Adrenal-tumors
🧬 Secondary Hypertension · Adrenal Gland Tumors
Pheochromocytoma · Conn's Syndrome · Cushing's Syndrome — predict the tumor from the physiology.
The adrenal glands are hormonal powerhouses. Depending on which layer develops a tumor, you get a completely different type of severe hypertension, driven by distinct physiological mechanisms.
Anatomy 101: The Adrenal Gland Layers
Adrenal Cortex (Outer layer)
- Aldosterone (Mineralocorticoid)
- Cortisol (Glucocorticoid)
- Androgens (Sex hormones)
Function Regulates salt/water balance, metabolism, stress response.
Adrenal Medulla (Inner core)
- Epinephrine (Adrenaline)
- Norepinephrine (Noradrenaline)
Function "Fight or Flight" — controls HR, contractility, vascular tone.
Tumor 1: Adrenal Medulla — PHEOCHROMOCYTOMA
The "Spiker" — paroxysmal surges of catecholamines
What it is: Tumor of chromaffin cells in the medulla that dumps uncontrolled surges of Epinephrine and Norepinephrine.
Pathophysiology (connecting to our cheat sheet):
- HR: Norepinephrine → Beta-1 → tachycardia.
- SV: Epinephrine → Beta-1 → ↑ contractility → ↑ SV.
- TPR: Norepinephrine → Alpha-1 → massive vasoconstriction.
- Calcium: Alpha-1 → Gq → IP3 → SR calcium release → violent constriction.
Clinical Prediction:
- BP: Paroxysmal spikes (e.g., 240/140 mmHg).
- HR: Very fast (110–140 bpm) during spikes.
- Symptoms: Pounding headache, sweating (diaphoresis), palpitations, pallor.
- Metabolic clue: Hyperglycemia (glycogen breakdown).
⚠️ Treatment order: Alpha-blocker first (Phenoxybenzamine) to dilate vessels. Wait 1 week, then add Beta-blocker to control HR. Then surgical resection.
Tumor 2: Adrenal Cortex (Zona Glomerulosa) — PRIMARY ALDOSTERONISM
Conn's Syndrome — relentless volume-driven hypertension
What it is: Tumor (or hyperplasia) producing excessive Aldosterone → kidney retains Na⁺, excretes K⁺.
Pathophysiology:
- Volume / SV: Na⁺ retention → water follows → ↑ blood volume → ↑ preload → ↑ SV (Frank-Starling).
- TPR: Volume expands → stretches arterioles → myogenic response → vasoconstriction.
- Na/K pump: High extracellular Na⁺ → pump struggles → intracellular Na⁺ rises → NCX reverses → Ca²⁺ influx → chronic constriction.
Clinical Prediction:
- BP: Sustained, severe (e.g., 160–180/100–110).
- HR: Normal or slow (reflex bradycardia).
- Metabolic clue: Hypokalemia (low K⁺) → muscle cramps, weakness, fatigue. Metabolic alkalosis.
💊 Treatment: Spironolactone or Eplerenone (aldosterone receptor blockers) — directly block Na⁺ retention, reduce volume. Amiloride (blocks sodium channels downstream).
Tumor 3: Adrenal Cortex (Zona Fasciculata) — CUSHING'S SYNDROME
Cortisol excess — mimics aldosterone + amplifies RAAS
What it is: Tumor (or pituitary ACTH-driven) producing excessive Cortisol.
Pathophysiology:
- Volume / SV: Cortisol mimics aldosterone → Na⁺/water retention → ↑ preload → ↑ SV.
- TPR: Cortisol ↑ hepatic Angiotensinogen → floods RAAS → ↑ Angiotensin II → vasoconstriction.
- Vessels: Cortisol ↑ Alpha-1 receptors → hyper-reactivity to norepinephrine.
Clinical Prediction:
- BP: Moderate to severe systemic hypertension (both systolic and diastolic).
- HR: Normal or slightly elevated.
- Physical clues: Central obesity, "Moon face," "Buffalo hump," purple striae, easy bruising, high blood sugar (steroid-induced diabetes).
💊 Treatment: Surgical resection (adrenal or pituitary). Control BP with ACE inhibitors (block RAAS) + diuretics (reduce volume).
📋 The Ultimate Differential Diagnosis Cheat Sheet
| Feature | Pheochromocytoma (Medulla) | Conn's Syndrome (Cortex - Aldosterone) | Cushing's Syndrome (Cortex - Cortisol) |
|---|---|---|---|
| BP Pattern | Paroxysmal spikes (normal in between) | Sustained, severe | Sustained, moderate |
| Heart Rate | Very Fast (Tachycardia) | Normal / Slow | Normal / Slightly Fast |
| Key Physical Sign | Sweating, pounding headache, pallor | Muscle cramps, weakness, fatigue | Moon face, buffalo hump, purple striae |
| Serum Potassium | Normal | Very LOW (Hypokalemia) | Normal or slightly low |
| Serum Sodium | Normal | Normal or High | Normal or High |
| Blood Sugar | High (during spikes) | Normal | Very High (Diabetes) |
| Underlying Mechanism | Massive ↑ in CO and TPR (Sympathetic) | Massive ↑ in Volume (SV) and Myogenic TPR | Massive ↑ in RAAS (Angiotensin II) and Volume |
| Best First Drug | Alpha-blocker (then Beta-blocker) | Aldosterone Antagonist (Spironolactone) | ACE Inhibitor + Diuretic |
| Definitive Cure | Surgical resection | Surgical resection (or Spironolactone lifelong) | Surgical resection (Adrenal or Pituitary) |
🧠 The "Suprarenal" Summary
A tumor in the adrenal gland doesn't just "cause high blood pressure." It hijacks a specific physiological pathway:
- Medulla (Pheochromocytoma): Hijacks the Sympathetic Nervous System (Calcium, HR, TPR).
- Cortex - Aldosterone (Conn's): Hijacks the Kidney/Volume (Na/K pump, Preload, Myogenic tone).
- Cortex - Cortisol (Cushing's): Hijacks the RAAS System (Angiotensinogen, TPR, Volume).
clinical endocrinology · physiology