A 66-year-old man is in the ICU after a cardiac arrest. During resuscitation he received several ampules of 8.4% sodium bicarbonate, and since then 3% saline for cerebral edema. Over 3 days his weight has risen by 4 kg, and he has leg edema. Results: sodium 161 mmol/L, potassium 3.9 mmol/L, chloride 124 mmol/L, glucose 118 mg/dL [6.5 mmol/L], BUN 16 mg/dL [5.7 mmol/L]. Urine output is 1.8 L/day, urine osmolality 610 mOsm/kg and urine sodium 165 mmol/L. The most likely mechanism of the hypernatremia is:

Sodium gain from hypertonic infusions

Insensible water loss from skin and lungs

Osmotic diuresis from glucose or urea

Central diabetes insipidus after the arrest

A 41-year-old man with HIV infection is treated for Pneumocystis pneumonia with high-dose trimethoprim-sulfamethoxazole. On day 5: sodium 134, potassium 6.3, chloride 108 and HCO3- 19 mmol/L; creatinine 1.3 mg/dL [115 µmol/L] (1.0 mg/dL [88 µmol/L] on admission); glucose 96 mg/dL [5.3 mmol/L]. The sample is not hemolyzed, and a heparin plasma sample gives the same potassium. Morning cortisol is 21 µg/dL [580 nmol/L] and rises normally after cosyntropin, and aldosterone is high for the potassium. He takes no other drugs. What is the most likely cause of the hyperkalemia?

Trimethoprim blocking distal sodium channels

Acute kidney injury with a falling GFR

Potassium release from cells in the tube

A 66-year-old with type 2 diabetes and creatinine 1.7 mg/dL (150 µmol/L) has sodium 138, potassium 6.0, chloride 112 and bicarbonate 17 mmol/L. Plasma renin and aldosterone are both low. Which disorder best explains these results?

Hyporeninemic hypoaldosteronism

Pseudohyperkalemia from hemolysis

A patient on a long-term proton pump inhibitor has potassium 2.9 mmol/L that has not risen after 3 days of oral potassium. Magnesium is 0.8 mg/dL (0.33 mmol/L) [reference 1.7-2.4 mg/dL]. Why does the hypokalemia persist?

Low magnesium keeps the kidneys losing potassium

Proton pump inhibitors block potassium absorption

The potassium result is falsely low from hemolysis

Low magnesium drives potassium into the red cells

Electrolytes: interpretation and disease correlation

16 ASCP MLS practice questions on Electrolytes: interpretation and disease correlation, part of Chemistry. The first 16 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

