## Why "Increased lipoprotein lipase activity in dorsocervical adipose tissue stimulated by glucocorticoid excess" is right The buffalo hump (dorsocervical fat pad marked **A**) is a pathognomonic sign of Cushing syndrome resulting from cortisol excess. The mechanism is direct glucocorticoid stimulation of lipoprotein lipase (LPL) in central, dorsocervical, and facial adipose tissue, promoting triglyceride uptake and fat accumulation in these glucocorticoid-sensitive depots. This occurs alongside glucocorticoid-induced protein catabolism in muscle, explaining the clinical picture of central/dorsocervical obesity with thin extremities and proximal myopathy. (Robbins 10e Ch 24; Harrison 21e Ch 386) ## Why each distractor is wrong - **Decreased hormone-sensitive lipase activity in visceral adipose tissue due to cortisol deficiency**: This is backwards — the patient has cortisol *excess*, not deficiency. Cortisol stimulates, not inhibits, fat mobilization in peripheral depots while promoting central accumulation. - **Increased growth hormone secretion leading to preferential central fat deposition**: Growth hormone excess causes acromegaly with coarse features and peripheral fat accumulation, not the characteristic dorsocervical fat pad and muscle wasting of Cushing syndrome. - **Thyroid hormone resistance causing impaired lipid mobilization from dorsal fat stores**: Thyroid dysfunction may cause weight gain, but it does not produce the specific pattern of dorsocervical fat accumulation with supraclavicular pads, moon facies, and proximal myopathy characteristic of glucocorticoid excess. **High-Yield:** Buffalo hump = glucocorticoid-stimulated lipoprotein lipase in dorsocervical fat + protein catabolism in muscle = central obesity + thin extremities (the pathognomonic pattern of Cushing syndrome). [cite: Robbins 10e Ch 24; Harrison 21e Ch 386]
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