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2010-03-09 16:43:26

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  1. · Insulin producing beta cells in the pancreas are destroyed by an autoimmune process
    · Requires insulin because little or no insulin is produced by body
    · Onset is acute and usually occurs before age 30
    · 5% to 10% of diabetes population is Type 1
    Type 1 DM
  2. · Decreased sensitivity to insulin (insulin resistance) and impaired beta bell function results in decreased insulin production
    · 90% to 95% of diabetic population
    · More common in persons over age 30 and obese
    · Slow, progressive glucose intolerance
    Type 2 DM
  3. · Groups of diseases characterized by increase in glucose resulting from defects in insulin secretion, insulin action or both
    · 20.8 million people
    · 3rd leading cause of death by disease (usually due to CV effects)
    · Leading cause of blindness among 20-74 years
    · Leading cause of nontraumatic amputations
    · Cost are estimated to be $100 million annually
  4. · Three P’s
    · Fatigue, weakness, vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, and recurrent infections
    · Type 1 may have sudden weight loss, nausea, vomiting and abdominal pain if DKA has developed
    · Type 2 present with a history of weight gain
  5. · Lack of insulin, absence of insulin or insulin resistance sets off a chain of problems
    -Type 1 – lack of insulin
    -Type 2 – not enough insulin
    · Insulin cannot be used properly
    · Glucose remains in the bloodstream because insulin cannot transport glucose into cells for use as energy
    · Chain reaction
    ->Hyperglycemia -> produces osmotic effect and leads to…
    -Fluid and electrolyte imbalance
    -Three P’s
    -Fat and protein breakdown -> Type 1 -> Ketoacidosis problems (ketones spill over into urine: can also find glucose, protein)
    Patho of DM
  6. · Polyuria
    · Polydipia
    · Polyphagia
    · Weight loss
    · Fatigue
    · Increase frequency of infections
    · Rapid onset
    · Insulin dependent
    · Early onset
    S/S of Type 1 DM
  7. · Sedentary lifestyle
    · Familial tendency
    · Average age 50 years
    · History of increase BP
    · Fatigue
    · Decrease energy
    · Recurrent infections
    S/S of Type 2 DM
  8. · Symptoms and casual plasma glucose concentration = greater or equal to 200 mg/dl (> 1 test)
    · Fasting plasma glucose (FPG) = greater than or equal to 126 mg/dl (> 1 test)
    · 2 hr postload glucose = greater than or equal 200 mg/dl
    Diagnostic findings for DM
  9. · HbA1C (A1C)
    · Amount of glucose stored in hemoglobin
    · 4% to 7%
    · 7% = BGL 150 mg/dl
    Glycosylated hemoglobin
  10. · High carb/high fiber plays role in lowering total cholesterol
    · Alcoholism in moderation
    -Because of the potential for alcohol-induced hypoglycemia, the client is instructed to ingest alcohol only with or shortly after meals.
    · Sweeteners acceptable
    -Sweeteners-acceptable for patients with diabetes
    -Nutritive (contain calories) and nonnutritive (no calories)

    · Glycemic control and carb count
    · Fibers helps to bring down high glycemic index
    · Orange high in fiber
    Alcohol, fiber, sweeteners
  11. · Protein 10% to 20%
    · Fats 20% to 30%
    -Fats can aggregate and affect the long term complications
    · Carbohydrates 50% to 60%
    Caloric distributions
  12. · Carb count
    -Carbohydrate counting- provides flexibility in food choices, and allows more accurate management with multiple daily injections. Know allowances for each meal.
