Medicine — Adrenal and Pituitary Disease, NMC MBBS licence examination syllabus (Nepal Medical Council).
Adrenal and pituitary disease
One of these conditions kills quickly, is easily treated, and is usually mistaken for something else.
Most endocrine disease is chronic and unhurried. Adrenal insufficiency is the exception: an adrenal crisis presents as shock that does not respond to fluid, looks convincingly like sepsis or an acute abdomen, and is fatal if the diagnosis is not considered. The treatment is a steroid injection that is cheap, widely available and harmless if given unnecessarily.
That asymmetry — high cost of missing it, near-zero cost of treating it — is why the rule in this chapter is unusually blunt. Give the steroid, then confirm the diagnosis. Everything else here is important; that is the part that saves a life on a night shift.
🩺 Where this lives: The commonest cause of adrenal crisis is not a rare adrenal disease — it is a patient on long-term steroids who became unwell and did not increase the dose, or who stopped taking them. Long-term steroids suppress the adrenal axis, so the body cannot mount its own cortisol response to illness. A chest infection, a bout of vomiting, an operation, or simply running out of tablets can precipitate collapse. This makes it a prescribing problem as much as an endocrine one, and it is entirely preventable by two rules that every such patient should know.
💡 A note on numbers. This chapter gives no doses, no steroid equivalence tables, no sick-day dose multipliers, no stress-dose regimens, no cortisol or ACTH reference values and no dynamic test protocols. Steroid dosing is guideline-specific and getting it wrong in either direction causes harm. Take every figure from your national guidance. Thyroid disease and the cortisol-before-thyroxine rule are covered in the Thyroid chapter, hyponatraemia and hyperkalaemia in the Fluids chapter, and steroid adverse effects in the Prescribing Safety chapter.
Adrenal crisis
The presentation that should trigger the thought is shock that does not respond as expected to fluid, particularly with vomiting, abdominal pain and confusion, and with the biochemical triad of low sodium, high potassium and low glucose. It is mistaken for sepsis and for an acute abdomen because it genuinely resembles both — and the two can coexist, since infection is the commonest trigger. Give the steroid immediately. Take a cortisol sample if you can do so without delay, but never wait for the result.
WHY THE THRESHOLD FOR TREATING IS SO LOW
CONSIDER THE TWO ERRORS.
If you GIVE a steroid to someone who did not need it:
a single dose of hydrocortisone in an acutely unwell
adult is essentially harmless.
If you WITHHOLD it from someone in adrenal crisis:
they may die, and they will die of something entirely
treatable.
The asymmetry is so extreme that the correct behaviour is
to treat on suspicion. This is the same logic as antibiotics
in suspected meningococcal disease.
THE PRACTICAL RULE
In any shocked patient who is not responding as expected,
ASK WHETHER THEY TAKE STEROIDS — and ask about inhaled,
topical and injected preparations too, not only tablets.
Patients frequently do not regard these as "medicines",
exactly as with over-the-counter analgesics.
MANAGEMENT PRINCIPLES
STEROID immediately, by a parenteral route
FLUID resuscitation
GLUCOSE — hypoglycaemia is common
Look for and treat the PRECIPITANT, usually infection
Correct electrolytes; the sodium and potassium usually
improve with treatment
Doses come from your national guideline
AND AFTERWARDS: the patient needs education, a steroid
card, and clear sick-day instructions — because the crisis
will otherwise recur.
The two rules for long-term steroids
💡 Exam angle: these two rules are examined because breaking either causes a preventable crisis. Never stop long-term steroids abruptly — the suppressed axis cannot take over, so withdrawal must be gradual. And the dose goes up when the patient is ill, not down: fever, infection, surgery and trauma all increase requirement, and a vomiting patient needs a parenteral route because tablets will not be absorbed. Every patient on long-term steroids should carry a steroid card and know both rules.
Primary and secondary insufficiency
THE FEATURE THAT LOCALISES THE PROBLEM
PIGMENTATION MEANS PRIMARY.
In primary adrenal failure the adrenal cannot produce
cortisol, so negative feedback is lost and ACTH rises
sharply. ACTH and related peptides stimulate melanocytes —
producing pigmentation in skin creases, recent scars,
buccal mucosa, pressure areas and the palmar creases.
In SECONDARY insufficiency the problem is the pituitary, so
ACTH is LOW — and there is NO pigmentation. The patient may
look pale rather than tanned.
THE SECOND DIFFERENCE IS ALDOSTERONE
PRIMARY — the whole adrenal cortex fails, so
aldosterone is lost too. Hence salt loss,
volume depletion, LOW SODIUM and HIGH
POTASSIUM.
