1. Diabetes Mellitus

2. WHAT is Diabetes ?
Diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion , insulin action , or both.
Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient, and it is often unclear which abnormality, if either alone, is the primary cause of the hyperglycemia.
Symptoms of marked hyperglycemia include polyuria , polydipsia, weight loss, sometimes with polyphagia, and blurred vision . Impairment of growth and susceptibility to certain infections may also accompany chronic hyperglycemia.

3. Diabetes Mellitus (DM)
In its most severe forms, ketoacidosis or a non–ketotic hyperosmolar state may develop and lead to stupor, coma and, in absence of effective treatment, death.
Often symptoms are not severe, or may be absent, and consequently hyperglycemia sufficient to cause pathological and functional changes may be present for a long time before the diagnosis is made.

5. Diabetes Long –term Effect
The long–term effects of diabetes mellitus include progressive development of the specific complications of retinopathy with potential blindness, nephropathy that may lead to renal failure, and/or neuropathy with risk of foot ulcers, amputation, Charcot joints, and features of autonomic dysfunction, including sexual dysfunction.
People with diabetes are at increased risk of cardiovascular, peripheral vascular and cerebrovascular disease.

6. Diabetic Amputation

7. Diabetic Amputation

8. Diabetic Amputation

9. Diabetic Amputation

10. Diabetic Amputation

11. Burden of Diabetes
The development of diabetes is projected to reach pandemic proportions over the next10-20 years.
International Diabetes Federation (IDF) data indicate that by the year 2025, the number of people affected will reach 333 million –90% of these people will have Type 2 diabetes.
In most Western societies, the overall prevalence has reached 4-6%, and is as high as 10-12% among year-old people.
The annual health costs caused by diabetes and its complications account for around 6-12% of all health-care expenditure.

12. Types Of Diabetes Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus
Gestational Diabetes
Other types:
LADA (Latent Autoimmune Diabetes in Adults)
MODY (maturity-onset diabetes of youth)
Secondary Diabetes Mellitus

13. DM Type 1
Type 1 diabetes develops when the body’s immune system destroys pancreatic beta cells, the only cells in the body that make the hormone insulin that regulates blood glucose ; characterized by hyperglycemia, breakdown of body fats and protein and development of ketosis
Accounts for 5 – 10 % of cases of diabetes; most often occurs in childhood or adolescence
Formerly called Juvenile-onset diabetes or insulin-dependent diabetes (IDDM)
Risk factors for type 1 diabetes may include autoimmune, genetic, and environmental factors.
This form of diabetes usually strikes children and young adults, although disease onset can occur at any age.

14. DM Type 1
Pathophysiology 1. Autoimmune reaction in which the beta cells that produce insulin are destroyed 2. Alpha cells produce excess glucagons causing hyperglycemia Risk Factors 1. Genetic predisposition for increased susceptibility; HLA linkage 2. Environmental triggers stimulate an autoimmune response a. Viral infections (mumps, rubella, coxsackievirus B4) b. Chemical toxins

16. DM Type 2
Was previously called non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes.
Type 2 diabetes may account for about 90% to 95% of all diagnosed cases of diabetes.
It usually begins as insulin resistance, a disorder in which the cells do not use insulin properly. As the need for insulin rises, the pancreas gradually loses its ability to produce insulin.
Type 2 diabetes is increasingly being diagnosed in children and adolescents.

17. DM Type 2
Pathophysiology
1. Sufficient insulin production to prevent DKA; but insufficient to lower blood glucose through uptake of glucose by muscle and fat cells
2. Cellular resistance to insulin increased by obesity, inactivity, illness, age, some medications
Risk Factors
1. History of diabetes in parents or siblings; no HLA
2. Obesity (especially of upper body)
3. Physical inactivity

18. DM Type 2
4. Race/ethnicity: African American, Hispanic, or American Indian origin 5. Women: history of gestational diabetes, polycystic ovary syndrome, delivered baby with birth weight > 9 pounds 6. Clients with hypertension; HDL cholesterol < 35 mg/dL, and/or triglyceride level > 250 mg/dl.

20. Diagnosis Of Diabetes

21. Diagnosis Of Type 1
1. Casual plasma glucose (non-fasting) is 200 mg/dl OR 2. Fasting plasma glucose (FGP) of 126 mg/dl or higher OR 3. Two hour plasma glucose level of 200 mg/dl or greater during an oral glucose tolerance test 4. Detection of antibodies against islet antigens (insulin, beta cells, etc.) in the serum.

