2. It is a chronic systemic clinical syndrome , which is
characterized by hyperglycemia that reflect to either lack
of the insulin or there is peripheral resistance to insulin.
As a result there is elevation of the serum glucose level,
the consequence of the elevated glucose level is that there
is non – enzymatic glycosylation of the protein that have
lot of the pathology of the diabetes
4. Diabetes mellitus is diagnosed by there is elevation of the fasting
glucose level more than 126 on two separate occasion
Or
There glucose tolerance test (GTT) is positive
These can make the diagnosis
5. There are two types
-Primary diabetes mellitus
-Secondary diabetes mellitus
6. Primary Diabetes mellitus is categorized as
1) Type I DM it is also called as insulin dependant diabetes
mellitus IDDM
2) Type II DM it is also called as non – insulin dependant
diabetes mellitus NIDDM
The most common is type II DM (about 90 – 95% of the
cases)
7. The Diabetes mellitus is secondary to other diseases such as
1) Pancreatic Disease
2) Endocrine Disease
3) Drug – Induced Diabetes
4) Associated With The Genetic Syndrome
5) Gestational Diabetes
13. Definition:
There is absolute lack of the insulin due to autoimmune
destruction beta cells
It accounts for about 5 – 10% of the diabetes mellitus
It is most common in children & adolescence usually below the
age of the 20
The peak age of the occurrence of the type I diabetes is 10 – 13
years of the age
14. Person who have Northern European ancestors
- HLA System: (HLA DR 3, 4 & DQ)
- Genetic Susceptibility
- Inheritance (child of insulin dependent diabetes have increase
chances)
- Viral Infection (Coxsackie’s virus B4)
- Pancreatic Pathology
- Immunological Factors (T – cell mediated immune disease)
15. Islet autoantibodies are appears in the circulation in the first
few year of the life in first degree relatives of type I diabetes
demonstrating that the process culminating in diabetes is
initiated very early and many year before the diagnosis
16. There is absolute lack of the insulin because of autoimmune
destruction of the islets beta cells
As a result these persons are totally depend on insulin
With out insulin they develop the
Diabetic Ketoacidosis
Coma
17. The autoimmune destruction of the beta cells is triggered by the
infection & certain environmental factors in genetic susceptible
individuals
As a result beta – cells destroyed insulin production become
stop there is absolute lack of the insulin the pts not able use
the glucose their serum glucose level is elevated
18. On biopsy there is lot of the lymphocytes infiltration within
the pancreas surround the islets cells so called as “insulitis”
There is gradually loss of the beta cells and produce fibrosis
ultimately these person develop diabetes mellitus
19. Most of these pts are present with the 3P
*Polyuria
*Polyphagia
*Polydipasia
Other Features:
-Weight Loss
-Blurring Of The Vision
- Postural hypotension & Paraethiasis
- Ketoacidosis
There is also electrolytes imbalance dehydration
metabolic ketoacidosis coma death
These Pts totally depend on insulin injection
20. It is most common type of the diabetes mellitus
It accounts for about 90 – 95% of the cases
It is most common in individual age above 30
It is most common in obese individual, there is peripheral
resistance to insulin
Initially there may be increase serum insulin level
Type II diabetes mellitus is silence disease because world wide
half of the cases of type II DM are undiagnosed
21. - Obesity
- Genetic susceptible individual (Positive family history)
- Environmental factors
- Old age
22. It is rare variant of the type – 2 diabetes mellitus and is
strongly inherited.
The disease should be suspected in young peoples presenting
with a typical family history and in whom other features of
the type 1 are lacking
23. There is reduction of the insulin secretion
But most important is that there is peripheral resistance to the
insulin, peripherally there is decrease tissues sensation to the
insulin
Microscopic Appearance:
Microscopically there is non – specific changes in pancreas
There is little bit atrophy
Amyloid deposition
24. Frequently the pts with the type II diabetes are asymptomatic
They also develop 3P
Polyuria
Polyphagia
Polydipasia
Lack Of The Energy
Delayed Wound Healing
Blurring Of The Vision
Fungal infection (Pruritis vulvae, Balanitis)
Finally they also develop coma but this time there is
“Hyperosmolar non – ketotic diabetic coma
25. Major organs affected in diabetes are following
-Vascular system (Microangiopathy)
-Kidney (Nephropathy)
-Eye (Retinopathy)
-Peripheral (Neuropathy)
-There is increase risk of the infection
-Diabetic Foot
26. Diabetes mellitus is a major risk factor for the development of the
atherosclerosis
Most of the diabetes pts are die because of the MI (No. 1 killer)
There is also development of the peripheral vascular disease
Small Vessels: (microvascular disease)
There is thickening of the basement membrane and hyaline
arteriolar sclerosis
Other causes of the hyaline arteriolar sclerosis in small vessels are
-Hypertension
-Aging
27. There is development of the renal artery atherosclerosis as a result
lumen become narrow (stenosis)
In small vessels there is hyaline sclerosis changes
There is granular appearance on the surface of the kidney
Glomerular Diseases In DM:
Two most common glomerular diseases
*Diffuse glomerular sclerosis (Nephrotic syndrome)
*Nodular glomerular sclerosis (Kimmelstiel-Wilson lesion)
There is thickening of the basement membrane
Nephrotic Syndrome
