Level I W2013

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amelia.m.norton
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199232
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Level I W2013
Updated:
2013-02-17 19:40:44
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Diabetes
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Diabetes, Level I
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  1. Diabetes Insipidus
    disorder of the posterior love of the pituitary gland and excretion of large volumes of dilute urine
  2. Islets of Langerhans
    tiny, irregular structures distributed throughout the pancreas and comprising its endocrine portion
  3. Ketoacidosis
    accumulation of ketones in the blood, associated with uncontrolled diabetes and resulting in metabolic acidosis
  4. Metabolic Syndrome
    group of abnormalities (including high levels of glucose and triglycerides) associated with an increased risk of type 2 diabetes and coronary heart disease
  5. Microalbuminuria
    early sign of renal disease involving the presence of albumin in the urine in amounts greater than expected but too low to be detected by dipstick testing
  6. Nephropathy
    long-term complication of diabetes that involves damage to the cells of the kidneys and eventually leads to end-stage renal disease
  7. Neuropathy
    any of numerous disturbances or pathologic changes int he peripheral nervous system, most often affecting sensation, and often a long-term complication of diabetes
  8. Non-sulfonylurea secretagogue
    type of oral anti-diabetic agent that stimulates insulin release; glinide
  9. Polydipsia
    excessive thirst and fluid intake
  10. Polyphagia
    excessive hunger
  11. Polyuria
    excretion of abnormally large amounts of urine
  12. Sulfonylurea
    • type of oral antidiabetic agent that stimulates insulin release
    • glipizide/glucotrol
    • glyburide/micronase, diabeta, glynase
    • glimepiride/amaryl
    • increase insulin production from pancreas & sensitivity at receptor sites
    • may decrease hepatic glucose production
  13. Thiazolidinedione
    type of oral antidiabetic agent that reduces insulin resistance
  14. Type I diabetes
    • disorder involving the complete destruction of the insulin-producing beta cells in the pancreas and resulting in a lifelong need for daily insulin replacement therapy
    • less than 30yrs at onset
    • non-obese
  15. Type 2 diabetes
    disorder involving insulin resistance and impaired insulin secretion and resulting in the need for therapy that includes diet, exercise, oral medications, and possibly injectable medications
  16. Rapid acting insulin
    • Humalog (lispro)
    • NovoLog (aspart)
    • Glulisine (apidra)
    • Onset: 10-30 min, <15min
    • Peak: 30 min - 3 hr, 1-2hr
    • Duration: 3-5hr, 3-4hr
  17. Short acting insulin
    • Humulin R
    • Novolin R
    • Onset: 30-60 min
    • Peak: 1-5 hr, 2-4hr
    • Duration: up to 10hr, 6-8hr
    • IV or subQ
    • inject 30-45 min ac
  18. Alpha Cells of Pancreas
    secrete glucagon
  19. Beta Cells of Pancreas
    secrete insulin
  20. Diabetes & Pancreas
    Endocrine functions
  21. Insulin
    • anabolic hormone-beta cells
    • Islet of Langerhans
    • promotes glucose transport from the bloodstream to the cytoplasm of cell
    • inhibits gluconeogenesis
    • facilitates glycogenesis
    • increases transport of aa into cells & their synthesis into protein (healing)
  22. Basal rate of Insulin
    continuously released into the bloodstream in small increments
  23. Bolus of Insulin
    increased release after food ingestion
  24. Stable glucose
    70-140mg/dL
  25. Fasting glucose
    70-109mg/dL
  26. Insulin resistant
    when taking more than 100 units of insulin at one time
  27. Directly Insulin dependent tissue
    skeletal muscle and adipose tissue
  28. Gluconeogenesis
    the synthesis of glucose from molecules that are not carbohydrates, such as amino and fatty acids.
