1. Diabetes Mellitus
(DM)
Bhaumika Sharma
Lecturer
College of Nursing
Chitwan Medical College
03/12/12 1

2. INSULIN SECRETION AND
FUNCTION
• Insulin is a hormone secreted by the beta cells
of the islet of Langerhans in the pancreas.
• Increased secretion or a bolus of insulin,
released after a meal, helps maintain
euglycemia.
• Through an internal feedback mechanism
(pancreas and liver), circulating blood glucose
levels are maintained at a normal range of 60
to 110 mg/dL.
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3. Contd.
• Insulin is essential for the utilization of glucose
for cellular metabolism as well as for the
proper metabolism of protein and fat.
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4. Contd.
• Carbohydrate metabolism: insulin affects the
conversion of glucose into glycogen for
storage in the liver and skeletal muscles, and
allows for the immediate release and
utilization of glucose by the cells.
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5. Contd.
• Protein metabolism: amino acid conversion
occurs in the presence of insulin to replace
muscle tissue or to provide needed glucose
(gluconeogenesis).
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6. • Fat metabolism: storage of fat in adipose
tissue and conversion of fatty acids from
excess glucose occurs only in the presence of
insulin.
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7. Diabetic Mellitus (DM)
• Diabetes mellitus is a group of metabolic
diseases characterized by elevated levels of
glucose in the blood (hyperglycemia) resulting
from defects in insulin secretion, insulin
action, or both.
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8. Epidemiology
• Diabetes mellitus affects about 17 million
people, 5.9 million of whom are undiagnosed.
• In the United States, approximately 800,000
new cases of diabetes are diagnosed yearly
• Diabetes is especially prevalent in the elderly,
with up to 50% of people older than 65
suffering some degree of glucose intolerance.
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9. Contd.
• In the United States, diabetes is the leading
cause of nontraumatic amputations, blindness
among working-age adults, and end-stage
renal disease
• Diabetes is the third leading cause of death by
disease, primarily because of the high rate of
cardiovascular disease (myocardial infarction,
stroke, and peripheral vascular disease)
among people with diabetes.
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10. Classification of DM
Type 1 Diabetes Mellitus:
• Formerly known as insulin dependent diabetes
mellitus and juvenile diabetes mellitus.
• Five to 10% of all diabetic patients have type 1.
• Most commonly seen in patients under age 30
but can be seen in older adults.
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11. Contd.
• Etiology: autoimmunity, viral, and certain
histocompatibility antigens as well as a
genetic component.
• Clinical Features: usual presentation is rapid
with classic symptoms of polydipsia,
polyphagia, polyuria and weight loss.
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12. Type 2 Diabetes Mellitus
• Formerly known as noninsulin dependent diabetes
mellitus or adult onset diabetes mellitus.
• Approximately 90% of diabetic patients have type
2.
• It is caused by a combination of insulin resistance
and relative insulin deficiency
• Found primarily in adults over age 30; however,
may be seen in younger adults and adolescents
who are overweight.
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13. Contd.
• Etiology: strong hereditary component
commonly associated with obesity.
• Clinical Features: usual presentation is slow
and typically insidious with symptoms of
fatigue, weight gain, poor wound healing, and
recurrent infection.
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14. Gestational Diabetes Mellitus
(GDM)
• GDM is defined as carbohydrate intolerance
occurring during pregnancy.
• Occurs in approximately 4% of pregnancies
and usually disappears after delivery.
• Women with GDM are at higher risk for
diabetes at a later date.
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15. Contd.
• GDM is associated with increased risk of fetal
morbidity.
• Screening for GDM for all pregnant women
should occur between the 24th and 28th
weeks of gestation.
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16. Diabetes Associated with Other
Conditions
• Certain drugs can decrease insulin activity
resulting in hyperglycemia: corticosteroids,
thiazide diuretics, estrogen, phenytoin.
• Disease states affecting the pancreas or
insulin receptors: pancreatitis, cancer of the
pancreas, Cushing's disease or syndrome,
acromegaly, pheochromocytoma, muscular
dystrophy, Huntington's chorea.
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17. Etiology and Risk Factors
Type I
• Identical twins 25% to 50% inherited
• Siblings 6% and offspring 5% risk
• Virus appear to trigger autoimmune process:
islet cell antibody, autoimmunity
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18. Contd.
Type II
• Identical twins: 58% to 50% inherited
• Obesity
• Prevalence of coronary artery disease
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19. PHYSIOLOGY AND
PATHOPHYSIOLOGY OF DIABETES
• Type I DM
– 5 stages
Stage I: genetic predisposition
Stage 2: environmental trigger
Stage 3: active autoimmunity
Stage 4: progressive beta cell destruction
Stage 5: overt diabetes mellitus
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20. Contd.
• Blood Glucose
• Fasting blood sugar (FBS): drawn after at least
an 8-hour fast, to evaluate circulating
amounts of glucose
• Postprandial test (PP): drawn usually 2 hours
after a well-balanced meal, to evaluate
glucose metabolism; and random glucose,
drawn at any time, nonfasting.
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21. Contd.
• People with gene marker DR3 or DR4 HLA
indicate risk for type I DM
• Environmental triggers: coincidence of various
viral diseases
• Slow, progressive insult to beta cells and
endogenous insulin molecules
• Acute illness and stress: leads to
hyperglycemia, when acute illness resolves,
client my revert to compensated state of
variable duration, honeymoon period.
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22. Contd.
Type II
• 1st: Beta cells chronically exposed to high
blood levels of glucose become progressively
less efficient when responding to further
glucose elevations, phenomenon termed as
desensitization, is reversible by normalizing
glucose levels
•
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23. Contd.
• 2nd: Resistance to biologic activity of insulin in
both the liver and peripheral tissues, state
known as insulin resistance
• In type II DM there is decreased sensitivity to
glucose levels, which results in continued
hepatic glucose production, even with high
plasma glucose level
• Also inability of muscle and fat tissues to
increase glucose uptake aids
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24. 03/12/12 24

