Adrenal Disorders - Cheat Sheet
Your 30-minute rapid-fire reference for Cushing's syndrome, Addison's disease, adrenal crisis, and pheochromocytoma. Master the pathophysiology, electrolyte patterns, and nursing priorities that the NLE tests most frequently.
Adrenal Gland Anatomy & Physiology
Common values
Value
10–20 mcg/dL
Symbol
F
Quantity
Normal fasting cortisol (8 AM)
Value
<3–5 mcg/dL
Symbol
F
Quantity
Normal midnight cortisol
Value
20–90 mcg/24 hr
Symbol
UFC
Quantity
Normal 24-hour urinary free cortisol
Value
10–50 pg/mL (peak 6–8 AM)
Symbol
ACTH
Quantity
Normal ACTH
Important facts
- Cortisol has a diurnal rhythm: highest 6–8 AM, lowest 11 PM–midnight.
- Negative feedback: high cortisol suppresses ACTH; low cortisol stimulates ACTH.
- Hyperpigmentation in primary Addison's is due to HIGH ACTH stimulating melanin production.
- The HPA axis explains why abrupt steroid withdrawal causes adrenal crisis: the gland is suppressed and cannot respond to stress.
- Catecholamines (epinephrine/norepinephrine) account for ~5% of adrenal hormone output but produce dramatic symptoms when excess.
Key definitions
Adrenal Cortex
Example
Cortisol is regulated by ACTH in a negative-feedback loop: high cortisol → low ACTH; low cortisol → high ACTH.
Outer layer producing glucocorticoids (cortisol), mineralocorticoids (aldosterone), and androgens under hypothalamic-pituitary-adrenal (HPA) axis control.
Adrenal Medulla
Example
Released during acute stress, causes tachycardia, hypertension, and increased blood glucose.
Inner layer producing catecholamines (epinephrine and norepinephrine) for fight-or-flight response.
Cortisol (Glucocorticoid)
Example
Elevated fasting cortisol >18 mcg/dL or loss of diurnal variation suggests Cushing's syndrome.
Primary stress hormone that raises blood glucose, suppresses immunity/inflammation, and affects fat/protein metabolism; follows diurnal rhythm (peak 6–8 AM, nadir 11 PM–midnight).
Aldosterone (Mineralocorticoid)
Example
Primary hyperaldosteronism → hypertension + hypokalemia + metabolic alkalosis.
Hormone that retains sodium and water while excreting potassium; controls blood volume and pressure.
Diagrams to know
- The HPA axis: Hypothalamus (CRH) → Pituitary (ACTH) → Adrenal cortex (Cortisol) with negative feedback
- The two zones of the adrenal cortex and their hormones
- Diurnal cortisol curve (peak AM, nadir PM)
Cushing's Syndrome (TOO MUCH Cortisol)
Common values
Value
>90 mcg/24 hr (often much higher)
Symbol
UFC
Quantity
24-hour UFC in Cushing's
Value
>7.5 mcg/dL (loss of suppression)
Symbol
F midnight
Quantity
Midnight cortisol in Cushing's
Value
50–200+ pg/mL
Symbol
ACTH
Quantity
ACTH in Cushing's disease
Value
>200 pg/mL (often >1000)
Symbol
ACTH ectopic
Quantity
ACTH in ectopic ACTH
Value
<3.0 mEq/L (marked hypokalemia)
Symbol
K+
Quantity
Potassium in severe Cushing's (ectopic)
Important facts
- EXOGENOUS steroids are the MOST COMMON cause of Cushing's syndrome (prednisone, dexamethasone, etc.).
- Clinical hallmarks: MOON FACE, BUFFALO HUMP, central/truncal obesity with thin extremities, purple striae, thin skin, easy bruising.
- Metabolic effects: HYPERglycemia, HYPERtension, HYPOkalemia, metabolic alkalosis, fluid/sodium retention, edema.
- Psychiatric effects: mood changes, anxiety, insomnia, psychosis (especially with ectopic ACTH or high ACTH levels).
- Immune suppression: increased infection risk, but signs are MASKED because cortisol suppresses inflammation—watch for low-grade/atypical presentations.
- In women: hirsutism, acne, clitoromegaly, male-pattern baldness (excess androgens).
- Osteoporosis is universal; pathologic fractures are common even in younger patients.
- Dexamethasone suppression test (low-dose): normal cortisol suppresses; in Cushing's, cortisol remains elevated. High-dose suppression helps localize: pituitary disease suppresses (ACTH tumor responds to high dose); ectopic/adrenal do not.
