Addison’s disease is primary adrenal insufficiency — the destruction or dysfunction of the adrenal cortex itself, producing a deficiency of both cortisol and aldosterone. It affects roughly 1 in 10,000 people in the United States, with autoimmune adrenalitis accounting for approximately 80% of cases. The hallmark finding that distinguishes primary from secondary adrenal insufficiency is hyperpigmentation: excess ACTH (the pituitary’s response to low cortisol) exerts MSH-like activity on melanocytes, producing bronze or darkening of the skin and mucous membranes. Secondary adrenal insufficiency involves pituitary ACTH deficiency and does not produce hyperpigmentation. The life-threatening complication, Addisonian crisis, requires immediate IV hydrocortisone and fluid resuscitation. This reference covers pathophysiology, clinical presentation, laboratory findings, adrenal crisis management, nursing interventions, medications, patient education, and six NCLEX-style questions.
Use this page alongside the Cushing’s syndrome nursing reference for the full cortisol excess vs. deficiency comparison, the electrolyte imbalances reference for hyponatremia and hyperkalemia management, the diabetes mellitus nursing reference for hypoglycemia management, and the nursing lab values cheat sheet for cortisol and ACTH interpretation.
| Fast-scan summary | Key fact |
|---|---|
| Definition | Primary adrenal insufficiency — adrenal cortex destruction → cortisol + aldosterone deficiency |
| Most common cause | Autoimmune adrenalitis (~80% of cases in developed countries) |
| Pathognomonic sign | Hyperpigmentation — bronze darkening of skin, buccal mucosa, scars, pressure points (primary only; excess ACTH → MSH-like stimulation) |
| Electrolyte pattern | Hyponatremia + hyperkalemia (aldosterone deficiency → Na+ wasting, K+ retention) |
| Gold standard diagnostic test | ACTH (cosyntropin) stimulation test — measure cortisol at 0 and 60 min; failure to rise to ≥18 mcg/dL confirms insufficiency |
| Lab pattern in primary | Low cortisol + HIGH ACTH (pituitary compensates by overdriving); in secondary: low cortisol + LOW ACTH |
| Chronic cortisol replacement | Hydrocortisone 15–25 mg/day in 2–3 divided doses (largest dose in morning) |
| Mineralocorticoid replacement | Fludrocortisone 0.05–0.2 mg/day (primary Addison's only — secondary does not require mineralocorticoid) |
| Adrenal crisis treatment | Hydrocortisone 100 mg IV bolus STAT + normal saline resuscitation |
| Non-negotiable patient education | Medical alert bracelet + steroid ID card + emergency hydrocortisone injection kit |
Pathophysiology and etiology
The adrenal cortex has three zones, each producing distinct hormones. In Addison’s disease, destruction of the cortex impairs production of glucocorticoids (primarily cortisol, from the zona fasciculata), mineralocorticoids (primarily aldosterone, from the zona glomerulosa), and androgens (primarily DHEA, from the zona reticularis). The medulla, which produces catecholamines (epinephrine, norepinephrine), may also be affected depending on the underlying cause, but the cortisol and aldosterone deficiencies dominate the clinical picture.
When the adrenal cortex is destroyed, cortisol falls. The anterior pituitary detects this via loss of negative feedback and releases large amounts of ACTH in an attempt to drive adrenal output. ACTH shares structural homology with melanocyte-stimulating hormone (MSH): both derive from the precursor proopiomelanocortin (POMC). Excess ACTH binds to melanocortin-1 receptors (MC1R) on melanocytes, stimulating melanin production. This produces the characteristic hyperpigmentation that distinguishes primary from secondary adrenal insufficiency. In secondary adrenal insufficiency, the problem originates at the pituitary (ACTH deficiency), so ACTH is LOW — hyperpigmentation does not occur.