    · Exchange lists
    -6 main exchange lists
    o Foods included on one list contain = numbers of calories and @ = in grams of protein, fat and CHO
    o See page 1159 table 41-2 for sample
    · Food guide pyramidFood Guide Pyramid- used only as a first step teaching tool for pts to learn how to control food portions and how to identify foods containing CHO, Protein, and fat
    Meal planning
  13. · Describes how much food increases blood glucose
    · Combining starchy food with protein and fat containing food slows absorption and glycemic response
    · Raw or whole foods tend to have lower response than cooked, chopped or pureed foods
    · Eating whole fruits rather than juices decreases the glycemic response due to fiber slowing absorption
    · Adding food with sugars may produce lower response if eaten with foods that are more slowly absorbed
    Glycemic index
  14. · Benefits
    o Increase uptake of glucose by muscles
    o Lower BGL by increasing uptake of glucose by body muscles
    o Decrease amount of insulin needed
    o Reduce cardiovascular risk factors – exercise alters body lipids, decreasing total cholesterol

    · Precautions/recommendations
    o BGL of 250 mg or > with ketones – check with MD before exercise
    o 15 gram carb snack with protein – people who requires insulin should be taught to eat a 15 gram CHO exchange to prevent unexpected hypoglycemia (the decrease in circulating insulin that normally occurs with exercise cannot occur in patients treated with insulin)
    o Exercise at same time when BGL are at their peak
    o Proper footwear – poor circulation
  15. · ½ cup of fruit juice
    · 1 cup of milk
    · 1 TBS sugar
    · ½ cup regular soda
    · 5 lifesavers
    · 3-4 glucose tablets
    15 gram carb
  16. · Insulin or oral medications as usual
    · Frequent blood sugar monitoring – stress causes blood sugar levels to rise
    · Frequent small meals
    · Liquids every ½ to 1 hour
    · Report N/V/D
    Sick day rules
  17. · SMBG – self monitoring of blood glucose
    · Frequency
    o Insulin 2-4 times daily (usually before meals (ac) and at bedtime (hs)
    o Insulin before each meal = 3 times daily before each meal to determine insulin amount (sliding scale)
    o No insulin = 2-3 times a week when hypo or hyperglycemia is expected
    · Wash hands
    · Warm hands – increase blood flow
    · Lower hand – increase blood flowPuncture side of finger pad
    Monitoring glucose levels
  18. · Insulin
    o Insulin regimens for type 1 try to duplicate the normal release pattern of insulin from the pancreas. Normal patter page 1166 table 41-4 (when blood glucose levels rise after a meal insulin release is increased and continues at slow steady rate between meals).
    · Oral antidiabetic agents
    o Oral antidiabetic agents are used with type 2 diabetic pts who don’t have blood glucose control with dietary and exercise modification
    Pharmacological therapy
  19. · Rapid acting
    o Humalog – peak 1 hour
    o Novalog – peak 40 – 50 min
    o At risk for hypoglycemia: cool and clammy -> they need candy
    o Blood sugar needed for brain function -> explains neuro changes
    · Short acting (regular)
    o Novolin R – 2 – 3 hours
    · Intermediate acting (NPH)
    o NPH – peak 4 – 14 hours
    · Long acting
    · Very long acting
    · Page 1398 Table 41-3***
    Categories of insulin
  20. · Vials not in use should be refrigerated
    · Extreme temps avoided
    · Insulin in use should be in room temp up to 4 weeks
    · Mix cloudy insulin – intermediate and long acting
    · Extra dose available
    Storing insulin
  21. · Standard insulin administration involves subcutaneous injections with syringes marked in insulin units. Syringes are manufactured in .25, .3, .5, and 1 ml capacity
    · Needle size is .5 inches long
  22. "Clear before cloudy"
    · Mix intermediate acting
    · Inject air into intermediate acting (NPH)
    · Infect air into regular acting
    · Remove amount from regular acting
