DIABETES

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farevalo2
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113027
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DIABETES
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2011-11-01 16:15:42
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Diabetes drugs
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study for exam 1
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  1. what is diabetes?
    metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia)
  2. what is Insulin?
    a hormone produced by the pancrease (beta cells), controls levels of glucose in the blood by regulating the production & storage of glucose
  3. glucagon?
    hormone produced by the alpha islet cells of the pancreas, serves to complete gluconeogensis in the hypoglycemic state
  4. Glycogen
    stored glucose in liver and muscles
  5. What are 1st generation sulfonylureas? what is their action?
    antidiabetic; stimulates secretion of insulin.

    Chlorpropamide (Diabinese)

    Long lasting: 24-72 hrs
  6. What are 2nd generation sulfonylureas and their action?
    antidiabetic: stimulates the release of insulin and increases sensitivity to insulin.

    Glipizide (Glucatrol)

    Short half life, good in elderly
  7. What is common between 1st and 2nd generation sufonylureas?
    Both for Type II, both taken with first meal of the day.

    SE: hypoglycemia
  8. Why is Glucagon given?
    • raise blood sugar
    • treatment of severe hypoglycemia in diabetes and adjunct for GI radiography.
  9. What are thiazolidinediones?
    • Improves insulin sensitivity in Type II in liver, muscle and fat cells.
    • Pioglitazone (Actos)
    • Rosiglitazone (Avandia)
  10. what are adverse/side effects of thiazolidendiones?
    hepatotoxicity: liver function, and fluid overload, edema
  11. What are biguanides:
    Metformin (Glucophage)
    inhibitors of intestinal flucose production and absorption. Target is liver, small intestine and peripheral tissues. Has no effect on pancreatic beta cells
  12. What are SE of biguanides such as metformin?
    Lactic Acidosis. Must avoid it in renal failure or uncontrolled HF. Not to be used w/sulfonylureas or the pt will go hypoglycemic.
  13. What are alpha glucosidase inhibitors such as acarbose (Precose)?
    Type II- delays absorptoin of glucose from GI tract - target is small intestine. lowers BS by inhibiting alphaglucosidase in GI tract.
  14. what are nursing implications for Acarbose/Precose (alpha-glucosidase inhibitor)?
    • flatulence diarrhea, abdominal pain
    • must be taken immidiatly before meal
    • delays absorption of glucose in intestinal system
  15. What are s/s of hypoglycemia?
    dizziness, tremors, tachycardia, anxiety, sweating, hunger, weakness
  16. What are Non Sulfonylureas?
    • These are for Type II, and stimulates the secretion of insulin.
    • Target - pancreatic beta cells.
    • Fast Acting
    • Repaglinide (Prandin)
    • neteglide (Starlix)
  17. s/s of ketoacidosis (DKA)?
    polydipsia, polyuria, headache, N&V, ABD pain, air hunger, acetone/fruity breath, dim vision, drowsiness, unconsciousness, dehydration
  18. causes of hypoglycemia?
    • delayed or omission of a meal, excessive exercise, insulin overdose
    • injection-unused tissue, ASA
  19. causes of ketoacidosis?
    infection, trauma, stress, omitted insulin, loss of pancreatic insulin secretion
  20. Hypoglycemia compared to DKA
    • hypoglycemia:
    • BS <50, ketones 0-norm, HCO2 24-32-norm.
    • DKA:
    • BS >300, ketones 4+, HCO2 low (Met Res) 4-16
  21. treatment for hypoglycemia?
    glucose, glucagon, oral forms of sugar, D50W IVP
  22. Treatment for DKA?
    insulin, HCO2, fluid replacement, Potassium replacement is usually required after acid/base balance, Foley catheter
  23. Difference between Type I and Type II?
    • T1DM: is no insulin production, HLA (destruction of beta cells)
    • T2DM: is decreased insulin or insulin resistant
  24. difference between DKA and HHNS?
    • DKA: hyperglycemia in a Type 1
    • Hyperglycemic hyperosmolar nonketotic syndrome: Type 2: hyperglycemia, no ketones are produced.
  25. chronic complications of diabetes mellitus?
    • Macrovascular: coronary artery disease, cerebrovascular disease, peripheral vascular disease
    • Microvascular: Kidney and eye disease, Neuropathic complications
  26. what stimulates the liver to make glucose available to cells?
    Glucogon hormone
  27. Where is glucose stored and as what?
    liver as glycogen
  28. what are some other functions of insulin?
    • enhance storage of dietary fat in adipose tissue
    • accelerates transport of amino acids into cells
    • inhibits breakdown of stored glucose, protein and fat
  29. what happens during fasting such as sleeping at night in regards to insulin?
    during fasting, the pancreas releases a small amount of insulin on a continuous basis for our basal levels
  30. what happens during fasting in regards to glucose?
    glucose is released by the liver to provide energy to keep us breathing such as using the diaphragm
  31. glycogenolysis
    production of glucose from glycogen
  32. gluconeogenesis
    glucose from the breakdown of non carb substances such as proteins
  33. T1DM has a possible genetic tendency called ___, environmental factors of _____?
    HLA human leukocyte antigen

