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Nursing Field Notes / Endocrine · Adrenal · Med-Surg
⚗️ ENDOCRINE SET NG-284 Hyperthyroid NG-285 Hypothyroid NG-286 Parathyroid NG-287 Addison vs Cushing NG-289 Conn's & Pheo

Conn’s & Phaeochromocytoma 💥

Two adrenal tumors, two very different shapes of high blood pressure

NG-289 ENDOCRINE · ADRENAL ADHD-friendly visual edition

Both of these are secondary causes of hypertension — the kind you must not miss. Hyperaldosteronism (Conn’s) comes from the outer layer of the adrenal cortex: sustained high blood pressure with low potassium and metabolic alkalosis. Phaeochromocytoma comes from the adrenal medulla: a catecholamine-secreting tumor that throws out paroxysms of crushing headache, drenching sweat and pounding palpitations. And palpating the abdomen can set a phaeo off.

🧂 CONN’S = HYPER ALHTN · Yielding reflexes & bowels · Polyuria/polydipsia · ECG U wave & ST depression · Raining dilute urine · Adding sodium · Losing potassium.
🧠 A·LAldosterone ADDS sodium & water in and LETS potassium out. Every Conn’s finding comes from that one line.
💥 PHAEO TRIADPounding Headache + drenching Sweating + Palpitations, in paroxysms, with severe hypertension.
❌ Don’t pressNever palpate the abdomen in suspected phaeochromocytoma — it can squeeze out a catecholamine surge and trigger a crisis.
🫘

THE SAME GLAND, THE OUTER AND INNER LAYERS

STEP 1 · FOUNDATION

Conn’s is the outermost shell. Phaeo is the core. Everything else follows from that.

🫘 The adrenal cutaway — where each disease lives

THE ADRENAL GLAND · where Conn’s and phaeo come fromOne picture that explains Conn’s, Cushing’s, Addison’s and phaeochromocytomaADRENAL sits ON the kidneykidney (context)a. artery · v. vein · ureteradrenal vein drains to IVC / renal v.cut open and magnified →capsulefibrous coatZona GLOMERULOSAALDOSTERONE · salt &waterZona FASCICULATACORTISOL · sugar &stressZona RETICULARISANDROGENS · sexhormonesMEDULLAEPINEPHRINE /NOREPINEPHRINE🧠 “Salt · Sugar · Sex — the deeper you go, the sweeter it gets”GFR outside-in = Glomerulosa (salt) · Fasciculata (sugar) · Reticularis (sex)then the MEDULLA in the middle = the fight-or-flight core.

Conn’s syndrome = too much aldosterone from the outermost layer (zona glomerulosa). Phaeochromocytoma = too much epinephrine / norepinephrine from the medulla right in the middle.

🧠 GFR · Salt · Sugar · Sex, then the fight-or-flight core. Outer shell = salt problem. Core = epinephrine problem.
SAME DRAWINGAlso used on NG-287 · Addison’s vs Cushing’s, where the middle layer (cortisol) is the one in trouble.

⚙️ Aldosterone in one line

AADDS sodium and water back into the blood
LLETS potassium (and hydrogen) out into the urine

Normally it is released when blood pressure or blood volume falls, through the renin–angiotensin–aldosterone system. In Conn’s the gland makes it regardless of pressure — so renin is suppressed.

🧠 Primary Conn’s: aldosterone HIGH, renin LOW. That single pairing is the diagnostic test.

⚙️ Catecholamines in one line

The medulla is really a modified sympathetic nerve ending. Epinephrine and norepinephrine are fight-or-flight in a syringe:

  • Heart rate and contractility up → palpitations, chest pain
  • Vasoconstriction → severe hypertension, pallor
  • Glycogen breakdown → hyperglycemia
  • Metabolic rate up → sweating, heat intolerance, tremor, weight loss
  • Pupils dilate, gut slows → blurred vision, nausea, constipation
🧠 Phaeo = a bear jumps out at you, over and over, for no reason.

