This has been a tough concept for me to get, but I think I'm finally there:

The stem is describing primary adrenal insufficiency, or Addison's.

• ACTH is being over-produced to stimulate the adrenals to produce cortisol, but they can't respond, either due to atrophy or destruction (TB, autoimmune: DR4, etc.)
• The first 13 amino acids of ACTH can be cleaved to form α-MSH, which stimulates melanocytes, causing hyperpigmentation

The stem is describing primary adrenal insufficiency, or Addison's.

ACTH is being over-produced to stimulate the adrenals to produce cortisol, but they can't respond, either due to atrophy or destruction (TB, autoimmune: DR4, etc.) The first 13 amino acids of ACTH can be cleaved to form α-MSH, which stimulates melanocytes, causing hyperpigmentation. Cortisol helps with BP and his is low.

Patients also have low aldosterone. Low Na and high K is a sign of hypoaldosteronism. Patients retain H and lose HCO3. Losing HCO3 causes Cl- retention in the PCT. This all leads to metabolic acidosis. Loss of cortisol causes anorexia, hypoglycemia, and a low BP as seen in this patient.