NUR 265 Exam 1 V1, V2 and V3| Questions and Answers | 2026
Update | 100% Correct - Galen College of Nursing - 137
Questions
This exam assesses mastery of fluid and electrolyte imbalances, including pathophysiology, clinical
manifestations, diagnostic interpretation, and evidence-based interventions. Questions integrate advanced
pathophysiology, pharmacology, and clinical decision-making at a level expected of senior nursing students in a
rigorous US university program. It contains 137 multiple-choice questions, each with four distractors and a fully
worked rationale that explains why the keyed answer is correct. Content is organized into 8 focused sections:
Fluid & Electrolyte Imbalances, Acid-Base Balance, Perioperative Nursing, Pain Management, Shock & Sepsis,
Respiratory Disorders, Cardiovascular Disorders, Neurological Disorders. Targeted learning outcomes include:
Analyze the etiology and compensatory mechanisms for major electrolyte disturbances.; Interpret diagnostic lab
values and subtle clinical signs to differentiate imbalances.; Prioritize nursing interventions and evaluate
outcomes for patients with complex fluid and electrolyte disorders.. Every item has been reviewed for clinical
accuracy, current guidelines, and clarity so that students can study with confidence and self-correct as they work
through the bank. Use it as a high-yield review immediately before the exam, or as a structured practice tool
during the unit - the rationales double as concise teaching notes. The recommended writing time is 3 hours, with a
passing score of 90%. Aligned with Meets AACN BSN Essentials and CCNE accreditation standards for a top-tier
US nursing program. standards and reflects the question style commonly seen on accredited program
Section 1: Fluid & Electrolyte Imbalances (Questions 1-24)
1 A patient with diabetes insipidus presents with serum sodium of 160 mEq/L.
Using the formula for water deficit (TBW deficit = 0.6 x weight (kg) x [1 -
140/Na]), the calculated deficit is 6 L. Which of the following infusion
strategies is most appropriate to avoid complications?
A) Administer 0.9% NaCl at 250 mL/h until the deficit is replaced
B) Administer 5% dextrose in water at a rate to replace half the deficit over
24 hours
C) Administer 0.45% NaCl at 150 mL/h for the first 12 hours
D) Give desmopressin and replace the deficit with oral water only
Answer: B
Rationale: Correct: B. In hypernatremia (Na >150), rapid correction risks
cerebral edema. Half the deficit should be replaced over the first 24 hours using
hypotonic fluids (D5W or 0.45% NaCl). Option A uses isotonic saline, which
won't lower Na sufficiently. Option C may still be too rapid. Option D: oral
replacement may be insufficient in insipidus, and desmopressin alone doesn't
correct deficit.
,2 A patient receiving loop diuretics develops hypokalemia (2.8 mEq/L). ECG
shows flattened T waves and a prominent U wave. Which of the following
mechanisms best explains the increased risk of ventricular arrhythmias in
this setting?
A) Delayed repolarization due to prolonged action potential duration
B) Enhanced automaticity from increased resting membrane potential
excitability
C) Inhibition of the Na+/K+ ATPase pump, reducing outward potassium
current
D) Accelerated repolarization due to shortened refractory period
Answer: B
Rationale: Correct: B. Hypokalemia increases the resting membrane potential
(less negative), bringing it closer to threshold, enhancing automaticity and
predisposing to ectopic pacemakers and reentrant arrhythmias. Option A:
hypokalemia prolongs repolarization (QT prolongation), not delayed-flattened
T wave is early repolarization. Option C: Na+/K+ pump is actually inhibited,
but that's not the main arrhythmogenic mechanism. Option D: repolarization is
slowed, not accelerated.
3 A patient with metastatic breast cancer has serum calcium of 13.5 mg/dL.
Which of the following physiological alterations most likely contributes to
the impaired myocardial contractility observed?
