1. Interventions for Clients with Diabetes Mellitus
2009
Chapter 68 in Iggy

2. DEFINITION
Group of disorders
Glucose intolerance common thread

3. GOAL FOR NURSE Have patient control blood glucose levels
Prevent acute and long term complications
Develop self care habits (priority)

4. NORMAL ANATOMY/PHYSIOLOGY
SOURCES OF GLUCOSE:
From food
From liver
From pancreas

5. WHEN A MEAL IS EATEN Insulin secretion increases
Glucose is moved from the blood into muscle, liver, and fat cells

6. INSULIN Hormone Produced by pancreas
Controls level of glucose in blood
Secreted by beta cells in islets of Langerhans in pancreas

7. EFFECT OF INSULIN AFTER IT IS MOVED
Glucose is used for energy
Stimulates storage of glucose in the liver and muscle in the form of glycogen
Promotes storage of dietary fat in adipose tissue
Speeds up the transport of amino acids coming from dietary protein into cells

8. DURING FASTING PERIODS
Continuous release of small amount of insulin
Glucagon secreted from alpha cells of islets of Langerhans
The liver produces glucose through breakdown of glycogen (glycogenolysis)
After 8-12 hours the liver forms glucose from the breakdown of noncarbohydrate substances eg: amino acids (gluconeogenesis)

9. STATISTICS About 17 million people
Cultural prevalence: Hispanics, *African Americans, Native Americans
Costs: As of 2002 $132 billion annually for diabetic related costs
Prevalent in elderly

10. CLASSIFICATION
Type I: Characterized by destruction of pancreatic cells (beta cells die); no production of insulin
Type II: Insulin resistance/impaired insulin secretion
Gestational: (GDM) increased blood glucose during pregnancy

