1. Corticosteroid s

2. 2Contents Introduction History Functional anatomy and histology of adrenal glands Biosynthesis of steroids Fate of steroids Mineralocorticoids (source, action, regulation) Glucocorticoids (source, action, regulation) Mechanism of action at cellular level 3. 3Classification of steroidsUses in medicine Steroids in dentistry Adverse effects Drug interactions PrecautionsPathologies of adrenal gland 4. 4Introduction The adrenal gland is the source of a diverse group of hormones essential for metabolic control, regulation of water and electrolyte balance, and regulation of bodys response to stress. Using cholesterol as a substrate, the adrenal cortex produces a large number of substances collectively known as corticosteroids. 5. 5History By the middle of 19th century it was demonstrated that adrenal glands were essential for life Later, it was appreciated that the cortex was more important than the medulla A number of steroidal active principles were isolated and their structures were elucidated by kendall and his coworkers in the 1930s. 6. 6However, the gate to their great therapeutic potential was opened by Hench (1949) who obtained striking improvement in rheumatoid arthritis by using cortisone. The nobel prize was awarded the very next year to kendall and Hench. Currently, corticosteroids are drugs with one of the broadest spectrum of clinical utility. 7. 7Functional anatomy and histology of adrenal glands 8. 8 9. 9 10. 10Zones of adrenal cortex Zona glomerulosaHormones Aldosterone DesoxycorticosteroneZona fasciculataCortisone CortisolZona reticularisDehydroepiandrosterone Androstenidione Traces of estrogensEssentials Of Medical Physiology 3rd Edition, K Sembulingam 11. 11Biosynthesis of steroids CholesterolPregnenoloneProgesterone17 Hydroxy pregnenoloneDehydroepiandrosterone11- Deoxy corticosterone17 Hydroxy progesteroneAndrostenidioneCorticosterone11 Desoxyhydro cortisoneAldosterone HydrocortisoneTestosterone 12. 12MineralocorticoidsGlucocorticoids CortisolAldosteroneCorticosterone 11- Deoxy corticosteroneCortisoneEssentials Of Medical Physiology 3rd Edition, K Sembulingam 13. 13Rate of secretion of the principal steroids Glucorticoids 10-20 mg daily Mineralocorticoids 0.125 mg dailyTextbook of Medical Physiology 11th Edition, Arthur C. Guyton, John E. Hall - 2006 14. 14REGULATION OF SECRETION Regulation by Hypothalamus (CRH) & Pituitary (ACTH)Negative feedback effect from plasma cortisol levelsPulsatile secretion of ACTH based on Circadian rhythmNeural effects on HPA axis due to emotional / physical stress 15. 15Fate of corticosteroids Degraded mainly in liver Conjugated to form glucuronides and to a lesser extent form sulphates 25% - excreted in bile and feces 75% - excreted in urine 16. 16MECHANISM OF ACTION plasma memb CYTOPLASMICCorticosteroidsRECEPTOR PROTEIN GLUCOCORTICOID RESPONSE ELEMENTTranscription of m - RNANew protein synthesisNucleusTOTAL TIME 30 60 mins 17. 17Mineralocorticoid s 18. 18Mineralocorticoids Source : Zona glomerulosa Functions: 90% of mineralocorticoid activity is provided by aldosterone Aldosterone life saving hormoneEssentials Of Medical Physiology 3rd Edition, K Sembulingam 19. 19ActionsOn Na+ metabolism Increase in the reabsorption of sodium from renal tubules Essentials Of Medical Physiology 3rd Edition, K Sembulingam 20. 20On ECF volume Na reabsorption from renal tubules Simultaneous water reabsorption Increase in ECF volumeEssentials Of Medical Physiology 3rd Edition, K Sembulingam 21. 21On BP Increases ECF volume Increases BPEssentials Of Medical Physiology 3rd Edition, K Sembulingam 22. 22On K+ ionsIncrease in the excretion of potassium from renal tubules Essentials Of Medical Physiology 3rd Edition, K Sembulingam 23. 