A) Calcium binding to troponin C is excessive, causing sustained contraction
B) Elevated calcium levels antagonize potassium channels, prolonging
diastole
C) Hypercalcemia decreases the slope of phase 0 depolarization in cardiac
myocytes
D) Calcium overload leads to increased intracellular cAMP and altered
excitation-contraction coupling
Answer: C
Rationale: Correct: C. Hypercalcemia reduces the transmembrane gradient for
sodium, slowing phase 0 depolarization (decreased dV/dt max), which delays
conduction and impairs contractility. Option A: hypercalcemia does increase
calcium binding but not to the point of sustained contraction; that would
actually increase contractility. Option B: hypercalcemia shortens the action
potential (QTc shortening), not prolong diastole. Option D: cAMP is not
,directly increased by calcium; hypercalcemia actually inhibits adenylyl cyclase
in some tissues.
4 A patient with chronic alcoholism presents with tetany and a positive
Chvostek sign. Serum magnesium is 1.2 mg/dL. After administration of 2 g
of IV magnesium sulfate, the tetany persists. Which of the following most
likely explains the lack of response?
A) Concomitant hypocalcemia unmasked by magnesium depletion
B) Magnesium replacement was given too slowly to raise serum levels
C) The tetany is due to metabolic alkalosis rather than hypomagnesemia
D) Intracellular magnesium remains depleted despite normalizing serum
levels
Answer: A
Rationale: Correct: A. Hypomagnesemia often coexists with hypocalcemia
because magnesium is needed for PTH secretion and action. Tetany in
hypomagnesemia may persist until both magnesium and calcium are corrected.
Option B: 2 g IV is a standard dose and should raise serum Mg if given
appropriately. Option C: metabolic alkalosis can cause tetany, but
hypomagnesemia is likely the primary issue given the Chvostek sign and
alcoholism. Option D: Intracellular depletion takes longer to correct, but tetany
usually resolves with serum Mg correction if calcium is normal.
5 A patient with severe pancreatitis develops oliguria, hemoconcentration (Hct
50%), and hypovolemic shock despite a positive fluid balance. Which of the
following best explains this paradoxical finding?
A) Increased insensible losses from hyperventilation and fever
B) Redistribution of fluid into the peritoneal cavity and retroperitoneal space
C) Compensatory activation of the renin-angiotensin-aldosterone system
D) Impaired renal concentrating ability due to medullary ischemia
Answer: B
Rationale: Correct: B. In severe pancreatitis, third-spacing of fluid into the
peritoneal and retroperitoneal spaces reduces effective circulating volume
despite a positive net intake. This leads to hemoconcentration and hypovolemic
shock. Option A: insensible losses may increase but not enough to cause such
severe hemoconcentration. Option C: RAAS activation is a response to
hypovolemia, not the cause of the paradox. Option D: renal concentrating
, ability may be impaired, but that would cause dilute urine, not oliguria with
hemoconcentration.
6 A patient with heart failure and EF 25% is receiving furosemide 80 mg IV
BID. He develops worsening dyspnea, jugular venous distention, and a chest
X-ray shows pulmonary edema. Serum sodium is 130 mEq/L, B-type
natriuretic peptide (BNP) > 5000 pg/mL. Which of the following is the most
likely cause of hyponatremia in this context?
A) Excessive free water intake due to increased thirst
B) Impaired renal diluting capacity due to reduced renal perfusion
C) Non-osmotic release of antidiuretic hormone (ADH)
D) Sodium loss from diuretic therapy exceeding water excretion
Answer: C
Rationale: Correct: C. In heart failure, decreased effective circulating volume
stimulates non-osmotic ADH release, leading to water retention and dilutional
hyponatremia. Option A: thirst may be increased, but ADH-mediated water
reabsorption is the primary driver. Option B: impaired diluting capacity is a
factor, but it is largely due to ADH and reduced distal delivery. Option D:
furosemide causes isotonic urine, so water loss equals sodium loss;
hyponatremia is usually not due to diuretics unless there is concomitant water
intake.
7 A 70 kg patient with renal failure and hyperkalemia (K+ 6.8 mEq/L) is about
to receive emergency treatment. Which of the following medication orders
should the nurse question?
A) Intravenous calcium gluconate 10 mL
B) Albuterol nebulization 10 mg
C) Sodium polystyrene sulfonate 30 g rectally
D) Potassium chloride 20 mEq IV
Answer: D
Rationale: Correct: D. Administering potassium chloride to a patient with
severe hyperkalemia is contraindicated and would worsen the condition.
Options A (calcium stabilizes cardiac membranes), B (albuterol shifts
potassium into cells), and C (removes potassium via gut) are all appropriate
acute interventions.
