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Endocrine disease in dentistry /certified fixed orthodontic courses by Indian dental academy


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Endocrine disease in dentistry /certified fixed orthodontic courses by Indian dental academy

  1. 1. Endocrine disease and Dentistry
  2. 2. INDIAN DENTAL ACADEMY Leader in continuing dental education
  3. 3. Mechanism of hormone action  ACTH, TSH, PTH, ADH, FSH, LH H + R→ ATP→cAMP→increased protein kinase activity.  Insulin, IGF increase intracellular Ca from EC/ER/mitochondria; combines with calmodulin which alters str and fn of enz.
  4. 4. Mechanism of hormone action  Steroid hormones H enters the cell, combines with R; H+R combine with acceptor site on human DNA→mRNA→protein synthesis.
  5. 5. Acromegaly  High index of suspicion necessary  Peak incidence 30-50 years.  Insidious onset  Causes- acidophil tumor of anterior pituitary, hyperplasia.
  6. 6. Acromegaly –clinical features  Coarse facial features- broad nose,thick lips,enlarged supra-orbital ridges.  Enlarged hands, carpal tunnel syndrome  Type 2 DM.  CVS- IHD, Cardiomyopathy, CCF.
  7. 7. Acromegaly – clinical features
  8. 8. Acro-megaly- oral features  Macro-glossia, inter-dental spacing  “Shrunk dentures”  Prognathism, mal-occlusion – class II.  Thick lips.
  9. 9. Acromegaly- X- Ray Skull
  10. 10. Acromegaly- contd.  Visual field defects  III, IV and VI th cranial nerves.  Hyper-prolactinemia  Investigations- IGF-1 assay - CT scan. - Perimetry. - GH levels after 75 g. oral glucose.
  11. 11. HYPERTHYROIDISM  Causes- - Grave’s disease (70-80%) Toxic multi-nodular goitre Toxic adenoma Ca thyroid Ectopic secretion from ovarian tumors Pituitary tumors.
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  13. 13.
  14. 14. Hyperthyroidism- effects  Weight loss, heat intolerance,muscle weakness, sweating,diarrhea,anxiety.  Tachycardia,Atrial fibrillation,CCF, increased systolic BP.  Tremors, hyper-reflexia.  Lid retraction, lid lag and exophthalmos
  15. 15. Hypothyroidism  Causes- Hashimoto’s thyroiditis,Radioiodine therapy,surgery,Iodine deficiency drugs like amiodarone,lithium etc. -Hashimoto’s thyroiditis- common in middle age, presents with goitre and hypothyroidism.
  16. 16. Hypothyroidism- C/F  Tiredness,cold intolerance,weight gain,constipation,”Slow”,poor memory  Hoarse voice,cool coarse skin, hair loss  Bradycardia, angina, pericardial effusion.  Confusion, Psychosis, delayed relaxation of DTR.
  17. 17. Investigations for thyroid  T3, T4 and TSH  Ultrasonography  Radio-active Iodine Uptake  FNAC  ECG  Lipid profile.
  18. 18. Thyroid- dental implications  Goitre visible to dentist  Hyperthyroidism- pain, anxiety and psychiatric problems  Hypothyroidism- avoid sedation  Treated patients are normal.
  19. 19. ADRENALS  Zona glomerulosa- Aldosterone  Zona fascicularis- Cortisol  Zona reticularis-Adrenal androgens
  20. 20. Actions of Cortisol  Steroids diffuse passively through the cell membrane and bind to intracellular receptors .  The steroid-receptor complex is transported to the nucleus, where it binds to specific sites on steroidregulated genes, altering levels of transcription.
  21. 21. Action on CHO metabolism  Glucocorticoids raise the blood glucose level by acting as an insulin antagonist and by suppressing the secretion of insulin, thereby inhibiting peripheral glucose uptake, which promotes gluconeogenesis.
  22. 22. The actions on protein metabolism Mainly catabolic in effect, resulting in an increase in protein breakdown and nitrogen excretion.  Mobilization of glycogenic amino acid precursors from peripheral supporting structures, such as bone, skin, muscle, and connective tissue, due to protein breakdown. Hyper aminoacidemia also facilitates gluconeogenesis. 
