A 52-year-old man presents to the endocrinology clinic with progressive coarsening of facial features, macroglossia, and markedly enlarged hands with a "spade-like" appearance (shown as **A** in the diagram). His wife reports he has required progressively larger shoe and ring sizes over the past 8 years. Serum IGF-1 is elevated at 680 ng/mL (normal: 90–360 ng/mL for his age). An oral glucose tolerance test shows failure of growth hormone to suppress below 1 ng/mL after 75 g glucose load. Pituitary MRI reveals a 2.2 cm sellar mass with suprasellar extension. Which of the following is the MOST LIKELY pathophysiology underlying the clinical phenotype marked **A**?
A. Chronic excess prolactin causing galactorrhea and secondary hypogonadism with facial edema
B. Chronic excess thyroid hormone causing metabolic acceleration and tissue hypertrophy
C. Chronic excess cortisol causing central obesity and proximal myopathy with facial plethora
D. Chronic excess growth hormone stimulating hepatic IGF-1 production, driving progressive somatic and soft tissue overgrowth
Explanation
Why "Chronic excess growth hormone stimulating hepatic IGF-1 production, driving progressive somatic and soft tissue overgrowth" is right
The clinical phenotype marked A — coarse facies with supraorbital ridge prominence, macroglossia, prognathism, and spade-like hands — is the pathognomonic presentation of acromegaly. This syndrome results from chronic GH excess in adults after epiphyseal closure. The mechanism is direct: excess GH stimulates hepatic production of insulin-like growth factor-1 (IGF-1), which drives progressive somatic and visceral overgrowth, manifesting as the characteristic coarsening of facial features, enlargement of the tongue and jaw, and the distinctive spade-shaped hands with reported progressive increase in shoe and ring size over years. This is the textbook pathophysiology of acromegaly (Endocrine Society 2014; AACE/ACE 2020).
Why each distractor is wrong
Chronic excess thyroid hormone: Thyrotoxicosis causes tachycardia, weight loss, tremor, and heat intolerance—not the progressive coarsening of facial features, macroglossia, or spade hands seen in acromegaly. Thyroid hormone does not drive the characteristic soft tissue and skeletal overgrowth pattern of acromegaly.
Chronic excess cortisol: Cushing syndrome presents with central obesity, proximal myopathy, facial plethora (moon facies), and buffalo hump—a distinctly different clinical phenotype (shown as B in the diagram). Cortisol excess does not produce macroglossia, prognathism, or the progressive spade-like hand enlargement characteristic of acromegaly.
Chronic excess prolactin: Hyperprolactinemia causes galactorrhea, amenorrhea/hypogonadism, and erectile dysfunction, with possible facial edema from fluid retention—not the progressive skeletal and soft tissue overgrowth, macroglossia, or spade hands of acromegaly. Prolactin does not drive the IGF-1–mediated somatic overgrowth seen here.
High-YieldNEET PG
Acromegaly = GH excess → IGF-1 ↑ → progressive coarse facies, macroglossia, spade hands, and soft tissue overgrowth over 5–10 years; >95% caused by GH-secreting pituitary macroadenoma.
Endocrine Society Acromegaly Guidelines 2014; AACE/ACE 2020 Update
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