Guide — Endocrine
Adrenal Disorders for Nurses
Cushing's syndrome, Addison's disease, adrenal crisis, and pheochromocytoma — pathophysiology, assessment findings, labs, nursing priorities, and NCLEX pearls.
11 min read · Endocrine
Educational use only. Adrenal crisis is a life-threatening emergency. Follow institutional protocols and provider orders for all endocrine emergencies. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Adrenal Gland Overview
| Region | Layer | Hormones | Primary Action |
|---|---|---|---|
| Cortex (outer) | Zona glomerulosa (outer) | Aldosterone (mineralocorticoid) | Na⁺ retention, K⁺ excretion, water retention, blood pressure |
| Zona fasciculata (middle) | Cortisol (glucocorticoid) | Stress response, glucose regulation, immune suppression, anti-inflammatory | |
| Zona reticularis (inner) | Androgens (DHEA) | Sex hormone precursors; minor in adults | |
| Medulla (inner) | Chromaffin cells | Epinephrine, norepinephrine (catecholamines) | Fight-or-flight: ↑HR, ↑BP, ↑glucose, bronchodilation |
Memory aid: GFR → Glomerulosa (salt/mineralocorticoids) → Fasciculata (sugar/glucocorticoids) → Reticularis (sex hormones)
Cushing's Syndrome — Cortisol Excess
Most common cause: Exogenous corticosteroid use (iatrogenic — most common overall). Endogenous causes: pituitary adenoma secreting ACTH (Cushing's disease, most common endogenous), adrenal tumor, ectopic ACTH production (small-cell lung cancer).
| System | Clinical Findings | Mechanism |
|---|---|---|
| Appearance | Moon face, buffalo hump (dorsal fat pad), central obesity (truncal), supraclavicular fat pads, thin extremities | Fat redistribution from cortisol excess |
| Skin | Purple/violaceous abdominal striae, thin fragile skin, easy bruising, poor wound healing, hirsutism | Cortisol-induced collagen breakdown; androgen effects |
| Metabolic | Hyperglycemia (steroid-induced diabetes), hypertension, hypokalemia, weight gain | Gluconeogenesis promotion; mineralocorticoid activity of cortisol |
| Musculoskeletal | Proximal muscle weakness (difficulty rising from chair), osteoporosis, pathologic fractures | Protein catabolism; cortisol inhibits calcium absorption |
| Immune | Immunosuppression, increased infection risk, masked fever, poor wound healing | Anti-inflammatory and immunosuppressive effects of cortisol |
| Psychiatric | Depression, anxiety, emotional lability, psychosis in severe cases | Cortisol effects on CNS neurotransmitter systems |
Diagnostics
- 24-hour urine free cortisol (↑ in Cushing's)
- Overnight low-dose dexamethasone suppression test — 1mg dex at midnight; cortisol measured at 8am; normal: cortisol suppressed; Cushing's: cortisol fails to suppress
- Late-night salivary cortisol (high in Cushing's — cortisol normally lowest at midnight)
- ACTH level differentiates ACTH-dependent (pituitary, ectopic) from ACTH-independent (adrenal tumor, exogenous steroids)
Nursing Priorities
- Monitor blood glucose — steroid-induced hyperglycemia common
- Infection precautions — immunosuppressed, fever may be masked
- Skin care — fragile skin, avoid tape trauma, assess for bruising
- Fall precautions — proximal muscle weakness, osteoporosis
- Fluid/electrolyte monitoring — hypokalemia, hypertension
- Psychological support — body image changes, emotional lability
- Steroid taper education — NEVER abruptly stop corticosteroids (risk of adrenal crisis)
Addison's Disease — Adrenal Insufficiency
Primary adrenal insufficiency (Addison's): Adrenal gland fails to produce cortisol/aldosterone. Most common cause: autoimmune destruction. Other causes: TB, bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome from meningococcemia), adrenal metastasis, fungal infection.