25. Clinical Manifestations
• Hyperglycemia
• 3 P’s
– Polyuria (increased urination)
– Polydipsia (increased thirst)
– polyphagia (increased appetite)
• Weight loss, fatigue
• Blurred vision
• Poor wound healing
• Recurrent infections, particularly of the skin
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26. Diagnostic Evaluation
• Diabetes can be diagnosed in any of the
following ways (and should be confirmed on a
different day by any of these tests):
– FBS of ≥126 mg/dL
– Random blood glucose of ≥200 mg/dL with classic
symptoms (polyuria, polydipsia, polyphagia,
weight loss)
– OGTT greater than or equal to 200 mg/dL on the
2-hour sample
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27. Contd.
• Tests for glucose control over time are
glycated hemoglobin and fructosamine assay.
• These tests are not used for diagnosis.
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28. Management
Diet
• Dietary control with caloric restriction of
carbohydrates and saturated fats to maintain
ideal body weight.
• The goal of meal planning is to control blood
glucose and lipid levels.
• Weight reduction is a primary treatment for
type 2 diabetes.
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29. Contd.
Exercise
• Regularly scheduled, moderate exercise
performed for at least 30 minutes most days
of the week promotes the utilization of
carbohydrates, assists with weight control,
enhances the action of insulin, and improves
cardiovascular fitness.
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30. Contd.
Medication
• Oral antidiabetic agents for patients with type
2 diabetes who do not achieve glucose control
with diet and exercise only.
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31. Oral hypoglycemic Drugs
Second-Generation Sulfonylureas
Glyburide (Micronase, 1.25-20 mg in single or divided dose with
DiaBeta) meals
Glyburide, micronized 0.75-12 mg in single or divided dose
(Glynase)
Glipizide (Glucotrol) 2.5-40 mg in single dose or divided dose with
meals
Glipizide (Glucotrol 5-20 mg in single dose before breakfast
XL)
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32. Contd.
Agents Dose
Biguanides
Metformin (Glucophage) 500-2,550 mg in 2-3 divided
doses with meals
Metformin (Glucophage XR) 500-2,000 mg daily with evening
meal
Alpha-Glucosidase Inhibitors
Acarbose (Precose) 150-300 mg in 3 doses with
meals; if < 60 kg, maximum dose
50 mg tid
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33. Contd.
Agents Dose
Meglitinide Analogue
Repaglinide (Prandin) 0.5-16 mg in 2-4 divided doses within
30 minutes of starting meal; if meal is
skipped, do not take dose
Amino Acid Derivative
Nateglinide (Starlix) 120-360 mg in 3 divided doses within
30 minutes of starting meal; if meal is
skipped, do not take dose
Thiazolidinediones
Rosiglitazone (Avandia) 4-8 mg in a single dose or 2 divided
doses
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34. Contd.
Agents Dose
Combination Agents
Glyburide/metformin Up to 20/2,000 mg/day in
(Glucovance) single dose or divided doses
Glipizide/metformin Up to 20/2,000 mg/day in
(Metaglip) single dose or divided doses
Rosiglitazone/metformin Up to 8/2,000 mg/day in
(Avandamet) divided doses
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35. Sites of Action of Oral Anti-diabetic Drugs
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36. Insulin Therapy
INSULIN ONSET PEAK DURATION
Immediate-acting
(lispro, 0.25 hour 0.5-1 hour 5 hours
aspart)
Short-acting
(regular, 0.5-1 hour 2-4 hours 5-7 hours
semilente)
Intermediate-acting
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37. INSULIN ONSET PEAK DURATION
Long-acting
(ultralente) 4-6 hours 10-30 hours 24-36 hours
(insulin 1 hour none 24+1 hours
glargine)
Mixed
(Regular 0.5 hour 2-12 hours 24 hours
30%, NPH
70%)
(Regular 0.5 hour 3-5 hours 24 hours
50%, NPH
50%)
(Lispro 25%,0.25 hour 0.5-1.5 hours 24 hours
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NPH 75%)

