← Common Core coursesNU 237 · Medical Pathology I
NU 237 · NursingSection 5.9 · Digestive and endocrine disorders
Section 25 of 25

Endocrine assessment, diagnostics and nursing management

Explain why a hormone result is read together with the hormone that controls it, describe how the endocrine history, physical signs, imaging and dynamic tests fit together, and apply the five nursing tasks — daily weight, measured intake and output, electrolyte and glucose surveillance, safe hormone replacement and patient teaching — to any patient with a gland disorder.

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Why this matters

Endocrine disease is easy to misread, because the sick gland often produces a value that looks ordinary while the controlling hormone is shouting. The patient in front of you may be tired, thirsty, cold, confused or simply “not themselves”, and the diagnosis is made by putting four things together: what the patient reports, what you see and feel at the bedside, what the laboratory measures, and what happens when the axis is deliberately disturbed. This section is the toolkit that turns the individual gland disorders of this unit into a repeatable clinical method. It also carries the nursing rules that prevent the two disasters of endocrine care — a missed airway after neck surgery and a missed adrenal crisis in a patient whose steroid was stopped.

What you need to know first

You need only the everyday idea that glands release chemical messengers into the blood and that these messengers act on organs elsewhere in the body. The names of the hormones, the tests and the clinical signs are all defined below, so no previous endocrinology course is assumed.

Words to know (5)
Hormone
A chemical messenger released by a gland into the blood, which travels to distant cells and changes what they do. Thyroid hormone reaches almost every cell and sets the speed at which the body burns energy.
Negative feedback
The control principle in which the hormone produced at the end of a chain switches off the signal that produced it, so the level stays within range. When the thyroid makes enough T4, the rising level suppresses the pituitary signal, and TSH falls.
Tropic hormone
A hormone whose target is another gland rather than a working tissue, such as TSH acting on the thyroid or ACTH acting on the adrenal cortex. A high TSH with a low T4 means the pituitary is stimulating a thyroid that cannot answer.
Dynamic test
A diagnostic test that gives a stimulating or suppressing substance and measures the response, instead of measuring one level at rest. The overnight dexamethasone suppression test shows whether cortisol production can still be switched off.
Orthostatic vital signs
Blood pressure and pulse measured with the patient lying, then sitting, then standing, to detect a fall in pressure on standing. A pressure that falls with a rising pulse when the patient stands suggests a failing adrenal cortex.
One idea at a timeIdea 1 / 5

In one sentence Because each gland is switched on and off by the hormone above it, a single level means little: it becomes a diagnosis only when it is read with the hormone that controls it.

Every endocrine result is read as a pair, never as a single number

A gland is a group of cells that releases a hormone, a chemical messenger carried in the blood to act on a distant target. Endocrine glands are not controlled one at a time; they sit in chains called axes. The hypothalamus signals the pituitary, the pituitary signals a target gland such as the thyroid or the adrenal cortex, and the target gland releases the hormone that does the work. That hormone then travels back and switches off the signal which produced it.

This is negative feedback, and it is the most useful idea in endocrine diagnosis, because it means two different faults produce two opposite patterns. If the target gland fails, the pituitary loses its brake and the controlling hormone rises: a failing thyroid gives a low T4 with a high TSH. If the controlling gland fails instead, both hormones fall together: a failing pituitary gives a low T4 with a low TSH.

The same logic applies to the adrenal axis, read as ACTH with cortisol, and to the parathyroid axis, where calcium itself is the controlled variable, so PTH is read with calcium.

A value inside the reference range can still be wrong for the situation: a TSH of 2.0 mIU/L is normal in a healthy adult and inappropriately low when the free T4 is low.

For example

Two patients both have a low free T4. The first has a TSH of 18 mIU/L, so the thyroid itself has failed. The second has a TSH of 0.1 mIU/L, so the pituitary is the gland at fault.

Pause and check yourself

A patient has a low free T4 and a low TSH. Which gland has failed, and why?

Show the answer

The pituitary or the hypothalamus, because a healthy pituitary would raise TSH to stimulate a failing thyroid. A low TSH with a low T4 means the thyroid is not being told to work.