- ACTH level is the KEY to localization: HIGH ACTH = pituitary or ectopic (ectopic is usually VERY high); LOW/NORMAL ACTH = adrenal tumor.
- Midnight cortisol or late-night salivary cortisol loss of suppression is a screening test (loss of diurnal variation).
Key definitions
Cushing's Syndrome
Example
Patient on prednisone 20 mg daily for 6 months develops moon face, central obesity, and easy bruising.
Chronic excess glucocorticoid from any source (exogenous or endogenous); most common cause is long-term corticosteroid therapy.
Cushing's Disease
Example
ACTH-secreting pituitary adenoma → high ACTH → high cortisol.
Endogenous Cushing's syndrome specifically caused by a pituitary ACTH-secreting tumor; accounts for ~60% of endogenous cases.
Ectopic ACTH Syndrome
Example
Small cell lung cancer secreting ACTH → very high ACTH + very high cortisol with marked hypokalemia.
Non-pituitary tumor (often small cell lung cancer) secreting ACTH; causes severe hypokalemia and metabolic alkalosis.
Diagrams to know
- Dexamethasone suppression testing algorithm (low-dose vs. high-dose)
- ACTH-driven vs. non-ACTH-driven Cushing's decision tree
- The feedback loop: exogenous steroids → suppress ACTH → suppress native adrenal production
Cushing's Syndrome - Nursing Management & Pharmacology
Important facts
- NEVER STOP STEROIDS ABRUPTLY—always taper to prevent adrenal crisis.
- Take steroids with food (ulcer/GI irritation risk) and in the MORNING (mimics natural peak, reduces insomnia).
- Increase steroid dose during stress: illness, fever, surgery, trauma, or severe emotional stress.
- Monitor blood glucose, blood pressure, weight, I&O, and electrolytes (especially K+, Na+) closely.
- PROTECT FROM INFECTION: fragile skin, poor healing, masked infection signs, immunosuppression; high infection risk despite absent or low-grade signs.
- Fall/injury prevention: osteoporosis + thin, fragile skin → easy fracture/bruising.
- Diet: LOW SODIUM (reduce hypertension/fluid retention), HIGH PROTEIN (combat muscle loss), HIGH POTASSIUM (replace losses), HIGH CALCIUM + VITAMIN D (bone protection).
- Post-adrenalectomy: becomes dependent on lifelong steroid replacement; monitor closely for hypotension/adrenal insufficiency or over-replacement effects.
- After unilateral adrenalectomy: the remaining gland is suppressed (high endogenous cortisol suppressed ACTH) and may take months to recover function.
- Post-op adrenalectomy care: HIGH-DOSE IV steroids peri-operatively (100–200 mg hydrocortisone), then taper as cortisol recovers; monitor vital signs for hemorrhage/shock (adrenal glands are highly vascular).
Key definitions
Steroid Taper
Example
Reduce prednisone by 2.5–5 mg every 1–2 weeks depending on dose and duration; never stop abruptly.
Gradual reduction of exogenous corticosteroids to allow the suppressed HPA axis to recover and resume cortisol production; prevents adrenal crisis.
Stress Dosing
Example
Patient on hydrocortisone 20 mg daily during surgery receives 50–100 mg IV/IM before and during procedure, then tapers post-op.
Temporary increase in corticosteroid dose during physical/emotional stress to meet increased cortisol demand; required during illness, surgery, or trauma.
Diagrams to know
- Steroid taper schedule (gradual reduction timeline)
- Post-operative steroid dosing in adrenalectomy
- HPA axis recovery timeline after adrenalectomy (months to years)
Addison's Disease (TOO LITTLE Cortisol & Aldosterone)
Common values
Value
<3–5 mcg/dL
Symbol
F
Quantity
Fasting cortisol in Addison's
Value
>100 pg/mL (often 200–1000+)
Symbol
ACTH
Quantity
ACTH in primary Addison's
Value
<10 pg/mL
Symbol
ACTH
Quantity
ACTH in secondary insufficiency
Value
<130 mEq/L (hyponatremia)
Symbol
Na+
Quantity
Sodium in Addison's
Value
>5.5 mEq/L (hyperkalemia)
Symbol
K+
Quantity
Potassium in Addison's
Value
<70 mg/dL (hypoglycemia, fasting)
Symbol
Glc
Quantity
Glucose in Addison's
Important facts
- PRIMARY ADDISON'S (autoimmune, ~90% of cases in developed countries) presents with cortisol AND aldosterone deficiency.
