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Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
Diabetes Mellitus
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Diabetes Mellitus

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  • congratulation great information.. but nowdays a coupple of things have already changed...
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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
  • 41.  
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