Diabetes mellitus type 2, nursing prespective

1. DIABETES MELLITUS
TYPE 2
PRESENTER:
Esther Mary Mathew
M.Sc Nursing 1st year
MODERATOR :
Ms. Ujjwal Dahiya
Lecturer, CON AIIMS.

2. INTRODUCTION
 Type 2 diabetes is sometimes called a “life style” disease as it
more common in people who don’t do enough exercise, have an
unhealthy diet and obese.
 Type 2 Diabetes was previously seen mainly in older adults,
however it is becoming more common in young children due to
obesity and overweight children.

3. HISTORY
The earliest known
record of diabetes was
written on 3rd Dynasty
Egyptian papyrus by
physician ‘Hesy-Ra’.
He stated recurring
urination as a sign of
this illness

4. HISTORY
The Indian physician
Sushruta in the 6th
century B.C. noticed
the sweet nature of
urine in such patients
and termed the
condition
MADHUMEHA.

5. Diabetes
mellitus
Greek word
"diabainein"
meaning "to siphon or
pass through"
Latin word "mellitus"
meaning "sweetened
with honey"
"to pass through sweetened with
honey"

6. DIABETIC MELLITUS
Diabetes is a group of metabolic diseases characterized by
hyperglycemia resulting from defects in insulin secretion,
insulin action, or both.

7. EPIDEMIOLOGY
Globally
382 million people had diabetes in
2013
By 2035, this number will rise to 592
million
In India
65.1 million people had diabetes in
2013
By 2035, this number will increase by
70.6%

8. Courtesy: 2015 International Diabetes Federation
Epidemiology

9. ANATOMY OF PANCREAS
 The adult pancreas is a transversely oriented retroperitoneal
organ extending from the "C " loop of the duodenum to the
hilum of the spleen
EXOCRINE secretion
 pancreatic juice enzymes promote the digestion of
carbohydrates, proteins and fats
ENDOCRINE secretion
 Insulin and glucagon- enter portal vein – transported directly to
the liver – regulate metabolism of carbohydrates, proteins and
fats.

10. PANCREAS
 15- 20% α cells synthesize and secrete GLUCAGON
 70- 80% β cells synthesize and secrete INSULIN
 1-8% δ cells synthesize and secrete STOMATOSTATIN
and GASTRIN
 1-2% F- cells secrete PANCREATIC POLYPEPTIDE
which decreases the absorption of food from the GIT

11. INSULIN
 Polypeptide hormone produced by β- cells of islets of
Langerhans of pancreas
 Insulin is a protein made of 2 chains- alpha and beta
 Anabolic hormone
STRUCTURE OF INSULIN

12. REGULATION OF INSULIN SECRETION
 Factors stimulating insulin secretion :
 Glucose: The effect is more predominant when glucose is
administered orally. Arise in blood glucose level is a signal for
insulin secretion.
 amino acids:
 gastrointestinal hormones: Gastrointestinal hormones (secretin,
gastrin) enhance the secretion of insulin.

13. REGULATION OF INSULIN SECRETION
 Factors inhibiting insulin secretion
• Epinephrine is the most potent inhibitor of insulin release.
• In emergency situations like stress, extreme exercise and
trauma, the nervous system stimulates adrenal medulla to
release epinephrine.
• Epinephrine suppresses insulin release and promotes energy
metabolism by Mobilizing energy-yielding compounds-glucose
from liver and fatty acids from adipose tissue

14. Gluconeogenesis : The synthesis of glucose from non-
carbohydrate precursors( e.g. amino acids, glycerol)
Glycogenesis: The formation of glycogen from
glucose.
Glycogenolysis : The breakdown of glycogen to
glucose

15. ACTIONS OF INSULIN
Stimulation of the activity of glycolytic enzymes
Reduces the activity of the enzymes of gluconeogenesis
Increased synthesis of glycogen
Increased uptake of of glucose by resting skeletal muscles
Reduction of blood glucose level
Reduction of lipolysis and stimulation of lipid synthesis