- SECONDARY insufficiency (pituitary/hypothalamic) preserves some aldosterone function (from adrenal responsiveness to angiotensin II).
- Manifestations are the MIRROR IMAGE of Cushing's: HYPOtension (not hypertension), HYPONATREMIA (not hypernatremia), HYPERKALEMIA (not hypokalemia), HYPOglycemia (not hyperglycemia).
- HYPERPIGMENTATION (bronze/tan skin) is pathognomonic for primary Addison's; skin darkening in creases, lips, gums, and knuckles.
- Salt craving is a classic sign (low aldosterone → sodium loss).
- GI symptoms: anorexia, nausea, vomiting, diarrhea, abdominal pain (can mimic acute abdomen).
- Fatigue and muscle weakness are universal and profound.
- Loss of adrenal androgens in women causes loss of axillary/pubic hair.
- ACTH STIMULATION TEST: give synthetic ACTH (cosyntropin)—in primary Addison's, cortisol FAILS TO RISE (gland is destroyed); in secondary, cortisol RISES (gland is intact but not stimulated).
- ACTH level: HIGH in primary (gland destroyed, pituitary trying to stimulate), LOW in secondary (pituitary/hypothalamic failure).
- Early morning fasting cortisol <3 mcg/dL is highly suggestive; combined with high ACTH = primary Addison's.
Key definitions
Primary Addison's Disease
Example
Autoimmune destruction of adrenal cortex → hypotension, hyponatremia, hyperkalemia, hyperpigmentation, and high ACTH.
Adrenal cortex hypofunction (usually autoimmune destruction) → deficient cortisol AND aldosterone; ACTH is HIGH (trying to stimulate the dead gland).
Secondary Adrenal Insufficiency
Example
Patient on long-term prednisone suddenly stops → low cortisol, low ACTH, and risk of crisis; or pituitary tumor removes ACTH.
Pituitary ACTH deficiency or abrupt withdrawal of long-term steroids → low cortisol but LOW ACTH (no pituitary stimulation); aldosterone may be preserved (still has some adrenal responsiveness).
Hyperpigmentation (Bronze Skin)
Example
Patient with Addison's has bronze discoloration of skin, especially in sun-exposed areas and creases; knuckles and lips darkened.
In primary Addison's, the chronically HIGH ACTH stimulates melanocytes to produce excess melanin, causing a distinctive tan/bronze appearance.
Diagrams to know
- Comparison of primary vs. secondary Addison's (ACTH levels, aldosterone, clinical presentation)
- ACTH stimulation test interpretation algorithm
- Timeline of symptom development in Addison's (acute vs. chronic onset)
Addison's Disease - Nursing Management & Patient Teaching
Common values
Value
15–25 mg/day (divided 10–15 AM + 5–10 PM)
Symbol
Hydrocortisone
Quantity
Hydrocortisone maintenance dose
Value
0.1 mg/day
Symbol
Fludrocortisone
Quantity
Fludrocortisone dose
Value
25–50 mg/day extra
Symbol
HC stress
Quantity
Hydrocortisone stress dose (minor surgery/illness)
Value
50–100 mg IV/IM q 6–8 hr
Symbol
HC major
Quantity
Hydrocortisone dose (major surgery/ICU)
Important facts
- GLUCOCORTICOID replacement: hydrocortisone 15–25 mg/day (in divided doses: 10–15 mg AM, 5–10 mg PM) or prednisone 5–7.5 mg/day.
- MINERALOCORTICOID replacement: fludrocortisone 0.05–0.2 mg/day (usually 0.1 mg); suppresses renin and maintains sodium/BP.
- MUST INCREASE DOSE during stress, illness, surgery, trauma, fever, or severe emotional stress to prevent crisis.
- NEVER STOP STEROIDS ABRUPTLY—taper any changes over weeks.
- MEDICAL ALERT BRACELET is mandatory; patient must carry it always.
- EMERGENCY HYDROCORTISONE KIT (injectable): patient should carry a syringe/kit to self-inject 50–100 mg IM/IV during crisis or if unable to take oral meds.
- Dietary sodium is encouraged (low aldosterone → sodium loss); patient should add salt to meals and avoid sodium restrictions.
- Monitor electrolytes regularly: Na+, K+, and glucose; adjust fludrocortisone if persistent hyponatremia or hypokalemia.
