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Q1: Definition and diagnosis (2 min)
- Define adrenal insufficiency and distinguish primary (Addison), secondary (pituitary ACTH deficiency) and tertiary (hypothalamic CRH deficiency, most often chronic exogenous steroid therapy).
- Why does primary AI produce hyponatraemia WITH hyperkalaemia while secondary AI produces hyponatraemia WITHOUT hyperkalaemia? (Aldosterone is regulated by the RAAS (angiotensin II, potassium), not by ACTH — preserved in secondary AI.)
- How would you confirm AI biochemically? (Morning cortisol: above 500 nmol/L excludes; below 138 nmol/L highly suggestive. Confirm with the 250 mcg short Synacthen test — peak cortisol above 500 nmol/L is normal.)
- How do you localise the level? (Plasma ACTH — high in primary, low in secondary; renin and aldosterone — renin high + aldosterone low in primary, normal in secondary.)
Q2: Causes and classification (2 min)
- Classify the causes of primary AI: autoimmune (West, anti-21-hydroxylase Ab, APS-1/APS-2); tuberculosis (worldwide); congenital adrenal hyperplasia (21-OHD, raised 17-OH-progesterone); bilateral adrenal haemorrhage (Waterhouse-Friderichsen in meningococcaemia, anticoagulation); infiltrative (amyloid, sarcoid, haemochromatosis); metastases; infections (HIV, fungal); drugs (etomidate, ketoconazole, metyrapone, mitotane, mifepristone).
- Distinguish APS-1 (AIRE gene, candidiasis + hypoparathyroidism + Addison) from APS-2 / Schmidt syndrome (Addison + autoimmune thyroid + type 1 diabetes).
- What are the causes of secondary AI? (Pituitary adenoma, surgery/radiotherapy, apoplexy, Sheehan, infiltrative, trauma, genetic — PROP1.)
- What is the commonest AI of all? (Tertiary — chronic exogenous glucocorticoid therapy suppressing CRH/ACTH.)
Q3: Management (3 min)
- Chronic replacement in primary AI: hydrocortisone 15 to 25 mg/day in divided doses (10 mg waking, 5 mg noon, 5 mg evening) + fludrocortisone 50 to 200 mcg/day (primary only) — how do you titrate fludrocortisone? (blood pressure including postural, electrolytes, plasma renin to upper normal).
- Why is fludrocortisone not needed in secondary AI? (the RAAS is intact).
- Reproduce the sick-day rules: minor febrile illness — double the hydrocortisone; severe illness, vomiting or surgery — triple or hydrocortisone 100 mg IM/IV.
- Reproduce the surgical stress-dose steroid schedule: minor 50 mg, moderate 75 to 100 mg, major 100 mg at induction then 200 mg/24 h for 24 to 48 h then taper.
- What does the patient carry? (Steroid Emergency Card, medical alert bracelet, emergency hydrocortisone 100 mg IM injection kit.)
- Why does patient education halve crisis rates? (the commonest cause of crisis is non-adherence during illness or failure to escalate during vomiting.)
Q4: Adrenal crisis (3 min)
- Clinical tetrad: shock, abdominal pain/vomiting, hypoglycaemia, hyponatraemia ± hyperkalaemia.
- The resuscitation bundle: ABCDE; hydrocortisone 100 mg IV STAT then 100 mg/24 h; 0.9 percent saline 1 L STAT then 2 to 3 L/24 h + dextrose if hypoglycaemic; treat the precipitant (cultures and broad-spectrum antibiotics for sepsis); ICU; taper daily once stable.
- Why is fludrocortisone NOT needed acutely in crisis? (high-dose hydrocortisone above 50 to 100 mg/day saturates the mineralocorticoid receptor.)
- Why draw cortisol and ACTH BEFORE the first hydrocortisone but treat empirically? (the in-crisis cortisol and ACTH are diagnostic.)
- Why does vasopressor-refractory shock respond to hydrocortisone? (cortisol restores vascular catecholamine sensitivity.)
- Name five precipitants of crisis: infection (commonest), omitted dose or vomiting, surgery/trauma, MI/stroke, pregnancy/labour, abrupt steroid withdrawal.
Q5: Special situations and pitfalls (2 min)
- Pregnancy in AI — increase hydrocortisone in the third trimester; hydrocortisone 100 mg IM q6-8h in labour; fludrocortisone often reduced postpartum.
- CAH 21-OHD in neonates — salt-wasting crisis with ambiguous genitalia in females; raised 17-OH-progesterone; newborn screen.
- CIRCI / septic shock — hydrocortisone 200 mg/day for vasopressor-refractory shock (Annane 2002 — benefit in SST non-responders; CORTICUS 2008 — no overall mortality benefit).
- Pitfalls: never treat SIADH with fluid restriction before excluding AI; never give thyroxine before hydrocortisone in panhypopituitarism (thyroxine accelerates cortisol clearance → crisis); rifampicin accelerates cortisol metabolism (double the hydrocortisone); etomidate inhibits 11β-hydroxylase (avoid in septic shock).