P

DrV.MEERA
PROF&HOD
 INTRODUCTION
Diabetes is a group of metabolic disorders
characterized by abnormal metabolism, which results
most notably in hyperglycemia , due to defects in
insulin secretion, insulin action, or both.
Diabetes is a serious chronic disease without a cure,
and it is associated with significant morbidity and
mortality.
Diabetes is a serious disease associated with acute
(due to hyperglycemia) and chronic (due to vascular
damage) complications.
 Diabetes mellitus
"Diabetes" comes from the Greek word for "siphon",
and implies that a lot of urine is made.
The second term,"mellitus" comes from the Latin
word, "mel" which means "honey", and was used
because the urine was sweet.
 Diabetes in india
According to the Indian Council of Medical Research-
Indian Diabetes study (ICMR-INDIAB), a national
diabetes study, India currently has 63 million people
with diabetes.
India represents the world’s second largest diabetes
population after China.
This is set to increase to over 100 million by 2030.
The majority of people with diabetes (>90%) have
Type 2 diabetes (T2DM).
Learning Objectives
At the end of this talk you should understand:
What diabetes mellitus means
The difference between types-1 and -2 diabetes
How the different types are treated
The reasons for the current epidemic of diabetes and
how it can be prevented
What the complications of diabetes are and how they
can be prevented
 TYPESOFDIABETES
 TYPE -- 1 Diabetes Mellitus
 TYPE --2 Diabetes Mellitus
 Gestational Diabetes Mellitus
 Other uncommon types like
1. Genetic defects of beta cell function
2. Genetic defects in insulin action
3. Exocrine pancreatic defects
4. Infections
5. Drugs
6. Genetic syndromes like Down syndrome
PATHOPHYSIOLOGY
 ETIOLOGYOFDIABETES
Both type 1and type 2 diabetes share one
central feature: elevated blood sugar
(glucose) levels due to absolute or relative
insufficiencies of insulin, a hormone
produced by the pancreas.
Type 1-Beta cell destruction completely
leading to absolute insulin deficiency
Type 2 –combination of insulin
resistance and Beta cell dysfunction
BASICUNDERSTANDINGOF
GLUCOSEMETABOLISM AND
INSULIN ACTION
 Action of insulin
 It works in the following way:
•During and immediately after a meal, digestion
breaks carbohydrates down into sugar molecules
(of which glucose is one) and proteins into amino
acids.
•Right after the meal, glucose and amino acids are
absorbed directly into the bloodstream, and blood
glucose levels rise sharply. (Glucose levels after a
meal are called postprandiallevels.)
The rise in blood glucose levels signals important cells
in the pancreas, called beta cells, to secrete insulin,
which pours into the bloodstream. Within 20 minutes
after a meal insulin rises to its peak level.
Insulin enables glucose to enter cells in the body,
particularly muscle and liver cells. Here, insulin and
other hormones direct whether glucose will be burned
for energy or stored for future use.
When insulin levels are high, the liver stops producing
glucose and stores it in other forms until the body
needs it again.
 Blood sugar and health
Sugar (glucose) is
an important source Insulin is produced
of energy by the pancreas when
blood sugar ishigh

