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  1. 1. Adrenocorticosteroids and Adrenocortical Antagonists Ma. Victoria M. Villarica, M.D. Fatima College of Medicine
  2. 2. Objectives <ul><li>Review briefly the adrenal gland </li></ul><ul><li>Name the different adrenocorticotropic hormones and discuss their effects </li></ul><ul><li>Identify uses of adrenocorticotropic hormones </li></ul>
  3. 4. Types of steroid hormones <ul><li>Glucocorticoids ; cortisol is the major representative in most mammals </li></ul><ul><li>Mineralocorticoids ; aldosterone being most prominent </li></ul><ul><li>Androgens such as testosterone </li></ul><ul><li>Estrogens , including estradiol and estrone </li></ul><ul><li>Progestogens (also known a progestins) such as progesterone </li></ul>
  4. 5. Adrenal Gland <ul><li>Adrenal cortex – mineralocorticoids, glucocorticoids, adrenal androgens </li></ul><ul><li>Adrenal medulla - catecholamines </li></ul>
  5. 7. Adrenal Cortex <ul><li>Outer zone (zona glomerulosa) – secretes mineralocorticoids </li></ul><ul><li>- receptors for angiotensin II and express aldosterone synthase; do not atrophy </li></ul><ul><li>Inner zone (zona fasciculata and reticularis) – secrete glucocorticoids and adrenal androgens </li></ul><ul><li>- expresses 17 α - hydroxylase and 11 β - hydroxylase; results in atrophy </li></ul>
  6. 8. ACTH <ul><li>a peptide of 39 amino acids </li></ul><ul><li>amino acids 15 – 18: high affinity binding </li></ul><ul><li>amino acids 6 – 10: receptor activation </li></ul><ul><li>synthesized from pro-opiomelanocortin (POMC) </li></ul>
  7. 9. ACTH <ul><li>Stimulates the synthesis and release of adrenocortical hormones </li></ul><ul><li>Human ACTH – G-protein coupled receptor family -> activates adenyl cyclase -> ↑ intracellular cyclic AMP (2 nd messenger for most steroidogenesis) </li></ul>
  8. 10. Regulation of ACTH secretion <ul><li>Hypothalamic – Pituitary – Adrenal axis (HPA axis) </li></ul><ul><li>- 3 levels of regulation: </li></ul><ul><li>1. diurnal rhythm in basal steroidogenesis </li></ul><ul><li>2. negative feedback regulation </li></ul><ul><li>3. marked increases in steroidogenesis in </li></ul><ul><li>response to stress </li></ul>
  9. 11. Control of Endocrine Activity <ul><li>The physiologic effects of hormones depend largely on their concentration in blood and extracellular fluid. </li></ul><ul><li>Almost inevitably, disease results when hormone concentrations are either too high or too low, and precise control over circulating concentrations of hormones is therefore crucial. </li></ul>
  10. 14. <ul><li>All steroid hormones are derived from cholesterol and differ only in the ring structure and side chains attached to it. </li></ul><ul><li>All steroid hormones are lipid soluble </li></ul>Steroid hormones
  11. 15. cholesterol Extracellular lipoprotein Cholesterol pool LH ATP cAMP PKA+ Pregnenolone Progesterone Androstenedione TESTOSTERONE 3  HSD P450c17 17  HSD acetate
  12. 16. Steroid hormone production <ul><li>rate limiting step – conversion of cholesterol to pregnenolone </li></ul><ul><li>sources of cholesterol : circulating cholesterol (LDL), cholesterol esterase, de novo biosynthesis </li></ul><ul><li>Lack of : </li></ul><ul><li>21- β -hydroxylase -> virilization </li></ul><ul><li>11- β - hydroxylase -> hypertension </li></ul><ul><li>17- α -hydroxylase -> hypogonadism </li></ul>
