NURS 3209 FLUID AND ELECTROLYTE BALANCE EXAM PRACTICE
QUESTIONS AND CORRECT ANSWERS (VERIFIED ANSWERS)
PLUS RATIONALES Q&A INSTANT DOWNLOAD PDF
150 QUESTIONS
TABLE OF CONTENTS
# TOPIC
1 Analyze the regulatory mechanisms of fluid and electrolyte balance and their disruptions
2 Interpret laboratory data and hemodynamic parameters to guide clinical decisions
3 Evaluate the appropriateness of nursing and medical interventions for fluid and electrolyte imbalances
4 Synthesize knowledge to prioritize care in complex, multi-system clinical situations
5 NURS 3209 Fluid and Electrolyte Balance Exam Practice Questions And Correct Answers
6 Verified Answers
7 Plus Rationales Q&A Instant Download Pdf
8 Foundations of Nursing - Fluid and Electrolyte Balance
9 Applied Nursing - Fluid and Electrolyte Balance
10 Advanced Nursing - Fluid and Electrolyte Balance
11 Nursing - Fluid and Electrolyte Balance Review
Page 1
,Q1 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
A patient with syndrome of inappropriate antidiuretic hormone (SIADH) presents
with severe hyponatremia (Na+ 115 mEq/L) and neurological symptoms. Which
combination of therapies is most appropriate for immediate management?
A. Hypertonic saline (3%) plus furosemide, with strict fluid restriction and frequent serum sodium
monitoring CORRECT
B. Normal saline (0.9%) bolus followed by fluid restriction
C. Vaptans (tolvaptan) alone, avoiding any sodium replacement
D. Demeclocycline and fluid restriction, avoiding hypertonic saline
RATIONALE: In severe symptomatic hyponatremia, hypertonic saline (3%) is indicated to raise
serum sodium at a controlled rate, while furosemide helps prevent fluid overload and corrects the
dilutional state. Vaptans are used for chronic SIADH, not acute severe symptoms. Normal saline
may worsen hyponatremia in SIADH. Demeclocycline is too slow for emergency management.
Q2 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
Which physiological mechanism primarily explains the development of
hyperkalemia in a patient with tumor lysis syndrome?
A. Increased renal excretion of potassium due to aldosterone stimulation
B. Massive release of intracellular potassium from lysed tumor cells overwhelming renal
excretory capacity CORRECT
C. Shift of potassium into cells due to insulin and beta-adrenergic stimulation
D. Decreased dietary intake and increased gastrointestinal losses
RATIONALE: Tumor lysis syndrome causes rapid lysis of malignant cells, releasing large
amounts of intracellular potassium into the circulation. If renal excretion cannot keep pace,
hyperkalemia ensues. Aldosterone would increase excretion, not cause hyperkalemia. Insulin
and beta-agonists shift potassium into cells, lowering serum levels. Dietary intake and GI losses
are not primary factors.
Page 2
,Q3 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
A postoperative patient has a nasogastric tube on low intermittent suction. Arterial
blood gas shows: pH 7.50, PaCO2 45 mm Hg, HCO3- 34 mEq/L. Which intravenous
fluid is most appropriate to address the underlying acid-base disturbance?
A. Lactated Ringer's
B. 0.45% sodium chloride with potassium chloride
C. 0.9% sodium chloride CORRECT
D. D5W
RATIONALE: The ABG indicates metabolic alkalosis due to loss of hydrogen ions and chloride
via gastric suction. Normal saline (0.9% NaCl) provides chloride to correct the hypochloremic
metabolic alkalosis. Lactated Ringer's contains lactate and may worsen alkalosis. Hypotonic
fluids and D5W do not adequately replace chloride. Potassium may be needed but is not the
primary fluid.
Q4 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
Which set of findings is most consistent with hypermagnesemia?
