Diabetes Mellitus: The Health Relevance Of Its Pathological Changes In Retinopathy And Renal Lesions
A General Overview
In diabetes Mellitus, the beta cells of the islets of Langerhands show reduction in number, degranulation and hyalinization. In recent onset IDDM lymphocytic infiltration of the islets occurs and this may be caused by viral inflammation or autoimmune processes. Round cell infiltration is seen particularly around the beta cells and not around the alpha cells which produce glucagon, delta cells which produce somatostatin and the “pp” cells which produce pancreatic polypeptides.
Vascular Changes: Diabetics show a predisposition to develop vascular lesions affecting the small and the large vessels. In microangiopathy, there is a specific involvement of the small blood vessels. The basement membrane is thickened. Ultimately, there is vascular occlusion. Microangiopathy is most marked in IDDM developing early in life. Various factors like endothelial damage, increased plasma viscosity, erythrocyte aggregation, reduced red cell deformity and increased platelet adhesion have been incriminated to lead to microangiopathy. The problem is more complex and the entire process is still not fully understood. Microangiopathy affects several organ systems and this manifests as dysfunction of many organs.
In macroangiopathy, the processes occurring in microangiopathy develop but in addition, there is smooth muscle proliferation, lipid accumulation and plaque formation. Apart from specific diabetic angiopathies, a diabetic is very prone to develop atherosclerosis much earlier than the non-diabetic. Both sexes are affected similarly in this process.
Diabetese mellitus produces a classical retinopathy. A specific change occurs in the vessels leading to loss of mural cell (pericytes) and the formation of microaneurysms. The occurrence of retinopathy is related to the duration and not the severity of the disease. Once initiated, the fundus changes are usually progressive. The early changed are venous dilatation and the appearance of small, dot-like microaneurysms in the perimacular area. Arterial blood is shunted and this leads to ischemia of the retina. Increased vascular permeability accounts for the formation of exudates. In the next stage dot and blot hemorrhages are produced along with hard yellow exudates. In a few cases, hemorrhages predominate. When large subhyaloid hemorrhages occur along the vein or vitreous vision is seriously impaired. Such hemorrhages are due to rupture of newly formed blood vessels. As these hemorrhages are absorbed, organizations by fibrous tissue occurs and multiple bands of retinitis proliferans develop. These lead to permanent visual impairment. The fibrous bands may contract giving rise to retinal detachment. Leaking vessels in the retina can be demonstrated by fluorescein angiography. Retinopathy is usually associated with advanced nephropathy. The changes occur in the renal glomeruli and blood vessels. Sometimes in diabetic ketoacidosis with severe hyperlipidemia, the fat gives a milky white appearance to the retinal arteries called “lipemia retinalis”.
These are invariably seen in subjects who have had diabetes for over 20 years. Vascular changes include
- Arterio-sclerosis of the renal artery,
- 2. Sclerosis of the arterioles, and
Glomerulosclerosis may be nodular (Kimmelsteil Wilson lesions) or diffuse. There is accumulation of a PAS positive eosinophilic material within the mesangium. There is thickening of the glomerular capillary basement membrane. The establishment of glomerulosclerosis is indicated by the presence of proteinuria. Further damage to the glomeruli results in the development of chronic renal failure.
The diabetic is predisposed to develop urinary infection and therefore acute and chronic pyelonephritis are very common. Fulminant urinary infection leads to ischemic necrosis of the renal papillae. This presents as acute anuric renal failure. Fleshy masses may be passed in urine. These represent the necrosed papillae.
© 2014 Funom Theophilus Makama