Pathophysiology of diabetes

Retinopathy. Microaneurysm formation is the earliest manifestation of diabetic retinopathy. Microaneurysms may form due to the release of vasoproliferative factors, weakness in the capillary wall, or increased intra-luminal pressures. Microaneurysms can cause vascular permeability in the macula, which can lead to macular edema that threatens central vision. Obliteration of retinal capillaries can lead to intraretinal microvascular abnormalities. As capillary closure becomes extensive, intraretinal hemorrhages develop.
Proliferative retinopathy develops due to ischemia and release of vasoactive substances, such as vascular endothelial growth factor, which stimulate new blood vessel formation as a progression of nonproliferative retinopathy. These vessels may erupt through the surface of the retina and grow on the posterior surface of the vitreous humor. These vessels are very friable and can lead to vitreous hemorrhages. The vitreous humor can contract and lead to retinal detachment.
Nephropathy. Two pathophysiologic pathways for diabetic nephropathy have been identified. First, diabetic nephropathy can result from increased glomerular capillary flow that, in turn, results in increased extracellular matrix production and endothelial damage. This leads to increased glomerular permeability to macromolecules. Mesangial expansion and interstitial sclerosis can ensue, which have the potential to cause glomerular sclerosis. A second pathway termed nonalbuminuric renal impairment is due to macrovascular and/or repeated unresolved episodes of acute kidney injury. Reduced glomerular filtration rate (GFR) and albuminuria are risk factors for cardiovascular events whereas albuminuria predicted death and progression to end-stage renal disease better than GFR loss.
Neuropathy. The pathophysiology of neuropathy is complex. Diabetes is associated with dyslipidemia, hyperglycemia, and low insulin and growth factor abnormalities. These abnormalities are associated with glycation of blood vessels and nerves. In addition, autoimmunity may affect nerve structure. Trauma and nerve entrapment can lead to structural nerve damage including segmental demyelination, axonal atrophy and loss, and progressive demyelination. These effects cause neuropathy.
Macrovascular. The macrovascular complications of diabetes result from hyperglycemia, excess free fatty acid, and insulin resistance. These cause increased oxidative stress, protein kinase activation, and activation of the receptor for advanced glycation end products, factors that act on the endothelium.

  • First decreased nitric oxide, increased endothelin, and increased angiotensin II cause vasoconstriction that results in hypertension and vascular smooth muscle cell growth.
  • Second, decreased nitric oxide, activated nuclear factor-KB, increased angiotensin II, and activation of activated protein-1 increase inflammation, which results in the release of chemokines, cytokines, and expression of cellular adhesion molecules.
  • Third decreased nitric oxide, increased tissue factor, increased plasminogen activator inhibitor-1, and decreased prostacyclin result in thrombosis, hypercoagulation, platelet activation, and decreased fibrinolysis.

  • Insulin-Pancreatic hormone
  • Gluconeogenesis
  • Insulin Receptors
  • Glucose and Glucagon
  • Insulin Resistance
  • Metabolic Acidosis
  • Translocation of glucose

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