  23. 23. Actions on fat metabolism Glucocorticoids regulate fatty acid mobilization by enhancing the activation of cellular lipase.  The actions of cortisol on protein and adipose tissue vary in different parts of the body. Cortisol depletes the protein matrix of the vertebral column (trabecular bone), not long bones. Peripheral adipose tissue mass decreases, whereas abdominal and interscapular fat expand. 
  24. 24. Anti-inflammatory effects  Effects on the microvasculature and to suppression of inflammatory cytokines.  Cortisol maintains vascular responsiveness to circulating vasoconstrictors and opposes the increase in capillary permeability during acute inflammation.
  25. 25. Anti-inflammatory effects  Glucocorticoids produce a depletion of circulating eosinophils and T cells. Thus, cortisol impairs cell-mediated immunity.
  26. 26. Anti-inflammatory effects  Glucocorticoids also inhibit the production and action of the mediators of inflammation, such as the lymphokines and prostaglandins. Glucocorticoids inhibit the production and action of interferon by T lymphocytes and the production of IL-1 and IL-6 by macrophages.
  27. 27. Anti-inflammatory effects  Glucocorticoids inhibit the production and inflammatory effects of bradykinin, platelet-activating factor, and serotonin.  Antibody production is reduced and lysosomal membranes are stabilized,
  28. 28. Actions of cortisol-contd. Glucocorticoids also have weak mineralocorticoid-like properties, and high doses promote renal tubular sodium re-absorption and increased urine potassium excretion.  Glucocorticoids also can influence behavior; emotional disorders may occur with either an excess or a deficit of cortisol. 
  29. 29. LABORATORY EVALUATION OF ADRENOCORTICAL FUNCTION Urinary excretion of free cortisol, 17 ketosteroids.  Plasma levels of cortisol, aldosterone- max values in morning, low levels in evening.  Stimulation tests ( for detecting hypofunction) 25 units of Cosyntropin i.v./i.m., measure plasma cortisol levels before, 30 minutes after and 60 minutes after inj.If stimulated level >7 microgm/dl- normal 
  30. 30. Tests of Mineralocorticoid Reserve These tests use protocols designed to create a programmed volume depletion, such as sodium restriction, diuretic administration, or upright posture.  A simple, potent test consists of severe sodium restriction and upright posture. After 3 to 5 days of a 10-mmol/d sodium intake, rates of aldosterone secretion or excretion should increase two- to threefold over the control values. Supine morning plasma 
  31. 31. LABORATORY EVALUATION OF ADRENOCORTICAL FUNCTION  1) 2) Suppression test for hyper-functionOral dexametasone 1 mg at midnight of previous day, 8 a.m. plasma cortisol should be < 5 microgm/dl in normal persons. Definitive test- 0.5 mg Dexa-methasone 6 hrly for 2 days, plasma cortisol < 5 microgm/dl, urinary excretion of cortisol in 24 hrs < 30 microgm.
  32. 32. Tests of Mineralocorticoid Suppressibility  These tests rely on an expansion of extra-cellular fluid volume, which should decrease circulating plasma renin activity and decrease the secretion and/or excretion of aldosterone.
  33. 33. TESTS OF PITUITARY-ADRENAL RESPONSIVENESS Insulin-induced hypoglycemia – In this test, regular insulin (0.05 to 0.1 U/kg body weight) is given intravenously as a bolus to reduce the fasting glucose level to at least 50% below basal. The normal cortisol response is a rise to more than 500 nmol/L (18 ug/dL).  Other tests are metyrapone test and CRH test. 
  34. 34. Addison’s disease-causes  Tuberculosis  Histoplasmosis  Coccidioidomycosis  Cryptococcosis.  frequent cause-Idiopathic atrophy- an autoimmune mechanism- Other autoimmune diseases maybe present.
  35. 35. Addison’s disease-causes  Rarely, Adrenoleukodystrophy, bilateral hemorrhage, tumor metastases, HIV, cytomegalovirus (CMV), amyloidosis, adrenomyeloneuropathy, familial adrenal insufficiency, or sarcoidosis.  Pituitary failure- Chromophobe adenoma and Sheehan’s syndrome.
