IDDM
IDDM is associated with inflammation of the ilets of the pancreas and appears to be an autoimmune response.
Infection with Coxsackie’s viruses B has been shown to be the likely trigger of the autoimmune response
Other Etiological factor is inherited susceptibility after infection with virus, the beta cells inappropriately express an antigen.
The antigens on the beta cells are recognized and destroyed by circulating T cells.
The process of cellular destruction is marked by the appearance of Islet cell antibodies.
Some time the Pancreas will attempt to produce near – normal or normal levels of insulin during a “Honey Moon” Phase. Usually noticed after initial diagnosis. This phase may last upto 6 months or longer, but in true DM, the patient will develop signs of hyperglycemia again.
NIDDM
Refractoriness to insulin in the cell membrane receptors causes NIDDM
In Obesity, the pancreas cannot compensate for problems in the receptors by increasing insulin production. Some newer theories suggest that over time, the high levels of circulating insulin that occur with obesity “Insulinise” the cells, making them resistant to the action of insulin
DIAGNOSTIC ASSESSMENT:
1. Blood Glucose
2. Fasting Blood Sugar
3. Post Prandial Blood Sugar
4. Blood Glucose finger sticks
5. Glycosyloted haemoglobin
6. Glucose tolerance test. (GTT).
MEDICAL MANAGEMENT:
There is No cure for Diabetes.
Diabetes control depends on the proper interaction of 3 factors.
1) Diet.
2) Insulin or oral medication to lower blood glucose.
3) Exercise.
DIETARY:
The dietary management is the cornerstone for diabetes. The balanced nutritional plan for patients with diabetes has a two fold purpose
1) To discourage the ingestion of food with high sugar and fat content
2) To correct or avoid Obesity
The current recommendation for the distribution of calories are
-55 to 60 % of CHO
-30 % of FAT
-12 to 20 % of PROTEIN
PHARMOCOLOGICAL MANAGEMENT:
Oral hypoglycemic agents:
Oral hypoglycemic agents are not insulin. They lower the Blood glucose in part by stimulating the pancreatic beta cells to release insulin.
IDDM is associated with inflammation of the ilets of the pancreas and appears to be an autoimmune response.
Infection with Coxsackie’s viruses B has been shown to be the likely trigger of the autoimmune response
Other Etiological factor is inherited susceptibility after infection with virus, the beta cells inappropriately express an antigen.
The antigens on the beta cells are recognized and destroyed by circulating T cells.
The process of cellular destruction is marked by the appearance of Islet cell antibodies.
Some time the Pancreas will attempt to produce near – normal or normal levels of insulin during a “Honey Moon” Phase. Usually noticed after initial diagnosis. This phase may last upto 6 months or longer, but in true DM, the patient will develop signs of hyperglycemia again.
NIDDM
Refractoriness to insulin in the cell membrane receptors causes NIDDM
In Obesity, the pancreas cannot compensate for problems in the receptors by increasing insulin production. Some newer theories suggest that over time, the high levels of circulating insulin that occur with obesity “Insulinise” the cells, making them resistant to the action of insulin
DIAGNOSTIC ASSESSMENT:
1. Blood Glucose
2. Fasting Blood Sugar
3. Post Prandial Blood Sugar
4. Blood Glucose finger sticks
5. Glycosyloted haemoglobin
6. Glucose tolerance test. (GTT).
MEDICAL MANAGEMENT:
There is No cure for Diabetes.
Diabetes control depends on the proper interaction of 3 factors.
1) Diet.
2) Insulin or oral medication to lower blood glucose.
3) Exercise.
DIETARY:
The dietary management is the cornerstone for diabetes. The balanced nutritional plan for patients with diabetes has a two fold purpose
1) To discourage the ingestion of food with high sugar and fat content
2) To correct or avoid Obesity
The current recommendation for the distribution of calories are
-55 to 60 % of CHO
-30 % of FAT
-12 to 20 % of PROTEIN
PHARMOCOLOGICAL MANAGEMENT:
Oral hypoglycemic agents:
Oral hypoglycemic agents are not insulin. They lower the Blood glucose in part by stimulating the pancreatic beta cells to release insulin.
First generations:
1) Talbutamide (orinage)
2) Tolazamide ( tolinage)
3) Acetohexamide (dymelor)
4) Chlorpropamide ( diabinase)
Second generation:
1) Glyburide
2) Glipizide
Insulin therapy:
Patients with IDDM must inject insulin daily to survive. Some patients with NIDDM may require insulin if diet , exercise & oral hypoglycemic agents are ineffective.
Some medications such as Prednisone may elevate blood glucose levels & necessitate insulin injection for a time.
Insulin lower blood glucose by
1) Promoting the transport of glucose into cells
2) Inhibiting the conversion of glycogen & amino acids to glucose.
TYPES OF INSULIN:
1) Rapid Acting – eg Hunulin R ( 6- 8) hrs duration
2) Intermediate Acting -eg Lente insulin ( 6- 12) hrs
3) Long Acting -eg Protamine zincinsulin ( 18 – 24) hrs
If Blood glucose is difficult to control, two different insulin can be mixed & administerd as a single injection.
EXERCISE:
A program of planned exercise can greatly benefit the patient with diabetes.
1) Lower blood glucose by increasing CHO metabolism
2) Facilitates weight reduction & proper weight maintainence
3) decrease Blood Pressure
4) Decrease Stress & tension
SURGICAL MANAGEMENT:
Pancreas transplants
