Cushing's syndrome nursing: assessment, interventions, and NCLEX review

Cushing’s syndrome is a clinical disorder caused by prolonged exposure to elevated cortisol, producing a constellation of findings that nursing students must recognize immediately: central obesity, moon face, buffalo hump, purple striae, easy bruising, and proximal muscle weakness. It is a high-yield NCLEX topic because cortisol excess affects virtually every body system — cardiovascular, musculoskeletal, metabolic, immune, and psychiatric — and because the post-operative care after surgical correction carries life-threatening adrenal insufficiency risk. Understanding the Cushing’s disease vs Cushing’s syndrome distinction, interpreting the diagnostic test sequence, and knowing how to safely care for a patient with hypercortisolism are all expected nursing competencies. This reference covers the complete clinical picture from pathophysiology through NCLEX preparation.

Use this page alongside the diabetes mellitus nursing reference for hyperglycemia management, the electrolyte imbalances reference for hypokalemia and fluid volume excess, the hypothyroidism nursing reference and hyperthyroidism nursing reference for the full endocrine cluster, and the nursing lab values cheat sheet for serum cortisol and ACTH interpretation.

Cushing’s syndrome vs Cushing’s disease

This distinction is one of the most tested NCLEX concepts related to adrenal pathology. Many students use the terms interchangeably — but they are not synonymous.

Memory anchor: Cushing’s disease = pituitary disease. If the question specifies a pituitary adenoma, the correct term is Cushing’s disease. If it specifies an adrenal tumor, ectopic ACTH, or steroid use, it is Cushing’s syndrome.

Pathophysiology

Cortisol is produced by the zona fasciculata of the adrenal cortex under regulation of the hypothalamic-pituitary-adrenal (HPA) axis. The hypothalamus releases corticotropin-releasing hormone (CRH), which signals the anterior pituitary to secrete adrenocorticotropic hormone (ACTH). ACTH then stimulates the adrenal cortex to produce cortisol. Rising cortisol levels normally feed back to suppress both CRH and ACTH, maintaining tight physiological control.

In Cushing’s syndrome, this negative feedback loop is overridden. The result is persistently elevated cortisol regardless of physiological need. The downstream effects are global:

• Metabolic: Cortisol increases gluconeogenesis and hepatic glycogenolysis while driving insulin resistance → hyperglycemia and secondary diabetes mellitus
• Protein catabolism: Muscle breakdown → proximal myopathy, thin skin, poor wound healing, purple striae (rapid subcutaneous fat accumulation with skin tearing due to collagen loss)
• Fat redistribution: Visceral and dorsocervical fat accumulation → central obesity, moon face, buffalo hump — with paradoxical loss of fat in extremities
• Mineralocorticoid cross-reactivity: At high concentrations, cortisol activates mineralocorticoid receptors → sodium and water retention, hypokalemia, hypertension
• Immune suppression: Cortisol inhibits lymphocyte proliferation, reduces IL-2 and TNF-alpha, decreases neutrophil migration → increased infection susceptibility
• Bone: Cortisol inhibits osteoblast activity and increases osteoclast activity while reducing intestinal calcium absorption → osteoporosis and fracture risk
• Psychiatric: Glucocorticoid receptors in the hippocampus and prefrontal cortex → depression, cognitive impairment, emotional lability, psychosis in severe cases

Etiology and classification

Clinical differentiator — ectopic ACTH: Ectopic ACTH secretion produces a more severe, rapid-onset syndrome. Because ACTH also stimulates melanocyte-stimulating hormone (MSH), patients often develop hyperpigmentation — a finding not seen in adrenal causes (where ACTH is suppressed) and less prominent in Cushing’s disease. Profound hypokalemia is a hallmark, as markedly elevated cortisol saturates 11β-HSD2 enzyme, allowing cortisol to freely activate mineralocorticoid receptors.

Clinical manifestations

The classic “cushingoid” appearance is one of the most recognizable presentations in all of endocrinology — and a high-yield visual recognition item on NCLEX.

