Corticosteroids

A patient on prednisone for two weeks now has a blood glucose of 248 mg/dL and no diabetes history. Corticosteroids mimic Cushing syndrome — and every side effect traces back to that single idea.

Corticosteroids (prednisone, dexamethasone, hydrocortisone) suppress inflammation by flooding the body with exogenous glucocorticoid. The adverse effects mirror Cushing syndrome because that is exactly what you are pharmacologically creating. Metabolic effects hit first: hyperglycemia from gluconeogenesis, fluid retention and hypokalemia from mineralocorticoid activity, and weight gain with redistribution (moon face, buffalo hump, truncal obesity). Immune suppression raises infection risk — monitor for subtle signs because the drug masks fever and inflammation. Bone loss (osteoporosis) occurs with long-term use; calcium, vitamin D, and baseline DEXA scans matter. GI irritation increases peptic ulcer risk, especially combined with NSAIDs. Psychiatric effects range from euphoria to psychosis. Adrenal suppression is the most dangerous long-term consequence: the HPA axis downregulates, so abrupt discontinuation triggers adrenal crisis (hypotension, shock, cardiovascular collapse). Taper — never stop suddenly after more than 7-10 days of use. Monitor blood glucose, electrolytes (especially potassium), weight, blood pressure, and signs of infection at every visit.

Key Distinctions

Don't confuse corticosteroid-induced hyperglycemia with new-onset diabetes — the glucose elevation is drug-driven and may resolve after tapering. Students often think infection risk means the patient gets more infections; the real danger is that signs of infection are masked by the drug's anti-inflammatory action. Adrenal crisis from abrupt withdrawal is not a side effect of taking the drug — it is a side effect of stopping it.

Clinical Pearl

Think "Cushing in a bottle." If you can picture moon face, high glucose, thin skin, and a suppressed immune system, you already know every major corticosteroid adverse effect.

Clinical Use & Administration

Corticosteroids (prednisone, hydrocortisone, methylprednisolone, dexamethasone) are synthetic versions of cortisol produced by the adrenal cortex. Their mechanism is suppression of the inflammatory and immune cascade — they induce lipocortin (annexin A1), which inhibits phospholipase A2, shutting down prostaglandin and leukotriene production upstream of where NSAIDs act. This makes them far more potent anti-inflammatory agents. Indications split into two categories: physiologic replacement (Addison's disease, adrenal insufficiency after surgery) and pharmacologic suppression (asthma exacerbations, autoimmune flares, organ transplant rejection, allergic reactions, cerebral edema). Administration timing matters — give oral doses in the morning to mimic the body's natural cortisol peak (6–8 AM), which minimizes HPA axis suppression. Doses taken with food reduce GI irritation. For acute situations, IV methylprednisolone provides rapid onset. Dose tapering is mandatory after use exceeding 1–2 weeks because exogenous steroids suppress the hypothalamic-pituitary-adrenal axis; abrupt withdrawal can trigger life-threatening adrenal crisis. Potency varies: dexamethasone has roughly 25 times the anti-inflammatory potency of hydrocortisone with no mineralocorticoid effect, making drug selection indication-specific.

Key Distinctions

Don't confuse replacement therapy (low physiologic doses for adrenal insufficiency) with immunosuppressive therapy (high pharmacologic doses for inflammation) — indications and risk profiles differ significantly. Students mix up corticosteroids with anabolic steroids; corticosteroids cause muscle wasting, not building. Prednisone is a prodrug converted to prednisolone in the liver — impaired liver function may require prescribing prednisolone directly.

Clinical Pearl

Morning dose, with food, never stop cold turkey. Think of the adrenal glands as employees — if steroids do their job too long, the glands stop showing up to work.