Pathophysiology of Diabetic retinopathy
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Diabetic retinopathy is caused by pathological changes to the retina due to hyperglycemia. The breakdown of the blood-retinal barrier leads to vascular permeability and leakage. This results in retinal edema, hemorrhages, and exudates. Over time, there is loss of pericytes and endothelial cells, capillary nonperfusion, and upregulation of growth factors like VEGF. Eventually, this causes the development of proliferative retinopathy characterized by neovascularization and fibrovascular proliferation. The pathological effects of hyperglycemia are mediated through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and increased oxidative stress - all of which disrupt the normal vascular physiology in
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& function of
various intra
&extracellular
proteins
Reducing
sugars
Amino groups
of proteins,
lipids & NA
Schiff base
Amadori
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AGEs
VEGF
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- 1. PATHOPHYSIOLOGY OF DIABETIC RETINOPATHY Dr. NIKHIL GOTMARE @ eyeamnikhil
- 4. - BRB compartmentalises the neurosensory retina from the vascular component of the eye. Inner BRB is formed by tight junctions between the retinal vascular endothelial cells and glial cells . Outer BRB by tight junctions between RPE ( zonula occludens
- 5. - The pericytes are wrapped around the capillaries and are thought to be responsible for the structural integrity of the vessel wall.
- 8. Hard exudate (Circinate pattern) Degeneration and loss of pericytes Plasma leakage Capillary wall weakening microaneurysm Retinal edema outpouching of capillaries at structurally weak points
- 9. microaneurysm Intraretinal hemmorhage Dot blot hage Flame shaped hage rupture (outer plexiform and inner nuclear) (nerve fiber layer)
- 10. Pericyte loss Endothelial loss Changes in tight junctions AGELeukostasis Breakdown of blood retinal barrier Inflow of fluid > outflow EDEMA - Development of retinal edema requires accumulation of fluid which occurs if : Leakage : Absorption : - Microanurerysms. - Incompetent capillaries - Uptake from adjusent capillaries - Healthy RPE cells
- 11. Increased plasma viscosity Deformation of RBC Increased platelets stickiness Decreased capillary blood flow and perfusion Endothelial cell damage and proliferationCapillary basement membrane thickening Retinal hypoxia VEGF Proliferative retinopathy Neovascularization and fibrovascular proliferation Rubeosis iridis A-V shunt IRMA* *intraretinal microvascular abnormalities
- 12. New vessel proliferationFibrous glial tissue proliferaion Tractional RD RD IRMA
- 16. Glucose Sorbitol Fructose NADPH NADP NAD NADH Damaging effects on pericytes & endothelial cells Aldose reductase Sorbitol dehydrogenas e
- 17. Alters structure & function of various intra &extracellular proteins Reducing sugars Amino groups of proteins, lipids & NA Schiff base Amadori product [eg: HbA1c] AGEs VEGF Endothelins Leukostasis
- 19. VEGF Phosphorylation of tight junction & cytoskeletal proteins Fenestraion in endothelial cell membranes Breakdown of BRB + bFGF, Angiotensin II, IGF New vessel formation Neovascularisati on
- 22. Cross linking, Fragmentation, oxidation of proteins, lipids, nucleic acids Cellular dysfunction, Leukostasis, vascular permeability Enzymatic reactions Electron transport Oxidases Auto-oxidation in hyperglycemia scavengers Reactive oxygen species
- 23. Disruption of nitric oxide regulation VEGF PKC vascular permeability Leukostasis Vasoconstriction blood flow
- 26. HYPERGLYCEMIA PKC ROS AGEs SORBITOL VEGF LEUKOSTASIS PERICYTE & ENDOTHELIAL CELL LOSS Breakdown of BRB RAAS Microaneurysms & BM thickening Neovascula risation
- 28. THANK YOU