What is eaten is
absorbed into Insulin keeps blood
the blood sugar level within
the normal range
for health
PATHOPHYSIOLOGYOFTYPE1
Pathophysiology of Type1
Type 1diabetes is characterized by destruction of the
pancreatic beta cells. Most likely cause of these
conditions is combined genetic, immunologic and
possibly environmental (e.g. viral) factors contribute
to cell destruction.
This is abnormal response of the body in which the
antibodies are direct against the normal tissues as if
they were foreign and eventually can damage Islet of
Langerhans , specific area of the pancreas that produce
insulin, reducing the production of insulin or totally
no production of insulin.
PATHOPHYSIOLOGYOFTYPE2
PATHOPHYSIOLOGYOFTYPE2
Type 2 Diabetes Mellitus is a adult onset, and non-
insulin dependent. There are 2 main problems related
to insulin in type 2 diabetes, first one is “insulin
resistance “ (insulin do not bind with the special
receptor on cell surface) and impaired insulin
secretion (insulin secreting glands release irregular
amount of insulin).
 Gestational Diabetes
•Diabetes diagnosed during pregnancy
•Gestational diabetes is caused when the insulin
receptors do not function properly.
•This is likely due to pregnancy related factors such as
the presence of human placental lactogen that
interferes with susceptible insulin receptors.
•Increased health risk to mother and baby
•Big baby,jaundice,still birth can occur for untreated
cases
•Goes away after birth, but increased risk of
developing Type 2 DM for mother and child
Differences between type-1 andtype-2
Diabetes Mellitus
Type 1 Type 2
Young age Middle aged, elderly
Normal BMI, not obese Usually overweight/obese
No immediate family Family history usual
history Symptoms may be present
Short duration of for months/years
symptoms (weeks) Do not present with
Can present with diabetic diabetic coma
coma (diabetic Insulin not necessarily
ketoacidosis) required
Insulin required Previous diabetes in
pregnancy
These differences are not absolute
RISKFACTORS&SYMPTOMS
RISKFACTORS
Symptoms of Diabetes
Symptoms of new onset
Polyurea
Polydipsia
Polyphagia
Weight loss
Fatigue
 Symptoms
Hypoglycemia Hyperglycemia
Tremor Polyurea
Headache Polydipsia
Pallor Dry mouth
Dizziness Ketoacidosis (shortness of
Paresthesia breath)
Loss of coordination Hyperosmolar hyperglycemic
Anxiety non ketotic
syndrome(fever,confusion,
Mood confusion
weakness)
seizure
 INVESTIGATION
Fasting blood sugar
Post prandial blood sugar
HbA1C
Lipid Profile – To diagnose dyslipidaemia

RBS can be done only if the patient follows up for the

diagnostic tests after a meal
 FASTINGBLOODSUGAR
•Person to be tested should be on a normal diet for at least 3 days
prior to testing.
•The test should be done after an overnight fast of 8 – 10 hours (no
beverages including tea or coffee should be consumed),
•Draw a sample of blood after confirming fasting state of the patient.

Fasting Serum Glucose Diagnosis

(mg/dl)

Below 110 Normal

Between 110and 126 Pre-diabetes

Above 126 Diabetes (Must be confirmed with a

second fasting test)
 Post prandial blood sugar
Following the collection of the fasting blood sample
for analysis of fasting serum glucose (FSG). Patient is
advised to have a normal meal and return to the clinic
after 2 hours following the meal.
Draw a sample of blood after confirming the time of
meal.
Post prandial blood sugar Diagnosis

< 140mg/dl Normal

140-200mg/dl Pre -diabetic

>200mg/dl Diabetic
 HbA1C
Person to be tested should be on a normal diet for at
least 3 days prior to testing.
The test should be done after an overnight fast of 8 –
10 hours
Draw a sample of blood after confirming fasting state
of the patient.
HbA1C Levels Diagnosis