There is also increase risk for the development of the
pyelonephritis, necrotizing papilitis & ultimately renal failure
28. There is tremendous amount of the pathology in the retina
1) Non – proliferative phase:
There is development of the microaneurysm in retinal vessel
these become rupture retinal hemorrhage & retinal exudate
As a consequence of the retinal hemorrhage there is development
of the new vessels (neovascularization) & fibroblast growth thus
granulation tissues formation
2) Fibrotic Phase: There is formation of the scar over the time
the scar become contract and pull the retina blindness
There is also increase risk of the development of the cataract &
glaucoma as well
29. Lower Extremities:
Peripheral neuropathy
Non – healed ulcer (There is non – traumatic ulcer in
diabetic patients)
Focal neurologic impairment is most likely due to the
micrangiopathy
Bladder:
Neurogenic bladder
Increase risk of the development of the
Cystitis
Pyelonephritis
30. Diabetes Pts develop one special type of the infection
The infection is caused by the fungus mucor mycosis
There is necrotizing infection of the sinuses the problem
with that there is increase chances of the transformation of
the infection to the brain that cause very serious
complication
31. -Fasting Blood Sugar (FBS)
-Random Blood Sugar (RBS)
-Glucose Tolerance Test (GTT)
-Glycosylated Hemoglobin (Hemoglobin A1c)
-Serum Fructosamine
-Urinalysis to detect glucose in the urine
-Urine For Proteinuria
-Complete Blood Count (CBC)
-Urea, Creatinine & Electrolytes
-Fasting Serum Cholesterol & Triglyceride
32. Normal Fasting Glucose level is less the 110mg/dl
Impaired fasting Glucose is >110 but < 126 mg/dl
If fasting blood sugar is greater than 126mg/dl on more than
one occasion, diabetes is confirmed
33. If random blood sugar is greater than 200 mg/dl on two
separate occasion, the diabetes is confirmed, however the
more reliable test is FBS
34. After the overnight fast, 75 gm of the glucose is taken in 250
– 300 ml of the water
Normally 2 – hour after the glucose load is < 140 mg/dl
Impaired glucose tolerance test is labeled, when 2 – hour
after glucose is > 140mg/dl but < 200 mg/dl
Diabetes is confirmed if two hours after glucose is > 200mg/
dl
- GTT is confirmatory test, require only when the FBS
glucose level is greater than normal
35. Level of the glycosylated HB reflect the state of the
glycemia over the preceding 8 – 12 weeks
Normal level is 4 – 6%
Therapy is require when the HB A1c is above the normal
The sensitivity of the test is about 85%
The test is quite is specific in 91% of the cases
36. Serum fructosamine is formed by nonenzymatic
glycosylation of the serum protein predominantly the
albumin
Serum fructosamine level reflect the state of the glycemic
control for preceding 2 weeks.
Normal values are 1.5 – 2.4 mmol/L
38. Type I:
- Diet Modification
- Insulin Injection
Type II:
- Oral hypoglycemic Agents
Sulphonylureas (Thin pts)
Biguanides (Obese Pts)
Oral hypoglycemic agents are contraindicated in pregnancy
Vascular complication of the diabetes can be reduced by the
low dose aspirin
39. - Modification Of The Diet
- Reduction Of The Weight
- Diet & Oral Hypoglycemic Agents
- Diet & Oral hypoglycemic Agents
40. -Fasting Blood Sugar (FBS)
-Random Blood Sugar (RBS)
-Glucose Tolerance Test (GTT)
-Glycosylated Hemoglobin (Hemoglobin A1c)
-Serum Fructosamine
-Urinalysis to detect glucose in the urine
-Urine For Proteinuria
-Complete Blood Count (CBC)
-Urea, Creatinine & Electrolytes
-Fasting Serum Cholesterol & Triglyceride
41. Achieve Good Glycemic Control
Reduce Hyperglycemia & Avoid Hypoglycemia
Assist With The Weight management
Reduce The Risk Of The Micro & macrovascular
complication
Ensure The adequate nutrition intake
Avoid the athrogenic diet or those that aggravate
complication (e.g. High protein intake in nephropathy)
42. Carbohydrate: ( 45 – 60%)
Sucrose up to 10%
Fat: (< 35%)
n – 6 polyunsaturated < 10%
n – 3 Polyunsaturated (eat oily fish once or twice weekly)
Monounsaturated 10 – 20%
Saturated < 10%
Protein: (10 – 15%)
Protein do not exceed 1g/kg of the body weight
43. In patient with the diabetes the weight management is key
factor as a high percentage of the peoples with the type II
diabetes are obese or overweight
many anti – diabetic medication and insulin encourage
weight gain
Abdominal obesity with increase waist circumference also
predict insulin resistance and CVS risk
Weight loss can be achieved through a reduction in energy
intake and an increase in energy expenditure through
physical activity
44. Alcohol can be consumed in moderation unless there is a co
– existing medical problem that require abstinence
Alcohol precipitate the hypoglycemia particularly in patients
taking insulin or sulphonylureas because alcohol inhibit the
gluconeogenesis
45. Peoples With diabetes should follow the advice given to the
general population
Reduce sodium intake to no more than 6 – g/day
Further restriction of the sodium intake 3 g/day is important in
treating hypertensive diabetic patient
46. Low – calories and sugar free drinks are useful for patient
with the diabetes
These drinks usually contain non – nutritive sweeteners
many diabetes foods are contain sarbitol and are expensive,
high in calories and may cause the gastrointestinal side –
effects
47. Various drugs are effective in reducing the hyperglycemia in
patient with the type – II diabetes such as
- Sulphonylureas
- Biguanides
- Alpha – Glucosidase Inhibitors
- Thiazolidinediones
- Meglitinides & Amino Acids derivatives
- Combined Oral anti – diabetic therapy & Insulin