Diabetes

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  1. Rapid acting insulin: names (clarity, onset, peak , and duration)
    • Rapid acting:
    • Names:Lispro (Humalog) Aspart (Novolog) Glulisine (Apidra)

    clear, onset: 10 - 30 minutes, Peak: 30 min - 3 hour, Duration: 3 - 5 hour
  2. Short acting insulin: names (clarity, onset, peak, duration)
    • Short acting:
    • Regular (Humulin R, Novolin R)
    • clear, onset: 30 min - 1 hour, peak: 2 - 5 hour, Duration: 5 - 8 hour
  3. Intermediate acting: name (clarity, onset, peak, duration)
    • Intermediate acting:
    • NPH (Humulin N, Novolin N)
    • cloudy, onset: 1.5 - 4 hour, peak: 4 - 12 hour, duration: 12 - 18 hour
  4. Long acting: names (clarity, onset, peak, duration)
    • Long acting:
    • Glargine (Lantus) Determir (Levemir)
    • clear, onset: 0.8 - 4 hour, peak: no pronounced peak, duration: 24+ hour
  5. Diabetes mellitus: chronic multi system disease r/t
    • Abnormal insulin production 
    • Impaired insulin utilization 
    • Both
  6. Causes of Diabetes Mellitus:
    • Genetic
    • Autoimmune 
    • Environmental: Virus, obesity
  7. Pancreas (endocrine): alpha cells secrete:
    glucagon (raises Blood sugar concentration)
  8. Pancreas (endocrine): Betta cells secrete:
    • Insulin (Lowers blood sugar concentration) 
    • Amylin (inhibits release of glucagon)
  9. Glucagon works on the ________ nervous system.
    Sympathetic nervous system (Fight or flight)
  10. Insulin works on the ______ nervous system.
    Parasympathetic (rest and digest)
  11. Counter regulatory hormones that increase blood sugar are:
    • Catecholamines (Epinephrine, Nor epinephrine)
    • Growth hormones
    • Glucocorticoid hormones (steroids)
  12. Stress hyperglycemia: corticosteroids and catecholamines increase. 
    Production of glucose in liver _____. 
    Production of glucagon _____. 
    functioning insulin receptors on cell ______.
    • production of glucose in liver increases
    • Production of glucagon increases
    • Functioning insulin receptors on cell decreases.
  13. Glucagon increases blood glucose by stimulating ________.
    Glucagon synthesized in response to low levels of blood glucose, protein ingestion, and exercise.
    Gluconeogenesis (generation of glucose)
  14. ______: hormone produced by betta cells in islets of Langerhans.
    Insulin
  15. Insulin metabolism: Stimulates the storage of glucose as glycogen in ______ and ______. 
    Inhibits _________. 
    Enhances fat deposition of adipose tissues. 
    Increases protein synthesis.
    • Glucose stored as glycogen in Liver and Muscle.
    • Inhibits glyconeogenesis.
  16. Type 1 diabetes: __________ of beta cells in pancreas.
    Destruction (complete lack of insulin)
  17. Type 2 diabetes: ______ of beta cells and insulin ______.
    • dysfunction and insulin resistance.
    • (same as gestational diabetes)
  18. Risk factors for diabetes: 
    Age >45 (35 with other risk factors) 
    Women with polycystic ovarian syndrome
    Obesity
    Prior gestational diabetes or baby weighing > 9 pounds
    Prior IGT and IFG or _______. 
    History of ______. 
    • Prior impaired glucose tolerance or impaired fasting glucose or family history
    • History of HTN or vascular disease.
  19. IGT: fasting glucose levels higher than normal