  29. Glycogenesis
    the conversion of glucose to glycogen for storage in the liver
  30. Counter-regulatory hormones to Insulin
    • glucagon, epinephrine, growth hormone, cortisol
    • opposes the effects of insulin
    • increase blood glucose levels
    • provide a regulated release of glucose for energy
    • help maintain normal blood glucose levels
  31. Diabetes Mellitus
    • chronic metabolic disease resulting in hyperglycemia from
    • -abnormal insulin production (decreased/absent)
    • -impaired insulin utilization (insulin resistance)
    • -or both
  32. Diabetes Mellitus Types
    • Type I (5-10%)
    • Type II (90%)
    • Gestational @ 28 weeks
    • Pre-diabetes
    • Secondary diabetes
  33. Diabetes Mellitus complications
    • end stage renal disease
    • adult blindness
    • non-traumatic lower limb amputation
    • heart disease
    • stroke
    • 75% w/ diabetes have hypertension
    • neuropathy
  34. Diabetes Type I causes/risk factors
    • Genetic: genetic susceptibility for antibody production; related to human-leukocyte antigen
    • Autoimmune
    • Environmental: virus, toxins
    • All causes result in beta cell destruction
  35. Type I Diabetes Patho
    • progressive destruction of pancreatic beta cells by the body's own T-cells
    • Auto-antibodies reduce normal beta cell function 80-90% before symptoms occur
  36. Clinical manifestations Type I
    • recent/sudden weight loss
    • weakness
    • fatigue/irritability
    • polyphagia
    • polydipsia
    • polyuria
  37. Type I why s/s occur
    BG becomes hypertonic -> body attempts to dilute w/ fluid from intracellular space -> extracellular space floods increasing blood volume -> polyuria -> cellular dehydration triggers polydipsia -> starving cells trigger polyphagia and weight loss
  38. Diabetic Ketoacidosis Characteristics
    • type of metabolic acidosis
    • Absence/deficiency of insulin
    • -hyperglycemia
    • -ketosis (fat breakdown ketones) ACETONE (fruity smell)
    • -acidosis
    • -dehydration
  39. DKA Causes
    • undiagnosed type I diabetes
    • illness
    • infection
    • inadequate insulin dosage
    • poor self management
    • neglect
  40. DKA clinical Presentation
    • Early: lethargy/weakness, N/V, fruity breath odor
    • As dehydration occurs: poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension, abdominal pain
    • Late: Kussmaul breathing (rapid/deep)
    • Possible sodium/potassium loss
  41. DKA lab findings
    • Glucose: >250mg/dL
    • pH: <7.30 ABG
    • Serum HCO3-: <15mEq/L
    • Ketones in blood and urine
  42. Insulin Therapy
    Action
    Therapeutic Effect
    • Action: lowers blood glucose by stimulating glucose uptake in skeletal muscle and fat, inhibiting hepatic glucose production
    • Therapeutic effect: control of glucose in diabetic patients
  43. Nursing Implications for Insulin Therapy
    • onset, peak, duration
    • dosing instructions
    • s/s of hypoglycemia
    • injection sties
    • which insulins can & can't be mixed
    • standards of practice-2nd nurse double check
    • Regular insulin only one as IV
  44. Intermediate-acting (cloudy)
    • NPH (Humulin N; Nobolin N; ReliOn N)
    • Lente
    • Onset: 2-4hr
    • Peak: 4-10hr
    • Duration: 10-16hr
  45. Long-Acting (clear)
    • Glargine (Lantus)
    • Onset: 3-4hr
    • Peak: none
    • Duration: 24hr
    • Detemir (Levemir)
    • Onset: 3-4hr
    • Peak: 3-14hr
    • Duration: 6-24hr
  46. Combination INsulin Therapy
    • NPH/Regular: 70/30, 50/50
    • Lispro protamine/lispro 75/25
    • Aspart protamin/aspart 70/30
  47. Insulin Site absorption
    • fastest/steadiest
    • Abdomen
    • arm
    • thigh
    • buttock
  48. Somogyi effect
    • rebound effect in which an overdose of insulin induces hypoglycemia
    • monitor BG between 2am & 4am
    • Counter regulatory hormones with bounce it back toward hyperglycemia and ketosis
    • night sweats-nightmares
    • trtmt: less insulin
  49. Dawn Phenomenon
    • hyperglycemia on awakening in mroning due to release of counter
    • regulatory hormones in predawn hours
    • monitor BG between 2 & 4am
    • trtmt: insulin timing or more insulin
  50. Sliding Scale + Formula
    • 1 unit Humalog for every 10points of BG over 120
    • 1 unit of Humalog insulin for every 5grams of carbs
  51. Hypoglycemia mild symptoms
    • palpitations/tachycardia
    • irritability/nervousness
    • diaphoresis
    • tremors