- Patient education on signs of under-replacement (fatigue, weakness, nausea, hypotension) vs. over-replacement (insomnia, mood changes, hyperglycemia, hypertension).
- Pregnancy: steroid dose may need to increase; coordinate with endocrinologist; risk of crisis during labor/delivery.
Key definitions
Lifelong Hormone Replacement
Example
Typical regimen: hydrocortisone 20 mg AM + 10 mg PM + fludrocortisone 0.1 mg daily; doses adjusted based on symptoms and electrolytes.
Patient with Addison's requires permanent glucocorticoid (hydrocortisone/prednisone) and mineralocorticoid (fludrocortisone) replacement therapy.
Sick-Day Rules
Example
Patient with flu doubles steroid dose until fever breaks; patient undergoing dental procedure takes extra hydrocortisone before and after.
During illness, fever, surgery, or stress, the patient increases steroid dose to meet elevated cortisol demand; failure to do so risks adrenal crisis.
Diagrams to know
- Steroid dosing adjustments during stress (sick-day rules)
- Hydrocortisone + fludrocortisone replacement regimen
- Patient safety checklist for Addison's management
Addisonian (Adrenal) Crisis - EMERGENCY
Common values
Value
50–100 mg IV push
Symbol
HC STAT
Quantity
IV hydrocortisone STAT dose
Value
50–100 mg IV q 6–8 hr
Symbol
HC acute
Quantity
Hydrocortisone maintenance (acute phase)
Value
<120 mEq/L (severe hyponatremia)
Symbol
Na+
Quantity
Sodium in adrenal crisis
Value
>6.5 mEq/L (severe hyperkalemia)
Symbol
K+
Quantity
Potassium in adrenal crisis
Value
<50 mg/dL (severe hypoglycemia)
Symbol
Glc
Quantity
Glucose in adrenal crisis
Important facts
- PRECIPITATING FACTORS: infection, trauma, surgery, acute illness, dehydration, abrupt steroid withdrawal, heat stress, or emotional trauma in a patient with adrenal insufficiency.
- HALLMARK SIGNS: profound HYPOTENSION → cardiogenic shock, severe HYPONATREMIA + HYPERKALEMIA, severe HYPOGLYCEMIA, high fever, severe vomiting/diarrhea/dehydration.
- CARDIAC RISK: hyperkalemia → peaked T waves, widened QRS, arrhythmias, cardiac arrest.
- IMMEDIATE PRIORITY MANAGEMENT: (1) IV HYDROCORTISONE 50–100 mg STAT, then 50–100 mg IV q 6–8 hr; (2) IV normal saline with 5% dextrose to correct hypovolemia, hyponatremia, and hypoglycemia; (3) Treat hyperkalemia (calcium gluconate, insulin/glucose, sodium bicarbonate, furosemide, kayexalate); (4) Monitor cardiac rhythm and vital signs continuously; (5) Identify and treat the trigger; (6) Minimize all stressors.
- FLUIDS: start with RAPID IV normal saline (500 mL to 1 L over 30–60 min), then add 5% dextrose (correct hypoglycemia); may need 3–5 L in first 24 hours depending on volume deficit.
- ELECTROLYTES: severe hyponatremia often CANNOT be corrected rapidly (risk of cerebral edema); sodium rises as volume is repleted and steroids work. Hyperkalemia must be treated urgently (peaked T waves → arrhythmia risk).
- GLUCOSE: may be profoundly low (<40 mg/dL); monitor fingerstick glucose frequently and correct with IV dextrose.
- After initial stabilization: hydrocortisone dose is gradually tapered as patient improves; transition to oral maintenance doses.
- Monitor urine output (may be oliguric if severely dehydrated); watch for signs of infection/sepsis (the likely trigger).
- PREVENTION is KEY: patient education on sick-day rules, emergency kit, and medical alert bracelet.
Key definitions
Addisonian Crisis (Adrenal Crisis)
Example
Patient with undiagnosed Addison's develops fever/infection → sudden hypotension, severe hyponatremia (Na+ 120), hyperkalemia (K+ 6.5), hypoglycemia, and vascular collapse.
Acute, life-threatening deficiency of cortisol and aldosterone triggered by stress, infection, trauma, surgery, or abrupt steroid withdrawal; presents as shock with severe electrolyte abnormalities.
