Mastering Adrenal Insufficiency Guidelines for MRCP PACES
Why Adrenal Insufficiency Is a PACES Favourite
Adrenal insufficiency is one of the highest-yield endocrinology topics in the MRCP PACES examination. It can appear in Station 2 (history taking with fatigue, weight loss, or collapse), Station 4 (communication scenarios involving new diagnosis or steroid education), and Station 5 (brief consultation with a patient who has Addison's disease or is on long-term steroids). What makes this topic particularly attractive to examiners is the rich intersection of pathophysiology, clinical examination findings, guideline-based management, and patient safety communication — all of which are assessed across multiple marking domains in the revised PACES23 format.
As a registrar-level candidate, you are expected not merely to recognise adrenal insufficiency but to demonstrate a senior, guideline-concordant approach to diagnosis, acute management, and long-term patient education. This guide consolidates the essential guidelines and clinical pearls you need to present with confidence.
Classification: Know Your Definitions
Before discussing management, you must be able to classify adrenal insufficiency correctly. This is a frequent examiner question in the discussion phase:
| Type | Site of Defect | Common Causes |
|---|---|---|
| Primary | Adrenal cortex | Autoimmune Addison's disease, TB, adrenal haemorrhage, metastases, congenital adrenal hyperplasia |
| Secondary | Anterior pituitary | Pituitary tumours, pituitary surgery/radiotherapy, Sheehan's syndrome |
| Tertiary | Hypothalamus | Chronic exogenous steroid suppression (most common in practice) |
Examiner Pearl: In PACES, if the patient is on long-term glucocorticoids, the most likely cause of adrenal insufficiency is tertiary (iatrogenic) HPA axis suppression. Always ask about inhaled, nasal, and topical steroids, not just oral prednisolone.
Recognising the Clinical Presentation
History Clues (Station 2 and Station 5)
The presentation of adrenal insufficiency is notoriously insidious. Key features to elicit:
Fatigue and weakness (present in nearly all patients)
Weight loss (often 5–10 kg)
Gastrointestinal symptoms — nausea, vomiting, abdominal pain, anorexia
Postural dizziness or syncope (suggests mineralocorticoid deficiency)
Salt craving (classic in primary AI)
Skin pigmentation — especially palmar creases, buccal mucosa, scars, and gingival mucosa (primary AI only — due to elevated POMC/MSH)
Vitiligo (autoimmune association)
Loss of axillary and pubic hair (women — due to loss of adrenal androgens)
Amenorrhoea in women
Examination Clues (Station 1 or Station 3)
Hyperpigmentation — the single most important sign to elicit actively
Postural hypotension — check lying and standing BP
Signs of associated autoimmune conditions — vitiligo, thyroid enlargement, features of type 1 diabetes
Signs of underlying cause — e.g., cachexia (malignancy), neck scar (thyroidectomy suggesting polyglandular failure)
PACES23 Marking Tip: In the clinical examination stations, actively stating "I would like to check for postural drop in blood pressure" and "I would examine the buccal mucosa and palmar creases for pigmentation" demonstrates safe, thorough clinical reasoning and directly contributes to the Clinical Examination skill domain.
Diagnostic Guidelines: A Stepwise Approach
The diagnostic pathway should follow a logical, guideline-concordant sequence. You should be able to articulate this clearly during examiner discussion.
Step 1: Screening Test
Morning (9 AM) serum cortisol
If cortisol < 100 nmol/L → adrenal insufficiency is likely; proceed to confirmatory testing
If cortisol > 400–450 nmol/L → adrenal insufficiency is excluded (in the absence of severe stress)
If cortisol 100–400 nmol/L → equivocal; proceed to short Synacthen (ACTH stimulation) test
Step 2: Confirmatory Test
Short Synacthen Test (250 µg IV/IM ACTH analogue)
Measure cortisol at 0, 30, and 60 minutes
Normal response: peak cortisol ≥ 500–550 nmol/L
Subnormal response: confirms adrenal insufficiency
Step 3: Differentiate Primary from Secondary/Tertiary
-
Plasma ACTH level (taken at 9 AM with cortisol):
Primary AI: ACTH is markedly elevated (> 300 ng/L) due to loss of negative feedback
Secondary/Tertiary AI: ACTH is low or inappropriately normal
-
Plasma renin and aldosterone:
Primary AI: Renin elevated, aldosterone low (zona glomerulosa also destroyed)
Secondary/Tertiary AI: Renin and aldosterone typically normal (RAAS is ACTH-independent)
Step 4: Identify the Underlying Cause
Adrenal autoantibodies (21-hydroxylase antibodies) — confirms autoimmune Addison's
** adrenal CT** — to identify haemorrhage, infiltration, calcification (suggesting TB), or masses
Pituitary MRI — if secondary cause suspected
Consider TB screening (Quantiferon, chest X-ray) in high-risk populations
Check other autoimmune conditions (TFTs, HbA1c, B12, thyroid antibodies) if autoimmune Addison's confirmed
Examiner Pearl: Always mention the importance of checking DHEA-S and 17-OH progesterone if congenital adrenal hyperplasia is suspected, particularly in younger patients or those with hyperandrogenism.
