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Pathophysiology
Process
In Type 2 there is interference with the body's utilization of available insulin. Insulin resistance is a decreased responsiveness to sufficient concentration of insulin. The primary causes of insulin resistance are considered genetics and weight gain. This first phase of resistance stimulates an increase in insulin production by ß-cells. ß-cells are unable to make enough insulin to meet the body's perceived need. As the insulin resistance continues hyperglycemia ensues. ß-cell failure due to "exhaustion" or "glucose toxicity" is believed to follow. Autoimmune destruction of ß-cells does not occur in individuals with Type 2. (3,18)
Although similar to the scenario of Type 1, Type 2 is not identical in its pathophysiologic process. The classic triad of polyuria, polydypsia and polyphagia may be present, but not as striking. Ketoacidosis is less likely, but possible. In Type 2, the presence of insulin prevents the lipogenesis that would lead to the production of ketones. Hyperglycemic Hyperosmolar Syndrome (HHS) is a life-threatening outcome of neglected hyperglycemia in Type 2s. Severe hyperglycemia and extreme dehydration characterize this condition. This outcome is unlikely but may be seen in older populations whose diabetes is not well managed (3,18)
Signs and Symptoms of Type 2 Diabetes
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