Etiology and Pathophysiology
- Progressive destruction of pancreatic b cells
- Autoantibodies cause a reduction of 80% to 90% of normal b cell function before
manifestations occur
- Causes:
- Genetic predisposition
- Related to human leukocyte antigens (HLAs)
- Exposure to a virus
Combined genetic, immunologic, and possibly environmental (eg, toxins, viral)
factors are thought to contribute to beta cell destruction. There is also evidence of an autoimmune response in type 1 diabetes. This is an
abnormal response in which antibodies are directed against normal tissues of the
body, responding to these tissues as if they were foreign.Onset of Disease
- Manifestations develop when the pancreas can no longer produce insulin
- Rapid onset of symptoms
- Present at ER with ketoacidosis
Type 1 Diabetes Mellitus Onset of Disease
- Weight loss
- Polydipsia
- Polyuria
- Polyphagia
- Diabetic ketoacidosis (DKA)
- Occurs in the absence of exogenous insulin
- Life-threatening condition
- Results in metabolic acidosis
The destruction of the beta cells results in decreased insulin production,
unchecked glucose production by the liver, and fasting hyperglycemia.
In addition, glucose cannot be stored in the liver but instead remains in the
bloodstream and contributes to postprandial (after meals) hyperglycemia.