    Impaired glucose tolerance: >100 mg/dL but <126 mg/dL
  20. Oral glucose tolerance test (OGTT): 2 hour plasma glucose higher than normal
    </= 200 mg/dL
  21. Type 1 Diabetes: "I___ D____ D____"
    • Insulin dependent diabetes 
    • Autoimmune 
    • Destruction of Beta cells: absence of insulin 
    • causes: genetics, virus
  22. Type 1 Diabetes manifestations
    3 P's: ________
    weight loss
    fatigue
    • 3 P's: Polyuria, Polydipsia, Polyphagia
    • Ketoacidosis (fruity breath)
  23. S/S More common in type 1 diabetes
    • Lethargy
    • Stupor  
    • Nausea 
    • vomiting 
    • Abdominal pain 
    • Kussmaul breathing 
    • Weight loss
  24. Type 2 diabetes Mellitus: "N__ I___ D__"
    Risk factors:
    • Overweight 
    • Age >45 (35 with other risk factors) 
    • Family history 
    • Race
  25. Type 2 Diabetes Mellitus: pancreas continues to produce some insulin. (Not enough or poorly used by tissues) 
    Genetic link:
    • Insulin resistance
    • Beta cells fatigue and produce less insulin 
    • Haphazard release of glucose by liver 
    • adipokines- chronic inflammation
  26. Type 2 DM manifestations:
    • Recurrent infections 
    • Prolonged wound healing 
    • 3 P's: Polyuria, polydipsia, polyphagia
    • Fatigue 
    • Visual changes: chronic hyperglycemia
  27. Type 1 Diabetes: age at onset, type of onset, environmental factors, insulin
    • Age: young
    • Type of onset: Abrupt
    • Environmental factors: Virus, toxins 
    • Insulin: required
  28. Type 2 diabetes: age at onset, type of onset, environmental factors, insulin
    • Age: >45 (35 if other risk factors) 
    • Type of onset: Gradual 
    • Environmental factors: obesity, lack of exercise
    • Insulin: may be necessary as disease progresses
  29. Diagnositcs
    A1C: ___
    Fasting Plasma glucose: _____
    2 hour plasma glucose: ______
    Islet cell antibody testing: Type ___
    • A1C: 6.5% or higher (monitor for diabetes) 
    • (7% is generally acceptable) 
    • Fasting plasma glucose: >/= 126 mg/dL 
    • 2 hour plasma glucose: >/= 200 mg/dL
    • Islet cell antibody t esting: Type 1 DM
  30. Meal time insulin:_______ 
    Control between meals and night time:____
    Carbohydrate counting:____
    • Meal time insulin: rapid or short acting (before meal) 
    • control between meals and night time: Basal insulin(long/intermediate acting) 
    • Carb counting: allows to adjust the amount of insulin based on how many grams of carbs are eaten.
  31. Insulin adverse effects:
    • Hypoglycemia
    • Allergic reaction 
    • Lipodystrophy 
    • Somogyi effect 
    • Dawn phenomenon
  32. Somogyi Effect: Requires _____ insulin.
    Counterregulatory hormone response to high insulin dosage.
    • Somogyi effect: requires less insulin. 
    • Morning hyperglycemia.
  33. Dawn phenomenon: Adjust insulin administration time or ______ dose. 
    Growth hormone and cortisol excreted in increased amount (counterregulatory hormones)
    • Dawn phenomenon: adjust insulin administration time or increase dose. 
    • *requires more insulin 
    • Most common in adolescents
  34. Plasma blood glucose & HGB A1C goals for type 1 DM 
    Toddlers & preschoolers <6 years: before meals, bed time, HGB A1C
    Toddlers & Preschoolers <6 years: 

