182. Diabetes mellitus type I and II : definition, etiology, macro- and microscopic changes in the pancreas, blood vessels, kidneys, liver.

Diabetes mellitus is a disease caused by relative or absolute insulin deficiency.

Etiological and pathogenetic factors (risk factors) of diabetes mellitus:

– genetically determined decrease in the number of β-cells and functional disorders: decreased insulin synthesis, impaired conversion of proinsulin to insulin, synthesis of abnormal insulin;

– environmental factors that violate the integrity and function of beta cells: viruses, autoimmune reactions;

– nutrition that leads to obesity;

– increased activity of the adrenergic nervous system.

Macro- and microscopic changes:

The pancreas is often reduced, its lipomatosis and sclerosis occur. Most islets are prone to atrophy and hyalinosis, some islets are compensatorily hypertrophied. However, sometimes the gland looks unchanged, and only special methods of histochemical and electron microscopic studies detect degranulation of β-cells.

The liver is usually slightly enlarged, glycogen in hepatocytes is not detected, and obesity of liver cells is noted.

The vascular bed changes due to its reaction to latent and obvious metabolic disorders and to immune complexes circulating in the blood. Diabetic macro- and microangiopathy develops. Diabetic macroangiopathy is manifested by atherosclerosis of elastic and muscular-elastic arteries. Changes in diabetic microangiopathy are plasmorrhagic damage to the basement membrane of the microcirculatory bed with a friendly reaction of the endothelium and perithelium, culminating in sclerosis and hyalinosis, while lipogyalin, characteristic of diabetes, appears. Sometimes pronounced proliferation of the endothelium and perithelium is combined with lymphohistiocytic infiltration of the microvascular wall — vasculitis.

The most pronounced and specific morphological manifestations of diabetic microangiopathy in the kidneys are diabetic glomerulonephritis and glomerulosclerosis. They are based on the proliferation of mesangial cells in response to the clogging of the mesangium with "ballast" metabolic products and immune complexes, and their increased formation of a membrane-like substance. In the final, hyalinosis mesangia and glomerular death develop. Diabetic glomerulosclerosis can be diffuse, nodular, or mixed. It has a definite clinical expression in the form of Kimmelsteel–Wilson syndrome, manifested by high proteinuria, edema, and hypertension.

Possible exudative manifestations of diabetic nephropathy are the formation of "fibrin caps" on the capillary loops of the glomeruli and a "capsule drop". These glomerular changes are complemented by a peculiar change in the epithelium of the narrow segment of the nephron, where glucose polymerization into glycogen occurs — glycogen infiltration of the epithelium. The epithelium becomes high, with a light translucent cytoplasm, in which glycogen is detected by special staining methods.