Long-Term Management Guidelines
Glucocorticoid Replacement
The backbone of management is oral hydrocortisone, dosed to mimic the physiological cortisol circadian rhythm:
-
Standard regimen: 15–25 mg/day in 2–3 divided doses
Common schedule: 10 mg on waking, 5 mg at midday, 5 mg at 4–5 PM
Largest dose in the morning to mimic the physiological dawn cortisol rise
-
Alternative agents:
Prednisolone 5 mg once daily (longer half-life; useful for once-daily dosing)
Dexamethasone — rarely used for maintenance (no physiological equivalence; used in acute settings)
Mineralocorticoid Replacement (Primary AI Only)
Fludrocortisone 50–200 µg once daily (typically 100 µg)
Not needed in secondary/tertiary AI (RAAS axis is intact)
Dose adjusted based on blood pressure, electrolytes, and plasma renin
Monitoring
Patients should be reviewed at least annually in specialist endocrinology clinics, with assessment of:
Symptoms of over- or under-replacement
Blood pressure (including postural)
BMI
Electrolytes (Na+, K+)
Plasma renin (to guide fludrocortisone dosing)
Bone health (DEXA scan — glucocorticoids increase osteoporosis risk)
Sick Day Rules: The Communication Essential
This is the most commonly tested communication point in adrenal insufficiency PACES scenarios. Whether in Station 4 or Station 5, you must be able to clearly and confidently explain sick day rules.
The Sick Day Rules Protocol
| Situation | Action |
|---|---|
| Mild-moderate illness (e.g., URTI, fever > 37.5°C) | Double the normal oral hydrocortisone dose for 2–3 days until recovered |
| Severe illness / vomiting / diarrhoea / unable to take oral medication | 100 mg IM hydrocortisone (self-administered or by carer) → seek urgent medical attention |
| Surgical procedure — minor (e.g., under local anaesthesia) | Double hydrocortisone on the day |
| Surgical procedure — moderate (e.g., general anaesthesia, joint replacement) | Hydrocortisone 100 mg IM at induction → 50 mg IM/IV every 8 hours for 24–48 hours → taper to normal |
| Major surgery / ITU admission | Hydrocortisone 100 mg IV stat → continuous infusion 200 mg/24 hours or 50 mg IV every 6 hours → taper over 2–3 days |
Additional Safety Netting for Patients
Carry a steroid emergency card (or wear medical alert jewellery)
Keep an emergency hydrocortisone injection kit at home and know how to use it
Ensure family members/carers know how to administer IM hydrocortisone
Register with the UK Addison's Disease Self-Help Group for support resources
PACES23 Communication Tip: When explaining sick day rules in a communication station, use teach-back — ask the patient to repeat the instructions back to you. This demonstrates the patient-centred communication skills that examiners score in the Managing Patients' Concerns domain.
Adrenal Crisis: Emergency Management
Adrenal crisis is a life-threatening emergency and a high-yield scenario for acute medicine discussion in PACES. You must know the emergency protocol cold.
Recognition
Suspect adrenal crisis in any patient with known adrenal insufficiency (or risk factors) presenting with:
Hypotension (often refractory to fluids)
Abdominal pain, vomiting, diarrhoea (can mimic acute abdomen — do NOT operate until treated!)
Altered consciousness / confusion
Hyponatraemia, hyperkalaemia, hypoglycaemia
Unexplained fever
Emergency Protocol (NICE-Concordant)
ABCDE approach — secure airway, high-flow oxygen, IV access (2 large-bore cannulae)
Immediate IV/IM hydrocortisone 100 mg — do NOT wait for cortisol results to treat
IV fluids: 1 litre 0.9% sodium chloride stat → continue with 1 litre every 4–6 hours (adjust based on clinical response and sodium level)
Correct hypoglycaemia: if glucose < 4 mmol/L, give 25–50 mL of 50% dextrose IV (or 100 mL of 10% dextrose)
Treat precipitating cause: sepsis (blood cultures + broad-spectrum antibiotics), MI, etc.
Monitor: electrolytes (Na+, K+), glucose, urea, creatinine every 4–6 hours; continuous cardiac monitoring (hyperkalaemia risk)
Supportive care: urinary catheter for fluid balance, consider VTE prophylaxis
Key Don'ts
Do NOT delay hydrocortisone while waiting for confirmatory cortisol/ACTH levels (but do take bloods first if possible)
Do NOT give fludrocortisone acutely — at high hydrocortisone doses (> 100 mg/day), the mineralocorticoid effect of hydrocortisone is sufficient
Do NOT perform surgery for an acute abdomen until adrenal crisis is treated — the abdominal pain often resolves with steroid replacement
Examiner Pearl: A classic PACES question is: "A patient with Addison's disease presents with vomiting and hypotension. What is your immediate management?" The expected answer must include: IM/IV hydrocortisone 100 mg immediately, IV fluids, bloods including cortisol/ACTH before steroids if possible but treatment must not be delayed, identify and treat precipitant.