Update | 100% Correct - Galen College of Nursing - 137
Questions
This exam assesses mastery of fluid and electrolyte imbalances, including pathophysiology, clinical
manifestations, diagnostic interpretation, and evidence-based interventions. Questions integrate advanced
pathophysiology, pharmacology, and clinical decision-making at a level expected of senior nursing students in a
rigorous US university program. It contains 137 multiple-choice questions, each with four distractors and a fully
worked rationale that explains why the keyed answer is correct. Content is organized into 8 focused sections:
Fluid & Electrolyte Imbalances, Acid-Base Balance, Perioperative Nursing, Pain Management, Shock & Sepsis,
Respiratory Disorders, Cardiovascular Disorders, Neurological Disorders. Targeted learning outcomes include:
Analyze the etiology and compensatory mechanisms for major electrolyte disturbances.; Interpret diagnostic lab
values and subtle clinical signs to differentiate imbalances.; Prioritize nursing interventions and evaluate
outcomes for patients with complex fluid and electrolyte disorders.. Every item has been reviewed for clinical
accuracy, current guidelines, and clarity so that students can study with confidence and self-correct as they work
through the bank. Use it as a high-yield review immediately before the exam, or as a structured practice tool
during the unit - the rationales double as concise teaching notes. The recommended writing time is 3 hours, with a
passing score of 90%. Aligned with Meets AACN BSN Essentials and CCNE accreditation standards for a top-tier
US nursing program. standards and reflects the question style commonly seen on accredited program
Section 1: Fluid & Electrolyte Imbalances (Questions 1-24)
1 A patient with diabetes insipidus presents with serum sodium of 160 mEq/L.
Using the formula for water deficit (TBW deficit = 0.6 x weight (kg) x [1 -
140/Na]), the calculated deficit is 6 L. Which of the following infusion
strategies is most appropriate to avoid complications?
A) Administer 0.9% NaCl at 250 mL/h until the deficit is replaced
B) Administer 5% dextrose in water at a rate to replace half the deficit over
24 hours
C) Administer 0.45% NaCl at 150 mL/h for the first 12 hours
D) Give desmopressin and replace the deficit with oral water only
Answer: B
Rationale: Correct: B. In hypernatremia (Na >150), rapid correction risks
cerebral edema. Half the deficit should be replaced over the first 24 hours using
hypotonic fluids (D5W or 0.45% NaCl). Option A uses isotonic saline, which
won't lower Na sufficiently. Option C may still be too rapid. Option D: oral
replacement may be insufficient in insipidus, and desmopressin alone doesn't
correct deficit.
,2 A patient receiving loop diuretics develops hypokalemia (2.8 mEq/L). ECG
shows flattened T waves and a prominent U wave. Which of the following
mechanisms best explains the increased risk of ventricular arrhythmias in
this setting?
A) Delayed repolarization due to prolonged action potential duration
B) Enhanced automaticity from increased resting membrane potential
excitability
C) Inhibition of the Na+/K+ ATPase pump, reducing outward potassium
current
D) Accelerated repolarization due to shortened refractory period
Answer: B
Rationale: Correct: B. Hypokalemia increases the resting membrane potential
(less negative), bringing it closer to threshold, enhancing automaticity and
predisposing to ectopic pacemakers and reentrant arrhythmias. Option A:
hypokalemia prolongs repolarization (QT prolongation), not delayed-flattened
T wave is early repolarization. Option C: Na+/K+ pump is actually inhibited,
but that's not the main arrhythmogenic mechanism. Option D: repolarization is
slowed, not accelerated.
3 A patient with metastatic breast cancer has serum calcium of 13.5 mg/dL.
Which of the following physiological alterations most likely contributes to
the impaired myocardial contractility observed?
A) Calcium binding to troponin C is excessive, causing sustained contraction
B) Elevated calcium levels antagonize potassium channels, prolonging
diastole
C) Hypercalcemia decreases the slope of phase 0 depolarization in cardiac
myocytes
D) Calcium overload leads to increased intracellular cAMP and altered
excitation-contraction coupling
Answer: C
Rationale: Correct: C. Hypercalcemia reduces the transmembrane gradient for
sodium, slowing phase 0 depolarization (decreased dV/dt max), which delays
conduction and impairs contractility. Option A: hypercalcemia does increase
calcium binding but not to the point of sustained contraction; that would
actually increase contractility. Option B: hypercalcemia shortens the action
potential (QTc shortening), not prolong diastole. Option D: cAMP is not
,directly increased by calcium; hypercalcemia actually inhibits adenylyl cyclase
in some tissues.
