1 03 of live births are type 1 type 2 is unknown but

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Unformatted text preview: produced ketosis ketoacidosis diabetic ketoacidosis (DKA) • lowered pH Insulin dekiciency Glucose dekicient tissue Body thinks starving Burn Fatty Acids Make Ketones Blood pH increases Hyperapnea Brain uses ketones Stupor Coma Overview of Type 2 • 85- 90% of DM – most common type • disease of ageing and obesity o more common in older adults, but happens in all age groups o more common with overweight and obesity • insulin resistance • insulin insufficiency (beta cell dysfunction) Natural History of Type 2 • genetic predisposition – certain ethnic groups – Ojibwe Cree, Pima Indians • large environmental influence o lifestyle factors – nutrition and physical activity • cells become resistant to insulin • hyperinsulinemia results • pancreatic exhaustion and loss of insulin secretion Insulin Resistance • something decreases effectiveness of intracellular signal that tells the GLUT4 transporters to be inserted into the plasma membrane • problem with signalling inside cell Type%2%Diabetes%E.ology % Insulin Insulin Insulin Normal Glucose and Insulin levels Insulin Insulin resistance Hyperinsulinemia PREDIABETES Impaired Glucose Tolerance Type 2 Diabetes Impaired Fasting Glucose Worsening Beta-cell dysfunction Progression to Type 2 Diabetes overtime Why does insulin resistance happen? • theories – high blood lipid levels and markers of inflammation o obesity o high fat diet o low fruit and vegetable diet o high fructose diet o high glycemic index or glycemic load diets o low physical activity levels • metabolically active fat tissue (visceral fat tissue) more blood lipids circulating increased levels of lipids in the blood seem to interfere with signalling inside cell • inflammation – markers of lowgrade inflammation are higher than those in a person without diabetes • both blood lipid levels and inflammation seems to interfere with signalling inside the cell Insulin Sensitivity • in normal individuals – decreased insulin sensitivity compensated by increased insulin release hyperinsulinemia (may never get diabetes) • can be insulin insensitive, but as long as beta cells produce insulin, will have normal function Why does Beta Cell Dysfunction Happen? • genetic o 45- 96% of monozygotic twins • high insulin production o beta cells may “wear out” o too much insulin may be damaging to beta cells • glucotoxicity o increased glucose levels may damage beta cells • lipotoxicity o high lipid levels could be toxic to beta cells • inflammation o inflammatory markers might damage beta cells Type 2 Signs and Symptoms • may have no signs and symptoms (silent) • may have classic symptoms similar to those in type 1 DM • mild fatigue • mild or no weight loss • mild ketosis, usually no DKA o ketosis is not extreme like in type 1 Diabetes in Pregnancy • gestational DM o 2- 3% of pregnancies o high blood glucose levels develop during pregnancy develops during pregnancy and goes away after • pre- existing DM o 0.1- 0.3% of live births are type 1, type 2 is unknown but increasing o glucose control more difficult during pregnancy • for both, poor blood glucose control could lead to poor maternal and infant outcomes Gestational Diabetes • risk factors: o obesity o older age o history of macrosomia (large birth weigh...
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This document was uploaded on 03/03/2014.

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