| Cause | Mechanism | Notes |
|---|---|---|
| Autoimmune adrenalitis | Antibodies against 21-hydroxylase enzyme destroy the adrenal cortex | Most common cause (~80% in developed countries); anti-21-hydroxylase antibodies are diagnostic; often part of autoimmune polyendocrine syndrome (APS) — co-occurs with thyroid disease, type 1 diabetes, celiac disease |
| Tuberculosis | Granulomatous destruction of the adrenal glands; may calcify on imaging | Leading infectious cause worldwide; consider in patients from endemic regions or with prior TB; bilateral adrenal calcification on CT is a classic finding |
| Fungal infections | Histoplasma, Cryptococcus, Blastomyces invade adrenal tissue | Associated with immunocompromised states (HIV/AIDS); histoplasmosis is a classic cause in endemic regions (Ohio/Mississippi River valleys) |
| Metastatic cancer | Bilateral adrenal metastases destroy functional cortical tissue (typically requires >90% destruction for insufficiency) | Most common primary tumors: lung, breast, colon, kidney, melanoma; often an incidental finding on staging CT |
| Adrenal hemorrhage | Bilateral adrenal infarction, often from anticoagulant therapy, septicemia (Waterhouse-Friderichsen syndrome with meningococcemia), or antiphospholipid syndrome | Waterhouse-Friderichsen syndrome: acute bilateral adrenal hemorrhage in septicemia — dramatic onset, often fatal without early recognition |
| Medications | Etomidate (inhibits adrenal steroidogenesis), ketoconazole, metyrapone, mitotane, rifampin (accelerates cortisol metabolism) | Etomidate used for rapid sequence intubation can suppress adrenal axis for 24–48 hours; clinically significant in critically ill patients |
| Congenital adrenal hyperplasia (CAH) | Enzyme deficiency (most often 21-hydroxylase) impairs cortisol and aldosterone synthesis from birth | Different from autoimmune Addison's but same cortisol/aldosterone deficiency outcome; usually diagnosed in infancy with salt-wasting crisis |
Primary vs secondary vs tertiary adrenal insufficiency
| Feature | Primary (Addison's) | Secondary (pituitary) | Tertiary (hypothalamic) |
|---|---|---|---|
| Problem location | Adrenal cortex | Anterior pituitary | Hypothalamus |
| Deficient hormone | ACTH (response: elevated), CRH elevated | ACTH (response: low), CRH elevated | CRH (response: low), ACTH low |
| Cortisol | Low | Low | Low |
| ACTH level | HIGH (pituitary drives compensation) | Low | Low |
| Aldosterone | Low (adrenal destruction) | Normal (RAAS intact — renin drives aldosterone independently) | Normal |
| Hyperpigmentation | YES — excess ACTH stimulates MC1R | No — ACTH is low | No — ACTH is low |
| Salt craving / hypovolemia | Yes — aldosterone deficiency | Mild — SIADH-like hyponatremia possible but no aldosterone deficit | Mild |
| Mineralocorticoid replacement needed | Yes (fludrocortisone) | No | No |
| Most common cause | Autoimmune adrenalitis | Long-term exogenous steroid use (HPA axis suppression) | Long-term exogenous steroid use (CRH suppression) |
Clinical presentation
Addison’s disease develops insidiously over months to years. Because the adrenal cortex must be more than 90% destroyed before overt insufficiency appears, patients often present with vague symptoms that are initially attributed to depression, chronic fatigue, or gastrointestinal illness. Recognizing the constellation — fatigue + weight loss + hyperpigmentation + orthostatic hypotension + salt craving — is essential for both clinical practice and NCLEX.
Glucocorticoid deficiency (cortisol) manifestations:
- Fatigue and generalized weakness (most common, often profound)
- Anorexia, nausea, vomiting, abdominal pain
- Weight loss
- Hypoglycemia (cortisol is a counter-regulatory hormone — its absence reduces gluconeogenesis)
- Depression, irritability, cognitive difficulties
- Amenorrhea and loss of libido (adrenal androgens depleted, affecting sex hormone balance)
- Increased sensitivity to insulin (hypoglycemia risk particularly in patients also on insulin)
Mineralocorticoid deficiency (aldosterone) manifestations:
- Hyponatremia — aldosterone normally promotes Na+ reabsorption in the distal nephron; without it, Na+ is wasted in the urine
- Hyperkalemia — aldosterone normally drives K+ excretion; without it, K+ accumulates
- Hypovolemia and hypotension — Na+ wasting leads to volume depletion
- Orthostatic hypotension — drop in systolic BP ≥20 mmHg and/or diastolic BP ≥10 mmHg on standing
- Salt craving — a classic history clue; patients describe craving salty foods
- Dizziness on standing, palpitations
Androgen deficiency manifestations (more prominent in women):
- Loss of axillary and pubic hair (adrenal androgens are the primary source in women)
- Decreased libido
- Dry skin
Hyperpigmentation (primary Addison’s only): This is the most NCLEX-important physical finding. Excess ACTH activates MC1R on melanocytes, producing bronze or tan discoloration, particularly prominent at:
- Sun-exposed areas (face, neck, dorsum of hands)
- Pressure points (elbows, knees, knuckles)
- Skin folds (axillae, groin)
- Buccal mucosa and gingiva (important: darkening of the inner cheeks is pathognomonic)
- Scars and areolae
- Palmar creases
New darkening of existing scars is a classic NCLEX clue — scars formed before the disease developed now darken as ACTH rises.
