In hypocorticism : decrease work capacity & weakness are due to hypodynamic circulation.
In hypercorticism : weakness is due to hypokalemia (excess of mineralocorticoid), & muscle wasting and myopathy (excess of glucocorticoids).
Catabolic and antianabolic effects :
Stimulate protein and RNA synthesis in liver, but have catabolic and antianabolic effect on lymphoid tissue, connective tissue, muscle, fat and skin dec. muscle mass, thinning of skin and osteoporosis. In children- retardation of growth .
Nonspecific suppression of all components, stages and cardinal signs of inflammation .
Produce vasoconstriction, reduce capillary permeability, local exudation, cellular infiltration, phagocytic activity& late responses like capillary proliferation, collagen deposition, fibroblastic activity, & scar formation- action is direct and local .
Action on inflammatory cells.
Decrease migration & reduced activity of neutrophils & macrophages .
(thinning of the skin, striae, telangiectases ,superficial fissures and purpura)
Allergic contact dermatitis (uncommon)
Masking or aggravation of dermatophytoses, impetigo or scabies
Adverse skin reactions to topical glucocorticoids
Drug interactions of glucocorticoids Glucocorticoid dosage is decreased: Antibiotics (erythromycin, trioleandomycin), cyclosporin, isoniazid and ketoconazole reduce the metabolic clearance of glucocorticoids. Estrogens increase the levels of corticosteroid binding protein and thus reduce the free fraction; they also reduce the clearance. Cholestyramine decreases the intestinal absorption. Antiepileptic drugs(barbiturates, phenytoin, carbamazemine), rifampicin,, aminoglutethimide increase the metabolism by inducing hepatic microsomal enzymes. Antianxiety and antipsychotic drugs: Recurrent or poor control of CNS symptoms due to inherent glucocorticoid effects. Glucocorticoid dosage is increased: Glucocorticoid dosage needs adjustment: Anticholinesterases: May precipitate myasthenic crisis Anticoagulants: Effectiveness of anticoagulants decreases Antihypertensives: Their effectiveness decreases Oral hypoglycemics: Their effectiveness decreases Sympathomimetics: Their effectiveness increases Salicylates: Their clearance is increased
Principles of treatment of acute adrenal insufficiency
Precautions during glucocorticoid therapy Before starting therapy Enquire about and check for: peptic ulcer, diabetes mellitus, tuberculosis, any other infection (especially one not amenable to chemotherapy). During therapy Prescribe the drug with food Diet low in calories and sodium, and high in potassium
Check periodically for: weight gain, edema, hyperglycemia, hypertension, infection, GI bleeding, hypokalemia, ocular changes
Monitor growth in children
Instruct the patient not to stop the drug abruptly (severe infection, major surgery)
Prescribe oral calcium and vitamin D supplements; alendronate; antacids; H 2 receptor blockers