  13. 18. Steroidogenic Enzymes Common name &quot;Old&quot; name Current name Side-chain cleavage enzyme; desmolase P450 SCC CYP11A1 3 beta-hydroxysteroid dehydrogenase 3 beta-HSD 3 beta-HSD 17 alpha-hydroxylase/17,20 lyase P450 C17 CYP17 21-hydroxylase P450 C21 CYP21A2 11 beta-hydroxylase P450 C11 CYP11B1 Aldosterone synthase P450 C11AS CYP11B2 Aromatase P450 aro CYP19
  14. 19. Adrenocorticosteroids <ul><li>Classification : </li></ul><ul><li>A. Mineralocorticoids </li></ul><ul><li>B. Glucocorticoids </li></ul><ul><li>C. Adrenal Androgens </li></ul>
  15. 20. A. Mineralocorticoids <ul><li>Aldosterone – electrolyte-balance regulating, salt-retaining activity </li></ul><ul><li>- promotes reabsorption of Na+ from the distal convoluted tubules and proximal collecting tubules; loosely coupled with K+ and H+ ions excretion </li></ul><ul><li>- secreted at a rate of 100-200ug/d </li></ul><ul><li>- t ½ 15-20mins </li></ul><ul><li>- excreted in the urine as tetrahydroaldosterone and 3-oxo-glucoronide </li></ul>
  16. 21. B. Glucocorticoids <ul><li>Cortisol – carbohydrate metabolism regulating,; intermediary metabolism; immune function </li></ul><ul><li>- 10-20 mg daily; circadian rhythm </li></ul><ul><li>- bound to CBG (90%), albumin (5%) </li></ul><ul><li>- t ½ =60-90 mins.; </li></ul><ul><li>- liver (glucoronic acid or sulfates) </li></ul><ul><li>- 1/3 excreted as 17-hydroxysteroids while 1% is unchanged </li></ul>
  17. 22. CBG (transcortin) <ul><li>Elevated: pregnancy, hyperthyroidism, estrogen administration </li></ul><ul><li>Diminished: hypothyroidism, protein deficiency, genetic defects </li></ul>
  18. 23. C. Adrenal Androgens <ul><li>- Dehydroepiandrosterone (DHEAs) and </li></ul><ul><li>androstenedione – androgenic-estrogenic activity </li></ul><ul><li>- they do not stimulate or support major androgen dependent pubertal changes in humans) </li></ul><ul><li>- used in SLE and women with adrenal insufficiency </li></ul>
  19. 24. <ul><li>Dynamics: </li></ul><ul><li>MOA - bind to cytosol receptors (steroid receptor complex) </li></ul><ul><li>- alters gene expression by binding to glucocorticoid-response element (GREs) </li></ul>
  20. 25. Physiologic effects <ul><li>Carbohydrate metabolism : </li></ul><ul><li>- protect glucose-dependent tissues from starvation </li></ul><ul><li>- stimulate gluconeogenesis, glycogen synthesis in the fasting state -> ↑ glucose -> lipolysis ↑ FFA -> insulin release -> periphery: ↓glucose utilization and lipogenesis ( fat deposition) </li></ul><ul><li>Protein metabolism: </li></ul><ul><li>- ↑ protein breakdown (amino acids) </li></ul><ul><li>- catabolic effects : decrease muscle mass, atrophy of lymphoid tissue, negative nitrogen balance, thinning of the skin </li></ul>
  21. 26. Physiologic effects (cont.): <ul><li>Lipid metabolism: </li></ul><ul><li>- redistribution of body fat (buffalo hump, moon facies, supraclavicular area with loss of fat in the extremities) </li></ul><ul><li>- induce lipolysis in adipocytes ( FFA) </li></ul><ul><li>- lipogenesis </li></ul><ul><li>Electrolyte and water balance : </li></ul><ul><li>- enhances the reabsorption of Na (aldosterone) and renal excretion of free water and interferes with Ca uptake, while there is ↑ Ca excretion by the kidneys (glucocorticoids) </li></ul>
