Match each patient's adrenal and pituitary laboratory profile with the most likely underlying pathophysiologic diagnosis.
- Low AM serum cortisol, elevated plasma ACTH, hyponatremia, hyperkalemia, and elevated plasma renin activityPrimary adrenal insufficiency (Addison disease)
- Low AM serum cortisol, inappropriately normal or low plasma ACTH, normal serum electrolytes, and normal plasma renin activitySecondary adrenal insufficiency (Pituitary dysfunction)
- Elevated -hour urine free cortisol, suppressed plasma ACTH, and lack of cortisol suppression with low-dose dexamethasoneACTH-independent Cushing syndrome (Adrenal adenoma)
- Elevated -hour urine free cortisol, elevated plasma ACTH, and suppression of serum cortisol following a high-dose dexamethasone suppression testACTH-dependent Cushing syndrome (Pituitary corticotroph adenoma)
Cevap
The profiles match as follows: primary adrenal insufficiency shows pan-cortical failure (high ACTH, high renin, abnormal electrolytes); secondary adrenal insufficiency shows isolated glucocorticoid failure (low ACTH, normal renin/electrolytes); ACTH-independent Cushing syndrome shows high cortisol with suppressed ACTH; and pituitary Cushing disease shows high cortisol, high ACTH, and suppression with high-dose dexamethasone.
Correct matching requires applying principles of endocrine feedback loops. Primary gland failures (adrenal insufficiency, adrenal adenoma) show an inverse relationship between the stimulating hormone (ACTH) and the peripheral hormone (cortisol). Central defects (pituitary failure, Cushing disease) show concordant changes. Furthermore, the functional independence of the zona glomerulosa (aldosterone) from ACTH allows distinction between primary and secondary adrenal insufficiency, while the relative feedback resistance of pituitary adenomas allows distinction from ectopic ACTH syndromes.
Adım Adım Çözüm
Anahtar Kavram
The diagnostic approach to adrenal axis disorders relies on paired hormone testing (Cortisol/ACTH) to localize the defect and assessing parallel pathways (renin-aldosterone) or feedback sensitivity (dexamethasone suppression) to determine the exact etiology.