16. INSULIN
 Pancreas secretes 40-50 units of insulin daily in two steps:
• Secreted at low levels during fasting ( basal insulin
secretion
• Increased levels after eating (prandial)
• An early burst of insulin occurs within 10 minutes of
eating
• Then proceeds with increasing release as long as
hyperglycemia is present

18. GLUCOSE HOMEOSTASIS

20. CLASSIFICATION
 Classification by American diabetic association 2009 :
• Type 1 diabetes
• Type 2 diabetes
• Gestational diabetes mellitus (GDM)
• Secondary DM:
Hormonal problems, pancreatic disorders, drugs

21. TYPE 1 DM
 Juvenile / IDDM (5 to 10%)
 Autoimmune destruction of pancreatic beta cells.
 Individual has an absolute insulin deficiency and no longer
produces insulin.
 Such patients are absolutely dependent on exogenously
administered insulin for survival.

23. TYPE 2 DIABETES
MELLITUS

24. TYPE 2 DM
 Most common type
 Comprises 90 to 95% of DM cases
 Most type 2 DM patients are overweight, and most are
diagnosed as adults.
 Approximately half of the patients are unaware of their
disease

25. Peripheral
resistance to
insulin, especially
in muscle cells
Increased
production of
glucose by the
liver
Insulin secretary
defect of the beta
cells
• Obesity contributes greatly to insulin resistance
• Insulin resistance generally decreases with weight loss
TYPE 2 DM
The underlying pathophysiologic defect in type 2 DM is
characterized by the following three disorders:

26. COMPONENTS OF DM-II
Type 2
diabetes
Insulin
resistance
-cell
dysfunction

28. RISK FACTORS
 NON-MODIFIABLE:
 Age: 45 or more
 Race : African American, Asian American, Hispanic or
Latino.
 Familial history : a parent, or siblings with diabetes.

29. RISK FACTORS
 MODIFIABLE:
 Pre diabetes
 Heart and blood disease
 Hypertension
 Low HDL cholesterol and high triglycerides.
 Obesity
 Polycystic ovary syndrome
 Physical inactivity

30. RESEARCH INPUT
 High Bone Mineral Density and Fracture Risk in Type
2 Diabetes as Skeletal Complications of Inadequate
Glucose Control.
 Ling Oei, Abbas, Karol Estrada et al
 Journal : Diabetes Care 2013 Jun; 36(6)
 Objective: To examine the influence of glucose control
on skeletal complications.

31. RESEARCH INPUT
 RESEARCH DESIGN AND METHODS: prospective
population-based study
 420 participants with type 2 diabetes were classified by
glucose control - according to HbA1c
 adequately controlled diabetes (ACD: n = 203;
HbA1c <7.5%)
 inadequately controlled diabetes (ICD; n = 217;
HbA1c≥7.5%)
 no diabetes (n = 3,715)

32. RESEARCH INPUT
 RESULTS : The ICD group had 1.1–5.6% higher BMD,
and 1.2 to −1.8% narrower femoral necks than ACD
and ND, respectively.
 Participants with ICD had 47–62% higher fracture risk
than individuals without diabetes whereas those with
ACD had a risk similar to those without diabetes.
 CONCLUSIONS : Poor glycemic control in type 2
diabetes is associated with fracture risk.

34. CLINICAL PRESENTATION
 Patients can be asymptomatic
 Polyuria
 Polydipsia
 Polyphagia
 Fatigue
 Weight loss
 Most patients are discovered while performing urine
glucose screening

36. DIAGNOSIS
 Fasting Plasma Glucose
 Oral Glucose Tolerance Test
(OGTT)
 Glycoselated Hemoglobin (HbA1c)
 Urinalysis
• Glycosuria
• Ketone bodies

38. HBA1C
•Measures the amount of glycated haemoglobin in blood.
•HbA1c is not sensitive enough to detect DM but is the gold
standard for the long term monitoring.