    • before meals 100 - 180 
    • bedtime 110 - 200
    • HGB A1C </= 8.5% but >/=7.5%
  35. Plasma blood glucose & HGB A1C goals for type 1 DM

    School age 6 - 12 years
    School age 6 - 12 years 

    • before meals 90 - 180
    • before bed 100 - 180 
    • HGB A1C <8%
  36. Plasma blood glucose & HGB A1C goals for type 1 DM

    Adolescents >12 years and young adults
    Adolescents >12 years and young adults 

    • Before meals 90 - 130 
    • Before bed 90 - 150
    • HGB A1C <7.5%
  37. _____ insulin (Long/intermediate) 
    Control b/w meals and nighttime.
    Basal insulin
  38. Combination of insulin: Mix _____ and _____ in same syringe. (Clear to cloudy)
    Short and Intermediate
  39. Oral Antidiabetics work on 3 defects of type 2 diabetes

    Insulin ______. 
    ______ insulin production. 
    ______ hepatic glucose production.
    • Insulin resistance
    • Decreased insulin production 
    • Decreased hepatic glucose production
  40. Oral antidiabetics:
    • Metformin: 
    • Glucophage 
    • Glucophage XR
    • Fortamet 
    • Riomet
  41. Biguanides: trade names, action, adverse effects
    • Trade names: Metformin (Glucophage)
    • Action: Reduces glucose production in liver enhance insulin sentivity @ tissue
    • Adverse effects: Kidney injury, lactic acidosis

    (D/C Metformin 24 - 48 hours before contrast CT scan, restart metformin 48 hours later.)
  42. Sulfonylureas: trade names, action, adverse effects
    • Trade names: Glipizide, Glyburide
    • Action: Increases insulin production by pancreas 
    • Adverse effects: Hypoglycemia
  43. Meglitinides: trade names, action, adverse effects
    • Trade names: Starlix, prandin 
    • Action: Increases insulin production by pancreas
    • Adverse effects: Weight gain, hypoglycemia
  44. Dipeptidyl peptidase-4 inhibitors: trade names, action, adverse effects
    • Trade names: Trajenta, Onglyza, Januvia 
    • Action: Block DPP-4 enzyme increases insulin release, decreases glucagon secreation, decreases hepatic glucose production
    • Adverse effects: Pancreatitis
  45. Nutritional therapy

    Total carbs: fruits, vegs, grains, legumes, low fat milk.
    Minimum ______ g/day.
    Carbs minimum 130 g/day
  46. Nutritional therapy 

    Fiber intake _____ g/day
    Fiber intake 25 - 30 g/day
  47. Nutritional therapy 
    Protein: ______ % total calories 
    No high protein diets
    Protein: 15 - 20% total calories
  48. Nutritional therapy
    Fat : _____ total calories 
    Dietary cholesterol: _____
    ______ servings fish/week
    • Fat: <7% total calories 
    • Dietary cholesterol: <200 mg/day 
    • >/= 2 servings of fish/week
  49. Nutritional therapy
    Alcohol limit ___ drink/day for women, ___ drink/day for men
    • Alcohol limit 1 drink/day for women 
    • Alcohol limit 2 drink/day for men
  50. Nutritional Therapy 
    Education
    Dietitian initially provides education 
    should include ____. 
    _____ method: helps patient visualize the amount of vegetable, starch, and meat that should fit a 9 inch plate.
    • Should include Family
    • Plate method
  51. Exercise
    _____ blood glucose during and after exercise. 
    Causes uptake of glucose by ______. 
    Improves insulin ______ and insulin _______. 

    lasts _____ hours.
    • Lowers blood glucose. 
    • Uptake of glucose by muscles. 
    • Improves insulin Utilization and insulin sensitivity
    • last 2 - 48 hours 
  52. Diabetic complications
    DKA: _______
    HHNS:________
    H:_________
    Morning H: ______
    • Diabetic ketoacidosis
    • Hyperosmolar Hyperglycemic NonKetotic Syndrome
    • Hypoglycemia 
    • Morning Hyperglycemia
  53. DKA is ____________.
    Most common in Type __ DM
    Type _ DM possible in overwhelming _____ or ____.
    • DKA is a Profound deficiency of insulin. 
    • Most common in Type 1 DM
    • Type 2 DM possible in overwhelming infection or stress.
  54. DKA: Precipitating Factors 

    Illness and _____. 
    Inadequate ____ dosage. 
    Undiagnosed _______. 
    _______ self management. 
    Neglect.
    • Illness and infection
    • Inadequate insulin dosage.
    • Undiagnosed Type 1 DM
    • Neglect.
  55. DKA: Pathophysiology 

