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2. PRESENTED BY : 09Z31R0003
09Z31R0005
09Z31R0028
09Z31R0033
09Z31R0039
G.VANI
M.Pharm,Pharmacology
GUIDED BY: Mrs.
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3.  Introduction
To Diabetes Mellitus
Epidemiology
Blue Circle
Types Of Diabetes Mellitus
Pathophysiology
Clinical Manifestations Of Diabetes
Mellitus
Diagnosis Of Diabetes Mellitus
Management Of Diabetes Mellitus
Complications Of Diabetes Mellitus
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4. INTRODUCTION
TO
DIABETES
MELLITUS
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5. Diabetes mellitus is a group of metabolic diseases in
which a person has high blood sugar, either because the
pancreas does not produce enough insulin or because
cells do not respond to the insulin that is produced.
This high blood sugar produces the classical symptoms of
polyuria (frequent urination), polydipsia (increased thirst)
and polyphagia (increased hunger).
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6. EPIDEMIOLOGY
About 16 million have diabetes. Around the world, the prevalence
of diabetes is expected to double between 1994 and 2010, at which
time about 240 million people will have the disease. The incidence of
diabetes rises as the population ages and as the prevalence of obesity
increases.
Unfortunately, about half of those with diabetes are presently
unaware that they have the disease. Most dental practices have a
significant number of diabetic patients in their population. Based on
data, an "average" practice would have between 60 and 70 diabetic
individuals for every 1,000 patients, and 30 to 35 of these patients
would be undiagnosed.
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7. Continue…….
Gestational diabetes occurs during pregnancy and usually
resolves after delivery. Other types of diabetes may occur in
individuals with certain genetic disorders, pancreatic
diseases, infections, injuries to the pancreas, and endocrine
diseases. Drug therapy with certain agents may also induce
a diabetic state.
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8. WORLD DIABETES DAY
World Diabetes Day commemorates the global
awareness campaign, which is held on NOV 14.
It was introduced in 1991 by the
International diabetes federation and the world health
organization...In response to the alarming rise of diabetes around the
world.
The day also marks the birthday of FREDERICKBANTING
who, along with CHARLES BEST, first conceived the idea to
the discovery of insulin in 1922.
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10. TYPES OF DIABETES MELLITUS
TYPE-I
DIABETES
MELLITUS
TYPE-II
GESTATIONAL
DIABETES
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11. Type 1 diabetes is an autoimmune destruction of pancreatic beta
cells.
Hence the individual has an absolute insulin deficiency and no longer
produces insulin.
Autoimmune beta cell destruction is thought to be triggered by an
environmental event, such as a viral infection.
Most type 1 diabetic individuals are of normal weight or are thin in
stature.
Since the pancreas no longer produces insulin, a type 1 diabetes patient is
absolutely dependent on exogenously administered insulin for
survivalwith type 1 diabetes are highly susceptible to diabetic
People
ketoacidosis.
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13. Most type 2 diabetes patients are overweight, and most are diagnosed as
adults. The genetic influence in type 2 diabetes is greater than that seen with
type 1.
In addition to genetic influences, acquired risk factors for type 2 diabetes
include obesity, advancing age, and an inactive lifestyle.
pathophysiologic defect in type 2 diabetes does not involve autoimmune
beta-cell destruction.
Type 2 diabetes is characterized by the following three disorders:
(1) peripheral resistance to insulin, especially in muscle cells;
(2) increased production of glucose by the liver
(3) altered pancreatic insulin secretion
TYPE 2 DIABETIC PATIENTS OFTEN HAVE A GROUP OF DISORDERS THAT HAS BEEN CALLED
"INSULIN RESISTANCE SYNDROME" OR SYNDROME X.
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15. It usually develops during the third trimester and significantly increases
 The proper diagnosis and management of gestational diabetes improves
pregnancy outcomes.
As with type 2 diabetes, the pathophysiology of gestational diabetes is
associated with increased insulin resistance.
 Most patients with gestational diabetes return to a normoglycemic state
after parturition; however, about 30 to 50% of women with a history of
gestational diabetes will develop type 2 diabetes within 10 years.
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17. Pathophysiology of diabetes rests upon of the basics of carbohydrate
metabolism and insulin action.
consumption of food, carbohydrates are broken down into glucose molecules
in the gut.
Glucose is absorbed into the bloodstream elevating blood glucose levels. This
rise in glycemia stimulates the secretion of insulin from the beta cells of the
pancreas
Insulin is needed by most cells to allow glucose entry. Insulin binds to
specific cellular receptors and facilitates entry of glucose into the cell, which
uses the glucose for energy.
The increased insulin secretion from the pancreas and the subsequent cellular
utilization of glucose results in lowered of blood glucose levels. Lower glucose
levels then result in decreased insulin secretion
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18. Continue…….
If insulin production and secretion are altered by disease blood glucose
dynamics will also change.
Following meals, the amount of glucose available from carbohydrate
breakdown often exceeds the cellular need for glucose.
Excess glucose is stored in the liver in the form of glycogen, which serves as a
ready reservoir for future use. When energy is required, glycogen stores in the
liver are converted into glucose via glycogenolysis
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19. Continue…….
The liver also produces glucose from fat (fatty acids) and proteins (amino
acids) through the process of gluconeogenesis. Glycogenolysis and
gluconeogenesis both serve to increase blood glucose levels. Thus, glycemia is
controlled by a complex interaction between the gastrointestinal tract, the
pancreas, and the liver
Insulin is the only hormone that lowers blood glucose levels. The counterregulatory hormones such as glucagon, catecholamine's, growth hormone,
thyroid hormone, and glucocorticoids all act to increase blood glucose levels
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22. CLINICAL
MANIFESTATION
The symptoms are similar in type 1 & Type 2, but may vary in their intensity. (Common symptoms
include polyuria and polydipsia, which are a consequence of osmotic diuresis. Blurred vision may
occur due to a change in refraction. Weight loss despite normal or increased appetite is also
common feature).
Type 1
Type 2
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24. Patient's Blood glucose
conditio
levels
n
Inferences
Fasting
Fasting
<110 mg/dl
Normal value
110-126 mg/dl
Impaired fasting glucose (IFG) value.
Likely to develop NIDDM in later
stages.
Fasting
2hrs after
glucose
administration
126 mg/dl
DM is indicated & must be confirmed
(a) <140 mg/dl
(b) 140-200 mg/dl
(c) 200 mg/dl
Normal glucose tolerance
Impaired glucose tolerance (IGT)
Diabetes mellitus is confirmed
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25. HbA1c- THE BLOOD TEST
What is HbA1c?
Hemoglobin is a protein that makes your red
blood cells red-colored.
When hemoglobin picks up glucose from your
bloodstream, the hemoglobin becomes
glycosylated.
HbA1c in your bloodstream
Glycosylated hemoglobin is HbA1c. The
HbA1c test measures the percentage of HbA1c in
your blood—
a number that corresponds to your average blood
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glucose for the previous 3 months.

