Diabetes Mellitus patients in dental management


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Diabetes Mellitus patients in dental management

  1. 1. Diabetes Mellitus patients in dental management Reporter : 吳和泰 Modulator: Dr. 雷文天
  2. 2. Introduction <ul><li>Diabetes mellitus is a metabolic disorder characterized by relative or absolute insufficiency of insulin , and resultant disturbances of carbonhydrate metabolism . </li></ul><ul><li>The major function of insulin is to counter the concerted action of a number of hyperglycemia-generating hormones and to maintain low blood glucose levels. </li></ul>
  3. 3. Epidemiology <ul><li>6% (16 million persons) of the general population in the US have diabetes mellitus. </li></ul><ul><li>Almost 20% of adult older than 65 y/o have DM. </li></ul><ul><li>A dental practice serving an adult population of 2,000 can expect to encounter 40-80 persons with diabetes, about half of whom will be unaware of their condition. </li></ul>National Institutes of Health, Aug 2001
  4. 4. 國人之糖尿病盛行率
  5. 5. Etiologic classification of DM <ul><li>There are two types of Diabetes Mellitus: </li></ul><ul><ul><li>Type 1 , insulin-dependent or, juvenile-onset diabetes (IDDM) </li></ul></ul><ul><ul><li>Type 2 , non-insulin-dependent, adult-onset diabetes (NIDDM) </li></ul></ul><ul><ul><li>Other specific types </li></ul></ul>JADA, Oct 2001
  6. 6. Type 1 (IDDM) <ul><li>Autoimmune destruction of the insulin-producing beta cells of pancreas. </li></ul><ul><li>5-10% of DM cases. </li></ul><ul><li>Common occurs in childhood and adolescence , or any age. </li></ul><ul><li>Absolute insulin deficiency. </li></ul><ul><li>High incidence of severe complications . </li></ul><ul><li>Prone to autoimmune diseases . (Grave’s, Addison, Hashimoto’s thyroiditis) </li></ul>
  7. 7. Type 2 (NIDDM) <ul><li>Result from impaired insulin function . (insulin resistance) </li></ul><ul><li>Constitutes 90-95% of DM </li></ul><ul><li>Specific causes of this form are unknown . </li></ul><ul><li>Risk factors : age, obesity, alcohol, diet, family Hx and lack of physical activity ..etc. </li></ul>
  8. 8. mild beta-cell depletion severe beta-cell depletion   focal atrophy and amyloid deposits marked atrophy and fibrosis   no insulitis insulitis early Islet Cells relative insulin deficiency severe insulin deficiency   insulin resistance autoimmunity, immunopathologic mechanisms Pathogenesis No HLA association human leukocyte antigen (HLA)-D linked   ketoacidosis rare ketoacidosis common Genetics no anti-islet cell antibodies anti-islet cell antibodies   normal or increased blood insulin decreased blood insulin   obesity normal weight   onset >30 years onset <20 years Clinical Type 2 Type 1 Comparison
  9. 9. Other specific types <ul><li>Genetic defects of beta-cell functions </li></ul><ul><li>Decrease of exocrine pancreas </li></ul><ul><li>Endocrinepathothies </li></ul><ul><li>Drug or chemical usage </li></ul><ul><li>Infections </li></ul><ul><li>………… . </li></ul>
  10. 10. Gestational diabetes mellitus (GDM) <ul><li>Defined as any degree of glucose intolerance with onset or first recognition during pregnancy. </li></ul><ul><li>4% of pregnancy in US. </li></ul>
  11. 11. Pathophysiology <ul><li>Healthy people blood glucose level maintained within 60 to 150 mg/dL . </li></ul><ul><li>Insulin synthesized in beta cells of pancreas and secreted rapidly into blood in response to elevations in blood sugar. </li></ul><ul><li>Promoting uptake of glucose from blood into cells and its storage as glycogen </li></ul><ul><li>Fatty acid and amino acids converted to triglyceride and protein stores. </li></ul>
  12. 12. Pathophysiology <ul><li>Lack of insulin or insulin resistance, result in inability of insulin-dependent cells to use glucose . </li></ul><ul><li>Triglycerides broken down to fatty acids  blood ketones ↑  diabelic ketoacidosis . </li></ul>