23On H+ ion concentration Causes tubular secretion of hydrogen ions Essential to maintain acid - base balance Essentials Of Medical Physiology 3rd Edition, K Sembulingam 24. 24On intestineGreatly enhances sodium absorption from the intestine Essentials Of Medical Physiology 3rd Edition, K Sembulingam 25. 25Regulation of aldosterone secretion Increase in K+ concentration Decrease in Na+ Concentration Decrease in ECF volumeDecrease in K+ concentration Increase in Na+ Concentration Increase in ECF volume Feedback inhibitionStimulationangiotensinogenAngiotensin - 1Angiotensin - 2ReninConverting enzymeJuxtaglomerular apparatusExcretion of K+ Retention of Na+ Retention of waterLungskidneysAdrenal cortexAldosteroneEssentials Of Medical Physiology 3rd Edition, K Sembulingam 26. 26Glucocorticoids 27. 27Glucocorticoids Source : zona fasciculata Functions: HormoneGlucocorticoid activityCortisol95%Corticosterone4%Cortisone1%Cortisol Life protecting hormone Essentials Of Medical Physiology 3rd Edition, K Sembulingam 28. 28Actions: On carbohydrate metabolism Increases blood glucose level in two ways, Promotes gluconeogenesis Inhibits glucose uptake and utilization by peripheral cells Essentials Of Medical Physiology 3rd Edition, K Sembulingam 29. 29On protein metabolism Promote catabolism of protein in cell Increase plasma amino acid and protein content in the cell. Essentials Of Medical Physiology 3rd Edition, K Sembulingam 30. 30On fat metabolism Causes mobilization and redistribution of fat Actions are - Mobilization of fatty acids from adipose tissue - Increase the concentration of fatty acids in blood - Increases the utilization of fat for energy Essentials Of Medical Physiology 3rd Edition, K Sembulingam 31. 31On mineral metabolism Enhances sodium retention Slightly increase potassium excretion Decreases blood calcium by inhibiting absorption from intestine Essentials Of Medical Physiology 3rd Edition, K Sembulingam 32. 32On water metabolism Accelerate the excretion of waterEssentials Of Medical Physiology 3rd Edition, K Sembulingam 33. 33On muscles Increase the release of aminoacids from muscles by catabolism of proteins Essentials Of Medical Physiology 3rd Edition, K Sembulingam 34. 34On blood vessels Decreases the number of circulating eosinophills in retculoendothelial cells Decrease the number of basophils and lymphocytes Increase the number of neutrophills, RBCs and platelets. Essentials Of Medical Physiology 3rd Edition, K Sembulingam 35. 35On vascular response Glucocorticoids is essential for the constrictor action of adrenaline and noradrenaline In adrenal deficiency, the blood vessels fail to respond to Adr and NA leading to vascular collapse. Essentials Of Medical Physiology 3rd Edition, K Sembulingam 36. 36On CNS Essential for normal functioning Insufficiency causes personality changes like irritablity and lack of concentration Essentials Of Medical Physiology 3rd Edition, K Sembulingam 37. 37Permissive action of glucocorticoids The action of some hormones are executed only in the presence of glucocorticoids. Eg: Calorigenic effect of glucagon Lipolytic effect of catecholamines Pressor effects of catecholamines Bronchodialation by catecholamines Essentials Of Medical Physiology 3rd Edition, K Sembulingam 38. Anti-inflammatory actions LipocortinRecruitment of WBC & monocytemacrophage into affected area & elaboration of chemotactic substances ELAM & ICAM in endothelial cells TNF from phagocytic cells IL1 from monocyte-macrophage Expression of cyclooxygenase II GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006)38 39. CorticosteroidsLipocortin Phospholipids Phospholipase A2 Arachidonic acidslipoxygenaseLeukotrieneCycylooxygenaseProstaglandins, Thromboxane Prostacyclins39 40. On resistance to stress Physical or mental stress Increases ACTH Increase in glucocorticoid secretion High resistance to body against stress GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006)40 41. 