🔬 What aldosterone actually does at the tubule

WHAT ALDOSTERONE ACTUALLY DOES🧠 “A·L” = ADDS sodium & water in · LETS potassium outglomerulusdistal tubule + ductmagnify →principal cellURINE side(tubule lumen)BLOOD side(peritubular capillary)Na⁺ + H₂O → reabsorbedK⁺ → excretedH⁺ → excreted (→ alkalosis)ALDNa⁺ ↑over 145 mEq/LWATER retainedvolume ↑ → BP over 140/90K⁺ ↓3.5 mEq/L or lessH⁺ lostmetabolic ALKALOSIS⭐ CONN’S SYNDROME = primary hyperaldosteronismThe classic trio: HYPERTENSION + HYPOKALEMIA + METABOLIC ALKALOSIS —and, unusually for a fluid-overloaded state, the patient is usually NOT edematous.
🧠 Sodium in, potassium and hydrogen out — that is hypertension + hypokalemia + metabolic alkalosis in one sentence.
🧂

HYPERALDOSTERONISM (CONN’S)

SIDE A · TOO MUCH SALT HORMONE

Sustained hypertension that will not respond to the usual drugs — plus a stubbornly low potassium.

⭐ Patho & causes

Primary (inside the adrenal) — the gland itself overproduces aldosterone:

  • Conn’s syndrome — a benign aldosterone-producing adenoma. The classic cause.
  • Bilateral adrenal hyperplasia
  • Rare familial/genetic forms

Secondary (outside the adrenal) — something else is telling the gland to make more:

  • Renal artery stenosis — the kidney thinks pressure is low and pumps out renin
  • Heart failure, cirrhosis with ascites, nephrotic syndrome

The distinction shows up in the labs: primary has a low renin; secondary has a high renin.

🧠 Primary: gland shouting on its own. Secondary: the kidney is shouting at it.

🧠 “HYPER AL” — the whole picture

H — HypertensionSustained, often over 140/90, and resistant to several drugs
Y — YieldingReduced deep tendon reflexes and hypoactive bowel sounds — everything slow
P — Polyuria & polydipsiaThe kidney cannot concentrate urine when potassium is low
E — ECGST depression and a U wave from hypokalemia
R — Raining urineLarge volumes of dilute urine, low specific gravity
A — Adding sodiumSodium high or high-normal (over 145 mEq/L)
L — Losing potassium3.5 mEq/L or less

Typical adult reference ranges: potassium ≈ 3.5–5.0 mEq/L, sodium ≈ 135–145 mEq/L — ranges vary by laboratory, so confirm the range printed on the result.

Also: muscle weakness and cramps, paraesthesia, headache, fatigue, a swollen dry tongue, and metabolic alkalosis from losing hydrogen ions.

Despite retaining sodium and water, Conn’s patients are typically NOT edematous — an “aldosterone escape” mechanism limits the fluid gain.

🧠 High BP + low K⁺ + alkalosis = think Conn’s. Three findings, one diagnosis.

💓 What low potassium looks like on the monitor

LOW POTASSIUM ON THE MONITORConn’s dumps potassium in the urine — the ECG shows it before the patient feels itNORMALcrisp T wave, flat ST segment, no U waveHYPOKALEMIA (K⁺ ≤ 3.5 mEq/L)flattened T · ST depression · prominent U wave — then arrhythmiasU
🧠 U wave = potassium Used up. It shows on the strip before the patient feels weak.
SEE ALSOFull potassium content is on NG-088 (Potassium · Sodium · Chloride) and NG-003 (All Electrolytes).

✅ Treatment — the goal is less fluid and more potassium

  • Spironolactone — an aldosterone antagonist and potassium-sparing diuretic. It blocks the hormone at the receptor, which is exactly the problem.
  • Potassium supplements as ordered while potassium is low
  • Sodium restriction
  • Other antihypertensives as needed
  • Adrenalectomy for a single adenoma — often curative

Spironolactone teaching: it can cause hyperkalemia, so avoid salt substitutes (they are potassium chloride) and potassium-rich supplements once the level normalizes. It can also cause gynaecomastia, breast tenderness and menstrual changes.

🧠 Spironolactone SPARES potassium — it is the antidote to the whole “L” in HYPER AL.
SEE ALSONG-181 · Potassium-sparing diuretics.

⭐ Nursing monitoring

  • Blood pressure — lying and standing, both arms initially
  • Potassium and sodium with every set of bloods
  • Strict intake and output, daily weight, urine specific gravity
  • Cardiac rhythm — watch for U waves, ST depression and ectopy
  • Assess muscle strength, reflexes and bowel sounds
  • After starting spironolactone, watch the potassium climb the other way
🧠 You are chasing two numbers: the BP and the K⁺.
💥

PHAEOCHROMOCYTOMA

SIDE B · THE EPINEPHRINE TUMOR

A rare tumor of the adrenal medulla — and one of the few conditions where your examination can kill.

💥 The tumor and the surge

PHAEOCHROMOCYTOMA · a tumor of the adrenal MEDULLAThe medulla is basically a sympathetic nerve ending — a tumor here squirts epinephrine💥 CATECHOLAMINE SURGEepinephrine + norepinephrine straight into the bloodBP can rocket past 200 systolic in minutes →stroke, MI, arrhythmia, retinal hemorrhageadrenal CORTEXadrenal MEDULLAPHAEO TUMORkidney❌ DO NOT PALPATE THE ABDOMENsqueezing the tumor sets off a crisis🔺 WHAT ELSE SETS IT OFF• Deep abdominal palpation or massage• Sudden position change / bending• Straining, coughing, vomiting• Anesthesia induction · surgery• Smoking, caffeine, other stimulants• Some drugs & foods — check before giving• Emotional stress and pain⭐ THE CLASSIC TRIAD — pounding HEADACHE + profuse SWEATING + POUNDING HEARTin short paroxysms, with severe hypertension. Add pallor, tremor, anxiety, chest pain, nausea and high blood sugar.Diagnosis is by measuring catecholamine breakdown products (metanephrines) in plasma or a 24-hour urine collection.
🧠 Squeeze the tumor, squeeze out the epinephrine. That is why the abdomen is off-limits.

🚨 The classic triad

H — HeadacheSudden, pounding, severe
S — SweatingDrenching, out of nowhere
P — PalpitationsPounding heart, chest pain, tachycardia

…arriving together in paroxysms lasting minutes to an hour, on a background of severe hypertension. Between attacks the patient can look completely normal, which is exactly why it gets missed.

Also expect: pallor (not flushing), tremor, marked anxiety or a sense of doom, nausea and vomiting, blurred vision, heat intolerance, weight loss, constipation, and hyperglycemia.

🧠 “The 3 P’s” — Pressure, Pain in the head, Perspiration. Plus Palpitations and Pallor if you want five.

📈 Two different shapes of hypertension

TWO SHAPES OF HIGH BLOOD PRESSUREConn’s pushes the whole line up. Phaeo throws spikes out of a near-normal line.NORMALstable around 120/80normaltime →CONN’S (hyperaldosteronism)persistently high, hard to control, with low K⁺normaltime →PHAEOCHROMOCYTOMAparoxysms: pounding HEADACHE + SWEATING + PALPITATIONSnormalcrisiscrisiscrisistime →
🧠 Conn’s lifts the whole line. Phaeo throws spikes off a near-normal line.

❌ What can trigger a hypertensive crisis

  • Never palpate the abdomen deeply in a suspected or confirmed phaeochromocytoma — pressure on the tumor releases a bolus of catecholamines.
  • Sudden position changes, bending over, or vigorous movement
  • Straining, coughing, vomiting, or a Valsalva maneuver
  • Anesthetic induction and surgery — which is why patients are blocked with drugs first
  • Stimulants: smoking, caffeine, decongestants, some cold remedies
  • Emotional stress and uncontrolled pain
  • Certain drugs and foods — check before administering anything new

Blood pressure can pass 200 systolic within minutes, risking stroke, MI, arrhythmia, retinal hemorrhage and acute heart failure.

🧠 Hands off the belly, and no stimulants.

✅ Nursing care & diagnosis

  • Monitor blood pressure closely — this is the priority assessment; use continuous monitoring during a crisis
  • Quiet room, minimal stimulation, rest, and no interruptions during attacks
  • Change position slowly; assist with all transfers
  • Avoid all stimulants; smoking and caffeine are out
  • Adequate hydration and a nutritious diet — these patients often lose weight
  • Give ordered alpha-blockade first, then beta-blockade — the order matters

Diagnosis: measure catecholamine breakdown products — plasma free metanephrines or a 24-hour urine collection for metanephrines and catecholamines — then CT or MRI to find the tumor. For the urine collection, keep the container on ice/with preservative and discard the first void, then collect everything for a full 24 hours including the final void.