39. ADDITIONAL INVESTIGATIONS;
 Lipid profile
 Fundoscopic examination
 LFT ,
 Urine analysis
 ECG
 Test to assess other complications

40. Any one test should be
confirmed with a
second test, most often
fasting plasma glucose
(FPG).
DIAGNOSTIC CRITERIA
• Classic signs of HYPERGLYSEMIA with CPG ≥200mg/D
• OGTT ≥200mg/dL
• FPG ≥126mg/dL
• A1C ≥ 6.5%

41. “WHO” DIAGNOSTIC CRITERIA
CONDITION 2 HRS GLUCOSE FASTING
GLUCOSE
HbA1C
UNIT Mg/dl Mg/dl %
Normal <140 <110 <6
Impaired fasting
glycemia
<140 110 – 126 6 -6.4
Impaired glucose
tolerance
>140 <126 6 – 6.4
DM >200 >126 > 6.5

42. MANAGEMENT OF DIABETES
MELLITUS

43. The major components of the treatment of diabetes are:
MANAGEMENT OF DM
• Medical Nutrition Therapy(Diet and
Exercise)A
• Oral hypoglycaemic therapyB
• InsulinC

44.  Dietary treatment should aim at:
 Ensuring weight control.
 Providing nutritional requirements.
 Allowing good glycaemic control with blood glucose
levels as close to normal as possible.
 Correcting any associated blood lipid abnormalities.
A. DIET

45. DIETARY MANAGEMENT
DIETARY MANAGEMENT
 Follow individualized meal plan and snacks as scheduled
 Balanced diabetic diet – 50% CHO, 30% fats, 20% CHON,
vitamins and minerals
 diet based on pts. size, wt., age, occupation and activity.
 Meal should include more fiber and starch and fewer
simple or refined sugars.

46. DIETARY MANAGEMENT
 If taking insulin, eat extra food before periods of vigorous
exercise
 Routine blood glucose testing before each meal and at
bedtime is necessary during initial control, during illness and
in unstable pts.
 Excessive salt intake is to be avoided. It should be particularly
restricted in people with hypertension and those with
nephropathy

47.  Eat grains in the least processed state possible.
 Limit potatoes and refined grain products.
 Avoid concentrated sweets (jellies, jams, cakes, ice
cream)
 Choose foods with healthy fats.
 Have 3 meals and one or two snacks each day
 Eat slowly and stop when full.
 Avoid periods of fasting and feasting, Do not skip
meals
How to eat low GI food

48.  Physical activity promotes weight reduction and improves
insulin sensitivity, thus lowering blood glucose levels.
 Exercise same time and duration of day.
 People should, however, be educated about the
potential risk of hypoglycaemia and how to avoid it.
 Avoid during poor metabolic control.
 Avoid trauma to extremities.
EXERCISE

50. EXERCISE PRECAUTIONS
 Patients who have BS >250mg/dl and who have urine
ketones should not begin exercise until urine tests are
NEGATIVE.
 Use of proper footwear.
 Avoid exercise in extreme heat or cold
 Have snacks after the exercise , to avoid post exercise
hypoglycemia.

51.  There are currently four classes of oral anti-diabetic
agents:
i. Biguanides
ii. Insulin Secretagogues – Sulphonylureas
iii. Insulin Secretagogues – Non-sulphonylureas
iv. α-glucosidase inhibitors
v. Thiazolidinediones (TZDs)
vi. DPP4i
B. ORAL ANTI-DIABETIC AGENTS

52. MAJOR CLASSES
• Body to insulin +/-
control hepatic
glucose production
• Stimulate the
pancreas to make
more insulin
• Slow the absorption
of starches
Thiazolidinediones
Biguanides
Sulfonylureas
Meglitinides
Alpha-glucosidase
inhibitors

53. Oral Anti-diabetic Agents

54. BIGUANIDES
 Metformin : is the only drug of this class presently available
in market
 It does not cause hypoglycaemia
 MOA : They increase glucose uptake and utilisation in
skeletal muscle (thereby reducing insulin resistance) and
reduce hepatic glucose production (gluconeogenesis).
 Pharmacokinetic : Metformin has a half-life of about 3
hours and is excreted unchanged in the urine.

