Harr - Clinical Chemistry

Electrolytes

1. Which condition results in metabolic acidosis with severe

hypokalemia and chronic alkaline urine?

A. Diabetic ketoacidosis
B. Phenformin-induced acidosis
C. Renal tubular acidosis
D. Acidosis caused by starvation

2. In which condition would hypochloremia be expected?

A. Respiratory alkalosis
B. Metabolic acidosis
C. Metabolic alkalosis
D. All of these options

3. Given the following serum electrolyte data, determine the anion gap.

Na = 132 mmol/L Cl = 90 mmol/L HCO3 – = 22 mmol/L

A. 12 mmol/L
B. 20 mmol/L
C. 64 mmol/L
D. Cannot be determined from the information provided

4. Which of the following conditions will cause an increased anion gap?

A. Diarrhea
B. Hypoaldosteronism
C. Hyperkalemia
D. Renal failure

5. Which of the following conditions is associated with an increase in

ionized calcium (Caᵢ) in the blood?
A. Alkalosis
B. Hypoparathyroidism
C. Hyperalbuminemia
D. Malignancy

6. Which of the following laboratory results is consistent with primary

hypoparathyroidism? A. Low calcium; high inorganic phosphorus Pᵢ
B. Low calcium; low Pᵢ
C. High calcium; high Pᵢ
D. High calcium; low Pᵢ

7. Which of the following conditions is associated with

hypophosphatemia?
A. Rickets
B. Multiple myeloma
C. Renal failure
D. Hypervitaminosis D

8. Which of the following tests is consistently abnormal in osteoporosis?

A. High urinary calcium
B. High serum Pᵢ
C. Low serum calcium
D. High urine or serum N-telopeptide of type 1 collagen

9. Which statement best describes testing recommendations for vitamin

D?
A. Vitamin D testing should be reserved only for those persons who
demonstrate hypercalcemia of an undetermined cause
B. Vitamin D testing should be specific for the 1,25(OH)D3 form
C. Testing should be for total vitamin D when screening for deficiency
D. Vitamin D testing should not be performed if the patient is receiving a
vitamin D supplement

10. What is the percentage of serum calcium that is ionized (Cai )?

A. 30%
B. 45%
C. 60%
D. 80%

11. Which of the following conditions is associated with a low serum

magnesium?
A. Addison’s disease
B. Hemolytic anemia
C. Hyperparathyroidism
D. Pancreatitis

12. Which of the following conditions is associated with hypokalemia?

A. Addison’s disease
B. Hemolytic anemia
C. Digoxin intoxication
D. Alkalosis

13. Which of the following conditions is most likely to produce an

elevated plasma potassium?
A. Hypoparathyroidism
B. Cushing’s syndrome
C. Diarrhea
D. Digitalis overdose

14. Which of the following values is the threshold critical value (alert or
action level) for low plasma potassium?
A. 1.5 mmol/L
B. 2.0 mmol/L
C. 2.5 mmol/L
D. 3.5 mmol/L
 15. Which electrolyte is least likely to be elevated in renal failure?
A. Potassium
B. Magnesium
C. Inorganic phosphorus
D. Sodium

16. Which electrolyte measurement is least affected by hemolysis?

A. Potassium
B. Calcium
C. Pi
D. Magnesium

17. Which of the following conditions is associated with hypokalemia?

A. Addison’s disease
B. Hemolytic anemia
C. Digoxin intoxication
D. Alkalosis

18. Which of the following conditions is associated with hypernatremia?

A. Diabetes insipidus
B. Hypoaldosteronism
C. Burns
D. Diarrhea

19. Which of the following values is the threshold critical value (alert or
action level) for high plasma sodium?
A. 150 mmol/L
B. 160 mmol/L
C. 170 mmol/L
D. 180 mmol/L

20. Which of the following conditions is associated with total body

sodium excess?
A. Renal failure
B. Hyperthyroidism
C. Hypoparathyroidism
D. Diabetic ketoacidosis