  22. 27. Physiologic effects (cont.) <ul><li>Cardiovascular system : </li></ul><ul><li>- mineralocorticoid-induced changes – hpn </li></ul><ul><li>- enhance vascular reactivity to other vasoactive substances </li></ul><ul><li>Skeletal muscle: </li></ul><ul><li>- normal function (steroid myopathy) </li></ul><ul><li>CNS: </li></ul><ul><li>- neurosteroids (regulate neuronal excitability) </li></ul>
  23. 28. Physiologic effects (cont.): <ul><li>Formed elements of blood: </li></ul><ul><li>- minor effects on hgb and erythrocyte production </li></ul><ul><li>- affect circulating WBC </li></ul><ul><li>(Addison’s: lymphocytosis, ↑ mass of lymphoid tissue) </li></ul><ul><li>Anti-inflammatory and Immunosuppressive action </li></ul><ul><li>- alter immune response of lymphocytes , monocytes </li></ul><ul><li>and basophils </li></ul><ul><li>- ↓ release of vasoactive and chemoattractive </li></ul><ul><li>factors </li></ul><ul><li>- ↓ extravasation of leukocytes to injury </li></ul><ul><li>- ↓ secretion of lipolytic and proteolytic enzymes </li></ul><ul><li>- effect on cytokine production </li></ul><ul><li>- ↓fibrosis </li></ul>
  24. 29. <ul><li>Other effects: </li></ul><ul><li>↑ amounts : </li></ul><ul><li>- insomnia, euphoria, depression, </li></ul><ul><li>pseudomotor cerebri, “roid rage” </li></ul><ul><li>- peptic ulcer, promote fat redistribution </li></ul><ul><li>- vit D antagonist on Ca absorption (bone </li></ul><ul><li>resorption) </li></ul><ul><li>- ↑ # of platelets and RBCs </li></ul><ul><li>↓ amounts: </li></ul><ul><li>- psychiatric depression </li></ul><ul><li>absence: </li></ul><ul><li>- impaired renal function and fetal lung effects </li></ul>
  25. 30. Synthetic Steroids <ul><li>source – cholic acid (cattle) or steroid sapogenins (diosgenin, hecopenin); </li></ul><ul><li>absorption: oral, IV, IM, sites of local administration </li></ul><ul><li>- prolonged effects with occlusive dressing </li></ul><ul><li>- large areas – may cause suppression of HPA axis </li></ul>
  26. 31. Classification of Glucocorticoids <ul><li>I. Short to medium-acting glucocorticoids: </li></ul><ul><li>a. Hydrocortisone (cortisol) </li></ul><ul><li>b. Cortisone </li></ul><ul><li>c. Prednisone </li></ul><ul><li>d. Prednisolone </li></ul><ul><li>e. Methylprednisolone </li></ul><ul><li>f. Meprednisone </li></ul>
  27. 32. II. Intermediate-acting glucocorticoids <ul><li>a. Triamcinolone </li></ul><ul><li>b. Paramethasone </li></ul><ul><li>c. Fluprednisolone </li></ul><ul><li>III. Long-acting glucocorticoids </li></ul><ul><li>a. Betamethasone </li></ul><ul><li>b. Dexamathasone </li></ul>
  28. 33. <ul><li>Deoxycortisone (DOC) – serves as precursor of aldosterone </li></ul><ul><li>2. Fludrocortisone – most widely used; </li></ul><ul><li>both mineralocorticoid and glucocorticoid activity; potent salt-retaining activity </li></ul><ul><li>- treatment of adrenocortical insufficiency </li></ul>IV. Mineralocorticoids
  29. 34. Uses: <ul><li>A. Diagnosis and treatment of disorders of adrenal function </li></ul><ul><li>B. Treatment of inflammatory and immunologic disorders </li></ul>