Laboratory findings
| Lab value | Expected finding | Mechanism | Clinical significance |
|---|---|---|---|
| Serum cortisol (AM) | Low (<3 mcg/dL is highly suggestive; <18 mcg/dL is suboptimal response) | Adrenal cortex cannot produce adequate cortisol | Draw before 9 AM (peak of diurnal rhythm); random cortisol alone is insufficient for diagnosis |
| Plasma ACTH | High (>100 pg/mL, often >200 pg/mL) in primary | Loss of cortisol negative feedback drives pituitary ACTH hypersecretion | High ACTH + low cortisol = primary; Low ACTH + low cortisol = secondary/tertiary |
| ACTH stimulation test (gold standard) | Cortisol fails to rise to ≥18 mcg/dL at 30–60 min post-cosyntropin 250 mcg IV/IM | Adrenal cortex cannot respond to ACTH stimulation | Normal response: cortisol ≥18 mcg/dL at 30–60 min; subnormal = adrenal insufficiency confirmed |
| Serum sodium (Na+) | Low (hyponatremia, typically 120–135 mEq/L) | Aldosterone deficiency → sodium wasting via the kidney | Can cause confusion, seizures at very low levels; distinguish from SIADH (which has different urine findings) |
| Serum potassium (K+) | High (hyperkalemia, typically 5.0–7.0 mEq/L) | Aldosterone normally drives K+ secretion in distal nephron; without it, K+ accumulates | Monitor for cardiac dysrhythmias (peaked T waves, widened QRS); extreme hyperkalemia is life-threatening |
| Serum glucose | Low (hypoglycemia) | Cortisol promotes gluconeogenesis and glycogenolysis; its absence impairs glucose maintenance | Particularly dangerous in patients with diabetes taking insulin; fasting hypoglycemia is a hallmark |
| Serum aldosterone | Low | Aldosterone is produced by the adrenal cortex (zona glomerulosa) — destroyed in primary disease | Measured alongside plasma renin activity (PRA); in primary Addison's: low aldosterone + high PRA (renin is upregulated trying to drive aldosterone) |
| Plasma renin activity (PRA) | High | Low aldosterone → volume depletion → renin/angiotensin system activated | High renin + low aldosterone = primary adrenal problem; confirms mineralocorticoid deficiency |
| Blood urea nitrogen (BUN) | Elevated (pre-renal azotemia) | Volume depletion from aldosterone deficiency reduces renal perfusion | BUN:creatinine ratio >20:1 suggests pre-renal cause |
| Eosinophil count | Elevated (eosinophilia) | Cortisol normally suppresses eosinophils; cortisol deficiency removes this suppression | Eosinophilia in the context of chronic fatigue and hyponatremia is a subtle clue to adrenal insufficiency |
| Lymphocyte count | Elevated (lymphocytosis) | Same mechanism — cortisol suppresses lymphocyte proliferation; its absence allows lymphocytosis | CBC may show eosinophilia + lymphocytosis as soft signs of cortisol deficiency |
| Metabolic acidosis | Mild hyperchloremic metabolic acidosis (non-anion gap) | Aldosterone deficiency impairs H+ and K+ secretion in the distal nephron → H+ retention | ABG: pH <7.35, HCO3 low, normal anion gap; see [ABG interpretation guide](/nursing-tips/abg-interpretation/) |
| Anti-21-hydroxylase antibodies | Positive in autoimmune Addison's | Autoantibodies target 21-hydroxylase, the enzyme essential for cortisol and aldosterone synthesis | Present in ~80–90% of autoimmune cases; confirms autoimmune etiology but does not replace ACTH stimulation test for functional diagnosis |
Adrenal crisis (Addisonian crisis)
Adrenal crisis is the most dangerous and time-critical complication of Addison’s disease. It is a life-threatening emergency characterized by severe hypotension, cardiovascular collapse, and acute cortisol deficiency. Without immediate treatment, it is fatal. Nursing recognition and rapid response are essential.
Triggers
Any significant physiologic stressor can precipitate a crisis in a patient with adrenal insufficiency, because these patients cannot mount the normal cortisol stress response:
- Infection (most common trigger — bacterial infections, pneumonia, urinary tract infections, sepsis)
- Surgery or invasive procedures (without stress-dose steroid coverage)
- Trauma
- Missed steroid doses (skipping scheduled hydrocortisone, vomiting unable to keep medication down)
- Sudden steroid discontinuation (including in patients on long-term exogenous steroids who develop HPA axis suppression)
- Gastrointestinal illness with vomiting/diarrhea (unable to absorb oral steroids)
- Extreme psychological stress
Signs and symptoms of adrenal crisis
- Severe hypotension — systolic BP often <90 mmHg; may progress to shock
- Profound weakness and lethargy — patient may be unable to stand or move
- Severe nausea, vomiting, abdominal pain — can mimic an acute abdomen
- High fever — often disproportionate to any identified infection
- Altered mental status — confusion, disorientation, coma in severe cases
- Tachycardia — compensatory response to volume depletion
- Hypoglycemia — severe, may cause seizures
- Severe hyponatremia and hyperkalemia — electrolyte crisis can cause cardiac dysrhythmia
Immediate nursing actions for adrenal crisis
- Call for immediate provider/rapid response — this is a life-threatening emergency requiring IV hydrocortisone immediately
- Establish IV access — large-bore IV (16–18 gauge) in at least one peripheral vein