    ______ circulating insulin, glucose not properly used for ______. 
    Body compensates breaks down ____ stores.
    _____: acidic by products of ____ break down. 
    _____ alters PH balance. 
    Patient goes into _____ acidosis. 
    ______ is _____ spilling into urine. 
    When ____ spill into urine ___ become depleted. 
    Insulin deficiency leads to impaired _____ synthesis. 
    Increased _____ degradation. 
    Increased _____ loss from tissues. 
    Increased production of glucose from ______ in liver leads to _________. 
    Due to insulin deficiency, blood glucose increases leading to _________. 
    Due to _______: Na, K, Cl, Mg, and Phos are _______. 
    Fluid volume is ________ (_________)
    Could lead to __________ shock, ____ failure, and death.
    • Decreased circulating insulin, glucose not properly used for energy
    • Body compensates breaks down Fat stores. 
    • Ketones: acidic by products of fat break down. 
    • Ketones alters PH balance. 
    • Patient goes into metabolic acidosis. 
    • Ketonuria is ketones spilling into urine. 
    • When ketones spill into urine electrolytes become depleted. 
    • Insulin deficiency leads to impaired protein synthesis. 
    • Increased protein degradation. 
    • Increased nitrogen loss from tissues. 
    • Increased production of glucose from amino acids in liver leads to hyperglycemia
    • Due to insulin deficiency, blood glucose increases leading to Osmotic diuresis
    • Due to osmotic diuresis: Na, K, Cl, Mg, and Phos serum levels are decreased
    • Fluid volume is decreased (hypervolemia)
    • Could lead to hypervolemic shock, renal failure, and death.
  56. DKA: clinical manifestations 

    ______ skin turgor.
    _____ mucous membranes.
    Tachycardia
    ________ hypotension
    Lethargy
    Soft ____ eyes
    Anorexia 
    _______ respirations
    ______ breath
    Nausea/______
    _____ pain (linked to accumulating acids) 
    Blood glucose >/=______
    Arterial blood PH < _______ (acidotic) 
    ______ in urine
    • Poor skin turgor
    • Dry mucous membranes
    • Tachycardia
    • Orthostatic hypotension 
    • Lethargy 
    • Soft sunken eyes
    • Anorexia 
    • Kussmaul respirations 
    • Acetone breath (fruity) 
    • Nausea/Vommiting 
    • Abdominal pain (linked to accumulating acids)
    • Blood glucose >/= 250
    • Arterial blood PH < 730
    • Ketones in urine
  57. DKA Treatment 

    _______: maintain tissue perfusion 
    ______ replacement 
    ______: reverses acidosis by inhibiting ___ breakdown. 
    Monitor: Vitals, Cardiac rhythm, __ levels, I&O:____ 
    Treat ____ if present
    O2
    IV: 0.9% or 0.45% NaCl solution until ___ stable and urine output ____ mL/hr
    When blood glucose reaches ______, begin 5% or 10% dextrose solution. 
    (Sudden drop in glucose causes _____)
    • Rehydration: maintain tissue perfusion
    • Electrolytes replacement 
    • Insulin: reverses acidosis by inhibiting fat breakdown. 
    • Monitor: vitals, cardiac rhythm, K+ levels, I&O: Kidneys 
    • O2: Oxygen 
    • IV: 0.9% or 0.45% NaCl solution until Blood pressure is stable and urine output 30 - 60 mL/hr 
    • When blood glucose reaches 250 mg/dL, begin 5% or 10% dextrose solution 
    • (sudden drop in glucose causes cerebral edema)
  58. DKA treatment: insulin 

    Crucial in restoring _______ balance and eliminating _______. 
    Standard rate ____ U/kg/hr
    Rate of insulin remains _____ while dextrose fluid ______ to achieve desired Serum glucose levels. 
    _______ and early identification. 
    Changes in mental status should ______. watch for ________. 
    _______ checks every 1 hour. 
    Monitor ______.
    • Crucial in restoring Acid-base balance and eliminating ketoacidosis
    • Standard rate o.1 U/kg/hr
    • Rate of insulin remains constant while dextrose fluid titrated to achieve desired serum glucose levels. 
    • Prevention and early identification
    • Changes in mental status should improve. Watch for cerebral edema. 
    • Neurological checks every 1 hour. 
    • Monitor respiration.
  59. Hyperosmolar hyperglycemic syndrome

    Type __ DM
    Age >___ years
    Less common than ____ 
    Produces enough insullin to prevent ____ but not enough to prevent 
    Severe _______
    Osmotic ______
    extracellular fluid ____
    • Type 2 DM 
    • Age > 60 years 
    • Less common than DKA 
    • Produces enough insulin to prevent DKA but not enough to prevent 
    • Severe hyperglycemia 
    • Osmotic diuresis 
    • extracellular fluid depletion
  60. HHS Causes 