    · Remove amount from intermediate acting (NPH)
    · Given with 5 minute
    Mixing insulin
  23. BGL Insulin dose
    80 – 150 None
    151 – 200 5 units
    201 – 250 10 units
    251 – 300 15 units
    301 – 350 20 units
    >350 Notify MD
    Sliding scale usually with short/rapid acting
  24. · Self care issues
    o Give up control
    o Re educate
    o Demonstrate and re demonstrate
    o Hygiene especially important with bedridden patients
    · Hyperglycemia
    o Change in treatment regimen (time of meals and insulin, decrease activity)
    o IV fluids (D5W)
    o Mismatch timing of meals and insulin
    · Hypoglycemia
    o Lack of dosage change with dietary intake is changed
    o Delay in meal after administration of insulin
    o Overuse of sliding scale
    · NPO (procedure or surgery)
    o Not OK to skip insulin dose with type 1 b/c may lead to DKA
    o Might be OK to skip with type 2 because there is some production of insulin
    · Clear liquids (gelatin and juice)
    o Have more simple CHO which contribute to rapid rise in glucose
    Hospitalized DM
  25. · Intrasite rotation
    · To prevent inadequate absorption = lipodystrophy
    Injection sites
  26. o Progressive rise in BGL from bedtime to am
    o ***Increase evening dose of intermediate of long-acting insulin
    Insulin waning
  27. o relatively normal BGL until 3am when they begin to rise due to surge in growth hormone secretion)
    o Rise in BGL at 3 am
    o ***Change time of intermediate-acting insulin from dinner to bedtime
    Dawn phenomenon
  28. o Decrease at 3 am
    o normal or elevated BGL at bedtime, decrease at 2 -3 am followed by a rebound hyperglycemia
    o ***Decrease evening intermediate-acting insulin or increase bedtime snack
    Somogyi effect
  29. · Effective for Type 2
    · Not used during pregnancy
    · Sulfonylureas
    · Biguanidea
    · Alpha glucosidase inhibitors
    · Thiazolidinediones
    · Meglitinides
    · Page 1499 table 41-6
    Oral antidiabetic agents
  30. · Used for patients with type 2 diabetes who cannot be treated with diet and exercise alone
    · Combinations of oral drugs may be used
    · Major side effects: hypoglycemia
    · Nursing interventions: monitor blood glucose and assess for hypoglycemia and the potential side effects
    · Patient teaching
    Oral antidiabetic agents
  31. · Cardiovascular complications
    o CAD
    o Cerebrovascular disease
    o Peripheral vascular disease
    · Retinopathy
    · Nephropathy
    · Neuropathy
    Long term complications
  32. · Atherosclerosis
    o Coronary artery
    o Cerebrovascular disease
    o Peripheral vascular
    · Management
    o Diet and exercise
    o HTN
    o Smoking
    o BGL
    Cardiovascular disease
  33. Deterioration of small blood vessels that nourish the retina
    Leading cause of blindness in 20-74 yrs
    Occurs in Type 1 and 2
    Other visual complications:
    o Cataracts
    o Lens changes
    o Extraocular muscle palsy
    o Glaucoma
  34. Increase BGL
    filtration mechanism is stressed
    increased pressure
  35. · Peripheral
    o Sensation changes in feet and hands
    o Proprioception
    · Autonomic
    o Orthostatic hypotension
    o Delayed gastric emptying
    o Urinary retention
    o Diminished symptoms of hypoglycemia
    o Decrease sweating of hand and feet
    o Sexual dysfunction
  36. · Factors contributing include:
    o Neuropathy
    o Peripheral vascular disease
    o Immunocompromised
    · Sequence of events
    Soft tissue injury -> formation of callus -> infection -> amputation
    Foot infections
  37. Keep BGL within normal range
    Inspect feet daily
    Wash and dry feet
    Closed toe shoes
    Trimming toe nails
    Do not smoke
    Do not cross legs
    Foot care
  38. · Hypoglycemia
    · Hyperglycemia
    · Diabetic Ketoacidosis
    · Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)
    Acute complications
  39. · Diet should always be considered as nursing consideration!!