55. METFORMIN
 Side effects :
-Dose-related gastrointestinal disturbances
-lactic acidosis is a rare but potentially fatal toxic effect
-Long-term use may interfere with absorption of vitamin B12
 Contra indications:
• Renal failure
• Hepatic disease
• Hypoxic pulmonary disease
• Heart failure or shock
Temporarily discontinued before any
radiographic procedure involving
intravenous iodinated contrast,
as patients are at an increased risk
of lactic acidosis.

56. INSULIN SECRETAGOGUES
SULFONYLUREAS : Inhibit KATP Channel of ß-cells
First-generation agents
 Tolbutamide
 Acetohexamide
 Tolazamide
 Chlorpropamide
Second-generation
Glipizide
Glyburide
Glimepiride

57. SULFONYLUREAS
 Hypoglycemia is the most common and most serious adverse
event associated with SU therapy
 Weight gain, regarded as a class effect of Su’s
 Contraindicaton: liver failure, renal failure patients.
 Most sulfonylureas cross the placenta and enter breast milk; as
a result, use of sulfonylureas is contraindicated in pregnancy and
in breast feeding
 P’kinetics : Orally given, Some is oxidised in the liver to
moderately active products and is excreted in urine; 50% is
excreted unchanged in the faeces.

58. NON-SULFONYLUREA SECRETAGOGUES
 MEGLITINIDES
• MOA: Inhibit KATP Channel of ß-cells
• Very fast onset of action, rapidly metabolized by liver
enzymes, with a peak effect within 1 hour, the duration of
action is 5–8 hr.
• Short duration of action and a low risk of hypoglycaemia
• Medications in this Class: repaglinide ,nateglinide

59. THIAZOLIDINEDIONES
 ↓ Insulin resistance by making muscle and adipose cells
more sensitive to insulin. They also suppress hepatic
glucose production.
 Side effects: weight gain, oedema, Hypoglycemia (if taken
with insulin)
 Contraindication: patients with abnormal LFT or CHF
 Medications in this class: pioglitazone , rosiglitazone,

60. Α-GLUCOSIDASE INHIBITORS
 Acarbose : An inhibitor of intestinal α-glucosidase.
 MOA : It delays carbohydrate absorption, reducing the
postprandial increase in blood glucose .
 Unwanted effects : flatulence, loose stools or diarrhoea, and
abdominal pain and bloating.
 Like metformin, it is helpful in obese type 2 patients, and it
can be co-administered with metformin.

61. TREATMENT OF TYPE 2 DIABETES
Diagnosis
Therapeutic Lifestyle Change
Combination Therapy - Oral Drug with Insulin
Combination Therapy - Oral Drugs Only
Monotherapy

62.  If glycaemic control is not achieved (HbA1c > 6.5%) with lifestyle
modification within 1 –3 months, ORAL ANTI-DIABETIC AGENT should
be initiated.
 In the presence of marked hyperglycaemia in newly diagnosed
symptomatic type 2 diabetes (HbA1c > 8%, FPG > 11.1 mmol/L), oral
anti-diabetic agents can be considered at the outset together with
lifestyle modification.
MONOTHERAPY

63. Combination oral agents is indicated in:
 Newly diagnosed symptomatic patients with HbA1c >10
 Patients who are not reaching targets after 3 months on
monotherapy
COMBINATION ORAL AGENTS

64. DIABETES MANAGEMENT ALGORITHM

65. Short-term use:
 Acute illness, surgery, stress and emergencies
 Pregnancy
 Breast-feeding
 Insulin may be used as initial therapy in type 2 diabetes
 Severe metabolic decompensation (diabetic ketoacidosis,
hyperosmolar nonketotic coma, lactic acidosis, severe
hypertriglyceridaemia).
INSULIN THERAPY

