## Primary Pathophysiology of Type 1 Diabetes **Key Point:** Type 1 Diabetes is fundamentally an **autoimmune disease** characterized by selective destruction of insulin-producing beta cells in the pancreatic islets of Langerhans. ### Mechanism of Beta Cell Destruction 1. **Autoimmune attack**: CD8+ T cells and B cells target beta cell antigens (GAD65, IA-2, insulin) 2. **Insulitis**: Inflammatory infiltration of islets leads to progressive beta cell loss 3. **Result**: Absolute insulin deficiency requiring lifelong insulin replacement ### Key Distinguishing Features | Feature | Type 1 | Type 2 | | --- | --- | --- | | **Primary defect** | Beta cell destruction (autoimmune) | Insulin resistance + relative insulin deficiency | | **Insulin levels** | Absent or very low | Initially normal/high, later declining | | **Onset** | Acute (days to weeks) | Insidious (years) | | **Ketosis risk** | High (prone to DKA) | Low (HHS more common) | | **C-peptide** | Low/absent | Normal or elevated | **High-Yield:** At diagnosis of Type 1 DM, approximately 80–90% of beta cell mass has already been destroyed. The remaining beta cells may produce residual insulin ("honeymoon phase") for weeks to months, but complete loss follows. **Clinical Pearl:** Presence of **diabetes-associated autoantibodies** (anti-GAD, anti-IA2, anti-insulin) confirms autoimmune beta cell destruction and distinguishes Type 1 from Type 2 DM. **Mnemonic: LADA** — **L**atent **A**utoimmune **D**iabetes in **A**dults. A slowly progressive form of Type 1 DM presenting in adults >30 years, often initially misdiagnosed as Type 2.
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