Adult I - Quiz 2

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Adult I - Quiz 2
2011-08-02 15:14:19

Ch. 67 Diabetes
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  1. Diabetes mellitus is the leading cause of ____________, ________________, ____________, ___________, and ______________.
    • Heart disease
    • Cerebral vascular accidents
    • Renal failure
    • Blindness
    • Non-traumatic limb amputation
  2. Complications of diabetes is reduced by _____________
    glycemic control
  3. Treatment of __________ and ___________ is essential
    • hypertension
    • hyperlipidemia
  4. Diabetes Mellitus
    • Disorder of glucose metabolism related to absent or insufficient insulin supply, and/or poor utilization of the insulin available.
    • Theories: genetic, autoimmune, viral, and environmental
  5. Serum Glucose
    • ... is controlled by the emptying rate of the stomach and delivery of nutrients into the small instestines
  6. Bloog Glucose Range
    70 - 100 mg/dL
  7. Basal Insulin Secretion
    Insulin that is continuously released in small pulsaatile increments during fasting
  8. Prandial Insulin Secretion
    Increased levels of insulin after eating
  9. Counter Regulatory Hormones
    • Glucagon, Epinephrine, Growth Hormone, and Cortisol
    • Oppose the effects of insulin
    • Increase blood glucose by stimulating glucose production and liver output
    • Combination of insulin and above hormones provide a sustained release of glucose energy during food intake and periods of fasting
    • Abnormal levels of hormones may produce DM
  10. Physiology of INSULIN
    • Released from pancreatic Beta cells
    • Promotes transport of glucose from the bloodstream across the cell membrane to the cytoplasm of the cell
    • Impacted by Incretin hormone
  11. Rise in insulin after a meal
    • Stimulates storage of glucose as glycogen in the liver and muscle (glycogenesis)
    • Inhibits conversion of proteins to glucose (gluconeogenesis)
    • Enhances fat cells to store triglycerides
    • Increases protein synthesis
  12. Incretin Hormone
    • Produced in the intestines
    • Secreted in response to the presence of food
    • INCREASES insulin, DECREASES glucagon, and SLOWS the rate of gastric emptying
  13. Fall in insulin during normal overnight
    • Release stored glucosed from the liver
    • Protein from muscle
    • Fat from adipose tissue
  14. Type I Diabetes
    • Formely known as "juvenile diabetes", or "insulin dependent"
    • Failure of the pancreas
    • Maybe be genetic - recessive (possible mutation on chromosome 11)
    • Viral (pt with HLA have exposure to viral infection)
    • 5 - 10% of all diabetics
    • Usually under age 30
    • Peaks from ages 11 - 13
    • Incidence is higher in whites
    • Same incidence in males & females
    • Patients are usually thin/lean, but may be obese
    • Progressive destruction of Pancreatic B cells
    • Require Exogenous Insulin
    • Diabetic Ketoacidosis
  15. Type I DM: Acute Onset 3 P's
    • Polydipsia: excessive thirst
    • Polyphagia: excessive hunger
    • Polyuria: increased frequency of urination
    • weight loss
  16. Prediabetes (Impaired Glucose Tolerance [IGT]) (Impaired Fasting Glucose [IFG])
    • Beta cells become fatigued from overproduction
    • Beta cell dysfunction is mild - with slight increase in glucose
    • Paitents with IGT are at increased risk for DM II, usually within 10 years
    • Approximately 20 million Americans (ages 40 - 75 yrs) have IGT
  17. Prediabetes
    • Fasting Plasma Glucose Level above 100
    • Studies show that people with pre-diabetes can prevent or delay the development of type 2 diabetes through changes to their lifestyle that include modest weight loss and regular exercise
    • Research has shown that long-term damage, especially to the cardiovascular system, already may be occuring during prediabetes
  18. Type II Diabetes
    • Formerly known as "Adult Onset"
    • Most prevalent (90% of patients)
    • Correlated with obesity
    • Over the age of 35
    • Also identified in younger people (especially with increased childhood obesity)
    • Genetics - dominant and multifactorial (linked to chromosomes 20, 7, 12)
    • Insulin resistance
    • Highest among Native American and Hispanics followed by African Americans
    • Pancreas usually continues to form some insulin
    • Insulin amount is usually insufficient to meet the needs of the body, AND/OR insulin is poorly utilized by tissues
    • Results in HHNK
  19. DM Type II: Insulin Resistance
    • Body tissues do not respond to insulin
    • Insufficent number of receptors or receptors are unresponsive to insulin
    • Hyperglycemia and Hyperinsulinemia
  20. Metabolic Syndrome
    Cluster of abnormalities working synergistically to greatly increase the risk for CV disease and diabetes
  21. Abonormalities of Metabolic Syndrome
    • Elevated insulin levels (insulin resistance)
    • High triglycerides
    • Decreased HDL
    • Increased LDL
    • Hypertension
    • Obesity (esp. central obesity)
    • Sedentary lifestyle
    • Esitmated that 34% of Americans fit this criteria
    • Can be treated with weight loss and exercise
