NUR 2063: Essentials of Pathophysiology Exam 2 | Rasmussen University 2026-2027 75 Questions
NUR 2063 / NUR2063: Essentials of Pathophysiology
Exam 2 (Latest ) - Rasmussen University
Modules 4, 5, and 6: GI, Genitourinary, and Endocrine Systems
Section 1: Fluid, Electrolyte, and Acid-Base Imbalances (Q1-Q15)
Q1: A patient is admitted with a serum sodium level of 128 mEq/L. The nurse observes
confusion and lethargy. Which pathophysiological mechanism best explains these
neurological symptoms?
A. Water shifts from the extracellular fluid into the intracellular fluid, causing brain cell
swelling and cerebral edema [CORRECT]
B. Water shifts from the intracellular fluid into the extracellular fluid, causing brain cell
dehydration and neuronal shrinkage
C. Sodium ions directly stimulate neuronal excitability, and low levels reduce neurotransmitter
release
D. Sodium depletion triggers aldosterone release, which causes vasoconstriction and reduced
cerebral perfusion
Correct Answer: A
Rationale: In hyponatremia (Na < 135 mEq/L), the decreased extracellular sodium concentration creates an
osmotic gradient that drives water from the ECF into the ICF, including brain cells. This causes cerebral edema,
which manifests as confusion, lethargy, and in severe cases, seizures. Option B describes the mechanism of
hypernatremia, not hyponatremia. Option C incorrectly describes sodium's role, as sodium primarily affects
osmolality rather than direct neurotransmitter stimulation. Option D is incorrect because aldosterone would be
released in response to hyponatremia to promote sodium reabsorption, not cause vasoconstriction.
Q2: A patient with a serum sodium level of 152 mEq/L presents with extreme thirst and
restlessness. What cellular mechanism is responsible for these clinical manifestations?
A. Neuronal shrinkage due to water movement from the intracellular fluid into the
extracellular fluid [CORRECT]
B. Neuronal swelling due to water movement from the extracellular fluid into the intracellular
fluid
C. Increased sodium-potassium pump activity causing rapid cellular depolarization
D. Sodium-induced activation of the renin-angiotensin-aldosterone system
Correct Answer: A
Rationale: In hypernatremia (Na > 145 mEq/L), the elevated extracellular sodium concentration creates an
osmotic gradient that pulls water out of cells, including neurons. This intracellular dehydration causes
neuronal shrinkage, which manifests as extreme thirst, restlessness, and neurological changes such as
confusion. Option B describes the hyponatremia mechanism. Option C is incorrect because the Na+/K+ pump
does not directly cause these manifestations. Option D describes a compensatory mechanism rather than the
primary cellular pathophysiology.
Q3: A patient with a serum potassium level of 2.8 mEq/L has an electrocardiogram ordered.
Which ECG finding is most consistent with this electrolyte imbalance?
A. Peaked T waves and widened QRS complex
B. Flat T waves and prominent U waves [CORRECT]
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,NUR 2063: Essentials of Pathophysiology Exam 2 | Rasmussen University 2026-2027 75 Questions
C. Prolonged PR interval and shortened QT interval
D. Elevated ST segment and inverted P waves
Correct Answer: B
Rationale: Hypokalemia (K < 3.5 mEq/L) characteristically produces flat or inverted T waves and prominent U
waves on ECG due to altered repolarization of cardiac muscle cells. The decreased extracellular potassium
affects the resting membrane potential and prolongs repolarization. Option A describes the ECG changes seen
in hyperkalemia, not hypokalemia. Option C is not a classic finding of potassium imbalance. Option D is more
consistent with myocardial ischemia or pericarditis, not hypokalemia.
Q4: A patient presents with muscle weakness and an electrocardiogram showing peaked T
waves. The serum potassium level is 6.2 mEq/L. Which pathophysiological process poses
the greatest immediate risk to this patient?
A. Cardiac arrest due to ventricular fibrillation caused by altered myocardial repolarization
[CORRECT]
B. Respiratory failure due to weakened diaphragmatic muscle contraction
C. Neurological damage due to cerebral edema from osmotic fluid shifts
D. Renal tubular necrosis due to direct potassium toxicity on kidney cells
Correct Answer: A
Rationale: Hyperkalemia (K > 5.0 mEq/L) causes peaked T waves by accelerating cardiac repolarization. The
most life-threatening risk is the development of ventricular fibrillation and cardiac arrest, as the elevated
potassium depolarizes the resting membrane potential of cardiac cells, making them more excitable and prone
to fatal arrhythmias. Option B describes a risk of hypokalemia, not hyperkalemia. Option C describes the risk of
hyponatremia. Option D is not the primary mechanism of hyperkalemia's danger.