  30. 35. Therapeutic Uses : <ul><li>A. Replacement Therapy </li></ul><ul><li>1. Adrenal Insufficiency </li></ul><ul><li>a. Acute adrenal insufficiency (acute adrenal crisis) </li></ul><ul><li>ssx: GIT symptoms, dhn, hypoNa, hyperK, weakness, lethargy, hypotension </li></ul><ul><li>cause: </li></ul><ul><li>- destructive lesions secondary to surgery; TB of the adrenals; </li></ul><ul><li>bilateral adrenal hgge </li></ul><ul><li>- abrupt withdrawal of glucocorticoids at high doses or prolonged use </li></ul><ul><li>mgt : IV : D5 0.3%NaCl solution </li></ul><ul><li>Monitor for fluid overload </li></ul><ul><li>Hydrocortisone (cortisol) 100mg bolus, ffed by 100mg every 8 hrs. ; once stable, may give 25mg IM hydrocortisone every 6-8hrs.; thereafter, same mgt with chronic adrenal insufficiency </li></ul>
  31. 36. 1. Adrenal Insufficiency (cont.) <ul><li>b. Chronic Adrenal Insufficiency (Addison’s disease) </li></ul><ul><li>ssx: hyperpigmentation, wt. loss, inability to </li></ul><ul><li>maintain fasting blood sugar, weakness, fatigue, </li></ul><ul><li>hypotension </li></ul><ul><li>cause: APECED (autoimmune polyendocrinopathy-candidiasis ectodermal dystrophy) </li></ul><ul><li>mgt: Hydrocortisone 20-30mg/day BID + </li></ul><ul><li>Fludrocortisone acetate 0.05 – 0.2mg/day </li></ul><ul><li>( valuable indicator of adequate replacement : </li></ul><ul><li>disappearance of hyperpigmentation and resolution of </li></ul><ul><li>electrolyte abnormalities) </li></ul><ul><li>-monitor plasma ACTH levels or measure urinary free </li></ul><ul><li>cortisol; dosage adjustments for stress </li></ul>
  32. 37. <ul><li>          Addison described :           . general languor and debility           . remarkable feebleness of the heart's action           . irritability of the stomach           . peculiar change of the color of the skin  </li></ul>
  33. 39. Therapeutic Uses (cont.) 2. Adrenocortical hypofunctioning and hyperfunctioning <ul><li>a. Congenital Adrenal Hyperplasia </li></ul><ul><li>ssx: - after puberty with infertility, hirsutism, amenorrhea and </li></ul><ul><li>acne; female pseudohermaphroditism; accelerated </li></ul><ul><li>linear growth but height at maturity is reduced; </li></ul><ul><li>- salt wasters – CV collapse (volume depletion) </li></ul><ul><li>cause: Genetic disorder; activity of enzymes required for </li></ul><ul><li>the biosynthesis of corticosteroid is deficient (21 β hydroxylase) </li></ul><ul><li>mgt: 1 st seen as acute adrenal crisis </li></ul><ul><li>oral hydrocortisone 0.6mg/kg/day BID or TID </li></ul><ul><li>fludrocortisone acetate 0.05-0.2mg/day </li></ul><ul><li>treatment in-utero: mothers at risk – glucocorticoid </li></ul><ul><li>therapy is initiated before 10 weeks gestation ffed by </li></ul><ul><li>genotyping and sex determination </li></ul>
  34. 40. Therapeutic Uses 2. Adrenocortical hypofunctioning and hyperfunctioning (cont.) <ul><li>b. Cushing’s syndrome </li></ul><ul><li>cause: pituitary adenoma, tumors of the adrenal gland </li></ul><ul><li>ssx: round, phletoric face, truncal obesity, </li></ul><ul><li>muscle wasting, thinning, purple striae and </li></ul><ul><li>easy bruising of the skin, poor wound healing, </li></ul><ul><li>osteoporosis </li></ul><ul><li>mgt: surgery </li></ul><ul><li>hydrocortisone 300 mg IV on the day of the </li></ul><ul><li>surgery, then maintenance oral dose </li></ul>