66. Long-term use:
 If targets have not been reached after optimal dose of
combination therapy, consider change to multi-dose insulin
therapy.
INSULIN THERAPY

68. INSULIN INJECTION SITES

69. ROUTES OF ADMINISTRATION
 Subcutaneous for long term regular use
 Intravenous infusion in acute conditions- diabetes
Ketoacidosis, Perioperative period, Hyperosmolar
Nonketotic state ONLY NEUTRAL/ CLEAR INSULIN CAN BE
USED
 Intraperitoneal – Peritoneal dialysis patients
 Inhaled insulin- experimental

71. COMPLICATIONS OF INSULIN
THERAPY
 Hypoglycemia
 Lipodystrophy
 Systemic allergic reactions
 Insulin resistence
 Dawn phenomenon
 Somagyi's phenomenon

72. METHODS OF INSULIN THERAPY
 Insulin syringe:
 Insulin pens
 Jet injectors
 Insulin Pumps

73. PATIENT EDUCATION
 Taking care of diabetes will help to reduce blood glucose, blood
pressure, and cholesterol levels in target ranges.
 Caring for your diabetes can also help prevent other health
problems over the years.
 Follow your healthy eating plan every day.
 Be physically active every day.
 Take your medicines every day.
 Check your blood glucose levels every day.

74. COMPLICATIONS OF
DIABETES

75. COMPLICATIONS OF DIABETES MELLITUS
I. Acute complications:
diabetic ketoacidosis
hypoglycemia
diabetic nonketotic hyperosmolar coma
II. Chronic complications:
 a. Microvascular
retinopathy
nephropathy
neuropathy
diabetic foot
dermopathy
 b. Macrovascular
Cerbro-vascular.
Cardio-vascular.
peripheral vascular
disease.

76. HYPOGLYCEMIA
 Hypoglycemia is the most frequent acute complication in
diabetes.
 Signs and symptoms are most common when blood
glucose levels fall <60 mg/dL
 CAUSE:
 Missing meals or excessive exercise
 Alterations or errors in insulin dosage
 Alcohol ingestion

77. CLINICAL MANIFESTATIONS OF
HYPOGLYCEMIA:
 Autonomic dysfunctions:
1. Hunger
2. Tremor
3. Palpitation
4. Anxiety
5. Pallor
6. Sweating
Neurologic dysfunctions:
1. Impaired thinking
2. Change of mood
3. Irritability
4. Headache
5. Convulsion
6. Coma

79. MANAGEMENT
 MILD (Self treated)
 Oral fast acting carbohydrate (10- 15gm) – taken as
glucose drink or candy
 Severe :(semi conscious or comatose patient)
 IV hypertonic glucose 25% or 50% concentration
 Glucagons injection- i.m Glucagon (1mg)

81. DIABETIC KETOACIDOSIS
- It is a true emergency
- CAUSES: Omitting insulin in type 1 DM or increase insulin
requirements,
 Infection
 Trauma
 Myocardial Infarction
 Stroke
 Surgery
 Emotional stress
 Mortality rate is around 5%.

82. CLINICAL PRESENTATION

83. MANAGEMENT
 Fluid replacement: 0.9% NaCl IV
 Insulin therapy for hyperglycemia: To restore the metabolic
abnormalities. Titrate the dose according to the blood glucose level.
• 50U insulin in 50 ml NS iv via infusion pump
 6U/hr initially
 3U/hr when blood glucose < 270mg/dl
 2U/hr when blood glucose < 180mg/dl
 Electrolyte correction.
 Acidosis correction.
 Treatment of precipitating cause.

