Diabetes Mellitus

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The islets of Langerhans are destroyed in type I diabetes mellitus. This occurs probably as a consequence of a genetic susceptibility, followed by the onset of autoimmune destruction triggered by some environmental factor such as a viral infection. Heavy lymphocytic infiltrates appear in and around islets. The number and size of islets are eventually reduced, leading to decreased insulin production and glucose intolerance.

The islets of Langerhans are normal in number or somewhat reduced with type II diabetes mellitus. Fibrosis and deposition of amylin polypeptide within islets are most characteristic of the chronic states of type II diabetes.

  1. Normal islets of Langerhans, with immunohistochemical stains (right, insulin and left, glucagon), microscopic.
  2. Islet of Langerhans, insulitis, microscopic.
  3. Islet of Langerhans, deposition of amyloid, microscopic.

Renal Complications

There are a variety of complications involving the kidney. Both nodular and diffuse glomerulosclerosis can lead to chronic renal failure. Diabetics are prone to infections, particularly pyelonephritis. Both bacterial and fungal infections can occur.

  1. Renal glomerulus, nodular glomerulosclerosis, microscopic.
  2. Renal glomerulus, nodular glomerulosclerosis, hyaline arteriolosclerosis, PAS stain, microscopic.
  3. Kidney, acute pyelonephritis, microscopic.
  4. Renal pelvis, infection with Candida albicans, PAS stain, microscopic.

Ocular Complications

The eyes can be affected in several ways by diabetes mellitus. Diabetic retinopathy is one of the leading causes for irreversible blindness in the United States. This retinopathy can occur with either type I or type II diabetes mellitus, usually a decade or so after the onset of diabetes. Most persons with type I diabetes and many of those with type II diabetes develop some background (non-proliferative ) retinopathy. Proliferative retinopathy is more ominous and is more likely to occur when diabetes mellitus is poorly controlled.

In severe retinopathy, neovascularization may lead to adhesions (synechiae) between iris and cornea or iris and lens. Neovascularization of the iris leads to secondary glaucoma with blindness.

Cataracts are more common in diabetics. This predilection for development of cataracts is felt to result from hyperglycemia leading to accumulation of sorbitol that results in osmotic damage to the crystalline lens.

  1. Normal appearance, retina on funduscopic examination.
  2. Diabetic retinopathy on funduscopic examination.
  3. Proliferative diabetic retinopathy on funduscopic examination.
  4. Glaucoma, cupping of the optic disk on funduscopic examination.
  5. Glaucoma with excavation of the optic cup, microscopic.
  6. Cataract of the crystalline lens, gross.


Persons with diabetes mellitus, either type I or type II, have early and accelerated atherosclerosis. The most serious complications of this are atherosclerotic heart disease, cerebrovascular disease, and renal disease. The most common cause of death with diabetes mellitus is myocardial infarction.

Peripheral vascular disease is a particular problem with diabetes mellitus and is made worse through the development of diabetic neuropathy, leading to propensity for injury.

  1. Left anterior descending coronary artery, advanced atherosclerosis, gross.
  2. Left anterior descending coronary artery, recent thrombus, microscopic.
  3. Interventricular septum, recent myocardial infarction, gross.
  4. Aortic atherosclerosis demonstrated in three aortas, gross.
  5. Foot with previous healed transmetatarsal amputation and recent ulcer, gross.
  6. Gangrenous necrosis and ulceration, lower extremity, gross.


This is a feared complication of diabetes mellitus. Diabetic ketoacidosis helps to potentiate the growth of Mucor. The site of involvement is typically the nasopharyngeal region, but the infection can spread to involve soft tissues and bone of the face, orbit, skull, and brain.

  1. Nasopharynx, mucormycosis (zygomycosis), H and E stain, microscopic.

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