By Dr Ashok Jaisingani

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

The Prevalence Of the diabetes is 2 – 3%

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

There are two types

-Primary diabetes mellitus

-Secondary diabetes mellitus

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)

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

Pancreatitis

Hemochromatosis

Cystic Fibrosis

Pancreactomy

Cushing Syndrome

Acromegaly

Thyrotoxicosis

Pheochromocytoma

Glucagonoma

Following Drugs May causing The Diabetes

Corticosteroid Therapy

Thiazide Diuretics

Phenytoin

Freidreich Syndrome

Myotonic Dystrophy

Down’s Syndrome

Klinefelter’s Syndrome

Turner’s Syndrome

Pregnancy induced Diabetes

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

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)

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

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 KetoacidosisComa

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

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

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

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

- Obesity - Genetic susceptible individual (Positive family history) - Environmental factors - Old age

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

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

Frequently the pts with the type II diabetes are asymptomatic They also develop 3P Polyuria Polyphagia PolydipasiaLack 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

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

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

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

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 exudateAs 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

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

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

-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

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

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

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/dlDiabetes 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

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

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

Strips are used for detection of the glucose in the urine

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

- Modification Of The Diet

- Reduction Of The Weight

- Diet & Oral Hypoglycemic Agents

- Diet & Oral hypoglycemic Agents

-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

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)

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

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

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

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

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

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

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