NCLEX clinical pearls:

• Purple striae wider than 1 cm are characteristic; pink/white striae from pregnancy or obesity are narrower and lack the violaceous color
• Proximal myopathy (weakness in hips and shoulders) but intact distal strength distinguishes Cushing’s from peripheral neuropathy
• Hypokalemia in Cushing’s is particularly severe with ectopic ACTH; watch for muscle cramps, weakness, and cardiac arrhythmias

Diagnostic workup

Diagnosis proceeds in two stages: confirm hypercortisolism, then localize the source.

Stage 1 — Confirm hypercortisolism

The Endocrine Society recommends at least two of the following first-line tests:

24-hour urinary free cortisol (UFC): The patient collects all urine over 24 hours; elevated UFC indicates excess cortisol production. Levels more than four times the upper limit of normal are virtually diagnostic of Cushing’s syndrome (this degree of elevation rarely occurs in pseudo-Cushing states). Creatinine is collected simultaneously to verify completeness of collection. False positives occur with high fluid intake (>5 L/day), which dilutes urine but raises total UFC volume.

Late-night salivary cortisol (×2): Cortisol normally reaches its nadir between 11 PM and midnight. In Cushing’s syndrome, this nocturnal nadir is lost — salivary cortisol remains elevated. Two separate measurements on different nights increase reliability. False positives: shift workers with disrupted circadian rhythm, acute illness, tobacco use (nicotine elevates salivary cortisol).

1 mg overnight dexamethasone suppression test (DST): The patient takes 1 mg of dexamethasone at 11 PM; serum cortisol is measured at 8 AM the following morning. Normally, dexamethasone suppresses pituitary ACTH → adrenal cortisol falls below 1.8 mcg/dL. In Cushing’s syndrome, cortisol fails to suppress. Sensitivity is high (~95%); false positives occur with medications that accelerate dexamethasone metabolism (phenytoin, rifampin, carbamazepine), obesity, depression, or alcoholism.

Low-dose DST (2-day): 0.5 mg dexamethasone every 6 hours for 48 hours; cortisol measured 6 hours after final dose. Abnormal if cortisol >1.8 mcg/dL. More specific than the 1 mg test.

Stage 2 — Localize the source

Once hypercortisolism is confirmed, ACTH measurement separates ACTH-dependent from ACTH-independent causes:

• Low ACTH (<10 pg/mL): ACTH-independent → adrenal source → adrenal CT/MRI
• Normal or elevated ACTH (≥20 pg/mL): ACTH-dependent → pituitary vs ectopic → next step is pituitary MRI

High-dose DST (8 mg overnight): 8 mg dexamethasone at 11 PM; cortisol measured at 8 AM. Pituitary adenomas retain some suppressibility (cortisol decreases by ≥50%) because they express glucocorticoid receptors. Ectopic ACTH tumors are autonomous and do not suppress. Sensitivity ~70%; used when imaging is inconclusive.

CRH stimulation test: IV CRH given; ACTH and cortisol measured at intervals. Pituitary adenomas respond with an exaggerated ACTH rise; ectopic sources do not respond. Often combined with inferior petrosal sinus sampling.

Inferior petrosal sinus sampling (IPSS): The gold standard for distinguishing pituitary from ectopic ACTH. Catheters placed in both inferior petrosal sinuses (which drain the pituitary); blood drawn simultaneously from central and peripheral veins before and after CRH. A central-to-peripheral ACTH ratio ≥2:1 (basal) or ≥3:1 (post-CRH) confirms pituitary origin. Side-to-side gradient localizes which half of the pituitary is affected. Invasive procedure — nursing consideration: monitor for venous thrombosis and neurological changes post-procedure.

Imaging:

• Pituitary MRI with gadolinium: First-line imaging for Cushing’s disease; microadenomas (<10 mm) in 40% may be too small to visualize
• Adrenal CT: First-line for ACTH-independent causes; characterizes adenoma vs carcinoma by size and lipid content
• Chest CT: Rules out bronchial carcinoid or small cell lung cancer in ectopic ACTH

Priority nursing assessment

When caring for a patient with Cushing’s syndrome, systematic assessment priorities include:

Vital signs and cardiovascular: Blood pressure (hypertension is universal and often severe), heart rate, oxygen saturation. Fluid retention and hypernatremia drive hypertension. Monitor for hypokalemia-associated dysrhythmias.