41Anti allergic action Suppress all types of hypersensitivity and allergic phenomena. Suppression of recruitment of leucocytes at the site of contact with antigen and of inflammatory response to immunological injury.GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 42. 42Immunosuppresive effects Suppress the immune system of the body by decreasing the number of circulating T lymphocytes. Prevent release of interleukin-2 by T cells GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 43. 43Regulation of cortisol secretion Emotion, stress, traumaFeedback inhibitionHypothalamusCorticotropin releasing factorAnterior pituitary ACTH Adrenal cortex Cortisol 44. 44Mechanism of action at cellular level 45. 45Mechanism of action at cellular level Translocation of glucose transporters from plasma membrane to deeper sitesDecreased glucose uptake and utilization in peripheral tissues GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 46. 46Induction of hepatic gluconeogenetic enzymesIncreased production of glucose from aminoacids GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 47. 47Induction of hepatic glycogen synthetaseDeposition of glycogen in hepatocytes GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 48. 48Site specific changes in sensitivity of adipocytes to GH, Adr, insulinAltered distribution of body fat GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 49. 49Decreased expression of POMC gene in pituitary corticotropesDecreased production of ACTH GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 50. 50Induction of lipocortins in macrophages, endothelium and fibroblastsLipocortins inhibit phospolipase A2 decreased production of PGs,LTs&PAF GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 51. 51Negative regulation of genes for cytokines in macrophages, endothelial cells and lymphocytesDecreased production of IL1,2,3,6,TNF,GM-CSF, Interferon Fibroblast proliferation and T lymphocyte function are suppressed. chemotaxis interfered.GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 52. 52Decreased production of acute phase reactants from macrophages and endothelial cellsComplement function is interfered. GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 53. 53Decreased production of ELAM-1 and ICAM-1 in endothelial cellsAdhesion and localization of leukocytes is interfered. GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 54. 54Inhibit IgE mediated histamine and LT-C4 release from basophilsEffects of antigen antibody reaction not mediated GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 55. 55Classificatio n 56. 56Classification of steroids based on their relative activity Glucocorticoids:Short acting (t1/2 < 12 hr) Hydrocortisone CortisoneIntermediate acting: (t1/2 12 36) Prednisole Methyl prednisole TriamcinoloneLong acting: (t1/2 > 36 hrs) Paramethasone Dexamethasone Betamethasone 57. 57Mineralocorticoids Desoxycorticosterone acetate(DOCA) Fludrocortisone Aldosterone 58. 58 PotencyExamplesHighest0.05% Clobetasol propionate 0.05%Betamethasone dipropionateHigh0.1% Halcinonide 0.25% Desoximethasone 0.05% Fluocinonide 0.5% Triamcinolone acetinode 0.05% Betamethasone dipropionate 0.05% Diflorasone diacetate creamIntermediate0.2% Fluo-cinolone acetonide 0.05% Desoxymethasone 0.025% Betamethasone benzoate 0.2% Hydrocortisone valerateLow0.025% Fluo-metholone 0.025% Triamcinolone acetonide 0.03% Fluocinolone pivalate 0.01% Betamethasone valerateLowest0.25-2.5% Hydrocortisone 0.5% Prednisolone 0.2% Betamethasone Handbook of Applied therapeutics 8th Edition, 2007 59. 59According to Potency AgentAntiinflammator yTopicalEquivalent oral dose (mg)Forms AvailableHydrocortisone1120O, I, TCortisone0.8025OPrednisolone545O, ITriamcinolone554O, I, TFlu-prednisolone1571.5OBetamethasone25-40100.6O, I, TDexamethasone30100.75O, I, TBasic and Clinical Pharmacology LANGE-11th Edition 60. 