Diabetes - test 4

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Anonymous
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41698
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Diabetes - test 4
Updated:
2010-10-12 16:25:40
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Diabetes test
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DM 1 & 2
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  1. where is insulin produced?
    pancreas
  2. true or false?
    type 1 diabetes is considered an autoimmune disease
    true
  3. what are the clinical manifestations of diabetes?
    Polydypsia, polyuria, polyphasia along with fatigue, weakness, sudden vision changes, tingling/numbness in hands and feet, dry skin, skin wounds/lesions that are slow to heal and recurrent infections.
  4. Along with all the other symptoms, type 1 diabetes has another symptom specific to this type. What is it?
    sudden weight loss, nausea, vomitting or abdominal pain.
  5. What is the patho for type 1 DM?
    destruction of pancreatic beta cells by an autoimmune process. This pt has no insulin.
  6. What is the patho for type 2 DM?
    Decreased sensitivity to insulin & impaired beta cell functioning, resulting in decreased insulin production.
  7. What is the typical age of onset for type 1 DM?
    younger than 30
  8. What is the typical onset age for type 2 DM?
    Over 30
  9. What people are more at risk for developing Diabetes?
    • * family history of diabetes
    • * obesity
    • * race/ethnicity (black, hispanic, native, asians and pacific islanders)
    • * previous problems w/ fasting glucose tolerance
    • * hypertension
    • * history of gestational diabetes or baby over 9lbs
  10. What are the effects of Carbs on insulin?
    Carbs have the greatest effect on blood glucose levels because they are faster digested than other foods and are converted into glucose rapidly. 50 to 60% of calories should be from carbs and 100% of carbs are converted into glucose.
  11. What are the effects of protein on insulin?
    50% of protein foods are converted into glucose and only 10 to 20% of a meal should be protein.
  12. What are the effects of fat metabolism on insulin?
    20 to 30% of meals should come from fat; this is to limit the development of CAD.
  13. What is the leading cause of death and disability in Diabetes patients?
    CAD
  14. How is type 1 diabetes diagnosed?
    • * Casual plasma glucose concentration of 200mg/dl or more
    • * polydypsia, polyuria and unexplained weight loss
  15. How is type 2 DM diagnosed?
    • * Slow progressive glucose intolerance, usually detected at routine exams
    • * Casual plasma glucose concentration of 200mg/dl on more than one occassion
  16. What lab test can identify if a client is using the prescribed dietary meds and excercise intervention for diabetes?
    Hemoglobin A1C - determines how well sugar has been controlled over the previous 3 to 4 months.
  17. True or False:
    Pts w/ glucose level of 250mg/dl and above & who have ketones in urines shouldn't begin excercising til' tests come back negative for ketones & blood glucose level is closer to normal.
    True
  18. Pts who are planning to excercise and take insulin should eat a 15g carb snack to prevent __________.
    hypoglycemia
  19. If a diabetic pt is excercising to lose weight than a _______ in insulin may be indicated.
    decrease
  20. What should a pt with diabetes that takes insulin and is excercising for prolonged periods of time do to a avoid postexcercise hypoglycemia?
    eat a snack at the end of excercise and monitor blood glucose more frequent
  21. True or false:
    pts participating in extended periods of excercise may want to monitor blood glucose before, during, after excercise and take carb snack as needed.
    True
  22. True or False:
    pts w/ type 2 diabetes who excercise have a better chance of glucose tolerance going back to normal.
    True
  23. What is the blood glucose level for hypoglycemia?
    50 to 60mg/dl
  24. What is hypoglycemia caused by?
    • too much insulin or oral hypoglycemic agents
    • too little food or excessive physical activity
  25. When does hypoglycemia occur?
    • it can occur at anytime of day or night
    • often occurs before meals; if delayed or if snacks are omitted.
  26. What is diabetic ketoacidosis caused by?
    an absence or marketly inadequate amount of insulin; this deficit in available insulin results in disorders in the metabolism of carbohydrate, protein and fat.
  27. 3 main clinical features of DKA are:
    • Hyperglycemia
    • dehydration and electrolye loss
    • acidosis
  28. What is Hyperglycemic hyperosmolar nonketotic syndrome (HHNS)
    a metobolic disorder of type 2 Diabetes resulting from a relative insulin deficiency initiated by an intercurrent illness that raises the demand for insulin; associated with polyuria and dehydration.
  29. Is the onset of Diabetic ketoacidosis rapid or slow?
    It is rapid. less than 24 hours
  30. Is the onset of hyperglycemic hyperosmolar nonketotic syndrome (HHNS) rapid or slow?
    slow. usually over several days.
