A 58-year-old man with a 15-year history of poorly controlled type 2 diabetes mellitus presents for a routine eye examination. He denies eye pain but reports gradually worsening vision over the past year. Funduscopic examination reveals microaneurysms, dot-and-blot hemorrhages, and hard exudates. No neovascularization is seen.
Which of the following is the most likely pathophysiologic mechanism responsible for this patient’s retinal findings?
The correct answer is:
A) Breakdown of the blood-retinal barrier due to pericyte loss
This patient’s findings are consistent with non-proliferative diabetic retinopathy, characterized by microaneurysms, dot-and-blot hemorrhages, and hard exudates without neovascularization. Chronic hyperglycemia leads to pericyte loss and basement membrane thickening in retinal capillaries, resulting in increased vascular permeability and breakdown of the blood-retinal barrier.
Answer choice B: Immune-mediated destruction of retinal ganglion cells, is incorrect. This mechanism is characteristic of glaucoma, which presents with optic nerve cupping and progressive peripheral vision loss rather than retinal hemorrhages and exudates.
Answer choice C: Ischemic necrosis of the optic nerve head, is incorrect. Ischemic optic neuropathy presents with sudden vision loss and optic disc swelling, not the gradual retinal changes seen here.
Answer choice D: Neovascularization driven by vascular endothelial growth factor, is incorrect. Vascular endothelial growth factor (VEGF)-mediated neovascularization occurs in proliferative diabetic retinopathy, which is defined by the presence of new, fragile blood vessels. No neovascularization is described in this patient.
Answer choice E: Obstruction of venous outflow from the retina, is incorrect. Central retinal vein occlusion causes widespread retinal hemorrhages and dilated tortuous veins, not microaneurysms and hard exudates.
Key Learning Point
Non-proliferative diabetic retinopathy results from pericyte loss and breakdown of the blood-retinal barrier, leading to microaneurysms, hemorrhages, and hard exudates without neovascularization.
