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Diabetes Mellitus
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Diabetes Mellitus

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  • 1. Diabetes Mellitus Barbara S. Hays Winter, 2006
  • 2. Blood Glucose ( normal serum level 65 – 105 mg )
    • Inside CNS
      • Brain uses glucose as primary fuel
      • Brain cannot store/produce glucose
    • Outside CNS
      • Fatty acids: stored as
        • Glycogen (liver/muscles)
        • Triglycerides (fat cells)
  • 3. Blood glucose, cont.
    • Outside CNS, continued
      • Endocrine portion of pancreas: Islets of Langerhans
        • Alpha cells make glucagon
          • “ counterregulatory”, acts opposite of insulin
        • Beta cells make insulin
          • Allows body cells to store and use carbohydrate, fats, and protein
  • 4. Hyperglycemia
    • When blood glucose becomes high
      • INSULIN allows glucose to enter cells
        • Liver
          • Production /storage of glycogen
          • Inhibits glycogen breakdown
          • Increased protein & fat synthesis (VLDL formation)
        • Muscles
          • Promotes protein and glycogen synthesis
        • Fat cells
          • Promotes storage of triglycerides
  • 5. Hyperglycemia
    • Drowsy
    • Flushed
    • Thirsty
  • 6. Hypoglycemia
    • Glucagon: causes release of glucose from liver
      • “ glycogenolysis (breakdown of glycogen to glucose)
      • “ glyconeogenesis of glucose not available
        • Lipolysis (breakdown of fat)
        • Proteolysis (breakdown of amino acids)
  • 7. Hypoglycemia
    • Weak, sweaty
    • Confused/irritable/ disoriented
  • 8. Diabetes Mellitus (problem with glucose metabolism)
    • Major health problem US/worldwide
    • Complications [lousy blood vessels]
      • Blindness
      • Renal failure
      • Amputations
      • [heart attacks and strokes]
      • [OB/neonatal complications]
  • 9. Diabetes Mellitus
    • The good news:
      • Blood glucose control reduces complications of Diabetes!
  • 10. Diabetes Mellitus
    • Absence (or ineffectiveness of ) insulin
    • Cellular resistance
    • Cells can’t use glucose for energy
      • Starvation mode
        • Compensatory breakdown of body fat/protein
        • Ketone bodies from faulty fat breakdown
            • Metabolic acidosis, compensatory breathing (Kussmal’s breathing)
  • 11. Diabetes Mellitus
    • HYPERGLYCEMIA : fluid/electrolyte imbalance.
      • Polyuria
        • Sodium, chloride, potassium excreted
      • Polydipsia from dehydration
      • Polyphagia : cells are starving, so person feels hungry despite eating huge amounts of food. Starvation state remains until insulin is available.
  • 12. Diabetes Mellitus
    • Complications of chronic hyperglycemia
      • Macrovascular complications
        • Cardiovascular disease (heart attack)
        • Cerebrovascular disease (strokes)
      • Microvascular
        • Blindness (retinal proliferation, macular degeneration)
        • Amputations
        • Diabetic neuropathy (diffuse, generalized, or focal)
        • Erectile dysfunction
  • 13. Classifying Diabetes Mellitus
    • Type I Diabetes: autoimmune
      • Beta cell destruction in genetically susceptible person
      • Some viral infections
  • 14. Classifying Diabetes Mellitus
    • Type II Diabetes
      • Reduction in ability of most cells to respond to insulin
      • Poor control of liver glucose output
      • Decreased beta-cell function (eventual failure)
  • 15. Diabetes Mellitus
    • Major risk factors
      • Family history
      • Obesity
      • Origin (Afro-American, Hispanic, Native American, Asian-American)
      • Age (older than 45)
      • History of gestational diabetes
      • High cholesterol
      • Hypertension
  • 16. Diabetes Mellitus
    • Prevention of effects: combination approach
      • Increased exercise
        • Decreases need for insulin
      • Reduce calorie intake
        • Improves insulin sensitivity
      • Weight reduction
        • Improves insulin action
  • 17. Triad of Treatment
    • Diet
    • Medication
      • Oral hypoglycemics
      • Insulins
    • Exercise
  • 18. Diabetes treatment
    • Exercise
      • Under physician supervision
      • Check glucose prior
  • 19. Diabetes treatment
    • Diet
      • Lower calorie
      • Fewer foods of “high glycemic index”
      • Spread meals evenly
  • 20. Diabetes treatment
    • Anti-Diabetic medications
      • Oral hypoglycemic agents (“Easy” p 297)