Metabolic: Blood glucose (hyperglycemia expected; glucose intolerance progresses to secondary diabetes in 20–40% of cases), daily weight, intake and output, edema assessment.

Musculoskeletal and safety: Muscle strength testing — specifically proximal strength (ask patient to rise from chair without arm support, raise arms overhead). Fall risk assessment. Height measurement for vertebral fracture screening. Assess for bone pain.

Skin: Thorough skin assessment including all pressure points, striae distribution and color, existing bruising, wound healing status. Assess skin turgor. Note any areas of breakdown.

Immune and infection: Baseline temperature (cortisol blunts fever response — a normal temperature does not exclude serious infection). Assess for subtle infection signs: increased fatigue, minimal localized warmth, mild WBC elevation. Monitor CBC differential: leukocytosis with neutrophilia and lymphopenia is expected.

Neuropsychiatric: Mood assessment, depression screening, cognitive status. Document baseline psychiatric symptoms. Involve social work or psychiatric consultation early.

Reproductive: Menstrual history in women; sexual function history in men. Document any changes.

Nursing diagnoses and interventions

Risk for infection

Rationale: Cortisol suppresses lymphocyte proliferation, neutrophil migration, and inflammatory cytokine production. The patient is broadly immunocompromised.

Interventions:

• Maintain strict hand hygiene; apply to all staff and visitors
• Limit exposure to individuals with known infections
• Monitor for atypical infection presentations — fever may be absent or minimal despite serious infection; rely on WBC trends, localized symptoms, and subtle behavioral changes
• Assess catheter sites, IV lines, and wound sites at every shift
• Ensure up-to-date vaccinations (coordinate with provider — live vaccines contraindicated in immunosuppressed patients)
• Educate patient to report any symptom that might indicate infection, however mild

Risk for injury (falls and fractures)

Rationale: Proximal myopathy impairs balance and ability to catch oneself; osteoporosis increases fracture risk from minimal trauma.

Interventions:

• Implement fall precautions: non-slip footwear, bed in lowest position, call light within reach
• Assist with ambulation as needed; physical therapy referral for strengthening
• Avoid activities that require spinal flexion (increases vertebral compression fracture risk)
• Ensure calcium and vitamin D are supplemented per orders
• Request bone density (DEXA) scan per protocol
• Educate patient on fracture risk and movement modifications

Impaired skin integrity

Rationale: Collagen loss, fragile capillaries, thin skin, and poor wound healing create multiple skin integrity risks.

Interventions:

• Handle skin gently — avoid tape directly on skin; use foam or silicone-backed dressings
• Reposition every 2 hours for immobile or low-activity patients
• Assess striae sites for skin breakdown; treat any open areas per wound care protocol
• Avoid constrictive clothing
• Ensure adequate protein intake to support tissue repair
• Document wound healing trajectory — healing is delayed and should be tracked carefully

Fluid volume excess

Rationale: Mineralocorticoid activity causes sodium and water retention; hypertension, edema, and hypokalemia result.

Interventions:

• Monitor daily weight (same scale, same time, same clothing) — 2 lb/day gain indicates fluid retention
• Strict intake and output; assess for dependent edema
• Administer diuretics and antihypertensives per orders; monitor for hypokalemia with diuretics
• Sodium-restricted diet as ordered
• Monitor serum sodium and potassium; potassium replacement per protocol
• Elevate edematous extremities

Disturbed body image

Rationale: Physical changes — central obesity, moon face, buffalo hump, hirsutism, striae — are rapid, dramatic, and distressing.

