result of stenos is in the arteries.