  13. 13. Pathophysiology <ul><li>As blood sugar levels became elevated ( hyperglycemia ), glucose is excreted in the urine and excessive of urination occurs due to osmotic diuresis ( polyuria ). </li></ul><ul><li>Increased fluid loss leads to dehydration and excess thirst ( polydipsia ) . </li></ul><ul><li>Since cells are starved of glucose, the patient experiences increased hunger ( polyphagia ). </li></ul><ul><li>Paradoxically, the diabetic patient often loss weight , since the cells are unable to take up glucose. </li></ul>
  14. 14. Complications <ul><li>People with DM have an increased incidence of both microvascular and macrovascular complications. </li></ul>peripheral vascular atherosclerosis; infections; gangrene Peripherals autonomic neuropathy; peripheral neuropathy Nervous system retinopathy; cataracts; glaucoma Eyes nephrosclerosis; glomerulosclerosis; arteriosclerosis; pyelonephritis Kidneys islet cell loss; insulitis (Type 1); amyloid (Type 2) Pancreas myocardial infarct; atherosclerosis; hypertension; microangiopathy; cerebral vascular infarcts; cerebral hemorrhage Cardiovascular system: heart, brain, blood vessels Long term complications Major organs/systems showing changes
  15. 15. Diagnosis <ul><li>A casual plasma glucose level of 200 mg/dL or greater with symptoms presented. </li></ul><ul><li>Fasting plasma glucose level of 126 or greater.(Normal <110 mg/dL,IGT,IFG) </li></ul><ul><li>Oral glucose tolerance test (OGTT) value in blood of 200 mg or greater. </li></ul><ul><li>ADA recommend >45 y/o screened every 3 years. </li></ul>Diabetes Care, 2000 National Institutes of Health, Aug 2001
  16. 16. Medical management <ul><li>Objective : maintain blood glucose levels as close to normal as possible. </li></ul><ul><li>Good glycemic control inhibits the onset and delay of type 1 DM, similar in type 2 DM. </li></ul>
  17. 17. Medical management <ul><li>Glycated hemoglobin assay (HbA 1c ) reflects mean glycemia levels over the proceding 2~3 months. (normal < 7%) </li></ul><ul><li>HbA 1c also a predictor for development of chronic complications. </li></ul>
  18. 18. Medical management <ul><li>Exercise and diet control </li></ul><ul><li>Insulin : rapid, short, intermediate, long acting. </li></ul><ul><li>Oral antidiabetic agents </li></ul>
  19. 19. Oral manifestations and complications <ul><li>No specific oral lesions associated with diabetes. However, there are a number of problems by present of hyperglycemia . </li></ul><ul><li>Periodontal disease </li></ul><ul><ul><li>Microangiopathy altering antigenic challenge. </li></ul></ul><ul><ul><li>Altered cell-mediated immune response and impaired of neutrophil chemotaxis. </li></ul></ul><ul><ul><li>Increased Ca + and glucose lead to plaque formation. </li></ul></ul><ul><ul><li>Increased collagen breakdown . </li></ul></ul>
  20. 20. Oral manifestations and complications <ul><li>Salivary glands </li></ul><ul><ul><li>Xerostomia is common , but reason is unclear. </li></ul></ul><ul><ul><li>Tenderness, pain and burning sensation of tongue. </li></ul></ul><ul><ul><li>May secondary enlargement of parotid glands with sialosis. </li></ul></ul><ul><li>Dental caries </li></ul><ul><ul><li>Increase caries prevalence in adult with diabetes. (xerostomia, increase saliva glucose) </li></ul></ul><ul><ul><li>Hyperglycemia state shown a positive association with dental caries. </li></ul></ul>
  21. 21. Oral manifestations and complications <ul><li>Increased risk of infection </li></ul><ul><ul><li>Reasons unknown, but macrophage metabolism altered with inhibition of phagocytosis . </li></ul></ul><ul><ul><li>Peripheral neuropathy and poor peripheral circulation </li></ul></ul><ul><ul><li>Immunological deficiency </li></ul></ul><ul><ul><li>High sugar medium </li></ul></ul><ul><ul><li>Decrease production of Ab </li></ul></ul><ul><ul><li>Candical infection are more common and adding effects with xerostomia </li></ul></ul>