Diagrams to know
- Adrenal crisis management flowchart (immediate steps and ongoing monitoring)
- Electrolyte changes in adrenal crisis and treatment priorities
- Timeline of hydrocortisone dosing and tapering post-crisis
Pheochromocytoma (Catecholamine Excess)
Common values
Value
<90 mcg/24 hr
Symbol
Metanephrines
Quantity
Normal 24-hour urine metanephrines
Value
<8 mg/24 hr
Symbol
VMA
Quantity
Normal 24-hour urine VMA
Value
<50 pg/mL
Symbol
Epi
Quantity
Plasma epinephrine (supine)
Value
<400 pg/mL
Symbol
NE
Quantity
Plasma norepinephrine (supine)
Value
>180 mmHg systolic (often 200–250+)
Symbol
BP crisis
Quantity
BP during pheochromocytoma crisis
Important facts
- RULE OF 10s: ~10% are bilateral, ~10% are extra-adrenal, ~10% are malignant, ~10% are familial (associated with MEN 2A/2B, NF1, VHL syndrome).
- MANIFESTATIONS: CLASSIC TRIAD (headache + palpitations + diaphoresis), SEVERE PAROXYSMAL HYPERTENSION, anxiety, tremor, chest/abdominal pain, pallor, flushing, hyperglycemia, weight loss.
- Episodes are EPISODIC (paroxysmal), lasting minutes to hours; may be triggered by abdominal pressure, exercise, certain foods (tyramine), or medications.
- Between episodes: patient may be asymptomatic or have sustained hypertension.
- DANGER: uncontrolled pheochromocytoma can cause hypertensive crisis, myocardial infarction, stroke, arrhythmias, pulmonary edema, or acute coronary syndrome.
- DIAGNOSIS: 24-hour urine metanephrines + VMA (plasma catecholamines less reliable due to episodic release); CT/MRI to locate tumor; avoid palpating the abdomen (can trigger release).
- Avoid triggers before diagnosis: NSAIDs, decongestants, tricyclic antidepressants, metoclopramide, and tyramine-rich foods.
- TREATMENT: surgical adrenalectomy is definitive.
- PRE-OP management is CRITICAL: ALPHA-BLOCKERS FIRST (phenoxybenzamine or doxazosin) to block alpha-adrenergic effects and prevent hypertensive crisis. ONLY AFTER alpha-blockade is controlled, add BETA-BLOCKERS (e.g., propranolol) if tachycardia persists. NEVER give beta-blocker first/alone—unopposed alpha stimulation causes severe hypertensive crisis.
- POST-OP: monitor for HYPOTENSION (catecholamine levels drop dramatically after tumor removal), arrhythmias, and adrenal insufficiency if bilateral.
Key definitions
Pheochromocytoma
Example
Patient with episodic severe headache, palpitations, and diaphoresis found to have 24-hour urine metanephrines 5× normal; CT shows 3 cm adrenal mass.
Catecholamine-secreting tumor of the adrenal MEDULLA (95% of cases) or extra-adrenal paraganglia (5%); releases excess epinephrine and norepinephrine causing episodic hypertensive crises.
Classic Triad
Example
Patient experiences sudden-onset severe frontal headache with heart racing and soaking sweats; event lasts 15–30 minutes then resolves; happens episodically.
The pathognomonic presentation of pheochromocytoma: SEVERE HEADACHE + PALPITATIONS/TACHYCARDIA + PROFUSE DIAPHORESIS.
Paroxysmal Hypertension
Example
BP baseline 140/90 mmHg, but during attack spikes to 220/120 mmHg for 20 minutes; returns to baseline post-episode.
Episodic, severe elevations in blood pressure (often >180 mmHg systolic) triggered by catecholamine surges; between episodes BP may be normal or mildly elevated.
Diagrams to know
- Pre-operative pharmacological management algorithm (alpha-blocker FIRST, then beta-blocker)
- Pheochromocytoma episode cascade (trigger → catecholamine release → symptoms)
- 24-hour urine metanephrine test collection and interpretation
Primary Hyperaldosteronism (Conn's Syndrome)
Common values
Value
0.5–1.5 ng/mL/hr
Symbol
PRA
Quantity
Normal plasma renin activity
Value
5–15 ng/dL
Symbol
Aldo
Quantity
Normal aldosterone
Value
>20–30
Symbol
Aldo/PRA
Quantity
Renin/aldosterone ratio (diagnostic)
Value
<3.5 mEq/L (hypokalemia)
Symbol
K+
Quantity
Potassium in Conn's syndrome
Important facts
- MANIFESTATIONS: HYPERTENSION (often difficult to control, resistant to standard drugs), HYPOKALEMIA (muscle weakness, cramping, palpitations, polyuria/nocturia), METABOLIC ALKALOSIS, headache.
