NU 237 · NursingSection 5.7 · Digestive and endocrine disorders
Section 23 of 25
Adrenal disorders: Addison’s disease and Cushing’s disease
Explain what cortisol and aldosterone do, describe how destruction of the adrenal cortex causes Addison’s disease and how an excess of cortisol causes Cushing’s syndrome, recognise an adrenal crisis, and outline the tests, the treatment and the nursing care of both conditions.
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Why this matters
Adrenal disease is the clearest lesson in the endocrine unit about how one chemical messenger can be wrong in two opposite directions. Too little cortisol and aldosterone produce a patient who is tired, dizzy on standing and unable to survive an infection; too much cortisol produces a patient whose face, bones, skin, glucose and mood all change, often because of a medicine we prescribed ourselves. Both pictures are common in hospital practice, both are dangerous when missed, and both are first recognised by a nurse who takes a blood pressure standing up, weighs the patient, or notices that a small infection is behaving strangely. Learn the two hormones here and the rest of adrenal care follows logically.
What you need to know first
You need only the everyday ideas that a gland releases hormones into the blood, that the body must hold its blood pressure and its blood sugar steady, and that a medicine can act like a natural hormone. The words cortisol, aldosterone, ACTH and steroid are all defined below, so no previous endocrinology course is assumed.
Words to know (5)
Adrenal cortex
The outer layer of the adrenal gland, which makes the steroid hormones cortisol, aldosterone and androgens; the inner medulla makes adrenaline. Damage confined to the cortex removes cortisol and aldosterone but leaves adrenaline production intact.
Cortisol
The main glucocorticoid, released in response to ACTH; it raises blood glucose, maintains blood pressure, restrains inflammation and helps the body survive stress. A patient who cannot make cortisol becomes hypoglycaemic when a meal is missed.
Aldosterone
The main mineralocorticoid; it makes the kidney reabsorb sodium and excrete potassium, and because water follows sodium, it defends blood volume and blood pressure. Without aldosterone the serum potassium rises and the blood pressure falls on standing.
Addison’s disease
Primary adrenal insufficiency: destruction of the adrenal cortex, so both cortisol and aldosterone are deficient. A patient with Addison’s disease needs both hydrocortisone and fludrocortisone replaced for life.
Cushing’s syndrome
The signs produced by chronic excess of glucocorticoid, whether from prescribed steroids or from overproduction by the pituitary or the adrenal gland. A patient on long-term prednisolone develops a moon face, thin skin and a raised blood glucose.
One idea at a timeIdea 1 / 6
In one sentence The adrenal cortex makes cortisol, which handles stress and blood sugar, and aldosterone, which keeps sodium, potassium and blood pressure steady.
The adrenal cortex makes two hormones with two different jobs
The adrenal glands are two small glands sitting on top of the kidneys. Each has an outer cortex and an inner medulla. The medulla makes adrenaline, the rapid fight-or-flight hormone; the cortex makes steroid hormones, and two of them matter here. Cortisol is the glucocorticoid: it raises blood glucose between meals, keeps blood vessels responsive so that blood pressure holds, restrains inflammation and the immune response, and helps the body survive physical stress. Aldosterone is the mineralocorticoid: it acts on the kidney tubule to reabsorb sodium and excrete potassium, and because water follows sodium, it defends blood volume and blood pressure.
Cortisol is switched on by adrenocorticotropic hormone (ACTH) from the pituitary, while aldosterone is controlled mainly by the renin–angiotensin system and by the potassium level.
Because the two hormones have separate controls and separate jobs, they can fail together or separately, and that is what makes adrenal disease predictable at the bedside.
For example
A person who misses breakfast still has a normal blood glucose because cortisol raises it; a patient whose cortex is failing becomes hypoglycaemic after the same missed meal.
Pause and check yourself
Which hormone defends blood pressure by keeping sodium in the body, and what controls it?
Show the answer
Aldosterone, made by the adrenal cortex and controlled mainly by the renin–angiotensin system and by the potassium level rather than by ACTH.
Read detailed explanations
Primary, secondary and tertiary insufficiency: the same shortage from three different places
Two glands share one conversation. Neurons in the hypothalamus release corticotropin-releasing hormone into the portal blood of the pituitary stalk. Anterior pituitary corticotroph cells answer by making proopiomelanocortin, a precursor that is cleaved into ACTH and several smaller peptides, including one that stimulates melanocytes. ACTH reaches the adrenal cortex and drives the zona fasciculata to synthesise cortisol, and cortisol travels back to the hypothalamus and pituitary to switch its own production down.