SECONDARY — aldosterone is largely regulated by the
renin-angiotensin system rather than by ACTH,
so it is preserved. Hyperkalaemia is
therefore less prominent.
CAUSES WORTH KNOWING
PRIMARY: autoimmune adrenalitis; TUBERCULOSIS, which
remains an important cause in this region; adrenal
haemorrhage, including in severe meningococcal sepsis;
metastases; HIV-related infection.
SECONDARY: EXOGENOUS STEROID WITHDRAWAL — much the
commonest — pituitary tumour, surgery, irradiation,
infarction, and postpartum pituitary necrosis.
THE CHRONIC PRESENTATION IS VAGUE: fatigue, weight loss,
anorexia, nausea, dizziness on standing, salt craving,
low mood. It is frequently attributed to depression or a
chronic infection for months before anyone measures a
sodium.
Cortisol excess
Before investigating Cushing's syndrome, look at the drug chart — prescribed glucocorticoid is by a wide margin the commonest cause, including inhaled and topical preparations that patients do not report. When it is not iatrogenic, the discriminating features are the ones that simple obesity does not produce: proximal myopathy (difficulty rising from a chair or climbing stairs), thin easily bruised skin, and wide purple striae. Central obesity and hypertension alone are far too common to be useful.
Pituitary disease
TWO WAYS A PITUITARY LESION PRESENTS
MASS EFFECT
The optic chiasm lies directly above the gland, so an
expanding lesion classically compresses the crossing
fibres and produces a BITEMPORAL HEMIANOPIA — loss of
the outer half of each visual field. Patients describe
bumping into things on both sides. Headache is common.
HORMONE EFFECT — excess or deficiency
PROLACTIN excess: galactorrhoea, amenorrhoea, reduced
libido, infertility.
GROWTH HORMONE excess: acromegaly — enlarging hands,
feet and facial features, often noticed by comparing
old photographs rather than by the patient.
DEFICIENCY: hypopituitarism, which may affect several
axes at once.
PITUITARY APOPLEXY — haemorrhage or infarction into the
gland. Sudden severe headache, visual disturbance,
ophthalmoplegia and collapse. It causes ACUTE ADRENAL
INSUFFICIENCY, so the immediate action is to GIVE STEROID
and refer urgently.
THE RULE THAT LINKS THIS TO THE THYROID CHAPTER
In hypopituitarism, REPLACE CORTISOL BEFORE THYROID
HORMONE. Thyroxine increases metabolic demand, and giving
it to a cortisol-deficient patient can precipitate an
adrenal crisis. This is examined in both chapters because
it is a genuine and avoidable harm.
Investigation and replacement regimens are specialist and
follow national guidance.
Clinical reasoning: four presentations
🔍 Case 1 — shock that will not lift
PresentationA woman presents with vomiting, abdominal pain and hypotension that persists after several litres of fluid. Sodium is low, potassium high, glucose low. She is treated for presumed sepsis and abdominal imaging is arranged. Nobody asks about medication.
Missed diagnosisAdrenal crisis.
ReasoningFluid-unresponsive shock with hyponatraemia, hyperkalaemia and hypoglycaemia is adrenal crisis until excluded. It resembles sepsis closely — and infection is often the trigger, so both may be present.
AnswerGive steroid immediately by a parenteral route, with fluid and glucose, take a cortisol sample only if it causes no delay, and treat the precipitant. Ask specifically about steroid use of any kind.
🔍 Case 2 — ran out of tablets
PresentationA man on long-term prednisolone for a chronic condition runs out of tablets while travelling and stops for four days. He then develops a febrile illness and collapses.
Two failuresAbrupt cessation, and no sick-day plan.
ReasoningLong-term steroids suppress the adrenal axis, so the body cannot generate its own cortisol response. Stopping abruptly removes the supply, and intercurrent illness raises demand at the same moment.
AnswerTreat as adrenal crisis. Then address prevention: never stop abruptly, increase the dose during illness, use a parenteral route if vomiting, and issue a steroid card with written sick-day rules.
🔍 Case 3 — tired, thin and tanned
PresentationA 40-year-old has six months of fatigue, weight loss, nausea and dizziness on standing. He craves salty food. He looks tanned despite little sun exposure, with dark buccal mucosa and palmar creases. He is being treated for depression.
Key signPigmentation.
ReasoningPigmentation of creases and mucosa indicates high ACTH, which means primary adrenal insufficiency. Salt craving and postural dizziness reflect aldosterone loss. The vague chronic picture is commonly attributed to depression.
AnswerCheck electrolytes and glucose, arrange cortisol testing per protocol, and treat urgently if he becomes unwell. Investigate the cause — in this region tuberculosis must be considered alongside autoimmune disease.
