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Your Patient's Na+ is 125
GATE QUESTIONBefore you do anything else — before you fluid-restrict, before you give saline, before you even think about SIADH — answer this:
Is this even real hyponatremia? What's the FIRST lab you check?
Exactly. Serum osmolality tells you if the sodium is truly low (hypotonic) or just looks low because something else is pulling water into the vascular space. Without this, you're treating a number, not a patient.
Good instinct, but those come later. Serum osmolality is step one — it tells you if this is real (hypotonic) hyponatremia or just a lab artifact from hyperglycemia or hyperlipidemia pulling water around. If you skip this, you might treat something that doesn't need treating.
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Step 1: Serum Osmolality
TRUE vs PSEUDO vs FACTITIOUSSerum osmolality splits hyponatremia into three buckets. This is the fork in the road — get it wrong and everything downstream is wrong too.
| Serum Osm | Type | What's Happening | Examples |
|---|---|---|---|
| < 280 | Hypotonic (TRUE) | Real low sodium. Water is diluting everything. | SIADH, CHF, cirrhosis, psychogenic polydipsia |
| 280-295 | Isotonic (PSEUDO) | Lab artifact. Lipids or proteins take up plasma volume, fooling the analyzer. | HyperlipidemiaMassive triglycerides or cholesterol displace plasma water. The ion-selective electrode (direct measurement) won't be fooled — only flame photometry or indirect ISE gets tricked., multiple myeloma (paraproteins) |
| > 295 | Hypertonic (FACTITIOUS) | Something osmotically active is pulling water INTO the vessels, diluting Na+. | HyperglycemiaEvery 100 mg/dL glucose above normal drops Na+ by ~1.6 mEq/L. The water shifts are real, but the Na+ isn't "lost" — it's diluted. Fix the sugar, fix the sodium., mannitol |
Hyperglycemia is the classic board trap. They give you Na+ 128 with glucose 600, and you're supposed to realize: correct the sodium first. For every 100 mg/dL glucose above 100, add 1.6 to the Na+. If corrected Na+ is normal, there's no real hyponatremia.
Quick — serum osm comes back 270. What does that tell you?
That's it. Osm < 280 = hypotonic = real deal. Now you need to figure out why the water is sticking around — and that means checking if ADH is appropriately on or off.
Not quite. 270 is below 280, which means hypotonic — this is real hyponatremia. Isotonic (pseudo) would be 280-295, and hypertonic would be above 295. The low osm confirms the sodium truly is diluted.
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Step 2: Urine Osmolality
IS ADH ON OR OFF?You've confirmed true hyponatremia. Now: is ADHAntidiuretic hormone (vasopressin). Released from the posterior pituitary when osmolality is high or volume is low. It inserts aquaporin-2 channels in the collecting duct — more ADH = more water reabsorption = concentrated urine. doing its job? If serum is dilute, the kidneys should be dumping water — making maximally dilute urine.
| Urine Osm | ADH Status | Meaning | Think... |
|---|---|---|---|
| < 100 | ADH OFF (appropriate) | Kidneys are doing their job — dumping free water | Primary polydipsia — patient is drinking so much water that even maximal dilution can't keep up |
| > 100 | ADH ON (inappropriately) | Kidneys are holding onto water when they shouldn't be | Everything else: SIADH, volume depletion, CHF, cirrhosis, hypothyroid, adrenal insufficiency |
The dilutional cut-off is 100 mOsm/kg. Below that = the kidneys got the memo. Above that = something is forcing ADH to stay on.
Urine osm is 450. Is ADH appropriately suppressed?
Right. The serum is already dilute (hypotonic), so the brain should be telling ADH to shut off. The kidneys should be making dilute urine (< 100). Urine osm 450 = ADH is ON when it shouldn't be. Now you figure out why — and that's volume status.
Think about it again. The serum is already dilute — the body has too much water relative to sodium. In that situation, ADH should turn OFF so the kidneys dump the extra water (urine osm < 100). A urine osm of 450 means ADH is stuck ON. That's inappropriate.