21. Which of the following conditions is associated with hyponatremia?

A. Diuretic therapy
B. Cushing’s syndrome
C. Diabetes insipidus
D. Nephrotic syndrome

22. Which of the following conditions involving electrolytes is described

correctly?
A. Pseudohyponatremia occurs only when undiluted samples are measured
B. Potassium levels are slightly higher in heparinized plasma than in serum
C. Hypoalbuminemia causes low total calcium but does not affect Caᵢ
D. Hypercalcemia may be induced by low serum magnesium
 23. Which of the following laboratory results is usually associated with
cystic fibrosis?
A. Sweat chloride greater than 60 mmol/L
B. Elevated serum sodium and chloride
C. Elevated fecal trypsin activity
D. Low glucose

24. Which electrolyte level best correlates with plasma osmolality?

A. Sodium
B. Chloride
C. Bicarbonate
D. Calcium

# Answer Explanation

1 C Metabolic acidosis can be caused by any condition that lowers bicarbonate. In nonrenal
causes, the kidneys will attempt to compensate by increased acid excretion. However,
in renal tubular acidosis (RTA), an intrinsic defect in the tubules prevents bicarbonate
reabsorption. This causes alkaline instead of acidic urine. Excretion of bicarbonate as
potassium bicarbonate (KHCO3) results in severe hypokalemia.

2 C Chloride is the major extracellular anion and is retained or lost to preserve

electroneutrality. Low chloride will occur in metabolic alkalosis because excess
bicarbonate is present. Low chloride also will occur in partially compensated
respiratory acidosis because the kidneys compensate by increased retention of
bicarbonate.

3 B The anion gap is defined as unmeasured anions minus unmeasured cations. It is

calculated by subtracting the measured anions (bicarbonate and chloride) from the
serum sodium (or sodium plus potassium). A normal anion gap is approximately 8–16
mmol/L (12–20 mmol/L when potassium is used).

Anion gap = Na – (HCO3 + Cl)

Anion gap = 132 – (90 + 22) = 20 mmol/L

4 D An increased anion gap occurs when there is production or retention of anions other
than bicarbonate or chloride (measured anions). For example, in renal failure, retention
of phosphates and sulfates (as sodium salts) increases the anion gap. Other common
causes of metabolic acidosis with an increased anion gap are diabetic ketoacidosis and
lactate acidosis. The anion gap may also be increased in the absence of an acid–base
disorder. Common causes include hypocalcemia, drug overdose, and laboratory error
when measuring electrolytes.

5 D Increased Caᵢ occurs in hyperparathyroidism, malignancy, and acidosis. Caᵢ is elevated

in primary hyperparathyroidism due to resorption of calcium from bone. Many
non-parathyroid malignancies create products called parathyroid hormone-related
proteins that stimulate the parathyroid receptors of cells. Acidosis alters the equilibrium
 between bound and free calcium, favoring ionization. Hyperalbuminemia increases the
total calcium by increasing the protein bound fraction, but does not affect the Caᵢ.

6 A Parathyroid hormone deficiency causes reduced resorption of calcium from bone,

increased renal excretion of calcium, and decreased renal excretion of phosphorus. It is
distinguished from other causes of hypocalcemia by Cai , which is reduced only by
primary hypoparathyroidism and alkalosis.

7 A Rickets can result from dietary phosphate deficiency, vitamin D deficiency, or an

inherited disorder of either vitamin D or phosphorus metabolism. Vitamin D–dependent
rickets (VDDR) can be reversed by megadoses of vitamin D. Type 1 is caused by a
deficiency in renal cells of 1-α-hydroxylase, an enzyme that converts 25
hydroxyvitamin D to the active form, 1,25 hydroxyvitamin D. Type 2 is caused by a
deficiency in the vitamin D receptor of bone tissue. Vitamin D–resistant rickets
(VDRR) is caused by a deficiency in the renal reabsorption of phosphate.
Consequently, affected persons (usually men because it is most commonly X-linked)
have a normal serum calcium and a low Pᵢ.

