SWEET

NOON TO ALL
Universal Symbol
For Diabetes
 CONTENTS:
 INTRODUCTION
 REVIEW OF ANATOMY AND
PHYSIOLOGY
 DEFINITION
 RISK FACTORS
 TYPES
 PATHOPHYSIOLOGY
 SIGN AND SYMPTOMS
 DIAGNOSTIC EVALUATION
 COMPLICATIONS
 MANAGEMENT
 PREVENTION
 Review of Anatomy and Physiology
PANCREAS
HORMONES:

• INSULIN BY BETA CELLS

• GLUCAGON BY ALPHA CELLS

• 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
INTRODUCTION
 Diabetes mellitus (DM), is a group of metabolic
diseases in which there are high blood sugar levels over
a prolonged period.

 Symptoms of high blood sugar include frequent urination,

increased thirst, and increased hunger.
DEFINITION OF DIABETES MELLITUS

Diabetes mellitus is a group of metabolic

diseases characterized by hyperglycemia resulting
from defects in insulin secretion, insulin action, or
both.
 If left untreated, diabetes can cause many complications.

Acute complications can include diabetic


ketoacidosis, nonketotic hyperosmolar coma, or death.

Serious long-term complications include heart

disease, stroke, chronic kidney failure, foot ulcers,
and damage to the eyes.
 Diabetes is due to either the pancreas not producing
enough insulin or the cells of the body not responding
properly to the insulin produced.
Risk Factors
• Obesity
• Race
• History of CVD
• HTN
• Physical inactivity
• Familial history
• Polycystic Ovary Syndrome
• Gestational Diabetes

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 There are three main types of diabetes
mellitus:
 Type 1 DM
 Type 2 DM
 Gestational Diabetes
 Type 1 DM
Results from the pancreas's failure to produce enough
insulin.

This form was previously referred to as "insulin-

dependent diabetes mellitus" (IDDM) or "juvenile
diabetes".

The cause is unknown.

 Type 2 DM
 Begins with insulin resistance, a condition in which
cells fail to respond to insulin properly.

This form was previously referred to as "non insulin-

dependent diabetes mellitus" (NIDDM) or "adult-onset
diabetes".
 The primary cause is excessive body weight and not
enough exercise.
 Gestational Diabetes

Is the third main form

and occurs in
pregnant women
without a previous
history of diabetes
 COMPARISON OF TYPE 1 AND 2 DIABETES
Feature Type 1 diabetes Type 2 diabetes
Onset Sudden Gradual
Age at onset Mostly in children Mostly in adults
Body size Thin or normal Often obese
Ketoacidosis Common Rare
Autoantibodies Usually present Absent
Normal,
Endogenous
Low or absent decreased
insulin
or increased
Concordance
50% 90%
in identical twins
Prevalence ~10% ~90%
Causes Type 1 diabetes

Type 1 diabetes is caused by the immune system destroying

the cells in the pancreas that make insulin. This causes
diabetes by leaving the body without enough insulin to
function normally.

This is called an autoimmune reaction, or autoimmune cause,

because the body is attacking itself.

There is no specific diabetes causes, but the following

triggers may be involved:

•Viral or bacterial infection

•Chemical toxins within food
•Unidentified component causing autoimmune reaction
Underlying genetic disposition may also be a type 1 diabetes.
Type 2 diabetes causes
•Obesity
•Living a sedentary lifestyle
•Increasing age
•Bad diet
Gestational diabetes causes