11. Types of Diabetes Other types include:
Genetic defect of beta cell or insulin action
Disease of exocrine pancreas
Drug or chemical induced (glucocorticoids, thyroid hormone, beta-adrenergic agonists, thiazides, dilantin, etc
Infections
Others
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12. TYPE 1 AND TYPE 2 DIABETES Features Type 1 Type 2 Former name
Juvenile onset
Insulin dependent diabetes mellitus(IDDM)
Maturity onset
Non-insulin dependent diabetes mellitus (NIDDM)
Age at onset
Any age, usually under 30 yr
Starts in 40’s, Peaks in 50’s; may occur earlier, increase in childhood/adolescence due to obesity
Inheritance
Recessive
Dominant
Nutritional status
Usually nonobese
60-80% obese
Insulin
All dependent on insulin
Required 20-30%
Sulfonylurea therapy
None
Effective
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13. Usually no ketoacidosis Onset Abrupt Gradual Medical nutrition therapy
Features
Type 1
Type 2
Prevalence
Same for women and men
Symptoms
thirst, wgt loss,
None or thirst, fatigue, visual blurring, vascular or neural complications,
Usually no ketoacidosis
Onset
Abrupt
Gradual
Medical nutrition therapy
Mandatory
mandatory
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14. Absence of Insulin Hyperglycemia Polyuria Polydipsia Polyphagia
Hemoconcentration, hypervolemia, hyperviscosity, hypoperfusion, and hypoxia
Acidosis, Kussmaul respiration
Hypokalemia, hyperkalemia, or normal serum potassium levels
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15. Acute Complications of Diabetes
Diabetic ketoacidosis
Hyperglycemic-hyperosmolar-nonketotic syndrome
Hypoglycemia from too much insulin or too little glucose
ALL THREE PROBLEMS REQUIRE EMERGENCY TREATMENT AND BE FATAL IF NOT CORRECTED
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16. Chronic Complications of Diabetes
MACROVASCULAR: large vessels
Coronary heart disease, cerebrovascular disease, PVD, MI
MICROVASCULAR: small vessels
Retinopathy (vision) problems
Diabetic neuropathy
Diabetic nephropathy
Male erectile dysfunction
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17. CAUSE OF VASCULAR COMPLICATIONS
Chronic hyperglycemia
Glucose toxicity
Chronic ischemia
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18. Risk for Injury Related to Hyperglycemia FIRST GENERATION SULFONYLUREA AGENTS:
Used for clients with some pancreatic beta-cell function, stimulate insulin secretion
Acetohexamide (Dymelor, Dimelor):
Chloropropamide (Diabinase, Novo-Propamide)
SIDE EFFECTS: **hypoglycemia common in older, debilitated malnourished clients, CV, liver, kidney problem
SEVERE REACTION WITH ALCOHOL: flushing, pulsating HA, sweating, confusion, slurred speed CAN LEAD TO DEATH
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19. Risk for Injury Related to Hyperglycemia FIRST GENERATION SULFONYLUREA AGENTS:
Tolazamide (Tolinase): give with meals to avoid GI upset, do not give with alcohol
Tolbutamide( Orinase, Mobenoi): if client on a beta blocker, hypoglycemia S&S masked, no alcohol
A lot of drug interactions with this class of drug
Chloropropamide (Diabinase, Novo-Propamide)
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20. SECOND GENERATION SULFONYLUREA AGENTS
Glipizide (Glucotrol): give 30 min before meals to improve absorption, don’t crush, or chew tablet, designed to be absorbed slowly, if eat low calorie increased hypoglycemia
Glyburide (DiaBeta, Micronase): give with food decrease GI upset and enough calories to decrease hypoglycemia
Glimepiride (Amaryl): give with 1st main meal, debilitated or malnourished clients have more hypoglycemia
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21. Meglitinide Analogs
Actions and SE like sulfonylureas, rapid onset with limited duration
HOW: lowers blood glucose by triggering insulin secretion via beta cells in 20 min
SE: hypoglycemia
Repaglinide (Prandin): take 30 min before each meal; best reduction of postmeal hyperglycemia
Nateglinide (Starlix): 30 min before meals, omit med if meal skipped, add a dose if an extra meal eaten
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22. Biguanides
Lowers glucose by decreasing liver glucose release and decreasing cellular insulin resistance. Does not stimulate insulin release
Metformin (Glucopohage): give with food, check renal function, do not give with renal disease; Hold for 48 hrs before iodinated contrast materials used for radiographic tests
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23. Alpha-Glucosidase Inhibitors:
Reduce hyperglycemia after meals by lowing intestinal digestion and absorption of CHO
Inhibit enzymes in the intestinal tract delaying CHO digestion
Acarbose (Precose); Miglitol (Glyset)
take at the first bite of each of the three main meals, GI SE common, may accumulate in renal dysfunction, increases serum transaminase levels; NO HYPOGLYCEMIA unless given with sulfonylureas or insulin
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24. Thiazolidinediones
Enhances insulin action promoting glucose utilization in peripheral tissues, called insulin sensitizers and inhibit gluconeogenesis. Can be used with sulfonylureas or insulin to improve blood glucose control
Ploglitazone (Actos); Rosiglitazone (Avandia)
Rare cases liver failure, reduces effect of contraceptives, SE: fluid retention, wgt gain, CHF
Liver function tests checked
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25. Fixed Combinations
By combining drugs with different mechanisms of action may be highly effective in maintaining desired blood glucose control
Some clients need combination of oral agents and insulin to control blood glucose levels
Glucovance (Glyburide and metformin)
Avandamet (Rosiglitazone and metformin)
Metaglip (Glipizide and metformin)
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26. Drug Therapy
Drug administration: started at lowest effective dose and increased every 1-2 wks until blood glucose levels are controlled
Drug selection: age, cost, response
(Continued)
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27. RAPID ACTING iNSULINS Marked: NovoLog, Humalog, Apidra
Onset: hr
Peak: NovoLog – 1-3 hrs; Humalog: hrs; Apidra: hrs
Duration: NovoLog – 3-5 hrs; Humalog: 3-4 hrs; Apidra: 5 hrs
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28. SHORT ACTING INSULIN
Marked R on bottle for regular: Humulin R, Novolin R, Velosulin BR
Onset: ½ hour
Peak: Humulin: 2-4 hrs, Novolin R: hrs Velosulin BR is 1-3 hours
Duration: Humulin: 6-8 hrs, Novolin R: 8hrs Velosulin BR is 8 hrs
Usually given minutes before a meal
May be given alone or with longer acting insulin

