Overview
The Shared Injury Pattern
Persistent hyperglycaemia damages the smallest vessels that nourish the retina, the glomeruli and the peripheral nerves.
NCLEX-RN
NCLEX-RN
Persistent hyperglycaemia damages the smallest vessels that nourish the retina, the glomeruli and the peripheral nerves. Endothelial dysfunction, capillary basement-membrane thickening, inflammation and impaired blood flow leave these tissues vulnerable to leakage, ischaemia and progressive cell injury. The mechanism is the same in all three organs; what differs is what the tissue does when its blood supply fails, and therefore what the patient notices. The clinical consequences differ by organ: - In the retina, leaking and occluded capillaries cause retinopathy, macular oedema, ischaemia and abnormal new-vessel growth. - In the peripheral and autonomic nerves, metabolic injury and reduced microvascular perfusion impair sensory fibres, producing pain, numbness and loss of protective sensation, and impair the nerves that regulate blood pressure, the gut and the bladder. - In the kidneys, glomerular injury permits albumin to enter the urine before filtration necessarily declines. Glycaemic control matters, but it is not the only target. Elevated blood pressure accelerates capillary injury, and dyslipidaemia contributes to retinal and vascular disease. Effective prevention therefore combines glycaemic, blood-pressure, lipid, kidney and foot-risk management. The practical consequence for the...
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