84. HYPERGLYCEMIA HYPEROSMOLAR
NONKETONIC SYNDROME (HHNK)
 Occurs when there is insufficient insulin to prevent
hyperglycemia, but there is enough insulin to prevent
Ketoacidosis
 Occurs in all types of diabetes, Esp Diabetes Type 2
 Life threatening medical emergency
 Characterized by :
 Plasma osmolarity 340 mOsm/L or greater normal: 280 -300)
 Blood glucose severely elevated, 600 - 1000 or 2000 (normal 70-
110)
 Undetectable ketonuria and Absence of acidosis

85. HHNKS
 Major difference from diabetic ketoacidosis is the lack of
ketonuria because there is some residual ability to secrete
insulin in NIDDM.
CLINICAL MANIFESTATION:
 Altered level of consciousness (lethargy to coma)
 Neurological deficits: hyperthermia, motor and sensory
impairment, seizures
 Dehydration: dry skin and mucous membranes, extreme
thirst.

86. MACRO-VASCULAR COMPLICATIONS
 Ischemic heart diseases.
 Cerebrovascular diseases.
 Peripheral vascular diseases.
Diabetic patients have a 2 to 6 times higher risk for development of
these complications than the general population

87. HYPERTENSION IN DM
 Mostly present at diagnosis
 Affects about 60% of patients
 Secondary to insulin resistance
 Increases risk for retinopathy, nephropathy
 Dyslipidaemia in DM
 Most common abnormality is  HDL and  Triglycerides
 A low HDL is the most constant predictor of Cardiovascular
disease in DM.

88. PERIPHERAL VASCULAR DISEASE
 Increased risk for Types 1 and 2 diabetics.
 Development of arterial occlusion and thrombosis resulting
in gangrene.
 Gangrene from diabetes is themost common cause of non-
traumatic lower limb amputation

89. SCREENING FOR MACROVASCULAR
COMPLICATIONS
1. Examine pulses for cardiovascular diseases.
2. Lipid profile.
3. ECG.
4. Blood pressure.

90.  Microvascular complications are specific to longstanding
hyperglycaemia.
 Both Type1 DM and Type2 DM are susceptible to
microvascular complications.
 The duration of diabetes and the quality of diabetic control
are important determinants of microvascular abnormalities.
MICROVASCULAR COMPLICATIONS

91. DIABETIC RETINOPATHY
 Affects 60 % of Type 2 diabetics
 progressive, irreversible vision loss.
 Damage to the tiny blood
vessels that supply the eye
• Micro aneurysms
• Scattered exudates
• Cotton wool spots (<5)
• Venous dilatations
NORMAL RETINA
Cotton wool spots

92. DIABETIC NEPHROPATHY (DN)
Diabetic nephropathy is defined by persistent albuminuria (>300
mg/day), decrease glomerular filtration rate and rising blood
pressure.
About 20 – 30% of patients with diabetes develop diabetic nephropathy
- Manifested as:
- Microalbuminuria
- Progressive diabetic nephropathy leading to end-stage
renal disease

93. TREATMENT TO PREVENT PROGRESSION TO DN
 All diabetic patients should be screened annually for
microalbuminurea.
 Tight glycemic control and management of the blood pressure
 ACE-inhibitors are recommended to decrease the progression of
nephropathy
 Smoking cessation.
 Proteins restriction.
 Lipid reduction.

94. DIABETIC NEUROPATHY
 Damage to the Nerves due to hyperglycemia
 Types of Neuropathies…
 Sensory-Motor Polyneuropathy
• Numbness, paresthesias.
• Feet are mostly affected, hands are seldom affected.
• Complicated by ulceration (painless), charcot arthropathy
• Decreased deep tendon reflexes

95. DIABETIC NEUROPATHY
 Autonomic neuropathy
 Can affect almost any system
- Manifested by orthostatic hypotension, diabetic diarrhea,
erectile dysfunction, and difficulty in urination.

96. RESEARCH INPUT
 Effect of mechanical vibration on transcutaneous oxygen
levels in the feet of type 2 diabetes mellitus patients.
 Núñez Carrera L, Alessi Montero A ,et al
 Journal of clinical medicine: 2016 Nov 18.
 objective : To determine whether whole body vibration
favors some parameters of interest related
to complications associated with the diabetic foot
syndrome.(Transcutaneous oxygen levels (TcPO2)>40mmHg in cases of
diabetic foot syndrome are associated with a good prognosis in the
resolution of ulcers.)

