Mechanism of Action

Synthetic versions of cortisol from the adrenal cortex. They suppress the inflammatory and immune cascade by inducing lipocortin (annexin A1), which inhibits phospholipase A2 — shutting down prostaglandin AND leukotriene production UPSTREAM of where NSAIDs act, making them far more potent anti-inflammatories. Dosing splits into physiologic replacement (Addison's, adrenal insufficiency) and pharmacologic suppression (asthma flares, autoimmune disease, transplant rejection, cerebral edema). Potency varies widely: dexamethasone is ~25× hydrocortisone with no mineralocorticoid effect. Prolonged use suppresses the HPA axis, so a taper is mandatory.

Common Medications

prednisonePrototype

prodrug → prednisolone in liver

methylprednisolone

IV for acute/rapid onset

dexamethasone

~25× potency, no mineralocorticoid effect

hydrocortisone

physiologic replacement; stress-dose in adrenal crisis

Indications

adrenal insufficiency

physiologic replacement (e.g., Addison's)

asthma exacerbation

COPD exacerbation

autoimmune flares

lupus, rheumatoid arthritis

organ transplant rejection

allergic reactions

cerebral edema

Side Effects

hyperglycemia Hallmark

gluconeogenesis + insulin resistance; may occur without prior diabetes

fluid retention

mineralocorticoid activity → hypertension

hypokalemia

weight gain

increased appetite

cushingoid fat redistribution

moon face, buffalo hump, truncal obesity

osteoporosis

long-term use; calcium, vitamin D, baseline DEXA

thin skin and easy bruising

mood changes

euphoria to psychosis

proximal muscle weakness

cataracts

posterior subcapsular; glaucoma also possible long-term

Contraindications & Interactions

Contraindications

systemic fungal infection

live vaccines during therapy

immunosuppression; non-live vaccines need a prescriber order

abrupt discontinuation after >1–2 weeks

precipitates adrenal crisis — taper required

Interactions

NSAIDs

additive GI ulceration/bleeding risk

potassium-wasting diuretics

additive hypokalemia

insulin / oral hypoglycemics

raises glucose — may need dose increase

Administration & Monitoring

give oral dose in the morning

matches 6–8 AM cortisol peak; minimizes HPA suppression and insomnia

give with food

reduces GI irritation

monitor blood glucose

monitor potassium

monitor blood pressure

monitor weight

assess for signs of infection

fever may be masked

schedule bone density scan with long-term use

never stop abruptlyHold

taper after >7–10 days of use

give stress-dose steroids in acute illness

IV when oral cannot be tolerated, to prevent crisis

Patient Teaching

take in the morning with food

do not stop abruptly

provider-guided taper; risk of adrenal crisis

finish the entire taper

even after symptoms improve

report signs of infection without fever

sore throat, drainage

monitor blood glucose more frequently

avoid NSAIDs

additive GI bleeding

carry medical identification

stress-dose steroids may be needed in emergency/surgery

seek care if unable to keep pills down

may need IV steroids during illness

Report Nowescalate immediately

adrenal crisis Hallmark

from ABRUPT withdrawal / acute stress in an HPA-suppressed client; hypotension, shock, hyponatremia, hypoglycemia — needs stress-dose hydrocortisone + IV fluids

masked infection

anti-inflammatory action hides fever — report sore throat / purulent drainage even without fever

severe hyperglycemia

report markedly elevated glucose, especially in diabetics

GI bleeding

peptic ulcer risk, amplified with concurrent NSAIDs

steroid psychosis

Clinical Pearl

Think 'Cushing in a bottle' — moon face, high glucose, thin skin, suppressed immune system, and every major adverse effect falls out. Morning dose, with food, never stop cold turkey: if steroids do the adrenals' job too long, the glands stop showing up to work.