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Adrenal insufficiency & diabetes mellitus /certified fixed orthodontic courses by Indian dental academy


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Adrenal insufficiency & diabetes mellitus /certified fixed orthodontic courses by Indian dental academy

  1. 1. ADRENAL INSUFFICIENCY Leader in continuing dental education INDIAN DENTAL ACADEMY
  2. 2. ADRENAL INSUFFICIENCY Adrenal Insufficiency is a true medical emergency in which victim is in immediate danger because of Glucocorticoid deficiency  Acute
  3. 3. CORTISOL A Glucocrticoid  Secreted – Adrenal Cortex  Helps the body adapt to stress  Hypersecretion – Cushing’s Syndrome  Deficiency – Addison’s Disease 
  4. 4. ADRENAL INSUFFICIENCY PRIMARY Addison’s Disease  SECONDARY Chronic Exogenous Glucocorticoid administration 
  5. 5. In primary Adrenal Insufficiency  Clinical manifestation do not develop until at least 70% - 80% of adrenal cortex is destroyed  Patient is capable of maintaining endogenous cortisol for day to day living  In stress full situation ( Dental appointments ) Adrenal cortex is unable to produce additional quantity of cortisol needed to adapt to stress . 
  6. 6. SECONDARY ADRENAL INSUFFICIENCY Glucocorticoids drugs are widely prescribed for variety of disorders  It produces diffuse atrophy of adrenal cortex diminishing the ability to increase corticosteroid levels in respose to stressful situation 
  7. 7. PRE DISPOSING FACTORS Sudden withdrawal of steroid harmones  Physiologic or Psychological Stress  Bilateral adrenelectomy  Injury to Adrenal gland due to Trauma, infection 
  8. 8. CLINICAL MANIFESTATION  If a patient with Addison's disease is challenged by stress (e.g., illness, infection, surgery), an adrenal crisis may be precipitated. The most common complaints are  weakness, fatigue, and abnormal pigmentation of the skin and mucous membranes  Hypotension, anorexia, and weight loss are additional common findings.
  9. 9.  This medical emergency manifests as severe exacerbation of the patient's condition, including  If not treated rapidly, the patient may develop hypothermia, severe hypotension, hypoglycemia, and circulatory collapse that can result in death.  sunken eyes, profuse sweating, hypotension, weak pulse, cyanosis, nausea, vomiting, weakness, headache, dehydration, fever, dyspnea, myalgias, arthralgia, hyponatremia, and eosinophilia.
  10. 10. PATIENT PAST HISTORY OF SYSTEMIC CORTICOSTEROID USE  Evaluate the patient. Determine whether systemic corticosteroid was taken within the past 2 weeks and the reason for discontinuing usage.  Identify signs and symptoms of possible adrenal insufficiency.  If major invasive oral procedure is planned and corticosteroid was taken within the past 2 weeks, consult with the physician regarding status and stability  If adrenal insufficient, implement steroid supplementation protocol. 
  11. 11. PATIENT CURRENTLY TAKING SYSTEMIC CORTICOSTEROIDS Identify signs and symptoms of possible adrenal insufficiency.  For diagnostic and minimally invasive procedures, have patient take the usual daily dose, and perform oral procedure in the morning, shortly after the corticosteroid is taken.  Stress reduction measures should be implemented, blood pressure recorded during the procedure.   For major invasive oral procedures, consult with the physician 
  12. 12. PATIENT NOT TAKING SYSTEMIC CORTICOSTEROIDS, BUT MAY HAVE ADRENAL INSUFFICIENCY  Evaluate the patient for historical findings associated with risk for adrenal insufficiency. Identify signs and symptoms of adrenal insufficiency.  Refer to the physician for ACTH testing.  If the patient is found to be adrenally insufficient, defer dental treatment until stabilized with corticosteroid treatment. 
  13. 13. STEROID SUPPLEMENTATION PROTOCOL FOR MAJOR SURGICAL PROCEDURE: Discontinue drugs that decrease cortisol levels (e.g., ketoconazole, metyrapone) at least 24 hours before surgery with the consent of the patient's physician.  Have patient take usual morning dose and provide supplemental hydrocortisone preoperatively and intraoperatively to achieve 100 mg within first hour of surgery. Give hydrocortisone 25 mg every 8 hours subsequent to surgery for 24 to 48 hours. Provide adequate operative and postoperative analgesia.   
  14. 14.   Communicate with the patient at the end of the appointment and within 4 hours postoperatively to determine whether features of weak pulse, hypotension, dyspnea, myalgias, arthralgia,  Monitor blood pressure (BP) and blood loss throughout the procedure. If BP drops to below 100/60 mm Hg and the patient is unresponsive to fluid replacement and vasopressive measures, administer supplemental steroids.
