Type 2 diabetes is sometimes called a “life style” disease as it
more common in people who don’t do enough exercise, have
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 Indian physician
Sushruta in the 6th
century B.C. noticed
the sweet nature of
urine in such patients
and termed the
siphon or pass
"To pass through sweetened with
Diabetes is a group of metabolic diseases characterized by
hyperglycemia resulting from defects in insulin secretion,
insulin action, or both.
382 million people had diabetes in 2013
By 2035, this number will rise to 592
65.1 million people had diabetes in 2013
By 2035, this number will increase by
Courtesy: 2015 International Diabetes Federation
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
15- 20% α cells synthesize and secrete GLUCAGON
70- 80% β cells synthesize and secrete INSULIN
1-8% δ cells synthesize and secrete
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
STRUCTURE OF INSULIN
REGULATION OF INSULIN
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.
gastrointestinal hormones: Gastrointestinal hormones
(secretin, gastrin) enhance the secretion of insulin.
REGULATION OF INSULIN
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
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
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
• 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
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.
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:
COMPONENTS OF DM-II
Age: 45 or more
Race : African American, Asian American, Hispanic
Familial history : a parent, or siblings with diabetes.
Heart and blood disease
Low HDL cholesterol and high triglycerides.
Polycystic ovary syndrome
Patients can be asymptomatic
Most patients are discovered while performing urine
•Measures the amount of glycated haemoglobin in
blood.•HbA1c is not sensitive enough to detect DM but
is standard for the long term monitoring.
Test to assess other complications
Any one test should be
confirmed with a second
test, most often fasting
plasma glucose (FPG).
• Classic signs of HYPERGLYSEMIA with CPG ≥200mg/
• OGTT ≥200mg/dL
• FPG ≥126mg/dL
• A1C ≥ 6.5%
The major components of the treatment of
MANAGEMENT OF DM
• Medical Nutrition Therapy(Diet and Exercise)A
• Oral hypoglycaemic therapyB
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
Follow individualized meal plan and snacks as
scheduled diet based on pts. wt., age, occupation and
Balanced diabetic diet – 50% CHO, 30% fats, 20%
CHON(Co2, H2o, O2, Nitrogen), vitamins and
Meal should include more fiber and starch and fewer
simple or refined sugars.
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
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 Glycemic Index food
Physical activity promotes weight reduction and
improves insulin sensitivity, thus lowering blood
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.
Patients who have BS >200mg/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
There are currently four classes of oral anti-diabetic
ii.Insulin Secretagogues – Sulphonylureas
iii.Insulin Secretagogues – Non-sulphonylureas
B. ORAL ANTI-DIABETIC
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
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
Heart failure or shock.
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.
• 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
• Medications in this Class: Repaglinide, Nateglinide.
↓ 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
Medications in this class: Pioglitazone,
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.
TREATMENT OF TYPE 2 DIABETES
Therapeutic Lifestyle Change
Combination Therapy - Oral Drug with Insulin
Combination Therapy - Oral Drugs Only
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.
Combination oral agents is indicated in:
Newly diagnosed symptomatic patients with
Patients who are not reaching targets after 3
months on monotherapy
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 hypertriglyceridaemia).
If targets have not been reached after optimal
dose of combination therapy, consider change to
multi-dose insulin therapy.
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
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 medicines every day.
Check blood glucose levels every day.
COMPLICATIONS OF DIABETES
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)
- It is a true emergency
- CAUSES: Omitting insulin in type 1 DM or increase
Mortality rate is around 5%.
Fluid replacement: 0.9% Na.
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.
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
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
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
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
A low HDL is the most constant predictor of
disease in DM.
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.
SCREENING FOR MACROVASCULAR
1. Examine pulses for cardiovascular
2. Lipid profile.
4. Blood pressure.
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
Affects 60 % of Type 2 diabetics
progressive, irreversible vision loss.
Cotton wool spots
Damage to the tiny blood vessels that supply the eye
• Micro aneurysms
• Scattered exudates
• Cotton wool spots (<5)
• Venous dilatations
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
- Manifested as:
- Progressive diabetic nephropathy leading to end-
stage renal disease
TREATMENT TO PREVENT
PROGRESSION TO DN
All diabetic patients should be screened annually for
Tight glycemic control and management of the blood
ACE-inhibitors are recommended to decrease the
progression of nephropathy
Damage to the Nerves due to hyperglycemia
Typses of Neuropathies…
• Numbness, paresthesias.
• Feet are mostly affected, hands are seldom affected.
• Complicated by ulceration (painless), charcot arthropathy
• Decreased deep tendon reflexes
Can affect almost any system
- Manifested by orthostatic hypotension, diabetic
diarrhea, erectile dysfunction, and difficulty in
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?
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
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.
2. 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 hypoglycemia.
Treat hypoglycemia promptly with 15 to 20 gm of fast
Encourage patients to carry sugar candy all times.
Encourage patient to wear identification bracelet
3. Deficit knowledge related to use of oral hypoglycemic
Assess level of knowledge of disease and ability to care
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.
4. Risk for impaired skin integrity related to decreased
sensation and circulation to lower extremities.
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
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
5. Ineffective coping related to chronic disease and
complex self care regimen.
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.
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
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.