Diabetic Retinopathy, the Cause of New Blindness

The ocular- tear barrier restricts the passage of large-mouthed blood proteins and various smaller molecules out of the capillary lumen. In addition to the endothelial cell layer, retinene capillaries also mystify a surrounding cell layer composed of pericytes imbed in the basement membrane. The ratio of pericytes to endothelial cells is approximately 1:2 (Mandarino, 1992, p. 1892). Pericytes whitethorn be involved in contractility. In addition, various evidence suggests that the cells also control endothelial proliferation. Together, the devil cell types may coordinate "the maintenance of retinal capillary structure and function (Mandarino, 1992, p. 1893)."

In diabetic retinopathy, the retinal capillaries permit both morphologic and functional alteration. Perhaps the earliest pathophysiologic swap involves the loss of pericytes. Subsequent to this loss, the basement membrane thickens and a crack-up in capillary integrity occurs. These changes eventually lead to a dysfunctional ocular-blood barrier and increased permeability (Mames, 1994, p. 241). Such morbid phenomena are thought to response from chronic metabolic injury. root cellar membrane thickening may be caused by nonenzymatic glycosylation and increased cross-linking of extracellular matrix proteins. Further abnormalities may include increased platelet aggregability, decreased red cell de nisusability, and bony blood flow. The retina responds to progressive ischemia by growing ne

Parnes, R. E., & Singerman, L. J. (1994, April). Diabetic retinopathy. Preserving your patient's sight. Journal of the Florida Medical Association, 81, 236-239.

The lifelike progression of diabetic retinopathy involves five fundamental pathologic processes. It begins with the physical composition of retinal capillary microaneurysms. Excessive vascular permeability hence results in leakage and retinal edema. Thirdly, vascular occlusion may occur (Davis, 1992, p. 1843). Increasing ischemia then can result in blood vessel proliferation. These capillaries, and their accompanying fibrous tissue, draw to accumulate on the retina surface. Should these proliferations contract, retinal detachment may prove (Mames, 1994, p. 240).

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Existing endothelial cells migrate and proliferate to form new vascular lumens (Mames, 1994, p. 241). Such neovascularization may impair retinal function.

Retinopathy is essentially divided into two general subgroups: these include nonproliferative and proliferative diabetic retinopathy. Each of these individual subgroups comprises an array of pathological features. Terms much(prenominal) as "non-retinopathy" and "pre-proliferative retinopathy" may connote different levels of the two subgroups, respectively. Nonproliferative diabetic retinopathy typically involves the following: (1) various levels of microaneurysms; (2) lipid exudation; (3) bleed; (4) venous changes; and (5) microinfarcts, or "cotton wool spots (Mames, 1994, p. 240)." In contrast, the more vision-threatening, proliferative retinopathy, consists of nonproliferative disease plus the growth of new blood vessels. "High risk characteristics" in proliferative disease may additionally include such things as "severe disc neovascularization alone, or moderate neovascularization and/or moderate neovascularization elsewhere accompanied by preretinal or vitreous hemorrhage (Parnes & Singerman, 1994, p. 237)."

Two therapeutic modalities apply against the disea
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