  17. 17. DIABETES MELLITUS  Diabetes mellitus is a metabolic disorder characterized by relative or absolute insufficiency of insulin, and resultant disturbances of carbonhydrate metabolism
  18. 18. Type 1, insulin-dependent or, juvenile-onset diabetes (IDDM)  Type 2, non-insulin-dependent, adult-onset diabetes (NIDDM)  Gestational diabetes mellitus (GDM 
  19. 19.  TYPE 1:  TYPE 2:   Result from impaired insulin function. (insulin resistance) GDM:  Defined as any degree of glucose intolerance with onset or first recognition during pregnancy  Autoimmune destruction of the insulin-producing beta cells of pancreas.
  20. 20. PATHOPHYSIOLOGY     Healthy people blood glucose level maintained within 60 to 150 mg/dL. Insulin synthesized in beta cells of pancreas and secreted rapidly into blood in response to elevations in blood sugar. Promoting uptake of glucose from blood into cells and its storage as glycogen Fatty acid and amino acids converted to triglyceride and protein stores.
  21. 21. Lack of insulin or insulin resistance, result in inability of insulin-dependent cells to use glucose.  Triglycerides broken down to fatty acids blood ketones↑  diabelic ketoacidosis. 
  22. 22. As blood sugar levels became elevated (hyperglycemia), glucose is excreted in the urine and excessive of urination occurs due to osmotic diuresis (polyuria).  Increased fluid loss leads to dehydration and excess thirst (polydipsia).  Since cells are starved of glucose, the patient experiences increased hunger (polyphagia).  Paradoxically, the diabetic patient often loss weight, since the cells are unable to take up glucose. 
  23. 23. COMPLICATIONS Major organs/systems showing changes Long term complications myocardial infarct; atherosclerosis; hypertension; microangiopathy; cerebral vascular infarcts; cerebral hemorrhage Pancreas islet cell loss; insulitis (Type 1); amyloid (Type 2) Kidneys nephrosclerosis; glomerulosclerosis; arteriosclerosis; pyelonephritis Eyes retinopathy; cataracts; glaucoma Nervous system autonomic neuropathy; peripheral neuropathy Peripherals peripheral vascular atherosclerosis; infections; gangrene Cardiovascular system: heart, brain, blood vessels
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  25. 25. MEDICAL MANAGEMENT Sulfonyl ureas  Bigaunides  Meglitidines  Thiazoledinediones  Exercise and diet control  Insulin : rapid, short, intermediate, long acting.  Oral antidiabetic agents 
  26. 26. MANAGEMENT: • Lifestyle intervention (HbA1c ↓1–2%) • Metformin (HbA1c ↓1.5%) STEP 2 After 2–3 months select 1 additional agent STEP 3 Adjust therapy • Basal insulin HbA1c ≥ 7% (HbA1c ↓1.5–2.5%) • Sulfonylureas (HbA1c ↓1.5%) • Thiazolidinedione (HbA1c ↓0.5–1.4%) HbA1c ≥ 7% •Start or intensify insulin therapy STEP 1 Initial therapy • Add a third oral agent if cost-effective • Adapted from Nathan DM, et al. Diabetologia 2006;49:1711–21
  27. 27. ORAL MANIFESTATIONS  Periodontal disease     Salivary glands    Xerostomia is common, but reason is unclear. Tenderness, pain and burning sensation of tongue. Dental caries  Increase caries prevalence in adult with diabetes. (xerostomia, increase saliva glucose)  Microangiopathy altering antigenic challenge. Altered cell-mediated immune response and impaired of neutrophil chemotaxis. Increased Ca+ and glucose lead to plaque formation. Increased collagen breakdown.
  28. 28.  Increased risk of infection:    Delayed wound healing:   Due to microangiopathy and ultilisation of protein for energy, may retard the repair of tissues. Increase prevalence of dry socket.  advanced glycation end- products (AGE) synthesized due to hyperglycemia, can convert macrophages into cells with a destructive phenotype, producing high levels of interleukin-1β, interleukin 6(IL-6) and tumour necrosis factor- α (TNF-α).
  29. 29. DENTAL MANAGEMENT CONSIDERATIONS     Glucose levels Frequency of hypoglycemic episodes Medication, dosage and times. Consultation To minimize the risk of an intraoperative emergency, clinicians need to consider some issues before initiating dental treatment  Medical history : take hx and assess glycemic control at initial appt.
  30. 30. DENTAL MANAGEMENT CONSIDERATIONS  Scheduling of visits Morning appt. (endogeneous cortisol)  Do not coincide with peak activity.  Diet   Blood glucose monitoring   Ensure that the patient has eaten normally and taken medications as usual. Measured before beginning. Prophylactic antibiotics    Established infection Pre-operation contamination wound Major surgery 
  31. 31. DENTAL MANAGEMENT CONSIDERATIONS  During treatment   After treatment    Infection control Dietary intake Medications : salicylates increase insulin secretion and sensitivity avoid aspirin.  The most complication of DM occur is hypoglycemia episode. Hyperglycemia
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  33. 33. Thank you Leader in continuing dental education