        • Sulfonylureas
        • Thiazolidinediones
        • Biguanides
        • Alpha-glucosidase inhibitors
        • D-phenylalinine derivatives
        • Combinations
      • Insulins (“Easy” Prototype Pro p 393)
  • 21. Sulfonylureas
    • Stimulate pancreas to secrete insulin
      • Glyburide (Diabeta) [Prototype Pro p 393]
        • Glucotrol (Glipizide)
        • Diabenese (chlorpropamide)
    • Adverse reactions
      • Hypoglycemia
      • Water retention/edema
      • Photosensitivity
    • May need to add insulin in times of stress
  • 22. Biguanides
    • Decreases liver production of glucose
    • Decreases intestinal absorption of glucose
    • Improves cell sensitivity to insulin
    • Example: Metformin
      • GI upset, flatulence
      • Cardiac (CHF, MI)
  • 23. Thiazolidinediones
    • Increase cellular sensitivity to insulin
      • Pioglitazone (Actos)
      • Rosiglitazone (Avandia)
    • Client should have liver enzymes
    • checked periodically
  • 24. D-Phenylalanine derivatives
    • Nateglinide (Starlix)
    • Rapid onset, short half-life
      • Good for those with rapid post prandial rise in blood glucose
  • 25. Combinations
    • Glucovance
      • Glyburide and Metformin
    • Avandamet
      • Avandia and Metformin
    • [come tell me when you run into this question…]
  • 26. Insulin
    • Made in beta cells of the pancreas
    • Moves glucose into cells (thus acts like growth hormone in a way)
    • Moves potassium into cells (can buy time in emergencies)
  • 27. Insulin preparations (“Easy” p 390) given ONLY with syringes marked in “units”
    • Rapid acting (lispro, asparte)
    • Short acting (regular)
    • Intermediate acting (NPH)
    • Long acting
      • Ultralente
      • [Glargine/Lantus]
  • 28. Your learning
    • Onset of action
    • Peak (blood glucose will be lowest then)
    • Duration
  • 29. Rapid acting insulin
    • Lispro ( Humolog, Novolog Aspart)
      • Onset of action
        • “ 15-30” minutes [may come on in 5 minutes…]
      • Peak of action
        • 1 - 2 hours
      • Duration
        • 3 – 4 hours
  • 30. Short acting insulins
    • Regular (clear so can be given IV)
      • Onset of action
        • 0.5 to 1 hour
      • Peak of action
        • 2 – 4 hours
      • Duration of action
        • 6 – 8 hours
  • 31. Intermediate acting insulins
    • NPH , Lente (chemicals added. Cloudy)
      • Onset of action
        • 1 – 4 hours
      • Peak of action
        • 4 – 12 hours
      • Duration of action
        • 18 – 24 hours
  • 32. Long acting insulins
    • Ultralente
      • Onset of action
        • 4 – 8 hours
      • Peak of action
        • 18 hours
      • Duration of action
        • 24 – 36 hours
  • 33. Once a day insulin
    • Glargine/Lantus
      • Cannot be diluted or mixed in syringe with any other insulin
      • Slow, steady release
      • Daily dosing [usually at bedtime]
      • Refrigerated or tosses every 14 days
  • 34. Combination insulins
    • 70/30 (70% NPH and 30% regular)
    • Humolog 70/30 (Humolog and regular)
    • Fewer injections
    • Rotate sites to decrease lipodystrophy
  • 35. Miscellaneous
    • Byetta for type II Diabetics taking sulfonylureas or combination
      • Mimics physiologic glucose control
        • Inhances insulin secretion only in presence of hyperglycemia
        • Insulin secretion decreases as blood glucose approaches normal
    • Neutontin for Diabetic nerve pain
  • 36. Some things to know
    • Insulin moves potassium into cells
      • Good for emergency situations
      • Dangerous if potassium level already low
  • 37. Some things to know…
    • HHNK ( H yperglycemic H yperosmolar N on- K etotic Coma). Also called
      • HHNK
      • HNKS [syndrome]
        • Like dibetic ketoacidosis, without the ketones
        • Type II diabetic, makes enough insulin to avoid ketones, but sugar guilds up to dangerous levels -> cellular dehydration
  • 38. Some things to know…
    • Dawn Phenomenon vs Somogi’s effect
      • Dawn phenomenon
        • Blood sugar rises in early morning
      • Somogi’s (rebound) effect
        • Blood sugar rise in morning as reaction to hypoglycemic time during the night
  • 39. Some things to know…
    • Diabetic foot care
      • Dry, cracked skin + poor circulation could = loss of a limb
      • For the most part nurses don’t trim nails of diabetic clients. Refer to Podiatrist.
  • 40. Typical diabetic foot ulcer
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