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Diabetes Mellitus
 

Diabetes Mellitus

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    Diabetes Mellitus Diabetes Mellitus Presentation Transcript

    • Diabetes Mellitus Barbara S. Hays Winter, 2006
    • 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)
    • 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
    • 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
    • Hyperglycemia
      • Drowsy
      • Flushed
      • Thirsty
    • 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)
    • Hypoglycemia
      • Weak, sweaty
      • Confused/irritable/ disoriented
    • 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]
    • Diabetes Mellitus
      • The good news:
        • Blood glucose control reduces complications of Diabetes!
    • 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)
    • 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.
    • 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
    • Classifying Diabetes Mellitus
      • Type I Diabetes: autoimmune
        • Beta cell destruction in genetically susceptible person
        • Some viral infections
    • 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)
    • 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
    • Diabetes Mellitus
      • Prevention of effects: combination approach
        • Increased exercise
          • Decreases need for insulin
        • Reduce calorie intake
          • Improves insulin sensitivity
        • Weight reduction
          • Improves insulin action
    • Triad of Treatment
      • Diet
      • Medication
        • Oral hypoglycemics
        • Insulins
      • Exercise
    • Diabetes treatment
      • Exercise
        • Under physician supervision
        • Check glucose prior
    • Diabetes treatment
      • Diet
        • Lower calorie
        • Fewer foods of “high glycemic index”
        • Spread meals evenly
    • 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)
    • 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
    • Biguanides
      • Decreases liver production of glucose
      • Decreases intestinal absorption of glucose
      • Improves cell sensitivity to insulin
      • Example: Metformin
        • GI upset, flatulence
        • Cardiac (CHF, MI)
    • Thiazolidinediones
      • Increase cellular sensitivity to insulin
        • Pioglitazone (Actos)
        • Rosiglitazone (Avandia)
      • Client should have liver enzymes
      • checked periodically
    • D-Phenylalanine derivatives
      • Nateglinide (Starlix)
      • Rapid onset, short half-life
        • Good for those with rapid post prandial rise in blood glucose
    • Combinations
      • Glucovance
        • Glyburide and Metformin
      • Avandamet
        • Avandia and Metformin
      • [come tell me when you run into this question…]
    • 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)
    • 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]
    • Your learning
      • Onset of action
      • Peak (blood glucose will be lowest then)
      • Duration
    • 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
    • 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
    • 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
    • Long acting insulins
      • Ultralente
        • Onset of action
          • 4 – 8 hours
        • Peak of action
          • 18 hours
        • Duration of action
          • 24 – 36 hours
    • 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
    • Combination insulins
      • 70/30 (70% NPH and 30% regular)
      • Humolog 70/30 (Humolog and regular)
      • Fewer injections
      • Rotate sites to decrease lipodystrophy
    • 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
    • Some things to know
      • Insulin moves potassium into cells
        • Good for emergency situations
        • Dangerous if potassium level already low
    • 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
    • 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
    • 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.
    • Typical diabetic foot ulcer
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