What is the most likely diagnosis in a 48‑year‑old female with progressive weight gain, moon face, central obesity, thin fragile skin with purple abdominal striae, easy bruising, proximal muscle weakness, hypertension, hyperglycemia, hypokalemia, and elevated serum cortisol and ACTH?

Cushing's Disease (ACTH-Dependent Cushing's Syndrome)

This patient has Cushing's disease—a pituitary adenoma secreting excessive ACTH, driving bilateral adrenal cortisol overproduction. The combination of classic cushingoid features (moon face, central obesity, purple striae >1 cm, proximal muscle weakness, easy bruising), hypertension, hyperglycemia, hypokalemia, and critically, elevated ACTH with elevated cortisol definitively indicates ACTH-dependent Cushing's syndrome, with pituitary adenoma being the cause in 75-80% of cases 1, 2.

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CJMM Phase 1: Recognize Cues

Four Abnormal Assessment Findings:

• Moon face with central (truncal) obesity and thin extremities – pathognomonic redistribution of fat from chronic hypercortisolism 3, 2
• Wide purple abdominal striae – striae ≥1 cm are a key discriminator distinguishing pathologic Cushing's from simple obesity or metabolic syndrome 2
• Proximal muscle weakness – glucocorticoid-induced myopathy affecting hip flexors and shoulder girdle, causing difficulty rising from chairs 2
• Hypertension (162/94 mm Hg) – occurs in 70-90% of Cushing's patients due to mineralocorticoid receptor activation by excess cortisol and multiple cardiovascular pathways 2

Two Abnormal Laboratory Values:

• Elevated serum cortisol with elevated ACTH – this combination confirms ACTH-dependent Cushing's syndrome; any ACTH >5 ng/L with hypercortisolism indicates pituitary or ectopic source rather than adrenal adenoma 1
• Hypokalemia (3.1 mEq/L) – results from mineralocorticoid effects of excess cortisol on renal sodium/potassium handling 3, 2

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CJMM Phase 2: Analyze Cues

How Elevated Cortisol Contributes to Physical Appearance and Symptoms:

Cortisol excess causes multisystem pathophysiologic changes 2, 4:

• Fat redistribution: Glucocorticoids promote central adiposity (truncal obesity, moon face, buffalo hump, supraclavicular fat pads) while causing peripheral fat wasting and muscle breakdown 2
• Skin changes: Cortisol inhibits collagen synthesis, causing thin fragile skin, easy bruising, and wide purple striae from dermal tearing 2, 4
• Muscle weakness: Direct catabolic effects on skeletal muscle protein, particularly affecting proximal muscle groups 2
• Hypertension: Multiple mechanisms including mineralocorticoid receptor activation (increasing renal sodium absorption), renin-angiotensin system activation, vascular sensitization to catecholamines, and impaired nitric oxide bioavailability 2
• Mood changes: Direct glucocorticoid effects on brain neurotransmitter systems 2, 4

Relationship Between Cortisol and Elevated Blood Glucose:

Cortisol is a counter-regulatory hormone that antagonizes insulin action 2, 4:

• Stimulates hepatic gluconeogenesis (new glucose production from amino acids)
• Promotes peripheral insulin resistance in muscle and adipose tissue
• Inhibits glucose uptake by peripheral tissues
• Result: Glucose abnormalities occur in >80% of Cushing's patients, with fasting glucose of 178 mg/dL indicating impaired fasting glucose or diabetes 2

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CJMM Phase 3: Prioritize Hypotheses

Most Likely Health Problem:

Cushing's disease (pituitary ACTH-secreting adenoma) – accounts for 75-80% of ACTH-dependent cases, making it statistically most likely given elevated ACTH with classic cushingoid features 1, 2.

One Potential Complication:

Cardiovascular events (myocardial infarction, stroke, pulmonary embolism) – Cushing's syndrome carries increased mortality from these complications, with average diagnostic delay of 3 years significantly increasing cardiovascular risk 2, 4.

Priority Concern at This Time:

Hypertension (162/94 mm Hg) with hypokalemia – this combination requires immediate attention as it increases risk for acute cardiovascular events and arrhythmias; the severely elevated blood pressure needs urgent control 3, 2.