    U--
    P-------
    S-----
    A---- I------
    Newly diagnosed Type - --
    • UTI
    • Pneumonia 
    • Sepsis 
    • Acute illness 
    • Newly diagnosed Type 2 DM 
  61. HHS clinical manifestations 

    Elevated _______: ____ mg/dL 
    _____ PH
    _____ of Ketones
    _____ of urine glucose 
    Abnormal levels of Na, K, CL caused by ______
    • Elevated Blood glucose: >600 mg/dL 
    • Normal pH
    • Absence of Ketones 
    • Presence of urine glucose 
    • Abnormal levels of Na, K, Cl caused by Osmotic diuresis
  62. HHS Treatment 

    Same as DKA except HHS requires greater _______ replacement.
    Greater fluid volume replacement 

    • DKA treatment: 
    • Maintain tissue perfusion 
    • Electrolyte replacement 
    • Insulin 
    • Oxygen 
    • IV therapy
  63. These symptoms are for DKA or HHS? 
    Common 
    Type 1 
    Precipitated by infection 
    Ketoacidosis 
    Short prodromal sympts 
    MOrtality 5 - 10% 
    Age 20 - 29
    DKA
  64. These symptoms are for DKA or HHS? 
    Uncommon
    Type 2 
    More severe illness 
    NOt ketoacidotic 
    Longer prodromal sympts 
    Mortality 40 - 60%
    Age 57 - 70
    HHS
  65. Hypoglycemia is too _____ glucose in blood stream. <___ mg/dL
    Hypoglycemia is too little glucose in blood stream. <70 mg/dL
  66. Hypoglycemia Pathophysiology: 
    Blood glucose decreases to _______
    _______ hormones are released
    Insulin production is ________
    Glucagon and epinephrine are ________
    • Blood glucose decreases to <70 mg/dL 
    • Counterregulatory hormones are released
    • Insulin production is decreased
    • Glucagon and epinephrine are increased 
  67. Hypoglycemia manifestations: 

    No ____ signs 
    Hypoglycemia reaches ______ point 
    Patient c________, i_____ or u_______.
    Autonomic neuropathy (problem with _____ secretion)
    • No warning signs 
    • Hypoglycemia reaches critical point 
    • Patient combative, incoherent or unconscious
    • Autonomic neuropathy (problem with epinephrine secretion)
  68. Rule of 15
    Eat/Drink ____ g of ____ carbs
    ___ oz soda, orange jice
    ___ life savers 
    ___ Tbs syrup/honey 
    ___ tsp jelly 
    Wait ___ minutes
    Check glucose 
    If blood glucose _____, repeat 
    If glucose ______, feed snack 
    _____ carb + protein
    • Eat/drink 15 g of quick carbs 
    • 4 - 6 oz soda, orange juice
    • 8 - 10 life savers 
    • 1 Tbs syrup/honey 
    • 4 tsp jelly 
    • wait 15 minutes 
    • If blood glucose <70 mg/dL, repeat 
    • If glucose >70 mg/dL, feed snack 
    • complex carb + protein
  69. Macrovascular diseases include: 

    ______vascular disease
    ______vascular disease 
    _____  vascular disease
    • Cerebrovascular disease 
    • Cardiovascular disease 
    • Peripheral vascular disease
  70. Macrovascular risk factors 

    S______
    O_____
    H_____
    H_____
    S_____
    Macrovascular risk factors 

    • Smoking 
    • Obesity 
    • Hypertension 
    • High fat intake 
    • Sedentary lifestyle
  71. Microvascular 

    Specific to ______ 
    ______ of vessel membranes in ______ and _______ in response to chronic _________. 
    ______pathy
    ______pathy
    ______pathy
    Microvascular: 

    • Specific to diabetes 
    • Thickening of vessel membranes in capillaries and arterioles in response to chronic hyperglycemia
    • Retinopathy (retina damage) 
    • Nephropathy 
    • Dermopathy
  72. Diabetic Retinopathy 

    Microvascular damage to _____ aas result of _________. 
    Classifications: 
    ___________
    ___________
    Diabetic retinopathy