    · Insulin – know fast/slow acting, intermittent and actions
    · Oral hypoglycemic agents
    · Exercise
    Treatment for DM
  40. · Leads to unrecognized hypoglycemia
    · Patient does not recognize fight flight situation
    Autonomic nervous damage
  41. · Classified as beta blocker used for heart problems
  42. Med that hides/mask S/S of hypoglycemia: Inderal (Propranolol)
  43. · Abnormally low blood glucose level (below 50 to 60 mg/dL)
    · Causes include too much insulin or oral hypoglycemic agents, too little food, and excessive physical activity
  44. o Adrenergic symptoms: sweating, tremors, tachycardia, palpitations, nervousness, and hunger, cool and clammy skin
    o Central nervous system symptoms: inability to concentrate, headache, confusion, memory lapses, slurred speech, numbness of lips and tongue, irrational or combative behavior, double vision, and drowsiness
    o Severe hypoglycemia may cause disorientation, seizures, and loss of consciousness
    S/S of hypoglycemia
  45. · MD ordered
    · Administered IM/SubQ to reverse severe hypoglycemia (>50 and unconscious) in home setting
    · Followed by FSBS
    Glucagon (Tx for hypoglycemia)
  46. · IV push for severe hypoglycemia (>50 and unconscious) in hospital setting
    · Irritating to vein
    · Followed by FSBS
    50% Dextrose (Tx for hypoglycemia)
  47. · Onset is abrupt and may be unexpected
    · Symptoms vary from person to person
    · Symptoms also vary related to the rapid decrease in blood glucose and usual blood glucose range
    · Decreased adrenergic response may affect symptoms in persons who have had diabetes for many years probably related to autonomic neuropathy
    Assessment of hypoglycemia
  48. · Treatment must be immediate
    · Give 15 g of fast-acting, concentrated carbohydrate
    o 3 or 4 glucose tablets
    o 4 to 6 ounces of juice or regular soda (not diet soda)
    o 6 to 10 hard candies
    o 2 to 3 teaspoons of honey
    · Retest blood glucose in 15 minutes, retreat if <70 mg/dL or if symptoms persist more than 10 to 15 minutes and testing is not possible
    · Provide a snack with protein and carbohydrate unless the patient plans to eat a meal within 30 to 60 minutes
    Mangement of hypoglycemia
  49. · If the patient cannot swallow or is unconscious:
    o Subcutaneous or intramuscular glucagon 1 mg
    o 25 to 50 mL 50% dextrose solution IV
    Emergency measures for hypoglycemia
  50. o SNS – as BGL fall, the SNS is stimulated resulting in a surge of epinephrine and norephinephrine causings symptoms such as sweating, tachycardia, palpitations, nervousness, hunger
    o CNS - As BGL falls, the brain cells are deprived of needed fuel for functioning causing symptoms inability to concentrate, headache, lightheadiness, confusion, memory lapses, numbness of lips and tongue, slurred speech
    S/S of hypoglycemia
  51. · BGL less than 50 to 60
    · Causes
    o Too much insulin
    o Too much OHA
    o Too little food
    o Excessive physical activity
    o Delay of snacks or meals
    o Peak action of insulin
    Occurs before meals
  52. · Caused by an absence of or inadequate amount of insulin resulting in abnormal metabolism of carbohydrate, protein, and fat
    · Clinical features
    o Hyperglycemia
    o Dehydration
    o Acidosis
  53. · Manifestations include polyuria, polydipsia, blurred vision, weakness, headache, anorexia, abdominal pain, nausea, vomiting, acetone breath, hyperventilation with Kussmaul respirations, and mental status changes
    S/S of DKA
  54. · 15 gm CHO
    · 3-4 Glucose tablets
    · ½ cup fruit juice
    · 6 to 10 life savers
    · 2 to 3 tsp sugar/honey
    Management of hypoglycemia
  55. · Sick day rules
    · Decrease stress
    · Change or decrease intermediate acting insulin
    · Exercise
    · Smaller portions
  56. · Caused by absence or markedly inadequate amount of insulin. Seen more commonly in type 1.
    · Clinical features
    o Hyperglycemia - Without insulin the amt of glucose entering the cells is reduced and the liver increases glucose production which in turn lead to hyperglycemia (>300)
    o Dehydration and electrolyte loss - In the attempt to rid the body of excess glucose the kidneys excrete glucose along with water and electrolytes (sodium, potassium and chloride) this leads to excessive urination which in turn leads to dehydration and electrolyte loss
    § Potassium levels much be monitored. In early DKA, K level may be elevated but in time will decrease so K will be ordered IV.
