Steroids

What are glucocorticoids?

Glucocorticoids (corticosteroids) are steroid hormones produced by the adrenal cortex that regulate carbohydrate metabolism, suppress inflammation, and suppress the immune response.

What are the two major types of corticosteroids?

Mineralocorticoids (regulate salt and water balance; aldosterone) and glucocorticoids (regulate carbohydrate metabolism; cortisol).

What is the primary endogenous glucocorticoid?

Cortisol.

What is the primary endogenous mineralocorticoid?

Aldosterone.

How do glucocorticoids support the body's stress response?

They work with epinephrine to maintain blood pressure, support cardiovascular function, and help the body respond to physiologic stress.

How do glucocorticoids affect the central nervous system?

They may cause insomnia, wakefulness, and agitation.

What role do glucocorticoids play in fetal development?

They promote fetal lung maturation and reduce the risk of respiratory distress syndrome in preterm infants.

How do glucocorticoids affect carbohydrate metabolism?

They work opposite insulin by increasing gluconeogenesis, decreasing glucose uptake and utilization, and increasing glycogen storage, resulting in hyperglycemia.

How do glucocorticoids affect protein metabolism?

They increase protein breakdown, which can lead to muscle wasting and thin skin with long-term therapy.

How do glucocorticoids affect fat metabolism?

They promote lipolysis and cause fat redistribution, producing moon face, buffalo hump, and central obesity.

How do glucocorticoids affect blood vessels and blood pressure?

They decrease capillary permeability, promote vasoconstriction, and help maintain blood pressure.

How do glucocorticoids affect blood cell counts?

They increase red blood cells and neutrophils while decreasing lymphocytes, eosinophils, basophils, and monocytes.

What is the difference between physiologic and pharmacologic glucocorticoid doses?

Physiologic doses replace normal cortisol; pharmacologic doses suppress inflammation and immune function.

What are the major clinical indications for glucocorticoids?

Autoimmune diseases, allergic reactions, inflammatory disorders, asthma, transplant rejection prevention, and adrenal insufficiency.

Which glucocorticoid drug name patterns should you recognize?

Many glucocorticoids end in -sone, -solone, or -asone.

How are glucocorticoids administered?

They may be given orally, IV, IM, subcutaneously, topically, or intranasally.

How are glucocorticoids metabolized and eliminated?

They are metabolized by the liver and excreted by the kidneys.

What are the general dosing principles for glucocorticoids?

Start low for non-life-threatening conditions, start high for emergencies, use the lowest effective dose long-term, increase doses during stress, and taper when discontinuing.

Why are glucocorticoids usually administered before 9 AM?

To mimic the body's normal cortisol secretion and reduce adrenal suppression.

Why should glucocorticoids never be stopped abruptly?

Sudden discontinuation can cause adrenal insufficiency and potentially life-threatening adrenal crisis.

What are the major adverse effects of long-term glucocorticoid therapy?

Hyperglycemia, infection, osteoporosis, adrenal suppression, muscle weakness, fluid retention, hypokalemia, mood changes, cataracts, glaucoma, peptic ulcers, and Cushing syndrome.

Why do glucocorticoids increase infection risk?

They suppress immune function and decrease inflammatory responses.

How do glucocorticoids affect bone health?

Long-term therapy increases the risk of osteoporosis and fractures.

How do glucocorticoids affect glucose levels?

They raise blood glucose and may cause glycosuria.

How do glucocorticoids affect fluid and electrolyte balance?

They cause sodium and water retention, potassium loss, edema, hypernatremia, and hypokalemia.

What eye complications can occur with long-term glucocorticoid use?

Cataracts and glaucoma; patients require regular eye examinations.

Why do glucocorticoids increase the risk of peptic ulcer disease?

They decrease protective prostaglandins and mucus while increasing gastric acid and pepsin.

What is iatrogenic Cushing syndrome?

A syndrome caused by long-term glucocorticoid therapy characterized by fat redistribution, hyperglycemia, muscle weakness, osteoporosis, infection risk, and characteristic body changes.

What are the classic physical findings of Cushing syndrome?

Moon face, buffalo hump, central obesity, striae, muscle weakness, hyperglycemia, osteoporosis, and increased infection risk.

Which medications commonly interact with glucocorticoids?

NSAIDs, insulin and oral diabetic medications, loop and thiazide diuretics, and live vaccines.

Why should live vaccines generally be avoided during glucocorticoid therapy?

Because immunosuppression increases the risk of infection from live vaccines.

Who should generally not receive glucocorticoids?

Patients with systemic fungal infections or those receiving live virus vaccines.

Why does adrenal suppression occur during long-term glucocorticoid therapy?

Exogenous steroids suppress the HPA axis, decreasing endogenous cortisol production.

How can adrenal suppression be prevented when discontinuing therapy?

Gradually taper the dose while monitoring for recovery of endogenous cortisol production.

What nursing assessments are most important during glucocorticoid therapy?

Monitor blood glucose, electrolytes, edema, infection, bone health, muscle strength, vision changes, and signs of adrenal insufficiency.

What patient teaching is essential for glucocorticoid therapy?

Take in the morning with food, never stop abruptly, report signs of infection or vision changes, monitor for black stools and severe weakness, and follow taper instructions.

What are the highest-yield NCLEX concepts for glucocorticoids?

Opposite of insulin (hyperglycemia), administer before 0900, never stop abruptly, taper therapy, monitor for infection and osteoporosis, avoid live vaccines, and recognize Cushing syndrome.