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CJMM Phase 4: Generate Solutions

Two Priority Nursing Interventions:

1. Monitor blood pressure every 4 hours and assess for hypertensive crisis symptoms (headache, visual changes, chest pain, neurological changes) – given BP 162/94 and increased cardiovascular risk 3, 2

2. Implement fall precautions and assist with ambulation – proximal muscle weakness significantly increases fall risk, and fragile skin increases injury severity from falls 2, 4

Anticipated Treatments or Medications:

Diagnostic workup 1:

• Morning (08:00-09:00h) plasma ACTH measurement to confirm ACTH-dependent disease (already done, showing elevation)
• Pituitary MRI with thin slices (3T preferred) as next definitive step to identify pituitary adenoma ≥6 mm 1
• If MRI shows no adenoma or lesion <6 mm: Bilateral inferior petrosal sinus sampling (BIPSS) to distinguish pituitary from ectopic ACTH source, with central-to-peripheral ACTH ratio ≥2:1 baseline or ≥3:1 post-CRH confirming pituitary source 1

Medical management pending surgery 3, 2, 5:

• Mineralocorticoid receptor antagonists (spironolactone or eplerenone) as first-line for hypertension control – directly blocks cortisol activation of mineralocorticoid receptors 2
• Potassium supplementation to correct hypokalemia (goal >3.5 mEq/L) 3
• Steroidogenesis inhibitors (ketoconazole, metyrapone) if severe hypercortisolism requires rapid control before surgery 5

Definitive treatment 4, 5:

• Transsphenoidal selective adenomectomy – first-line therapy with ~80% remission rate, though 30% long-term relapse 5

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CJMM Phase 5: Take Action

Immediate Nursing Actions:

1. Establish continuous cardiac monitoring – hypokalemia (3.1 mEq/L) increases arrhythmia risk; monitor for peaked T-waves, U-waves, or dysrhythmias 3

2. Initiate strict intake/output monitoring – assess for polyuria from hyperglycemia and monitor fluid balance given hypertension 2, 4

3. Perform comprehensive skin assessment and document all bruises/wounds – establish baseline given delayed wound healing and fragile skin 2, 4

4. Check capillary blood glucose every 6 hours – fasting glucose 178 mg/dL requires monitoring for further hyperglycemia 2

5. Implement infection control precautions – elevated WBC with hypercortisolism increases infection risk and masks inflammatory responses 4

Patient Education to Initiate Today:

1. Explain Cushing's disease diagnosis: "Your pituitary gland has a small tumor producing too much ACTH hormone, which signals your adrenal glands to make excessive cortisol. This explains your weight gain, high blood pressure, high blood sugar, and other symptoms" 1, 2

2. Discuss upcoming diagnostic testing: "You'll need a specialized MRI of your pituitary gland. If the tumor is too small to see, you may need a procedure called petrosal sinus sampling where we measure hormone levels directly from veins near the pituitary" 1

3. Emphasize fall prevention: "Your muscle weakness and fragile skin mean falls are dangerous. Always use call light for assistance, wear non-slip footwear, and move slowly when changing positions" 2, 4

4. Wound care importance: "Your body doesn't heal wounds normally right now. Report any cuts, sores, or skin breakdown immediately. Avoid trauma to skin" 2, 4

5. Infection risk: "Your immune system is suppressed. Avoid sick contacts, practice meticulous hand hygiene, and report fever, cough, or any infection symptoms immediately" 4

6. Treatment expectations: "Surgery to remove the pituitary tumor is the goal. After surgery, you'll need temporary steroid replacement while your body recovers its normal hormone production" 5

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CJMM Phase 6: Evaluate Outcomes

Findings Indicating Improvement:

• Blood pressure <140/90 mm Hg – indicates adequate hypertension control 3
• Potassium >3.5 mEq/L – correction of hypokalemia reduces arrhythmia risk 3
• Fasting glucose <126 mg/dL – improved glycemic control 2
• Post-surgical cortisol suppression – morning cortisol <5 μg/dL indicates successful adenoma removal and predicts long-term remission 5
• Resolution of proximal muscle weakness – patient able to rise from chair without assistance 2
• Improved mood and sleep – neuropsychiatric symptoms resolve with cortisol normalization 2, 4

Findings Requiring Urgent Reevaluation:

• Blood pressure >180/110 mm Hg or symptoms of hypertensive emergency (severe headache, visual changes, chest pain, altered mental status) – requires immediate intervention 3
• Potassium <3.0 mEq/L or new cardiac arrhythmias – critical hypokalemia needs urgent correction 3
• Signs of infection (fever >100.4°F, productive cough, wound drainage, dysuria) – immunosuppression from hypercortisolism masks typical inflammatory responses; any infection can rapidly progress 4
• Acute hyperglycemia (glucose >300 mg/dL, polyuria, polydipsia, altered mental status) – risk of hyperosmolar hyperglycemic state 2
• New neurological symptoms (severe headache, vision changes, diplopia) – may indicate pituitary apoplexy or tumor expansion 1
• Post-operative adrenal insufficiency symptoms (hypotension, nausea, vomiting, weakness, hyponatremia) – requires immediate glucocorticoid replacement 5
• Recurrent cushingoid features months/years post-surgery – 30% long-term relapse rate necessitates lifelong surveillance 5

Critical pitfall: Do not attribute symptoms to menopause, obesity, or metabolic syndrome when wide purple striae, proximal muscle weakness, and easy bruising are present—these features mandate Cushing's syndrome evaluation 2. Average diagnostic delay is 3 years, significantly increasing mortality from cardiovascular complications 2.