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Step 3: Volume Status
HYPO vs EU vs HYPERADH is on and it shouldn't be. Three reasons it stays on — and they split by how the patient looks clinically:
| Volume | Exam Findings | Why ADH Is On | Causes |
|---|---|---|---|
| Hypovolemic | Dry mucosa, tachycardia, poor skin turgor, orthostatics | Low volume triggers ADH — body prioritizes volume over osmolality | Vomiting, diarrhea, diuretics, salt-wasting nephropathy, cerebral salt wasting |
| Euvolemic | Looks normal. No edema, no dehydration signs. | ADH is on for no good volume reason | SIADH, hypothyroidism, adrenal insufficiency, psychogenic polydipsia (if ADH on) |
| Hypervolemic | Edema, JVD, crackles, ascites | Total body water is UP but effective circulating volume is DOWN — body thinks it's dry | CHF, cirrhosis, nephrotic syndrome |
The hypervolemic paradox: In CHF and cirrhosis, the body is flooded with fluid — but it's in the wrong compartment (interstitial, not vascular). The baroreceptors sense low effective volume and tell ADH to hold more water. Result: edema + hyponatremia. Total water up, effective volume down.
Your patient has Na+ 128, serum osm 265, urine osm 500. They look clinically normal — no edema, no dehydration. What's the volume status?
Nailed it. Euvolemic hyponatremia with high urine osm = SIADH until proven otherwise. But first, rule out hypothyroidism (TSH) and adrenal insufficiency (AM cortisol). Those are the two "mimickers" boards love to test.
Look at the exam again — "clinically normal, no edema, no dehydration." That's euvolemic. Hypovolemic would show tachycardia, dry mucosa. Hypervolemic would show edema/JVD. A euvolemic patient with inappropriate ADH activity = SIADH (after ruling out hypothyroidism and adrenal insufficiency).
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Step 4: Urine Sodium
RENAL vs EXTRARENALIf the patient is hypovolemic, urine sodium tells you where the sodium went:
| Urine Na+ | Source of Loss | Meaning | Causes |
|---|---|---|---|
| < 20 | Extrarenal | Kidneys are holding onto sodium (they see low volume and reabsorb everything) | Vomiting, diarrhea, third-spacing, burns |
| > 20 | Renal | Kidneys are wasting sodium despite low volume — something's overriding normal reabsorption | Diuretics (especially thiazides), cerebral salt wastingSeen after CNS injury (SAH, TBI). The brain releases natriuretic peptides that force renal sodium loss. Looks like SIADH but the patient is volume-depleted. Treatment: saline replacement (opposite of SIADH fluid restriction)., salt-wasting nephropathy, adrenal insufficiency (no aldosterone) |
For euvolemic patients (SIADH), urine Na+ is typically > 40 — the kidneys are dumping sodium because volume is "normal" and the extra water dilutes everything. 🔑 SIADH = Sodium gets Spilled (urine Na+ > 40). The kidneys see normal volume and don't bother saving sodium.
Cerebral salt wasting vs SIADH — both have low Na+, high urine Na+, high urine osm. The difference? Volume status. CSW = hypovolemic (dehydrated, tachycardic). SIADH = euvolemic. Treatment is opposite: CSW gets saline, SIADH gets fluid restriction.
The algorithm in one sentence: Serum osm (is it real?) → Urine osm (is ADH on?) → Volume status (why is ADH on?) → Urine Na+ (where's the sodium going?). Four labs. Four questions. That's the whole tree.
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SIADH Deep Dive
MOST TESTEDSIADH is the #1 tested cause of euvolemic hyponatremia. The board loves it because it has specific diagnostic criteria that students mix up.
Diagnostic Criteria (ALL must be present):
• Serum osm < 275
• Urine osm > 100 (usually > 300)
• Euvolemic clinically
• Urine Na+ > 40
• Normal thyroid and adrenal function
• No diuretics, no renal disease
• Serum osm < 275
• Urine osm > 100 (usually > 300)
• Euvolemic clinically
• Urine Na+ > 40
• Normal thyroid and adrenal function
• No diuretics, no renal disease
Common causes boards test:
| Category | Causes |
|---|---|
| CNS | Stroke, hemorrhage, meningitis, trauma |
| Pulmonary | Small cell lung cancer (ectopic ADH), pneumonia, TB |
| Drugs | SSRIs, carbamazepine, cyclophosphamide, opioids, MDMA |
| Pain / Nausea | Potent ADH stimulators — post-surgical is classic |
Treatment hierarchy:
1
Fluid restriction (800-1000 mL/day)
Less water in = less dilution. First-line for mild/chronic SIADH.
2
Salt tabs + loop diuretic
Salt tabs add sodium; furosemide wastes free water by blocking the concentrating mechanism. Together they raise Na+.
3
Vaptans (tolvaptan, conivaptan)
V2 receptor antagonists — block ADH at the collecting duct. Aquaresis (water loss without sodium). Reserved for refractory SIADH.
4
Hypertonic saline (3%) — ONLY for severe symptoms (seizures, coma)
Raises Na+ rapidly. Max correction: 8 mEq/L per 24 hours. Overcorrect and you get osmotic demyelination syndrome (ODS) — central pontine myelinolysis.
