🟠 Adrenal Glands
Anatomy, cortex zones, medulla, Cushing’s, Conn’s, phaeochromocytoma, adrenal insufficiency — MRCS high-yield.
Anatomy & Cortical Zones
Gross Anatomy
| Feature | Detail |
|---|---|
| Location | Retroperitoneal, superior to each kidney within Gerota’s fascia. Right gland: pyramidal, closely related to inferior vena cava (IVC). Left gland: crescent-shaped, closely related to left renal vein and splenic vessels. |
| Size/weight | ~4 × 3 × 1 cm; ~5g each. Larger in stress (physiological hypertrophy). |
| Structure | Outer cortex (80–90% of gland mass) — lipid-rich, yellow appearance. Inner medulla (10–20%) — reddish-brown; modified sympathetic ganglion cells (chromaffin cells). |
| Right adrenal relations | Medial: IVC (very closely applied — a key surgical hazard). Superior: right lobe of liver. Posterior: right diaphragmatic crus. Right adrenal vein drains directly into IVC — short, fragile, most dangerous step in right adrenalectomy. |
| Left adrenal relations | Medial: aorta. Superior: body of pancreas and splenic vessels. Left adrenal vein drains into left renal vein (longer than right — slightly easier to ligate). |
Blood Supply
| Vessel | Origin | Supply |
|---|---|---|
| Superior suprarenal artery | Inferior phrenic artery | Upper part of gland |
| Middle suprarenal artery | Aorta directly | Middle part |
| Inferior suprarenal artery | Renal artery | Lower part |
| Right adrenal vein | Drains to IVC directly | Short (~5 mm) — highest risk step in right adrenalectomy |
| Left adrenal vein | Drains to left renal vein | Longer, less hazardous than right |
- Mineralocorticoid
- Acts on DCT & collecting duct
- ↑ Na⁺ reabsorption
- ↑ K⁺ excretion
- ↑ H⁺ excretion
- Regulated by RAAS + serum K⁺ (not ACTH)
- Excess → Conn’s syndrome (hypertension + hypokalaemia)
- Glucocorticoid — “stress hormone”
- Regulated by ACTH (pituitary)
- ↑ gluconeogenesis → hyperglycaemia
- Anti-inflammatory (inhibits PLA₂)
- Immunosuppression
- ↑ protein catabolism → muscle wasting, thin skin, striae
- ↑ fat redistribution → central obesity, buffalo hump
- Excess → Cushing’s syndrome
- Weak androgens: DHEA and androstenedione
- Regulated by ACTH
- Peripheral conversion to testosterone/oestrogens
- Important in females (main androgen source post-menopause)
- Excess → virilisation in females (congenital adrenal hyperplasia); feminisation in males
- Modified postganglionic sympathetic neurons (chromaffin cells)
- Adrenaline (epinephrine): ~80%
- Noradrenaline (norepinephrine): ~20%
- Regulated by sympathetic nervous system (not ACTH)
- “Fight or flight” response
- ↑ HR, ↑ BP, ↑ glucose, bronchodilation
- Excess → phaeochromocytoma
Aldosterone — Primary Role is Potassium Excretion
Although aldosterone is often remembered primarily for sodium retention (and the consequent water retention and blood pressure rise), its primary physiological role is potassium excretion in the distal convoluted tubule (DCT) and collecting duct. This is why primary hyperaldosteronism (Conn’s syndrome) characteristically causes hypokalaemia — excess aldosterone drives potassium out into the urine.
Aldosterone also promotes H⁺ ion excretion → metabolic alkalosis. The triad of Conn’s is therefore: hypertension + hypokalaemia + metabolic alkalosis.
Regulation: aldosterone is controlled by the renin-angiotensin-aldosterone system (RAAS) and directly by serum potassium — NOT by ACTH (contrast with cortisol and androgens which are ACTH-dependent). This explains why in primary hyperaldosteronism, renin is suppressed (excess aldosterone provides negative feedback on renin via expanded blood volume).