Glucocorticoids and mineralocorticoids are endogenous hormones normally produced by the adrenal glands. In clients with impaired adrenal function, these hormones can be administered as replacement therapy.
Synthetic glucocorticoids, also commonly known as corticosteroids, are medications that can be used in clients with decreased adrenal function, such as in adrenal insufficiency; this is also known as Addison disease, and specifically occurs when the adrenal glands don't make enough endogenous glucocorticoids, so these clients need hormone replacement therapy with synthetic glucocorticoids. In addition, glucocorticoids are used in the treatment of numerous inflammatory conditions, such as asthma, rheumatoid arthritis, and inflammatory bowel disease, as well as preventing organ rejection in transplant recipients.
Alright, now, based on the duration of action, synthetic glucocorticoids can be classified into three groups. The first group are short-acting glucocorticoids, such as cortisone and hydrocortisone. Cortisone needs to be converted into hydrocortisone in the liver in order to be active, so it can only be taken orally; while hydrocortisone can be given orally, intravenously, intramuscularly, and topically. The second group are intermediate-acting glucocorticoids, which include prednisone, prednisolone, and methylprednisolone. Prednisone can only be taken orally; while prednisolone can be administered orally, intravenously, or topically; and methylprednisolone can be given orally, intravenously, intramuscularly, or injected intra-articularly. The third and final group are long-acting glucocorticoids, which include betamethasone and dexamethasone. Both of these medications can be taken orally, intravenously, intramuscularly, or intra-articularly. In addition, betamethasone is also available for topical use.
Once administered, glucocorticoids act by binding to intracellular glucocorticoid receptors and then migrating into the nucleus to modify the expression of many different genes, including those involved in regulating inflammatory processes. Among their anti-inflammatory actions, glucocorticoids inhibit the release of pro-inflammatory molecules, such as prostaglandins and leukotrienes; prevent the activation and migration of immune cells; and increase the production and release of anti-inflammatory molecules.
Now, side effects of glucocorticoids are more common in clients receiving high doses for a prolonged period of time. Most side effects are related to excess glucocorticoid activity, which can result in iatrogenic Cushing syndrome. Common symptoms include mood changes; weight gain predominantly in the back of the neck between the shoulder blades and face, respectively termed buffalo hump and moon facies; skin atrophy and stretch marks; muscle weakness; hyperglycemia; and increased risk of infections. Additionally, prolonged use of glucocorticoids can increase the risk of osteoporosis and pathological fractures, and inhibition of bone growth in children. Clients receiving glucocorticoids can develop ocular disorders, like cataracts and glaucoma, as well as peptic ulcer disease. Finally, when glucocorticoids are given at high doses, they can also act on mineralocorticoid receptors, causing sodium and water retention, which may result in hypertension and edema.
Glucocorticoids are contraindicated in clients with severe systemic fungal infections. Additionally, glucocorticoids should be used with caution in clients with infections such as varicella and tuberculosis, as well as in glaucoma, peptic ulcer disease, heart failure, diabetes mellitus, osteoporosis, or certain psychiatric conditions.
Now, switching gears, synthetic mineralocorticoids are used to treat conditions where mineralocorticoid levels are low, such as Addison disease and severe congenital adrenal hyperplasia. Additionally, they can be used to treat conditions like idiopathic orthostatic hypotension and severe septic shock. Now, synthetic mineralocorticoids include fludrocortisone, which can be taken orally.
Once administered, mineralocorticoids act primarily on intracellular mineralocorticoid receptors in the kidney tubules, where they favor the reabsorption of sodium and water, along with excretion of potassium and protons. It’s important to note that mineralocorticoids can also cause moderate activation of glucocorticoid receptors.
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