Secondary hypoadrenalism, or ACTH deficiency hypoadrenalism, is caused by diseases of the pituitary gland, which lead to adrenal failure as a secondary effect.
The ACTH specifically stimulates cells in this zone to secrete cortisol, which belongs to a class of steroids, or lipid-soluble hormones, called glucocorticoids.
With less ACTH floating around, the zona fasciculata gets less stimulation to make cortisol, and eventually, cortisol levels go back down to the normal range again.
When the ACTH binds to receptors on cells in an adrenal cortex, it triggers the release of a frenzy of different freak-out compounds known as glucocorticoid and mineralcorticoid hormones.
Unlike pituitary adenomas, ectopic sites of ACTH productions typically don't respond even to high doses of dexamethasone, and the serum cortisol remains high.
Normally, the hypothalamus, which is located at the base of the brain, secretes corticotropin-releasing hormone, known as CRH, which stimulates the pituitary gland to secrete adrenocorticotropic hormone, known as ACTH.
Apart from pituitary adenomas, there are ectopic sources of ACTH like small cell lung cancer, and in these cases the excess ACTH is coming from somewhere other than the pituitary.
To do that, the body uses negative feedback, which means that high levels of cortisol tell the hypothalamus and pituitary gland to decrease their secretion of CRH and ACTH, respectively.