97.  METHOD:54 patients with DM were included in a 12-week
exercise program based on whole body vibration.
Glycemic control was determined on the basis of the
patients' levels of (HbA1c); sensitivity and TcPO2 levels of
each foot were also recorded.
 RESULTS: A significant 7mmHg increase was observed in
the concentration of TcPO2.
 CONCLUSION: Whole body vibration may increase
TcPO2 levels with useful implications for the prevention or
management of complications associated with restricted
blood perfusion in the diabetic foot syndrome.

99. NURSING
MANAGEMENT

100. NURSING ASSESSMENT
Obtain history : it includes,
 Current problems and General health history
 Family history
 Has the patient experienced polyuria,polydipsia,
polyphagia, and any other symptoms?
 Number of years since diagnosis of DM?
 Symptoms of complications?

101. NURSING ASSESSMENT
 PHYSICAL EXAMINATION:
 General: Recent wt. loss or gain, fatigue, anxiety
 Skin: lesion, infections, dehydration,
 Eyes: changes in vision, “floaters, halos, cataracts…
 Cardiovascular: orthostatic hypotension, claudication
 GI: diarrhea, increased hunger and thirst
 GU: polyurea, nocturia
 Neurologic: numbness, and tingling of extremities

102. 1.Imbalanced nutrition : more than body
requirement related to intake of excess of
activity expenditures.
• Assess the current timings and content of meals
• Advise patient on the importance of an individualized
meal plan in meeting weight loss goals.
• Explain the importance of exercise in maintain /
reducing body weight.
• Assist the patient to establish goals for weekly weight
loss and incentives to assist in achieving them.

103. Risk for injury ( hypoglycemia) related to effects of
insulin, inability to eat.
• Closely monitor blood glucose levels to detect
hypoglycemia.
• Instruct the patient in the importance of accuracy in
insulin preparation and meal timings to avoid
hypoglycemia.
• Treat hypoglycemia promptly with 15 to 20 gm of fast
acting carbohydrates.
• Encourage patients to carry sugar candy all times.
• Encourage patient to wear identification bracelet

104. • Assess level of knowledge of disease and ability to
care self.
• Assess adherence to diet therapy, monitoring
procedures, medication, treatment, and exercise
regimen.
• Assess for signs for hyperglycemia or hypoglycemia.
• Perform skin and extremity assessment for peripheral
neuropathy or any injury in feet and lower extremities.
Deficit knowledge related to use of oral
hypoglycemic agents

105.  Assess feet and legs for skin temperature sensation,
soft tissue injures, corn, dryness, hammer toe,
 Maintain skin integrity by protecting feet from break down.
 Use heel protectors, special mattresses, foot cradles for
patient on bed rest.
 Avoid Appling drying agent to skin. (alcohol)
 Apply moisturizers to maintain suppleness and prevent
cracking and fissures.
 Instruct patient in foot care guidelines
Risk for impaired skin integrity related to decreased
sensation and circulation to lower extremities.

106. FOOT CARE
Patient should
 check feet daily
 Wash feet daily
 Keep toe nails short
 Protect feet
 Always wear shoes
 Look inside shoes before
putting them on
 Always wear socks
 Break in new shoes gradually

107.  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 DM self
care regimen
 Assist family in providing emotional support.
Ineffective coping related to chronic disease and complex
self care regimen.

108. SPECIAL PATIENT POPULATION
 1. Adolescent Type 2 DM
- Type 2 DM is increasing in adolescent
- Lifestyle modification is essential in these patients
- If lifestyle modification alone is not effective, metformin
the only labeled oral agent for use in children (10-16
years)

110. CONCLUSION
 Type 2 diabetes is a “life style” disease, characterized by
hyperglycemia resulting from defects in insulin secretion,
insulin action, or both. Caring for diabetes can also help
prevent other health problems over the years.