Overview
Introduction
Chronic glucocorticoid excess leaves a recognizable but uneven clinical pattern: central fat redistribution with thin limbs, proximal weakness, fragile skin, hypertension, hyper...
Chronic glucocorticoid excess leaves a recognizable but uneven clinical pattern: central fat redistribution with thin limbs, proximal weakness, fragile skin, hypertension, hyperglycemia, and psychological change. The excess may come from prescribed glucocorticoids or endogenous disease. Endogenous Cushing syndrome is ACTH-dependent when pituitary or ectopic ACTH drives cortisol production, and ACTH-independent when an adrenal lesion produces cortisol autonomously; Cushing disease refers only to a pituitary source. For nursing assessment, the combination matters more than any single feature. A patient struggling to rise from a chair, bruising easily, and developing resistant hypertension deserves a medication history and a properly sequenced workup. Treatment can uncover the opposite emergency: adrenal insufficiency when suppressed cortisol production cannot meet stress demands.