  36. 36. Addison’s disease- C/f  Asthenia is the cardinal symptom  weight loss, lethargy, weakness.  vitiligo, cutaneous and mucosal hyperpigmentation, loss of body hair.
  37. 37. Addison’s disease- C/f anorexia, nausea and vomiting, illdefined abdominal pain.  hypotension (postural)- 80/50, and occasionally hypoglycemia.  Personality changes-excessive irritability and restlessness.  Addisonian crisis- hypotension, hypovolemia, vomiting, coma 
  38. 38. Addison’s disease – Oral Pigmentation
  39. 39. Lab diagnosis  Adrenal stimulation with ACTH uncovers abnormalities.  Serum sodium, chloride, and bicarbonate levels are reduced, and the serum potassium level is elevated.  Normocytic anemia, a relative lymphocytosis, and a moderate eosinophilia.
  40. 40. Addison’s disease-treatment Hydrocortisone (cortisol) is the mainstay of treatment. The dose for most adults (depending on size) is 20 to 30 mg/d. To simulate the normal diurnal adrenal rhythm, two-thirds of the dose is taken in the morning, and the remaining one-third is taken in the late afternoon.  Fludrocortisone-0.05 to 0.1 mg per day by mouth 
  41. 41. Treatment of Addison’s disease  If vomiting for > few hours- iv fluids and iv hydro-cortisone.  If significant infection- double the dose of cortisol during illness.  Peri-operative management For GA- IV Hydrocortisone 100mg before induction, repeat every 8 hrs. Halve every 24 hrs till 5th day.
  42. 42. Cushing’s syndrome- Causes Pituitary adenoma  Defect in hypothalamus- increased CRH  Ectopic ACTH from primitive small cell (oat cell) type of bronchogenic carcinoma,tumors of the thymus, pancreas, or ovary; medullary carcinoma of the thyroid,bronchial adenomas, carcinoid tumors or pheochromocytomas  20 to 25% of patients with Cushing's syndrome have an adrenal neoplasm. 
  43. 43. Cushing’s syndrome  Centripetal obesity- moon-face, buffalo hump.  Thin skin, purpura, acne, hirsutism, easy bruisability of skin.  Muscle weakness, osteoporosis.  Depression,mental lability and psychosis.  Hypertension and Diabetes Mellitus.
  44. 44. Cushing’s syndrome
  45. 45. Evaluation of patient Signs and symptoms ↓ Screening test ( 1mg DXM previous MN) ↓ Dexa-methasone suppression test 0.5 mg DXM 6hrly for 2 days ↓ Abnormal response ↓ High ACTH Low ACTH ↓ ↓ Pituitary imaging Abdominal CT increased u. 17 ketosteroid increased u. DHEA.
  46. 46. Iatrogenic Cushing’s syndrome  Plasma and urinary cortisol reduced because of suppression of HPA axis by exogenous steroids.
  47. 47. Treatment for Adrenal Neoplasm When an adenoma or carcinoma is diagnosed, adrenal exploration is performed with excision of the tumor. Adenomas may be resected using laparoscopic techniques.  The principal drug for the treatment of adrenocortical carcinoma is mitotane< 6gm/d. This drug suppresses cortisol production and decreases plasma and urine steroid levels 
  48. 48. ACTH producing tumors Whether pituitary or ectopic- treatment is excision. Radio-therapy can also be tried.  If inoperable ACTH producing tumors present, bilateral adrenalectomy with lifelong steroid supplement is the treatment.  Steroidogenesis can be inhibited by ketoconazole 600 mg. 
  49. 49. Dental aspects of Adrenal disease  Precautions for steroids  Liaise with physician  DM,CVS disease  Oral candidiasis in Cushing’s syndrome  Oral pigmentation in Addison’s disease.