A. Hyperactive deep tendon reflexes, muscle twitching, and positive Trousseau's sign
B. Hypotension, bradycardia, lethargy, and respiratory depression CORRECT
C. Hypertension, tachycardia, diarrhea, and flushing
D. Muscle weakness, constipation, and prolonged QT interval
RATIONALE: Hypermagnesemia causes vasodilation and neuromuscular depression, leading to
hypotension, bradycardia, lethargy, and respiratory depression. Hyperactive reflexes and
twitching are signs of hypomagnesemia. Hypertension and tachycardia are not typical.
Constipation and QT prolongation are more associated with hypocalcemia or hypokalemia, not
hypermagnesemia.
Page 3
, Q5 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
A patient with chronic kidney disease (stage 4) is prescribed oral calcium acetate
as a phosphate binder. Which laboratory value is most important to monitor to
prevent a serious complication of this therapy?
A. Serum potassium
B. Serum calcium CORRECT
C. Serum magnesium
D. Serum phosphorus
RATIONALE: Calcium acetate can cause hypercalcemia, especially in patients with CKD who
may have altered vitamin D metabolism. Monitoring serum calcium is crucial to prevent
hypercalcemia and vascular calcification. Potassium, magnesium, and phosphorus are not
directly affected by calcium acetate, though phosphorus is the target of therapy.
Q6 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
Which statement best describes the primary role of the
renin-angiotensin-aldosterone system (RAAS) in fluid balance?
A. It directly stimulates the release of atrial natriuretic peptide to promote sodium excretion.
B. It increases sodium and water reabsorption in the distal nephron via aldosterone, conserving
extracellular volume. CORRECT
C. It primarily regulates calcium and phosphate balance through parathyroid hormone.
D. It suppresses antidiuretic hormone release to increase free water clearance.
RATIONALE: RAAS activation leads to aldosterone secretion, which enhances sodium and water
reabsorption in the distal tubule and collecting duct, thereby expanding extracellular fluid volume.
ANP is released in response to atrial stretch and opposes RAAS. RAAS is not involved in
calcium/phosphate regulation. ADH is regulated by osmolality and volume, but RAAS does not
directly suppress it.
Page 4
QUESTIONS AND CORRECT ANSWERS (VERIFIED ANSWERS)
PLUS RATIONALES Q&A INSTANT DOWNLOAD PDF
150 QUESTIONS
TABLE OF CONTENTS
# TOPIC
1 Analyze the regulatory mechanisms of fluid and electrolyte balance and their disruptions
2 Interpret laboratory data and hemodynamic parameters to guide clinical decisions
3 Evaluate the appropriateness of nursing and medical interventions for fluid and electrolyte imbalances
4 Synthesize knowledge to prioritize care in complex, multi-system clinical situations
5 NURS 3209 Fluid and Electrolyte Balance Exam Practice Questions And Correct Answers
6 Verified Answers
7 Plus Rationales Q&A Instant Download Pdf
8 Foundations of Nursing - Fluid and Electrolyte Balance
9 Applied Nursing - Fluid and Electrolyte Balance
10 Advanced Nursing - Fluid and Electrolyte Balance
11 Nursing - Fluid and Electrolyte Balance Review
Page 1
,Q1 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
A patient with syndrome of inappropriate antidiuretic hormone (SIADH) presents
with severe hyponatremia (Na+ 115 mEq/L) and neurological symptoms. Which
combination of therapies is most appropriate for immediate management?
A. Hypertonic saline (3%) plus furosemide, with strict fluid restriction and frequent serum sodium
monitoring CORRECT
B. Normal saline (0.9%) bolus followed by fluid restriction
C. Vaptans (tolvaptan) alone, avoiding any sodium replacement
D. Demeclocycline and fluid restriction, avoiding hypertonic saline
RATIONALE: In severe symptomatic hyponatremia, hypertonic saline (3%) is indicated to raise
serum sodium at a controlled rate, while furosemide helps prevent fluid overload and corrects the
dilutional state. Vaptans are used for chronic SIADH, not acute severe symptoms. Normal saline
may worsen hyponatremia in SIADH. Demeclocycline is too slow for emergency management.
Q2 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
Which physiological mechanism primarily explains the development of
hyperkalemia in a patient with tumor lysis syndrome?
A. Increased renal excretion of potassium due to aldosterone stimulation
B. Massive release of intracellular potassium from lysed tumor cells overwhelming renal
excretory capacity CORRECT
C. Shift of potassium into cells due to insulin and beta-adrenergic stimulation
D. Decreased dietary intake and increased gastrointestinal losses
RATIONALE: Tumor lysis syndrome causes rapid lysis of malignant cells, releasing large
amounts of intracellular potassium into the circulation. If renal excretion cannot keep pace,
hyperkalemia ensues. Aldosterone would increase excretion, not cause hyperkalemia. Insulin
and beta-agonists shift potassium into cells, lowering serum levels. Dietary intake and GI losses
are not primary factors.
Page 2
,Q3 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
A postoperative patient has a nasogastric tube on low intermittent suction. Arterial
blood gas shows: pH 7.50, PaCO2 45 mm Hg, HCO3- 34 mEq/L. Which intravenous
fluid is most appropriate to address the underlying acid-base disturbance?
A. Lactated Ringer's
B. 0.45% sodium chloride with potassium chloride
C. 0.9% sodium chloride CORRECT
D. D5W
RATIONALE: The ABG indicates metabolic alkalosis due to loss of hydrogen ions and chloride
via gastric suction. Normal saline (0.9% NaCl) provides chloride to correct the hypochloremic
metabolic alkalosis. Lactated Ringer's contains lactate and may worsen alkalosis. Hypotonic
fluids and D5W do not adequately replace chloride. Potassium may be needed but is not the
primary fluid.
Q4 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
Which set of findings is most consistent with hypermagnesemia?
A. Hyperactive deep tendon reflexes, muscle twitching, and positive Trousseau's sign
B. Hypotension, bradycardia, lethargy, and respiratory depression CORRECT
C. Hypertension, tachycardia, diarrhea, and flushing
D. Muscle weakness, constipation, and prolonged QT interval
RATIONALE: Hypermagnesemia causes vasodilation and neuromuscular depression, leading to
hypotension, bradycardia, lethargy, and respiratory depression. Hyperactive reflexes and
twitching are signs of hypomagnesemia. Hypertension and tachycardia are not typical.
Constipation and QT prolongation are more associated with hypocalcemia or hypokalemia, not
hypermagnesemia.
Page 3
, Q5 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
A patient with chronic kidney disease (stage 4) is prescribed oral calcium acetate
as a phosphate binder. Which laboratory value is most important to monitor to
prevent a serious complication of this therapy?
A. Serum potassium
B. Serum calcium CORRECT
C. Serum magnesium
D. Serum phosphorus
RATIONALE: Calcium acetate can cause hypercalcemia, especially in patients with CKD who
may have altered vitamin D metabolism. Monitoring serum calcium is crucial to prevent
hypercalcemia and vascular calcification. Potassium, magnesium, and phosphorus are not
directly affected by calcium acetate, though phosphorus is the target of therapy.
Q6 ANALYZE THE REGULATORY MECHANISMS OF FLUID AND ELECTROLYTE BALANCE
AND THEIR DISRUPTIONS
Which statement best describes the primary role of the
renin-angiotensin-aldosterone system (RAAS) in fluid balance?
A. It directly stimulates the release of atrial natriuretic peptide to promote sodium excretion.
B. It increases sodium and water reabsorption in the distal nephron via aldosterone, conserving
extracellular volume. CORRECT
C. It primarily regulates calcium and phosphate balance through parathyroid hormone.
D. It suppresses antidiuretic hormone release to increase free water clearance.
RATIONALE: RAAS activation leads to aldosterone secretion, which enhances sodium and water
reabsorption in the distal tubule and collecting duct, thereby expanding extracellular fluid volume.
ANP is released in response to atrial stretch and opposes RAAS. RAAS is not involved in
calcium/phosphate regulation. ADH is regulated by osmolality and volume, but RAAS does not
directly suppress it.
Page 4