8 D Commonly used markers for other bone diseases such as serum or urinary calcium,
inorganic phosphorus, total alkaline phosphatase (ALP), and vitamin D are neither
sensitive nor specific for osteoporosis. Calcium and phosphorus are usually within
normal limits. Although estrogen deficiency reduces formation of 1,25 hydroxyvitamin
D (1,25 hydroxycholecalciferol), promoting postmenopausal osteoporosis, the 1,25
hydroxyvitamin D is low in only 30%–35% of cases, and low levels may be caused by
other bone disorders. Serum markers for osteoporosis include both N-telopeptide of
type 1 collagen (NTx) and C-telopeptide of type 1 collagen (CTx). These can be used
to follow treatment with resorption antagonists (bisphosphonates) because they
decrease significantly when therapy is successful.

9 C Vitamin D deficiency is far more common than vitamin D excess, and screening for
vitamin D deficiency is advocated especially for dark-skinned persons and people who
do not get adequate sunlight. Provitamin D is a steroid, and vitamin D is now
considered a hormone rather than a vitamin. The hormone regulates transcription of
over 200 genes and has pronounced effects on both dendritic cells and T lymphocytes.
Deficiency is associated with many chronic diseases including autoimmune diseases,
cancers, hypertension, and heart disease. There are two forms of the vitamin,
ergocalciferol (D2) and cholecalciferol (D3). Active D2 and D3 are formed when two
hydroxyl groups are added, the first being at the 25 position by the liver and the second
at the α-1 position by the kidney. The majority of the circulating vitamin D is in the
25-hydroxylated form of D2 and D3, called 25(OH)D. The plasma 25(OH)D
concentration is an expression of both dietary and endogenous vitamin D and is the
most appropriate test for detecting nutritional vitamin D deficiency. Since the effect on
calcium is derived from the active 1,25 form of the vitamin, plasma 1,25(OH)D
concentration is a more specific test for hypervitaminosis D.

10 B Calcium exists in serum in three forms: protein bound, ionized, and complexed (as
undissociated salts). Only Cai is physiologically active. Protein bound and Cai each
account for approximately 45% of total calcium, and the remaining 10% is complexed.

11 D Low magnesium can be caused by gastrointestinal loss, as occurs in diarrhea and

 pancreatitis (loss of Mg and Ca as soaps). Hyperparathyroidism causes increased
release of both calcium and magnesium from bone. Addison’s disease
(adrenocorticosteroid deficiency) may be associated with increased magnesium
accompanying hyperkalemia. Hemolytic anemia causes increased release of
magnesium as well as potassium from damaged red blood cells (RBCs).

12 D Addison’s disease (adrenocortical insufficiency) results in low levels of adrenal

corticosteroid hormones, including aldosterone and cortisol. Because these hormones
promote reabsorption of sodium and secretion of potassium by the collecting tubules,
patients with Addison’s disease display hyperkalemia and hyponatremia. Hemolytic
anemia and digoxin intoxication cause release of intracellular potassium. Alkalosis
causes potassium to move from the extracellular fluid into the cells as hydrogen ions
move from the cells into the extracellular fluid to compensate for alkalosis.

13 D Digitalis toxicity causes potassium to leave the cells and enter the extracellular fluid,
resulting in hyperkalemia. Renal failure, hemolytic anemia and Addison’s disease are
other frequent causes of hyperkalemia. Hypoparathyroidism indirectly causes
hypokalemia by inducing alkalosis via increased renal retention of phosphate and
bicarbonate. Cushing’s syndrome (adrenal cortical hyperfunction) results in low
potassium and elevated sodium. Diarrhea causes loss of sodium and potassium.

14 C The reference range for potassium is 3.6–5.4 mmol/L. However, values below 2.5
mmol/L require immediate intervention because below that level there is a grave risk of
cardiac arrhythmia, which can lead to cardiac arrest. The upper alert level for potassium
is usually 6.5 mmol/L, except for neonatal and hemolyzed samples. Above this level,
there is danger of cardiac failure.

15 D Reduced glomerular filtration coupled with decreased tubular secretion causes

accumulation of potassium, magnesium, and inorganic phosphorus. Poor tubular
reabsorption of sodium offsets reduced glomerular filtration. Unfiltered sodium draws
both chloride and water, causing osmotic equilibration between filtrate, serum, and the
tissues. In renal disease, serum sodium is often normal, although total body sodium is
increased owing to fluid and salt retention.

