Facts and Figures Currently affects 18.2 million people
5.2 million are undiagnosed
1.3 million new cases per year
At the current rate, 1 out of every 3 children born in the year 2010 will get DM in their lifetime
Classifications Type 1
Previously juvenile-onset DM• Most cases diagnosed before 30 years of
age Autoimmune
• Beta cell destruction with resulting absolute deficiency of insulin
~10% of DM cases• Symptoms: significant weight loss, polyuria,
polydipsia
Type 1 Risk in general population: 1:400 to
1:1000 Combination of genes for disease
susceptibility and disease resistance 40% of caucasians express the genes,
less than 1% develop type 1 DM 50% discordance rate between identical
twins
Type 1 A trigger is necessary for gene
expression Immunological attack on beta cells
and insulin Hyperglycemia and symptoms
develop after >90% destruction of the secretory capacity of the beta cell
Type 1 “Honeymoon Period”
Noninsulin dependancy Maintains normal glycemia Continued beta cell destruction Insulin required in 3-12 months
Type 2 diabetes 90% of DM cases
30-50% of childhood-onset diabetes 50% of men and 70% of women are obese at
diagnosis Insulin resistance Endogenous insulin may be normal,
increased,or decreased Frequently asymptomatic at diagnosis
Type 2 30% remain undiagnosed Microvascular complications exist in
~20% at time of diagnosis May be present 6.5 years at time of
diagnosis Pima Indians have a 50% prevalence
rate
Type 2 Specific defects
Beta cell dysfunction resulting in insulin deficiency
Insulin receptor abnormalities Postreceptor defects
• Insulin resistance
Type 2 50% reduction in beta cell mass
Abnormal beta cell recognition of glucose
Beta cells chronically exposed to hyperglycemia become less efficient in their response
Type 2 Insulin resistance BG is maintained by hepatic glucose
production when fasting Insulin suppresses hepatic glucose Type 2: decrease in sensitivity and
response Type 2: persistant hepatic glucose
production
DM Diagnosis Prediabetes
Fasting: 110-125 mg/dL Random: 140-199 mg/dL
Diabetes Fasting: >126 Random: >200
• Confirmed with a second lab test and/or symptoms
Gestational Diabetes Affects 2-14% of pregnancies Glucose intolerance that develops or
is first discovered during pregnancy Diagnostic classification changes
after pregnancy Increased future risk for type 2 DM
50%-80% within 1 decade
GDM Pregnancy is an insulin resistant
state Resistance is progressive and is related
to circulating hormones (human placental lactogen, prolactin, estrogen, and cortisol)
Parallel to fetal and placental growth
GDM Risk Factors
Marked obesity History of GDM Strong family history of DM Glycosuria Ethnic group of high prevalence
• Hispanic, African American, Mexican, Native American, South or East Asian, Pacific Islands
GDM Screening
High risk: as early as possible Average risk: 24-28 weeks gestation
Diagnosis 1 hour 50g load: >140, 3 hour OGTT is
scheduled 3 hour 100g load: 2 or more BG’s meet or
exceed, GDM is diagnosed• Values: Fasting-95 mg/dL, 1 hour-180 mg/dL, 2 hour-
155 mg/dL, 3 hour-140 mg/dL
GDM Fetal risks
First trimester: congenital malformations
Increased endocrine system workload Macrosomia (<9 pounds)
• Shoulder dystocia and traumatic birth Hyperglycemia at birth
DM Risk Factors Genetics Age (>45 years) Overweight/Obesity Physical Inactivity Ethnicity Prior GDM or babies over 9#
Blood Sugar Testing Varying times per day
1-7 times BG goals:
Fasting 80-120 Preprandial: <110 2 hours postprandial: <140
DM Management Dietary
Carbohydrate control• Individualized recommendations• No standardized menus• Total carbohydrates- NOT sugar• Use of alternative sweeteners• NO SUGARY DRINKS!!!!!!!!!!!!!!!
DM Management Exercise
Improved BG control with weight loss of 10%
30 minutes/day as many days as possible• Doesn’t have to be consecutive
DM Management Oral Medications
Sulfonylureas, Meglitinides, Biguanides, Thiazolidinediones (TZD’s), Alpha-Glucosidase Inhibitors, Amylin Agonists• Secretagogues, sensitizers, suppress
hepatic glucose production, delay glucose absorption
Insulin Rapid-acting to long-acting
Oral Medications Sulfonylureas
Glyburide, Glipizide (Glucotrol), Glimepiride (Amaryl)
Increase insulin release from the pancreas
Can cause hypoglycemia • BG < 70
Oral Medication Meglitinides
Repaglinide (Prandin) and Nateglinide (Starlix)
Increases insulin release but the effect is glucose-dependant and diminishes at low blood glucose concentrations
Can cause hypoglycemia
Oral Medications Biguanides
Metformin (Glucophage), Glucovance (Glyburide/Metformin), Metaglip (Glipizide/Metformin), Avandamet ( Metformin/ Rosiglitazone)
Reduce hepatic glucose production and decrease insulin resistance
Not a hypoglycemic agent
Oral Medications Thiazolidinediones (TZD’s)
Pioglitazone (Actos), Rosiglitazone (Avandia)
Decrease insulin resistance Not a hypoglycemic agent
Oral Medications Alpha-Glucosidase Inhibitors
Acarbose (Precose) and Miglitol (Glyset) Inhibit alpha-glucosidase enzymes in
the small intestine and pancreatic alpha-amylase • Reduces the rate of starch digestion and
subsequent glucose absorption
Injectable Medications Symlin and Byetta
Synthetic Amylin: hormone secreted by the pancreatic cells in response to hyperglycemia• Inhibits gastric emptying and suppresses
glucagon secretion• Adjunctive therapy
Insulin Basal vs. bolus Variation in peak time and duration Vial and syringe vs. insulin pens Pump therapy
Insulin guidelines Absorbed most readily in the
abdomen, followed by the arms, thighs, and buttocks
Best injected at room temperature Keep backups in the refrigerator
Vials last ~1 month at room temperature, pens last ~2 weeks
Carbohydrate Counting 1500 Rule
Weight in kilograms• Wt (kg) X 0.6 = TDD (total daily dose)
• .6 (Type 1) – 1.0 (Type 2)• 1500/ TDD= BG1 (How much 1 unit of insulin
drops the BG)• BG1 X .33 = How many grams of carbohydrate is
equal to 1 unit of insulin