60Some Commonly Prescribed Steroids 61. 61Triamcinolone Kenacort, Tricort, kenalog, Tess buccal pasteOral:1,4,8mg syrup Topical:0.1% eye drops, ointment Parentral: 3,10,40 mg/ml for I.M, intraarticular, intralesional injections 62. 62Dexamethasone Decadron, Dexasone, WymesoneOral:0.25,0.5,0.75,1,2,4,6mg tablets Topical:0.1% eye drops, ear drops, skin ointment Parenteral: 4,8,10,20 mg/ml for IV, IM, intralesional and intraarticular. 63. 63Betamethasone Oral: oral drops 0.5 mg/ ml, tablets 0.5 to 1 mg. Betnesol, Betnovate, Topical 0.1% eye drops, Betnesol forte, ointment,0.05% nasal drops, Betawin forte, 0.12% skin creams Walacort, Parenteral:4 mg/ml for IM, Stemin IV, intralesional, intraarticular 64. 64Hydrocortisone Wycort, Hycort, Unicort, Cipcorlin, EfcorlinOral:5mg,10mg,20mgtab Topical: 1%eye drops 0.025%nasal drops 0.25-2.5%skin cream Parenteral:25, 50 mg/ml for IV,IM,SC Injections 65. 65Cortisone Oral: 5, 10, 25 mg tablets Corlin, Cortone Parentral:22,25 mg/ml of solution 66. 66Prednisolone Wysolone, Prelone, Nucort, Cecort,Oral:5,10, 20 mg tablets, 15mg/5 ml syrup, 5mg/ml suspension as pediatric drops Parenteral:25,50 mg/ml IM,IV,Intralesional 67. 67UsesIn medicineIn dentistry 68. 68MedicineReplacement therapy Pharmacotherapy 69. 69Replacement therapy: Acute adrenal insufficiencyChronic adrenal insufficiency : Hydrocortisone or dexamethasone are given i.v, first as a bolus injection and then as infusion along with istonic saline and glucose solutions. Hydrocortisone given orally is the most commonly used drug with adequate salt and water allowanceCongenital adrenal hypoplasia : 0.6 mg/kg daily in divided doses round the clock 70. 70Pharmacotherapy: Single dose (even excessive) is not harmful can be used to tide over mortal crisis even when benefit is not certain. Short courses (even high doses) are not likely to be harmful in the absence of contraindications. Starting doses can be high in severe illness 71. 71 Long term use is potentially hazardous: keep the dose to minimum which is found by trial and error, even partial relief may have to be tolerated. No abrupt withdrawal after a corticoid has been given for > 2 to 3 weeks: may precipitate adrenal insufficiency 72. 72Arthritis Rheumatoid arthritis Osteoarthritis Rheumatic feverGout 73. 73Collagen diseases SLE Polyarteritis nodosa Dermatomyositis Nephrotic syndrome Glomerulonephritis 74. 74Severe allergic reactions Used for short periods in anaphylaxis Angioneurotic edema UtricariaSerum sickness 75. 75Autoimmune disorders Autoimmune hemolytic anemia Thrombocytopenia Active chronic hepatitis Myasthenia gravis 76. 76Bronchial asthma Status asthmaticus Severe chronic asthma 77. 77Infective diseases Severe forms of tuberculosis Severe lepra reaction Certain form of bacterial meningitisPneumocystitis carini pneumonia with hypoxia in AIDS patients. 78. 78Eye diseases Effective in diseases of anterior chamberAllergic conjuctivitis Iritis keratitis 79. 79Skin diseases Eczematous skin diseases Pemphigus vulgaris Exfoliative dermatitisSteven johnsons syndrome 80. 80Intestinal diseasesUlcerative colitis Chrons disease 81. 81Others Cerebral edema Malignancies Organ transplantation and skin allograft Shock To test the adrenal pituitary axis 82. Steroids in DentistryUsed primarily to decrease postoperative edema and manage oral inflammatory diseases82 83. 83Steroids in oral surgery Prevention of postoperative pain, edema, trismus after 3rd molar surgeryPrevention of postoperative edema after orthognathic surgery Prevention of alveolar osteitis 84. 