Chronically high levels of glucose and free fatty acids Beta cell (in islet of langerhans) desensitization Insulin

resistance Increased beta cell secretion of insulin In time however, the insulin declines because of increasing beta cell dysfunction Impaired ability of the body to metabolize glucose Chronic elevation blood glucose level Tendency of kidney to excrete excess blood glucose Osmotic diuresis DM TYPE 2 Cortisol secretion due to decreased glucose utilization Glucocorticoid hormones stimulate gluconeogenesis glycoprotein cell wall deposits Production of excess glucagon Production of glucose from protein and fat stores Excess loss of fluid Wasting of lean body mass

Increased glucose level in blood (ideal for bacterial growth)

Decreased erythropoietin production (in nephropathy)

Altered balance between cell destruction and regeneration Disruption of normal blood composition Decreased erythrocyte number volume Decreased circulating leukocytes Impaired immune function Opportunistic Bacteria enter into the lower airway Activation of inflammatory reaction Release of cytokines WBC, mostly neutrophils, migrate into the site of infection Dead bacteria and macrophages or phagocytes form exudates exudates fill the normally air-filled spaces consolidation of the lobe PNEUMONIA Decreased production of thrombopoeitin Impaired coagulation

Increased intracellular concentration of glucose Increased formation of glycoproteins in the basement membrane of small blood vessels and capillaries Structural defects in basement membrane and microcirculation Vascular complication

Small vessel disease

Diabetic neuropathy

formation of abnormal blood sugar glycoproteins damage on the glomeruli NEPHROSCLEROSIS decrease GFR

Diabetic retinopathy

alteration in regulatory process Stressed kidney filtration mechanism

activation of renin-angiotensinaldosterone system Renin will be secreted by the kidney alteration in regulatory process angiotensin I production of the adrenal cortex Increased pressure of blood vessels conversion in the lungs by ACE I Angiotensin II Increase in Na and H2O retention RENAL HYPERTENSION
+

Blood protein leak in into the urine Thickening in the renal arteries Diabetic nephropathy Progression of irreversible renal damage Retention of uremic waste products CHRONIC RENAL DISEASE Impaired excretion of metabolic wastes

decreased erythropoietin production decreased red blood cell production ANEMIA

Accumulation of substances into the bloodstream

Medication

Drug Induced Hypoglycemia