Which disorders should the nurse identify as originating from the adrenal glands? (Select all that apply.) (Select All that Apply.)

The adrenal glands consist of an outer cortex and an inner medulla that synthesize essential steroid hormones, mineralocorticoids, and catecholamines. Autoimmune destruction of this tissue precipitates chronic adrenal insufficiency, characterized by severe cortisol and aldosterone deficits. Conversely, hypercortisolism driven by intrinsic neoplasia or pituitary adenomas induces glucocorticoid excess, leading to profound systemic metabolic and structural remodeling. A. Addison disease: This pathology involves autoimmune or infectious destruction of the adrenal cortex, destroying the body's ability to synthesize glucocorticoids and mineralocorticoids. The resulting primary adrenal insufficiency manifests as severe hypotension, electrolyte imbalances, and hyperpigmentation. It originates directly within these endocrine organs. B. Diabetes insipidus: This water-wasting disorder is caused by a deficiency in antidiuretic hormone synthesis in the hypothalamus or its release from the posterior pituitary. The condition alters renal water reclamation but shares zero physiological or anatomical links with adrenal tissue. It is a neurohypophyseal problem. C. Simple goiter: Glandular hypertrophy of the thyroid tissue stems from chronic iodine deficiencies or uninhibited thyroid-stimulating hormone overproduction. This localized cervical enlargement is entirely centered within the thyroid-axis feedback loop, running independently of adrenal steroid pathways. It is an isolated thyroid disorder. D. Cushing syndrome: This clinical state represents a prolonged, pathological exposure to high circulating levels of cortisol, often caused by adrenal adenomas or hyperplasia. The hormone excess manifests as central adiposity, dermal striae, and systemic hypertension. It represents a classic disorder of adrenal hyperfunction. E. Graves' disease: This autoimmune condition features thyrotropin receptor antibodies that mimic hormone signals, causing uninhibited thyroid hypersecretion and goiter formation. The resulting thyrotoxicosis represents a thyroid-specific autoimmune disease that does not arise from adrenal medullary or cortical tissue. It is an independent metabolic pathology.