    virus and toxins
  34. glycosuria
    • glucose spilled in the urine 180-200 mg/dl
    • Also loss of electrolytes
  35. When you have glycogenesis (production of new glucose from amino acids) ___ are produced from the breakdown of fats
    • KETONES
    • Increasing the Acid balance = DKA
  36. who ususally gets DKA?
    • usually under 30. They have no insulin, are very dehydrated and they feel like they have the flu - vomiting, no energy
    • Caused by: absence or inadequate amount of insulin, Hyperglycemia, acidosis, electrolyte loss. amount of glucose entering cells is reduced & liver produces more glucose.
  37. treatments for DKA?
    • fluid replacement Normal Saline
    • tx of hyperglycemia
    • electrolyte stabilizaiton
    • tx of underlying risks such as lack of education.
  38. What is the concern with K+ in DKA?
    usually K+ will correct when fluid replacement and regular insulin is given. Don't replace K+ until pt has stabalized
  39. Who normally gets type 2 diabetes?
    over 30 and obese
  40. How quickly does Type 2 advance?
    • slow and insiduous process of glucose intolerance or insulin resistance
    • 75% of cases dx incidentally
  41. What is pimary treatment of type 2?
    • weight loss (as most pts obese)
    • oral antidiabetic medications
    • then insulin if other measures are ineffective
  42. What is primary treatment of Type 1
    insulin
  43. Does HHNS have a slower or faster onset than DKA? Is insulin present? What about Dehydration?
    • HHNS is slower in onset
    • some insulin is present
    • profound dehydration
  44. treatment of a HHNS Crisis?
    • Fluid replacement if indicated
    • trmt of hyperglycemia, electrolyte stabilization
  45. Type 1 S/S?
    Fatigue, weak, sudden vision changes, tingling or numbness in hands or feet. dry skin and sores that are slow to heal due to poor circulation.recurrent infections, ABD pain , Nausea, Vomiting
  46. 3 clinical manifestations of diabetes?
    • polydipsia
    • polyuria
    • polyphalgia
  47. Fasting plasma glucose for diagnosis of DM ___ Random plasma glucose levels > ____ on more than one occasion
    • >126mg/dl FPG
    • >200 mg/dL Random PG
  48. What is the level of HgbA1C confirming hyperglycemia?
    7%+
  49. what is HgbA1C?
    • glycosylated hemoglobin measured every 3 months. It gives a tale of the last 90 days.
    • Normal is 4.4% - 6.4%
    • 12 is very bad
  50. What assessments & labs can be done for assessment and diagnosis of Diabetes?
    History (3 P's), Physical examination (eyes, cardiovscular, renal impairment), Labs: HgbA1C, Microalbuminuria or 24 hr urine q year (notes renal failing), Fasting lipids annually
  51. Diabetes management:
    • 1. nutrition therapy
    • 2. exercise
    • 3. monitoring
    • 4. Phrmacologic therapy
    • 5. education
  52. Main goal of diabetes?
    normalize insulin activity and blood glucose level to reduce the incident of vascular and neuropathic complications
  53. what are some important considerations on Sick Days in DM?
    • Take insulin/oral med as usual
    • test BS & urine ketones q 3-4 hrs
    • call MD if BS >300 or ketones present in urine
    • make sure to eat, take liquids
  54. What are advantages of patient control of DM? Disadvantages?
    • adv - allows pt control
    • dis - requires fine motor skills, visual acuity
  55. possible causes of elderly who have hyperglycemia are:
    poor nutrition, decrease in lean body mass, alterred insulin secretions, decrease in circulation
  56. dm pts need referrals to other health professionals such as (3):
    nutritionist, podiatrist, ophthalmologist
  57. how does exercise effect blood sugar?
    exercise lowers blood glucose levels by increasing uptake of glucose
  58. pts with blood glucose levels of > ___ or _____ in their urine should not begin exercising
    250... ketones
  59. rapid acting insulins?
    • Humalog, Novolog, Regular Insulin.
    • Onset 10-15 minutes
    • Peak 1-2 hrs
    • Duration 3 hrs
  60. intermediate acting insulins?
    • NPH & Lente (cloudy) must eat food near the onset and peak of action
    • Onset 3-4 hrs
    • peak 4-12 hrs
    • Duration 16-20 hrs
  61. SLOW acting insulins?
    • Long lasting: Ultralente
    • Onset is 6-8 hrs
    • peak 12-16 hrs
    • duration is 20-30 hrs
    • Needs to be supplemented w/short acting insulin
  62. What are complications of insulin therapy?
    • local & systemic allergic reactions
    • lipodystrophy, insulin resistance, morning hyperglycemia
  63. What do sulfonureas Type II oral antidiabetic agents do?
    stimulate pancreas to secrete insulin