Interventions:

• Acknowledge the patient’s feelings without minimization; validate that the changes are a medical consequence, not personal failing
• Educate that physical changes typically reverse after successful treatment
• Involve the patient in care decisions to restore a sense of control
• Consult social work or psychology for coping support
• Assess for depression; Cushing’s syndrome carries high rates of major depressive disorder

Activity intolerance

Rationale: Proximal myopathy, fatigue, hyperglycemia, and cardiovascular burden all reduce exercise tolerance.

Interventions:

• Pace activities with planned rest periods; avoid clustering care tasks
• Encourage low-impact activity as tolerated — walking, range of motion exercises
• Physical therapy referral for progressive strengthening program
• Monitor blood glucose before and after activity
• Evaluate for underlying anemia (may co-exist) as contributing factor

Risk for hyperglycemia

Rationale: Insulin resistance and gluconeogenesis drive glucose elevation; secondary diabetes mellitus develops in 20–40%.

Interventions:

• Monitor blood glucose per protocol; report values outside target range promptly
• Administer insulin or oral antihyperglycemic agents per orders
• Dietary consultation for low-glycemic, controlled-carbohydrate meal planning
• Educate patient on glucose monitoring if new-onset diabetes
• Recognize that glucose may normalize after cortisol-lowering treatment

Pharmacological management

Medical therapy is used when surgery is not possible, while awaiting surgery, or when surgery fails to achieve remission. Drugs are classified by their mechanism — steroidogenesis inhibitors (reduce cortisol production), glucocorticoid receptor antagonists, and neuromodulatory agents (reduce ACTH secretion).

Surgical management and post-operative care

Transsphenoidal surgery (TSS)

Transsphenoidal surgery is the first-line treatment for Cushing’s disease (pituitary adenoma). The neurosurgeon approaches the pituitary gland through the nose and sphenoid sinus, removing the adenoma while preserving surrounding normal pituitary tissue.

Remission rates: 65–90% with experienced pituitary surgeons; recurrence occurs in 15–25% within 10 years.

Post-operative nursing care:

• Positioning: Head of bed elevated 30 degrees to reduce cerebral edema and CSF pressure
• Nasal assessment: Monitor nasal packing/drainage; clear or watery discharge may indicate cerebrospinal fluid leak — report immediately (test with glucose dipstick: CSF contains glucose; mucus does not — note this is a bedside screening tool, not definitive)
• Headache management: Expected post-operatively; distinguish from signs of meningitis or increased ICP
• Fluid balance: Diabetes insipidus (DI) is a post-operative complication from disruption of ADH secretion; monitor for polyuria (>200–250 mL/hour), rising serum sodium, increasing serum osmolality, dilute urine (SG <1.005)
• Vision monitoring: Pituitary gland is adjacent to optic chiasm; assess visual fields and acuity post-operatively; any change → neurosurgery notification immediately
• Cortisol monitoring: Serum cortisol is measured at 8 AM on post-operative day 1–3; low cortisol (<2 mcg/dL) indicates successful removal of the adenoma (remaining adrenal glands are still suppressed from chronic ACTH excess)

Critical concept: adrenal insufficiency after surgery

This is the most clinically important post-operative nursing concept for Cushing’s syndrome — and heavily tested on NCLEX.

When cortisol levels have been chronically elevated, the HPA axis adapts by suppressing CRH and ACTH production. After surgical removal of the cortisol-secreting source, the axis cannot immediately recover. The remaining adrenal glands (which have been chronically suppressed) cannot produce adequate cortisol. The patient will develop adrenal insufficiency — this is expected, predictable, and potentially life-threatening if not anticipated.

Management:

• Hydrocortisone replacement is started immediately post-operatively (often as stress-dose IV hydrocortisone: 50–100 mg every 8 hours IV, then tapered over weeks to months as the HPA axis recovers)
• Patient is tapered to physiologic doses (15–25 mg/day in divided doses) as ACTH stimulation testing confirms recovery
• Adrenal recovery may take 6–24 months; some patients require permanent replacement

Signs of adrenal insufficiency / adrenal crisis to monitor post-operatively:

• Hypotension (often refractory to fluids alone)
• Nausea, vomiting, abdominal pain
• Fatigue, weakness, lethargy
• Hyponatremia and hyperkalemia (opposite of Cushing’s — note the reversal)
• Hypoglycemia
• Fever

Nursing action for suspected adrenal crisis: This is a medical emergency. Administer IV hydrocortisone (100 mg bolus) per emergency protocol, aggressive IV fluid resuscitation with normal saline, and glucose supplementation. Notify provider immediately.