  31. What is usually the blood glucose level of some in DKA?
    250mg/dl and up
  32. Even thought DKA can occur in either diabetes. In which is it most likely to occur?
    type 1 DM
  33. What is the mortality rate for DKA?
    5%
  34. Even though HHNS can occur in both type of diabetics. Which type is it most likely to occur in?
    type 2. especially in the elderly with type 2 diabetes
  35. What is the blood glucose levels for a person with HHNS?
    Greater than 600mg/dl
  36. Are ketones present present in pts with DKA?
    yes
  37. Are ketones present in patients w/ HHNS?
    NO
  38. What is the mortality rate for HHNS?
    10-40%
  39. What would you give apt w/ hypoglycemia?
    • 3 to 4 glucose tabs
    • 4 to 6oz of juice or regular soda
    • 6 to 10 hard candies
    • 2 to 3 tsp of sugar or honey
  40. What would you do for a patient with DKA?
    • rehydration
    • restore electrolytes
    • reverse acidosis
    • prevent fluid overload
  41. What would you do for a pt w/ HHNS?
    • rehydrate
    • restore electrolytes
    • administer insulin
    • prevent fluid overload
  42. True or False:
    ppl with type 1 DM have presence of islet cell antibodies.
    True
  43. Type 1 Diabetes medicine __________ insulin.
    replaces
  44. How do type 2 DM meds work in the body?
    • increase secretion of insulin by pancreatic beta cells
    • inhibit production of glucose by liver
    • or
    • delay absorption of complex carbs in intense and slow entry of glucose into systemic circulation
  45. What are the First generation sulfonylureas (4)
    • acetohexamide (Dymelor)
    • chlorpropamide (Diabenese)
    • tolazamide (Tolinase)
    • tolbutamide (Orinase)
  46. What is the action of first generation sulfonylureas (which are rarely used)
    stimulate beta cells of the pancreas to secrete insulin
  47. What are the second generation sulfonylureas (3)
    • glipizide (Glucatrol)
    • glyburide (Micronase, glynase, dia-beta)
    • glimepiride (Amaryl)
  48. What is the action of the second generation sulfonylureas?
    stimulate beta cells of the pancreas to secrete insulin
  49. What meds are the Biguanides?
    • Metformin (Glucophase, fortamet)
    • Metformin w/ glyburide (Glucovance)
  50. What is the mechanism of action of the biguanides?
    inhibits production of glucose by liver, increases tissue sensitivity to insulin and decreases hepatic synthesis of cholesterol
  51. Which meds are the alpha-glucosidase inhibitors?
    • acarbose (Precose)
    • miglitol (Glyset)
  52. What is the mechanism of action of the alpha-glucosidase inhibitors?
    delays absorption of complex carbs in the intestine and slows entry of glucose into sysyemic circulation
  53. What are the sulfonylurea insulin secretagogues?
    • repaglinide (Prandin)
    • neteglide (Starlix)
  54. what is the mechanism of action of the sulfonylurea insulin secretagogues?
    stimulate pancreas to secrete insulin
  55. Which meds are the thiazolidinediones (or glitazones)?
    • Pioglitazone (actos)
    • rosiglitazone (avandia)
  56. what is the mechanism of action of the thiazolidinediones?
    sensitize tissue to insulin; stimulate receptor sites to lower blood glucose
  57. Which are the rapid acting insulins?
    • Lispro (Humalog)
    • Aspart (Novolog)
  58. what is the onset for the rapid acting insulins like humalog and novolog?
    5 to 15 minutes
  59. what is the peak for rapid acting insulin?
    1 hour
  60. what is the duration of action for rapid acting insulin?
    2 to 4 hours
  61. What is the short acting insulin?
    Regular (humalog r, novolin r)
  62. what is the onset, peak and duration for short acting (aka regular insulin)?
    • onset: 1/2 hour to 1 hour
    • peak: 2 to 3 hours
    • duration: 4 to 6 hours
  63. What are the intermediate acting insulins?
    • NPH (nuetral protamine hagedorn)
    • Humilin N
    • Lente
  64. What is the onset, peak and duration time for intermediate acting insulin like NPH, Humulin N and Lente?
    • onset: 2 to 4 hours
    • peak: 4 to 12 hours
    • duration: 16 to 20 hours
  65. Which is the long acting insulin?
    Ultralente (UL)
  66. What is the onset, peak and duration time for long acting insulin, ultralente?
    • onset: 6 to 8 hours
    • peak: 12 to 16 hours
    • duration: 20 to 30 hours
  67. Which is the very long acting insulin?
    Glargine (Lantus)
  68. What is the onset, peak and duration time for very long acting insulin, Lanus?
    • onset: 1 hour
    • peak: No Peak
    • duration: 24 hours
  69. True or False:
    Pts who switch from animal to synthesized insulin should be monitored for low blood glucose level b/c human form insulin is used more effectively?
    True
  70. True or False:
    Don't mix Lantus with any other drugs.
    True
  71. True or False:
    Hypoglycemia occurs when a pt w/ diabetes doesn't eat but continues to take insulin or oral antidiabetics.
    True
  72. In an emergency case of hypoglycemia what should be given to the pt nad how long can it take for them to regain conciousness?
    • Glucagon SubQ or IM shot of 1mg
    • D50 IV Push
    • 20 minutes
  73. a blood glucose level of _____ and above is considered prediabetic.
    110mg/dl
  74. What is the ONLY insulin that can be given IV?
    Regular
  75. Macrovascular complications involve:
    • heart (CAD)
    • brain (TIA, CVA)
    • extremities (ulceration, gangrene)
  76. Microvascular complications involve
    • eyes (blindness)
    • kidneys (kidney failure)
    • nerves (amputation)

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