Question 1 · Hard
A 66-year-old man is in the ICU after a cardiac arrest. During resuscitation he received several ampules of 8.4% sodium bicarbonate, and since then 3% saline for cerebral edema. Over 3 days his weight has risen by 4 kg, and he has leg edema. Results: sodium 161 mmol/L, potassium 3.9 mmol/L, chloride 124 mmol/L, glucose 118 mg/dL [6.5 mmol/L], BUN 16 mg/dL [5.7 mmol/L]. Urine output is 1.8 L/day, urine osmolality 610 mOsm/kg and urine sodium 165 mmol/L. The most likely mechanism of the hypernatremia is:
1. AInsensible water loss from skin and lungs
2. BSodium gain from hypertonic infusions
3. COsmotic diuresis from glucose or urea
4. DCentral diabetes insipidus after the arrest
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Answer: B · Sodium gain from hypertonic infusions
Hypernatremia with weight gain and edema means the body has gained sodium rather than lost water. The urine is concentrated at 610 mOsm/kg, so ADH is being released and is acting, which excludes diabetes insipidus. A urine sodium of 165 mmol/L shows the kidneys excreting the sodium load, while normal glucose and BUN rule out an osmotic diuresis. Pure water loss would lower body weight and would not cause edema. Each 50-mL ampule of 8.4% sodium bicarbonate holds 50 mmol of sodium, and 3% saline holds about 513 mmol/L, so both are common hidden sources of sodium in critical care.
- A: Water loss would lower body weight, but he has gained 4 kg and has edema.
- C: Glucose and BUN are normal, so no solute is driving an osmotic diuresis.
- D: Diabetes insipidus gives dilute urine, but this urine is concentrated at 610 mOsm/kg.
Question 2 · Hard
A 41-year-old man with HIV infection is treated for Pneumocystis pneumonia with high-dose trimethoprim-sulfamethoxazole. On day 5: sodium 134, potassium 6.3, chloride 108 and HCO3- 19 mmol/L; creatinine 1.3 mg/dL [115 µmol/L] (1.0 mg/dL [88 µmol/L] on admission); glucose 96 mg/dL [5.3 mmol/L]. The sample is not hemolyzed, and a heparin plasma sample gives the same potassium. Morning cortisol is 21 µg/dL [580 nmol/L] and rises normally after cosyntropin, and aldosterone is high for the potassium. He takes no other drugs. What is the most likely cause of the hyperkalemia?
1. AAcute kidney injury with a falling GFR
2. BPotassium release from cells in the tube
3. CPrimary adrenal insufficiency
4. DTrimethoprim blocking distal sodium channels
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Answer: D · Trimethoprim blocking distal sodium channels
Trimethoprim acts like amiloride: it blocks the epithelial sodium channel in the collecting duct, so less sodium is reabsorbed and less potassium is secreted. High doses, as used for Pneumocystis, often raise potassium within days, especially in HIV infection. A high aldosterone shows that the hormone is present but the tubule cannot respond, and a normal cosyntropin response confirms adrenal function. The small creatinine rise is partly because trimethoprim also blocks tubular secretion of creatinine, and kidney function at this level would not by itself push potassium to 6.3 mmol/L. An unhemolyzed sample with a matching plasma potassium excludes pseudohyperkalemia.
- A: Creatinine rose only slightly, partly because trimethoprim blocks its secretion.
- B: The sample is not hemolyzed, and plasma gives the same potassium.
- C: Cortisol and its response to cosyntropin are normal, and aldosterone is high, not low.
Question 3 · Hard
A 66-year-old with type 2 diabetes and creatinine 1.7 mg/dL (150 µmol/L) has sodium 138, potassium 6.0, chloride 112 and bicarbonate 17 mmol/L. Plasma renin and aldosterone are both low. Which disorder best explains these results?
1. APrimary adrenal insufficiency
2. BPrimary hyperaldosteronism
3. CPseudohyperkalemia from hemolysis
4. DHyporeninemic hypoaldosteronism
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Answer: D · Hyporeninemic hypoaldosteronism
Diabetic kidney disease often damages the renin-producing juxtaglomerular cells, so little renin and therefore little aldosterone is made. Without aldosterone the collecting duct secretes less potassium and less acid, giving hyperkalemia with a normal anion gap acidosis: 138 - (112 + 17) = 9 mmol/L. This pattern is also called type 4 renal tubular acidosis. The hyperkalemia is often out of proportion to the mild loss of kidney function.
- A: In primary adrenal insufficiency, renin is high because aldosterone is low.
- B: Primary hyperaldosteronism causes low potassium with high aldosterone.
- C: Pseudohyperkalemia would not explain the acidosis or the low renin and aldosterone.
Question 4 · Hard
A 70-year-old smoker with small cell lung carcinoma is euvolemic, with sodium 122 mmol/L, serum osmolality 254 mOsm/kg, urine osmolality 480 mOsm/kg and urine sodium 55 mmol/L. TSH and cortisol are normal. What is the most likely cause?
1. ASIADH from ectopic ADH
2. BPrimary polydipsia
3. CPseudohyponatremia
4. DDiuretic-induced sodium loss
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Answer: A · SIADH from ectopic ADH
The serum osmolality is low, so the hyponatremia is hypotonic and real. Urine more concentrated than plasma, with a urine sodium above 30 mmol/L in a euvolemic patient, means ADH is acting when it should be suppressed. Small cell lung carcinoma is a classic source of ectopic ADH. Thyroid and adrenal function must be normal before SIADH is diagnosed, as they are here.