    • hunger
    • weakness
  52. Hypoglycemia
    • BG <70mg/dL
    • Dependent upon patient's 'normal'
    • too much insulin and not enough glucose in the blood
  53. Hypoglycemia moderate symptoms
    • difficulty concentrating
    • headache
    • lightheadedness
    • confusion/memory lapse
    • numbness of tongue/lips
    • slurred speech
    • emotional changes
    • irritable/combative
    • double vision
    • drowsiness
  54. Hypoglycemia severe symptoms
    • disorientation
    • difficulty arousing
    • loss of consciousness
    • seizures
  55. Meds/drugs to predispose to Hypoglycemia
    • aspirin ASA
    • ETOH alcohol
    • sulfonamides
    • oral contraceptives
    • monoamine oxidase inhibiitors
    • opiates
    • street drugs that increase metabolic rate
  56. Conscious trtmt of Hypoglycemia
    • -gm quick acting carb
    • 4-6 oz Oj/grape juice
    • soda, honey or syrup
    • Recheck in 15min. continue if need be
  57. Unconscious trtmt of Hypoglycemia
    • SQ/IM injection 1mg glucagon
    • IV admin 20-50mL 50% glucose
  58. Type 2 Diabetes
    • most common form of diabetes
    • non-insulin dependent
    • slow, gradual onset, hyperglycemia may go undetected
    • Phase of hyperinsulinemia
    • decreased prod of insulin & insulin resistance
  59. Risk factors Type 2
    • age
    • genetics
    • ethnicity
    • environmental: obesity, physical inactivity, drugs/toxic agents
    • central obesity
    • high blood pressure
    • high triglycerides
    • low HDL cholesterol
    • Insulin resistance
  60. Pathogenesis of type 2
    • beta cells produce insulin but body is unable to use effectively because cells of body are resistant to action of insulin
    • BG rises
    • Pancreas puts out more insulin that cant be used
    • pt is hyperglycemic & hyperinsulinemic
    • pancreas becomes exausted
  61. Pathophysiology of type 2
    • 4 major metabolic abnormalities
    • -insulin resistance
    • -pancreas decreased ability to produce insulin
    • -increased glucose production from liver
    • -alteration in production of hormones and fatty acids
  62. Clinical manifestations Type II
    • non-specific symptoms
    • polydipsia
    • polyuria
    • recurrent infections
    • recurrent vaginal yeast/monilla infections
    • H/A
    • weakness/fatigue
    • blurred vision
  63. Pre-diabetes
    • impaired fasting glucose, impaired glucose tolerance
    • risk for Type 2 within 10 years
    • not symptomatic but has damage
  64. Gestational Diabetes
    • during pregnancy of mother
    • is insulin resistance problem
    • no insulin from mom but gets BG level from mom causing hyperinsulinemia in baby developing large fat growth/deposition
    • may become hypoglycemic after birth
  65. Etiology of Secondary Diabetes
    • trtmts that cause abnormal BG
    • corticosteroids (prednisone)
    • thiazides
    • phenytoin (dilantin)
    • atypical antipsychotics (clozapine)
    • admin of total parenteral nutrition in IV central line
    • resolves after underlying condition treated
  66. Medical conditions that cause Secondary Diabetes
    • cushings
    • hyperthyroidism
    • pancreatitis
    • parenteral nutrition
    • cystic fibrosis
    • hemachromatosis
  67. Recognition of Type II
    • 2 results of fasting >126
    • random plasma BG >200
    • 2 hour OGTT >200
    • A1C >6.5%
  68. Recognition of PreDiabetes
    • Fasting BG 110-125
    • 2 hr OGTT 140-199
  69. Pre-Diabetes
    • Impaired fasting glucose
    • Impaired glucose tolerance
  70. Diabetes Interventions
    • Airway/Breathing
    • monitor BG
    • monitor urine-ketones, I&O
    • IV therapy
    • Insulin therapy
    • Electrolyte replacement
    • watch for hypoglycemic episodes
    • assess renal status
    • assess healing
  71. Oral Drug therapy for diabetes
    • works in 3 ways
    • insulin resistance
    • decreased insulin production
    • increased hepatic glucose production
  72. Most common OA for diabetes
    • Biguanides(metformin/glucophage)
    • reduce glucose production by liver & enhances insulin sensitivity to improve glucose transport in cells
  73. OA alpha-glucosidase inhibitors
    • acarbose/precose
    • miglitol/glyset
    • starch blocker
    • eat at meal, lowers postprandial BG by slowing absorption of starch in small intestines
  74. OA thiazolidinediones
    • pioglitazone/actos
    • rosiglitazone/avandia
    • insulin sensitizer
    • insulin sensitivity, transport, utilization
