hydrocortisone

Hydrocortisone is the synthetic/bioidentical form of cortisol, the primary endogenous glucocorticoid produced by the zona fasciculata of the adrenal cortex. Mechanism: binds intracellular glucocorticoid receptors, translocates to nucleus, alters gene transcription—inhibits NF-κB and AP-1, decreases production of inflammatory cytokines (IL-1, IL-2, IL-6, TNF-α), inhibits phospholipase A2 (reducing prostaglandin/leukotriene synthesis), and promotes lipocortin-1 synthesis. Has significant mineralocorticoid activity (unlike prednisone/dexamethasone), making it ideal for primary adrenal insufficiency (Addison's disease) where aldosterone is also deficient. Clinical uses: (1) Adrenal insufficiency replacement (primary and secondary), (2) Adrenal crisis (IV hydrocortisone, high-dose), (3) Stress-dose coverage during surgery/illness in patients with HPA axis suppression, (4) Septic shock (adjunct in refractory cases), (5) Topical for dermatologic inflammation, (6) Rectal/topical for IBD. Relative potency: hydrocortisone is the reference standard (glucocorticoid potency=1, mineralocorticoid potency=1), useful for comparing other steroids (e.g., prednisone 4x glucocorticoid potency, dexamethasone 25x with minimal mineralocorticoid activity). Side effects with chronic use: Cushingoid features, hyperglycemia, osteoporosis, immunosuppression, HPA axis suppression, hypertension (mineralocorticoid effect), skin thinning, mood changes, peptic ulcers. Abrupt withdrawal after chronic use can cause adrenal crisis due to HPA suppression—must taper. High-yield board concept: differentiate mineralocorticoid vs glucocorticoid potency among steroids and know hydrocortisone's dual activity profile, which is clinically exploited in Addison's disease management alongside fludrocortisone if needed.