- Obtain STAT labs — serum cortisol, ACTH, BMP (Na+, K+, glucose, BUN, creatinine), CBC with differential, blood cultures if infection suspected. Draw labs before giving steroids if possible — but do not delay steroids if labs will take time
- Administer hydrocortisone 100 mg IV bolus — this is the cornerstone treatment; give immediately without waiting for cortisol level results if clinical suspicion is high
- Initiate aggressive IV fluid resuscitation — isotonic normal saline (0.9% NaCl), typically 1–2 liters rapidly in the first hour; 5% dextrose in normal saline (D5NS) if significant hypoglycemia present
- Monitor and treat hypoglycemia — D50W 25–50 mL IV if blood glucose <60 mg/dL
- Continuous cardiac monitoring — hyperkalemia can cause dysrhythmias; watch for peaked T waves, widened QRS
- Identify and treat the precipitating cause — blood/urine cultures, broad-spectrum antibiotics if sepsis suspected
- Continue hydrocortisone maintenance — following the 100 mg bolus: hydrocortisone 50–100 mg IV every 6–8 hours OR 200 mg in 24-hour continuous infusion
- Position and safety — head of bed flat or reverse Trendelenburg to support BP; fall precautions for orthostasis and altered mental status
Steroid taper post-crisis
Once the patient is stable, oral intake is tolerated, and the precipitating cause is treated: taper parenteral hydrocortisone over 1–3 days to oral maintenance dose. Fludrocortisone may be added once the patient can tolerate oral medications (at hydrocortisone doses ≥50 mg/day, the mineralocorticoid activity of hydrocortisone itself is sufficient, so fludrocortisone is not needed acutely).
Nursing assessment
Vital signs
- Blood pressure with orthostatic measurements (key assessment): check BP and HR lying, sitting, and standing. A drop of ≥20 mmHg systolic or ≥10 mmHg diastolic on standing, or HR increase ≥20 bpm, confirms orthostatic hypotension. Document all three positions.
- Temperature: fever may indicate infection (a common crisis trigger) or may occur during the crisis itself
- Weight: daily weights detect fluid volume changes; weight loss trend supports chronic adrenal insufficiency
Skin assessment for hyperpigmentation
This is the most NCLEX-critical physical assessment finding in Addison’s disease. Inspect systematically:
- Buccal mucosa and gingiva — grayish-brown patches on the inner cheeks and gums are pathognomonic for primary adrenal insufficiency
- Pressure points — elbows, knees, knuckles, heels
- Skin folds — axillae, groin, abdominal folds
- Sun-exposed areas — face, neck, dorsum of hands and forearms
- Scars — existing scars become hyperpigmented as ACTH rises (a history clue: “my old scars are turning dark”)
- Areolae and genitalia
- Palmar creases
Document baseline color and any changes. In patients with darker baseline skin tones, compare unexposed areas with exposed areas; buccal mucosa assessment is most reliable across all skin tones.
Electrolyte and glucose monitoring
- Monitor serum Na+, K+, and glucose every 4–8 hours during acute illness or hospitalization
- In chronic outpatient management: check electrolytes every 6–12 months, or with any symptom change
- Monitor for signs of hyperkalemia: muscle weakness, palpitations, peaked T waves on ECG
- Monitor for hypoglycemia: diaphoresis, tremor, confusion, palpitations, hunger
- Maintain continuous glucose monitoring in patients with concurrent diabetes
Fluid balance
- Strict intake and output during acute illness
- Daily weights (same scale, same time of day)
- Assess for dehydration: skin turgor, mucous membrane moisture, urine output (target ≥0.5 mL/kg/hr), urine specific gravity
Nursing interventions
| Problem | Nursing interventions | Rationale |
|---|---|---|
| Fluid volume deficit (aldosterone deficiency) | Administer IV fluids as ordered (isotonic NS preferred); monitor I&O strictly; daily weights; assess orthostatic BP q shift; administer fludrocortisone as ordered | Aldosterone deficiency causes sodium and water wasting; volume repletion corrects hypovolemia; fludrocortisone replaces mineralocorticoid action |
| Risk for electrolyte imbalance | Monitor serum Na+, K+, and glucose frequently; cardiac monitoring for hyperkalemia dysrhythmias; administer ordered electrolyte supplements (Na+ replacement in hyponatremia); hold potassium supplementation; assess neuro status for signs of hyponatremia-related cerebral edema | Aldosterone deficiency → hyponatremia + hyperkalemia; cortisol deficiency → hypoglycemia; dysrhythmia risk with K+ >6.0 mEq/L |
| Activity intolerance (profound fatigue) | Schedule nursing activities around rest periods; assist with ADLs; implement fall precautions; educate patient on energy conservation techniques; assess fatigue level on validated scale | Cortisol deficiency causes profound weakness and fatigue; orthostatic hypotension elevates fall risk; cortisol replacement takes days to restore energy |
| Risk for hypoglycemia | Monitor blood glucose before meals and at bedtime; have D50W or oral glucose sources at bedside; administer glucocorticoids with food when possible; educate patient on hypoglycemia signs and treatment (15-15 rule) | Cortisol promotes gluconeogenesis; deficiency causes fasting hypoglycemia; risk increases with exercise, missed meals, or illness |
