Microvascular and Macrovascular Complications of Diabetes - Webnar - Article Example

In this article, the long term side effects of diabetes will be discussed. Any organ in the body can be damaged by diabetes. That is why it is very important to prevent diabetes and also keep it in control when contracted by this disease. In the long-term, diabetes leads to 3 main conditions, disease of the eyes (retinopathy), nerves (neuropathy), and kidneys (nephropathy). These effects are due to the damaging effect of hyperglycemia on the blood vessels in these tissues. Tissues like nerves, lenses, kidneys and blood vessels do not require insulin for transport of glucose.

Hence blood glucose can enter the cells without insulin. Hyperglycemia leads to increased intracellular glucose which is then metabolized by aldose reductase to sorbitol and then fructose. This process uses NADPH which gradually gets depleted resulting in oxidative stress in the cells. Thus damage to the organs occurs. In the retina, increased intracellular glucose stimulates the de novo synthesis of diacyl glycerol from glycolytic intermediates which further causes activation of protein kinase C.

Protein C causes revascularization in retina and diabetic retinopathy, increased depositon of extra cellular matrix, fibrinolysis and production of pro-inflammatory cytokines. Thus various tissues in the body are damaged as a result of blood hyperglycemia. Microvascular complications include diabetic retinopathy, diabetic nephropathy and diabetic neuropathy. . Osmotic stress secondary to accumulation of sorbitol is the main reasons for microvascular complications. Pathological studies in animal models have suggested that osmotic injury due to sorbitol can lead to thickening of the basement membranes, microaneurysms and loss of pericytes.

However, for some reason, aldose reductase inhibitors do not prevent this. Another important cause for cellular injury in hyperglcemia is oxidative stress. This is because, hyperglycemia can trigger production of free radicals and reactive oxygen species formation. Antioxidant therapy may help to some extent prevent vascular injury, but not the development or progression of microvascular complications. Growth factors like vascular endothelial growth factors have been proven to play an important role in diabetic retinopathy, especially in response to hypoxia.

The ocular manifestations of diabetes mellitus are numerous and include retinopathy, cataract, glaucoma, and neurophthalmic disorders. These associated conditions increase with age and duration of disease whether type-1 or type-2. It can be classified as background or proliferative. In background retinopathy, small hemorrhages are seen in the middle layers of retina. Whereas, in proliferative retinopathy, new blood vessels are formed on the surface of retina and that can lead to vitreous hemorrhage.

Diabetic nephropathy can lead to renal failure and is defined as proteinuria more than 500mg in 24 hours urine sample. Pathological changes include increased thickness of glomerular basement membrane, mesangial nodule formation, microaneurysm formation and other changes. ACE inhibitors may prolong the development of nephropathy. In diabetic neuropathy, peripheral nerve