Q5: A nurse is assessing a patient who reports tingling around the mouth and in the
fingertips. The nurse taps the patient's facial nerve anterior to the ear, and facial twitching
is observed. Which electrolyte imbalance is most likely present?
A. Hypercalcemia
B. Hypocalcemia [CORRECT]
C. Hypermagnesemia
D. Hypomagnesemia
Correct Answer: B
Rationale: The positive Chvostek sign (facial muscle twitching when the facial nerve is tapped) is a classic
assessment finding in hypocalcemia. Low serum calcium levels increase neuromuscular excitability, leading to
tingling (paresthesias), tetany, and positive Chvostek and Trousseau signs. Option A, hypercalcemia, presents
with constipation, kidney stones, and muscle weakness, not neuromuscular hyperexcitability. Options C and D
relate to magnesium imbalances, which have different clinical presentations.
Q6: A patient with hypocalcemia demonstrates a positive Trousseau sign after a blood
pressure cuff is inflated on the upper arm. Which pathophysiological process underlies this
finding?
A. Increased neuromuscular excitability due to reduced threshold for nerve and muscle
depolarization [CORRECT]
B. Decreased neuromuscular excitability due to impaired acetylcholine release at the
neuromuscular junction
C. Vascular spasms caused by direct calcium-mediated vasoconstriction of peripheral arteries
D. Enhanced muscle relaxation due to inadequate calcium availability for troponin binding
Correct Answer: A
Rationale: Trousseau sign (carpopedal spasm after cuff inflation) occurs in hypocalcemia because low
extracellular calcium lowers the threshold for nerve and muscle membrane depolarization, causing
Page 2
, NUR 2063: Essentials of Pathophysiology Exam 2 | Rasmussen University 2026-2027 75 Questions
spontaneous muscle contractions (tetany). Calcium normally stabilizes resting membrane potentials; when
calcium levels drop, nerves become hyperexcitable. Option B describes the opposite effect. Option C is incorrect
because calcium causes vasodilation, not vasoconstriction. Option D is incorrect because reduced calcium
impairs muscle relaxation but the spasm is due to hyperexcitability, not enhanced relaxation.
Q7: A patient is diagnosed with hypomagnesemia. The nurse notes that the patient also has
hypocalcemia that is difficult to correct. Which pathophysiological relationship explains
this finding?
A. Hypomagnesemia impairs parathyroid hormone (PTH) secretion and causes peripheral
PTH resistance [CORRECT]
B. Hypomagnesemia increases calcitonin release, which directly lowers serum calcium levels
C. Low magnesium stimulates the parathyroid glands to overproduce PTH, leading to bone
demineralization
D. Magnesium deficiency causes increased renal excretion of calcium through the distal tubules
Correct Answer: A
Rationale: Hypomagnesemia is a known cause of refractory hypocalcemia because magnesium is required for
both PTH secretion from the parathyroid glands and for PTH receptor responsiveness in target tissues (bone
and kidney). When magnesium is low, PTH release is impaired and tissues become resistant to the PTH that is
released, making hypocalcemia very difficult to correct without first addressing the magnesium deficiency.
Option B is incorrect because calcitonin is not the primary mediator. Option C is incorrect because
hypomagnesemia reduces, not increases, PTH. Option D describes a secondary effect but not the primary
mechanism.
Q8: A patient with severe hypomagnesemia is also found to have hypokalemia. Which
mechanism best explains the relationship between low magnesium and low potassium in
this patient?
A. Hypomagnesemia causes renal potassium wasting through increased potassium
secretion in the distal tubules [CORRECT]
B. Low magnesium levels inhibit the sodium-potassium ATPase pump, trapping potassium
inside cells
C. Magnesium deficiency stimulates aldosterone secretion, which increases potassium
reabsorption
D. Hypomagnesemia causes cellular shift of potassium from the extracellular fluid into the
intracellular fluid
Correct Answer: A
Rationale: Hypomagnesemia leads to renal potassium wasting because magnesium normally inhibits the renal
outer medullary potassium (ROMK) channels in the distal tubules. When magnesium is deficient, these
channels become overactive, increasing potassium secretion into the urine and causing hypokalemia. This is
why hypokalemia that is refractory to potassium replacement often resolves only after magnesium is corrected.
Option B is incorrect because the Na+/K+ pump is not directly inhibited. Option C is incorrect because
aldosterone would worsen hypokalemia through potassium excretion. Option D describes transcellular shifts
which are not the primary mechanism.
Q9: A malnourished patient is started on enteral feeding. The nurse monitors for refeeding
syndrome. Which electrolyte abnormality is most critical to assess in this condition, and
what is its pathophysiological consequence?
