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Pathology - Type 2 Diabetes Mellitus
Type 2 DM is a state of inappropriate hyperglycemia and abnormal metabolism caused by a combination of insufficient insulin production and insulin insensitivity in peripheral tissues. Long-term complications of DM, owing to small and large artery disease, include renal failure, blindness, amputations, myocardial infarction, stroke, and peripheral neuropathy. Most people with type 2 DM are overweight or obese. Insulin insensitivity correlates with visceral obesity (notice big waist circumference in this patient) rather than subcutaneous obesity. Adipose tissue releases cytokines (“adipokines”) including tumor necrosis factor and resistin that cause tissue insulin resistance and beta cell loss. A normal blood glucose concentration is initially maintained due to increased insulin secretion, but as the disorder progresses more beta cells are destroyed and this compensatory response begins to fail. Skin discoloration (acanthosis nigricans) is an indication of insulin resistance. Presenting signs such as vulvovaginitis, impaired vision, and peripheral neuropathy are more prevalent presentations of type 2 than type 1 DM. Ketoacidosis seldom develops in type 2 DM because a little insulin response is enough to prevent glucagon from triggering excess hepatic ketone production. Dyslipidemia frequently coexists with hyperglycemia as a consequence of insufficient insulin action. Treatment includes weight loss and exercise, both of which lower insulin resistance. Oral medicines include metformin to decrease hepatic glucose synthesis, sulfonylureas to stimulate insulin secretion, and incretin mimetics to both increase insulin secretion and inhibit glucagon secretion. Subcutaneous insulin injections may also need to be provided as the condition worsens.
Type 2 DM is a state of inappropriate hyperglycemia and abnormal metabolism caused by a combination of insufficient insulin production and insulin insensitivity in peripheral tissues. Long-term complications of DM, owing to small and large artery disease, include renal failure, blindness, amputations, myocardial infarction, stroke, and peripheral neuropathy. Most people with type 2 DM are overweight or obese. Insulin insensitivity correlates with visceral obesity (notice big waist circumference in this patient) rather than subcutaneous obesity. Adipose tissue releases cytokines (“adipokines”) including tumor necrosis factor and resistin that cause tissue insulin resistance and beta cell loss. A normal blood glucose concentration is initially maintained due to increased insulin secretion, but as the disorder progresses more beta cells are destroyed and this compensatory response begins to fail. Skin discoloration (acanthosis nigricans) is an indication of insulin resistance. Presenting signs such as vulvovaginitis, impaired vision, and peripheral neuropathy are more prevalent presentations of type 2 than type 1 DM. Ketoacidosis seldom develops in type 2 DM because a little insulin response is enough to prevent glucagon from triggering excess hepatic ketone production. Dyslipidemia frequently coexists with hyperglycemia as a consequence of insufficient insulin action. Treatment includes weight loss and exercise, both of which lower insulin resistance. Oral medicines include metformin to decrease hepatic glucose synthesis, sulfonylureas to stimulate insulin secretion, and incretin mimetics to both increase insulin secretion and inhibit glucagon secretion. Subcutaneous insulin injections may also need to be provided as the condition worsens.
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