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Dot and blot hemorrhages diabetic retinopathy
Dot and blot hemorrhages diabetic retinopathy









PDRĬontinued ischemia stimulates retinal cells to release pro-angiogenic factors such as VEGF. Macular edema can occur in NPDR, but it is more common in more severe cases of DR where the increased vascular permeability is more advanced. Sediment left behind from this edema leads to waxy, yellow lipid byproducts referred to as hard exudates. The pathologic process involved in DME is the resultant fluid leaking into the retina and depositing under the macula. Inflammatory cytokines are significantly up-regulated in diabetes, and as a result, chronic inflammation and endothelial damage lead to increased vascular permeability of blood vessels.

dot and blot hemorrhages diabetic retinopathy

This obstruction can cause infarction of the nerve fiber layer, resulting in cotton-wool spots. The fundamental pathologic process involved in capillary occlusion is believed to be the result of an activated leukocyte adhering to and damaging the retinal capillary wall, which results in eventual capillary occlusion. Microaneurysms consequently rupture to form hemorrhages deep in the retina, appearing as "dots" on retinal examination, more commonly known as dot and blot hemorrhages. The resulting endothelial damage compromises capillary walls and results in microaneurysms. Hyperglycemia results in damage to retinal capillaries through the formation of advanced glycation endproducts (AGEs). However, the most common cause of vision loss in type II diabetes patients is DME. In patients with type I diabetes, PDR is the most prevalent vision-threatening condition. DME is characterized by thickening of the macula due to the accumulation of fluid within 500 µm of the center of the macula and it can occur at any stage of DR. The new abnormal vessels may bleed into the vitreous or cause a tractional retinal detachment, severely impairing vision. PDR represents a more advanced stage of DR characterized by the presence of neovascularization. Lesions vary from microaneurysms, dot and blot hemorrhages, hard exudates, and cotton wool spots to venous beading and intra-retinal microvascular abnormalities (IRMAs). Based on the severity of retinal vascular lesions, NPDR is categorized into mild, moderate, and severe forms. NPDR represents the early stage of DR, with increased vascular permeability and capillary occlusion being the two main observations in retinal vasculature. Mechanisms of Diabetic Retinopathy Subtypes This article provides detail on the mechanisms and pathological processes involved in DR.ĭR can be classified clinically into non-proliferative (NPDR) and proliferative (PDR) forms, according to the presence or absence of retinal neovascularization, and it can present with or without macular edema (DME). įor more information on the disease entity, etiology, risk factors, diagnosis, and management, see Diabetic Retinopathy. The propensity of developing DR is directly proportional to the age of the patient and duration of diabetes as well as with poor glycemic control and hypertension. ĭR is the most common microvascular complication in diabetic patients and the leading global cause of vision loss in working middle-aged adults.

  • 2.4 Vascular abnormalities and angiogenesis pathwaysĭiabetic retinopathy (DR) is a microvascular disorder caused by vision-threatening damage to the retina, a long-term sequela of diabetes mellitus.
  • 2.1.5 Poly(ADP-Ribose) Polymerase Activation.
  • dot and blot hemorrhages diabetic retinopathy

    2.1 Hyperglycemia and the regulation of metabolic pathways.1.1 Mechanisms of Diabetic Retinopathy Subtypes.











    Dot and blot hemorrhages diabetic retinopathy