A. Hyperphosphatemia leading to calcium phosphate precipitation in renal tubules
B. Hypophosphatemia leading to ATP depletion, which can cause cardiac and respiratory
muscle failure [CORRECT]
C. Hyperkalemia leading to peaked T waves and risk of ventricular fibrillation
Page 3
NUR 2063 / NUR2063: Essentials of Pathophysiology
Exam 2 (Latest ) - Rasmussen University
Modules 4, 5, and 6: GI, Genitourinary, and Endocrine Systems
Section 1: Fluid, Electrolyte, and Acid-Base Imbalances (Q1-Q15)
Q1: A patient is admitted with a serum sodium level of 128 mEq/L. The nurse observes
confusion and lethargy. Which pathophysiological mechanism best explains these
neurological symptoms?
A. Water shifts from the extracellular fluid into the intracellular fluid, causing brain cell
swelling and cerebral edema [CORRECT]
B. Water shifts from the intracellular fluid into the extracellular fluid, causing brain cell
dehydration and neuronal shrinkage
C. Sodium ions directly stimulate neuronal excitability, and low levels reduce neurotransmitter
release
D. Sodium depletion triggers aldosterone release, which causes vasoconstriction and reduced
cerebral perfusion
Correct Answer: A
Rationale: In hyponatremia (Na < 135 mEq/L), the decreased extracellular sodium concentration creates an
osmotic gradient that drives water from the ECF into the ICF, including brain cells. This causes cerebral edema,
which manifests as confusion, lethargy, and in severe cases, seizures. Option B describes the mechanism of
hypernatremia, not hyponatremia. Option C incorrectly describes sodium's role, as sodium primarily affects
osmolality rather than direct neurotransmitter stimulation. Option D is incorrect because aldosterone would be
released in response to hyponatremia to promote sodium reabsorption, not cause vasoconstriction.
Q2: A patient with a serum sodium level of 152 mEq/L presents with extreme thirst and
restlessness. What cellular mechanism is responsible for these clinical manifestations?
A. Neuronal shrinkage due to water movement from the intracellular fluid into the
extracellular fluid [CORRECT]
B. Neuronal swelling due to water movement from the extracellular fluid into the intracellular
fluid
C. Increased sodium-potassium pump activity causing rapid cellular depolarization
D. Sodium-induced activation of the renin-angiotensin-aldosterone system
Correct Answer: A
Rationale: In hypernatremia (Na > 145 mEq/L), the elevated extracellular sodium concentration creates an
osmotic gradient that pulls water out of cells, including neurons. This intracellular dehydration causes
neuronal shrinkage, which manifests as extreme thirst, restlessness, and neurological changes such as
confusion. Option B describes the hyponatremia mechanism. Option C is incorrect because the Na+/K+ pump
does not directly cause these manifestations. Option D describes a compensatory mechanism rather than the
primary cellular pathophysiology.
Q3: A patient with a serum potassium level of 2.8 mEq/L has an electrocardiogram ordered.
Which ECG finding is most consistent with this electrolyte imbalance?
A. Peaked T waves and widened QRS complex
B. Flat T waves and prominent U waves [CORRECT]
Page 1
,NUR 2063: Essentials of Pathophysiology Exam 2 | Rasmussen University 2026-2027 75 Questions
C. Prolonged PR interval and shortened QT interval
D. Elevated ST segment and inverted P waves
Correct Answer: B
Rationale: Hypokalemia (K < 3.5 mEq/L) characteristically produces flat or inverted T waves and prominent U
waves on ECG due to altered repolarization of cardiac muscle cells. The decreased extracellular potassium
affects the resting membrane potential and prolongs repolarization. Option A describes the ECG changes seen
in hyperkalemia, not hypokalemia. Option C is not a classic finding of potassium imbalance. Option D is more
consistent with myocardial ischemia or pericarditis, not hypokalemia.
Q4: A patient presents with muscle weakness and an electrocardiogram showing peaked T
waves. The serum potassium level is 6.2 mEq/L. Which pathophysiological process poses
the greatest immediate risk to this patient?
A. Cardiac arrest due to ventricular fibrillation caused by altered myocardial repolarization
[CORRECT]
B. Respiratory failure due to weakened diaphragmatic muscle contraction
C. Neurological damage due to cerebral edema from osmotic fluid shifts
D. Renal tubular necrosis due to direct potassium toxicity on kidney cells
Correct Answer: A
Rationale: Hyperkalemia (K > 5.0 mEq/L) causes peaked T waves by accelerating cardiac repolarization. The
most life-threatening risk is the development of ventricular fibrillation and cardiac arrest, as the elevated
potassium depolarizes the resting membrane potential of cardiac cells, making them more excitable and prone
to fatal arrhythmias. Option B describes a risk of hypokalemia, not hyperkalemia. Option C describes the risk of
hyponatremia. Option D is not the primary mechanism of hyperkalemia's danger.
Q5: A nurse is assessing a patient who reports tingling around the mouth and in the
fingertips. The nurse taps the patient's facial nerve anterior to the ear, and facial twitching
is observed. Which electrolyte imbalance is most likely present?
