Diabetes Mellitus

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Pathophysiology of Type I IDDM and Type II NIDDM
Type I Insulin dependent Diabetes Mellitus (IDDM) and Type II Non-Insulin dependent Diabetes Mellitus (NIDDM) are two separate pathophysiological features that separate them from one another.
Type I Insulin dependent Diabetes Mellitus (IDDM) "results from immune-mediated destruction of the insulin-producing beta cells of the pancreas" (Kantárová, 2007, p. 1). Individuals that are genetically susceptible to IDDM produce autoantibodies that becomes triggered after a viral infection affects the body. The autoantibodies targets and destroys the pancreas ' insulin-producing beta cells which results in a decline in secretion of insulin and insulin deficiency.
Type II Non-insulin dependent Diabetes
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Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS)
Diabetic ketoacidosis (DKA) is an acute, life threatening condition where blood glucose levels exceed 300 mg/dL resulting in the breakdown of body fat for energy, which leads to accumulation of ketones in the blood and urine. Onset of DKA is rapid with a mortality rate of less than 5%. DKA is associated with undiagnosed or untreated Type I DM. The most common cause of DKA with an individual with Type I DM is any factors that increase carbohydrate metabolism and an increased in need of insulin such as: infection, trauma, surgery, illness, physical or emotional stressors.
Hyperosmolar hyperglycemic state (HHS) is an acute life threatening condition where blood glucose exceeds 600 mg/dL. HHS is associated with Type II DM. Older adult who has residual insulin secretion which is enough to prevent the production of ketone bodies in the blood, but not enough to prevent excess blood glucose.

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