Must have exogenous insulin type ii diabetes results

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Unformatted text preview: endence. Must have exogenous insulin. Type II Diabetes---results from a decrease in beta cell weight or number or insulin resistance. Insulin receptors in target tissues become insensitive or resistant to insulin. May be controlled with diet and exercise or oral agents. Gestational Diabetes---disorder of glucose intolerance of variable severity with onset during pregnancy. Etiology Etiology Type I Diabetes---occurs as a result of genetic, environmental, ---occurs or immunological factors that damage the pancreatic beta cells. May be autoimmune. Absolute insulin deficiency caused by b-cell failure. May effect any age group. Prone to developing ketoacidosis. developing -Genetic susceptibility -Genetic Type II Diabetes---etiology is unknown but obesity is the ---etiology single most important risk factor. Decrease tissue sensitivity and responsiveness. Prone to developing nonketotic hyperglycemic hyperosmolar coma. hyperglycemic -Genetic predisposition -Genetic Risk Factors Type I Risk Generally in younger, thinner, “acute” onset. Generally “acute” 20% of type 1 develop DM after age 30. Variants with more latent onset- years. Environmental influence Heredity Risk Factors for Type 2 Risk Obesity (% body fat) Family history/ currently thought to occur in genetically Family predisposed individuals who are exposed to a series of environmental influences that precipitate the onset of clinical disease. History gestational diabetes, hypertension, dyslipidemia, high triglycerides. high Sex (female), age, and ethnic background are important Sex factors in determining risk for the development of type 2 diabetes. diabetes. Sedentary life style. Pathophysiology---Type I Pathophysiology---Type Caused by selective T lymphocyte–mediated autoimmune destruction of the B cells of the pancreatic islets. Insulin deficiency caused by pancreatic B cell failure. Damage to the beta cells leads to uncontrolled glucose production by the liver resulting in hyperglycemia. Glucose spills into the urine causing osmotic diuresis which leads to excessive amounts of urine(polyuria). Loss of fluids leads to excessive thirst (polydipsia). Due to the lack of insulin, the body is unable to use carbs so uses proteins and fats for energy leading to weight loss. Fat metabolism produces ketone bodies leading to acidosis. Breakdown of nutritional stores leads to excessive hunger (polyphagia). DKA---severe metabolic, fluid, and electrolyte disturbances. Pathogenesis of Insulin Resistance Resistance Tissue resistance to insulin with high insulin Tissue secretion is at the root of disorder. secretion 2. Insulin targets many cell types and triggers Insulin intracellular cascades linked to cell growth, lipid dysregulation, cytokine production. lipid 3. Common concurrent disorders: 1. • Vascular effects: hypertension, atherosclerosis • High triglyceride, low HDL (total cholesterol and LDL High are not good indicators of CV risk in this group) are • Increased BMI, abdominal adiposity Pathophysiology---Type II Pathophysiology---Type Persons with Type 2 diabetes demonstrate three cardinal Persons abnormalities: abnormalities: 1) resistance to the action of insulin in peripheral tissues, particularly muscle and fat but also liver particularly 2) defective insulin secretion, particularly in response to a glucose stimulus glucose 3) increased glucose production by the liver Relative insulin deficiency caused by decreased tissue sensitivity and decreased r...
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This document was uploaded on 03/25/2014.

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