- DISTINCTIVE FEATURE: edema is typically ABSENT despite sodium retention (the 'aldosterone escape' phenomenon—initial sodium retention → plasma expansion → increased ANP and pressure natriuresis → excretion of excess sodium, but potassium loss continues).
- DIAGNOSIS: suppressed plasma renin activity (<1 ng/mL/hr) + elevated aldosterone (>15 ng/dL); ratio of aldosterone to renin >20–30 is diagnostic; adrenal imaging (CT/MRI) to identify adenoma.
- MANAGEMENT: potassium-sparing diuretic SPIRONOLACTONE (aldosterone antagonist) or amiloride (ENaC blocker) to block aldosterone effects; correct hypokalemia with potassium supplementation; reduce sodium intake.
- SURGICAL adrenalectomy for confirmed adenoma; medical management (spironolactone) for bilateral hyperplasia.
- Monitor blood pressure, potassium, and acid-base status closely during treatment.
Key definitions
Primary Hyperaldosteronism (Conn's Syndrome)
Example
Patient with hypertension refractory to 3 antihypertensive drugs found to have low renin, high aldosterone, and hypokalemia; adrenal CT shows 1 cm nodule.
Aldosterone-secreting adrenal adenoma causing excess sodium/water retention and potassium loss; manifests as resistant hypertension with hypokalemia but often WITHOUT edema.
Diagrams to know
- Aldosterone excess pathophysiology and the aldosterone escape phenomenon
- Diagnostic algorithm: plasma renin + aldosterone ratio interpretation
Corticosteroid Therapy - The Cross-Cutting Teaching Point
Important facts
- GOLDEN RULE: NEVER STOP STEROIDS ABRUPTLY—always TAPER (gradual reduction over weeks to months).
- Tapering prevents adrenal crisis by allowing the HPA axis to recover and native cortisol production to resume.
- Take steroids WITH FOOD (reduce GI ulceration/irritation risk) and in the MORNING (mimics natural peak, reduces insomnia).
- INCREASE dose during STRESS: fever, infection, illness, surgery, trauma, emotional stress—the 'stress response' requires extra cortisol.
- Manifestations of OVER-replacement: hyperglycemia, hypertension, hypokalemia, fluid retention, mood changes, insomnia, osteoporosis (chronic).
- Manifestations of UNDER-replacement: fatigue, weakness, nausea, hypotension, hypoglycemia, salt craving.
- INFECTION RISK: steroids suppress immune response and inflammation—infections may be atypical, low-grade, or present late with minimal signs (e.g., pneumonia without fever/cough).
- MASKING effect: steroids suppress fever and inflammatory signs; monitor carefully for hidden infection.
- MONITOR: blood glucose, blood pressure, weight, I&O, electrolytes (K+, Na+), and signs of infection (ask about subtle symptoms).
- LONG-TERM effects: osteoporosis (prophylaxis with calcium/vitamin D), GI ulcers (PPI use), myopathy (muscle weakness), psychiatric effects, cataract formation.
Key definitions
Steroid Suppression
Example
Patient on prednisone 20 mg daily for 3 months stops abruptly; the adrenal glands are shrunken and cannot respond to stress → adrenal crisis within days.
Long-term exogenous corticosteroids suppress the HPA axis by negative feedback, causing the pituitary to reduce ACTH and the adrenal cortex to atrophy and stop producing cortisol; can persist for months after discontinuation.
Diagrams to know
- Timeline of HPA axis suppression and recovery with long-term steroid therapy
- Steroid tapering schedule example
- Stress dosing algorithm during acute illness/surgery
Must remember
- CUSHING'S = TOO MUCH cortisol: moon face, buffalo hump, truncal obesity with thin limbs, purple striae, easy bruising, HYPERglycemia, HYPERtension, HYPOkalemia, osteoporosis. Most common cause is long-term corticosteroid therapy (exogenous).
- ADDISON'S = TOO LITTLE cortisol/aldosterone: HYPOtension, HYPONATREMIA, HYPERKALEMIA, HYPOglycemia, weight loss, HYPERPIGMENTATION (bronze skin), salt craving. Most common endogenous cause is autoimmune; most common iatrogenic cause is abrupt steroid withdrawal.
