Transcript DIABETES MELLTIUS - Rawal College Of Dentistry

DIABETES MELLTIUS
Dr. Ayisha Qureshi
Assistant Professor
MBBS, MPhil
DIABETES MELLITUS
Definition:
Diabetes mellitus is a syndrome of impaired
carbohydrate, protein & fat metabolism
caused by either lack of insulin secretion
or decreased sensitivity of the tissues to
insulin.
The word “Diabetes Mellitus” literally means
“excessive secretion of sweet urine”
DIABETES MELLTIUS
• In 2000, diabetes affected 150 million people
worldwide
• This number is expected to climb to 220 million
by 2010.
• Third leading cause of death
• Leading cause of blindness
• Diabetes is a very prevalent disease, has a huge
economic toll, forces individuals to change their
lifestyle thus affecting their quality of life &
predisposes the affected to a variety of
troublesome & even life threatening conditions.
Diabetes Mellitus
Type I
Juvenile onset/
Insulin Dependant
Type II
Adult onset/
Insulin Independent
TYPE I/ Juvenile Onset/ Insulin Dependant
It is the more severe from of diabetes.
DEFINITION:
It is a catabolic disorder in which circulating insulin is virtually
absent, plasma glucose is elevated & the pancreatic beta cells
fail to produce any insulin in response to all insulinogenic
stimuli.
Cause: Lack of insulin secretion from the beta cells of the islets
of langerhans
• It is an autoimmune disorder in which there is selective destruction
of the pancreatic beta cells by T lymphocytes.
• Mostly it seems to have an immunological basis & circulating islet
cell antibodies & anti-insulin antibodies may be demonstrated.
• Usually there is a genetic predisposition to this type of diabetes
which may be triggered off by:
- Viral infections e.g. rota virus, coxsackie virus
- Environmental triggers.
TYPE II DIABETES/ Non-Insulin
Dependant/ Adult Onset Diabetes
It is further classified into:
1. Non-obese type II
2. Obese type II
•
•
•
It is the most common type of diabetes, accounting for
about 90% of all cases of diabetes mellitus.
The age of onset is usually after 30, often b/w 50 & 60
years of age.
It develops gradually & is the less severe form of
diabetes.
Cause: Decreased sensitivity of target tissues to the
metabolic effects of insulin. This reduced sensitivity to
insulin is often called INSULIN RESISTANCE.
TYPE II DIABETES
Factors that can lead to Insulin resistance include:
1. Anti-insulin antibodies
2. Autoantibodies to the insulin receptor
3. Mutation of insulin receptor
4. Down-regulation of insulin receptors by sustained
hyperinsulinism
5. Primary hyperinsulinism (Beta cell adenoma)
6. Secondary hyperinsulinism (Cushing’s syndrome,
acromegaly, pregnancy or diabetes mellitus)
In both # 5 & 6 Poor response of the target organs is due to
reduced numbers of insulin receptors
7. Obesity/overweight especially excess fat deposits
around the abdomen
PATHOPHYSIOLOGY
• Diabetes type I is far more rapid in onset
occurring over a few days as compared to type II
which has a more gradual onset.
• Type I also shows far more complications as
compared to Type II which rarely shows
complications
• Type I requires Insulin while Type II can usually
be controlled by simple changes in lifestyle as
diet, exercise & weight control
• Type I insulin is more prone to Ketoacidosis
while Type II is not!
COMPLICATIONS
In long standing diabetes mellitus, following complications
may arise:
1. Neuropathies
2. Peripheral vascular disease
3. Gangrene
4. Atherosclerosis
5. Ischemic heart disease
6. Renal disease
7. Early cataract
8. Retinopathy
9. Skin infections
10. Neuropathies affecting the ANS
Diabetic foot showing ulcer
Gangrene that must be treated with
an amputation
DIAGNOSIS OF DIABETES
1. Blood sugar random ( 80-120 mg/100ml)
2. Blood sugar fasting (80-90 mg/100ml)
3. GTT or Glucose Tolerance Test:
When a normal fasting person is given 1g of glucose /kg
body weight, his plasma glucose levels rise to 120-140
but fall back to normal within 2 hours
In a prediabetic or diabetic, not only is the fasting plasma
glucose on the higher side but also the post meal
plasma glucose rises to as high as 140-200 & fails to
come back to normal within 2 hours of giving conc.
glucose solution. Even after 4-6 hours it rarely comes
back to the normal range!
NORMAL MEAN BLOOD GLUCOSE IS APP. 110 !
POINT TO REMEMBER!
WHY IS ORAL GLUCOSE A MORE
POWERFUL STIMULANT THAN
INJECTABLE GLUCOSE FOR INSULIN
SECRETION?
Glucose Tolerance Test
DIAGNOSIS OF DIABETES
4. Presence of glucose in urine (glucosuria)
5. Acetone breath
6. Lab test for assessing control of diabetes:
TREATMENT
•
Type I diabetes
WHY CANNOT INSULIN BE GIVEN BY MOUTH?
WHY IS ONLY CHO RESTRICTION NOT VERY EFFECTIVE?
Administer enough insulin so that metabolism of fat, proteins & CHO proceed
as normally as possible!
Insulin is available in various forms:
1.
Insulin preparations are available with rapid (regular), intermediate & long
durations of action:
- regular: duration of action is 3-8 hours
- Intermediate (NPH) not used during ER
- Long: duration of action is 10-48 hours
Individualized insulin schedules which consist of one injection of longer acting
insulin followed by regular insulin when the glucose level is expected to
rise .i.e. at meals.
Insulin is administered subcutaneously (s/c) except in the case of
emergencies when it is given intravenously (i/v).
The less soluble an insulin preparation is, the longer it acts!
INSULIN SYRINGES
TREATMENT
Type II diabetes:
• Diet
• Exercise
• Weight loss
The chief goal is to attain patient’s ideal weight!
• Drugs to increase sensitivity of different organs to insulin
- sulfonylureas
• Insulin injections
• Portable infusion pump
SULFONYLUREAS!
NIDDM patients above the age of 40 years & having h/o
diabetes of less than 5 years are given Oral
Hypoglycemics!
Mechanism of Action:
1. Stimulate release of Insulin from beta cells of pancreas
2. Reduction of serum Glucagon!
3. Increased binding of Insulin to target tissues &
receptors
E.g. Tolbutamide
Glyburide
Glipizide