The causes of diabetes in pregnancy also known as

gestational diabetes remain unknown. However, there are a
number of risk factors that increase the chances of
developing this condition:
•Family history of gestational diabetes
•Overweight or obese
•Suffer from polycystic ovary syndrome
•Have had a large baby weighing over 9lb
Other diabetes causes
There are a variety of other potential diabetes causes. These
include the following:
•Pancreatitis or pancreatectomy as a cause of diabetes.
Pancreatitis is known to increase the risk of developing
diabetes, as is a pancreatectomy.
•Polycystic Ovary Syndrome (PCOS). One of the root causes
of PCOS is obesity-linked insulin resistance, which may also
increase the risk of pre-diabetes and type 2 diabetes.
•Cushing’s syndrome. This syndrome increases production of
the cortisol hormone, which serves to increased blood
glucose levels. An over-abundance of cortisol can cause
diabetes.
•Glucagonoma. Patients with glucagonoma may experience
diabetes because of a lack of equilibrium between levels of
insulin production and glucagon production.
•Steroid induced diabetes (steroid diabetes) is a rare form of
diabetes that occurs due to prolonged use of glucocorticoid
SIGNS AND SYMPTOMS OF DIABETES
SIGNS AND SYMPTOMS
 The classic symptoms of untreated diabetes are
 weight loss
 polyuria (increased urination)
 polydipsia (increased thirst) and
 polyphagia (increased hunger).

Symptoms may develop rapidly (weeks or months) in

type 1 DM, while they usually develop much more slowly
and may be subtle or absent in type 2 DM.
SIGNS AND SYMPTOMS
In addition they also include:
 Blurry vision
 Headache

 Fatigue

 Slow healing of cuts and

 Itchy skin.

 Prolonged high blood glucose can cause glucose

absorption in the lens of the eye, which leads to changes
in its shape, resulting in vision changes.

 A number of skin rashes that can occur in diabetes are

collectively known as diabetic dermadromes
Diagnostics
 PHYSICAL EXAMINATION

Weight / BMI Injection sites

Retinal examination Vibratory sensation

Foot examination Tooth examination

Orthostatic blood Peripheral pulses

pressure
Investigations during Follow up
1.Urine sugar,2 hr PP (once a week)

2.Blood Sugar-FBS,PPBS (once in 3-6 months)

3.Lipid profile (Once in a yr)

4.ECG (Once a yr)

5.Urine albumin

6.Blood Urea, Serum creatinine

7.Retinoscopy (Once in a yr)

8.Glycated Hb (Once in 3-6 months)

DIAGNOSIS
 Can be diagnosed by demonstrating any one of the
following:

 Fasting plasma glucose level ≥ 7.0 mmol/l (126 mg/dl)

 Plasma glucose ≥ 11.1 mmol/l (200 mg/dl) two hours

after a 75 g oral glucose load as in a glucose tolerance
test.

 Symptoms of high blood sugar and casual plasma

glucose ≥ 11.1 mmol/l (200 mg/dl)
DIAGNOSIS
 Oral Glucose Tolerance Test (OGTT)

Measures the body's ability to metobolise

glucose
Most commonly done to check for gestational
diabetes.
The patient is asked to take a glucose
drink and their blood glucose level is
measured
before and at intervals after the sugary drink is
taken.
For the standard glucose tolerance test,
we should drink 75 grams or 100 grams.
Fasting Plasma Glucose
Oral Glucose Tolerance Test (OGTT)
 OGTT RESULT’S :
 People without diabetes
Fasting value (before test): under 6 mmol/L
At 2 hours: under 7.8 mmol/L

 People with impaired glucose tolerance (IGT)

Fasting value (before test): 6.0 to 7.0 mmol/L
At 2 hours: 7.9 to 11.0 mmol/L

 Diabetic levels
Fasting value (before test): over 7.0 mmol/L
At 2 hours: over 11.0 mmol/L
WHO DIABETES DIAGNOSTIC CRITERIA
2 Hour Fasting
Condition HbA1c
Glucose Glucose
mmol/l mmol/l mmol/m
Unit DCCT %
(mg/dl) (mg/dl) ol

Normal <7.8 (<140) <6.1 (<110) <42 <6.0

Diabetes
≥11.1 (≥200) ≥7.0 (≥126) ≥48 ≥6.5
mellitus
Glycoselated Hemoglobin (HbA1c)