Adrenalectomy

Unilateral adrenalectomy is performed for adrenal adenoma or adrenal carcinoma. Bilateral adrenalectomy (BLA) is reserved for ectopic ACTH tumors that cannot be resected or for refractory Cushing’s disease after failed TSS.

Bilateral adrenalectomy considerations:

• Requires lifelong glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone) replacement — permanent adrenal insufficiency
• Risk of Nelson’s syndrome in Cushing’s disease: without cortisol feedback, the residual pituitary adenoma may grow aggressively, causing mass effects and markedly elevated ACTH with resulting hyperpigmentation
• Patients must carry injectable hydrocortisone (Solu-Cortef) emergency kit and wear medical alert identification

Patient and family teaching

Medication safety:

• Never stop corticosteroids abruptly — this risks adrenal crisis. Taper is always required; patients must understand this is a safety issue, not optional
• If vomiting prevents oral medication, parenteral hydrocortisone (IM/IV) is required — patients should have an injectable form at home and know when to use it
• Teach “sick day rules”: double or triple steroid dose during illness, fever, or physical stress per provider guidance

Medical alert identification: All patients on long-term corticosteroids or with adrenal insufficiency post-surgery must wear a medical alert bracelet/necklace stating “adrenal insufficiency — requires cortisol in emergency”

Monitoring:

• Daily weight — same time, same scale; report 2 lb/day gain to provider
• Blood pressure monitoring at home
• Blood glucose monitoring if hyperglycemia has developed
• Signs to report: severe fatigue, nausea/vomiting, dizziness, confusion — may signal adrenal insufficiency

Infection prevention:

• Report any sign of infection promptly — even mild symptoms may indicate serious infection
• Avoid close contact with sick individuals
• Keep vaccinations up to date (discuss live vaccine restrictions with provider)

Physical changes:

• Reassure patient that most physical changes (moon face, central obesity, buffalo hump, striae fading) will gradually improve after successful cortisol normalization — this may take months to years
• Address psychiatric symptoms: depression and cognitive changes often predate physical findings and require specific treatment; counsel that mental health support is an appropriate part of Cushing’s care

Bone health:

• High-calcium, high-vitamin D diet; weight-bearing exercise as tolerated
• Avoid activities with high fall or spinal-load risk until bone density is confirmed

Cushing’s syndrome vs Addison’s disease: comparison table

This comparison table is a high-yield NCLEX anchor — the two classic adrenal cortex disorders are often presented as SATA or prioritization items requiring students to distinguish them rapidly.

Memory anchor: Cushing’s = TOO MUCH cortisol → everything is excessive (hypertension, hyperglycemia, hypernatremia, central obesity, immunosuppression). Addison’s = TOO LITTLE cortisol → everything falls (hypotension, hypoglycemia, hyponatremia, weight loss). Potassium moves opposite to sodium in both cases.

NCLEX practice questions

Question 1

A patient is diagnosed with Cushing’s disease after pituitary MRI reveals a 6 mm adenoma. The nurse understands that which of the following best describes why this condition is called “Cushing’s disease” rather than “Cushing’s syndrome”?

A. Cushing’s disease refers specifically to cases caused by adrenal tumors B. Cushing’s disease is a subtype of Cushing’s syndrome caused by a pituitary ACTH-secreting adenoma C. Cushing’s disease is the term used when the cause is exogenous corticosteroid use D. Cushing’s disease and Cushing’s syndrome are interchangeable terms for the same condition

Correct answer: B

Rationale: Cushing’s syndrome is the broader clinical disorder describing hypercortisolism from any cause. Cushing’s disease is a specific subtype defined by a pituitary ACTH-secreting adenoma (corticotroph adenoma) that drives adrenal cortisol overproduction. Option A is incorrect — adrenal tumors cause ACTH-independent Cushing’s syndrome (not Cushing’s disease). Option C is incorrect — exogenous steroid use causes iatrogenic Cushing’s syndrome, not Cushing’s disease. Option D is incorrect — the terms are not interchangeable and the distinction is clinically meaningful for treatment planning.

