Adrenal Gland Secrets: From GFR Layers to Addison’s Bronze Killer – A MSRA Revision Guide

examiner mla
Jul 1
2 min read

Updated: Sep 2

Adrenal Gland Anatomy & Function – Layer by Layer

🧠 The Adrenal Gland: Two Regions

Adrenal Cortex (outer): produces steroid hormones
Adrenal Medulla (inner): produces catecholamines

🧱 Adrenal Cortex: 3 Layers (Mnemonic: "GFR – Salt, Sugar, Sex")

Layer	Hormones	Type	ACTH Dependent?
Zona Glomerulosa	Aldosterone	Mineralocorticoid	❌ (RAAS-regulated)
Zona Fasciculata	Cortisol	Glucocorticoid	✅
Zona Reticularis	DHEA, Androstenedione	Androgens	✅

⚡ Adrenal Medulla

Hormones	Stimulus
Epinephrine, Norepinephrine	Sympathetic nervous system (ACh)

Summary:

ACTH stimulates: Cortisol (fasciculata) and androgens (reticularis)
Not ACTH-dependent: Aldosterone (glomerulosa – regulated by RAAS & potassium)
Medulla is independent of ACTH

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Addison’s Disease – The Bronze Killer

⚡ Why is Addison’s Disease Important?

Because it:

Presents insidiously with non-specific symptoms.
Can lead to life-threatening adrenal crisis.
Has classic signs that are easy to clinch marks in your exams if you recognise them.

🔑 What is Addison’s Disease?

▶️ Primary adrenal insufficiency due to destruction of the adrenal cortex.

Top Causes:

UK/US: Autoimmune adrenalitis (most common)
Worldwide: Tuberculosis (still a major cause globally)
Others: HIV, fungal infections (e.g. histoplasmosis in immunocompromised), adrenal hemorrhage (Waterhouse–Friderichsen syndrome from meningococcal sepsis).

👩‍⚕️ Key Clinical Presentation – The Exam Triggers

✅ Fatigue + Weight Loss + Salt Craving → Think Addison’s Disease.

✅ Hyperpigmentation:

Palmar creases
Buccal mucosa
Scar areas, hip creases

➡️ Due to ↑ ACTH + MSH from Pro-opiomelanocortin cleavage.

✅ Postural Hypotension

Due to volume depletion (lack of aldosterone).

✅ Electrolyte Clues:

Hyponatremia (↓ Na+)
Hyperkalemia (↑ K+)
Hypoglycemia (especially in children)
Mild hypercalcemia (10-20%)

✅ Mood & GI Symptoms:

Nausea, vomiting, abdominal pain, constipation or diarrhoea.
Low mood, irritability, confusion.

🚨 Adrenal Crisis – Life-Threatening Emergency

🆘 Presentation:

Severe hypotension, hypovolemic shock
Vomiting, acute abdominal pain
Reduced consciousness

💡 Triggers: Infection, surgery, trauma.

🔑 Management:

Urgent IV hydrocortisone + IV fluids.

🧪 Investigations – What Exams Test You On

🔬 8 AM Serum Cortisol:

>500 nmol/L: Adrenal insufficiency unlikely
<100 nmol/L: Suggestive
100–500 nmol/L: Needs Synacthen (ACTH stimulation) test.

🧪 Synacthen Test:

250 μg tetracosactide IV/IM
Measure cortisol before and 30 mins after.
Normal: Rise to >500-550 nmol/L.

✅ Other Key Tests:

Adrenal autoantibodies: Anti-21 hydroxylase, adrenal cortex antibodies.
U&E: Hyponatremia, hyperkalemia
CT abdomen: Adrenal calcifications (TB), hemorrhage.
High ACTH + high renin + low aldosterone in primary insufficiency.

💊 Management Essentials

Glucocorticoid Replacement:
- Hydrocortisone 15-25 mg/day in 2-3 divided doses.
- Stress dosing: Double dose during illness, surgery, or strenuous exercise.
Mineralocorticoid Replacement:
- Fludrocortisone to maintain BP and sodium.
Emergency Measures:
- Medical alert bracelet + steroid card (blue).
- Emergency hydrocortisone IM injection kit.

🧠 Associated Autoimmune Syndromes

▶️ APS Type 2 (Schmidt’s): Addison’s + autoimmune thyroid disease ± Type 1 DM.

▶️ APS Type 1 (APECED): Addison’s + hypoparathyroidism + mucocutaneous candidiasis.

👶 Paediatric Pearl

Congenital Adrenal Hyperplasia (CAH) mimics Addison’s in infants (vomiting, dehydration) but no hyperpigmentation.

🔑 High-Yield Exam Clinchers Summary

✔️ Bronze skin (palmar creases, buccal mucosa) + salt craving + postural hypotension.

✔️ Hyponatremia + hyperkalemia + raised ACTH.

✔️ No cortisol rise on Synacthen test confirms diagnosis.

✔️ Always stress dose steroids during illness to avoid adrenal crisis.

✨ Final Pearl for MSRA

“If you see fatigue, weight loss, hyperpigmentation, and hypotension – Addison’s is your best answer choice.”

📚 References: