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Type 1 Diabetes Mellitus
1. Type 1 diabetes is also called insulin-dependent diabetes.
2. It used to be called juvenile-onset diabetes, because it often begins in childhood.
3. This type accounts for 5-10 percent of people with diabetes.
4. The pathogenesis of Type 1 diabetes mellitus underlie as follows:
- Immunological activation: Type 1 diabetes is an autoimmune disorder is based on the presence, at the onset, of lymphocytic cells which infiltrate in and around the islets of the pancreas, as well as the occurrence of autoantibodies to islet-cell proteins ICA, IA-2, GAD (glutamic acid decarboxylase) and insulin autoantibodies.
- Progressive beta-cell destruction: The progressive destruction of the beta cells is rapidly progressive in children and slowly progressive in adults and result in Insufficient beta-cell function
- Genetic susceptibility: There is evidence that type 1 diabetes is a genetic disorder. Siblings of a person with type 1 diabetes are about 15 times more likely to develop diabetes than the general population. This translates into a risk of approximately 6% up to age 35 years. Interestingly, children in families with a mother with type 1 diabetes have a lower risk (~3%) than children in families with a father who has type 1 diabetes; the reasons for this are unknown.
- Environmental trigger: The epidemiological patterns of type 1 diabetes, including geographic, seasonal, and temporal variations in incidence suggest that viruses may be important risk factors. Viruses are thought to act as initiators, accelerators or precipitators of the disease. These may attack and destroy the beta cells of the pancreas and directly cause diabetes. While multiple viruses appear to be associated with type 1 diabetes, most infected people never develop the disease. It is therefore unlikely that specific antiviral vaccines would significantly reduce the burden of type 1 diabetes in a community.
Pathophysiology of type 1 diabetes
1. In type 1 diabetes, there is severe to total insulin deficiency.
2. This results in the following:
- A decrease in glucose uptake by the muscle cells.
- The breakdown of muscle into amino acids – then taken up by the liver and converted into new glucose (gluconeogenesis).
- An increase in the breakdown of triglycerides, leading to an increase in the release of free fatty acids – also taken up by the liver and converted into a usable energy form, ketones.
- A reduction in the uptake of glucose by the liver and an increase in the breakdown of glycogen (glycogenolysis).
Risk Factors
- Being ill in early infancy
- Having a parent with type 1 diabetes (the risk is greater if a father has the condition)
- Having a mother who had preeclampsia during pregnancy
- Having other autoimmune disorders such as Grave's disease, Hashimoto's thyroiditis (a form of hypothyroidism), Addison's disease, multiple sclerosis (MS), or pernicious anemia
Signs and Symptoms
| Polyuria
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| Polydipsia
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| Polyphagia
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| Weight loss
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| Weakness
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| Dry skin
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| Ketoacidosis
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| Blurred vision
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