1. Diabetes Normal Anatomy andPhysiology

2. Pancreas Pancreas : abdominal organ responsible for exocrine secretion of digestive enzymes into the gut And Endocrine secretion of hormones of glucose control: insulin and glucagon

3. Pancreas : Exocrine And Endocrine: Islets of Langerhans

4. Glucose Glucose : 6 carbon sugar that is the principle source of energy for cellular metabolism Glucose circulates in the blood and is transported into cells for use as an energy source

5. Glucose Glucose concentration in the blood is normally controlled between 3.6 and 11 mmol/L by various hormonal influences including: Insulin and Glucagon

6. Insulin Insulin : peptide hormone released by beta cells of the Islets of Langerhans in response to rising levels of blood glucose Acts by increasing cellular transport of glucose and increased storage of glucose

7. Glucagon Glucagon : peptide hormone released by alpha cells of the Islets of Langerhans in response to falling levels of blood glucose Acts by increasing release of glucose from the liver by breakdown of glycogen

8. Alpha cells: Glucagon Beta cells: Insulin

9. Diabetes mellitus Diabetes mellitus : A metabolic disease caused by an absolute or relative lack of insulin resulting in abnormalities in carbohydrate, protein and lipid metabolism.

10. Diabetes mellitus: Prevalence: 6% of the population (estimate 30,000 in London area) (120 diabetics in a 2,000 patient practice)

11. Diabetes mellitus: Classfication: Type 1 10% of diabetics (estimate 3,000 in London area) Type 2 90% of diabetics (estimate 27,000 in London area)

12. Pathophysiology   Type 1 diabetes – beta cells are immunologically destroyed, eventually no insulin is produced   Type 2 diabetes – insulin secretion is reduced, target cells become relatively insulin resistant ( receptors and post- receptor activity

13. Comparison of type 1 and 2 Type 1   10% of diabetics   Age of onset – young   Severe   Requires insulin   Normal build   Little genetic component   Autoimmune Type 2   90% of diabetics   Age of onset – 40+   Mild   May require insulin, usually diet or oral hypoglycemics   Obese   Strong genetic component

14. Diabetes Diabetes is characterized by: Hyperglycemia Loss of glucose (and water) in the urine Paradoxical cellular starvation

15. Symptoms of diabetes   Polyuria (increased urination)   Polydipsia (increased drinking)   Weight loss   Weakness   Increased infections and impaired healing   Blurred vision

16. Lab tests - diagnosis   Normal range of fasting blood glucose: 3.9 to 6.1 mmol/L Diagnosis of DIABETES is based on   Random glucose   >11.0 mmol/L + symptoms or   Fasting glucose   >6.9 mmol/L on 2 occasions

17. Medical management   The tighter the glycemic control, the fewer complications– BUT – the more risk of getting hypoglycemic   IDEAL management   Fasting glucose 4.0 – 7.0 mmol/L   Infection, stress, pregnancy, surgery will all disturb control

18. Treatment: Type 1   Diet and physical acitivity plus   Insulin: usual starting dose about 20 units/day (OD, BID, multiple, continuous infusion pump)   Testing 2-5 x/day   ACE inhibitors (captopril / ramipril) to control nephropathy   Cholesterol lowering drugs

19. Treatment: Type 2   Diet and physical activity only (testing 2x/month)   +/- Oral hypoglycemics (increase insulin secretion, receptors or post-receptor activity)   Sulphonylureas (glyburide = Diabeta) (can induce hypoglycemia)   Biguanides (metformin = Glucophage)   Gamma-glucosidase inhibitor (acarbose = Prandase   +/- Insulin

20. Lab tests - monitoring   Daily (or more) finger pick and glucometer readings   Hb A1c (Normal = 4.0 to 6.0)   A long term (3 month) measure of diabetic control (glycosylated Hb)   Good <7.0   Fair7.0 to 8.9   Poor>9.0

21. Diabetic complications Related to the strictness of glycemic control and are characterized as: Macrovascular complications atherosclerosis Microvascular complications eye and kidney

22. Complications   Macrovascular   Stroke (2-5 X increased risk)   MI(2-5 X increased risk)   Cutaneous ulcers (PVD)   Amputation(40 X increased risk)

23. Complications   Microvascular   Retinopathy – blindness (20 X increased risk)   Cataracts (5 X risk)   Nephropathy – renal failure (25 X increased risk)

24. Complications   Neuropathy – numbness, tingling, pain, glove and stocking sensory deficits   Autonomic involvement   Infections secondary to impaired vascularity and PMN defects   Decreased duration and quality of life

25. Emergencies: ketoacidosis   In type 1 patients only   Marked hyperglycemia (high serum glucose) causes osmotic diuresis   Patient loses excess water, Na, K, and ketones released from the liver cause a metabolic acidosis   Precipitated by an infection, insulin error or omission, or occurs in a previously undiagnosed patient

26.   Treated with insulin, fluid replacement, K replacement   Type 2 diabetics can have a much less serious variant of this called: Hyperglycemic hyperosmolar nonketotic state secondary to dehydration Emergencies: ketoacidosis

27. Emergencies: hypoglycemia May occur with an overdose of insulin / oral medication or a missed meal   Only some oral medications cause hypoglycemia – (Sulfonylureas) Glyburide, Glicazide, Chlorpropamide   Patient gets diaphoretic, weak, shaky, palpitations, difficulty thinking, aggressive, vision changes and may lose consciousness

28. Emergencies: hypoglycemia   Patient needs glucose – a glass of juice, a candy, or if comatose, IV 50% glucose solution or IM glucagon (1 mg)   Some patients are totally unaware of their hypoglycemia until they lose consciousness

29. Dental management   Assess control / severity / compliance (CSC)   Treatment plan modification (based on CSC)   Possibly … None   AM appointments   Normal meds and diet pre-op   Limit treatment duration   Antibiotic coverage???   Post-op diet instructions   Hospitalization / GA and NPO status   Consultation with the MD

30. Dental management   Assess control / severity /compliance   When were they first diagnosed   Type 1 vs Type 2   What medications are they taking (or diet only)   How much insulin do they use / how frequently   How often do they measure their glucose and what are their usual measurements

31. Dental management   Assess control / severity / compliance   Frequency of hypoglycemic reactions (can they feel them coming on?)   Complications: brain, eye, heart, kidney, toes   How often and when last did they see their MD   Did they take meds and have meals today   Be alert to changes in “control”

32. Dental management   Assess control / severity / compliance   BRITTLENESS: poor control of diabetes as a function of the nature of the disease or other complicating factors such as infection (?dental abscess?)   COMPLIANCE: an indication of the patient’s willingness or ability to manage his/her medications or diet for optimal control

33. Dental conerns:   Hypoglycemia during a procedure   Oral surgeries that will prevent the patients from getting their usual caloric requirements   Brittle diabetics (extreme fluctuations of hypo/hyperglycemia) – usually occurs after years of high dose insulin therapy

34. Dental conerns:   Acute oral infections that precipitate hyperglycemia   Be more aggressive with antibiotics in patients with high sugars

35. Oral complications   Xerostomia secondary to dehydration   Mucosal fungal infection: candidiasis   Increased caries and periodontal disease

36. Oral complications   Poor post surgical wound healing   “Burning mouth syndrome” …diabetic neuropathy   Consult MD in suspicious patients

37. Questions?