NLE Endocrine & Metabolic Nursing — Adrenal DisordersCheat Sheet

Common Values

Section Title

Adrenal Gland Anatomy & Physiology

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

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)

Common Values

Section Title

Cushing's Syndrome (TOO MUCH Cortisol)

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

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

Section Title

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

Diagrams To Know

• Steroid taper schedule (gradual reduction timeline)
• Post-operative steroid dosing in adrenalectomy
• HPA axis recovery timeline after adrenalectomy (months to years)

Common Values

Section Title

Addison's Disease (TOO LITTLE Cortisol & Aldosterone)

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

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)

Common Values

Section Title

Addison's Disease - Nursing Management & Patient Teaching

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

Diagrams To Know

• Steroid dosing adjustments during stress (sick-day rules)
• Hydrocortisone + fludrocortisone replacement regimen
• Patient safety checklist for Addison's management

Common Values

Section Title

Addisonian (Adrenal) Crisis - EMERGENCY

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

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

Common Values

Section Title

Pheochromocytoma (Catecholamine Excess)

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

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

Common Values

Section Title

Primary Hyperaldosteronism (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

Diagrams To Know

• Aldosterone excess pathophysiology and the aldosterone escape phenomenon
• Diagnostic algorithm: plasma renin + aldosterone ratio interpretation

Section Title

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

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

Rows

Columns

• Feature
• Cushing's (TOO MUCH Cortisol)
• Addison's (TOO LITTLE Cortisol)

Table Title

Cushing's Syndrome vs. Addison's Disease - Mirror Images

Rows

Columns

• Feature
• Primary Addison's (Cortex Destroyed)
• Secondary (Pituitary/Hypothalamic Failure)

Table Title

Primary vs. Secondary Adrenal Insufficiency

Rows

Columns

• Electrolyte
• Addisonian Crisis
• Septic Shock
• Hypovolemic Shock

Table Title

Adrenal Crisis vs. Other Shock States - Electrolytes Tell the Story

Rows

Columns

• Agent
• Mechanism
• Timing
• Why This Order?

Table Title

Pheochromocytoma Pre-Op Pharmacology - Critical Sequencing