Common PACES Scenarios: What to Expect
Scenario 1: Station 5 — Newly Diagnosed Addison's Disease
Patient brief: A 42-year-old woman recently diagnosed with autoimmune Addison's disease attends for follow-up.
Your tasks: Take a focused history, address concerns, discuss management plan.
Key points to cover:
Confirm understanding of the diagnosis
Review symptoms — is the replacement adequate?
Explain sick day rules clearly
Ensure the patient has a steroid emergency card and IM hydrocortisone kit
Discuss associated autoimmune conditions (thyroid, B12, type 1 diabetes)
Address psychological impact and support groups
Safety netting regarding adrenal crisis
Scenario 2: Station 2 — Fatigue and Weight Loss
Patient brief: A 55-year-old man presents with 3 months of progressive fatigue, 8 kg weight loss, and dizziness on standing.
Key historical features to elicit:
Timeline and progression of symptoms
Associated GI symptoms (nausea, vomiting, abdominal pain)
Skin changes (has the patient or family noticed darkening of skin?)
Salt craving
Medication history — especially any steroid exposure (inhaled, topical, oral)
Other autoimmune conditions
Family history of autoimmune disease
Sexual symptoms (loss of libido, erectile dysfunction, amenorrhoea)
Presentation structure to examiner:
"My differential diagnosis includes adrenal insufficiency, given the constellation of fatigue, weight loss, postural symptoms, and the possibility of hyperpigmentation on examination. I would also consider..."
State your investigation plan clearly (morning cortisol → Synacthen test → ACTH level → cause identification)
Scenario 3: Station 4 — Breaking Bad News and Steroid Education
Patient brief: A 28-year-old woman with newly diagnosed Addison's disease needs education about lifelong steroid replacement.
Communication skills to demonstrate:
Use the SPIKES protocol for delivering the diagnosis
Explore the patient's understanding before explaining
Chunk and check — deliver information in manageable portions and confirm understanding
Acknowledge emotions — this is a chronic, lifelong diagnosis that will affect daily life
Empower the patient — with appropriate education, Addison's disease is fully compatible with a normal life and normal life expectancy
Provide written information and signpost to support groups
High-Yield Exam Facts: Quick Revision
| Fact | Detail |
|---|---|
| Most common cause of primary AI in the UK | Autoimmune Addison's disease (~80%) |
| Most common cause worldwide | Tuberculosis |
| Drug causing AI | Exogenous glucocorticoids (iatrogenic — tertiary AI) |
| Cortisol level excluding AI (unstressed) | > 400–450 nmol/L |
| Cortisol level suggesting AI | < 100 nmol/L |
| Synacthen test — adequate response | Peak cortisol ≥ 500 nmol/L at 30 or 60 min |
| ACTH in primary AI | Markedly elevated |
| Electrolyte pattern in primary AI | Hyponatraemia, hyperkalaemia, hypoglycaemia |
| Electrolytes in secondary AI | Hyponatraemia possible (cortisol deficiency); K+ is normal (aldosterone preserved) |
| Hydrocortisone replacement dose | 15–25 mg/day in divided doses |
| Fludrocortisone dose | 50–200 µg/day (primary AI only) |
| Adrenal crisis — hydrocortisone dose | 100 mg IV/IM immediately |
| Adrenal crisis — IV fluid | 1L 0.9% NaCl stat |
| Sick day rule — mild illness | Double hydrocortisone |
| Sick day rule — vomiting | 100 mg IM hydrocortisone → seek help |
Common Candidate Mistakes to Avoid
Forgetting to mention ACTH level when discussing differentiation between primary and secondary AI
Not knowing sick day rules — this is essentially guaranteed marks in a communication scenario
Overlooking iatrogenic (steroid-induced) AI — always ask about ALL steroid forms
Recommending fludrocortisone for secondary/tertiary AI — it is only needed when the adrenal cortex (zona glomerulosa) is destroyed
Failing to safety-net adequately — the emergency injection kit, steroid card, and family education are essential
Not mentioning autoimmune screening for associated conditions in primary AI
Confusing the electrolyte patterns — hyperkalaemia is specific to primary AI (mineralocorticoid deficiency)
Summary Checklist for PACES
When faced with an adrenal insufficiency scenario, mentally run through this checklist:
☐ Have I classified the type of AI correctly?
☐ Can I state the diagnostic pathway (cortisol → Synacthen → ACTH → cause)?
☐ Do I know the hydrocortisone replacement regimen?
☐ Can I explain sick day rules clearly to a patient?
☐ Do I know the adrenal crisis emergency protocol?
☐ Have I mentioned fludrocortisone appropriately (primary only)?
☐ Have I screened for associated autoimmune conditions?
☐ Have I addressed patient safety netting (card, injection kit, alert bracelet)?
Mastering these guidelines will ensure you can approach any adrenal insufficiency scenario in PACES with the confidence and clinical maturity expected at registrar level. Good luck with your preparation!
Last reviewed: 2025. Guidelines referenced include NICE CKS Adrenal Insufficiency, Addison's Disease Clinical Practice Guideline (Endocrine Society), and the European Society of Endocrinology guidelines. Always check the latest local protocols for your examination centre.
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