Question 2

A nurse is reviewing morning labs for a patient with Cushing’s syndrome. Which set of findings is most consistent with this diagnosis?

A. Serum sodium 128 mEq/L, potassium 5.8 mEq/L, glucose 62 mg/dL B. Serum sodium 148 mEq/L, potassium 3.0 mEq/L, glucose 198 mg/dL C. Serum sodium 138 mEq/L, potassium 4.2 mEq/L, glucose 90 mg/dL D. Serum sodium 130 mEq/L, potassium 4.5 mEq/L, glucose 145 mg/dL

Correct answer: B

Rationale: Cushing’s syndrome produces characteristic electrolyte and metabolic abnormalities driven by cortisol’s mineralocorticoid activity and insulin resistance. Hypernatremia (sodium 148) results from sodium and water retention. Hypokalemia (potassium 3.0) results from potassium wasting as sodium is retained. Hyperglycemia (glucose 198) results from cortisol-driven insulin resistance and increased gluconeogenesis. Option A describes the pattern of Addison’s disease — hyponatremia, hyperkalemia, and hypoglycemia. Option C is normal. Option D shows hyponatremia with normal potassium and mild hyperglycemia — not consistent with the complete Cushing’s picture.

Question 3

A patient with Cushing’s syndrome reports difficulty rising from a chair without using arm support and difficulty raising arms above the head. The nurse interprets these findings as indicating which complication?

A. Peripheral neuropathy from hyperglycemia B. Proximal myopathy from protein catabolism C. Osteoporosis-related vertebral compression fracture D. Fluid retention causing extremity heaviness

Correct answer: B

Rationale: Proximal myopathy — weakness in the large proximal muscle groups of the hips, thighs, and shoulders — is a hallmark manifestation of Cushing’s syndrome caused by cortisol-driven protein catabolism and muscle wasting. The description of difficulty rising from a chair (hip flexor/quadriceps weakness) and difficulty reaching overhead (deltoid/shoulder girdle weakness) with presumably intact distal strength is the classic pattern. Option A (diabetic peripheral neuropathy) produces distal sensory loss and weakness, not proximal predominance. Option C (vertebral compression fracture) would present with back pain and height loss, not this pattern. Option D (fluid retention) would cause generalized heaviness and edema, not this selective proximal pattern.

Question 4

A patient with Cushing’s disease undergoes successful transsphenoidal surgery. On post-operative day 1, the 8 AM serum cortisol is 1.2 mcg/dL. The nurse recognizes this finding as:

A. A sign of surgical failure — cortisol should rise after removing the adenoma B. An expected finding indicating successful adenoma removal; adrenal insufficiency precautions are required C. A normal value requiring no intervention D. A sign of diabetes insipidus — serum cortisol and urine output should be correlated

Correct answer: B

Rationale: A low post-operative serum cortisol (below 2 mcg/dL on day 1–3) after transsphenoidal surgery indicates successful removal of the ACTH-secreting adenoma. The adrenal glands, which have been chronically suppressed by high ACTH and cortisol, cannot immediately recover — they are atrophic and will not produce adequate cortisol. This is an expected and potentially dangerous state of adrenal insufficiency that requires hydrocortisone replacement. The nurse should ensure cortisol replacement is ordered, monitor for signs of adrenal crisis (hypotension, nausea, hyponatremia, hyperkalemia, hypoglycemia), and educate the patient that this replacement may be required for 6–24 months. Option A is incorrect — a low cortisol after surgery is a sign of success, not failure. Option C is incorrect — 1.2 mcg/dL is critically low and requires intervention. Option D is incorrect — diabetes insipidus is monitored via urine output and osmolality, not cortisol.