4 A patient with chronic alcoholism presents with tetany and a positive
Chvostek sign. Serum magnesium is 1.2 mg/dL. After administration of 2 g
of IV magnesium sulfate, the tetany persists. Which of the following most
likely explains the lack of response?
A) Concomitant hypocalcemia unmasked by magnesium depletion
B) Magnesium replacement was given too slowly to raise serum levels
C) The tetany is due to metabolic alkalosis rather than hypomagnesemia
D) Intracellular magnesium remains depleted despite normalizing serum
levels
Answer: A
Rationale: Correct: A. Hypomagnesemia often coexists with hypocalcemia
because magnesium is needed for PTH secretion and action. Tetany in
hypomagnesemia may persist until both magnesium and calcium are corrected.
Option B: 2 g IV is a standard dose and should raise serum Mg if given
appropriately. Option C: metabolic alkalosis can cause tetany, but
hypomagnesemia is likely the primary issue given the Chvostek sign and
alcoholism. Option D: Intracellular depletion takes longer to correct, but tetany
usually resolves with serum Mg correction if calcium is normal.
5 A patient with severe pancreatitis develops oliguria, hemoconcentration (Hct
50%), and hypovolemic shock despite a positive fluid balance. Which of the
following best explains this paradoxical finding?
A) Increased insensible losses from hyperventilation and fever
B) Redistribution of fluid into the peritoneal cavity and retroperitoneal space
C) Compensatory activation of the renin-angiotensin-aldosterone system
D) Impaired renal concentrating ability due to medullary ischemia
Answer: B
Rationale: Correct: B. In severe pancreatitis, third-spacing of fluid into the
peritoneal and retroperitoneal spaces reduces effective circulating volume
despite a positive net intake. This leads to hemoconcentration and hypovolemic
shock. Option A: insensible losses may increase but not enough to cause such
severe hemoconcentration. Option C: RAAS activation is a response to
hypovolemia, not the cause of the paradox. Option D: renal concentrating
, ability may be impaired, but that would cause dilute urine, not oliguria with
hemoconcentration.
6 A patient with heart failure and EF 25% is receiving furosemide 80 mg IV
BID. He develops worsening dyspnea, jugular venous distention, and a chest
X-ray shows pulmonary edema. Serum sodium is 130 mEq/L, B-type
natriuretic peptide (BNP) > 5000 pg/mL. Which of the following is the most
likely cause of hyponatremia in this context?
A) Excessive free water intake due to increased thirst
B) Impaired renal diluting capacity due to reduced renal perfusion
C) Non-osmotic release of antidiuretic hormone (ADH)
D) Sodium loss from diuretic therapy exceeding water excretion
Answer: C
Rationale: Correct: C. In heart failure, decreased effective circulating volume
stimulates non-osmotic ADH release, leading to water retention and dilutional
hyponatremia. Option A: thirst may be increased, but ADH-mediated water
reabsorption is the primary driver. Option B: impaired diluting capacity is a
factor, but it is largely due to ADH and reduced distal delivery. Option D:
furosemide causes isotonic urine, so water loss equals sodium loss;
hyponatremia is usually not due to diuretics unless there is concomitant water
intake.
7 A 70 kg patient with renal failure and hyperkalemia (K+ 6.8 mEq/L) is about
to receive emergency treatment. Which of the following medication orders
should the nurse question?
A) Intravenous calcium gluconate 10 mL
B) Albuterol nebulization 10 mg
C) Sodium polystyrene sulfonate 30 g rectally
D) Potassium chloride 20 mEq IV
Answer: D
Rationale: Correct: D. Administering potassium chloride to a patient with
severe hyperkalemia is contraindicated and would worsen the condition.
Options A (calcium stabilizes cardiac membranes), B (albuterol shifts
potassium into cells), and C (removes potassium via gut) are all appropriate
acute interventions.