38. Five components of Diabetic
Management
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39. Patient Education: Self Insulin Injection
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40. 03/12/12 40

41. 03/12/12 41

42. 03/12/12 42

43. 03/12/12 43

44. Areas for Insulin Injection
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45. 03/12/12 45

46. Microfilaments for Testing of
Sensation
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47. Disposable Filament for Patient
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48. Insulin Pump
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49. DIAGNOSTIC TESTS
Blood Glucose
• Fasting blood sugar (FBS): drawn after at least
an 8-hour fast, to evaluate circulating
amounts of glucose
• Postprandial test (PP): drawn usually 2 hours
after a well-balanced meal, to evaluate
glucose metabolism; and random glucose,
drawn at any time, nonfasting.
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50. Contd.
Nursing and Patient Care Considerations
• Advise patient to refrain from smoking before
the glucose sampling because this affects the
test results.
• For postprandial test, advise patient that no
food should be eaten during the 2-hour
interval.
• For random blood glucose, note the time and
content of the last meal.
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51. Contd.
• Interpret blood values as diagnostic for
diabetes mellitus as follows:
– FBS greater than or equal to 126 mg/dL on two
occasions
– Random blood sugar ≥200 mg/dL and presence of
classic symptoms of diabetes (polyuria, polydipsia,
polyphagia, and weight loss)
• Fasting blood glucose result of ≥100 mg/dL
demands close follow-up and repeat
monitoring.
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52. Oral Glucose Tolerance Test
(OGTT)
• OGTT evaluates insulin response to glucose
loading. FBS is obtained before the ingestion
of a 50- to 200-g glucose load (usual amount is
75 g), and blood samples are drawn at ½, 1,
2, and 3 hours (may be 4- or 5-hour sampling).
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53. Contd.
Nursing and Patient Care Considerations
• Advice patient to use usual diet and exercise
pattern must be followed for 3 days before
OGTT.
• During OGTT, the patient must refrain from
smoking and remain seated.
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54. Contd.
• Oral contraceptives, salicylates, diuretics,
phenytoin, and nicotinic acid can impair
results and may be withheld before testing
based on the advice of the health care
provider.
• Diagnostic for diabetes mellitus if 2-hour value
is 200 mg/dL or greater.
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55. Glycated Hemoglobin
(Glycohemoglobin, HbA1c)
HbA1c measures glycemic control over a 60- to
120-day period by measuring the irreversible
reaction of glucose to hemoglobin through
freely permeable erythrocytes during their
120-day lifecycle.
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56. Contd.
Nursing and Patient Care Considerations
• No prior preparation, such as fasting or
withholding insulin, is necessary.
• Test results can be affected by red blood cell
disorders (eg, thalassemia, sickle cell anemia),
room temperature, ionic charges, and
ambient blood glucose values.
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57. C-Peptide Assay (Connecting
Peptide Assay)
• Cleaved from the proinsulin molecule during
its conversion to insulin, C-peptide acts as a
marker for endogenous insulin production.
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58. Contd.
Nursing and Patient Care Considerations
• Test can be performed after an overnight fast
or after stimulation with Sustacal, I.V. glucose
or 1 mg of glucagon subcutaneously.
• Absence of C-peptide indicates no beta cell
function, reflecting possible type 1 diabetes.
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59. Testing for Ketones
• When there is almost no effective insulin
available, the body starts to break down
stored fat for energy.
• Ketone bodies are byproducts of this fat
breakdown, and they accumulate in the blood
and urine.
• Ketones (or ketone bodies) in the urine signal
that control of type 1 diabetes is
deteriorating, and the risk of DKA is high.
03/12/12 59