29. INTERMEDIATE ACTING INSULIN
Eg: NPH, Lente
Onset NPH: 1.5 hrs; Lente: 2.5 hrs
Peak:NPH 4-12 hours; Lente: 7-15 hrs
Duration NPH: 24 hrs; Lente 22 hrs

30. LONG ACTING INSULINS Peakless insulin
Tends to have a long slow sustained action rather than sharp, definite peaks, used to control fasting glucose levels
Ultralente, lantus
Onset Ultralente 4-6 hrs: Lantus: 2-4 hrs
Peak: Ultralente: 8-20 hrs; Lantus: none
Duration : Ultralente: 24 hrs; Lantus: 24 hrs

31. Insulin Regimens Single daily injection protocol Two-dose protocol
Three-dose protocol
Four-dose protocol
Combination therapy
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32. Pharmacokinetics of Insulin
Injection site
Absorption rate
Injection depth
Time of injection
Mixing insulins
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33. Complications of Insulin Therapy
Hypoglycemia
Lipoatrophy
Dawn phenomenon
Somagyi's phenomenon
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34. SOMOGYII PHENOMENON
Hypoglycemia at night with hyperglycemia in morning
Cause: too much insulin, or increase of insulin sensitivity, check exercise programs
Treatment: gradual lowering of insulin dose and increase in diet at time of hypoglycemia reaction

35. DAWN PHENOMENON
Fasting hyperglycemia results from a nighttime release of growth hormone that causes blood glucose elevations at 5-6 AM
Common problem
Treatment: client controlled by altering time and dose of insulin of the evening dose of (NPH) by 1-2 units

36. Alternative Methods of Insulin Administration
Continuous subcutaneous infusion of insulin
Implanted insulin pumps
Injection devices
New technology includes:
Inhaled insulin
Transdermal patch (being tested)
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37. Client Education Storage and dose preparation Syringes
Blood glucose monitoring
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38. Client Education: glucose self monitoring devices
Frequent blood glucose monitoring allows the diabetic to adjust insulin to obtain optimal blood glucose control
Detects and prevents hypoglycemia and hyperglycemia
Maintains normal blood glucose levels decreasing long term complications
PROTOCOL: take blood glucose 2-4 times/day

39. GOALS OF DIET AND WEIGHT CONTROL
Provide all essential food constituents
Reasonable weight
Meeting energy needs
Glucose levels as close to normal as possible with few fluctuations
Decrease serum lipid levels

40. Diet Therapy Principles of nutrition in diabetes
Protein, fats and carbohydrates, fiber, sweeteners, fat replacers
Alcohol
Food labeling
Exchange system, carbohydrate counting
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41. RECOMMENDED TYPES OF FOOD
High complex carbohydrates (absorbed more gradually); eg: cereals, grains, pasta, potatoes, legumes, vegetables, and fruits
High soluble fiber foods (oat bran cereals, beans, peas, fruits) – help control blood glucose
Few simple or refined sugars
Limit Fats: meat, butterfat, lard, bacon, oils

42. GLYCEMIC INDEX
DEFINED: description of how much a given food raises the blood glucose level compared with an equivalent amount of glucose

43. GENERAL GUIDELINES RELATED TO GLYCEMIC INDEX
Combine starch foods with protein and fat foods to slow the absorption of the starch food and lower the glycemic response
Eat raw foods to lower the glycemic response (versus chopped, pureed or cooked foods)
Eat whole fruit to lower the glycemic response (avoid juice); the fiber slows the absorption of the food

44. GENERAL GUIDELINES R/T GLYCEMIC INDEX CONTINUED
If eating simple sugar foods, eat them with food that is more slowly absorbed to lower the glycemic response to the simple sugar food

45. SWEETNERS NUTRITIVE: contain calories eg: sorbitol, xylitol
NON NUTRITIVE: have minimal to no calories. Eg: asparatame, saccharin, acesulfame K, sucralose
NON NUTRITIVE: approved for diabetics

