Adrenal Disorders

Core Concepts

The HPA axis and the adrenal cortex

The cortex has three functional zones: the outer zone makes aldosterone; the middle zone makes cortisol; the inner zone makes androgens. Aldosterone is controlled mainly by the renin–angiotensin system (the body's blood-pressure sensor chain) rather than by ACTH — this matters because it explains why some adrenal failures lose cortisol but keep aldosterone, and vice versa. Cortisol is controlled by the HPA axis: CRH → ACTH → cortisol, with cortisol suppressing CRH and ACTH (negative feedback). This feedback is why someone taking long-term glucocorticoids has a suppressed axis: the outside steroid satisfies the feedback loop, so the hypothalamus and pituitary stop signaling, and the adrenal cortex shrinks in activity. If the steroid is stopped abruptly, the body may not be able to restart cortisol production in time to handle stress — the basis of adrenal crisis.

Cushing syndrome: too much cortisol

Cushing syndrome is the state of cortisol excess, from any cause. The most common cause overall is exogenous — long-term glucocorticoid therapy. Endogenous causes include a pituitary ACTH-producing adenoma (Cushing disease — the pituitary form, linking back to topic 4), an adrenal tumor, or ectopic ACTH from elsewhere in the body. The classic picture: central (truncal) obesity with thinner arms and legs, moon face, buffalo hump (fat pad at the base of the neck), thin fragile skin, easy bruising, purple striae (stretch marks) on the abdomen, high blood sugar, muscle weakness, bone loss, mood changes, and increased infection risk. Nursing care focuses on monitoring blood sugar and blood pressure, protecting fragile skin, fall prevention (muscle weakness and bone loss), infection precautions, and education. Person-first language: "person with Cushing syndrome," never "a Cushing's."

Adrenal insufficiency: too little cortisol

Primary adrenal insufficiency (Addison disease) means the adrenal cortex itself is destroyed — most often by autoimmune disease, but also by infection, hemorrhage, or infiltrative processes. Both cortisol and aldosterone are lost, producing weakness, fatigue, weight loss, low blood pressure (including orthostatic drops), hyperpigmentation of skin and mucous membranes (from high ACTH, which stimulates pigment cells — this appears only in primary disease), salt craving, low sodium, and high potassium. Secondary adrenal insufficiency comes from pituitary ACTH deficiency or from exogenous steroid suppression: cortisol is low but aldosterone is usually spared (it runs on the renin–angiotensin system), and there is no hyperpigmentation. Adrenal crisis is the acute, life-threatening decompensation: severe hypotension/shock, vomiting, abdominal pain, profound weakness, and altered mental status. Triggers include infection, surgery, trauma, and — critically — abruptly stopping glucocorticoids in someone whose axis is suppressed. Crisis management is an emergency and entirely provider- and protocol-driven; the nurse's role is rapid recognition, protecting the airway, and notifying the team immediately.

Pheochromocytoma: too much catecholamine

A pheochromocytoma is a tumor — usually in the adrenal medulla — that secretes epinephrine and norepinephrine. The hallmark is episodic hypertension with headache, palpitations, and profuse sweating ("spells"), sometimes with anxiety, pallor, or tremor. Spells can be provoked by physical activity, stress, or other triggers. The danger is the extreme swings in blood pressure; such patients need careful, calm handling and prompt provider notification of any hemodynamic change. Management (including pre-procedure blood pressure control) is provider-directed and institution-specific. (Educational overview only.)

Primary aldosteronism: too much aldosterone

Also called Conn syndrome, this is usually a small adrenal adenoma overproducing aldosterone. Excess aldosterone makes the kidneys hold sodium and water while wasting potassium, producing hypertension plus low potassium (hypokalemia) — the classic duo. Low potassium can cause muscle weakness, fatigue, cramping, and cardiac rhythm disturbances. Nursing care includes blood pressure monitoring, fall precautions (weakness), and reporting of any muscle complaints; treatment is provider-driven.

Nursing care across adrenal disorders

General nursing themes: careful blood pressure and heart-rate monitoring (orthostatic checks in insufficiency); safety precautions for weakness and bone loss; blood sugar monitoring in cortisol excess; skin care (thin skin, bruising, poor healing); infection surveillance; and — above all — medication education: people on long-term glucocorticoids should never stop abruptly, should carry medical-alert identification, and should have a provider-reviewed plan for illness or surgery (often called "sick-day rules"). Teach the person to report vomiting, diarrhea, fever, or inability to keep medication down, since these can precipitate crisis. Scope-of-practice note: stress-dose adjustments, fluid choices, and emergency protocols vary by institution and provider orders — nurses implement, verify, and escalate.

Clinical Scenario

Mr. Chen, 61, has taken a glucocorticoid medication for years to manage an autoimmune condition. He is admitted with pneumonia. The nurse recognizes that his long-term steroid therapy has suppressed his HPA axis: his adrenal glands have been "asleep" because the medication supplies the cortisol the body thinks it needs. In the stress of infection, his body cannot mount its own cortisol response. The nurse verifies that Mr. Chen's steroid medication is continued (never stopped abruptly), monitors his blood pressure and blood sugar, and watches closely for the red flags of adrenal crisis — sudden hypotension, vomiting, weakness, confusion. She reports any change immediately and later teaches him: never stop the medication suddenly, keep medical-alert identification, and contact his provider about any illness, vomiting, or surgery because the dose may need adjustment. This scenario describes recognition and education only — all dose decisions are provider- and institution-directed.

Common Confusions