Read detailed explanations
Anatomy of an axis: primary, secondary and tertiary failure

The hypothalamic–pituitary–target gland arrangement is repeated for almost every hormone, and each level has its own cell type and its own hormone. The hypothalamus releases releasing factors such as thyrotropin-releasing hormone and corticotropin-releasing hormone into a small portal circulation that carries them directly to the anterior pituitary, so they are not diluted in the general bloodstream. There, specialised cells answer: thyrotrophs make thyrotropin, corticotrophs make corticotropin, gonadotrophs make the gonadotropins and lactotrophs make prolactin, which is unusual because it is restrained rather than stimulated by hypothalamic dopamine.

The pituitary hormones are called tropic because their target is another gland, and the target gland hormones — thyroxine, triiodothyronine, cortisol, the sex steroids — are the ones that act on the tissues. The site of the fault is named by its level. Primary failure is disease of the target gland itself: the tropic hormone rises because the brake has gone, as in Hashimoto’s thyroiditis or autoimmune destruction of the adrenal cortex, where the high corticotropin also produces the characteristic bronzing of the skin. Secondary failure is disease of the pituitary: the tropic hormone and the target hormone fall together. Tertiary failure is disease of the hypothalamus above it.

The distinction changes treatment and monitoring. In primary hypothyroidism the replacement dose is followed with thyrotropin; in secondary hypothyroidism thyrotropin is useless as a guide because the pituitary cannot respond, so free thyroxine must be followed instead. The same trap exists for cortisol, where the morning value is interpreted against a rhythm: cortisol is highest at about 08:00 and lowest around midnight, and each laboratory sets its own reference range, which is why ranges travel poorly between hospitals and why the patient’s own previous results are the best comparison.

The dynamic tests, one by one, and the nursing safety rules they carry

Each dynamic test has a protocol, an interpretation and a hazard, and the nurse owns all three. The overnight low-dose dexamethasone suppression test gives one milligram of dexamethasone at about 23:00 and measures cortisol in the morning; a healthy axis is switched off, while autonomous production is not. Obesity, alcohol excess, depression and oestrogen-containing medicines can cause a false abnormal result, so interfering drugs are held only on a written order and the reason is documented.

The 24-hour urinary free cortisol measures total daily production and depends entirely on a complete collection with the exact start and finish times recorded and stored as the laboratory requires; a missed specimen invalidates the test, which is why the nurse, not the patient, controls the timing. The cosyntropin stimulation test gives 250 micrograms of synthetic corticotropin and measures cortisol at 30 and 60 minutes: a normal adrenal cortex rises, whereas a failing one does not, and the test must be done before steroid treatment is started because exogenous steroid suppresses the response.

The water deprivation test with desmopressin is the most dangerous of the group. Fluids are withheld under continuous supervision while weight, urine volume, urine osmolality and serum sodium are followed; the test is stopped if the patient loses about three to five per cent of body weight or if the sodium rises too far, and vasopressin is never given during the deprivation phase in the classic protocol. Interpretation separates central diabetes insipidus, in which the kidney concentrates urine once the hormone is supplied, from nephrogenic diabetes insipidus, in which it cannot, and from primary polydipsia, in which chronic overdrinking has washed out the medullary gradient.

The prolonged glucose tolerance test used when an insulinoma is suspected carries the opposite hazard: the patient is fasted and may become hypoglycaemic, so glucose is drawn up at the bedside and symptoms are watched continuously. Finally, imaging has its own rules: MRI requires screening for metal and for claustrophobia and the patient must lie still for a long scan, thyroid ultrasound is painless but fine-needle aspiration is explained first, and radioiodine scanning is avoided in pregnancy and breastfeeding. Thyroid medicines, antithyroid drugs and iodine-containing contrast can all distort an isotope study, so the ordering physician must know what the patient is taking.

Keeping the endocrine patient safe: fluid balance, steroid cover and teaching

Safety in endocrine nursing rests on a handful of quantitative rules that the nurse applies before the physician arrives. A litre of water weighs a kilogram, so daily weight is the reference measurement for fluid balance; urine output below about half a millilitre per kilogram per hour in an adult is a warning, and the intake and output chart must add up because the arithmetic is the assessment. In the syndrome of inappropriate antidiuretic hormone secretion, water is retained and the sodium is diluted, so the signs are neurological — headache, nausea, confusion, personality change, and ultimately seizure and coma — and the speed of the fall matters more than the absolute value. Fluid restriction is the first measure, which means documenting every mouthful, offering ice chips that are also counted, and giving frequent mouth care within the restriction.