60. Contd.
• Urine testing is the most common method
used for self-testing of ketone bodies by
patients.
• Urine ketone testing should be performed
whenever patients with type 1 diabetes have
glucosuria or persistently elevated blood
glucose levels (more than 240 mg/dL or 13.2
mmol/L for two testing periods in a row) and
during illness, in pregnancy with pre-existing
diabetes, and in gestational diabetes.
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61. General Health
The American Diabetes Association (2003)
recommends the following goals of treatment.
• Glycemic control
– HbA1c < 7%
– Preprandial glucose 90 to 130 mg/dL
– Peak postprandial glucose < 180 mg/dL
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62. Contd.
• BP < 130/80 mm Hg
• Lipid control
– Low-density lipoprotein < 100 mg/dL
– High-density lipoprotein > 40 mg/dL
– Triglycerides < 150 mg/dL
• Microalbumin (spot urine) < 30 mcg/mg
creatinine
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63. Complications of Diabetes
Mellitus
Acute
1. Hypoglycemia occurs as a result of an
imbalance in food, activity, and insulin/oral
antidiabetic agent.
2. Diabetic ketoacidosis (DKA) occurs primarily
in type 1 diabetes during times of severe
insulin deficiency or illness, producing severe
hyperglycemia, ketonuria, dehydration, and
acidosis.
63

64. Contd.
3. Hyperosmolar hyperglycemic nonketotic
syndrome (HHNKS) affects patients with type
2 diabetes, causing severe dehydration,
hyperglycemia, hyperosmolarity, and stupor.
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65. Contd.
Chronic
1.Macroangiopathy
– Cerebrovascular Disease
– Coronary Artery Disease (CAD)
– Peripheral Vascular Disease
1.Microangiopathy
– Retinopathy
– Nephropathy
– Peripheral Neuropathy
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66. Contd.
3. Autonomic Neuropathy
– Gastroparesis
– Impotence/Sexual Dysfunction
– Orthostatic Hypotension
03/12/12 66

67. Contd.
• In type 1 diabetes, chronic complications
usually appear about 10 years after the initial
diagnosis.
• The prevalence of microvascular
complications (retinopathy, nephropathy) and
neuropathy is higher in type 1 diabetes.
• Because of its insidious onset, chronic
complications can appear at any point in type
2 diabetes.
03/12/12 67

68. Contd.
• Macrovascular complications: in particular
cardiovascular disease, occurring in type 1 and
type 2 diabetes are the leading cause of
morbidity and mortality among persons with
diabetes.
03/12/12 68

69. Contd.
• Nursing Assessment
• Obtain a history of current problems, family
history, and general health history.
– Has the patient experienced polyuria, polydipsia,
polyphagia, and any other symptoms?
– Number of years since diagnosis of diabetes
– Family members diagnosed with diabetes, their
subsequent treatment, and complications
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70. Contd.
• Perform a review of systems and physical
– General: recent weight loss or gain, increased
fatigue, tiredness, anxiety
– Skin: skin lesions, infections, dehydration,
evidence of poor wound healing
– Eyes: changes in vision floaters, halos, blurred
vision, dry or burning eyes, cataracts, glaucoma
03/12/12 70

