Pathophysiology of Type 1 Diabetes

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Clinical onset generally acute, but T-cell mediated selective destruction of beta cells would have been progressive for many years prior to diagnosis – preclinical stage may be up to 5 – 7 years. The circulating islet cell antibodies can be detected in this preclinical stage even though they are still normoglycaemic (remaining beta-cells can produce enough insulin)

Hypothetical stages:
1. Genetic susceptibility
2. Triggering of immune response by environmental agent
3. Autoimmunity develops – antibodies detectable include ICA (islet cell antibodies), IAA (insulin autoantibodies) and anti-GAD.
4. Pre-diabetes (loose first phase insulin response)
5. Clinical diabetes
6. Remission (honeymoon phase)
7. Relapse – need insulin for survival

Pathological features of the pre-diagnosis pancreas are typically:
infiltration of the islets by mononuclear cells – macrophages, T lymphocytes, natural killer cells and B lymphocytes  indicative of inflammation (insulitis)
patchiness of lesion – areas are unaffected
beta cells are specifically attacked (other hormone secreting cells unaffected)

As insulin is deficient  increase in gluconeogenesis, lipolysis and ketogenesis  ketoacidosis (do not get ketoacidosis in type 2)

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