| Risk for adrenal crisis | Monitor for crisis triggers (infection, nausea/vomiting, missed doses); educate patient on sick day rules and crisis recognition; ensure emergency injection kit is available and patient/family trained; have crash cart accessible for hospitalized patients | Any physiologic stressor can precipitate crisis; early recognition and steroid dose escalation are life-saving; a patient who cannot take oral steroids due to vomiting needs IV hydrocortisone immediately |
| Knowledge deficit (steroid management) | Teach medication regimen, sick day rules, stress dosing; provide written steroid ID card; ensure medical alert bracelet is ordered; demonstrate emergency injection kit use; involve family in teaching; document comprehension | Patients must self-manage dose escalation during illness; failure to do so results in adrenal crisis; emergency responders need to know the diagnosis if patient is unconscious |
| Impaired skin integrity (hyperpigmentation and dry skin) | Assess skin systematically at each visit using consistent lighting; document and photograph baseline hyperpigmentation; assess buccal mucosa; use moisturizing skin care; protect from pressure injury in bedridden patients | Hyperpigmentation is a monitoring marker for disease control — darkening may indicate inadequate cortisol replacement (ACTH still rising); worsening hyperpigmentation = indicator to review steroid dosing |
| Body image disturbance | Acknowledge cosmetic impact of hyperpigmentation openly; provide realistic expectations about partial improvement with treatment (ACTH decreases with adequate replacement but hyperpigmentation may persist); refer to counseling if significant psychological distress | Hyperpigmentation affects quality of life; improved cortisol replacement lowers ACTH and can reduce melanocyte stimulation over time |
Medications
| Medication | Class | Dose and schedule | Nursing considerations |
|---|---|---|---|
| Hydrocortisone | Glucocorticoid (cortisol replacement) | Oral: 15–25 mg/day in 2–3 divided doses. Typical split: 10–15 mg on waking + 5–10 mg early afternoon. For crisis: 100 mg IV bolus, then 50–100 mg IV q6–8h or 200 mg/24h continuous infusion | Largest dose in morning to mimic diurnal cortisol rhythm (cortisol peaks at 8 AM). Give with food to prevent GI irritation. Never crush or chew extended-release formulations. Monitor for signs of over-replacement: hypertension, weight gain, hyperglycemia, insomnia — these mirror Cushing's symptoms |
| Fludrocortisone (Florinef) | Synthetic mineralocorticoid (aldosterone replacement) | 0.05–0.2 mg orally once daily. Typical starting dose: 0.1 mg/day | For PRIMARY Addison's only — secondary adrenal insufficiency retains RAAS function, no mineralocorticoid replacement needed. Monitor blood pressure (over-replacement → hypertension, edema, hypokalemia; under-replacement → hypotension, hyperkalemia). Dose may need to increase in summer heat (increased sweat sodium losses). Reassess dose based on plasma renin activity (target PRA in the upper normal range) |
| Stress-dose hydrocortisone (sick day rules) | Glucocorticoid — dose escalation | Minor illness (fever, URI, minor stress): double or triple the usual daily dose for 2–3 days. If vomiting prevents oral intake: administer IM/SC hydrocortisone 100 mg IMMEDIATELY, then go to emergency department. For surgery: minor procedures 25 mg IV; moderate surgery 50–75 mg IV; major surgery 100–150 mg IV in divided doses over 24–48 hours | Teach the "sick day rule" clearly: patients must know the threshold for dose escalation, when to inject themselves, and when to call 911. The most common cause of preventable crisis is a patient with vomiting who could not absorb oral steroids and did not seek emergency care in time |
| Hydrocortisone emergency injection kit | Glucocorticoid — emergency | 100 mg IM or SC hydrocortisone for self-administration or administration by trained caregiver during crisis when IV access is unavailable | Every patient must have a kit; must be trained in self-injection or have a trained caregiver. Prefilled syringe kits (e.g., Solu-Cortef Act-O-Vial) are preferred. Verify kit is not expired at every follow-up. Patient and at least one household member must demonstrate injection technique before discharge |
| Dexamethasone (if cosyntropin test pending) | Glucocorticoid — diagnostic alternative | 4 mg IV if crisis suspected but cosyntropin test has not been completed | Dexamethasone does NOT cross-react with cortisol assays (unlike hydrocortisone), so it allows the ACTH stimulation test to be performed without interference. Use dexamethasone as a bridge ONLY when the cosyntropin test is being arranged. Switch to hydrocortisone after test completion |
Patient education
Patient education in Addison’s disease is life-saving — not merely health-promoting. Patients who understand their disease and know how to manage acute stress can prevent crisis. Patients who do not understand their disease die of preventable adrenal crisis.