  50. 50. Managing a patient on steroids Minor surgery and GA- The usual oral dose of steroid is given on the morning of surgery, and the usual dose of oral steroid after surgery.  Moderate or major surgery and GA-Usual oral dose of steroid on the morning of surgery. + Hydrocortisone 25-50 mg at the time of induction + HCHS 25mg 3 times daily after surgery or for 72 hrs after major surgery.  Usual steroid dose after stopping injection 
  51. 51. Steroids and Dentistry  If pt. is on >10mg Prednisolone daily, no need to increase the dose.  If pt. is receiving 1-10 mg Prednisolone cover with double dose if required.  If pt has stopped steroids for last 3 months highest risk. Pre-operative day + day of surg + 2 post-op days
  52. 52. PARATHYROID    Parathormone binds to the receptors on osteoblast cells, and cytokines are released which stimulate osteoclast cells; causing osteoporosis. PTH decreases renal clearance of Ca, increases intestinal absorption,and causes bone resorption. Released in response to low Ca, Mg levels.
  53. 53. Hyperparathyroidism  Causes- solitary adenoma -chief cell hyperplasia, - Carcinoma parathyroid and -MEN I and II.
  54. 54. HYPERPARATHYROIDISMClinical features • • • • • Asymptomatic in 50% cases. Renal- calcification/stones. Bone- Osteitis fibrosa cystica- decreased trabeculae, giant multi-nucleated osteoclasts, punched out lesions. GIT- Peptic ulcers, pancreatitis, anorexia, nausea,constipation. CNS- Muscle weakness,mental changesdepression. Hypertension.
  55. 55. HyperparathyroidismTreatment Hydration, increased salt intake,mild and forced diuresis.  Phosphates, diphosphonates, Mithramycin, Steroids.  In young patients, surgery. 
  56. 56. Hypoparathyroidism  Causes- Hereditary  Acquired- due to surgery/radiotherapy for thyroid; auto-immune failure.  Ineffective PTH- CRF,Vitamin D deficiency and Pseudo-hypoparathyroidism. 
  57. 57. Hypoparathyroidism Clinical featuresMuscle spasm, carpo-pedal spasm, Trousseau’s sign, Chvostek’s sign laryngeal spasm, convulsions, cardiac arrhythmias, mal-absorption, Extra-osseous calcification.
  58. 58. Hypo-parathyroidismtreatment. • Vitamin D3 500 – 3000 micrograms/day or Calcitriol 0.25 –1 micrograms/day. • Calcium 2-3 gm/day. • Thiazide diuretics with salt restriction.
  59. 59. Diabetes Mellitus The magnitude of the problem- 3.5 crore diabetics in India. - 14% of the urban population. - Estimated to be 5.72 crore by 2025. - Only 10-12% of diabetics receive modern pharmacologic treatment. 
  60. 60. Diabetes Mellitus- definition  A syndrome characterized by chronic hyperglycemia and disturbances of carbohydrate, fat and protein metabolism associated with absolute or relative deficiency of insulin secretion and/or action.
  61. 61. Diabetes Mellitus-Diagnosis FPG 110 mg% Normal 110-126 mg% IFG >126mg% DM 2 hours after 75 g oral glucose <140 mg% Normal 140-200 mg% IGT >200mg% DM
  62. 62. DM-classification         Type 1 Insulin deficiency Type 2 Insulin resistance but can progress to insulin def.- lean type,obese type & MODY. Gestational Diabetes Pancreatic disease Hormonal Disorders Drugs and chemicals Insulin receptor abnormalities Genetic syndromes- Myotonic dystrophy, Lipodystrophy, Ataxia-Telangiectasia.
  63. 63. Type 1 DM Childhood/Adolescence or adult onset.  Childhood type- higher ICA and IAA more severe de-compensation.  Adult onset-Latent auto-immune diabetes in Adults. (LADA) GAD (Glutamic acid decaroboxylase) associated,lower antibody levels May masquerade as non-obese type 2. 
  64. 64. Type I DM Circulating auto-antibodies present -GAD glutamic acid decarboxylase -ICA islet cell antibodies -IAA insulin auto-antibodies Immune-mediated beta cell destruction - hyper-glycemia - Ketoacidosis.
  65. 65. Type 2 DM      Diagnosed by excluding type1. Most common form of DM( 90% cases). Strongly associated with obesity and inactivity. Usually > 40 yrs but MODY type possible. Strong family history.
  66. 66. Effects of DM Metabolic syndrome- hyper-insulinemia - hypertension. - Obesity with abdominal distribution. - Dyslipidemia. - Pro-coagulant epithelial markers. - Accelerated atherosclerosis. 