  22. Nonspecific Manifestations with Type II Diabetes
    • Can be the 3 P's
    • Fatigue
    • Recurrent Infections
    • Visual Changes
    • Prolonged healing times
  23. Methods of Diagnosis
    • Fasting Plasma Glucose
    • Random Glucose
    • Two Hour Oral Glucose Tolerance Test (OGTT)
    • Glycosylated Hemoglobin A1C (HbA1C)
  24. Fasting Plasma Glucose
    • No caloric intake for at least 8 hours
    • (>100 - <126) Impaired Fasting Glucose
    • Critical Values: < 60 mg/dL or > 500 mg/dL
  25. Random Glucose
    • Can be drawn at anytime
    • Meals, drugs, and stress can cause an increase
    • > 180 mg/dL on two occasions
  26. Two Hour Oral Glucose Tolerance Test (OGTT)
    • Multiple blood draws over 2 hours after a glucose load of 75 g
    • 200 mg/dL or more = Diabetes
    • > 140 and < 199 = Pre-Diabetes
  27. Glycosylated Hemoglobin A1C (HbA1C)
    • Glucose attaches to Hgb and remains attached to the RBC for it's lifespan (90 days)
    • Indicates overall glucose control for previous 90 days
    • Near-normal levels over time have greatly reduced the risk for development of complications
    • Normal range = 4 - 7%
    • Goal: A1C level of 6.5% or less
    • Condtions that effect RBC turnover may alter HbA1C (blood loss, hemolysis, etc.)
  28. Diagnostic Tests
    • Urine: check protein & ketones
    • Kidney Function Tests
    • BMI - concern with > 25
  29. Insulin Onset-Peak-Duration
  30. Insulin Sliding Scale
  31. Insulin Admixture
    • 1. wash hands
    • 2. gently rotate NPH insulin bottle
    • 3. wipe off tops of insulin vials with alcohol sponge
    • 4. draw back amount of air into the syringe that equals the TOTAL dose
    • 5. inject air equal to NPH dose into NPH vial; remove syringe from vial
    • 6. inject air equal to REGULAR dose into regular vial
    • 7. invert REGULAR insulin bottle and withdraw REGULAR insulin dose
    • 8. without adding more air to NPH vial, carefully withdraw NPH dose

    • [NR][RN]
    • [air][withdraw]
  32. Insulin Pump
    • Glucose monitor which can send wireless glucose value to insulin "smart" pump
    • The pump calculates complex math based on measures sent and recommends dosages to patient
    • Change site every two to three days
    • Check site for redness or other signs of infection
  33. Insulin Jet
    • Delivers insulin in fine pressurized steam through skin without needle
    • Peak onset & etc. occur earlier
    • Thorough training and monitoring needed
  34. Intensive Insulin Therapy
    • Consists of multiple daily insulin injections together with frequent self-monitoring of blood glucose
    • Glucose needs to be checked 4 to 6 times per day
  35. Oral Agents for Diabetes Treatment
    • Sulfonylurea
    • Meglitinides
    • Biguanidea
    • Alpha Glucosidase Inhibitors
    • Thiazolidinediones ((TZD's)
  36. Sulfonylurea
    • "Micronase"
    • Increase insulin from the pancreas
  37. Meglitinides
    • "Prandin"
    • Rapidly absorbed, increase insulin the the pancreas
  38. Biguanides
    • "Metformin"
    • Reduce glucose production by the liver
  39. Alpha Glucosidase Inhibitors
    • "Precose"
    • Slow down CHO absorption in small intestine
  40. Thiazolidinediones (TDZ's)
    • "Actose"
    • "Insulin Sensitizers"; use with caution with cardiac patients
  41. DDP-4 (Dipetidyl Peptidase) Inhibitors (Oral)
    • New class of glucose-lowering drugs
    • Galvus (vildagliptin)
    • DDP-4 normally inactivates incretin hormone
    • Incretin hormone is released from the intestines, it is released throughout the day, and in response to meals
    • Incretin increases insulin synthesis and release from the pancreas
    • Low risk of hypoglycemia
  42. Amylin Analog (Smylin)
    • Type I and II
    • Adjuct to insulin for better control
    • Thigh or abdomen SubQ injection
    • CANNOT be mixed with insulin
    • Slows gastric emptying and reduces post-prandial glucagon secretion
    • May cause severe hypoglycemia in Type I
  43. Incretin Mimetic (Byetta)
    • Type II in place of insulin
    • Similar to hormone
    • Suppression of glucagon, slows gastric emptying
    • Reducing intake by decreasing appetite
    • SubQ
    • Now approved as monotherapy
  44. Medications that effect blood glucose levels or interact with sulfonylurea drugs -- BE AWARE
  45. Pancreas, Pancreas-Kidney Transplantation, & Islet Cell Transplant Indications
    • Used for some patients with Type I diabetes
    • Some recieve kidney with pancreas due to nephropathy present with current kidney
  46. Complications of Diabetes
    • Hypoglycemia
    • Hyperglycemia
    • Somogyi Effect
    • Dawn Effect
    • Diabetic Ketoacidosis
    • Hyperosmolar Hyperglycemic State (HHS)
    • Lipodystrophy
  47. Somogyi Effect
    • Rebound effect in which an overdose of insulin induces morning hyperglycemia
    • Results in decreased blood sugar in the middle of the night as a response to increased insulin
    • Compensatory mechanisms occur to rain glucose (release of counterregulatory hormones -- lipolysis, gluconeogenesis, glycogenolysis)
    • Results in overcompensation
    • Leading to rebound hyperglycemia and ketosis noted in the A.M.