46. MEALS
Distribute food evenly throughout the day in 3-4 meals with snacks between meals and at bedtime

47. EXERCISE VERY IMPORTANT COMPONENT Walking is best form
WHAT DOES IT DO? Beneficial effect on CHO metabolism and insulin sensitivity
Lowers the blood glucose and reduces cardiovascular risk
HOW? By increasing the uptake of glucose by body muscles and by improving insulin utilization

48. OTHER BENEFITS OF EXERCISE
Improves circulation and muscle tone
Alters blood lipids

49. PROBLEMS WITH EXERCISE
HYPOGLYCEMIA after exercise
Eating snack after exercise and at bedtime
Exercise at same time of day preferably when blood glucose levels are at their peak

50. WHAT TO DO BEFORE EXERCISING
Check blood glucose levels before exercise; if exceed 250 test urine for ketones. Absence of ketones indicates enough insulin available for glucose transport
If ketones present client should not exercise; means current insulin levels are not adequate
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51. Assessment History & Blood tests
Fasting blood glucose test: two tests > 126 mg/dL says the client has diabetes
ADA says premeal glucose should be mg/dL
ADA says bedtime glucose should be mg/dl
Oral glucose tolerance test: blood glucose > 200 mg/dL at 120 minutes ( most sensitive test for dx diabetes)
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52. Assessment continued Glycosylated hemoglobin assays: nl 4-6%;
ADA says keep it at 7%
8%or more indicate poor diabetic control
Glucosylated serum proteins and albumin (GSP & GSA)
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53. Urine Tests Urine testing for ketones Urine testing for renal function
Urine testing for glucose
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54. Whole-Pancreas Transplantation
Operative procedure: all or part of it, or pancreas plus kidney transplant
Rejection management
Complications
Islet cell transplantation hindered by limited supply of beta cells and problems caused by antirejection drugs
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55. Risk for Delayed Surgical Recovery
Interventions include:
Preoperative care
Intraoperative care
Postoperative care and monitoring includes care of:
Cardiovascular
Renal
Nutritional
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56. Risk for Injury Related to Sensory Alterations
Interventions and foot care practices:
Cleanse and inspect the feet daily.
Wear properly fitting shoes.
Avoid walking barefoot.
Trim toenails properly.
Report nonhealing breaks in the skin.
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57. Wound Care Wound environment Debridement
Elimination of pressure on infected area
Growth factors applied to wounds
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58. Chronic Pain Interventions include:
Maintenance of normal blood glucose levels
Anticonvulsants: gabapentin (Neurontin)
Antidepressants:amitriptyline hydrochloride (Elavil, Levate), nortriptyline (Pamelor)
Capsaicin cream (Axsain, Zostrix))
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59. Risk for Injury Related to Disturbed Sensory Perception: Visual
Interventions include:
Blood glucose control
Environmental management
Incandescent lamp
Coding objects
Syringes with magnifiers
Use of adaptive devices
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60. Ineffective Tissue Perfusion: Renal
Interventions include:
Control of blood glucose levels
Yearly evaluation of kidney function
Control of blood pressure levels
Prompt treatment of UTIs
Avoidance of nephrotoxic drugs
Diet therapy
Fluid and electrolyte management
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61. Potential for Hypoglycemia
Blood glucose level < 70 mg/dL
Diet therapy: carbohydrate replacement
Drug therapy: glucagon, 50% dextrose, diazoxide, octreotide
Prevention strategies for:
Insulin excess
Deficient food intake
Exercise
Alcohol
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62. MILD HYPOGLYCEMIA Blood sugar drops to less than 60 mg/dL
Sympathetic nervous system stimulate; Surge of adrenalin
Causes sweating, tremor, tachycardia, palpitations, nervousness, hunger, shaky, headache, fully conscious
TREAT with g of CHO, glucose tablets or gel, fruit juice, regular soft drink, 8 oz of skim milk, 6-10 hard candies, 4 cubes of sugar, 6 saltines, 3 graham crackers, 1 tblsp of honey or syrup

