A 39-year-old woman presents with a 2-year history of progressive weight gain, easy bruising, and new-onset hypertension and diabetes. On examination, the structure marked **A** is noted—a rounded, plethoric face with marked facial fullness and bilateral malar redness. She also has wide violaceous abdominal striae (>1 cm), proximal myopathy, and a dorsocervical fat pad. Her 24-hour urine free cortisol is 380 mcg/24h (normal <50), late-night salivary cortisol is 8.2 ng/mL, and the 1 mg overnight dexamethasone suppression test shows a morning cortisol of 14 mcg/dL (not suppressed). Which of the following best describes the pathophysiological basis for the appearance marked **A** in this patient?
A. Chronic excess glucocorticoid causes facial adiposity, vasodilation, and increased skin fragility, resulting in rounded plethoric facies with facial fullness and easy bruising
B. Thyroid hormone deficiency causes myxedematous facial puffiness and loss of facial definition
C. Chronic mineralocorticoid excess from primary hyperaldosteronism causes facial edema and hypertension without glucocorticoid excess
D. Acute catecholamine excess from a pheochromocytoma causes facial flushing and edema independent of cortisol levels
Explanation
Why option 1 is correct
The structure marked A—rounded plethoric (moon) facies with facial fullness—is a hallmark clinical sign of Cushing syndrome caused by chronic glucocorticoid excess. Excess cortisol promotes redistribution of fat to the face and supraclavicular regions (lipodystrophy), increases skin vascularity and erythema (plethora), and impairs collagen synthesis, making skin fragile and prone to bruising. The combination of facial adiposity, malar redness (plethora), and easy bruising from minor trauma is pathognomonic for hypercortisolism. The patient's biochemical profile (elevated 24-hour urine free cortisol, elevated late-night salivary cortisol, and failure of dexamethasone suppression) confirms Cushing syndrome, and the clinical phenotype—including the moon facies, violaceous striae, proximal myopathy, and osteoporosis—is classic for this diagnosis. [Nieman LK et al. J Clin Endocrinol Metab 2008;93(5):1526-1540]
Why each distractor is wrong
Option 2 (pheochromocytoma): Catecholamine excess causes acute flushing and diaphoresis but does not produce the chronic facial adiposity, redistribution of fat, or the characteristic plethoric moon facies seen in Cushing syndrome. Pheochromocytoma does not cause the wide violaceous striae, proximal myopathy, or the degree of metabolic derangement (diabetes, hypertension, osteoporosis) seen here.
Option 3 (hypothyroidism): Thyroid hormone deficiency causes myxedematous facial puffiness from mucopolysaccharide deposition, which is non-pitting and associated with cold intolerance, weight gain despite low appetite, and bradycardia. It does not cause the plethora, easy bruising, violaceous striae, or proximal myopathy characteristic of Cushing syndrome.
Option 4 (primary hyperaldosteronism): Mineralocorticoid excess causes hypertension and peripheral edema but does not produce the facial adiposity, plethora, easy bruising, violaceous striae, proximal myopathy, or the metabolic complications (new diabetes, osteoporosis, amenorrhea) that are driven by glucocorticoid excess, not aldosterone alone.
High-YieldNEET PG
Moon facies + plethora + easy bruising + violaceous striae + proximal myopathy = Cushing syndrome until proven otherwise; the rounded plethoric face is a cardinal clinical sign reflecting chronic glucocorticoid-induced fat redistribution, vasodilation, and collagen breakdown.
Nieman LK et al. The Diagnosis of Cushing Syndrome: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2008;93(5):1526-1540
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