  35. 41. B. Stimulation of fetal lung maturation – betamethasone 12mg ffed by 12mg 18-24 hrs. later <ul><li>C. Non-Adrenal Diseases </li></ul><ul><li>1. Rheumatic disorders – suppress the disease </li></ul><ul><li>and minimize resultant tissue damage </li></ul><ul><li>mgt: oral prednisone 10 mg/kg/day (taper </li></ul><ul><li>thereafter by decreasing 1mg/kg/day every </li></ul><ul><li>2-3 wks) </li></ul><ul><li>- intraarticular injection: triamcinolone acetonide: </li></ul><ul><li>minimize complications (3-4x/year) </li></ul>
  36. 42. C. Non-Adrenal Diseases (cont.) <ul><li>2. Renal Disorders – nephrotic syndrome </li></ul><ul><li>mgt: prednisone: 1-2 mg/kg x 6 wks, ffed. by gradual tapering over 6-8 wks or alternate-day therapy (diminished proteinuria in 85% pts in 2-3 wks and 95% pts will have remission in 3 mos. </li></ul><ul><li>- membranous glomerulonephritis </li></ul><ul><li>mgt: alternate-day prednisone 8-10 wks ffed by 1-2 month period of tapering </li></ul>
  37. 43. C. Non- Adrenal Diseases (cont.) <ul><li>3. Allergic Disease: onset of action of glucocorticoid is delayed (6-12hrs.) </li></ul><ul><li>anaphylaxis: epinephrine 0.5ml of a 1:1000 solution IM or SQ, repeated every 15 mins up to 3 doses is needed (anaphylaxis) </li></ul>
  38. 44. C. Non-Adrenal Diseases (cont.) <ul><li>4. Bronchial Asthma – role of inflammation in the immunopathogenesis </li></ul><ul><li>- onset of action is delayed for 6 – 12 hrs. </li></ul><ul><li>mgt: IV methylprednisolone 60-120mg initially ffed. by oral prednisone 40-60mg daily as the attack resolves </li></ul><ul><li>inhaled steroids – reduces bronchial hyperreactivity with less suppression of adrenal function (SE: dysphonia or oropharyngeal candidiasis) </li></ul><ul><li>ex: beclomethasone dipropionate, budesonide phosphate, flunisolide, fluticasone, momethasone furoate, triamcinolone acetonide </li></ul>
  39. 45. C. Non-Adrenal Diseases (cont.) <ul><li>5. Infectious Disease – P. carinii pneumonia – increases oxygenation and decreases the incidence of respiratory failure and mortality </li></ul><ul><li>H. influenzae type b meningitis – decrease the long-term neurological impairment </li></ul><ul><li>6. Ocular disease – 0.1% dexamethasone </li></ul><ul><li>- C/I: herpes simplex keratitis (clouding of the cornea) , glaucoma </li></ul>
  40. 46. C. Non-Adrenal Diseases (cont.) <ul><li>7. Skin diseases – inflammatory dermatoses </li></ul><ul><li>8. GIT diseases – inflammatory bowel disease </li></ul><ul><li>9. Hepatic diseases – prednisolone – 80% </li></ul><ul><li>histologic remission in pts. with chronic, active </li></ul><ul><li>hepatitis </li></ul><ul><li>10. Malignancies – ALL, lymphomas </li></ul>
  41. 47. C. Non-Adrenal Diseases (cont.) <ul><li>11. Cerebral edema – neoplasms and parasitic infections but not in CVA or trauma </li></ul><ul><li>12. Miscellaneous dis – Sarcoidosis (induce remission), thrombocytopenia (decrease bleeding tendency), </li></ul><ul><li>organ transplantation (reduce Ag expression from grafted tissues, delayed revascularization, interferes with cytotoxic T-lymphocytes and generation of primary Ab formation), spinal cord injury (within 1st 8 hrs: inhibition of free-radical mediated cellular injury ffng ischemia and reperfusion) </li></ul>