84steroids in Endodontics Steroids are used as intracanal medicaments in endodontics Ledermix is corticosteroid- antibiotic intracanal paste Painful teeth with acute apical periodontitis that had been dressed with ledermix paste gave rise to less pain and it has proved to be an effective intracanal medicament for the control of postoperative pain associated with acute apical periodontitis with a rapid onset of pain reductionInternational Endodontic Journal,Volume 36 Issue12, Pages 868 - 75 85. 85Corticosteroids in Oral Medicine 86. 86 Eg: Erosive LP Ulcerative, Vesiculoerosive diseases RAS Benign lesions Salivary gland disorders TMJ DisordersNeuralgia Treatment Miscellanous Eg: CGCG Eg: Mucocele Eg: Osteoarthritis Rheumatiid arthritis Eg. Post herpatic neuralgia OSMF 87. 87Ulcerative Vesiculoerosive diseases Immunologically mediated diseases that affect the oral mucosa present with inflammation and loss of epithelial integrity, through cellular and/or humoralimmunity-mediated attack on epithelial connective tissue targets. Themainreddening, debilitating.clinicalwithfeaturespainthatarecanulcerationandbeandsevere 88. 88 Corticosteroids play a central role in the treatment of vesiculoerosive lesions. However, the frequency and severity of the adverse effects associated with the use of systemic corticosteroids have led to the increased use of topical corticosteroids (TCs) 89. 89Criteria for use short course of TCs Accelerate remission without adverse effectsTCs must be used for longer, less predictable periodsRecurrent aphthous stomatitis (RAS), some cases of erythema multiforme (EM), and Drug-induced ulceration.Severe RAS, Erosive oral lichen planus (OLP), specific forms of EM, and mucous membrane pemphigoid (MMP)Scully et al., 1999; Chan et al., 2002 90. 90 CODS Davangere24/01/2014very severe cases of ulcerationShort course of systemic corticosteroids followed by maintenance regimen of TCs and or can also be started simultaneously with the systemic therapyPemphigus vulgaris ,10-30% of Pemphigoid patients, Erosive lichen planusInevitably be treated with systemic corticosteroids and/or other immunosuppressant therapiesLaskaris and Angelopoulos, 1981; Nisengard and Neiders, 1981; Fine et al., 1984; Domloge-Hultsch et al., 1994; Dayan et al., 1999 91. 91Protocols for use When a TC is prescribed, and especially when a prolonged course is predicted, the basic rule is that a TC of a potency appropriate to the severity of the clinical symptoms should be used, at the lowest possible concentration and frequency, with maintaining the effectiveness of the treatment. It should always be taken into account that these drugs do not cure the disease but rather control or relieve the symptoms. JDR April 2005 vol. 84 no. 4 294-301 92. 92The key factors The specific diagnosis The severity of the oral disease The presence or absence of extra-oral lesions The medical history of the patientJDR April 2005 vol. 84 no. 4 294-301 93. 93Factors that influence the effectiveness of TCs:The intrinsic potency of the drugwhich can be significantly increased by the halogenation of the steroid; esterification, which makes the drug more lipophilic and gives it greater penetrability (Regezi and Sciubba, 1999).JDR April 2005 vol. 84 no. 4 294-301 94. 94Factors that influence the effectiveness of TCs:The contact time between the drug and lesion and the vehicle used to apply it;JDR April 2005 vol. 84 no. 4 294-301 95. 95Factors that influence the effectiveness of TCs:Concentrationwhich can increase its clinical effectiveness, although no additional advantage is obtained beyond certain limits. (Regezi and Sciubba, 1999). JDR April 2005 vol. 84 no. 4 294-301 96. 96Success of a topical medicineTwo main factors Number of applications per day High-potency (2-3 times)The vehicle usedLow potency (5-10 times)JDR April 2005 vol. 84 no. 4 294-301Various vehicles 97. 