🔍 Case 4 — the inhaler that was not mentioned
PresentationA woman has central weight gain, a round face, thin bruising skin, purple striae and difficulty rising from a chair. An extensive endocrine work-up for Cushing's syndrome is planned. Her regular high-dose inhaled steroid and topical steroid cream are not recorded as medication.
Step missedThe drug chart.
ReasoningPrescribed glucocorticoid is by far the commonest cause of Cushing's syndrome, and patients often do not report inhaled or topical preparations as drugs. Proximal myopathy with thin bruising skin is the useful combination distinguishing this from simple obesity.
AnswerTake a full medication history including inhaled, topical and injected steroids before investigating. Review the indication and dose with the prescriber, and do not stop long-term steroid abruptly.
Commonly confused
Confusion
The distinction
Why it matters
Adrenal crisis vs sepsis
Fluid-unresponsive shock with the biochemical triad
They resemble each other and often coexist.
Confirming vs treating
Give the steroid first
The asymmetry of harm is extreme.
Primary vs secondary insufficiency
PIGMENTATION means primary
High ACTH drives it.
Aldosterone lost vs preserved
Only primary loses it
Explains the hyperkalaemia.
Stopping steroids vs tapering
The axis cannot take over abruptly
A leading preventable cause of crisis.
Illness: dose down vs up
Requirement RISES when ill
The counterintuitive rule patients forget.
Cushing's vs simple obesity
Proximal myopathy and thin bruising skin
Central obesity alone is not useful.
Thyroxine vs cortisol first
Replace cortisol first
Thyroxine can precipitate a crisis.
Rapid revision
MUST-KNOW FACTS
1. ADRENAL CRISIS: shock that does not respond to fluid.
2. With vomiting, abdominal pain and confusion.
3. Biochemistry: LOW SODIUM, HIGH POTASSIUM, LOW GLUCOSE.
4. It closely resembles SEPSIS and an acute abdomen.
5. GIVE STEROID IMMEDIATELY — do not wait for cortisol results.
6. A single dose in an unwell adult is essentially harmless.
7. Withholding it from a crisis may be fatal.
8. ASK EVERY UNEXPLAINED SHOCKED PATIENT ABOUT STEROIDS.
9. Include inhaled, topical and injected preparations.
10. Give fluid and GLUCOSE alongside, and find the precipitant.
11. Infection is the commonest trigger.
12. NEVER STOP LONG-TERM STEROIDS ABRUPTLY.
13. This includes patients who simply run out of tablets.
14. SICK DAY RULE: the dose goes UP when the patient is ill.
15. Vomiting means a PARENTERAL route.
16. Every long-term steroid patient needs a card and written rules.
17. PIGMENTATION MEANS PRIMARY — high ACTH drives it.
18. Look in creases, scars, buccal mucosa and palmar creases.
19. SECONDARY has NO pigmentation — ACTH is low.
20. PRIMARY loses ALDOSTERONE — salt loss, low sodium, high potassium.
21. SECONDARY preserves aldosterone — hyperkalaemia is less prominent.
22. Primary causes: autoimmune, TUBERCULOSIS, haemorrhage, metastases.
23. Secondary: EXOGENOUS STEROID WITHDRAWAL is much the commonest.
24. Chronic insufficiency is vague — often labelled depression for months.
25. CUSHING'S: the commonest cause is PRESCRIBED STEROID.
26. Check the drug chart, including inhaled and topical preparations.
27. Useful signs: PROXIMAL MYOPATHY and THIN BRUISING SKIN.
28. Also purple striae, hypertension, diabetes, osteoporosis.
29. PITUITARY mass effect: BITEMPORAL HEMIANOPIA and headache.
30. Prolactin excess: galactorrhoea, amenorrhoea, infertility.
31. Growth hormone excess: acromegaly, often seen in old photographs.
32. PITUITARY APOPLEXY: sudden headache, visual loss, collapse.
33. Apoplexy causes acute adrenal insufficiency — GIVE STEROID and refer.
34. In hypopituitarism, REPLACE CORTISOL BEFORE THYROID HORMONE.
💡 Exam angle: if you remember one thing from this chapter, make it the steroid. Shocked and not responding to fluid, or collapsed on long-term steroids, or pituitary apoplexy — in each case the answer is give hydrocortisone now and confirm afterwards.
Syllabus points
Recognising adrenal crisis
Why it resembles sepsis
Treating before confirming
Asking every shocked patient about steroids
Never stopping steroids abruptly
Sick day rules
Why pigmentation means primary
Aldosterone loss and hyperkalaemia
Causes including tuberculosis
The vague chronic presentation
Cushing's and the drug chart
Signs that distinguish it from obesity
Pituitary mass effect and hormone effect
Apoplexy and cortisol before thyroxine
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