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Adrenocortical hormones The adrenal cortex synthesizes three kinds of steroids: 1.glucocorticoids(GCS),in human ,hydrocortisone(cortisol) is the main glucocorticoid , it was produced and released from the cells of zona fasciculata of adrenal cortex. 2.mineralocorticoids , aldosterone is the main mineralocorticoid, it was produced and released from the cells of zona glomerulosa of adrenal cortex.. 3.sex hormones, include androgen and estrogen , produced and released from the cells of zona reticularis of adrenal cortex. Glucocorticoids(GCS) physiological effects 1. Effects on carbohydrate: They can increase the blood glucose level by the following ways : ①stimulate glyconeogenesis from amino acid, lactic acid and glycerol. ②stimulate glycogen deposition in liver , ③in periphery tissues, it can decrease the oxidation and utilization of glucose by inhibiting the transport and uptake of glucose by muscle cells. 2. Effects on protein metabolism: ① Stimulate protein and RNA synthesis in the liver. ② Have catabolic effects in lymphoid and connective tissue, muscle, fat, and skin. ③ Supraphysiologic amounts: lead to decreased muscle mass and weakness. 3. Effects on fat metabolism: ① promote the lipolysis in adipocytes with increased release of fatty acids and glycerol into the circulation. ② it can cause dramatic redistribution of body fat. 4. Effects on electrolyte and water balance : Pharmacological effects 1. anti-inflammatory effects: three characters ①Glucocorticoids have strong anti-inflammatory action, ②This effect was nonspecific, they are effective to all kinds of inflammation such as those caused by radiant, mechanical , chemical, biological, infections and immunological stimuli. ③They are effective to both the early phase and later phase of inflammation: Mechanism of anti-inflammatory action 1) Regulating the production of cytokine, and reducing the cell response of inflammation. GCS can inhibit the production of some pro-inflammatory cytokine such as IL-1, IL-3, IL-8, TNF-α(tumor necrosis factorα)and GM-CSF(granulocyte-macrophage colony stimulating factor),they can also induce the production of some anti-inflammatory cytokine such as IL-10. 2) Inhibiting the metabolism of AA and inhibiting the production of PGs and LTs Membrane phospholipids GCS induce lipocortin-1 (-) PLA2 Arachidonic acid(AA) COX NSAIDs LOX 1 Prostaglandins(PGs) Leukotrienes(LTs) 3)↓ activity of NOS(nitric oxide synthase)→ ↓ NO 4) inducing ACE(angiotensin converting enzyme)→↑the degradation of bradykinin 2. immunosuppressive effects: 1) Inhibiting phagocytosis and management of macrophages on antigen 2) promoting the redistribution of lymphocyte in human blood→↓lymphocytes in circulation 3) small dose : inhibit the cellular immunity large dose: inhibit the humoral immunity 3. anti-shock effects: Supralarge dose of GCS can be used to treat any kind of shock, especially infectious-toxic shock. 1) relaxing the smooth muscle of spasmodic vessels and enhancing the contractility of myocardium 2) reducing the sensitivity of some vasoconstrictive substances on vessel 3) stabilizing the lysosomal membrane and decreasing the production and release of myocardial-depressant factor(MDF) 4)enhancing tolerance of body to bacterial endotoxins 4. effects on blood and hemopoietic system: 1) stimulate hemopoiesis →↑RBC, PLT, and Hb(hemoglobin) in circulation. 2)↓ lymphocytes, monocytes , eosinophils and basophils in blood 3) Increase the number of neutrophils but inhibiting their function 2. other effects: Central nervous system: stimulate the CNS and may cause euphoria, excitement and insomnia. Digestive system: stimulate the secretion of pepsin and gastric acid, and may induce peptic ulcer. Clinical uses replacement therapy in small dose acute or chronic hypofunction of adrenal cortex (such as addison’s disease), post adrenalectomy, hypofunction of anterior pituitary . Severe infection and inflammation severe acute bacterial infections : Fulminant epidemic meningitis, toxic pneumonia, toxic dysentery, scarlet fever and so on. Under such circumstance, large-dose, short-term treatment of GCS may help patients go through dangerous stage attention: must be combined with large-dose of effective antibilateral agents prevention of some inflammatory sequela: iritis, keratitis, retinitis, tuberculosis, meningitis, testitis. GCS must be used during the early stage of inflammation Allergic and autoimmune diseases allergic diseases: hay fever, serum sickness, urticaria, contact dermatitis, drug reactions ,bronchial asthma, angioneurotic-edema. Autoimmune diseases: such as rheumatic arthritis, rheumatic fever, systemic lupus erythematosus , autoimmune hemolytic anemia, rejection in organ transplatation, Shock infectious-toxic shock(first choice), anaphylactic shock, cardiogenic shock , hypovolemic shock and so on.. Blood disorders 2 Acute lymphatic leukemia, aplastic anemia, thrombocytopenia, granulocytopenia. topical uses some skin diseases and some eye diseases GCS are remarkably effacious in the treatment of a wide variety of skin disorders such as contact dermatitis, eczema. Adverse reactions continued use of supraphysiological doses of GCS Iatrogenic Cushing’s syndrome: mainly caused by metabolism disorder of lipid, protein, glucose and water-electrolyte. The symptoms include sodium retention, hypokalemia, hypertension, moon face, bump back, diabetes, muscle wasting . Induction and aggravation of infection Possible risk of peptic ulcers Cardiovascular complications Long-term use of GCS may cause hypertension and arteriolosclerosis Osteoporosis GCS decrease bone density by multiple mechanisms, including inhibition of gonadal steroid hormones, diminished gastrointestinal absorption of calcium and inhibition of bone formation Other complications Acute psychosis, hypomania , growth retardation and so on . Withdrawl reactions Iatrogenic adrenocortical insufficiency : adrenocortical atrophy and adrenal crisis acute adrenal insufficiency results from too rapid withdrawl of GCS after prolonged therapy, when the HPA axis has been suppressed. + + CRH ACTH GCS _ _ 3