  42. 48. D. Diagnostic Application – dexamethasone: suppress production of ACTH <ul><li>Dexamethasone suppression test – differentiates Cushing’s syndrome vs. stress and if Cushing’s syndrome, whether it’s an adrenal or a pituitary tumor </li></ul><ul><li>Baseline cortisol levels are determined </li></ul><ul><li>-urine: 17-hydroxycorticosteroids – LIDDLE’S test </li></ul><ul><li>Dexamethasone 0.5mg every 6hrs x 48 hrs. – measure urinary steroids ( if ↑, (+) Cushing’s) </li></ul><ul><li>Dexamethasone 2 mg every 6 hrs. x 48 hrs.- measure urinary steroids (if ↑, due to an adrenal tumor; if ↓, due to a pituitary tumor) </li></ul>
  43. 50. Toxicity: <ul><li>Withdrawal of therapy : </li></ul><ul><li>ssx: fever, myalgias, arthralgias, malaise, pseudomotor cerebri ( ↑ICP, papilledema) </li></ul><ul><li>Continued use at supraphysiologic doses </li></ul><ul><li>ssx: fluid and electrolyte abnormalities, hypertension, hyperglycemia, increased susceptibility to infection, myopathy, behavioral disturbances, cataracts, growth arrest and fat redistribution, acne, hirsutism, striae, ecchymoses, osteonecrosis, peptic ulcer </li></ul><ul><li>Adrenal suppression - >2 wks . </li></ul><ul><li>Contraindications: peptic ulcer, heart disease or Hpn with CHF, infections, psychoses, diabetes, osteoporosis, glaucoma or herpes simplex infection </li></ul>
  44. 51. Supplemental measures: <ul><li>Diet rich in potassium and low in sodium </li></ul><ul><li>Caloric mgt to prevent obesity </li></ul><ul><li>High protein intake </li></ul><ul><li>Appropriate antacid therapy </li></ul><ul><li>Calcium and vit D, physical therapy </li></ul><ul><li>Alendronate biphosphonate </li></ul>
  45. 52. Antagonists of Adrenocortical Agents <ul><li>Synthetic inhibitors and glucocorticoid antagonists </li></ul><ul><li>1. Metyrapone – inhibits 11-hydroxylation, interfering with cortisol and corticosterone synthesis (0.25g BID to 1g QID) </li></ul><ul><li>- used in tests of adrenal function (300-500mg q 4hrs. X 6doses, ffed by urine collection) -> there’s a 2-fold ↑ in urinary steroids </li></ul><ul><li>- treat hypercorticotism: 4 g/day </li></ul>
  46. 53. Synthetic inhibitors and glucocorticoid antagonists (cont.) <ul><li>2. Aminoglutethimide – blocks the conversion of cholesterol to pregnanenolone and causes a reduction in the synthesis of all hormonally active steroids </li></ul><ul><li>- breast Ca and Cushing’s syndrome due to adrenocortical Ca: 250 mg every 6hrs. </li></ul><ul><li>- enhances metabolism of dexamethasone </li></ul>
  47. 54. <ul><li>3. Ketoconazole – an antifungal imidazole derivative; potent, non-selective inhibitor of adrenal and gonadal steroid synthesis; hepatotoxic </li></ul><ul><li>- inhibits cholesterol side chain cleavage </li></ul><ul><li>- tx of Cushing’s syndrome –inoperable </li></ul><ul><li>(200-1000mg/d ) </li></ul><ul><li>4 . Mifepristone (RU 486) – </li></ul><ul><li>11 β -aminophenyl-substituted 19-norsteroid; </li></ul><ul><li>has strong anti-progestin activity; blocks </li></ul><ul><li>glucocorticoid receptor </li></ul>Synthetic inhibitors and glucocorticoid antagonists (cont.)
  48. 55. <ul><li>5. Mitotane – adrenal Ca; 12 g/daily results in reduction in tumor mass; caution: adverse effects (80%: LBM, nausea, vomiting, somnolence, skin rashes) </li></ul><ul><li>6. Trilostane - 3 β -17 hydroxysteroid dehydrogenase inhibitor that interferes with the synthesis of adrenal and gonadal hormones; 30 mg 4x a day </li></ul><ul><li>- comparable to aminogluthemide </li></ul>Synthetic inhibitors and glucocorticoid antagonists (cont.)