22. Diagnosis Of Type 1 less than 100 mg/dL normal 125 mg/dL to 100 mg/dL
pre-diabetes
126 mg/dL or greater
diabetes

23. Diagnosis Of Type 1

24. Diagnosis Of Type 2 1. Fasting Blood Glucose (normal: 70 – 110 mg/dL)
2. Glycosylated hemoglobin (c) (Hemoglobin A1C)
► Blood test analyzes excess glucose attached to hemoglobin. Since rbc lives about 120 days gives an average of the blood glucose over previous 2 to 3 months
3. Urine glucose and ketone levels (part of routine urinalysis)
► Glucose in urine indicates hyperglycemia (renal threshold is usually 180 mg/dL)
4. Urine albumin (part of routine urinalysis)
►Typical order is creatinine clearance testing
5. Cholesterol and Triglyceride levels
6. Serum electrolytes in clients with DKA or HHNS

25. Diabetes Therapeutics

26. Insulin A
1. Sources: standard practice is use of human insulin prepared by alteration of pork insulin or recombinant DNA therapy 2. Clients who need insulin as therapy: a. All type 1 diabetics since their bodies essentially no longer produce insulin b. Some Type 2 diabetics, if oral medications are not adequate for control (both oral medications and insulin may be needed) c. Diabetics enduring stressor situations such as surgery, corticosteroid therapy, infections, treatment for DKA, HHNS d. Women with gestational diabetes who are not adequately controlled with diet e. Some clients receiving high caloric feedings including tube feedings or parenteral nutrition

27. Insulin Injection Sites

28. Alternative Insulin Administration
Insulin pump
Continuous subcutaneous infusion of a basal dose with increases at meal times
Implanted pumps
Implanted into the peritoneal cavity

29. Insulin Pump

30. Internal insulin Pump

31. B 1. Used to treat Diabetes Type 2
Oral Hypoglycemic Agents B
1. Used to treat Diabetes Type 2
2. Client must also maintain prescribed diet and exercise program; monitor blood glucose levels
3. Not used with pregnant or lactating women
4. Several different oral hypoglycemic agents and insulin may be prescribed for the client
5. Specific drug interactions may affect the blood glucose levels
6. Must have some functioning beta cells

32. Classifications and action
A.Sulfonylureas
1. Action: Stimulates pancreatic cells to secrete more insulin and increases sensitivity of peripheral tissues to insulin
2. Used: to treat non-obese Type 2 diabetics
3. Example: Glipizide (Glucotrol), Chlorpropamide (Diabinese), Tolazamide (Tolinase

33. Classifications and action
B. Meglitinides
1. Action: stimulates pancreatic cells to secret more insulin
2. Taken just before meals, rapid onset, limited duration of action
3. Major adverse effects is hypoglycemia
4. Used in non-obese diabetics
5. Example: Repaglinide (Prandin), Nateglinide (Starlix)

34. Classifications and action
C. Biguanides
1. Action: decreases overproduction of glucose by liver and makes insulin more effective in peripheral tissues
2. Used in obese diabetics
3. Does not stimulate insulin release
4. Metabolized by the kidney, do not use with renal patients
5. Example: Metformin (Glucophage)

35. Classifications and action
D. Alpha-glucoside Inhibitors
1. Action: Slow carbohydrate digestion and delay rate of glucose absorption
2. Take with first bite of the meal or 15 min after
3. Adjunct to diet to decrease blood glucose levels
4. Example: Acarbose (Precose), Miglitol (Glyset)

36. Classifications and action
E. Thizaolidinediones (Glitazones)
1. Action: Sensitizes peripheral tissues to insulin
2. Used in obese diabetics
3. Inhibits glucose production
4. Improves sensitivity to insulin in muscle, and fat tissue
5. Example: Rosiglitazone (Avandia), Pioglitazone (Actos)

37. My Recommendation

38. Reference
National Diabetes Fact Sheet 2003, DEPARTMENT OF HEALTH AND HUMAN SERVICES Centres for Disease Control and Prevention
World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. Report of WHO. Department of Non-communicable Disease Surveillance. Geneva 1999
Canadian Dibetes Association ( )
Academy of Medicine. Clinical Practice Guidelines. Management of type 2 diabetes mellitus. MOH/P/PAK/87.04(GU), 2004
American Diabetes Association ( )
NHS. Diabetes - insulin initiation - University Hospitals of Leicester NHS Trust Working in partnership with PCTs across Leicestershire and Rutland, May 2008.