Hypertonic saline is given only on a specific order, at a controlled rate, with sodium checked at the prescribed intervals, because correcting hyponatraemia too quickly can cause permanent osmotic injury to the brain; isotonic saline alone can even worsen the problem, because the kidney excretes the salt and keeps the water. In diabetes insipidus the risk is the opposite: free access to water, a rising sodium, and teaching about desmopressin. In adrenal insufficiency the dangers are hypotension on standing, hypoglycaemia and hyperkalaemia, and the single most important teaching point is that steroid replacement must never be stopped abruptly. The body cannot increase its own cortisol output during stress, so the dose is increased during fever, vomiting, diarrhoea, dental work or surgery — the rule nurses call steroid cover — and the patient carries a card or bracelet explaining it. Adrenal crisis with profound weakness, vomiting, hypotension and low glucose is a medical emergency in which intravenous hydrocortisone and fluid are given without waiting for confirmatory tests.

In Cushing’s syndrome and in patients treated with corticosteroids, the nurse watches the glucose because steroids raise it, inspects the skin because healing is delayed, looks for the subtle signs of infection that the anti-inflammatory effect conceals, and protects the patient from falls because the bones are losing calcium.

After thyroid surgery the priorities are different again: keep oxygen, suction and a tracheostomy set at the bedside, place the patient semi-upright to reduce tension on the neck, inspect the wound for bleeding and for swelling that could obstruct the airway, and watch for the tingling that announces hypocalcaemia. Postoperative education closes the loop: lifelong replacement, the reason it is never omitted, the laboratory work that adjusts the dose, and the medical alert jewellery that speaks for the patient when the patient cannot.

Explore the diagram

Look at the whole drawing first. Then select one numbered part and connect it to the idea you just read.

Endocrine diagnosis: read the pair, then disturb the axis

The plate follows the method of this section in three columns. On the left, every gland sits in a feedback axis, so a hormone is always read with the hormone that controls it. In the middle, the three diagnostic moves are shown: read the pair, disturb the axis with a suppression, stimulation or deprivation test, and image the gland. On the right are the nursing tasks that repeat in every endocrine disorder. The band below compares the three dynamic tests, and the closing rule states why one level is never the whole diagnosis.

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01 / 5The feedback axis: why a pair is needed

Endocrine diagnosis: read the pair, then disturb the axisThe plate follows the method of this section in three columns. On the left, every gland sits in a feedback axis, so a hormone is always read with the hormone that controls it. In the middle, the three diagnostic moves are shown: read the pair, disturb the axis with a suppression, stimulation or deprivation test, and image the gland. On the right are the nursing tasks that repeat in every endocrine disorder. The band below compares the three dynamic tests, and the closing rule states why one level is never the whole diagnosis.Endocrine diagnosis in three movesRead the pair · disturb the axis · monitor the patient1. The feedback axisHypothalamus releases TRHPituitary releases TSHThyroid makes T4 and T3T4 and T3 act on every cellFeedback switches the axis off2. Three diagnostic movesRead the pairhormone + controlling hormoneDisturb the axissuppression or stimulationImage the glandMRI, ultrasound, isotope scanThe pair shows the fault site3. What the nursemonitorsDaily weight, same scaleMeasured intake and outputElectrolytes, calcium, glucosePressure lying and standingAirway after neck surgeryNever stop hormone treatmentTeaching and alert jewelleryHow the dynamic tests answer the questionSuppression: switch it offDexamethasone overnightStimulation: switch it onCosyntropin (ACTH) testDeprivation: can it hold water?Then desmopressin is givenOne level is never the diagnosis: the axis decidesA value inside the reference range can still be wrong for the situation —a low T4 with a low TSH means the pituitary has failed, not that the thyroid is normal.

If the drawing is wider than this panel, scroll it sideways. Labels stay readable; the numbered explanations below show the same ideas.