16 B Potassium, phosphorus, and magnesium are the major intracellular ions, and even slight
hemolysis will cause falsely elevated results. Serum samples with visible hemolysis (20
mg/dL free Hgb) should be redrawn

17 D Addison’s disease (adrenocortical insufficiency) results in low levels of adrenal

corticosteroid hormones, including aldosterone and cortisol. Because these hormones
promote reabsorption of sodium and secretion of potassium by the collecting tubules,
patients with Addison’s disease display hyperkalemia and hyponatremia. Hemolytic
anemia and digoxin intoxication cause release of intracellular potassium. Alkalosis
causes potassium to move from the extracellular fluid into the cells as hydrogen ions
move from the cells into the extracellular fluid to compensate for alkalosis

18 A Diabetes insipidus results from failure to produce ADH. Because the collecting tubules
are impermeable to water in the absence of ADH, severe hypovolemia and dehydration
result. Hypovolemia stimulates aldosterone release, causing sodium reabsorption,
which worsens the hypernatremia. Burns, hypoaldosteronism, diarrhea, and diuretic
therapy are common causes of hyponatremia.
19 B The adult reference range for plasma sodium is approximately 135–145 mmol/L.
Levels in excess of 160 mmol/L are associated with severe dehydration, hypovolemia,
and circulatory and heart failure. The threshold for the low critical value for sodium is
120 mmol/L. This is associated with edema, hypervolemia, and circulatory overload.
Alert levels must also be established for potassium, bicarbonate, calcium, pH, PO2,
glucose, bilirubin, hemoglobin, platelet count, and prothrombin time. When a sample
result is below or above the low or high alert level, respectively, the physician must be
notified immediately.

20 A Total body sodium excess often occurs in persons with renal failure, congestive heart
failure, and cirrhosis of the liver. When water is retained along with sodium, total body
sodium excess results rather than hypernatremia. Heart failure causes sodium and water
retention by reducing blood flow to the kidneys. Cirrhosis causes obstruction of hepatic
lymphatics and portal veins, leading to local hypertension and accumulation of ascites
fluid. Renal failure results in poor glomerular filtration and isosmotic equilibration of
salt and water.

21 A Diuretics lower blood pressure by promoting water loss. This is accomplished by

causing sodium loss from the proximal tubule and/or loop. Addison’s disease,
syndrome of inappropriate ADH release, burns, diabetic ketoacidosis, hypopituitarism,
vomiting, diarrhea, and cystic fibrosis also cause hyponatremia. Cushing’s syndrome
causes hypernatremia by promoting sodium reabsorption in the collecting tubule in
exchange for potassium. Diabetes insipidus and nephrotic syndrome promote
hypernatremia by causing water loss.

22 C When serum albumin is low, the equilibrium between bound and Cai is shifted,
producing increased Cai . This inhibits release of PTH by negative feedback until the
Cai level returns to normal. Potassium is released from platelets and leukocytes during
coagulation, causing serum levels to be higher than plasma. Pseudohyponatremia is a
measurement error caused by diluting samples containing excessive fat or protein. The
colloids displace plasma water, resulting in less electrolytes being delivered into the
diluent. Only ion-selective electrodes that measure whole blood or undiluted serum are
unaffected. Magnesium is needed for release of PTH, and PTH causes release of
calcium and magnesium from bone. Therefore, hypocalcemia can be associated with
either magnesium deficiency or magnesium excess.

23 A Cystic fibrosis causes obstruction of the exocrine glands including the sweat glands,
mucus glands, and pancreas. Newborns with pancreatic involvement demonstrate fecal
trypsin deficiency, which may be detected by a low fecal chymotrypsin or
immunoreactive trypsin result. However, these tests require confirmation. Serum
sodium and chloride levels are low. More than 98% of affected infants have elevated
sweat sodium and chloride and low serum levels. Sweat chloride in excess of 60
mmol/L confirms the clinical diagnosis. Some persons with the disease have insulin
deficiency and elevated blood glucose. Genetic tests are available to detect several
mutations that occur at the cystic fibrosis transmembrane conductance regulator
(CFTR) locus on chromosome 7.

24 A Sodium and chloride are the major extracellular ions. Chloride passively follows
sodium, making sodium the principal determinant of plasma osmolality.