- B: Primary polydipsia gives maximally dilute urine, below 100 mOsm/kg.
- C: Pseudohyponatremia has a normal serum osmolality.
- D: No diuretic is in the history, and diuretic loss usually causes volume depletion.
Question 5 · Hard
A patient on a long-term proton pump inhibitor has potassium 2.9 mmol/L that has not risen after 3 days of oral potassium. Magnesium is 0.8 mg/dL (0.33 mmol/L) [reference 1.7-2.4 mg/dL]. Why does the hypokalemia persist?
1. AProton pump inhibitors block potassium absorption
2. BThe potassium result is falsely low from hemolysis
3. CLow magnesium keeps the kidneys losing potassium
4. DLow magnesium drives potassium into the red cells
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Answer: C · Low magnesium keeps the kidneys losing potassium
Magnesium normally restrains potassium secretion through ROMK channels in the distal nephron. When magnesium is low, potassium keeps leaking into the urine, so potassium replacement fails until magnesium is corrected. Long-term proton pump inhibitors are a recognized cause of hypomagnesemia, as are diuretics and alcohol use. Magnesium should be checked in any hypokalemia that does not respond to treatment.
- A: Proton pump inhibitors lower magnesium; they do not block potassium absorption.
- B: Hemolysis releases potassium from cells and would raise, not lower, the result.
- D: The main problem is renal potassium loss, not a shift into red cells.
Question 6 · Hard
An outpatient with no symptoms and a normal ECG has potassium 9.2 mmol/L, calcium 2.8 mg/dL (0.70 mmol/L), and very low magnesium and alkaline phosphatase. The sample is not hemolyzed. The most likely cause is:
1. ADelayed separation of serum
2. BAcute kidney injury
3. CHypoparathyroidism
4. DContamination with K2EDTA
Answer and explanation in LearnFree account
Question 7 · Easy
Which hormone makes the distal nephron reabsorb sodium and secrete potassium?
1. AParathyroid hormone
2. BAtrial natriuretic peptide
3. CAntidiuretic hormone
4. DAldosterone
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Question 8 · Medium
Sodium 124 mmol/L, serum osmolality 258 mOsm/kg (reference 275-295) and urine osmolality 70 mOsm/kg. Which condition do these results most suggest?
1. APrimary polydipsia
2. BSevere hyperglycemia
3. CSIADH
4. DSevere hyperlipidemia
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Question 9 · Easy
Antidiuretic hormone (vasopressin) acts mainly on the collecting duct to:
1. AIncrease water reabsorption
2. BIncrease sodium reabsorption
3. CIncrease water excretion
4. DIncrease potassium secretion
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Question 10 · Medium
A patient in diabetic ketoacidosis has a serum potassium of 6.0 mmol/L. Total-body potassium in this patient is most likely:
1. AHigh, matching the serum level
2. BNormal, with no shift between spaces
3. CHigh, from reduced kidney excretion
4. DLow, despite the high serum potassium
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Question 11 · Medium
Glucose 900 mg/dL (50 mmol/L), sodium 126 mmol/L and a high measured serum osmolality. The low sodium is best explained by:
1. AInappropriate secretion of ADH
2. BWater shifting from cells into plasma
3. CSodium loss in the urine
4. DLipemia interfering with sodium measurement
Answer and explanation in LearnFree account
Question 12 · Hard
An 88-year-old nursing home resident with dementia has had a fever for 4 days. Sodium 158 mmol/L, BUN 58 mg/dL (20.7 mmol/L), creatinine 1.5 mg/dL (133 µmol/L), urine osmolality 820 mOsm/kg. The most likely cause of the hypernatremia is:
1. APrimary hyperaldosteronism
2. BCentral diabetes insipidus
3. CWater losses not replaced by drinking
4. DNephrogenic diabetes insipidus
Answer and explanation in LearnFree account
Question 13 · Medium
Two days after a head injury, a patient passes large volumes of urine with an osmolality of 110 mOsm/kg, and serum sodium is 154 mmol/L. What is the most likely cause?
1. ACentral diabetes insipidus
2. BSIADH
3. CPrimary hyperaldosteronism
4. DPrimary polydipsia
Answer and explanation in LearnFree account
Question 14 · Hard
Serum potassium is 6.4 mmol/L in a non-hemolyzed sample from a patient with essential thrombocythemia (platelets 1,350 × 10^3/µL; 1,350 × 10^9/L). Creatinine and the ECG are normal. The best next step is to:
1. ARepeat potassium on a fresh serum sample
2. BMeasure potassium in EDTA plasma
3. CMeasure potassium in heparinized plasma
4. DRepeat potassium after a longer clotting time
Answer and explanation in LearnFree account
Question 15 · Medium
After 4 days of severe diarrhea, a dehydrated patient has sodium 129 mmol/L, a low serum osmolality and a urine sodium of 8 mmol/L. What does this pattern point to?
1. ASodium loss through the kidneys
2. BWater retention from SIADH
3. CMineralocorticoid deficiency
4. DSodium loss through the intestine
Answer and explanation in LearnFree account
Question 16 · Medium
Which of these drugs is most likely to cause hyperkalemia?
1. AFurosemide (loop diuretic)
2. BHydrochlorothiazide (thiazide)
3. CLisinopril (ACE inhibitor)
4. DAlbuterol (beta-2 agonist)
Answer and explanation in LearnFree account