26. MANAGEMENT OF DM
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28. DIET
Fresh vegetables with out
salt & sugar
sweets and chronic alcohol intake
Green leafy vegetables
Whole fruits than juices
Citrus fruits
Whole grain foods
Beans-good source of fiber
Chicken with skin
Fish and lean cut beef
& pork
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29. Sulphonyl urea's
Biguanides
Meglitinides
Tolbutamide
Phenformin
Repaglinide
α-glucosidase
inhibitors
Chlorpropamide
Metformin
Nateglinide
Acarbose
Miglitol
Acetohexamide
Glibenclamide
Glipizide
Thiazolidinediones(TZD)/glitazones
Ciglitazone
Pioglitazone
Troglitazone
Rosiglitazone
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30. INSULIN THERAPY
Pancreas is an exocrine gland secreting pancreatic fluid
Into the duodenum after a meal.
Inside the pancreas are millions of clusters of cells called islets of Langerhans.
The islets are endocrine tissue containing four types of cells. In order of
abundance, they are:
Who need insulin
•Beta cells- insulin and amylin;
medicine????
Type I (insulin dependent) diabetes
•Alpha cells- glucagon;
patients whose body produces no
•Delta cells- somatostatin
insulin.
•Gamma cells/F cells- a polypeptide. Type 2 diabetes patients that do not
always produce enough insulin.
Treatment : subcutaneous
injection
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32. •It stimulates skeletal muscle fibers.
•It stimulates liver cells.
•It acts on fat cells
•It inhibits production of certain
Regular insulin's
Humulin
enzyme.
Novalin
•In each case, insulin triggers these Neutral protamine
hagedron
Lente insulin(Zn)
effects by binding to the insulin
receptor.
Insulin Analogs:
Fatty acid
acylated insulins
Insulin lispro
Insulin aspart
Insulin glargine
Insulin detemir
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33. Diabetes
Management
Algorithm
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34. Hypoglycemic coma
Diabetic ketoacidosis
Diabetic retinopathy
 Diabetic nephropathy
 Diabetic neuropathy
 Diabetic foot ulceration
 Diabetic Dermopathy
 Diabetic CV diseases
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37. DIABETIC NEPHROPATHY is initially
manifested by proteinuria & microalbuminuria.
•Subsequently, as kidney function declines, urea
and creatinine accumulate in the blood.
PROGRESSIVE DIABETIC NEPHROPATHY
consists of proteinuria of varying severity
occasionally leading to nephrotic syndrome
with hypoalbuminemia, edema, and an increase
in circulating LDL cholesterol
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38. •Loss of function appears which is due to an
axonal neuropathic process.
•Longer nerves are especially vulnerable, hence
the impact on the foot.
•Both motor and sensory nerve conduction is
delayed and ankle jerks may be absent.
•Sensory involvement usually seen which is
associated with dulled perception of vibration,
pain, and temperature.
PAINFUL DIABETIC NEUROPATHY
Erectile dysfunctioning is
Hypersensitivity to light touch and occasionally
severe "burning" pain, particularly at night, can
become physically and emotionally disabling.
Amitriptyline, 25-75 mg at bedtime, has been
recommended for pain associated with diabetic
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neuropathy

39. A foot ulcer in a diabetic patient, most probably due to nerve
damage. The callus (hard skin) around the ulcer, indicating
that the foot was subjected to excess pressure.
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40. Skin spots are uncommon in adult diabetics.
They are brownish, rounded, painless atrophic lesions of
the skin in the pretibial area.
Candidal infection can produce erythema and edema of
intertriginous areas below the breasts, in the axillas, and
between the fingers.
It causes vulvovaginitis in most chronically uncontrolled
diabetic women with persistent glucosuria and is a frequent
cause of pruritus.
While antifungal creams containing
miconazole or clotrimazole offer
immediate relief .
Vulvovaginitis, recurrence is
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41. •Cardiovascular disease risk is increased in patients with
type 1 diabetes & risk is lower than in patients with
type 2 diabetes.
• Premenopausal women who normally have lower rates
of coronary artery disease lose this protection once
diabetes develops.
•The increased risk in patients with type 2 diabetes
reflects the combination of hyperglycemia,
hyperlipidemia, abnormalities of platelet adhesiveness,
coagulation factors, hypertension, oxidative stress, and
inflammation.
•Lowering LDL cholesterol reduces without known
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coronary disease

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