Medical alert bracelet and steroid identification card (non-negotiable)
Every patient with Addison’s disease must wear a medical alert bracelet stating “Adrenal Insufficiency: Needs Hydrocortisone in Emergency.” This is not optional. If the patient is unconscious in an emergency department, this bracelet is the only information emergency clinicians have. The bracelet must:
- State the diagnosis (adrenal insufficiency or Addison’s disease)
- State the emergency medication (hydrocortisone)
- Be worn at all times
A steroid identification card (wallet card) complements the bracelet with more detail: diagnosis, maintenance dose, emergency dose (100 mg hydrocortisone IV/IM), prescribing provider contact information.
Sick day rules
Key principle: when the body is stressed, it needs more cortisol. A healthy adrenal gland increases cortisol output by 5–10x during illness or major surgery. Patients with Addison’s disease cannot do this. They must increase their dose manually.
- Fever, minor illness (URI, mild GI illness): Double or triple the daily hydrocortisone dose for 2–3 days, then return to maintenance dose when better
- Vomiting or inability to take oral medications: This is an emergency. Administer emergency injection (100 mg hydrocortisone IM/SC) immediately, then call 911 or go to the emergency department. Do not wait to see if vomiting resolves.
- Dental procedures, minor surgery: Take 25–50 mg hydrocortisone before the procedure
- Major surgery or serious trauma: Provider must administer IV hydrocortisone stress dosing (perioperative coverage)
When to call 911 vs. when to call the provider
Call 911 (emergency) if:
- Vomiting and cannot take oral medications (inject first, then call)
- Severe weakness, unable to stand
- Confusion or altered mental status
- Systolic BP <90 mmHg
- Loss of consciousness
Call the provider (within hours) if:
- Fever >100.4°F with no obvious cause
- Increasing fatigue or weakness despite dose adjustment
- Signs of over-replacement: swelling, weight gain, blood pressure elevation
Never abruptly stop steroids
Patients who have been on corticosteroid therapy for more than a few weeks develop HPA axis suppression. Abrupt discontinuation, even of prescribed therapeutic steroids for other conditions, can precipitate adrenal crisis. Any steroid dose reduction must be gradual and supervised by a provider.
Emergency injection kit education
- Store the kit at home, at work, and while traveling
- Keep a kit in a temperature-stable location (do not leave in a hot car)
- Teach a family member or close friend to administer the injection if the patient becomes too ill to self-administer
- Practice technique with a training device or with the provider team before discharge
- Check expiration dates at every provider visit and refill proactively
Exercise and activity
- Patients can exercise normally with stable disease on replacement therapy
- High-intensity exercise or prolonged endurance activity may require a small extra hydrocortisone dose (10–20 mg oral) before the activity
- Teach the patient to recognize early hypoglycemia symptoms during exercise and carry fast-acting glucose
Dietary guidance
- No strict dietary restrictions in well-managed Addison’s disease
- Liberal salt intake is encouraged (aldosterone deficiency increases sodium needs, especially in hot weather, during heavy exercise, or with significant sweating)
- Adequate carbohydrate intake to reduce hypoglycemia risk
- Patients on fludrocortisone who develop edema or hypertension may need dietary sodium reviewed with provider (possible dose adjustment)
Addison’s disease vs Cushing’s syndrome: comparison table
These two conditions represent opposite ends of the cortisol spectrum. Cushing’s syndrome is cortisol excess; Addison’s disease is cortisol deficiency. They are the two most commonly paired NCLEX endocrine questions. This table consolidates the key differentiators.
| Feature | Addison's disease (cortisol deficiency) | Cushing's syndrome (cortisol excess) |
|---|---|---|
| Cortisol level | LOW | HIGH |
| ACTH (primary) | HIGH (pituitary drives compensation) | HIGH if pituitary adenoma (Cushing's disease); LOW if adrenal tumor or exogenous steroids |
| Weight | Weight LOSS, anorexia | Weight GAIN, central obesity, moon face, buffalo hump |
| Blood pressure | HYPOTENSION, orthostatic changes | HYPERTENSION (cortisol has permissive vascular effects) |
| Blood glucose | HYPOGLYCEMIA (cortisol promotes gluconeogenesis) | HYPERGLYCEMIA (cortisol causes insulin resistance) |
| Sodium | HYPONATREMIA (aldosterone deficiency) | Hypernatremia (mild, cortisol has mineralocorticoid activity at high levels) |
| Potassium | HYPERKALEMIA (aldosterone deficiency) | HYPOKALEMIA (cortisol drives K+ loss) |
| Skin | Hyperpigmentation (excess ACTH → MSH-like activity) | Thin skin, easy bruising, purple striae, acne |
| Muscle | Weakness, fatigue (cortisol drives muscle energy) | Proximal muscle WASTING (catabolism), weakness |
| Immune function | Possible eosinophilia, lymphocytosis | Immunosuppression — increased infection risk |
| Bones | Not directly affected acutely | Osteoporosis (cortisol inhibits osteoblasts) |
| Mood | Depression, apathy, irritability | Euphoria, emotional lability, depression, psychosis |
| Aldosterone | LOW (adrenal cortex destroyed) | Normal to slightly elevated |
| Diagnostic test | ACTH stimulation test (cosyntropin) — confirm cortisol fails to rise | 24-h urine free cortisol, late-night salivary cortisol, 1-mg overnight dexamethasone suppression test |
| Treatment direction | REPLACE cortisol (hydrocortisone) + mineralocorticoid (fludrocortisone) | REMOVE or BLOCK cortisol source (surgery, adrenolytic agents) |
| Emergency | Addisonian crisis — severe hypotension, treat with hydrocortisone 100 mg IV + NS | Post-adrenalectomy adrenal crisis — same treatment |
For a full discussion of Cushing’s syndrome pathophysiology, diagnostic workup, and nursing care, see the Cushing’s syndrome nursing reference.