  49. 57. <ul><li>Mineralocorticoid Antagonists </li></ul><ul><li>1. Spirinolactone – diagnosis of aldosteronism (400-500mg/day for 5-8 weeks) </li></ul><ul><li>- preparing for surgery (300-40mg/day x 2 wks to reduce the incidence of arrhythmias) </li></ul><ul><li>- hirsutism in women (androgen antagonist at </li></ul><ul><li>50-200mg/d x 2-6 mos) </li></ul><ul><li>- diuretic </li></ul><ul><li>- treatment of primary hyperaldosteronism (Conn’s syndrome) </li></ul><ul><li>2. Eplerenone – in clinical trials </li></ul><ul><li>3. Drospirenone – progestin in a new oral contraceptive, antagonizes the effect of aldosterone </li></ul>
  50. 58. <ul><li>Hyperldosteronism </li></ul><ul><li>1. primary hyperaldosteronism – due to an adrenal adenoma (ssx: hypoK, alkalosis, hyperNa -> HPN, weakness and tetany </li></ul><ul><li>2. secondary hyperaldosteronism – due to low plasma renin, angiotensin II </li></ul>
  51. 59. Classification of topical corticosteroids based on their potencies <ul><li>Very potent </li></ul><ul><li>Clobetasol propionate 0.05% </li></ul><ul><li>Betamethasone dipropionate 0.05% </li></ul><ul><li>Diflucortolone valerate 0.3% </li></ul><ul><li>Halcinonide 0.1% </li></ul>
  52. 60. Classification of topical corticosteroids based on their potencies (continued) <ul><li>Potent </li></ul><ul><li>Beclomethasone dipropionate 0.025% and 0.05% </li></ul><ul><li>Betamethasone valerate 0.1% </li></ul><ul><li>Budesonide 0.025% </li></ul><ul><li>Desoxymethasone 0.25% </li></ul><ul><li>Difluocinolone 0.025% and 0.05% </li></ul><ul><li>Fluticasone propionate 0.05% </li></ul><ul><li>Hydrocortisone 17- butyrate 0.1% </li></ul><ul><li>Momethasone furoate 0.1% </li></ul><ul><li>Triamcinolone aceonide 0.1% </li></ul>
  53. 61. Classification of topical corticosteroids based on their potencies (continued) <ul><li>Moderately potent </li></ul><ul><li>Betamethasone valerate 0.025% and 0.05% </li></ul><ul><li>Clobethasone butyrate 0.05% </li></ul><ul><li>Fluocinolone acetonide 0.01% </li></ul><ul><li>Fludroxycortide 0.0125%-0.05% </li></ul><ul><li>Hydrocortisone 1% with urea </li></ul><ul><li>Triamcinolone acetonide 0.02% and 0.05% </li></ul>
  54. 62. Classification of topical corticosteroids based on their potencies (continued) <ul><li>Mildly potent </li></ul><ul><li>Aclomethasone dipropionate 0.05% </li></ul><ul><li>Desonide 0.05% </li></ul><ul><li>Fluocinolone base or acetate 0.1% - 2.5% </li></ul><ul><li>Methylprednisolone 0.25% </li></ul>
  55. 63. Common side effects of topical corticosteroids <ul><li>Skin atrophy </li></ul><ul><li>Striae (groin and axillae) </li></ul><ul><li>Slowed healing </li></ul><ul><li>Telangiectasia </li></ul><ul><li>Purpura </li></ul><ul><li>Rosacea </li></ul><ul><li>Acne </li></ul><ul><li>Perioral dermatitis </li></ul><ul><li>Hypertrichosis </li></ul>
  56. 64. Summary of adrenocortical agonists and antagonists…… <ul><li>Review briefly the adrenal gland </li></ul><ul><li>Name the different adrenocorticotropic hormones and discuss their effects </li></ul><ul><li>Identify uses of adrenocorticotropic hormones </li></ul>
  57. 65. <ul><li>Thank You </li></ul>