This loop explains why the site of the fault changes the signs. In primary insufficiency the adrenal gland is destroyed, so cortisol is low and the pituitary drives ACTH as high as it can; the accompanying melanocyte-stimulating peptide darkens the skin, and aldosterone is lost as well because the zona glomerulosa is damaged, giving hyperkalaemia, hyponatraemia and salt loss. In secondary insufficiency the pituitary fails, so ACTH is low: the skin does not darken, and aldosterone is largely preserved because the renin–angiotensin system still works, so hyperkalaemia is usually absent and the picture is dominated by fatigue and hypoglycaemia.
A third form, tertiary insufficiency, follows prolonged treatment with glucocorticoid medicines, which suppress the hypothalamus and pituitary and let the cortex atrophy. The cosyntropin stimulation test separates these: a gland destroyed by disease cannot answer even a large dose of synthetic ACTH, whereas a gland that has merely been idle may respond after repeated stimulation.
Why steroid treatment can never be stopped suddenly: the suppressed axis
Cortisol is not released evenly. It follows a diurnal rhythm: the level climbs during the night, peaks in the early morning and falls to a trough around midnight. Replacement is timed to imitate that pattern, with the largest dose in the morning, and the rhythm is also why samples for cortisol are taken early and why a late-night salivary sample is a sensitive test for excess.
The rhythm depends on the pituitary, and the pituitary depends on the hypothalamus, so any sustained supply of glucocorticoid from outside suppresses the whole axis. Within a few weeks of a supraphysiological dose, ACTH secretion falls, the adrenal cortex atrophies, and the gland becomes unable to mount the surge that injury or fever demands. If the medicine is then stopped abruptly, the patient may develop a withdrawal syndrome of weakness, nausea, joint pain and low mood; if they are also stressed, the result can be a full adrenal crisis with hypotension, hypoglycaemia and hyperkalaemia. This is why the dose is reduced in small steps over weeks or months rather than stopped, why the axis may take a year to recover, and why the patient must carry a steroid card and receive stress doses during intercurrent illness.
Replacement is always a balance: too little leaves the patient tired, hypotensive and hyperkalaemic, while too much recreates the features of Cushing’s syndrome, including osteoporosis, raised glucose and thin skin.
Finding and removing the source of a cortisol excess
Once excess cortisol is confirmed, the next question is where it comes from, because the treatment is completely different for each answer. The first step is to measure ACTH. A suppressed ACTH points to the adrenal gland itself, and adrenal imaging is arranged; a normal or high ACTH points above the adrenal, so the pituitary is imaged. A very high ACTH with rapid onset, hypokalaemia and no suppression at all suggests ectopic production, classically by a small-cell lung carcinoma, and the chest is imaged. When the pituitary scan is normal or ambiguous, inferior petrosal sinus sampling can measure ACTH close to the gland and show whether the pituitary is the source.
Cortisol excess is treated by removing its cause. A pituitary adenoma is resected through the nose by transsphenoidal surgery, sometimes followed by radiotherapy; an adrenal tumour is removed by adrenalectomy; an ectopic source is treated according to the underlying cancer.
When surgery must be delayed or has failed, adrenal enzyme inhibitors are used as a bridge: metyrapone blocks the last step of cortisol synthesis, ketoconazole blocks several steps, mitotane is adrenolytic, and aminoglutethimide reduces production. Each has its own monitoring, with liver enzymes, blood pressure, potassium and cortisol levels followed while the dose is adjusted.
Bilateral adrenalectomy removes the whole problem but leaves the patient steroid-dependent and carries the risk of Nelson’s syndrome, in which the pituitary adenoma enlarges and the skin darkens because it is no longer restrained by cortisol feedback. After pituitary surgery the nurse watches for diabetes insipidus, leakage of cerebrospinal fluid, and the need for temporary or permanent hormone replacement.
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One cortex, two opposite diseases: Addison’s and Cushing’s
The adrenal cortex makes cortisol and aldosterone, so disease can push it in either direction. On the left, a destroyed cortex leaves the body short of both hormones: sodium and glucose fall, potassium rises, blood pressure collapses on standing, and the skin darkens because the pituitary pours out ACTH. On the right, sustained cortisol excess reshapes the face, trunk, skin and bone, raises glucose and blood pressure, and hides infection. The same hormones explain both pictures, and the same nursing observations — fluid, glucose, potassium, safety and teaching — run through both.
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01 / 6The adrenal cortex: two steroid hormones
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The adrenal cortex: two steroid hormones
The cortex has three zones, and two of their products dominate the clinical picture. Cortisol is a glucocorticoid: it raises glucose between meals, keeps blood vessels responsive so blood pressure holds, and damps inflammation and immunity. Aldosterone is a mineralocorticoid: it reabsorbs sodium and excretes potassium in the distal nephron, and water follows the sodium, so it sets the circulating volume. Cortisol is driven by pituitary ACTH, while aldosterone is driven mainly by the renin–angiotensin system and by serum potassium. That separate control is why the two hormones can fail together, as they do in Addison’s disease; in Cushing’s syndrome cortisol alone is in excess, because aldosterone keeps obeying the renin–angiotensin system and the serum potassium.