Secondary adrenal insufficiency: Pituitary fails to secrete ACTH (pituitary tumor, surgery, radiation). No aldosterone deficiency (aldosterone regulated by renin-angiotensin, not ACTH). No hyperpigmentation.
| Finding | Clinical Details | Mechanism |
|---|---|---|
| Hyperpigmentation | Tanning of sun-exposed skin, buccal mucosa, scars, nipples, pressure points — HALLMARK of primary Addison's | High ACTH stimulates melanocytes (ACTH shares precursor with MSH) |
| Electrolytes | Hyponatremia, hyperkalemia, hypoglycemia (triad) | Aldosterone deficiency: Na⁺ wasting, K⁺ retention; cortisol deficiency: impaired gluconeogenesis |
| Cardiovascular | Hypotension (often orthostatic), tachycardia, dehydration, salt craving | Na⁺ loss → volume depletion; cortisol needed to maintain vascular tone |
| GI | Nausea, vomiting, abdominal pain, diarrhea, weight loss, anorexia | Cortisol deficiency effects on GI motility |
| Labs | Low morning cortisol, high ACTH (primary), low glucose, hyponatremia, hyperkalemia, eosinophilia | ACTH stimulation test: gold standard — normal response = cortisol rises > 18–20 mcg/dL |
Treatment
- Hydrocortisone (glucocorticoid replacement) — given in divided doses (mimics diurnal pattern: higher AM dose)
- Fludrocortisone (mineralocorticoid replacement) — for primary Addison's only
- Stress dosing: double or triple corticosteroid dose during illness, surgery, or significant stress
- Medical alert bracelet — mandatory for all patients on chronic steroid replacement
Adrenal (Addisonian) Crisis — Emergency
Life-threatening emergency — treat IMMEDIATELY
Triggers: Illness/infection, surgery, trauma, vomiting (unable to take oral steroids), abrupt steroid discontinuation, physiologic stress without dose increase in a patient on chronic steroids
Presentation: Severe hypotension/shock unresponsive to fluids, severe abdominal pain, nausea/vomiting, confusion, extreme weakness, high fever, hypoglycemia, hyponatremia, hyperkalemia
| Priority | Intervention | Rationale |
|---|---|---|
| 1st | IV Hydrocortisone (100 mg IV bolus) | Replace cortisol immediately — do NOT delay to confirm diagnosis; can be lifesaving |
| 2nd | IV Normal saline + Dextrose (D5NS) | Replace volume; correct hypoglycemia and hyponatremia |
| 3rd | Treat precipitating cause | Antibiotics for infection; address underlying trigger |
| Monitor | VS, glucose, Na⁺, K⁺, I&O | Hypotension, hypoglycemia, and electrolyte imbalances require continuous monitoring |
Pheochromocytoma
Definition: Catecholamine-secreting tumor of adrenal medulla (or extra-adrenal paraganglioma). Rare but dangerous — causes episodic or sustained hypertension and is curable with surgery.
Classic triad (3 Ps): Palpitations, Perspiration (diaphoresis), Pallor (pale) — with severe hypertension (often paroxysmal). Also: headache, tremor, anxiety/sense of doom.
Diagnosis: 24-hour urine metanephrines/catecholamines (or plasma free metanephrines) — most sensitive; CT/MRI for tumor localization.
Treatment: Alpha-blockade FIRST (phenoxybenzamine or doxazosin) before beta-blocker — beta-blocker alone in the presence of pheochromocytoma causes paradoxical severe hypertension (unopposed alpha); surgical resection (adrenalectomy) is curative.
NCLEX Key
Pheochromocytoma surgery risk: intraoperative hypertensive crisis (tumor handling) then hypotension (tumor removal). Have IV phentolamine (alpha-blocker) and fluids ready. Never palpate a suspected pheochromocytoma — can trigger crisis.
NCLEX Pearls
Adrenal crisis = hydrocortisone first: Treat before confirming diagnosis — delay can be fatal. Hydrocortisone has both glucocorticoid and some mineralocorticoid activity.
Never stop corticosteroids abruptly: Patients on chronic steroids require stress dosing during illness/surgery; abrupt discontinuation causes adrenal crisis — adrenals have atrophied.
Cushing's electrolytes: Hypokalemia, hypernatremia, hyperglycemia (cortisol excess mirrors aldosterone excess). Opposite of Addison's.
Addison's electrolytes: Hyponatremia, hyperkalemia, hypoglycemia. Remember: Addison's = lack of aldosterone = sodium low, potassium high.
Hyperpigmentation uniquely identifies primary Addison's: High ACTH drives melanocyte stimulation. Secondary adrenal insufficiency has LOW ACTH — no hyperpigmentation.
Steroid adverse effects to monitor: Glucose (hyperglycemia), BP (hypertension), K⁺ (hypokalemia), bones (osteoporosis), infection (masked fever), skin (thin/fragile), mood (depression/psychosis).
Related Resources
Standards & sources
Fact-checked Jun 20, 2026This page is written to align with American Diabetes Association (ADA) Standards of Care · American Association of Clinical Endocrinology (AACE). It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →