The Board Trap
45% of students pick the wrong answer on this one.
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.
Conn Syndrome
Primary Hyperaldosteronism
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. 🔑Conn = Can't stop making aldosterone. The Connection to renin is Cut.
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
Aldosterone tells the collecting duct to reabsorb Na+. More Na+ retained = more water follows = blood volume up = BP up. Simple plumbing.
Aldosterone reabsorbs Na+ by exchanging it for K+ and H+. More aldosterone = more K+ dumped into urine = blood K+ drops.
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+).
The RAAS in Conn · see what's suppressed:
Everything above the tumor is suppressed by negative feedback. The tumor doesn't need the RAAS cascade · it's autonomous.
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).
Primary vs Secondary
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 |
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).
The Adrenal Trio
Conn vs Cushing vs Pheo · three tumors, three hormones, three presentations.
If you can tell them apart, you get easy points.
| Feature | Conn (Aldo) | Cushing (Cortisol) | Pheo (Catecholamines) |
|---|---|---|---|
| Tumor location | Cortex (zona glomerulosa) | Cortex (zona fasciculata) | 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 | Serum/urine metanephrines |
| Key fact | #1 cause of resistant HTN | Can be subclinical (still causes osteoporosis, DM) | 10% malignant; alpha-block before surgery |
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.
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.
Board Traps
Don't fall for these.
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.
Both involve aldosterone and potassium. But they're opposites. Conn = TOO MUCH aldosterone (hypokalemia, alkalosis). Type 4 RTA = TOO LITTLE aldosterone (hyperkalemia, acidosis).
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.
Decreased renal blood flow causes SECONDARY hyperaldosteronism (high renin). Conn syndrome is PRIMARY · the tumor acts independently of renal perfusion.
Test Day Algorithm
Step-by-step decision tree for the exam.
Young patient + hypertension + hypokalemia + metabolic alkalosis? → Think Conn syndrome
Check renin.
Low renin = primary (tumor makes its own aldosterone)
High renin = secondary (kidney is responding to low perfusion)
If the question asks "what additional finding" · low renin is the answer. Not high Ang II (that's suppressed too).
If HTN is episodic with sweating/headache/palpitations → Pheo (check metanephrines).
If moon facies + striae + hyperglycemia → Cushing (check cortisol).
Decision Tree: Adrenal Incidentaloma Workup
Adrenal mass found on imaging. Follow the branch points.
Quiz
4 Adrenal Tumors Walk Into a Clinic · let's see if you can tell them apart.