Diabetic retinopathy. A pathogenesis

 Small blood vessels – such as those in an eye – are especially vulnerable for the weak control of a glucose of blood. Glucose and-or fructose superaccumulation (Kawasaki and others 2004) damages tiny blood vessels in a retina. During the initial stage termed as not proliferative diabetic retinopathy (NPDR), the majority of people does not note changes in their vision.

 Some people develop a Condition termed as an edema of maculae. It meets, when the defective blood vessels pass a fluid and lipids (Adeps) on maculae, a part of a retina which allows us to see details. The fluid does a tumor of maculae which stains vision.

 As illness advances, the serious not proliferative diabetic retinopathy arrives in premature, or proliferative, a stage. Shortage of oxygen (ischemia) in the parents of a retina, fragile, new, blood vessels to grow along a retina and in clear, gelepodobnom a vitreous which fills an interior part of an eye. Without timely treatment these new blood vessels can bleed, blackout vision and to blast a retina. The Sosudisto-fibrous proliferation can cause tractive amotio of a retina also. Not proliferative diabetic retinopathy is found out as maculae cotton wool, or cappilary disorders or as the superficial retinal hemorrhages. Even in this case, the premature proliferative diabetic retinopathy (PDR) can remain asymptomatic during very long time and so should be checked close with the regular checkouts.