  64. What do Biguanides T2DM oral antihyperglycemic agents do?
    • delay absorption of glucose
    • decreases glucose prodcution in liver (metformin) Glucophage
  65. long term complications of diabetes includes macrovascular complications such as
    • heart- coronary arteries
    • brain- cerebral vascular accident
    • main veins- peripheral vessels of lower limbs
  66. long term complications of diabetes includes microvascular complications such as
    retinopathy, nephropathy, neuropathies
  67. what may develop in a pt when ketone bodies accumulate?
    DKA
  68. What are s/s of DKA?
    ABD pain, nausea, vomiting, hyperventilation, fruity odor of breath
  69. a fasting plasma glucose greater than or equal to ____mg/dL would support checking blood levels for the diagnosis of DM
    126 mg/dL
  70. what type of T2DM Oral antidiabetic agents inhibit production of glucose by liver?
    biguanides
  71. what type of T2DM oral antidiabetic agent enhance insulin sensitivity in cells but not increasing insulin stimulation of pancreas?
    Thiazolidinediones such as Actos and Avan
  72. how do alpha-glucosiadase inhibitors work?
    • delay of absorption of glucose in the GI such as Acarbose (Precose)
    • lowers BS by inhibiting alphaglucosidase in GI tract
  73. when a pt has signs of hypoglycemia such as nervousness, tachycardia, diaphoresis and hunger, the nurse should provide what?
    15 g of fast acting simple carbs such as 3-4 commercially prepared glucose tabs. 6 oz fruit juice, regular soda, 6-10 hard candies
  74. What is considerred a macrovascular complication of DM?
    • Stroke, MI
    • CAD
    • cerebrovascular disease
    • peripheral vascular disease
  75. a normal pt BS level is
    60-120 in diabetic
  76. s/s of DKA?
    Kussmaul's respirations, dry skin, hypotension, and bradycardia are signs of diabetic ketoacidosis
  77. Cardinal signs of DM?
    Polyuria, polydipsia, polyphagia, and weight loss are classic signs
  78. s/s of hypoglycemia?
    anxiety, restlessness, headache, irritability, confusion, slurred speech, incoordiantion, diaphoresis, cool skin, tremors, coma, and seizures
  79. type 2 diabetes is described as:
    • insulin resistance (decreased sensitivity)or impaired insulin secretion
    • body tries to compensate by increasing the production of insulin
    • no ketones, rare
    • pts typically obese
    • pt has no islet antibodies
    • > 30
    • HHNS
  80. Type 1 diabetes is described as:
    • glucose derived from food cannot be stored in the liver and remains circulating in the blood, leading to postprandial hyperglycemia
    • desctruction of beta cells results in unchecked glucose production by the liver and fasting hyperglycemia
    • pt usually thin at Dx
    • pt needs insulin to preserve life
    • pt often has islet cell antibodies
    • onset can occur at any age
  81. what is lipotrophy?
    Lipotrophy is loss of subcutaneous fat and appears as a slight dimpling or more serious pitting of subcutaneous fat.
  82. Clinical manifestations of HHNS?
    • hypotension
    • profound dehydration
    • tachycardia
    • neuro- seizures
  83. leading cause of blindness in US in ages 20-74?
    diabetic retinopathy
  84. sensory neuropathy causes?
    loss of sensation to pain and pressure
  85. Autonomic neuropathy causes?
    • increased skin dryness
    • formation of skin fissures
  86. Motor neuropathy causes?
    muscular atrophy
  87. how does peripheral vascualar disease affect the progression of a foot infection and ulcer formation?
    inadequate and compromised lower extremity circulation interfers with ability to get nutrients to wound to promote healing and prevent gangrene.
  88. how does hyperglycemia affect the spread of a foot infection?
    hyperglycemia impairs leukocytes ability to destroy bacteria, thus lowering resistance to infection
  89. explain how insulin regulation is altered in the diabetic state
    insulin regulates the procution and storage of glucose: in diabetes the pancreas stops making insulin or the cells stop responding to it. hyperglycemia results and can lead to acute metabolic complications (DKA, HHNS)
  90. Describe the pathophysiologic difference between type 1 and type 2
    • type 1: characterized by an absence of insulin production and secretion due to autoimmune destruction of the beta cells
    • type 2: characterized by deficiency of insulin production and decreased insulin action as well as insulin resistance
  91. Glycemic index
    describes how much a given food increases the BG level compared with an equivalent amount of glucose

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