A. Hypercalcemia
B. Hypocalcemia [CORRECT]
C. Hypermagnesemia
D. Hypomagnesemia
Correct Answer: B
Rationale: The positive Chvostek sign (facial muscle twitching when the facial nerve is tapped) is a classic
assessment finding in hypocalcemia. Low serum calcium levels increase neuromuscular excitability, leading to
tingling (paresthesias), tetany, and positive Chvostek and Trousseau signs. Option A, hypercalcemia, presents
with constipation, kidney stones, and muscle weakness, not neuromuscular hyperexcitability. Options C and D
relate to magnesium imbalances, which have different clinical presentations.
Q6: A patient with hypocalcemia demonstrates a positive Trousseau sign after a blood
pressure cuff is inflated on the upper arm. Which pathophysiological process underlies this
finding?
A. Increased neuromuscular excitability due to reduced threshold for nerve and muscle
depolarization [CORRECT]
B. Decreased neuromuscular excitability due to impaired acetylcholine release at the
neuromuscular junction
C. Vascular spasms caused by direct calcium-mediated vasoconstriction of peripheral arteries
D. Enhanced muscle relaxation due to inadequate calcium availability for troponin binding
Correct Answer: A
Rationale: Trousseau sign (carpopedal spasm after cuff inflation) occurs in hypocalcemia because low
extracellular calcium lowers the threshold for nerve and muscle membrane depolarization, causing
Page 2
, NUR 2063: Essentials of Pathophysiology Exam 2 | Rasmussen University 2026-2027 75 Questions
spontaneous muscle contractions (tetany). Calcium normally stabilizes resting membrane potentials; when
calcium levels drop, nerves become hyperexcitable. Option B describes the opposite effect. Option C is incorrect
because calcium causes vasodilation, not vasoconstriction. Option D is incorrect because reduced calcium
impairs muscle relaxation but the spasm is due to hyperexcitability, not enhanced relaxation.
Q7: A patient is diagnosed with hypomagnesemia. The nurse notes that the patient also has
hypocalcemia that is difficult to correct. Which pathophysiological relationship explains
this finding?
A. Hypomagnesemia impairs parathyroid hormone (PTH) secretion and causes peripheral
PTH resistance [CORRECT]
B. Hypomagnesemia increases calcitonin release, which directly lowers serum calcium levels
C. Low magnesium stimulates the parathyroid glands to overproduce PTH, leading to bone
demineralization
D. Magnesium deficiency causes increased renal excretion of calcium through the distal tubules
Correct Answer: A
Rationale: Hypomagnesemia is a known cause of refractory hypocalcemia because magnesium is required for
both PTH secretion from the parathyroid glands and for PTH receptor responsiveness in target tissues (bone
and kidney). When magnesium is low, PTH release is impaired and tissues become resistant to the PTH that is
released, making hypocalcemia very difficult to correct without first addressing the magnesium deficiency.
Option B is incorrect because calcitonin is not the primary mediator. Option C is incorrect because
hypomagnesemia reduces, not increases, PTH. Option D describes a secondary effect but not the primary
mechanism.
Q8: A patient with severe hypomagnesemia is also found to have hypokalemia. Which
mechanism best explains the relationship between low magnesium and low potassium in
this patient?
A. Hypomagnesemia causes renal potassium wasting through increased potassium
secretion in the distal tubules [CORRECT]
B. Low magnesium levels inhibit the sodium-potassium ATPase pump, trapping potassium
inside cells
C. Magnesium deficiency stimulates aldosterone secretion, which increases potassium
reabsorption
D. Hypomagnesemia causes cellular shift of potassium from the extracellular fluid into the
intracellular fluid
Correct Answer: A
Rationale: Hypomagnesemia leads to renal potassium wasting because magnesium normally inhibits the renal
outer medullary potassium (ROMK) channels in the distal tubules. When magnesium is deficient, these
channels become overactive, increasing potassium secretion into the urine and causing hypokalemia. This is
why hypokalemia that is refractory to potassium replacement often resolves only after magnesium is corrected.
Option B is incorrect because the Na+/K+ pump is not directly inhibited. Option C is incorrect because
aldosterone would worsen hypokalemia through potassium excretion. Option D describes transcellular shifts
which are not the primary mechanism.
Q9: A malnourished patient is started on enteral feeding. The nurse monitors for refeeding
syndrome. Which electrolyte abnormality is most critical to assess in this condition, and
what is its pathophysiological consequence?
A. Hyperphosphatemia leading to calcium phosphate precipitation in renal tubules
B. Hypophosphatemia leading to ATP depletion, which can cause cardiac and respiratory
muscle failure [CORRECT]
C. Hyperkalemia leading to peaked T waves and risk of ventricular fibrillation
Page 3