  67. 67. Diabetes- management. Education  Targets - Pre-prandial 72-110mg% - Bed-time 110-145 mg% - HbA1c < 7% - Lipid profile- LDL cholesterol < 100 mg% - HDL cholesterol > 45 mg% - Triglycerides < 200 mg%. - Hypertension –Target BP 130/85 mm Hg.
  68. 68. DM –Nutrition Encourage regularity in meal timing and consistency about quantity of each meal.  Multi-vitamin supplements.  Calorie intake 1500 kcal/day in males and 1200 kcal/ day in females  Diet restriction -Avoid refined CHO and alcohol -Encourage high fiber food. -Reduce saturated fat,Sodium 2.4-3 gm/day. 
  69. 69. DM – Role of Exercise     Check-up for BP, CVS, CNS, eyes, feet and renal function before starting exercise. Tailor exercise to the patient’s needs and as per his limitations. Benefits of exercise- reduces insulin resistance, improves lipid profile, corrects obesity. Aerobic exercise with a warm-up of 3-5 minutes.
  70. 70. Type 2 DM-management  Oral hypoglycemic drugs 1) Insulin secretagoguesa) Sulfonylureasglibenclamide, gliclazide,glipizide b) Metiglinide deivatives- Repaglinide. 2) Insulin sensitizers a) Biguanides- Metformin. b) Thiozolidinedone- Pioglitazone,Rosiglitazone 3) Drugs delaying CHO absorption- Acarbose
  71. 71. Insulin in type 2 DM Not controlled with diet,exercise and OHA.  Pre-operatively.  During infection.  Pregnancy.  Diabetic keto-acidosis. Given pre- prandial with basal cover. 
  72. 72. Insulin therapy Sources of InsulinHuman,porcine and bovine.  Duration of ActionRapid acting –onset ½ hr; duration 8 hrs. Intermediate- NPH onset 1.5 hrs,duration 24 h Pre-mixed-50-50,30-70.onset ½h,duration24h Long acting.  Insulin delivery systems (Insulin pens, pump) 
  73. 73. Diabetes- complications Acute- hypoglycemia  Chronic-Atherosclerosis of large vessels-MI, CVA,gangrene,aneurysm. -infection risk -neuropathy-Sensori-motor, autonomic. -retinopathy, maculopathy, early cataract. -nephropathy. 
  74. 74. Diabetes and dentistry-1 Periodontopathy.  Wear and tear of gingival tissues due to dentures more in uncontrolled diabetes; chances of oral candidiasis.  Delayed healing and chances of infection after invasive dental procedures. 
  75. 75. Diabetes and dentistry- 2 High risk patients1) Poor metabolic control- FPG > 250 mg %, HbA1c > 9%.  Frequent episodes of hypoglycemia or ketoacidosis. 3) Multiple complications. 2)
  76. 76. Diabetes and dentistry-3 For type II – VI procedures, defer treatment until metabolic control is achieved.  Palliative rather than extensive restorative surgery preferred.  Aggressive control of oral infection – a must. 
  77. 77. Diabetes and surgery Metabolic changes during surgery-Hormone changes which aggravate DMAdrenaline,GH,cortisol. -More glucose production less muscle uptake. - metabolic acidosis likely.  Increased insulin requirements in type 1 DM  Type 2 DM may require insulin cover perioperatively. 
  78. 78. DM and Surgery-plan Target glucose level 7-11 mmol/lit during surgery.  IV fluids should not contain glucose.  Monitor electrolytes frequently (K +)  Ensure good analgesia- reduce stress.  GKI infusion10% Dextrose, 10 mmol K+,10 U actrapid. 
  79. 79. Sliding scale -GKI Blood glucose (mmol/lit) <4 4-6.9 7-10 11-16.9 > 17 Pump ml/hr stop 1 2 3 4
  80. 80. Dental Aspects of DM      Food intake maybe disrupted. Be aware of hypoglycemia and DKA. IHD, Neuropathy, eyes and dehydration. Infection risk. Poor wound healing.
  81. 81. Thank you Leader in continuing dental education