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.
The earliest known
record of diabetes was
written on 3rd Dynasty
Egyptian papyrus by
He stated recurring
urination as a sign of
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
pancreatic juice enzymes promote the digestion of
carbohydrates, proteins and fats
Insulin and glucagon- enter portal vein – transported directly to
the liver – regulate metabolism of carbohydrates, proteins and
15- 20% α cells synthesize and secrete GLUCAGON
70- 80% β cells synthesize and secrete INSULIN
1-8% δ cells synthesize and secrete STOMATOSTATIN
1-2% F- cells secrete PANCREATIC POLYPEPTIDE
which decreases the absorption of food from the GIT
Polypeptide hormone produced by β- cells of islets of
Langerhans of pancreas
Insulin is a protein made of 2 chains- alpha and beta
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
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
• 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
Glycogenolysis : The breakdown of glycogen to
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
Pancreas secretes 40-50 units of insulin daily in two steps:
• Secreted at low levels during fasting ( basal insulin
• Increased levels after eating (prandial)
• An early burst of insulin occurs within 10 minutes of
• Then proceeds with increasing release as long as
hyperglycemia is present
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
Such patients are absolutely dependent on exogenously
administered insulin for survival.
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
in muscle cells
glucose by the
defect of the beta
• 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:
28. RISK FACTORS
Age: 45 or more
Race : African American, Asian American, Hispanic or
Familial history : a parent, or siblings with diabetes.
29. RISK FACTORS
Heart and blood disease
Low HDL cholesterol and high triglycerides.
Polycystic ovary syndrome
30. RESEARCH INPUT
High Bone Mineral Density and Fracture Risk in Type
2 Diabetes as Skeletal Complications of Inadequate
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
420 participants with type 2 diabetes were classified by
glucose control - according to HbA1c
adequately controlled diabetes (ACD: n = 203;
inadequately controlled diabetes (ICD; n = 217;
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
Most patients are discovered while performing urine
40. Any one test should be
confirmed with a
second test, most often
fasting plasma glucose
• Classic signs of HYPERGLYSEMIA with CPG ≥200mg/D
• OGTT ≥200mg/dL
• FPG ≥126mg/dL
• A1C ≥ 6.5%
43. The major components of the treatment of diabetes are:
MANAGEMENT OF DM
• Medical Nutrition Therapy(Diet and
• Oral hypoglycaemic therapyB
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.
45. 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
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
47. Eat grains in the least processed state possible.
Limit potatoes and refined grain products.
Avoid concentrated sweets (jellies, jams, cakes, ice
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
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.
50. EXERCISE PRECAUTIONS
Patients who have BS >250mg/dl and who have urine
ketones should not begin exercise until urine tests are
Use of proper footwear.
Avoid exercise in extreme heat or cold
Have snacks after the exercise , to avoid post exercise
51. There are currently four classes of oral anti-diabetic
ii. Insulin Secretagogues – Sulphonylureas
iii. Insulin Secretagogues – Non-sulphonylureas
iv. α-glucosidase inhibitors
v. Thiazolidinediones (TZDs)
B. ORAL ANTI-DIABETIC AGENTS
52. MAJOR CLASSES
• Body to insulin +/-
• Stimulate the
pancreas to make
• Slow the absorption
Metformin : is the only drug of this class presently available
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.
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
• 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.
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
• 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
↓ Insulin resistance by making muscle and adipose cells
more sensitive to insulin. They also suppress hepatic
Side effects: weight gain, oedema, Hypoglycemia (if taken
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
Therapeutic Lifestyle Change
Combination Therapy - Oral Drug with Insulin
Combination Therapy - Oral Drugs Only
62. If glycaemic control is not achieved (HbA1c > 6.5%) with lifestyle
modification within 1 –3 months, ORAL ANTI-DIABETIC AGENT should
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
63. Combination oral agents is indicated in:
Newly diagnosed symptomatic patients with HbA1c >10
Patients who are not reaching targets after 3 months on
COMBINATION ORAL AGENTS
65. Short-term use:
Acute illness, surgery, stress and emergencies
Insulin may be used as initial therapy in type 2 diabetes
Severe metabolic decompensation (diabetic ketoacidosis,
hyperosmolar nonketotic coma, lactic acidosis, severe
66. Long-term use:
If targets have not been reached after optimal dose of
combination therapy, consider change to multi-dose insulin
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
Intraperitoneal – Peritoneal dialysis patients
Inhaled insulin- experimental
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.
75. COMPLICATIONS OF DIABETES MELLITUS
I. Acute complications:
diabetic nonketotic hyperosmolar coma
II. Chronic complications:
Hypoglycemia is the most frequent acute complication in
Signs and symptoms are most common when blood
glucose levels fall <60 mg/dL
Missing meals or excessive exercise
Alterations or errors in insulin dosage
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
Mortality rate is around 5%.
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
3U/hr when blood glucose < 270mg/dl
2U/hr when blood glucose < 180mg/dl
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
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-
Undetectable ketonuria and Absence of acidosis
Major difference from diabetic ketoacidosis is the lack of
ketonuria because there is some residual ability to secrete
insulin in NIDDM.
Altered level of consciousness (lethargy to coma)
Neurological deficits: hyperthermia, motor and sensory
Dehydration: dry skin and mucous membranes, extreme
86. MACRO-VASCULAR COMPLICATIONS
Ischemic heart 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
Gangrene from diabetes is themost common cause of non-
traumatic lower limb amputation
90. Microvascular complications are specific to longstanding
Both Type1 DM and Type2 DM are susceptible to
The duration of diabetes and the quality of diabetic control
are important determinants of microvascular abnormalities.
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
Cotton wool spots
92. DIABETIC NEPHROPATHY (DN)
Diabetic nephropathy is defined by persistent albuminuria (>300
mg/day), decrease glomerular filtration rate and rising blood
About 20 – 30% of patients with diabetes develop diabetic nephropathy
- Manifested as:
- Progressive diabetic nephropathy leading to end-stage
93. TREATMENT TO PREVENT PROGRESSION TO DN
All diabetic patients should be screened annually for
Tight glycemic control and management of the blood pressure
ACE-inhibitors are recommended to decrease the progression of
94. DIABETIC NEUROPATHY
Damage to the Nerves due to hyperglycemia
Types of Neuropathies…
• Numbness, paresthesias.
• Feet are mostly affected, hands are seldom affected.
• Complicated by ulceration (painless), charcot arthropathy
• Decreased deep tendon reflexes
95. DIABETIC 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.
100. NURSING ASSESSMENT
Obtain history : it includes,
Current problems and General health 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
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
• 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
• Instruct the patient in the importance of accuracy in
insulin preparation and meal timings to avoid
• Treat hypoglycemia promptly with 15 to 20 gm of fast
• Encourage patients to carry sugar candy all times.
• Encourage patient to wear identification bracelet
104. • Assess level of knowledge of disease and ability to
• Assess adherence to diet therapy, monitoring
procedures, medication, treatment, and exercise
• 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
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
check feet daily
Wash feet daily
Keep toe nails short
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
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
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.