Adrenal Adenomas Deep Dive

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Why This Question Was Tricky

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The question gave you a young, healthy woman with hypertension, hypokalemia, and metabolic alkalosis. No other symptoms. No meds. Normal glucose.

45% of students picked "increased angiotensin II" — because they know aldosterone is high and assumed the whole RAAS chain must be up. That's the trap.

⚠ In primary hyperaldosteronism, the tumor makes aldosterone on its own — it doesn't need renin or angiotensin II. The high aldosterone actually suppresses renin via negative feedback. Renin is LOW. Angiotensin II is LOW.

The correct answer is low plasma renin levels. The tumor bypasses the whole RAAS cascade.

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Conn Syndrome — Primary Hyperaldosteronism

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An aldosterone-secreting adenomaA benign tumor in the adrenal cortex (zona glomerulosa) that pumps out aldosterone independently of the RAAS system. It doesn't care what renin is doing — it just keeps making aldosterone. in the adrenal cortex. It makes aldosterone all by itself, ignoring the normal RAAS signals.

💡 The Classic Triad:
1. Hypertension (often resistant — won't respond to 3 drugs)
2. Hypokalemia (K+ < 3.5)
3. Metabolic alkalosis (bicarb > 29)

WHY each part of the triad happens:

🧬 Hypertension — Aldosterone tells the collecting duct to reabsorb Na+. More Na+ retained = more water follows = blood volume up = BP up. Simple plumbing.

🧬 Hypokalemia — Aldosterone reabsorbs Na+ by exchanging it for K+ and H+. More aldosterone = more K+ dumped into urine = blood K+ drops.

🧬 Metabolic alkalosis — Same exchange: Na+ in, H+ out. Dumping H+ into urine makes the blood more basic. Plus, hypokalemia itself causes alkalosis (H+ shifts into cells to replace K+).

🔑 Conn = Can't stop making aldosterone. The Connection to renin is Cut.

The RAAS in Conn — see what's suppressed:

Kidney senses low BP → Renin

↓

Angiotensinogen → Angiotensin I

↓

ACE → Angiotensin II

✘ bypassed

TUMOR → Aldosterone (unregulated)

↓

Na+ retained, K+ & H+ dumped

Everything above the tumor is suppressed by negative feedback. The tumor doesn't need the RAAS cascade — it's autonomous.

Diagnosis:

🔎 Aldosterone:Renin ratio — aldosterone is HIGH, renin is LOW. The ratio is elevated. This is the screening test. If the ratio is high, confirm with salt loading test (aldosterone stays high even when you flood the body with salt — because the tumor doesn't respond to feedback).

In Conn syndrome, renin levels are LOW because...

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Primary vs Secondary Hyperaldosteronism

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This is where most students get confused. Both have high aldosterone. The difference is WHY.

Feature	Primary (Conn)	Secondary
Source of aldosterone	Adrenal tumor (autonomous)	Normal adrenals responding to high renin
Renin	LOW (suppressed by feedback)	HIGH (driving the aldosterone)
Angiotensin II	LOW	HIGH
Aldosterone:Renin ratio	Very HIGH	Normal or low
Cause	Adrenal adenoma	Low renal perfusion (CHF, cirrhosis, renal artery stenosis)
The kidney is...	Fine — just suppressed by volume	Sensing low flow → cranking out renin

💡 The board question shortcut: Hypertension + hypokalemia + metabolic alkalosis? Check renin. Low renin = primary (Conn). High renin = secondary. That's it.

🔑 Primary = the price of renin drops (low). Secondary = the kidney secretes renin (high).

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The Adrenal Trio — Conn vs Cushing vs Pheo

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Three tumors, three hormones, three presentations. If you can tell them apart, you get easy points.

Feature	Conn (Aldosterone)	Cushing (Cortisol)	Pheo (Catecholamines)
Tumor location	Adrenal cortex (zona glomerulosa)	Adrenal cortex (zona fasciculata)	Adrenal medulla
Hormone	Aldosterone	Cortisol	Epi/NE/Dopamine
Presentation	Usually asymptomatic, found on labs	Moon facies, buffalo hump, striae, truncal obesity	Episodic headache, sweating, palpitations
HTN pattern	Resistant (won't budge on 3 drugs)	Sustained	Episodic (paroxysmal spikes)
BMP clue	Hypokalemia + met alkalosis	Hyperglycemia	Normal
Diagnosis	Aldosterone:renin ratio	Late-night salivary cortisol, dex suppression test	Serum/urine metanephrines
Key fact	#1 cause of resistant HTN	Can be subclinical (still causes osteoporosis, DM)	10% malignant; must alpha-block before surgery

⚠ Board trap: Pheo needs an alpha blocker BEFORE surgery. If you cut out a pheo without blocking alpha receptors first, the catecholamine surge during manipulation can cause a fatal hypertensive crisis. Phenoxybenzamine first, then surgery.

⚠ Board trap: All adrenal incidentalomasAn adrenal mass found accidentally on imaging done for something else (CT for kidney stones, etc.). Even if the patient has no symptoms, you must screen for all three functional tumors. must be screened for all three — Conn, Cushing, AND Pheo — regardless of symptoms. Subclinical Cushing is real and dangerous long-term.

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Board Traps — Don't Fall For These

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⚠ Trap 1: "Increased angiotensin II" in Conn. 45% of students picked this. In PRIMARY hyperaldosteronism, the RAAS cascade is suppressed. Renin LOW, Ang II LOW, aldosterone HIGH (from tumor). Only in SECONDARY would Ang II be high.

⚠ Trap 2: Conn vs Type 4 RTA. Both involve aldosterone and potassium. But they're opposites. Conn = TOO MUCH aldosterone (hypokalemia, alkalosis). Type 4 RTA = TOO LITTLE aldosterone (hyperkalemia, acidosis).

⚠ Trap 3: Normal glucose rules out Cushing. This patient has normal glucose, which helps point away from Cushing (which causes hyperglycemia). But remember — subclinical Cushing exists with normal-looking labs. Always screen incidentalomas.

⚠ Trap 4: "Decreased renal blood flow" as Conn's mechanism. Decreased renal blood flow causes SECONDARY hyperaldosteronism (high renin). Conn syndrome is PRIMARY — the tumor acts independently of renal perfusion.

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Test Day Algorithm

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1. Young patient + hypertension + hypokalemia + metabolic alkalosis?
→ Think Conn syndrome

2. Check renin.
Low renin = primary (tumor makes its own aldosterone)
High renin = secondary (kidney is responding to low perfusion)

3. If the question asks "what additional finding" — low renin is the answer. Not high Ang II (that's suppressed too).

4. If HTN is episodic with sweating/headache/palpitations → Pheo (check metanephrines).
If moon facies + striae + hyperglycemia → Cushing (check cortisol).

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Quiz — 4 Adrenal Tumors Walk Into a Clinic

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Let's see if you can tell these adrenal tumors apart without killing anyone.