• HbA1c is a test that measures the

amount of glycated hemoglobin in
your blood. Glycated hemoglobin is a
substance in red blood cells that is
formed when blood sugar (glucose)
attaches to hemoglobin.
(HbA1c)
 HbA1C
Percentage of HbA to which Glucose is
attached

Normal: <5.7 %

Pre-diabetic: 5.7-6.4 %

Diabetic: >6.5 %
Urinalysis
• Glycosuria
• Ketone bodies
Management of diabetes mellitus

TREATMENT OF
DIABETES

LIFESTYLE
DIET OHA INSULIN
MODIFICATIONS
Why Diet Management?

 To control weight

 To complete nutritional requirements

 To maintain blood glucose levels in normal limits

 To correct any associated blood lipid

abnormalities
Diet in Diabetes
Diet in diabetes

1. Calories from food

~55% from carbohydrate

~30% from fat
~15% from protein

2. Calorie calculation

Overweight (sedentary)- 20 kC/kg

Normal wt (sedentary)- 30 kC/kg
Normal wt (heavy worker)- 35 kC/kg
Underweight- 40 kC/kg
Diet in diabetes

1.Avoid sweets

2.Avoid overeating

3.Avoid fasting

4.Avoid alcohol
5. 4-5 small frequent meals (Same
amount, same time daily)

6. Almonds : to lower cholesterol level

7. Fruits: Take apple, guava

8. Avoid excessive salt

 Lifestyle modifications
Regular exercise
Walking

Other aerobic exercises

Maintenance of weight

Stop smoking

Foot care
 Oral anti-diabetic drugs

If satisfactory control is not possible with

Diet and Lifestyle changes alone

Sulfonylureas (Tolbutamide,Glibenclamide)
Biguanides (Metformin)
Alpha-glucosidase inhibitors (Acarbose)
Thiazolidinediones (Rosiglitazone,Pioglitazone)
 Insulin
 Different species
 Bovine -Human (recombinant)

 Different preparations
 Soluble insulin (“plain insulin”)
 Rapid-acting insulin analogues
» Lispro
» Aspart
 Prolonged acting insulins
» Protamine Insulin (NPH, Isophane)
» Zinc insulin
» Glargine
 INSULIN ROUTE

Ultra rapid acting IV/SC PRANDIAL/

Insulin analog/ Short- SUPPLEMENTAL
Acting
(Humalog)
Rapid acting: IV/SC PRANDIAL/
Regular (Semilente) SUPPLEMENTAL

Intermediate: SC BASAL
NPH (Lente)

Long acting: SC BASAL

Protamine Zinc
(Ultralente)
Insulin
injectio
n sites
 Technique of injection

• Painless 30/31G needles

• Subcutaneous
– Abdomen
– Thighs
– Arms

• Patients should be trained

 Insulin Therapy

• Subcutaneous
– ~30 min for onset of action
– 60-90 min for peak action

• Should be given 30 min BEFORE meals

• Start with small dose and increase as

needed
Factors that influence the body’s
need for insulin

1.  need : trauma, infection,

fever, severe psychological or
physical stress, other illnesses
2.  need : active exercise
 Complications of Insulin therapy
• Hypoglycemia
• Local
–Lipohypertrophy
–Injection site abscess
• Insulin resistance
–Insulin antibodies
• Weight gain
–In overdosage
–Insulin stimulates hunger
EMERGENCY MANAGEMENT

 Hypoglycemia

 Initial
signs : mood changes, decreased spontaneity,
hunger and weakness.

 Followed by sweating, incoherence, tachycardia.

 Resultsin unconsciousness, hypotension,

hypothermia, seizures, coma, even death.
EMERGENCY MANAGEMENT

 15 grams of fast-acting oral carbohydrate.

 Measured blood sugar.

 Loss of consciousness: 25-30ml 50% dextrose solution iv.

over 3 min period.