NCLEX-style practice questions
Question 1
A nurse is caring for a patient newly diagnosed with Addison’s disease. During skin assessment, which finding does the nurse expect that is pathognomonic for primary (not secondary) adrenal insufficiency?
A. Thin, translucent skin with easy bruising B. Grayish-brown discoloration of the buccal mucosa C. Periorbital edema and pretibial myxedema D. Yellowing of the sclerae and palms
Correct answer: B
Rationale: Hyperpigmentation of the buccal mucosa is pathognomonic for primary adrenal insufficiency. In primary Addison’s disease, the adrenal cortex is destroyed, removing negative feedback on the pituitary. The pituitary increases ACTH output dramatically. ACTH and melanocyte-stimulating hormone (MSH) share the same POMC precursor and both activate melanocortin-1 receptors (MC1R) on melanocytes, causing increased melanin production. This produces bronze-to-brown discoloration at sun-exposed areas, pressure points, skin folds, and most distinctively, the buccal mucosa and gingiva. Secondary adrenal insufficiency involves ACTH deficiency — no hyperpigmentation occurs. Option A describes findings in Cushing’s syndrome. Option C describes hypothyroid myxedema. Option D suggests jaundice, unrelated to adrenal function.
Question 2
A patient with known Addison’s disease is admitted with severe hypotension (BP 78/42 mmHg), vomiting, confusion, and a temperature of 39.8°C. The patient reports having vomiting for 12 hours and was unable to take their morning hydrocortisone. Which action is the nurse’s highest priority?
A. Obtain a serum cortisol level before initiating any treatment B. Administer hydrocortisone 100 mg IV bolus as ordered C. Initiate a 12-lead ECG to rule out MI D. Administer fludrocortisone 0.1 mg orally
Correct answer: B
Rationale: This patient is in adrenal crisis — a life-threatening emergency characterized by severe hypotension, vomiting, altered mental status, and fever in the context of missed steroid doses. The immediate priority is IV hydrocortisone 100 mg bolus. While it is ideal to draw labs before giving steroids, this must not delay treatment in a hemodynamically unstable patient. The nurse should draw labs (cortisol, ACTH, BMP) during IV placement — but the hydrocortisone bolus cannot wait. Option A is incorrect because waiting for a cortisol result in a crashing patient could be fatal. Option C is not the immediate priority given the clear clinical picture of adrenal crisis. Option D is incorrect because oral fludrocortisone is ineffective in crisis (patient is vomiting, unable to absorb oral medications, and fludrocortisone does not address glucocorticoid deficiency).
Question 3
A nurse is educating a patient with Addison’s disease about sick day management. Which statement by the patient indicates a need for further teaching?
A. “I will double my hydrocortisone dose if I develop a fever.” B. “If I start vomiting and can’t keep my pills down, I’ll use my injection kit and go to the ER.” C. “I wear my medical alert bracelet every day in case I’m in an accident.” D. “If I feel a little tired, I’ll skip my afternoon hydrocortisone dose to avoid over-replacement.”
Correct answer: D
Rationale: Skipping steroid doses based on symptom perception is extremely dangerous. Patients with Addison’s disease have no functional adrenal reserve — fatigue may reflect under-replacement (a signal to notify the provider) or normal fluctuation, but skipping doses risks precipitating adrenal crisis. Cortisol replacement must be taken consistently. Option A is correct — doubling the dose for febrile illness is appropriate sick day management. Option B is correct — vomiting that prevents oral absorption requires immediate injection and emergency evaluation; this is the exact scenario in which patients die without recognizing the urgency. Option C is correct and essential — the medical alert bracelet is non-negotiable for unconscious emergency situations.
Question 4
A nurse reviews morning lab results for a patient with suspected adrenal insufficiency. Which combination of findings is most consistent with primary Addison’s disease?