Comparison schematic, not anatomical: the gland is represented as one box, and only the cortical hormones that drive these two diseases are shown. Aldosterone deficiency belongs to primary insufficiency and is largely preserved in secondary insufficiency, which the single left-hand panel therefore does not separate.
Key points to remember
✓The adrenal cortex makes cortisol, which raises glucose, holds blood pressure and damps inflammation, and aldosterone, which retains sodium, excretes potassium and defends blood volume.
✓Addison’s disease is destruction of the cortex, usually autoimmune or tuberculous, giving weakness, weight loss, hyperpigmentation, low sodium and glucose, high potassium and postural hypotension.
✓An adrenal crisis is a medical emergency triggered by stress or by vomiting that prevents tablets being absorbed; it needs intravenous hydrocortisone and saline with dextrose before any test is confirmed.
✓Cushing’s syndrome is chronic cortisol excess, most often from prescribed steroids; Cushing’s disease is the specific case of an ACTH-secreting pituitary adenoma, and diagnosis uses urinary free cortisol and dexamethasone suppression.
✓Treatment replaces what is missing in Addison’s disease and removes the source of excess in Cushing’s syndrome; in both, the nurse watches fluid, glucose, potassium, bone, skin, infection and the safety of a patient whose hormones are no longer self-regulating.
Go deeper
Worked example
A patient with Addison’s disease who cannot keep her tablets down. A 52-year-old woman with known Addison’s disease has had influenza with vomiting for two days. She has taken none of her hydrocortisone since yesterday. She is drowsy, her lips are dry, her blood pressure is 82/54 mmHg lying and 66/40 mmHg standing, her pulse is 118 beats per minute, and her blood glucose is 3.1 mmol/L. Her sodium is 128 mmol/L and her potassium is 5.8 mmol/L.
Recognise the trigger and the mechanism. Influenza and vomiting are exactly the two things that cause an adrenal crisis: the demand for cortisol has risen with the infection, and the supply has stopped because the tablets are not being absorbed. The failing cortex cannot increase production on its own.
Read the biochemistry as two separate hormone failures. The sodium of 128 mmol/L, the potassium of 5.8 mmol/L and the postural fall in blood pressure are the signature of missing aldosterone: sodium is being lost and potassium retained, so the circulating volume is low. The glucose of 3.1 mmol/L is the signature of missing cortisol, which normally raises blood glucose between meals.
Act before confirming. This is a medical emergency, so blood is drawn for cortisol and ACTH while treatment begins, but treatment is never delayed for the results. Intravenous hydrocortisone is given at once, followed by 0.9% sodium chloride with dextrose to restore volume and glucose, and the potassium is treated according to the prescribed protocol with cardiac monitoring.
Look for and treat the precipitating infection. The crisis was triggered by influenza, so cultures and antibiotics may be needed, and the nurse continues to assess for a source throughout, because a fever may be blunted or absent in a patient with adrenal insufficiency.
Monitor and then teach. Blood pressure and pulse are checked lying and standing, intake and output and daily weight are recorded, and glucose and potassium are tracked while the dose is adjusted. Before discharge the patient is taught sick-day dosing, given an emergency hydrocortisone injection, reminded never to stop her replacement and to wear a medical alert bracelet.
The two clues that make this case unambiguous are the postural drop with hyperkalaemia, which points to aldosterone, and the hypoglycaemia, which points to cortisol. Together with the history they make adrenal crisis the working diagnosis, and the response is immediate intravenous steroid and fluid. The most important nursing lessons are that treatment comes before confirmation, that vomiting is a reason to give steroid by injection rather than by mouth, and that the crisis was preventable by the sick-day rule the patient had been taught.
Common misconception
A common belief, held by some patients as well as beginners, is that steroid tablets are safe to stop as soon as you feel better, and that natural adrenal disease and the side effects of steroid treatment are unrelated problems. They are the same hormone seen from opposite sides. Taking a glucocorticoid for more than a few weeks suppresses the pituitary and the adrenal cortex, so the gland shrinks and stops making cortisol on its own; stopping the tablets suddenly can then reproduce the picture of Addison’s disease, including a crisis. That is why steroids are reduced gradually, why the axis can take months to recover, and why a patient who has taken them for a long time must carry a steroid card and receive stress doses during illness even after the tablets are stopped.