🧠 Alpha before beta. Blocking beta first leaves alpha vasoconstriction unopposed and the pressure goes UP.
🔍

TELL THEM APART

STEP 4 · COMPARE

Both cause hypertension. Everything else is different.

📊 Side by side

 CONN’S 🧂 (aldosterone)PHAEOCHROMOCYTOMA 💥 (catecholamines)
Where in the glandCortex — zona glomerulosa (outermost)Medulla (the core)
HormoneAldosteroneEpinephrine / norepinephrine
Blood pressure patternSustained and drug-resistantParoxysmal spikes on a near-normal line
PotassiumLOW (≤3.5)Usually normal
SodiumHIGH / high-normal (>145)Usually normal
Acid–baseMetabolic alkalosisUsually normal
GlucoseNormal or mildly raisedHIGH — catecholamines mobilize glucose
Headline symptomsMuscle weakness, cramps, polyuria, thirst, constipationHeadache + sweating + palpitations, pallor, tremor, anxiety
SkinNothing specificPale and drenched in sweat during an attack
Reflexes / bowelsHypoactive (low potassium)Hyperactive sympathetic state, but constipated gut
ECGST depression, U wavesTachycardia, arrhythmias, ischemic changes
Key testAldosterone HIGH with renin LOWMetanephrines — plasma or 24-hour urine
Core drugSpironolactone (potassium-sparing)Alpha-blocker first, then a beta-blocker
Definitive treatmentAdrenalectomy for an adenomaSurgical removal after full blockade
The neverNever ignore a stubbornly low potassium in a hypertensive patientNever palpate the abdomen; never beta-block before alpha-blocking
🧠 Low potassium → Conn’s. Paroxysms → phaeo. Two words, two diagnoses.

⭐ When to suspect a secondary cause of hypertension

  • Hypertension that starts before about 30 or suddenly after 55
  • Blood pressure that stays high on three or more drugs
  • Unexplained hypokalemia — with or without a diuretic
  • Episodic symptoms: headache, sweating, palpitations, pallor
  • An adrenal mass found by accident on imaging
  • A family history of endocrine tumors
🧠 Young, resistant, or hypokalemic → look past “essential” hypertension.

🔗 How this page connects to NG-287

Four adrenal diseases, one gland, four layers:

Glomerulosa ↑Conn’s — salt and water retained, potassium dumped
Fasciculata ↑Cushing’s — sugar, fat and blood pressure up
Whole cortex ↓Addison’s — everything falls except potassium and pigment
Medulla ↑Phaeochromocytoma — epinephrine paroxysms
🧠 One drawing, four diseases. Learn the picture, not the four lists.
COMPANION NG-287 · Addison’s vs Cushing’s
💊

SURGERY, DRUGS & AFTERCARE

STEP 5 · CARE

Both can end with an adrenalectomy — and an adrenalectomy can create an Addison’s patient.

🔪 Around an adrenalectomy

Before:

  • Blood pressure must be controlled first. For a phaeo that means alpha-blockade for days to weeks, then a beta-blocker — never the reverse.
  • Correct potassium and volume; for Conn’s, expect spironolactone and potassium replacement.
  • Explain that handling the tumor during surgery can cause dramatic blood pressure swings.

After:

  • Blood pressure instability is expected — it can crash once the hormone source is removed. Continuous monitoring, and be ready for fluids and vasopressors.
  • Monitor glucose, potassium and sodium closely.
  • Watch for hemorrhage — the adrenals are very vascular. Check the dressing, vitals and abdomen.
  • Assess pain, bowel sounds and respiratory effort (a flank incision hurts to breathe through).
🧠 The pressure that was too high can become too low the moment the tumor leaves.

💊 If both adrenals go — lifelong steroids and the taper rule

WHY YOU TAPER STEROIDS · never stop them suddenlyWeeks of outside steroid put the adrenal glands to sleep — they need time to wake updosetime →SAFE: step down over weeksABRUPT STOPno drug · no own cortisol🚨 ADRENAL CRISIShypotension → shock → death⬆️ WHEN THE DOSE GOES UP• Infection or fever• Surgery or a procedure• Trauma or a burn• Severe emotional stress• Vomiting/diarrhea (can’t keep it down → call)✅ ALWAYS TEACH• Medical alert bracelet + emergency card• Never run out — get refills early• Take with food; report black stools• Daily weight and BP log🧠 “The adrenal glands are asleep, not dead — wake them slowly.”The same rule applies to anyone on more than about 2–3 weeks of systemic steroid for any reason — asthma, RA, IBD, transplant.

