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. 2017 Oct 1;14(9-10):4–10.

Table 3.

Comparing primary and secondary adrenal Insufficiency24-27

CLINICAL SYMPTOM PRIMARY ADRENAL INSUFFICIENCY SECONDARY ADRENAL INSUFFICIENCY MECHANISM OF SYMPTOM PRODUCTION
Hyper-pigmentation (+) (-) Lack of glucocorticoid negative feedback increases the release of ACTH and other POMC-peptides; these POMC-peptides are responsible for hyperpigmentation by acting on the MSH receptors in the skin
Hyperkalemia (+) (-) Due to mineralocorticoid deficiency
Signs of other pituitary hormone deficiencies (-) (+) Pan-hypopituitarism from lesions directly affecting pituitary gland
Headaches; visual field deficits (-) (+) From direct effect of pituitary lesion
Hyponatremia (+) (+) Due to mineralocorticoid deficiency, GC deficiency (leading to SIADH) in primary adrenal insufficiency, and dilutional in secondary adrenal insufficiency
Hypoglycemia (+) (++) Glucocorticoid deficiency
Orthostatic hypotension (+) (+) Mineralocorticoid deficiency is not seen in secondary adrenal insufficiency, as mineralocorticoids are principally regulated by the plasma renin-angiotensin system. Hypotension in secondary adrenal insuffiency occurs due to decreased vascular tone as a result of reduced vascular responsiveness to angiotensin II and norepinephrine
Anorexia; weight loss; fatigue; generalized malaise; decreased libido (+) (+) Glucocorticoid deficiency
Loss of axillary/pubic hair in women (+) (+) Loss of adrenal androgens