- ADRENAL CRISIS = EMERGENCY: hypotension → shock, severe hyponatremia + hyperkalemia, hypoglycemia, high fever, severe vomiting/diarrhea. IMMEDIATE treatment: IV hydrocortisone 50–100 mg STAT + IV normal saline with dextrose + treat hyperkalemia.
- NEVER STOP STEROIDS ABRUPTLY—always taper. Abrupt withdrawal → adrenal insufficiency/crisis because the HPA axis is suppressed and cannot respond to stress.
- PHEOCHROMOCYTOMA = Classic triad: SEVERE HEADACHE + PALPITATIONS + DIAPHORESIS + severe paroxysmal HYPERTENSION. Diagnosis: 24-hour urine metanephrines/VMA. Pre-op: ALPHA-BLOCKER FIRST, then beta-blocker (never beta-blocker alone—causes hypertensive crisis). DO NOT palpate abdomen (triggers release).
- Electrolytes tell the story: Cushing's = high Na+/low K+; Addison's = low Na+/high K+. Addisonian crisis = severe hyponatremia + severe hyperkalemia + hypoglycemia.
- ACTH localization: HIGH ACTH (pituitary or ectopic disease); LOW ACTH (adrenal tumor or secondary insufficiency). In PRIMARY Addison's, ACTH is very HIGH; in secondary, ACTH is LOW.
- ADDISON'S patient teaching (life-saving): NEVER stop steroids; INCREASE dose during stress/illness (sick-day rules); carry medical alert bracelet + emergency hydrocortisone kit; lifelong hydrocortisone + fludrocortisone replacement.
- POST-ADRENALECTOMY: become dependent on LIFELONG steroid replacement; peri-operative HIGH-DOSE IV steroids (100–200 mg hydrocortisone), then taper; monitor for hypotension/adrenal insufficiency or over-replacement.
- Corticosteroid teaching (applies to all steroid therapy): take with food + morning timing; increase during stress; monitor glucose, BP, K+, weight; watch for masked infection; osteoporosis risk; never stop abruptly.
Last minute tips
- READ THE ELECTROLYTES FIRST: Hypertension + hypokalemia = likely Cushing's. Hypotension + hyponatremia + hyperkalemia = likely Addison's or crisis. This single pattern often tells you the diagnosis before reading the clinical story.
- PHEOCHROMOCYTOMA PRE-OP SEQUENCE IS CRITICAL: If the question says 'alpha-blocker' and 'beta-blocker,' you MUST give alpha FIRST or you will trigger a hypertensive crisis. This is a high-yield, must-know detail that appears frequently on exams.
- ADDISONIAN CRISIS IS AN ACUITY LADDER: You will see a patient with Addison's → exposed to a stressor (surgery/infection/dehydration) → develops crisis. Recognize that the stressor triggers the crisis, and IV hydrocortisone + IV dextrose saline are the instant priorities—not vasopressors or dialysis.
- STEROID TAPER IS NON-NEGOTIABLE: Any question about stopping steroids, the answer involves tapering. Sudden withdrawal in a patient on long-term steroids = adrenal crisis. This concept is tested repeatedly.
- HYPERPIGMENTATION IN ADDISON'S = ACTH-DRIVEN: High ACTH stimulates melanocytes → bronze skin (especially in creases, lips, gums). This is pathognomonic for PRIMARY Addison's, not secondary. Use this clinical pearl to localize the problem quickly.