  22. 22. Oral manifestations and complications <ul><li>Delayed healing of wounds </li></ul><ul><ul><li>Due to microangiopathy and ultilisation of protein for energy, may retard the repair of tissues. </li></ul></ul><ul><ul><li>Increase prevalence of dry socket . </li></ul></ul><ul><li>Miscellaneous conditions </li></ul><ul><ul><li>Pulpitis : degeneration of vascular. </li></ul></ul><ul><ul><li>Neuropathies : may affect cranial nerves. (facial) </li></ul></ul><ul><ul><li>Drug side-effects : lichenoid reaction may be associated with sulphonylurea. (chlopropamide) </li></ul></ul><ul><ul><li>Ulcers </li></ul></ul>New Zealand Journal, Jan 1985
  23. 23. Dental management considerations <ul><ul><li>To minimize the risk of an intraoperative emergency, clinicians need to consider some issues before initiating dental tx. </li></ul></ul><ul><li>Medical history : take hx and assess glycemic control at initial appt. </li></ul><ul><ul><li>Glucose levels </li></ul></ul><ul><ul><li>Frequency of hypoglycemic episodes </li></ul></ul><ul><ul><li>Medication , dosage and times. </li></ul></ul><ul><ul><li>Consultation </li></ul></ul>
  24. 24. Dental management considerations <ul><li>Scheduling of visits </li></ul><ul><ul><li>Morning appt. (endogeneous cortisol) </li></ul></ul><ul><ul><li>Do not coincide with peak activity. </li></ul></ul><ul><li>Diet </li></ul><ul><ul><li>Ensure that the patient has eaten normally and taken medications as usual. </li></ul></ul><ul><li>Blood glucose monitoring </li></ul><ul><ul><li>Measured before beginning. (<70 mg/dL) </li></ul></ul><ul><li>Prophylactic antibiotics </li></ul><ul><ul><li>Established infection </li></ul></ul><ul><ul><li>Pre-operation contamination wound </li></ul></ul><ul><ul><li>Major surgery </li></ul></ul>
  25. 25. Dental management considerations <ul><li>During treatment </li></ul><ul><ul><li>The most complication of DM occur is hypoglycemia episode . </li></ul></ul><ul><ul><li>Hyperglycemia </li></ul></ul><ul><li>After treatment </li></ul><ul><ul><li>Infection control </li></ul></ul><ul><ul><li>Dietary intake </li></ul></ul><ul><ul><li>Medications : salicylates increase insulin secretion and sensitivity  avoid aspirin . </li></ul></ul>
  26. 26. Emergency management <ul><li>Hypo glycemia </li></ul><ul><ul><li>Initial signs : mood changes, decreased spontaneity, hunger and weakness. </li></ul></ul><ul><ul><li>Followed by sweating, incoherence, tachycardia. </li></ul></ul><ul><ul><li>Consequenced in unconsiousness, hypotention, hypothermia, seidures, coma, even death. </li></ul></ul>
  27. 27. Emergency management <ul><li>15 grams of fast-acting oral carbonhydrate . </li></ul><ul><li>Measured blood sugua. </li></ul><ul><li>Loss of conscious, 25-30ml 50% dextrose solution iv. over 3 min period. </li></ul><ul><li>Glucagon 1mg. </li></ul><ul><li>911, 119 </li></ul>
  28. 28. Emergency management <ul><li>Severe hyper glycemia </li></ul><ul><ul><li>A prolonged onset </li></ul></ul><ul><ul><li>Ketoacidosis may develop with nausea, vomiting, abdominal pain and acetone odor. </li></ul></ul><ul><ul><li>Difficult to different hypo- or hyper-. </li></ul></ul>
  29. 29. Emergency management <ul><li>Hyperglycemia need medication intervention and insulin administration . </li></ul><ul><li>While emergency, give glucose first ! </li></ul><ul><li>Small amount is unlikely to cause significant harm. </li></ul>JADA, Oct 2001
  30. 30. Conclusion
  31. 31. Thanks for ur attention !!
  32. 33. 1.Liver <ul><li>ketone body </li></ul><ul><li>ATP+co2 </li></ul><ul><li>acetyl coA </li></ul><ul><li>TG </li></ul><ul><li>FA </li></ul><ul><li>Glycerol-po4 </li></ul><ul><li>glucose </li></ul><ul><li>glucose </li></ul>glucose glucose TG glycerol-po4 glycerol +FA glycerol FA+ALB 2.Adipose glucose glucose 3.Muscle