The feedback axis: why a pair is needed

Each gland is switched on by the hormone above it and switched off by the hormone it makes itself, so the same laboratory value can mean two opposite things. In primary failure the target gland is destroyed and the controlling hormone rises, because the pituitary has lost its brake. In secondary failure the pituitary or hypothalamus is at fault and both hormones fall together. That is why thyrotropin is interpreted with free thyroxine, corticotropin with cortisol, and parathyroid hormone with calcium, where calcium itself is the regulated variable.

Schematic and simplified: the thyroid axis is drawn as the example, but the adrenal and parathyroid axes follow the same shape with different hormones. The hormone boxes show the principle of paired measurement, not the full biochemistry, and the nursing panel lists what is monitored rather than every possible observation.

Key points to remember

  • A hormone level is read with the hormone that controls it: a low target hormone with a high tropic hormone means the target gland has failed, while a low target hormone with a low tropic hormone means the pituitary or hypothalamus has failed.
  • Assessment comes before the laboratory: history, growth and weight, temperature tolerance, neck and eye inspection, visual fields, and blood pressure lying, sitting and standing.
  • Dynamic tests expose what a single sample hides: suppression tests ask whether the axis can be switched off, stimulation tests whether a gland can be switched on, and deprivation tests whether the kidney can concentrate urine.
  • Trousseau’s and Chvostek’s signs indicate latent tetany from hypocalcaemia after neck surgery, orthostatic vital signs detect aldosterone deficiency, and it is the glucose in the urine and the blood that separates water loss from sugar loss; the volume and colour of the urine only show whether the kidney is holding water.
  • The five recurring nursing tasks are daily weight on the same scale, measured intake and output, electrolyte and glucose surveillance, protection of lifelong hormone replacement, and teaching with a medical alert bracelet.
Go deeper

Worked example

Working up a patient who passes six litres of urine a day. A 52-year-old man reports that he drinks and passes urine constantly. A 24-hour collection contains 6 litres of pale urine with a specific gravity of 1.002, and he has lost two kilograms in a week. His random blood glucose is normal. He had a head injury in a road accident two years ago.

  1. Quantify the problem. Measure the 24-hour urine volume and the fluid intake, and weigh the patient on the same scale at the same time of day. Adult polyuria begins above roughly three litres a day; six litres is a real water loss and not a complaint. Check the sodium, the urea and the haematocrit, because a patient losing this much water becomes hypernatraemic and dehydrated.
  2. Exclude the common cause first. Check the blood glucose and the urine for glucose, because uncontrolled diabetes mellitus is the most frequent reason for polyuria and it is treated completely differently. A normal glucose with a very dilute urine moves the question away from sugar and towards water.
  3. Read what the target organ is doing. A specific gravity of 1.002 shows that the kidney is not concentrating the urine at all. Look for the reversible causes of a kidney that cannot answer vasopressin: a low potassium and a high calcium both make the tubule resistant to the hormone, and several medicines can do the same.
  4. Disturb the axis deliberately. Under supervision, fluids are withheld and the urine is measured, then desmopressin is given. If the urine becomes concentrated and the volume falls, the kidney can respond and the missing hormone is the problem — central diabetes insipidus, consistent with the old head injury. If the urine stays dilute, the kidney itself cannot respond. Stop the test and report if the patient loses more than about three to five per cent of body weight or if the sodium climbs sharply.
  5. Monitor and teach. Keep water within reach, record every millilitre of intake and output, weigh daily and follow the sodium, because replacing the hormone too generously causes water retention and a low sodium. Teach the patient that the medicine is taken every day, that the dose is adjusted on laboratory results, that a medical alert bracelet is worn, and what to do if the urine volume suddenly increases again.

The sequence is always the same shape: quantify the problem, rule out the common mimic, see what the target organ is doing, disturb the axis on purpose, and only then interpret a hormone level. The single most important safety point is that the dynamic test is a supervised procedure with a stopping rule, not an instruction to send the patient home thirsty. The nursing value of the case lies in the measurements — the collection, the weights and the sodium — because those are what make the diagnosis possible and what keep the patient safe while it is being made.

Common misconception

Many beginners believe that endocrine diagnosis works like any other blood test: find the hormone that is too high or too low and the disease names itself. That model fails for two reasons. Hormones are released in bursts and follow a daily rhythm, so a single value can be normal in a sick patient; and every gland is held in a feedback loop, so a value that is “normal” for a healthy person at rest can be grossly inappropriate for the situation. A low free T4 with a low TSH does not mean the thyroid is fine; it means the pituitary has stopped giving the order. This is why endocrine work-up uses pairs of hormones, timed samples, complete urine collections, imaging and dynamic tests rather than one number.

