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Our goals for today

Our goals for today. Define diabetes and subtypes Distinguish between the etiology of the prevalent forms of diabetes Discuss basic features of gestational diabetes Understand the pharmacological management of diabetes. Strange but true……….

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Our goals for today

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  1. Our goals for today • Define diabetes and subtypes • Distinguish between the etiology of the prevalent forms of diabetes • Discuss basic features of gestational diabetes • Understand the pharmacological management of diabetes

  2. Strange but true……… • Greeks noticed that urine of diabetics attracted flies (linked this to increased sugar) • Chinese tested for diabetes by noticing whether ants were attracted to urine • Europeans tasted urine for sweetness

  3. Our eating habits have changed…..

  4. Soft Drinks…… • A 50 ml pop drink contains 10 teaspoons sugar • 360 ml can of pop contains 160 calories • (and same caffeine as in a cup of coffee) • Between 1985 and 1997: • Schools purchased 30% less milk and • 1,100% more soft drinks

  5. We exercise less…….

  6. Famous People & Diabetes

  7. Watch the units!

  8. Increased sugar in urine leads to loss of water—THIRST • Loss of sugar in urine=loss of calories—WEIGHT LOSS • Hunger • Dry mouth • Increased urination • Blurred vision • Frequent infections • Slow healing of cuts, bruises

  9. Type 1 Diabetes • Previously called “juvenile onset diabetes” or “insulin dependent diabetes” • Canadian connection (Charles Best, medical student partner in discovery of insulin)

  10. Insulin (1) Things to remember: • Glucose UNITS: multiply or divide by 18 (mg/dL is larger than mmol/L) • Normal pancreas secretes half of insulin as bolus after a meal. To replace this: need a short acting insulin Secretes other half gradually during day and night (basal secretion). To replace this: need long acting insulin

  11. Insulin (2) Insulin to cover meals: short or rapidly acting insulin. NOVOLOG (insulin aspartate) HUMALOG (lispro) For later meal: intermediate acting insulin NPH (neutral protamine of Hagedorn) For basal insulin: long acting insulin INSULIN GLARGINE (Lantus) ULTRALENTE

  12. Time-effect relationship for different types of insulin following subcutaneous injection.

  13. Extent and duration of various types of insulin Figure 41-2 from Katzung, 8th edition, 2001 HYPOGLYCEMIA is the most prominent adverse effect of insulin.

  14. Type 2 Diabetes • Previously called “adult onset diabetes” or “maturity onset diabetes” or “non-insulin dependent diabetes”

  15. Evolutionary Pathway ?

  16. Pancreatic alpha and beta cell dysfunction in T2DM

  17. First thing to do…………. Lifestyle modifications: • Exercise (actually the mere attempt to exercise regularly—no weight loss—can be beneficial) • Diet(work with nutritionist)

  18. Pharmacological management(1) Oral medications initiated when 2-3 months of lifestyle modifications cannot maintain optimal plasma glucose * SULFONYLUREAS: First generation: tolbutamide Second generation: glyburide, glipizide *BIGUANIDES: Metformin used as monotherapy

  19. Pharmacological management(2) • ALPHA-GLUCOSIDASE INHIBITORS: (Acarbose) inbibits pancreatic alpha-glycosidase hydrolase enzymes in intestine. • THIAZOLIDINEDIONES (Rosiglatone, Pioglitazone)—adjunct to exercise and diet or as monotherapy (PPAR activators—nuclear peroxisome proliferator-activated receptors)

  20. PAPR activators • Activation of genes that mediate a variety of characteristic actions of insulin • PAPR receptors: regulate storage and catabolism of dietary fats. • PAPRγ highly expressed in adipose tissue: leads to induction of adipocyte genes—e.g. lipoprotein lipase and fatty acid transporter 1…………improves insulin action in muscle and liver.

  21. DPP-4 inhibitors (Januvia®)Canada: Approved for one a day use in 2007 • DPP found in all major organs—esp kidney, liver (also capillary surfaces, circulation (soluble form) • No weight gain or hypoglycemia

  22. Complications of diabetes.. • MACROVASCULAR: coronary artery disease, peripheral vascular disease, cerebrovascular disease • MICROVASCULAR: leading cause of blindness, kidney failure and amputations

  23. Gestational Diabetes

  24. Definition : “any degree of glucose intolerance with onset or first recognized during pregnancy”. IncludesPatients that may previously have undiagnosed diabetes, or may develop diabetes coincidentally with diabetes.Occurs in 5-10% of all pregnancies

  25. Risk Factors • Previous diagnosis of GDM or impaired glucose tolerance • Glycosurea, history of glucose intolerance • Family history (first relative with type 2 DM) • Maternal age (>35yr) • Ethnicity • Overweight/obese: BMI> 30kg/m2 (increases risk 2-8X) • Previous high birth weight child (>4000g)

  26. Mechanisms • Largely unknown. Main feature is insulin resistance. • Pregnancy hormones may modify binding of insulin to IR…plasma glucose levels rise and insulin release is increased (feedback). • Insulin resistance: secures glucose supply to fetus? • Normal pregnancy: nearly doubled insulin release

  27. Mediators • Prolactin? Estradiol? • Fat (Obesity) • Immune system? • Gene Mutations • Placental cytokines(TNF-α, resistin, leptin) increase IR • Placental hormones ( cortisol, progesterone, human placental growth hormone) increase IR. • Human chorionic somatomammotropin increases throughout pregnancy and increases maternal insulin release

  28. Complications • Most women with GDM don’t remain diabetic after birth of child • Risk to baby: Growth abnormalities and chemical imbalances (admit to ICU?). Maternal hyperglycemia during week 6-7 of pregnancy: embryo toxicity (CNS, MSK, CV, spontaneous abortion). Hypoglycemia at birth. Jaundice. Increased RBC. Poorly developed lungs (respiratory distress). Later develop diabetes (~50% chance) • Risk for mother: Hypertension, UTI and type 2 diabetes (50% chance). Cesarean sections. Increased risk for developing GDM in later pregnancies.

  29. Treatment (1) Non-pharmacological: Cornerstone treatment • Medical nutritional therapy (MNT) –caloric and nutritional support for pregnancy but maintain target blood glucose without excess weight loss/gain (frequent, smaller meals, foods with low glycemic index etc) • 30 min daily exercise ( insulin sensitivity, weight loss) • If exercise and diet (2 weeks) does not help, use drug treatment

  30. Treatment (2) Pharmacologic • Insulin: during excessive fetal growth or when maternal glucose levels are not maintained. Use human insulin (least immunogenic)—INJECT—need oral medication. Increase dosage in 3rd trimester • Glyburide: minimal placental transfer. Not approved for GDM • Metformin: crosses placenta. Many women still need insulin. Not approved for GDM

  31. Take Away Messages………. Diabetes is a progressive disease: high rates of morbidity and mortality. Most diabetics die of cardiovascular complications. Treatment of diabetes is a partnership: patient, physician, home support, nutritionist….others. Insulin types and use (type 1 and type 2 diabetes). Oral hypoglycemics (type 2 diabetes). Gestational diabetes—risks for baby and also for mother.

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