    • improve lipid levels/BP levels
    • not for CHG patients due to edema possibility
  75. Macrovascular disease
    • cerebrovascular/stroke
    • cardiovascular/MI
    • peripheral vascular/pain-cramping when walking
  76. Risk factors for Macrovascular
    • diabetes
    • genetics
    • obesity
    • smoking
    • hypertension
    • high fat intake
    • sedentary lifestyle
  77. Microvascular disease
    • specific to diabetes
    • chronic hyperglycemia
    • 10-20yr clinical manifestation
    • process through which very small branches of arteries and capillaries throughout body become damaged
    • thickening of vessel membranes in capillaries and arterioles
    • thickening results in occlusion of vessels and impairment of blood flow
  78. Microvascular causes
    • retinopathy
    • nephropathy
    • dermopathy-neuropathy
  79. Retinopathy
    damage to tiny blood vessels that nourish retina, tissue at back of your eye
  80. Mild retinopathy
    earliest stage, micro-aneurysms occur due to partial occlusions in small blood vessels, creating pressure
  81. Moderate retinopathy
    blood vessels that nourish the retina are blocked
  82. severe retinopathy
    many vessels blocked, depriving several areas of retina, body signals for new growth around areas
  83. Proliferative Retinopathy
    new blood vessels are abnormal and fragile
  84. Vision changes
    BG causes vitreous fluid shift, changing eye shape
  85. Nephropathy
    • damage to small blood vessels that supply glomeruli of kidney
    • leading cause of kidney failure & end stage renal disease
  86. Risk factors for Nephropathy
    • hypertension
    • genetic predisposition
    • smoking
    • chronic hyperglycemia
  87. Nephrotic Syndrome
    • increased glomerular permeability for protein
    • -edema, massive proteinuria, HTN, hypoalbuminemia; hyperlipidemia, increased triglycerides, compromised immune response, hypercoagulability-clot too much
    • Treatment: Ace inhibitors, decrease salt and protein diet d/t hypervolemia, diuretics, NSAIDS
  88. Hyperlipidemia
    • liver sees decreased protein so over synthesis of lipoproteins LDL, VLDL
    • decreased oncotic pressure- edema
  89. Neuropathy
    damage to peripheral nerves, sensory & autonomic
  90. Characteristics of Sensory Neuropathy
    • loss of protective sensation
    • abnormal sensation
    • pain
    • parasthesias
  91. Long term complications of DM
    • loss of sensitivity touch & temp
    • deformities - atrophy of hands and feet
    • foot injury
    • ulcerations
    • amputations
  92. Neuropathy Treatment
    • Prevention-tight glucose control
    • medication therapy-gabapentin
    • topical creams
    • tricyclic antidepressants: not used much anymore: metabolic acidosis
    • Selective serotonin & norepinephrine reuptake inhibitors-cymbalta
  93. Autonomic Neuropathy
    damage to the nerves that regulate the body functions  that you can't control, including the nerves that regulate your heart rate, BP, perspiration & digestion, among other functions
  94. Complications of autonomic neuropathy
    • hypoglycemic unawareness
    • bowel incontinenece=diarrhea
    • neurogenic bladder=urinary retention
    • Gastroparesis-triggers hypoglycemia delaying food absorption: anorexia, N/V, gastroesophageal reflux, feelings of fullness
    • Treatment with Reglan
    • Cardiovascular: postural HTN, resting tachycardia, painless MI
    • Sexual function
  95. FOOT COMPLICATIONS
    • peripheral arterial disease
    • sensory neuropathy
    • Examine DAILY
  96. ND for DM
    • Ineffective tissue perfusion (peripheral)
    • Impaired skin integrity
    • Impaired Adjustment (chronic disease)
  97. Infection & DM
    • greater chance of infection: defect in mobilization of inflammatory cells & impairment of phagocytosis by neutrophils and monocytes
    • circulation impaired -> slows neutrophils to site & to lymph once phagocytized
  98. Prevention of Complications in DM
    • health promotion & maintenance
    • identification
    • monitoring
    • education: self-monitoring, diet/exercise, S/S & trtmt of hyper/hypoglycemia
  99. Diabetic Diet
    • control BG
    • prevent extremes
    • consistent intake
    • AVOID high/low
    • 45-65% Carbs
    • max 20% fats
  100. Osmotic Diuresis
    blood hypertonic pulls H2O from cells -> increases blood volume -> increases perfusion to kidneys

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