63. MODERATE HYPOGLYCEMIA
Blood sugar drops: to 40 mg/dL
Deprives brain cells of fuel
Impaired function of CNS
Cold, clammy skin, pale, rapid pulse, rapid shallow respirations, marked change in mood
Treat with g of rapidly absorbed CHO
Take additional food such as low fat milk or cheese after min

64. SEVERE HYPOGLYCEMIA CNS CHANGES SO IMPAIRED NEED HELP
UNABLE TO SWALLOW, UNCONSCIOUSNESS, CONVULSIONS
BLOOD GLUCOSE USUALLY LESS THAN 20 MG/Dl
TREATMENT: 1 MG OF GLUCAGON AS im OR SUB q, ADMINISTER A SECOND DOSE IN 10 MINUTES IF STILL UNCONSCIOUS, GO TO ER

65. HYPOGLYCEMIA CONTINUED
Late food after insulin administration
Excessive insulin dose
GUIDELINE TO PREVENT HYPOGLYCEMIA:
FEED THE PEAK

66. DIABETIC KETOACIDOSIS
CAUSED by absence of insulin, illness, infection, initial S&S of undiagnosed untreated DM
RESULTS in disorders in metabolism of CHO, protein and fat
3 MAIN FEATURES: dehydration, electrolyte loss, acidosis

67. DKA Not enough insulin leads to
Decreased amount of glucose entering cells
Leads to liver making lots of glucose
RESULTS: hyperglycemia
Kidneys try to help by excreting glucose, but water and electrolytes get lost too (Na and K)

68. DKA CONTINUED
Excessive urination leads to DEHYDRATION AND MARKED ELECTROLYTE LOSS
In response to decreased insulin fats breakdown to FATTY ACIDS and GLYCEROL
The liver converts free fatty acids into KETONE BODIES
KETONE BODIES (are acids) accumulate and lead to METABOLIC ACIDOSIS

69. DKA CONTINUED Blood glucose could be 300 to 800 or 1000 or higher
KETOACIDOSIS reflected in following:
Low serum bicarb (0-15)
Low pH (6.8 to 7.3)
Low PCo2 (10-30)
REFLECTS RESPIRATORY COMPENSATION FOR METABOLIC ACIDOSES

70. DKA CONTINUED
Na and K may be low, normal or high depending on the water loss
High creatinine, high BUN, high Hgb, High Hct seen with dehydration

71. TREATMENT OF DKA
DEHYDRATION: rehydrate; may need 6-10 liters of NSS, 1 liter/hour for 2-3 hours then change to ½ NS
ELECTROLYTE LOSS: K may be low, normal or high initially, but there is a major loss of K during the dehydration; give 40 mEq KCl/hour for several hours

72. TREATMENT OF DKA CONTINUED
ACIDOSIS: insulin IV at slow rate 5 units/hour
Hourly blood glucose levels

73. MATH OF INSULIN DRIPS
Nurse must convert hourly rates of insulin infusion to IV gtt rates
Eg: 100 units Regular insulin mixed in 500cc of 0.9 NS
1 unit of insulin = 5 cc
Order is 5 units per hour
MATH: 5 units x 5 cc = 25 cc/hour

74. INSULIN DRIPS Infuse separately to allow for frequent changes
When mixing insulin drip, flush insulin solution through the entire IV infusion set and discard the first 50 cc fluid
WHY: inuslin molecules adhere to glass and plastic infusion sets, thus initial fluid has a decreased concentration of insulin

75. INSULIN DRIPS
Always run insulin continuously otherwise ketone bodies return
Even if blood glucose drops or returns to normal, keep insulin going

76. Potential for Hyperglycemic-Hyperosmolar Nonketotic Syndrome and Coma
Interventions include:
Monitoring
Fluid therapy: to rehydrate the client and restore normal blood glucose levels within 36 to 72 hr
Continuing therapy with IV regular insulin at 10 units/hr often needed to reduce blood glucose levels
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77. SICK DAY RULES Call MD Blood glucose q 4 hr
Urine for ketones when blood glucose is greater than 240 mg/dl
Take insulin/oral antidiabetic agents
Drink 8-12 oz sugar free liquids q hour awake
Eat regular meals
Call doctor for mod/lg ketones, N/V, uncontrolled blood glucose, high fever
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