71. Contd.
– Mouth: gingivitis, periodontal disease
– Cardiovascular: orthostatic hypotension, cold
extremities, weak pedal pulses, leg claudication
– GI: diarrhea, constipation, early satiety, bloating,
increased flatulence, hunger or thirst
03/12/12 71

72. Contd.
– Genitourinary (GU): increased urination, nocturia,
impotence, vaginal discharge
– Neurologic: numbness and tingling of the
extremities, decreased pain and temperature
perception, changes in gait and balance
03/12/12 72

73. Nursing Diagnoses
• Imbalanced Nutrition: More than Body
Requirements related to intake in excess of
activity expenditures
• Fear related to insulin injection
• Risk for Injury (hypoglycemia) related to
effects of insulin, inability to eat
03/12/12 73

74. Contd.
• Activity Intolerance related to poor glucose
control
• Deficient Knowledge related to use of oral
hypoglycemic agents
• Risk for Impaired Skin Integrity related to
decreased sensation and circulation to lower
extremities
• Ineffective Coping related to chronic disease
and complex self-care regimen
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75. Nursing Interventions
Improving Nutrition
• Assess current timing and content of meals.
• Advise patient on the importance of an
individualized meal plan.
• Reducing intake of carbohydrates may benefit
some patients
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76. Contd.
• Set a goal of a 10% (of patient's actual body
weight) weight loss over several months in
reducing blood sugar and other parameters.
• Assist patient to identify problems and their
solutions that may have an impact on dietary
adherence
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77. Contd.
• Emphasize that lifestyle changes should be
maintained.
• Explain the importance of exercise in
maintaining/reducing body weight.
03/12/12 77

78. Contd.
• Teaching About Insulin
• Assist patient to reduce fear of injection by
encouraging verbalization regarding insulin
injection, sense of empathy, and identifying
supportive coping techniques.
• Demonstrate and explain thoroughly the
procedure for insulin self-injection.
03/12/12 78

79. Contd.
• Help patient to master technique by taking a
step-by-step approach.
– Allow patient time to handle insulin and syringe to
become familiar with the equipment.
– Teach self-injection first to alleviate fear of pain
from injection.
– Instruct patient in filling syringe when he or she
expresses confidence in self-injection procedure.
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80. • Review dosage and time of injections in
relation to meals, activity, and bedtime.
Preventing Injury Secondary to Hypoglycemia
• Closely monitor blood glucose levels to detect
hypoglycemia.
• Instruct patient in the importance of accuracy
in insulin preparation and meal timing to
avoid hypoglycemia.
03/12/12 80

81. Contd.
• Assess patient for the signs and symptoms of
hypoglycemia.
– Adrenergic (early symptoms) sweating, tremor,
pallor, tachycardia, palpitations, nervousness from
the release of adrenalin when blood glucose falls
rapidly
– Neurologic (later symptoms) light-headedness,
headache, confusion, irritability, slurred speech,
lack of coordination, staggering gait from
depression of central nervous system as glucose
03/12/12 level progressively falls 81

82. Contd.
• Treat hypoglycemia promptly with 15 to 20 g
of fast-acting carbohydrates.
– Half cup (4 oz) juice, 1 cup skim milk, three
glucose tablets, four sugar cubes, five to six pieces
of hard candy may be taken orally.
– Nutrition bar specially designed for diabetics
supplies glucose from sucrose, starch, and protein
sources with some fat to delay gastric emptying
and prolong effect; may prevent relapse.
– Used after hypoglycemia treated with fact-acting
03/12/12 carbohydrate. 82

83. Contd.
– Glucagon 1 mg (subcutaneously or I.M.) is given if
the patient cannot ingest a sugar treatment.
Family member or staff must administer injection.
– I.V. bolus of 50 mL of 50% dextrose solution can
be given if the patient fails to respond to glucagon
within 15 minutes.
• Encourage patient to carry a portable
treatment for hypoglycemia at all times.
03/12/12 83

84. Contd.
• Assess patient for cognitive or physical
impairments that may interfere with ability to
accurately administer insulin.
• Between-meal snacks as well as extra food
taken before exercise should be encouraged
to prevent hypoglycemia.
• Encourage patients to wear an identification
bracelet or card that may assist in prompt
treatment in a hypoglycemic emergency.
03/12/12 84