A bilateral adrenalectomy removes all cortisol and aldosterone production, so the patient goes home on lifelong replacement with the same teaching as Addison’s: increase the dose during stress, carry an emergency kit, wear a medical alert bracelet, and never stop the steroid abruptly.

Even after a unilateral adrenalectomy for Cushing’s or Conn’s, the remaining gland may be suppressed and need temporary replacement.

🧠 REmove the organ → REplace the hormone.
SEE ALSOFull crisis and taper teaching is on NG-287.

💊 The drug list, sorted

Conn’sSpironolactone (aldosterone antagonist, potassium-sparing) · potassium supplements · sodium restriction · other antihypertensives
PhaeoAlpha-blocker FIRST · then a beta-blocker for rate · antihypertensives for crisis per protocol · surgery once blocked

Doses vary widely and are titrated to blood pressure — follow the order and the local protocol rather than a remembered number.

🧠 A before B. Alpha before beta, every time, in phaeochromocytoma.

🍽️ Diet & lifestyle teaching

  • Conn’s: restrict sodium; increase potassium-rich foods while potassium is low — but stop them once spironolactone has normalized the level, and avoid salt substitutes (they are potassium chloride)
  • Phaeo: no caffeine, no nicotine, no decongestants or other stimulants; adequate calories and fluid; plan rest between activities
  • Both: teach home blood pressure monitoring and when to seek help
  • Both: change position slowly and report dizziness
🧠 Conn’s = cut the salt. Phaeo = cut the stimulants.

🧠 Quiz yourself — no peeking

8 questions with answers
Q1: BP 178/104, potassium 2.9, sodium 148, metabolic alkalosis. Which diagnosis?
Primary hyperaldosteronism (Conn’s). Hypertension + hypokalemia + metabolic alkalosis is the classic trio, and aldosterone will be high with a suppressed renin.
Q2: Which diuretic class treats Conn’s, and why?
Potassium-sparing — spironolactone. It blocks the aldosterone receptor, so it lowers the blood pressure and holds on to potassium at the same time.
Q3: A patient with suspected phaeochromocytoma is due an abdominal assessment. What do you do?
Do not palpate the abdomen. Pressure on the tumor can release a bolus of catecholamines and trigger a hypertensive crisis. Inspect and auscultate only, and check with the provider.
Q4: Why is a beta-blocker alone dangerous in phaeochromocytoma?
Blocking beta receptors removes the vasodilating beta-2 effect and leaves alpha-mediated vasoconstriction unopposed, so the blood pressure rises further. Alpha-blockade must come first.
Q5: What ECG changes go with the potassium level in Conn’s?
Hypokalemia: flattened T waves, ST depression and a prominent U wave, with a risk of arrhythmias.
Q6: A patient describes 20-minute episodes of pounding headache, drenching sweat and a racing heart, and is normal in between. What are you thinking?
Phaeochromocytoma. The paroxysmal triad of headache, sweating and palpitations with severe hypertension is the classic presentation. Expect metanephrines to be ordered.
Q7: Immediately after an adrenalectomy, what hemodynamic change do you anticipate?
The blood pressure can fall sharply once the hormone source is removed. Monitor continuously and be prepared for fluids and vasopressor support.
Q8: Why must a patient after a bilateral adrenalectomy never stop their steroid?
They have no adrenal cortex left, so there is no endogenous cortisol at all. Stopping it causes adrenal crisis — profound hypotension and shock.
🧂 Conn’s trioHTN + LOW potassium + metabolic alkalosis, with sodium high and renin low. Usually NOT edematous.
💊 SpironolactoneBlocks aldosterone and spares potassium — then watch potassium climb too high. No salt substitutes.
💥 Phaeo = paroxysmsHeadache + sweating + palpitations + pallor, spiking off a near-normal line. Diagnose with metanephrines.
❌ Two absolute neversNever palpate the abdomen · never beta-block before alpha-blocking.