Comparison tables
Cushing's Syndrome vs. Addison's Disease - Mirror Images
| Feature | Cushing's (TOO MUCH Cortisol) | Addison's (TOO LITTLE Cortisol) |
|---|---|---|
| Blood Pressure | HYPERtension (often >150/90) | HYPOtension (often <90 systolic) |
| Sodium (Na+) | HIGH (retention, >145 mEq/L) | LOW (loss, <130 mEq/L) |
| Potassium (K+) | LOW (loss, <3.5 mEq/L) | HIGH (retention, >5.5 mEq/L) |
| Glucose | HIGH (hyperglycemia, impaired glucose tolerance) | LOW (hypoglycemia, fasting) |
| Weight | GAIN (central/truncal obesity, thin limbs) | LOSS (anorexia, GI symptoms) |
| Skin | Thin, fragile, purple striae, easy bruising, poor healing | Hyperpigmentation (bronze), salt craving, normal texture |
| Muscle | Wasting, weakness (proximal) | Weakness, fatigue |
| Mood | Mood changes, anxiety, insomnia, psychosis | Depression, apathy (from fatigue/malaise) |
| Infection Signs | MASKED (low fever, minimal inflammation) | May be profound but not masked |
| ACTH in Primary Disease | LOW-to-NORMAL (negative feedback from high cortisol) | HIGH (trying to stimulate dead gland) |
Primary vs. Secondary Adrenal Insufficiency
| Feature | Primary Addison's (Cortex Destroyed) | Secondary (Pituitary/Hypothalamic Failure) |
|---|---|---|
| Cause | Autoimmune (most), TB, adrenalectomy, infection | Pituitary tumor, surgery, radiation; abrupt steroid withdrawal |
| Cortisol | LOW (<3–5 mcg/dL) | LOW (<3–5 mcg/dL) |
| ACTH | HIGH (>100 pg/mL; gland is dead, pituitary trying) | LOW (<10 pg/mL; no pituitary stimulation) |
| Aldosterone | LOW (both zones destroyed) | Normal-to-low (adrenal still responsive to Ang II) |
| Electrolytes | Severe: Na+ <130, K+ >5.5 | Mild-to-moderate: Na+ 130–135, K+ mildly elevated |
| Hyperpigmentation | YES (high ACTH → melanin) | NO (low ACTH) |
| Salt Craving | YES (low aldosterone) | Usually NO (aldosterone preserved) |
| ACTH Stim Test | Cortisol FAILS to rise (gland destroyed) | Cortisol RISES (intact gland, needs stimulation) |
| Replacement | Glucocorticoid + MINERALOCORTICOID (fludrocortisone) | Glucocorticoid ONLY (aldosterone usually preserved) |
Adrenal Crisis vs. Other Shock States - Electrolytes Tell the Story
| Electrolyte | Addisonian Crisis | Septic Shock | Hypovolemic Shock |
|---|---|---|---|
| Sodium (Na+) | <120 mEq/L (severe) | Normal-to-low | High (hemoconcentration) or normal |
| Potassium (K+) | >6.5 mEq/L (severe) | Normal-to-low | High (hemoconcentration) or normal |
| Glucose | <40 mg/dL (profound hypoglycemia) | Variable (often high) | Normal-to-high |
| Cortisol | <3 mcg/dL (insufficient for stress) | High (appropriate response) | High (appropriate response) |
Pheochromocytoma Pre-Op Pharmacology - Critical Sequencing
| Agent | Mechanism | Timing | Why This Order? |
|---|---|---|---|
| Alpha-Blocker (Phenoxybenzamine/Doxazosin) | Blocks alpha-adrenergic receptors → prevents vasoconstriction | FIRST—start days to weeks before surgery | If not given first, unopposed alpha stimulation causes life-threatening hypertensive crisis |
| Beta-Blocker (Propranolol/Atenolol) | Blocks beta-adrenergic receptors → slows heart rate, reduces contractility | AFTER alpha-blocker is titrated and hypertension controlled | Prevents reflex tachycardia from alpha blockade; never give FIRST alone (causes hypertensive crisis) |
| Calcium Channel Blocker (Optional) | Additional BP control | May be added if alpha/beta insufficient | Provides additional vasodilation without adrenergic interaction |
Diagrams
Cushing's Syndrome - Diagnostic Algorithm: Localizing the Source
Step-by-step algorithm showing how to differentiate between pituitary Cushing's disease, ectopic ACTH, and adrenal tumors using dexamethasone suppression and ACTH measurement.
Addisonian Crisis - Immediate Management Flowchart
Critical step-by-step management flowchart for adrenal crisis showing immediate interventions, monitoring, and transition to maintenance therapy.
Adrenal Disorders Overview - All Four Major Conditions
Comprehensive mind map showing all four major adrenal disorders, their key pathophysiology, and management principles at a glance.
HPA Axis: Normal Feedback vs. Disruption in Adrenal Disease
State diagram showing how the HPA axis normally maintains balance and how it breaks down in Cushing's disease, Addison's disease, and steroid-induced insufficiency.
Pheochromocytoma Pre-Op Pharmacological Preparation - DO NOT REVERSE THE ORDER
Critical flowchart emphasizing the mandatory sequence: alpha-blocker FIRST, beta-blocker SECOND. Reversal of this order causes life-threatening hypertensive crisis.
Natural History and Complications - Cushing's vs. Addison's
Timeline showing the progressive nature of untreated Cushing's and Addison's disease and their major complications without intervention.