4-6 Normal for those without

diabetes
6.1-7 Target range fordiabetics

>7 Poor control

 Lipid profile
Results of lipid profile Classification
LDL
< 100 optimal
100-129 Near optimal
130-159 Borderline high
160-190 High
>190 Very high
Serum triglycerides
< 150 Optimal
150-199 Borderline high
200-499 High
>500 Very high
HDL cholesterol
< 40 Low
> 60 High
 TREATMENTGUIDELINES
Major Risk Factors (Exclusive of LDLCholesterol)
Cigarette smoking
Hypertension (BP >140/90 mmHg or on antihypertensive
medication)
Low HDL cholesterol (<40 mg/dL)
Family history of premature CHD
Age (men >45 years; women >55 years)
 TREATMENTGUIDELINES
LDL VALUES Risk factor Treatment goal
>_130 CHD Pharmacological
theraphy
>160 +2 risk factors Pharmacological
theraphy
>160-190 + 1risk factor Life style
modification
>190 +1 risk factor Pharmocological
theraphy
 PHYSICAL
EXAMINATION
 Complete physical examination
Examination
Weight/waist: – Body Mass Index (BMI)
– Waist circumference
Cardiovascular system:
– Blood pressure, ideally lying and standing
– Peripheral, neck and abdominal vessels
Eyes: – Visual acuity (with correction)
– Cataracts
– Retinopathy (examine with pupil dilation)
Feet: – Sensation and circulation
– Skin condition
– Pressure areas
– Interdigital problems
– Abnormal bone architecture
Peripheral nerves: – Tendonreflexes
– Sensation: touch
-vibration
Urinalysis: – Albumin
– Ketones
– Nitrites and/or leucocytes
TREATMENT
Management of DM
The major components of the treatment of diabetes
are:

A • Diet and Exercise

• Oral hypoglycaemic
B therapy

C • Insulin Therapy
A. Diet
Diet is a basic part of management in every case.
Treatment cannot be effective unless adequate
attention is given to ensuring appropriate nutrition.

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
Exercise
Physical activity promotes weight reduction and improves
insulin sensitivity, thus lowering blood glucose levels.

Together with dietary treatment, a programme of

regular physical activity and exercise should be
considered for each person. Such a programme must be
tailored to the individual’s health status and fitness.

People should, however, be educated about the

potential risk of hypoglycaemia and how to avoid it.
Nutritional Management for TypeI
Diabetes
Consistency and timing of
meals
Timing of insulin
Monitor blood glucose regularly
Nutritional Management for TypeII
Diabetes
Weight loss
Smaller meals and snacks
Physical activity
Monitor blood glucose and medications
MANAGEMENT OFTYPE1
DIABETES
MANAGEMENT OFTYPE2
DIABETES
COMPLICATIONS
 Chronic Complications
Systems Effected Disease Health Concern

Eyes • Retinopathy
• Blindness
• Glaucoma
• Cataracts

Blood Vessels • Coronary artery disease • Heart attack

• Cerebral vascular disease • Stroke
• Peripheral vascular disease • Poor circulation in feet
• Hypertension and legs
• Heart attack, stroke,
kidney damage
Kidneys • Renal insufficiency • Insufficient blood filtering
• Kidney failure • Loss of ability to filter blood

Nerves • Neuropathies • Chronic pain

• Poor nerve signaling to
• Autonomic neuropathy
organ systems

Skin, Muscle, Bone • Advanced infections

• Amputation
• Cellulitis
• Gangrene
 GENERAL TIPS
Steps to lower risk of diabetes complications:

• A1C < 7, which is an estimated average glucose of

154mg/dl
• Blood pressure < 130/80
• Cholesterol (LDL) < 100
• Cholesterol (HDL) > 40 (men) and > 50 (women)
• Triglycerides < 150
• Quitting smoking.
• Active life style.
• Healthy food choices.
Do’s and Don'ts of foot care
Patient should
check feet daily
Wash feet daily
Keep toenails short
Protect feet
Always wear shoes
Look inside shoes before
putting them on
Always wear socks
Break in new shoes gradually
FOLLOWUP
Fortnightly follow up for newly diagnosed cases
Monthly follow up for known diabetics
Quarterly review
Annual review
Health education
Self examination
 Quarterly review
Weight/waist
Height (children and adolescents)
Blood pressure
Feet examination without shoes, if new symptoms or
at risk
 Annual review
Weight/waist
Height (children and adolescents)
Blood pressure
Feet examination: without shoes, pulses,
monofilament check
Blood glucose at examination
Urinalysis
Visual acuity
Cornerstones of Diabetes
Management

 Healthy eating
 Exercise
 Monitoring
 Medication/Insulin
 Health Care Team
THANK
YOU