    • Problem: possible undetected hypoglycemia during the night
  48. Dawn Effect
    Hyperglycemia present on awakening impacted by release of growth hormone during sleep
  49. Lipodystrophy
    Hypertrophy or atrophy of s.c. tussie due to frequent use of the same injection site or an immune reaction to impurities in insulin
  50. HYPOglycemia Symptoms
    • Skin: cool & clammy
    • Perspiration: profuse
    • Mental Status: anxious, nervous, irritable, mental confusion, seizures, coma
    • Misc: Weakness, Double or blurred vision, Hunger, Tachycardia, Palpitations
    • Glucose: < 70 mg/dL
    • Ketones: negative
  51. Treatment for HYPOglycemia
    • Rapid acting sugars (OJ, candy)
    • IV Dextrose or Glucagon ... followed by complex CHO snack
  52. HYPERglycemia Symptoms
    • Skin: hot & dry
    • Dehydration: present
    • Respiration: Rapid, deep, acetone to breath
    • Mental Status: varies from alert to stuporous, obtunded, or frank coma
    • Glucose: > 250 mg/dL
    • Ketones: positive
  53. Treatment for Somogyi Effect
    • Check blood sugar between 2 and 4 AM
    • If this AM blood sugar is low ... then reduce PM dose of insulin or eat a more substantial bedtime snack
  54. Dawn Phenomenon
    • Hyperglycemia noted on awakening in AM due to release of hormones in predawn hours
    • Growth hormone is a possible factor
    • Affects majority of those with diabetes but most severe in adolescence and young adulthood
    • Problem: high blood sugar usually after 3 AM
  55. Treatment for Dawn Phenomenon
    • Check blood sugar between 2 and 4 AM
    • If high, then increase insulin and eat bedtime snack
    • Change timing of evening or intermediate acting insulin from dinnertime to bedtime
  56. Hyperglycemic Hyperosmolar State (HHS)
    Hyperosmolar Hyperglycemis Nonketotic State (HHNK)
    • (Formely HHNS)
    • Produce enough insulin to prevent DKA
    • Not enough insulin to prevent osmotic diuresis, hyperglycemia, or ECF depletion
    • Increse in serum osmolarity
    • BS > 400 mg/dL
    • High BG produces high serum osmolarity thus producing neurological manifestions (coma, seizures, etc.), strokelike symptoms
    • *** Fewer symptoms are seen earlier with HHNS so BS can get quite high
  57. Treatment of DKA and HHS
    • Medical emergency
    • IV administration of NSS of 1/2 NSS
    • Regular Insulin IV
    • When glucose falls < 250 ... add IV glucose (D5 1/2)
    • Electrolyte replacement
    • Bicarbonate for DKA in pH < 7.10
    • Treat underlying cause and complications
    • Cardiac monitoring
  58. Chronic Complications
    • Cataracts *
    • Retinopathy/Blindness *
    • Infections such as Gangrene *
    • Neuropathy
    • Arteriosclerosis
    • Myocardial Infarctions
    • Kidney disease
    • Valve disease
    • Cerebral Vascular Accidents
    • Erectile dysfunction

    * most common
  59. Exercise
    • Lowers blood glucose by increasing CHO
    • ** On occasion, exercise may be a stressor especially in Type I and may raise BS
    • Fosters weight reduction and maintenance
    • Increases insulin sensitivity
    • Increases LDL levels
    • Decreases triglceride levels
    • Lowers BP
    • Reduces stress & tension
  60. Patient Education
    • Medication
    • Follow-up visits to specialists
    • Foot care - risk of amputation 15x greater in diabetics; foot assessment; podiatrist
  61. Home care when illness cuases increased BS
    • Eat a regular diabetic diet
    • Increase noncaloric fluids
    • Continue with oral agents and/or insulin
    • Monitor BS every 4 hours ... if > 240 check urine for ketones, report + ketones to physician
  62. Home care if illness leads to decreased PO intake
    • Supplement CHO food intake with CHO-containing fluids while continuing with oral agents and/or insulin
    • Notify physician immediately if unable to keep and food or fluids down