97Various vehicles. Orabase (Stoy, 1966),Cyanoacrylate (Jasmin et al., 1993), Bioadhesive patches made of cellulose derivatives (Mahdi et al., 1996), Gels (Regezi and Sciubba, 1999), andDenture adhesive paste (Lo Muzio et al., 2001).JDR April 2005 vol. 84 no. 4 294-301 98. 98Patients prescribed TC in an adherent vehicle should be instructed to Apply a small amount to the target area after meals, and Not to eat or drink for at least 30 min. It is best not to rub the TC in, because this can produce irritation.JDR April 2005 vol. 84 no. 4 294-301 99. 100 For small and accessible erosive lesions, or those located on the gingiva and palate, the lesions can be treated by the Use of an adherent paste in a tray, Which allows for accurate control over the contact time and Ensures that the entire lesional surface is exposed to the drug. JDR April 2005 vol. 84 no. 4 294-301 100. 101Systemic steroids for ulcerative vesiculobullous diseases 101. 102major aphthae or severe multiple minor aphthae Prednisone therapy should be started at 1.0 mg/kg/day in patients with severe RAU and should be tapered after 1 to 2 weeks.Natah SS, Konttinen YT. IJOMS 2004;33:221-34. 102. 103Erythema multiformeMinor EMSevere or rapidly progressing lesions20 40 mg/day for 4 6 days60 mg/day slowly tapered by 10 mg/day over 6 weeksIndian J Ophthalmol Jan-Feb 2010;58(1):64-66 103. 104Pemphigus Vulgaris Mainstay 1-2mg/kg/d. Initial dose of treatment 0.5 mg/kg/day to 3 mg/kg/d Dose that achieves clinical control is maintained for 2-3 weeks and then gradually tapered.Burkits Oral Medicine, 11th edition 104. 105Pulse therapy Also called short term therapy High dose therapy involves a 48-72 hrs course of intensive steroid administration Single i.v injection of a supra-physiological dose of steroid Dose of 0.5-2g of prednisolone orequivalent 105. 106Benefits Avoids complications & side effects of long term steroid therapy To achieve immunosuppressive effects similar to those with higher doses of steroids 106. 108Cicatricial pemphigoid Predisolone 30 to 60 mg/day 2-3 weeks to stop new bullae formation Tapered by 20% every 2-3 weeks until the dose of 10 mg is reached Dose maintained on alternate days and reduced by 5 mg every 2 weeks, then stopped 107. 109Bullous pemphigoidClobetasol propionate 20 -40 mg/day is more effective for the treatment.JIAOMR, April-June 2011;23(2):128-131 108. 110Lichen planus Prednisolone 1mg/kg/d for 2 supplementatio weeks and ceased n needed < 1430 days ago, give previous maintenance dose If prior usage ceased > 1430 days ago, no supplementation neededCurrent Systemic Steroid UseDaily alternating Systemic Steroid UseCurrent topical Systemic Steroid UseTreat on No steroid dosage supplementatio day; no further n needed supplementatio n needed 139. 147Dental ProcedurePrevious Systemic Steroid UseCurrent Systemic Steroid UseExtractions, surgery, or extensive proceduresIf prior usage Double daily lasted > 2 weeks dose on day of and ceased < procedure 1430 days ago, give previous maintenance doseTreat on steroid dosage day, and give double daily dose on day of procedureIf prior usage ceased > 1430 days ago, no supplementatio n neededGive normal daily dose on first postoperative day when pain is anticipatedDouble daily dose on first postoperative day when pain is anticipatedDaily alternating Systemic Steroid UseCurrent topical Systemic Steroid UseNo supplementatio n needed 140. 148Scenario One Patient requiring extractions took a 7 day course of 20 mg. of prednisone for exacerbation of asthma one week agoNo supplementation required. Even though the dose was supraphysiologic, the course of time it was taken was less than 2 weeks Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001 141. 