    • Microvascular damage to retina as result of hyperglycemia
    • Classifications: 
    • nonproliferative
    • Proliferative 
  73. Nonproliferative Retinopathy

    Partial ______ of small blood vessels in _____. 
    __________ of capillary walls. 
    weak walls _____ fluid. 
    Retinal _______. 
    Intraretinal _______. 
    Visin affected if _____ involved.
    • Partial occlusion of small blood vessels in retina
    • microaneurysm of capillary walls. 
    • weak walls leak fluid. 
    • Retinal edema
    • Intraretinal hemorrhages 
    • Vision affected if macula involved.
  74. Proliferative Retinopathy

    Involves retina and _____. 
    Neovascularization.
    _____ occluded 
    Retinal _______.
    Proliferative Retinopathy 

    • Involves retina and vitreous 
    • Neovascularization 
    • Light occluded 
    • Retinal detachment.
  75. Retinopathy Treatment

    Blood glucose control
    P__________
    V_________
    Meds to supress Vascular ______ growth factor.
    Retinopathy Treatment 

    • Blood glucose control 
    • Photocoagulation 
    • Vitrectomy 
    • Meds to supress vascular growth factor
  76. Nephropathy

    Damage to small blood vessels of _____.

    (causes ______ to leak) 
    (_____ reduce risk of nephropathy)
    Damage to small blood vessels of Kidney. 

    • (causes protein to leak)
    • (Ace inhibitors reduce risk of Nephropathy)
  77. Nephropathy nursing interventions 

    S______
    __ control 
    Low _____/Low ____ diet 
    Education 
    H_______
    Renal _____
    • Symptomatic
    • BP control 
    • Low protein/ Low salt diet 
    • Education 
    • Hemodialysis 
    • Renal transplant 
  78. Diabetic Neuropathy 

    ________ r/t metabolic problems. 

    Calssifications: 
    S_______
    A______
    Diabetic Neuropathy 

    • Nerve damage r/t metabolic problems 
    • Classifications: 
    • Sensory 
    • Autonomic
  79. Sensory Neuropathy 

    ______ symmetric polyneuropathy.

    H____/F____
    S____ g_____ neuropathy. 
    Loss of or abnormla sensation 
    Pain 
    P______
    Ulcers 
    _____ gait
    Sensory Neuropathy 

    • Distal symmetric neuropathy 
    • Hands/Feet
    • Stocking glove neuropathy 
    • Loss of or abnormal sensation 
    • Pain 
    • Parasthesia 
    • Ulcers 
    • Unbalanced gait (walking on clouds/pillows)
  80. Autonomic Neuropathy 

    Damage to _____ of small blood vessels and _____ glands in skin, ___ system, ___ tract, and adrenergic system.
    Autonomic Neuropathy 

    Damage to nerves of small blood vessels and sweat glands in skin, CV system, GI tract, and adrenergic system.
  81. Autonomic Neuropathy Manifestations 

    Cardiovascular 
    _____ hypotension
    Resting _______
    Painless ____ 

    GI
    G______ (____ gastric emptying)
    GU
    ______ bladder (lose ____ in bladder) 
    Urinary ______ 
    ____ stream.
    • Autonomic Neuropathy Manifestations 
    • Cardiovascular 
    • Postural hypotension 
    • Resting tachycardia 
    • Painless MI 

    • GI
    • Gastroparesis (delayed gastric emptying) 
    • GU
    • Neurogenic bladder 
    • (lose sensation in bladder) 
    • Urinary retention 
    • Weak stream
  82. Diabetes complications of lower extremities

    A________.
    U________.

    Risk factors: 
    _____ neuropathy 
    PAD (Peripheral ______  _____)
    C_______ abnormalities
    S_______
    I_____ I______ system
    Diabetes complications of lower extremities 

    • Amputations 
    • Ulceration 


    • Risk Factors: 
    • Sensory neuropathy 
    • PAD (peripheral artery disease
    • Clotting abnormalities
    • Smoking 
    • Impaired immune system

Card Set Information

Author:
geoerguera
ID:
324058
Filename:
Diabetes
Updated:
2016-10-08 16:09:07
Tags:
Diabetes
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Description:
Diabetes exam
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