85. Caring for Patients With Diabetes
Mellitus
Improving Activity Tolerance
• Advise patient to assess blood glucose level
before and after strenuous exercise.
• Instruct patient to plan exercises on a regular
basis each day.
• Encourage patient to eat a carbohydrate
snack before exercising to avoid
hypoglycemia.
03/12/12 85

86. Contd.
• Advise patient that prolonged strenuous
exercise may require increased food at
bedtime to avoid nocturnal hypoglycemia.
• Instruct patient to avoid exercise whenever
blood glucose levels exceed 250 mg/day and
urine ketones are present.
03/12/12 86

87. Contd.
• Patient should contact health care provider if
levels remain elevated.
• Counsel patient to inject insulin into the
abdominal site on days when arms or legs are
exercised.
03/12/12 87

88. Contd.
• Providing Information About Oral Antidiabetic
Agents
• Encourage active participation of the patient
and family in the educational process.
03/12/12 88

89. Contd.
• Teach the action, use, and adverse effects of
oral antidiabetic agents.
– Sulfonylurea compounds promote the increased
secretion of insulin
– Potential adverse reactions include hypoglycemia,
photosensitivity, GI upset, allergic reaction,
reaction to alcohol, cholestatic jaundice, and
blood dyscrasias.
03/12/12 89

90. Contd.
– Metformin (Glucophage), a biguanide compound,
appears to diminish insulin resistance.
– Metformin must be used cautiously in renal
insufficiency, conditions that may cause
dehydration, and hepatic impairment.
– Potential adverse reactions include GI
disturbances, metallic taste, and lactic acidosis
(rare).
03/12/12 90

91. Contd.
– Alpha-glucosidase inhibitors (acarbose [Precose]
and miglitol [Glyset]) delay the digestion and
absorption of complex carbohydrates (including
sucrose or table sugar) into simple sugars, such as
glucose and fructose, thereby lowering
postprandial and fasting glucose levels.
03/12/12 91

92. Contd.
– Thiazolidinedione derivatives (rosiglitazone
[Avandia] and pioglitazone [Actos]) primarily
decrease resistance to insulin in skeletal muscle
and adipose tissue without increasing insulin
secretion.
– Secondarily, they reduce hepatic glucose
production.
– Ovulation may occur in anovulatory
premenopausal women.
– Adverse reactions include edema, weight gain,
03/12/12 anemia, and elevation in serum transaminases. 92

93. Contd.
• Meglitinide analogues (repaglinide [Prandin]) and
amino acid derivatives (nateglinide [Starlix])
stimulate pancreatic release of insulin in response to
a meal.
• They should not be taken when a meal is skipped or
missed.
• They should be used cautiously in patients with renal
and hepatic dysfunction, and may cause
hypoglycemia.
03/12/12 93

94. Contd.
Maintaining Skin Integrity
• Assess feet and legs for skin temperature,
sensation, soft tissue injuries, corns, calluses,
dryness, deep tendon reflex
– Use a monofilament to test sensation of the feet
and detect early signs of peripheral neuropathy.
03/12/12 94

95. Contd.
• Maintain skin integrity by protecting feet from
breakdown.
– Use heel protectors, special mattresses, foot
cradles for patients on bed rest.
– Avoid applying drying agents to skin (eg, alcohol).
– Apply skin moisturizers to maintain suppleness
and prevent cracking and fissures.
03/12/12 95

96. Contd.
• Advise the patient to stop smoking or reduce
if possible, to reduce vasoconstriction and
enhance peripheral blood flow.
• Help patient to establish behavior
modification techniques to eliminate smoking
in the hospital and to continue them at home
for smoking-cessation program.
03/12/12 96

97. Improving Coping Strategies
• Discuss with the patient the perceived effect of
diabetes on lifestyle, finances, family life,
occupation.
• Explore previous coping strategies and skills that
have had positive effects.
• Encourage patient and family participation in
diabetes self-care regimen to foster confidence.
• Identify available support groups to assist in
lifestyle adaptation.
• Assist family in providing emotional support.
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