Type 2 Diabetes –

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Basic overview and explanation of Type II Diabetes

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Type 2 Diabetes –

  1. 1. TYPE 2 DIABETES – THE #1 PREVENTABLE CHRONIC DISEASE! Dorothy D. Zeviar 17 April 2009
  2. 2. WHAT IS TYPE 2 DIABETES? <ul><li>The inability of insulin to act to get glucose into the cells </li></ul><ul><ul><li>Sometimes called “insulin resistance” </li></ul></ul><ul><ul><li>Causes hyperglycemia – too much glucose in the bloodstream and not enough in the cell </li></ul></ul><ul><li>“ Lock and key mechanism” </li></ul>
  3. 3. WHAT HAPPENS IN TYPE 2 DIABETES? <ul><li>Cells require glucose (sugar) and oxygen to survive </li></ul><ul><ul><li>Cellular respiration </li></ul></ul><ul><ul><li>C 6 H 12 O 6 + 6O 2  6CO 2 + 6H 2 O + 38 ATP </li></ul></ul><ul><li>Cells receive both from the bloodstream </li></ul><ul><li>When insufficient glucose is available to the cells, the liver tries to compensate by releasing glucagon (a counter-regulatory hormone). </li></ul><ul><li>When this is insufficient, the body compensates thru lipolysis and proteolysis (attempting to get its energy requirements thru breakdown of fats and proteins). </li></ul>
  4. 4. WHAT HAPPENS, con’t. <ul><li>Hyperglycemia in the bloodstream  fluid and electrolytes imbalances  osmotic diuresis  </li></ul><ul><ul><li>Polyuria  dehydration and loss of electrolytes  </li></ul></ul><ul><ul><li>Polydipsia  cell starvation  </li></ul></ul><ul><ul><li>Polyphagia  starvation mode  </li></ul></ul><ul><ul><li>Lipolysis  fatty acids  Kussmaul breathing/fruity breath  </li></ul></ul><ul><ul><li>Metabolic acidosis </li></ul></ul><ul><ul><li>Hyperviscosity of blood  </li></ul></ul><ul><ul><li>HTN  </li></ul></ul><ul><ul><li>Hypoperfusion  </li></ul></ul><ul><ul><li>Kidney and cardiac insufficiencies, etc </li></ul></ul><ul><ul><li>Neuropathies </li></ul></ul><ul><ul><li>Necrosis  amputations </li></ul></ul><ul><ul><li>Erectile dysfunction </li></ul></ul>
  5. 5. WHAT HAPPENS, con’t
  6. 6. WHAT HAPPENS IN VASCULATURE? <ul><li>Microvasculature </li></ul><ul><ul><li>Sugar “scars” the epithelium, making it more porous  </li></ul></ul><ul><ul><li>Large pores and structural changes in basement membrane </li></ul></ul><ul><ul><li>Chronic ischemia due to lack of oxygen exchange  </li></ul></ul><ul><ul><li>Tissue hypoxia  skin ulcers </li></ul></ul><ul><ul><li>Tissue hypoxia  necrosis  amputations </li></ul></ul><ul><ul><li>Retinopathy  blindness </li></ul></ul><ul><ul><li>Neuropathy  permanent loss of fx </li></ul></ul><ul><li>Macrovasculature </li></ul><ul><ul><li>Tissue hypoxia  coronary heart disease, CVA, PVD </li></ul></ul><ul><ul><li>Tissue “scarring”  platelet agglutination  clots/occlusion  </li></ul></ul><ul><ul><li>AS, MI  left ventricular dysfx, heart failure </li></ul></ul><ul><ul><li>Hyperglycemia  albuminuria  nephron occlusion  Kidney failure </li></ul></ul>
  7. 7. RISK FACTOR CORRELATES OF DIABETES <ul><li>Highly correlated with HTN, obesity, sedentary lifestyles, poor nutrition/poor glucose control </li></ul><ul><li>HTN > 140/90 mm Hg </li></ul><ul><li>BMI > 25 </li></ul><ul><li>LDL > 130 mg/dl </li></ul><ul><li>HDL < 40 mm/dl </li></ul><ul><li>Triglycerides > 250 mg/dl </li></ul><ul><li>History of frequent yeast infections </li></ul><ul><li>History of poor/slow wound healing </li></ul><ul><li>Increased risk for infection </li></ul><ul><li>Poor oral hygiene </li></ul>
  8. 8. EPIDEMIOLOGY OF TYPE 2 DIABETES <ul><li>Seventh leading cause of death in US </li></ul><ul><li>17 million people or 6+% of population </li></ul><ul><li>6 million people are undiagnosed with diabetes </li></ul><ul><li>Prevalence same for men and women </li></ul><ul><li>Incidence higher among African-Americans, Native Americans and Hispanic-Americans </li></ul><ul><li>20% of healthcare dollars is spent on people w/ diabetes </li></ul><ul><li>88 million disability days </li></ul><ul><li>176,000 cases of permanent disability -- $7.5 billion! </li></ul>
  9. 9. LABS AND DIABETES <ul><li>Blood glucose values dx Diabetes </li></ul><ul><li>Fasting blood glucose -- two separate test results > 126 mg/dL </li></ul><ul><li>Oral glucose tolerance test -- blood glucose > 200 mg/dL after 120 mins </li></ul><ul><li>Glycoselated hemoglobin assay -- HbA1c -- “sugar-coated” RBCs long-term glycemic control > 8% </li></ul><ul><li>Ketoneuria  ketoacidosis </li></ul><ul><li>Proteinuria  kidney failure </li></ul>
  10. 10. MEDICATIONS AND DIABETES <ul><li>Oral therapy </li></ul><ul><ul><li>Sulfonylurea agents stimulate remaining beta cells  insulin  risk of hypoglycemia </li></ul></ul><ul><ul><li>Caution w/ warfarin, beta-blockers, Ca+ channel blockers, H 2 antagonists, MAO inhibitors, NSAIDS, tetracycline, anti-fungals, steroids, thiazide diuretics, Lasix, estrogen, thyroxine </li></ul></ul><ul><ul><li>Biguanides (metformin) decrease cellular resistance, so no risk of hypoglycemia </li></ul></ul><ul><li>Insulin </li></ul><ul><ul><li>Short-acting (Humulin R), intermediate-acting (NPH, Humulin N), Lente (Humulin L), Long-acting (Humulin U, glargine) </li></ul></ul><ul><ul><li>Basal insulin levels = 40-50U daily; maintained by pancreas secretions </li></ul></ul>
  11. 11. KEY TEACHING POINTS FOR DIABETES <ul><li>Controlling glycemic levels </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Diet </li></ul><ul><li>Exercise </li></ul><ul><li>Foot care </li></ul>
  12. 12. THE END IS THE BEGINNING! 

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