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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
Type I Diabetes---occurs as a result of genetic, environmental,
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
Type II Diabetes---etiology is unknown but obesity is the
single most important risk factor. Decrease tissue sensitivity
and responsiveness. Prone to developing nonketotic
hyperglycemic hyperosmolar coma.
-Genetic Risk Factors Type I
Generally in younger, thinner, “acute” onset.
20% of type 1 develop DM after age 30.
Variants with more latent onset- years.
Heredity Risk Factors for Type 2
Obesity (% body fat)
Family history/ currently thought to occur in genetically
predisposed individuals who are exposed to a series of
environmental influences that precipitate the onset of
History gestational diabetes, hypertension, dyslipidemia,
Sex (female), age, and ethnic background are important
factors in determining risk for the development of type 2
Sedentary life style. Pathophysiology---Type I
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
DKA---severe metabolic, fluid, and electrolyte disturbances. Pathogenesis of Insulin
Tissue resistance to insulin with high insulin
secretion is at the root of disorder.
2. Insulin targets many cell types and triggers
intracellular cascades linked to cell growth,
lipid dysregulation, cytokine production.
3. Common concurrent disorders:
1. • Vascular effects: hypertension, atherosclerosis
• High triglyceride, low HDL (total cholesterol and LDL
are not good indicators of CV risk in this group)
• Increased BMI, abdominal adiposity Pathophysiology---Type II
Persons with Type 2 diabetes demonstrate three cardinal
1) resistance to the action of insulin in peripheral tissues,
particularly muscle and fat but also liver
2) defective insulin secretion, particularly in response to a
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.
- Spring '14