A. Low cortisol, low ACTH, hyponatremia, hypokalemia B. High cortisol, high ACTH, hypernatremia, hypokalemia C. Low cortisol, HIGH ACTH, hyponatremia, hyperkalemia D. Low cortisol, low ACTH, hypernatremia, hyperkalemia
Correct answer: C
Rationale: In primary adrenal insufficiency, the adrenal cortex is destroyed. Cortisol falls, removing negative feedback on the pituitary — ACTH rises dramatically (often >100–200 pg/mL). Aldosterone deficiency causes sodium wasting (hyponatremia) and potassium retention (hyperkalemia). This combination — low cortisol + HIGH ACTH + hyponatremia + hyperkalemia — is the classic electrolyte and hormonal pattern of primary Addison’s disease. Option A describes secondary/tertiary adrenal insufficiency (low ACTH, and hypokalemia is not expected). Option B describes Cushing’s disease (excess cortisol and ACTH). Option D cannot occur: low ACTH with hypernatremia and hyperkalemia is not consistent with any single adrenal disorder pattern.
Question 5
A patient with Addison’s disease is scheduled for an elective appendectomy. The patient asks the nurse why their hydrocortisone dose will be increased around the surgery. Which response by the nurse is most accurate?
A. “Higher steroid doses prevent the surgical wound from becoming infected.” B. “Your body normally increases cortisol output during surgical stress, but your adrenal glands cannot do this — we replace that increase artificially.” C. “The anesthesia medications break down cortisol faster than usual, so you need a larger dose.” D. “The IV fluids used in surgery dilute your cortisol level, so we compensate by giving more.”
Correct answer: B
Rationale: A healthy adrenal gland increases cortisol output significantly during physiologic stress such as surgery (the cortisol stress response can increase 5–10x above baseline). Patients with Addison’s disease have no functional adrenal reserve and cannot mount this response. Without supplemental hydrocortisone (stress dosing), the patient will develop adrenal crisis during or after surgery — severe hypotension refractory to vasopressors, hypoglycemia, and cardiovascular collapse. Stress dosing replaces the cortisol the patient’s own adrenal glands cannot produce. Option A is incorrect — glucocorticoids actually impair wound healing and immune function at high doses. Option C is clinically inaccurate. Option D is not a valid mechanism.
Question 6
The nurse is assessing a patient who has been treated for Addison’s disease for 5 years and is now on stable doses of hydrocortisone and fludrocortisone. The patient reports increasing fatigue, dizziness, salt cravings, and nausea over the past 3 weeks. Blood pressure is 94/58 mmHg. The nurse suspects which problem?
A. Over-replacement of fludrocortisone causing volume overload B. Under-replacement — inadequate steroid dosing relative to current needs C. Hyperglycemia from excess hydrocortisone D. Cushing’s syndrome from long-term steroid use
Correct answer: B
Rationale: The symptoms described — fatigue, dizziness, salt craving, nausea, and hypotension — are classic features of adrenal insufficiency and suggest the current replacement regimen is inadequate. This can occur because the patient’s needs have increased (illness, physiologic stress, life change), adherence has declined, or dosing simply needs adjustment over time. The priority nursing action is to notify the provider and review the current regimen. Option A is incorrect — over-replacement with fludrocortisone would cause hypertension, edema, and hypokalemia, the opposite of the findings. Option C is incorrect — hyperglycemia from excess hydrocortisone would present with polyuria, polydipsia, and elevated glucose. Option D describes findings of cortisol excess (moon face, central obesity, purple striae), which are not present.
Summary: high-yield NCLEX takeaways
- Hyperpigmentation = primary Addison’s = excess ACTH. No hyperpigmentation in secondary or tertiary adrenal insufficiency (ACTH is low in those).
- Lab pattern: low cortisol + HIGH ACTH + hyponatremia + hyperkalemia + hypoglycemia.
- Gold standard diagnosis: ACTH (cosyntropin) stimulation test — cortisol must rise to ≥18 mcg/dL; failure confirms insufficiency.
- Adrenal crisis = emergency: hydrocortisone 100 mg IV bolus + isotonic NS + treat the trigger.
- Stress dosing is mandatory — any illness, surgery, or major physiologic stress requires 2–3× dose increase; vomiting = inject + go to ER.
- Medical alert bracelet is non-negotiable — always on, contains diagnosis and emergency treatment.
- Fludrocortisone = mineralocorticoid, primary Addison’s only — secondary adrenal insufficiency does not require it.
- Hydrocortisone timing mirrors diurnal rhythm — largest dose on waking to peak with natural cortisol.
- Darkening of old scars = classic NCLEX clue for rising ACTH in primary Addison’s.
- Compare with Cushing’s: Addison’s = low BP, low glucose, low Na+, high K+, weight loss, hyperpigmentation. Cushing’s = high BP, high glucose, high Na+, low K+, weight gain, thin/fragile skin.
For further reading on related endocrine disorders, see the hypothyroidism nursing reference, hyperthyroidism nursing reference, Cushing’s syndrome nursing reference, and diabetes mellitus nursing reference. For electrolyte management in adrenal crisis, see the electrolyte imbalances reference and the nursing lab values cheat sheet.