    o Acidosis - Lack of insulin also leads to breakdown of fat because the body is trying to get energy. This breakdown leads to increased ketone bodies (ketone bodies are acids) which in turn leads to metabolic acidosis (increase acidity in blood due to accumulation of acids)
    · Causes (DKA is Type 1)
    o Decreased or missed insulin dose
    o Illness or infection
    o Untreated diabetes
  57. · Manifestations include polyuria, polydipsia, blurred vision, weakness, headache, anorexia, abdominal pain, nausea, vomiting, acetone breath, hyperventilation with Kussmaul respirations, and mental status changes
    S/S of DKA
  58. · Blood glucose levels vary between 300 to 800 mg/ dL
    · Severity of DKA is not related to blood glucose levelq
    · Ketoacidosis is reflected in low serum bicarbonate and low pH; low PCO2 reflects respiratory compensation
    · Ketone bodies in blood and urine ketonemia/ketouria
    · Electrolytes vary according to water loss and level of hydration
    Assessment of DKA
  59. · Hydration - Pts can loose up to 6.5 liters of fluid and therefore need 6-10 liters of IV fluids
    o Initially Normal Saline is administered rapidly-.2 to 1 liter per hour for 2-3 hrs
    o When glucose levels reach 250 - 300, changed to D5W to prevent fast decline of glucose
    o 0.9% Sodium Chloride and after patient starts to get better 0.45% Sodium Chloride
    · Insulin—IV insulin has a much shorter duration of action than subcutaneous insulin so if infusion is stopped , hyperglycemia will develop rapidly
    o Regular insulin can only be given IV
    o Acidosis that occurs in DKA is reversed with Insulin
    o Is usually infused IV at slow rate
    o BGL hourly
    · Electrolyte replacement
    o Major electrolyte of concern is K+
    o Replacement of K+ in order to avoid dysrhythmias that occur with hypokalemia
    Management of DKA "HI-E"
  60. · Rehydration with IV fluid
    · IV continuous infusion of regular insulin
    · Reverse acidosis and restoration of electrolyte balance
    · Note: rehydration leads to increased plasma volume and decreased K+; insulin enhances the movement of K+ from extracellular fluid into the cells
    · Monitor
    o Blood glucose and renal function/UO
    o EKG and electrolyte levels: potassiumVS, lung assessments, signs of fluid overload
    Treatment of DKA
  61. · More common in type 2 especially elderly type 2
    · The insulin level is too low to prevent hyperglycemia but high enough to prevent fat breakdown like in DKA therefore there is no ketoacidosis
    · Clinical features
    o Hyperglycemia > 800
    o Hypotension from dehydration
    o Dehydration – patient tolerate polyuria and polydipsia until neurological changes occurs
    o Tachycardia
    o Neurological signs – neuro altered sensory, seizures, and hemiparesis
    · Causes
    o Acute illness (pneumonia or CVA)
    o Medications that exacerbate hyperglycemia
    o Treatments (dialysis)- dialysis treatment contains sugar so patient is at risk for hyperglycemia
  62. · Hydration
    · Insulin
    · Electrolyte Replacement
    o K replacement
    · Similar to management of DKA but because older age, close monitoring of volume and electrolyte status is important to prevent fluid overload, heart failure, and cardiac dysrhythmias
    Management of HHNS
  63. · All Subcutaneous insulin doses may be withheld unless blood glucose level is greater than 200
    · Need to check with physician about orders prior to surgery for insulin
    · Healing!!!
    DM and SX
  64. · Live alone
    · Decreased renal function
    · Skip meals
    · Decreased visual acuity
    Gerontological considerations
  65. · Imbalanced Nutrition
    · Risk for Injury
    · Risk for Impaired Skin Integrity
    · Knowledge deficit
    · Risk for Infection
    · Risk for Ineffective Management
    Nursing dx
  66. · Group of diseases characterized by hyperglycemia due to defects in insulin secretion, insulin action, or both
    · Affects nearly 21 million people in US
    · Almost 1/3 of cases are undiagnosed
    · Prevalence is increasing
    · Minority populations and elderly are disproportionately affected
  67. · Someone who takes steroids for a long period of time at risk for diabetes.
    · TPN patients at risk for diabetes.
    At risk
  68. · Transports and metabolizes glucose for energy
    · Stimulates storage of glucose in liver and muscle as glycogen
    · Signals liver to stop release of glucose
    · Enhances storage of dietary fat in adipose tissue
    · Accelerates transport of amino acids into cells
    · Inhibits breakdown of store glucose, protein, and fat

    · Brain relies solely on sugar to function
    · Repeated attacks will cause
    Functions of insulin
  69. · High blood glucose -> pancreas release insulin -> cells take up glucose from blood and liver produces glycogen -> blood glucose falls
    · Low blood glucose -> pancreas releases glucagon -> liver breaks down glycogen -> blood glucose rises
    Insulin homeostatis