Question 5

A nurse is caring for a patient who takes long-term prednisone for rheumatoid arthritis. The patient is admitted for elective hip surgery. Which pre-operative nursing action has highest priority?

A. Advise the patient to stop prednisone 48 hours before surgery to reduce infection risk B. Confirm with the provider that stress-dose steroids are ordered for the perioperative period C. Switch the patient to a shorter-acting corticosteroid preoperatively D. Hold the morning prednisone dose on the day of surgery

Correct answer: B

Rationale: Patients on chronic exogenous corticosteroids develop HPA axis suppression — their adrenal glands are chronically suppressed and cannot mount an adequate cortisol stress response to surgical trauma. Without stress-dose steroid coverage (typically hydrocortisone 50–100 mg IV perioperatively), the patient risks adrenal crisis: refractory hypotension, hypoglycemia, and cardiovascular collapse. Confirming that stress-dose steroids are ordered is the highest priority pre-operative nursing action. Option A is critically dangerous — abrupt steroid cessation risks adrenal crisis and would precipitate the exact problem stress dosing prevents. Option C has no clinical basis. Option D is incorrect — holding the dose without replacement could precipitate adrenal insufficiency.

Question 6

A nurse is educating a patient newly diagnosed with Cushing’s syndrome about the 1 mg overnight dexamethasone suppression test ordered for outpatient completion. Which instruction is most important?

A. “Take the 1 mg dexamethasone tablet first thing in the morning and return to the lab within 2 hours” B. “Take the 1 mg dexamethasone tablet at 11 PM, then have your blood drawn at 8 AM the next morning” C. “Collect all urine for 24 hours in the container provided, starting after your first morning void” D. “Avoid eating or drinking anything after midnight before the morning blood draw”

Correct answer: B

Rationale: The 1 mg overnight dexamethasone suppression test requires specific timing: dexamethasone 1 mg is taken at 11 PM, and serum cortisol is measured at 8 AM the following morning. The timing exploits normal cortisol physiology — cortisol reaches its nadir at night, and dexamethasone given at 11 PM should suppress the subsequent early-morning cortisol rise via pituitary ACTH suppression. In normal individuals, the 8 AM cortisol falls below 1.8 mcg/dL. In Cushing’s syndrome, this suppression does not occur. Option A describes the wrong timing — dexamethasone must be taken at night, not morning. Option C describes the 24-hour urine free cortisol test, a different diagnostic study. Option D is incorrect — while fasting may be standard for some bloodwork, the key instruction for this test is the precise timing of dexamethasone ingestion and blood draw, not fasting status.

Summary

Cushing’s syndrome is the clinical consequence of sustained cortisol excess, producing a multi-system syndrome that nursing students must recognize, assess, and manage across acute, pre-operative, and post-operative settings. The core nursing priorities are:

1. Recognition: Central obesity, moon face, buffalo hump, purple striae, proximal myopathy, hypertension, hyperglycemia, and hypokalemia are the classic finding cluster
2. Safety: Infection risk (immunosuppression), fracture risk (osteoporosis), and fall risk (proximal myopathy) require systematic prevention strategies every shift
3. Terminology: Cushing’s disease = pituitary ACTH adenoma. Cushing’s syndrome = any cause of hypercortisolism
4. Diagnostics: First-line tests are 24-h UFC, late-night salivary cortisol (×2), and 1 mg overnight DST. ACTH level distinguishes ACTH-dependent (pituitary/ectopic) from ACTH-independent (adrenal) causes
5. Post-operative vigilance: After surgical removal of the cortisol source, adrenal insufficiency is expected and life-threatening if missed. Cortisol replacement is mandatory; adrenal crisis presents with hypotension, nausea, hyponatremia, hyperkalemia, and hypoglycemia
6. Comparison: Cushing’s syndrome and Addison’s disease are electrolyte and hemodynamic opposites — master this table for NCLEX prioritization questions

Use the ADPIE nursing process reference to structure formal nursing care plans for Cushing’s syndrome patients, and the nursing lab values cheat sheet for serum cortisol, ACTH, sodium, and potassium interpretation.