TYPE 2 DIABETES MELLITUS Cynthia Brown, MN, ANP, CDE.
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Transcript of TYPE 2 DIABETES MELLITUS Cynthia Brown, MN, ANP, CDE.
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TYPE 2 DIABETES MELLITUS
Cynthia Brown, MN, ANP, CDE
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Type 2 Diabetes Mellitus
Epidemiology: 25 million Americans or 8.3% 7 million undiagnosed 1.9 million older than 20 diagnosed in
2010 7th leading cause of death In 2007, cost of treating $174 billion 1.5 million >20 diagnosed per year
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Type 2 Diabetes Mellitus
Epidemiology: Leading cause of ESRD, blindness,
amputation, & impotence Heart disease & stroke 2-4 times more
common 90-95% of persons with diabetes have
Type 2
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Type 2 Diabetes Mellitus
Populations at risk: Those older than 30 Some children now diagnosed African Americans Native Americans Hispanics Asians Pacific Islanders
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Type 2 Diabetes Mellitus
Populations at risk: Family history in 1st or 2nd degree
relative Hx gestational diabetes or baby >9 lbs Signs of insulin resistance Hx pre-diabetes Hx vascular disease Physical inactivity
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Type 2 Diabetes Mellitus
Diagnosing: 1979: original WHO criteria-
FBS >140 2 hour >200
1997: ADA Type 1 Type 2 Eliminated all other references to age,
insulin usage
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Type 2 Diabetes Mellitus
Diagnosing: 1998: ADA
Lowered FBS to 126 Based on association between glucose
levels & development of retinopathy 2011: ADA accepted A1c >6.5% as
diagnostic; <6.5% does not exclude diagnosis
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Type 2 Diabetes Mellitus
Today’s testing methods: Fasting plasma glucose 1-2 hour post meal can be used; if
>140, further testing indicated FPG <100mg/dl=normal FPG >100 & <126 = IFG & pre-diabetes FPG >126=diabetes
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Type 2 Diabetes Mellitus
Oral glucose tolerance test still the gold standard 150 grams carb for 3 days prior 10-14 hour fast 75 gram glucose load No activity during test Do not perform in the ill, malnourished
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Type 2 Diabetes Mellitus
Impaired Glucose Tolerance (IGT) Impaired Fasting Glucose (IFG) Glucose higher than normal, but not
diagnostic of diabetes IGT: random or 2-hour glucose >140
but <200 IFG: FPG >100 but <126
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Type 2 Diabetes Mellitus
When to screen: Start at age 45; every 3 years if normal Start younger if overweight or risk
factors present Anytime fasting blood sugar not normal Easiest is a fingerstick Must note time of last food
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Type 2 Diabetes Mellitus
Metabolic Defects: Cellular resistance to effect of insulin Failing beta cells Loss of first phase response Decreased secretion of amylin Decreased secretion of incretins
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Type 2 Diabetes Mellitus
Each metabolic defect causes a different problem Cellular resistance causes high
circulating insulin levels Leads to fatigue and weight gain Low amylin-rapid emptying of stomach Low incretins-no sense of fullness Also problems with insulin secretion
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Type 2 Diabetes Mellitus
Chronic disease syndrome associated with insulin resistance: Metabolic Syndrome Dysmetabolic Syndrome Syndrome X
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Type 2 Diabetes Mellitus
Syndrome features: Central or visceral obesity Dyslipidemia Atherosclerosis Endothelial dysfunction Decreased fibrinolytic activity=pro-
thrombotic Hypertension Acanthosis
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Type 2 Diabetes Mellitus
Syndrome Features: PCOS Hyperuricemia Pre-diabetes
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Type 2 Diabetes Mellitus
Inherited defect in insulin action Abnormal insulin signaling Abnormal glucose transport Abnormal glycogen synthesis Abnormal mitochondrial oxidation
Hyperinsulinemia by downregulation of insulin receptor numbers & post-receptor events
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Type 2 Diabetes Mellitus
Enhanced lipolysis with elevation of free fatty acids aggravates insulin resistance
Impairs glucose uptake at muscle Enhances hepatic glucose
production Islet cell impaired in release of
insulin
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Type 2 Diabetes Mellitus
Impaired glucose tolerance & overt diabetes develop when beta cells fail
Cause of “pancreatic exhaustion” unknown
When FBS 115, first phase insulin secretion lost
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Type 2 Diabetes Mellitus
When FBS 180, all phases of insulin secretion markedly impaired.
Gastric emptying accelerated Post prandial hyperglycemia Defects in appetite control & satiety All treatments aimed at these
metabolic defects
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Type 2 Diabetes Mellitus
Insulin resistance: Start with insulin sensitizers-
Metformin (biguanide) Actos (TZD) Both re-sensitize person to own insulin Very different mechanisms Work at liver, muscle, islet cell
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Type 2 Diabetes Mellitus
Pancreatic stimulators: Glipizide, glyburide, glimepiride
(sulfonylureas) Prandin, Starlix (secretagogues) Rapid acting beta cell stimulators Interact with ATP-dependent potassium
channels of beta cells Glucose dependent action
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Type 2 Diabetes Mellitus
Januvia, Onglyza, Tradjenta (DPP-4 inhibitors) Slows inactivation of incretin hormones Concentrations of GLP-1 & GIP increase Enhances insulin release in glucose-
dependent manner Suppress hepatic glucose production Lowers post-meal glucose levels
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Type 2 Diabetes Mellitus
Byetta, Victoza (incretin mimetics) Glucoregulatory effects similar to
glucogon-like peptide-1 (GLP-1) Secreted by gut in response to food Very short half-life Restore first-phase insulin response Suppress post-meal glucagon Slows gastric emptying
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Type 2 Diabetes Mellitus
Precose, Glyset (alpha glucosidase inhibitors) Act locally in intestine Slows digestion of carbohydrates Delays absorption of glucose GI side effects
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Type 2 Diabetes Mellitus
Insulins: Basal: Lantus, Levemir, NPH Bolus: Humalog, Novolog, Apidra,
Regular Given in patterns to mimic mother
nature
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Type 2 Diabetes Mellitus
Thank you very much for your attention!
Questions?