Porth's Essentials of Pathophysiology, 4e
964
Nervous System
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the cause of neovascularization is uncertain, research links the process with a vascular endothelial growth fac- tor (VEGF) produced by the lining of blood vessels. 25–27 Hypoxia is a key regulator of VEGF-induced retinal neovascularization. It is likely that other growth factors and signaling systems are also involved. Opacities represent a loss of retinal transparency due to hemorrhages, exudates, cotton-wool spots, edema, and tissue proliferation. The development of exudates often results in the destruction of the underlying retinal pigment and choroid layer. Cotton-wool patches are ret- inal opacities with hazy, irregular outlines. They occur in the nerve fiber layer of the retina and are associated with retinal trauma, severe anemia, papilledema, and diabetic retinopathy. Diabetic Retinopathy. Diabetic retinopathy is one of the leading causes of blindness in the Western world, particularly among individuals of working age. 6,25–28 Chronic hyperglycemia, hypertension, hypercholesteremia, and smoking are all risk factors for the development and progression of the disorder. People with type 1 (insulin-dependent) diabetes do not usually
develop the disorder until at least 3 to 5 years after the onset of the disease, whereas those with type 2 diabetes may have retinopathy as a presenting symptom at the time of diagnosis. 25 Diabetic retinopathy can be divided into two types: nonproliferative (or background) and proliferative. 6,25 Nonproliferative retinopathy is confined to the retina. It involves engorgement of the retinal veins, thickening of the capillary endothelial basement membrane, and development of capillarymicroaneurysms (Fig. 38-8A,B). Small intraretinal hemorrhages may develop and microinfarcts may cause cotton-wool spots and leakage of exudates. The most common cause of decreased vision in persons with background retinopathy is macular edema. The edema is caused primarily by the breakdown of the blood-retina barrier at the level of the capillary endothelium, allowing leakage of fluid and plasma constituents into the surrounding retina. Proliferative diabetic retinopathy represents a more severe retinal change than background retinopathy (Fig. 38-8C,D). It is characterized by formation of new fragile blood vessels (i.e., neovascularization) at the optic disk and elsewhere in the retina, which is often the
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FIGURE 38-8. (A) Nonproliferative (background) retinopathy showing microaneurysms. (B) Ocular fundus of a patient with background diabetic retinopathy. Several yellowish “hard” exudates (which are rich in lipids) and several relatively small retinal hemorrhages are present. (C) Proliferative retinopathy. (D) Ocular fundus in a patient with proliferative retinopathy. A vascular frond (branching pattern of preretinal neovascularization) has extended anterior to the retina. (B and D from Klintworth GK.The eye. In: Rubin R, Strayer DS, eds. Rubin’s Pathology: Clinicopathologic Foundations of Medicine. 6th ed. Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams &Wilkins; 2012:1403.)
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