Check your reasoning

A patient has the typical appearance of excess cortisol, but a single morning blood cortisol is reported as normal. Explain to the patient why that does not exclude the diagnosis, and name the tests you expect the physician to order next.

Reveal an answer

Cortisol is not released at a steady rate: it comes in bursts and is highest in the early morning, so one sample can easily fall inside the reference range even when the total production over the day is far too high. That is why the diagnosis is made over time and against the feedback loop. The next tests are a 24-hour urinary free cortisol collection, which measures the total produced across a whole day and depends on the nurse obtaining a complete collection with the exact start and finish times, and an overnight low-dose dexamethasone suppression test, which checks whether the axis can still be switched off. Imaging of the pituitary and the adrenal glands follows once the excess is confirmed, because the source may be a pituitary tumour driving the adrenal cortex or an adrenal tumour producing cortisol on its own.

Where this comes from

  • Endocrine System Pathologies lecture notes (supplied), Level 200 nursing · “Assessment and Diagnostic Findings”, lines 97–102 (visual acuity and visual fields, CT and MRI of pituitary tumours, serum pituitary and target-organ hormones); “Diabetes insipidus”, lines 254–266 (normal blood glucose, low urine specific gravity, raised urea and sodium, vasopressin challenge, MRI) and lines 268–288 (desmopressin, fluid and electrolyte balance, daily weight, medical alert); “SIADH”, lines 313–328 (hyponatraemia, fluid restriction, daily weight, intake and output); “Hypothyroidism”, lines 367–380 (raised TSH unless the pituitary is the cause, low T3 and T4, autoantibodies, recheck at 6–8 weeks); “Hyperthyroidism”, lines 432–437 and 451–464 (T3, T4, antibodies, thyroid scan, laryngeal oedema, hypocalcaemia, semi-Fowler position); “Parathyroid”, lines 566–573 and 627–646 (calcium/PTH pair, Trousseau’s and Chvostek’s signs, IV calcium gluconate, quiet environment); adrenal axis, lines 654–661 (CRH–ACTH–cortisol negative feedback); “Cushing’s disease”, lines 737–742 (24-hour urinary free cortisol, low-dose dexamethasone suppression, imaging); “Diabetes mellitus”, lines 894–907 (fasting glucose 126 mg/dL = 7.0 mmol/L, OGTT 200 mg/dL = 11.1 mmol/L two hours after 75 g).
  • Beyond the supplied notes: standard test protocols and reference ranges · the 1 mg overnight dexamethasone suppression protocol; the 250 microgram cosyntropin stimulation test with cortisol at 30 and 60 minutes; the supervised water-deprivation protocol with desmopressin and its 3–5 per cent weight-loss stopping rule; the risk of osmotic demyelination when hyponatraemia is corrected too quickly and the caution that isotonic saline alone can worsen hyponatraemia in SIADH; the definition of orthostatic hypotension (a fall of at least 20 mmHg systolic or 10 mmHg diastolic on standing); a minimum adult urine output of about 0.5 mL/kg/h; the albumin correction for total calcium; reference ranges for TSH, free T4, total calcium, sodium and potassium; and the caveat that every laboratory sets its own ranges.
  • Corrections and clarifications applied to the supplied notes · Corrections: the notes require a fasting plasma glucose of 126 mg/dL (7.0 mmol/L) “on three different tests”, whereas standard practice confirms diabetes with two abnormal results from the same sample type, or one abnormal result together with classic symptoms; this section therefore states repeat confirmation rather than three tests. The notes also describe the vasopressin challenge in confusing wording (“will note a decrease in output and thirst”) and, for Cushing’s syndrome, give only the diagnosis line without explaining that dexamethasone is a suppression agent: both are rewritten here with the hormone language of the feedback axis. The notes’ spelling is corrected throughout for terms such as “hyrdrochlorothiazide”, “displagia”, “THYRIOD”, “PIYUITORY”, “parathormone” and “dessicated thyroid”.

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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.