Check your reasoning
Two patients arrive on the same shift. One is a man with darkening of his gums and a blood pressure that falls on standing; the other is a woman with a moon face and a blood glucose of 14 mmol/L. Before any laboratory result is back, what is your working explanation for each, and which one is at immediate risk of shock?
Reveal an answer
The man shows the classic direction of adrenal insufficiency: hyperpigmentation from a high ACTH level, together with postural hypotension from aldosterone deficiency, so the working diagnosis is Addison’s disease and he is the one at immediate risk, because a stress such as infection could turn this into an adrenal crisis with vascular collapse and hypoglycaemia. The woman shows the opposite direction — cortisol excess — and the raised glucose fits the glucocorticoid effect, while her moon face suggests Cushing’s syndrome; she is not at risk of acute collapse from the adrenal problem itself, but she is at risk of hyperglycaemia, infection, fracture and slow healing. The two presentations are mirror images of the same two hormones, and in both patients the nurse’s first useful act is to take a lying and standing blood pressure, check a glucose, and ask what steroid medicine has been taken.
Where this comes from
Medical Pathology I — lecture notes, unit 5 (endocrine): adrenocortical insufficiency and Cushing’s disease · endocrine-raw.txt lines 663–670 (definition of Addison’s disease, autoimmune and tuberculous causes, inadequate ACTH as a further cause, and Addisonian crisis as a medical emergency), 672–686 (signs, symptoms and diagnosis: weakness, weight loss, orthostatic hypotension, bronzing, anorexia, fatigue, emaciation, hypotension, low glucose, low sodium, high potassium), 689–710 (treatment with antibiotics, fludrocortisone, fluids and intravenous hydrocortisone with 5% dextrose in normal saline; nursing monitoring of lying, sitting and standing blood pressure and pulse, daily weight, bone density, daily medication and the medical alert bracelet), 712–719 (Cushing’s syndrome from steroid medication, adrenal hyperplasia, a pituitary ACTH-secreting tumour and an adrenal tumour), 721–742 (moon face, oily skin, acne, facial hair, buffalo hump, osteoporosis, kyphosis, backache, amenorrhoea, mental status changes, weakness; 24-hour urinary free cortisol, low-dose dexamethasone suppression, CT, MRI and ultrasound, raised glucose and sodium), 744–750 (transsphenoidal hypophysectomy, pituitary radiation, adrenalectomy and the adrenal enzyme inhibitors metyrapone, aminoglutethimide, mitotane and ketoconazole), 752–786 (protective environment, assisted ambulation, high-protein and high-calcium diet, subtle infection, urine glucose and acetone, skin trauma, bone densitometry, and post-operative care).
Beyond the supplied notes: adrenal physiology, testing and the hypothalamic–pituitary–adrenal axis · Beyond the supplied notes — standard endocrinology the notes do not state: the hypothalamic–pituitary–adrenal axis and the negative feedback of cortisol; the cleavage of proopiomelanocortin into ACTH and a melanocyte-stimulating peptide, which explains the hyperpigmentation of primary but not secondary insufficiency; the control of aldosterone by the renin–angiotensin system and potassium rather than by ACTH, which is why hyperkalaemia is typical of primary and not of secondary insufficiency; the diurnal rhythm of cortisol; the ACTH (cosyntropin) stimulation test, late-night salivary cortisol and the 1 mg overnight dexamethasone suppression test; the distinction between primary, secondary and tertiary insufficiency and the gradual taper required after prolonged steroid treatment; and the usual maintenance regimen of hydrocortisone plus fludrocortisone with stress-dose rules.
Beyond the supplied notes: corrections to the supplied lecture notes · Beyond the supplied notes — corrections: line 677 attributes the bronzing of the skin to the autoimmune disease, whereas hyperpigmentation is caused by the high ACTH level and its melanocyte-stimulating precursor peptide, which is why it is absent in secondary insufficiency; lines 712–719 use Cushing’s disease and Cushing’s syndrome interchangeably, whereas Cushing’s disease is specifically an ACTH-secreting pituitary adenoma and is only one cause of the syndrome, whose commonest cause is prescribed glucocorticoid medicine; line 707 advises a bone density test because of a decrease in mineralocorticoids, whereas mineralocorticoid deficiency does not thin bone and the relevant bone risk in adrenal disease comes from glucocorticoid excess or from over-replacement; and line 742 lists a raised serum sodium in Cushing’s syndrome, which is not a reliable finding and should not replace the diagnostic tests based on cortisol.
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About this course and its sources
The urinary and endocrine lessons build on the supplied Level 200 nursing notes (course instructor Bakume Jessey). Disease mechanisms, blood, lymphatic, cardiovascular and digestive lessons use cited external references. Diagrams are original educational schematics. Sections that go beyond the supplied notes say so in their sources. Specialist clinical and French-language editorial review remain pending.