The 8-per-day rule. Correct Na+ no faster than 8 mEq/L in 24 hours (some sources say 10-12, but 8 is safer for boards). Overcorrection causes osmotic demyelinationWhen sodium rises too fast, water rushes OUT of brain cells (which had adapted to low osmolality by losing organic osmolytes). The myelin in the pons is especially vulnerable. Result: quadriplegia, pseudobulbar palsy, "locked-in syndrome." Often irreversible. High-risk: chronic hyponatremia, alcoholism, malnutrition.. Who's at highest risk? Chronic hyponatremia, alcoholics, malnourished patients.
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Hyperkalemia
EKG CHANGES + TREATMENTPotassium is the "cardiac ion." Too much of it and the heart stops. The board tests two things: recognizing the EKG progression and knowing the treatment order.
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EKG Progression as K+ Rises
Each stage has a visual signature. The heart is telling you it's dying — learn to read the message.
| K+ Level | EKG Change | What's Happening |
|---|---|---|
| 5.5-6.5 | Peaked T waves | Accelerated repolarization. The T wave gets tall, narrow, pointy — like a tent. |
| 6.5-7.5 | PR prolongation + flattened P waves | Atrial conduction slows, then stops. The P wave disappears. |
| 7.0-8.0 | W i d e n e d Q R S | Ventricular conduction slows. The QRS stretches out, getting f a t a n d s l u g g i s h. |
| > 8.0 | Sine wave → V-fib/asystole | QRS and T merge into an undulating sine wave. This is pre-arrest. Act NOW. |
The progression: peaked T → lost P → wide QRS → sine wave → death. Each stage = more potassium poisoning the cardiac conduction system. 🔑 Peaked → lost P → Wide → Sine → Stop. The T gets excited first. The P gives up. The QRS gets fat. Then the whole thing just... waves goodbye.
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Treatment: Stabilize, Shift, Remove
Three goals, in order. Don't skip ahead.
1
Calcium gluconate (or chloride)
STABILIZE the membrane. Calcium antagonizes K+ at the cardiac membrane, raising the threshold for depolarization. Doesn't lower K+ — just buys time. Works in 1-3 minutes. Lasts 30-60 min.
2
Insulin + glucose / Bicarb / Albuterol
SHIFT K+ into cells. Insulin activates Na+/K+-ATPase (always give glucose to prevent hypoglycemia). Bicarb drives H+ out and K+ in (exchange). Beta-agonists also activate the pump. Temporary — K+ comes back out eventually.
3
Kayexalate / Patiromer / Lokelma / Dialysis
REMOVE K+ from the body. Kayexalate (sodium polystyrene sulfonate) exchanges Na+ for K+ in the gut. Patiromer and Lokelma are newer binders. Dialysis is the definitive removal for severe/refractory cases.
Your patient has K+ of 7.2 with widened QRS on EKG. What do you give FIRST?
Yes. Calcium first, always. It doesn't lower potassium — it protects the heart while you set up the things that actually lower K+ (insulin, bicarb). Think of it as the cardiac bodyguard: it doesn't solve the problem, but it keeps the patient alive while you do.
Good thought, but when there are EKG changes, calcium gluconate is ALWAYS first. It stabilizes the cardiac membrane in 1-3 minutes. Insulin+glucose shifts K+ into cells but takes 15-30 min. Kayexalate takes hours. Dialysis takes time to set up. None of those help if the heart fibrillates right now.
Pseudohyperkalemia — K+ comes back 6.8 but the patient looks fine with a normal EKG. Check: was the sample hemolyzed? Traumatic blood draw, prolonged tourniquet, or small-gauge needle can lyse red cells, releasing intracellular K+ into the sample. Always repeat the lab before treating a suspiciously high K+ in an asymptomatic patient.
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Elimination Game
DIAGNOSE BY EXCLUSIONSix patients, weird labs. Each clue eliminates a diagnosis. Watch the cards fall.
Case 1: 45F with Na+ 126. What's causing it?
Psychogenic polydipsia
SIADH
Hyperglycemia artifact
CHF
Case 2: 62M with Na+ 118. What's causing it?
Diuretic use
Cirrhosis
SIADH from lung mass
Adrenal insufficiency
Case 3: 30M with K+ 6.9 and EKG changes. Cause?
Hemolyzed sample
ACE inhibitor toxicity
Rhabdomyolysis
Addison's disease
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Board Practice
RANDOM FROM POOL5 patients just walked in with weird labs. Figure out what's wrong before their kidneys do.