Electrolytes: interpretation and disease correlation

A 66-year-old with type 2 diabetes and creatinine 1.7 mg/dL (150 µmol/L) has sodium 138, potassium 6.0, chloride 112 and bicarbonate 17 mmol/L. Plasma renin and aldosterone are both low. Which disorder best explains these results?

A 70-year-old smoker with small cell lung carcinoma is euvolemic, with sodium 122 mmol/L, serum osmolality 254 mOsm/kg, urine osmolality 480 mOsm/kg and urine sodium 55 mmol/L. TSH and cortisol are normal. What is the most likely cause?

A patient on a long-term proton pump inhibitor has potassium 2.9 mmol/L that has not risen after 3 days of oral potassium. Magnesium is 0.8 mg/dL (0.33 mmol/L) [reference 1.7-2.4 mg/dL]. Why does the hypokalemia persist?

An outpatient with no symptoms and a normal ECG has potassium 9.2 mmol/L, calcium 2.8 mg/dL (0.70 mmol/L), and very low magnesium and alkaline phosphatase. The sample is not hemolyzed. The most likely cause is:

Which hormone makes the distal nephron reabsorb sodium and secrete potassium?

Sodium 124 mmol/L, serum osmolality 258 mOsm/kg (reference 275-295) and urine osmolality 70 mOsm/kg. Which condition do these results most suggest?

Antidiuretic hormone (vasopressin) acts mainly on the collecting duct to:

A patient in diabetic ketoacidosis has a serum potassium of 6.0 mmol/L. Total-body potassium in this patient is most likely:

Glucose 900 mg/dL (50 mmol/L), sodium 126 mmol/L and a high measured serum osmolality. The low sodium is best explained by:

An 88-year-old nursing home resident with dementia has had a fever for 4 days. Sodium 158 mmol/L, BUN 58 mg/dL (20.7 mmol/L), creatinine 1.5 mg/dL (133 µmol/L), urine osmolality 820 mOsm/kg. The most likely cause of the hypernatremia is:

Two days after a head injury, a patient passes large volumes of urine with an osmolality of 110 mOsm/kg, and serum sodium is 154 mmol/L. What is the most likely cause?

Serum potassium is 6.4 mmol/L in a non-hemolyzed sample from a patient with essential thrombocythemia (platelets 1,350 × 10^3/µL; 1,350 × 10^9/L). Creatinine and the ECG are normal. The best next step is to:

After 4 days of severe diarrhea, a dehydrated patient has sodium 129 mmol/L, a low serum osmolality and a urine sodium of 8 mmol/L. What does this pattern point to?

Which of these drugs is most likely to cause hyperkalemia?