 Glucagon 1mg.
EMERGENCY MANAGEMENT

 Severe hyperglycemia

 A prolonged onset

 Ketoacidosismay develop with nausea, vomiting,

abdominal pain and acetone odor.

 Difficult
to different hypoglycemia or
hyperglycemia.
EMERGENCY MANAGEMENT

 Hyperglycemia needs medical intervention and

insulin administration.

 While emergency, give glucose first !

 Small amount is unlikely to cause significant

harm.
 Surgery

Pancreas transplant
kidney transplantation
Weight loss surgery
 COMPLICATIONS
 All forms of diabetes increase the risk
of long-term complications. These
typically develop after many years
(10–20)

 The major long-term complications

relate to damage to blood vessels.

 Diabetes doubles the risk

of cardiovascular disease

 About 75% of deaths in diabetics are

due to coronary artery disease.

 Other "macrovascular"
diseases (stroke)

 peripheral vascular disease.

COMPLICATIONS
The primary complications of diabetes due to damage in
small blood vessels include damage to the eyes, kidneys,
and nerves.

 Damage to the eyes, known as diabetic retinopathy, is

caused by damage to the blood vessels in the retina of
the eye, and can result in gradual vision loss
and blindness.

 Damage to the kidneys, known as diabetic nephropathy,

can lead to tissue scarring, urine protein loss, and
eventually chronic kidney disease, sometimes
requiring dialysis or kidney transplant.

Damage to the nerves of the body, known as diabetic

neuropathy, is the most common complication of diabetes.
 COMPLICATIONS
 The symptoms can include
numbness, tingling, pain, and altered
pain sensation, which can lead to
damage to the skin.

 Diabetes-related foot
problems (such as diabetic foot
ulcers) may occur, and can be
difficult to treat, occasionally
requiring amputation.

Additionally,
proximal diabetic
neuropathy causes painful muscle
wasting and weakness – Diabetic
Amyotrophy.
Primary Prevention

a. Population strategy

Primordial prevention
Weight maintenance
Diet
Exercise

b. High risk strategy

Avoid diabetogenic drugs (corticosteroids)

Reduce the factors causing atheroslerosis
(smoking,hypertension,high cholesterol)
Secondary Prevention
Early diagnosis and treatment
Maintain blood glucose level
Maintain ideal weight (Height in cm-100)
Blood pressure measurement
Routine blood glucose monitoring
Urine for ketones and proteins
Glycated Hb estimation
(6 monthly, should be <6%)
Secondary Prevention
Keep sugar in your pocket
Weight,Blood pressure measurement,Visual acuity
Feet care
Self Care: Adhere to diet,drugs,exercise,
investigations, periodic check–ups, recognition of
symptoms of hypoglycemia

Identification card with treatment details

44
 Feet Care

Wash feet daily,dry them,inspect them,

sprinkle talcum powder

Avoid walking bare foot,even at home

Wear soft cotton socks and canvas shoes

Avoid tight fitting shoes,chappals

Cut nails carefully after bath

See for the sensations

 Feet Care

Do not use hot water bottles or heating pads or any

electrical device for heating the feet

Do not use a pumice stone to remove callousness

Do not sit with your legs crossed

 Do not use commercial wart or corn removers on

your feet
 Feet Care

 Do not perform "bathroom surgery" by using

razor blades or other sharp instruments on your feet

 Do not ignore any(minor also) foot problem

 Use cream or lotion that keeps your skin soft and

free of cracks
 Regular Self Glucose Monitoring

Tertiary Prevention
Disability limitation if any disability

Diabetes clinic
REFERENCES:

 Harsh Mohan - Textbook of Pathology

 A Book Of Clinical Biochemistry-

Jay pee Brothers Medical Publishers

 Essentials of Medical Physiology

 K.D. Tripathi - Essentials of Medical Pharmacology

 Internet