Corticosteroids. Hawler Medical University College of Medicine Department of Pharmacology and Biophysics Dr.Susan Abdulkadir Farhadi MSc Pharmacology
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1 Corticosteroids Hawler Medical University College of Medicine Department of Pharmacology and Biophysics Dr.Susan Abdulkadir Farhadi MSc Pharmacology
2 Objectives By the end of this lecture you should be able to l Know the source & regulation of corticosteroids l Describe the effects of steroids on different body systems l List the therapeutic uses, PK and side effects of corticosteroids
3 l Adrenal gl. consists of cortex & medulla l Medulla secretes epinephrine l Cortex secretes 1. Adrenocorticosteroids (glucocorticoids & mineralocorticoids) 2. Adrenal androgenes
4 cortex Zona glomerulosa Zona fasciculata Zona reticularis Mineralocorticoids (e.g.) aldosterone Glucocorticoids (e.g.) cortisol Adrenal androgens (e.g.) dihydroepiandrosterone
5
6 Actions 1-Mineralocorticoids l Major endogenous mineralocorticoids is aldosterone. l Acts in distal convoluted tubule(dct) leading to Na + reabsorption, K + & H + excretion. l Excess can lead to sodium and water retention(ht & edema), hypokalemia and alkalosis.
7 2-Glucocorticoids l Cortisol is the principal human glucocorticoid l Normally has a diurnal production (a peak early in the morning, followed by a decline then a second smaller peak in the afternoon). l Factors like stress & levels of circulating steroids affect its secretion.
8 l Bind to specific intracellular cytoplasmic receptors in target tissue. l Receptor hormone complex translocates into nucleus. l Act as a transcription factor turning genes on and off. l Effects need time (except for lipolysis and bronchial muscle relaxation).
9 Effects of glucocorticoids I-Effects on metabolism Glucocorticoids are catabolic in nature and thus cause breakdown of carbohydrates (hyperglycemia),proteins (muscle wasting) and fat. 1.Promote gluconeogenesis through a) Increase a.a. uptake by liver and kidney b) Increase activity of gluconeogenic enzymes 2.Stimulate protein catabolism and lipolysis (more building blocks & energy for gs synthesis)
10 v Glucocorticoid insufficiency can lead to hypoglycemia (in fasting or stress). v Lipolysis results from glucocorticoids increasing the activity of hormone- sensitive lipase.
11 II-Increase resistance to stress 1. Increased plasma gs levels provides the body with needed energy(combat trauma, fright, bleeding etc.) 2. Enhance adrenergic stimulation on small blood vessels leading to vasoconstriction (increased blood pressure).
12 III-Effect on haematopoietic system l ê eosinophils,basophils, monocytes & lymphocytes. l é Hb, erythrocytes, platelets & polymorphonuclear leukocytes.
13 IV-Effect on inflammatory response l Glucocorticoids are powerful anti-inflammatory agents. l They inhibit chemotaxis (recruitment of cells at the site of inflammation. l Reduce inflammatory response and suppress immunity.
14 l Reduced peripheral lymphocytes and macrophages might be one factor l Inhibition of phospholipase A2 blocks the release of arachidonic acid (precursor of PG & LT). l Decreased mast cell degranulation è decreased histamine and capillary permeability
15 V-effects on other systems v Adequate level for normal glomerular filtration. Effects on other systems are more related to adverse effects 1. High dose leads to high gastric acid & pepsin resulting in ulcer formation 2. Bone loss on chronic use 3. Myopathy and weakness
16 Therapeutic uses 1-Replacement use A. Replacement for 1 adrenal insufficiency(addison s disease) B. Replacement for 2 &3 adrenocortical insufficiency
17 2-Diagnostic use l Dexamethasone suppression test used for A. Test the intactness of the HPA axis. B. Diagnosis of Cushing s syndrome.
18
19
20 3- Antenatal use l Betamethasone can be given to accelerate the fetal lung maturation, if delivery is anticipated before 32 weeks of gestation.
21 4-Non Adrenal uses A. Anti-inflammatory in RA,OA and gout when NSAIDs fail to provide analgesia. B. Anti-allergic in management of anaphylaxis, urticaria & angiodema. Used as inhalation in chronic asthma and IV in status asthmaticus. Also used in allergic skin conditions.
22 C. Immunosuppressive in organ transplantation to prevent graft rejection. D. Anti-cancer in ALL and lymphomas. Given with anti-neoplastic agents to decrease nausea and vomiting
23 E. Selective glucocorticoids (without Na + or water retaining activity) like betamethasone and dexamethasone are used to reduce cerebral oedema in primary or metastatic brain tumours or TB.
24 Pharmacokinetics l Synthetic glucocorticoids are used therapeutically. l Preparations given orally are well absorbed. l Selected compounds can be give I.V., I.M., intra-articular, topical or as an aerosol for inhalation.
25 l Topical administration decreases the likelihood of systemic toxicity. l More than 90% of the absorbed are bound to plasma proteins(corticosteroid binding globulin & albumin).
26 l Metabolized in the liver by liver microsomal oxidizing enzymes l Excreted by the kidney l Prednisone the only safe glucocorticoid during pregnancy ( prodrug not converted to active prednisolone in fetal liver).
27 Classification
28 Contraindications Contraindications to the use of corticosteroids for anti- inflammatory purposes: 1. Diabetes mellitus. 2. Peptic ulcer. 3. Tuberculosis. 4. Hypertension or heart failure. 5.Presence of infection.
29 Side effects l Large doses or prolonged administration rather than replacement therapy. l Oral thrush (candidiasis) frequently occurs when glucocorticoids are taken by inhalation. l Hyperglycemia can lead to D.M.
30
31 Withdrawal l Sudden withdrawal can be a serious problem because if the patient has HPA suppression (when used for more than 2 weeks), abrupt cessation of corticosteroids can be fatal (acute adrenal insufficiency syndrome). l The drug should be given on alternate days to avoid HPA suppression or should be tapered off gradually.
32 Inhibitors of glucocorticoid biosynthesis & antagonists 1-Metyrapone l Interferes with corticosteroid synthesis. It blocks the final step (11- hydroxylation) by inhibiting β-hydroxylase enzyme. l Used for treatment of pregnant women with Cushing's syndrome. l S.E. include salt and water retention, hirsutism and GI disturbances.
33 2-Aminoglutethimide l Inhibit conversion of cholesterol to pregnenolone (synthesis of all hormonally active steroids is reduced). l Used in treatment of breast cancer. l For treatment of malignant adrenocortical tumors (reduce steroid secretion).
34 3-Ketokonazole l Antifungal agent l Inhibits all gonadal and adrenal steroid hormone synthesis. l For treatment of Cushing's syndrome.
35 4- Mifepristone l At high doses a potent glucocorticoid(competitive receptor) antagonist as well as an antiprogestin. l Used for treatment of inoperable cases of ectopic ACTH syndrome (Small-cell carcinoma).
36 Summary l Glucocorticoids are secreted by the adrenal cortex along with aldosterone and androgens. l Increase response to stress and increases blood glucose levels. l Decreases immunity and inflammatory response. l Cushion's syndrome can be the result of endogenous increase of glucocorticoid levels or can be iatrogenic. l Inhibitors of synthesis or receptor blockers are used to treat high levels of glucocorticoids.
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