149Scenario Two Patient requiring extractions is taking 10 mg of prednisone for the past year to treat rheumatoid arthritisThis patients HPA axis is probably suppressed due to supraphysiologic dose of corticosteroids for longer than 2 weeks. Supplement with at least 100 mg of cortisol equivalent (25 mg prednisone) in the morning on the day of the surgeryClinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001 142. Scenario Three Patient requiring extractions is taking 2.5 mg of prednisone daily for the past 3 months to treat his psoriasisNo supplementation required. Even though the patient has been on prednisone for over 2 weeks, the dose is subphysiologic and will not adversely impact his stress response Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001150 143. Scenario Four Patient requiring extractions was previously taking 50 mg of prednisone for Crohns disease. He was on a 6-month course of prednisone but took his last dose 5 weeks agoNo supplementation needed. A functional stress response returns in 14-30 days after the last dose of steroids151 144. 152Scenario Five Patient requiring extractions is taking 75 mg of prednisone daily for the past 8 weeks to treat pemphigusNo supplementation needed as 75 mg of prednisone is the maximum dose equivalent to 300 mg of endogenous cortisol Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001 145. 153Pathology of Adrenal Gland 146. 154Pathologies of the adrenal gland Adrenal cortexHyperactivityHypoactivity 147. 155HyperactivityCushings syndromeHyperaldosteronismAdrenogenital syndrome 148. 156Cushings syndrome Hypersecretion of glucocorticoids particularly cortisol Due to pituitary originDue to adrenal originCushings diseaseCushings syndrome 149. 157Disproportionate body fat distribution Moon face Buffalo hump Pot bellyPurple striae Thinning of skin Pigmentation Facial redness Hirsutism Muscle weakness 150. 158Bone resorption Hyperglycemia HypertensionSusceptiblity to infections Poor wound healing 151. 159Hyperaldosteronism Hypersecretion of aldosterone PrimarySecondaryAdrenal causeExtra adrenal causes 152. 160Hyperaldosteronism Increase in ECF volume and blood volume Hypertension Severe depletion of potassium Muscle weakness Metabolic alkalosis 153. 163HypoactivityAddisons diseaseAdrenal crisisChronic adrenal hyperplasia 154. 164Addisons disease Failure of adrenal cortex to secrete all the corticosteroids PrimaryAdrenal causeSecondaryFailure of anterior pituitary to secrete ACTHTertiaryFailure of hypothalamus to secrete CRF 155. 165Pigmentation of skin and mucous membrane Muscle weakness Dehydration Hypotension Decreased cardiac output Hypoglycemia Nausea, vomiting, diarrhoea Inability to withstand stress 156. 166Adrenal crisis Common symptom of addisons disease characterized by sudden collapse associated with an increase in need forlarge quantities of glucocorticoids. Fatal if not treated in time 157. 167Adrenal crisisCauses Exposure to even mild stress Hypoglycemia due to fasting Surgical operation Sudden withdrawal of glucocorticoid treatment 158. 168Congenital adrenal hyperplasia Congenital disorder characterized by increase in size of adrenal cortex. Eventhough the size of the gland increases the cortisol secretion decreases. Congenital enzymes necessary for synthesis of cortisol, particularly 21- hydroxylase. 159. 169In boys: Precociousbodygrowth,causingstockyappearance called infant Hercules Precocious sexual development with enlarged penis even at age of 4 years. In girls: Produces MasculinizationFemale child born with external genitalia of male type. 160. 170Conclusion Corticosteroids play an important role in control of pain & inflammation associated with numerous disease states of oral cavity. Currently corticosteroids are drugs with one of the broadest spectrum of clinical utility. But it should never be used as a substitute to other treatments. Lets keep it mind that these drugs do not cure the disease but rather control or relieve the symptoms. It should be used cautiously as it is two edged sword.