RASMUSSEN UNIVERSITY | NURSING EDUCATION EXAMINATION PREPARATION
NUR 2063 / NUR2063: Essentials of Pathophysiology
EXAM 2 | VERIFIED QUESTIONS AND ANSWERS | A+ GRADED
Latest 2026/2027 Edition | 75 Questions | 6 Content Sections | Cognitive Levels: 25% Recall, 50% Application, 25% Analysis |
Aligned with Rasmussen University Essentials of Pathophysiology course objectives
Directions: Select the single best answer (A through D) for each of the 75 questions. Each question is immediately followed
by its verified correct answer and a comprehensive rationale grounded in NUR 2063 pathophysiology, explaining why the
correct option is correct and why the remaining options are wrong, with cellular mechanisms, physiologic processes, and
clinical implications. Content domains follow the NUR 2063 Exam 2 blueprint: fluid, electrolyte, and acid-base homeostasis
with arterial blood gas interpretation; cardiovascular, respiratory, renal and urinary, gastrointestinal and hepatic, and endocrine
system pathophysiology. Approximately 75% of items are clinical scenarios and 25% are direct recall or mechanism
identification, mirroring the cognitive distribution of the current blueprint.
SECTION 1 | QUESTIONS 1-20
Fluid, Electrolyte, and Acid-Base Imbalances
COVERAGE: Fluid compartments, osmolarity and tonicity, edema, dehydration, and third spacing | Sodium, potassium, calcium, magnesium, and
phosphate disorders | Metabolic and respiratory acidosis and alkalosis, compensation, mixed disorders, and ABG interpretation
Q1. A nursing student is reviewing body fluid compartment physiology. Which compartment contains
approximately two-thirds of total body water in a healthy adult?
A. Interstitial fluid
B. Intracellular fluid [CORRECT]
C. Intravascular (plasma) fluid
D. Transcellular fluid
Correct Answer: B
Rationale: Intracellular fluid (ICF) holds about two-thirds of total body water (roughly 25 to 28 of a 42-liter total)
because water distributes osmotically toward the compartment with the highest concentration of effective osmoles,
primarily potassium and phosphate. Extracellular fluid, composed of plasma and interstitial fluid, contains only
about one-third of body water. Interstitial fluid is the largest ECF subdivision but remains far smaller than the ICF,
plasma is the smallest functional ECF compartment, and transcellular fluid (cerebrospinal, synovial, and
gastrointestinal secretions) represents only a tiny fraction of total body water.
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Q2. A patient is receiving an infusion of 0.45% sodium chloride, a hypotonic solution. Which effect does this fluid
have at the cellular level?
A. Water shifts out of cells, causing them to shrink (crenation)
B. No net water movement occurs because the solution is isotonic
C. Water shifts from the extracellular fluid into cells, causing them to swell [CORRECT]
D. Sodium is actively transported out of cells, causing cellular dehydration
Correct Answer: C
Rationale: Because 0.45% NaCl has an effective osmolarity lower than that of intracellular fluid, it dilutes the
extracellular fluid and creates an osmotic gradient that pulls water from the ECF into cells, producing cellular
swelling and, in the brain, the risk of cerebral edema. Hypertonic solutions such as 3% NaCl draw water out of cells
and cause shrinkage, not hypotonic fluids. Option B describes isotonic solutions like 0.9% NaCl, which expand
volume without changing tonicity, and option D incorrectly implies movement of solute rather than free water, since
tonicity shifts are driven by water movement down an osmotic gradient.
Q3. A patient with right-sided heart failure develops progressive dependent ankle and sacral edema. Which
mechanism best explains this fluid accumulation?
A. Increased capillary hydrostatic pressure forcing fluid into the interstitium [CORRECT]
B. Decreased capillary hydrostatic pressure pulling fluid into the vessels
C. Increased plasma oncotic pressure holding fluid within the vasculature
D. Obstruction of lymphatic outflow with enhanced protein clearance
Correct Answer: A
Rationale: Right ventricular failure causes venous congestion that raises venous and capillary hydrostatic pressure,
pushing filtrate into the interstitial space faster than the lymphatics can return it, which produces dependent edema.
Decreased hydrostatic pressure and increased plasma oncotic pressure (as with normal or elevated albumin) would
favor fluid reabsorption into vessels rather than edema. Although lymphatic obstruction does cause edema, it does so
by blocking, not enhancing, protein and fluid clearance, and it is not the mechanism operating in congestive heart
failure.
Q4. A patient has experienced severe vomiting and diarrhea for three days. Which set of assessment findings best
indicates extracellular fluid volume deficit?
A. Bounding pulses, hypertension, and bradycardia
B. Weight gain of 2 kg in 24 hours with peripheral edema
C. Distended neck veins and crackles in the bilateral lung bases
D. Tachycardia, orthostatic hypotension, poor skin turgor, and elevated hematocrit [CORRECT]
Correct Answer: D
Rationale: Extracellular fluid volume deficit reduces circulating blood volume, triggering sympathetic
compensation (tachycardia), a fall in blood pressure that worsens with standing (orthostatic hypotension), and
hemoconcentration that elevates hematocrit and BUN; diminished interstitial fluid produces poor skin turgor and dry
mucous membranes. Bounding pulses with hypertension and bradycardia suggest volume excess or elevated
intracranial pressure, while weight gain, edema, distended neck veins, and crackles all reflect fluid overload rather
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than deficit.
Q5. A patient with severe acute pancreatitis develops hypotension and tachycardia despite adequate urine output
and no visible external fluid losses. Which phenomenon best explains this presentation?
A. Excessive renal sodium retention that expands plasma volume
B. Third spacing: fluid shifting from the intravascular compartment into inflamed interstitial spaces
[CORRECT]
C. Translocation of intracellular fluid into the intravascular compartment
D. Isolated fluid retention caused by elevated antidiuretic hormone
Correct Answer: B
Rationale: The intense inflammatory response in pancreatitis increases capillary permeability, allowing protein-rich
plasma to seep into the retroperitoneum and peritoneal cavity; this third-space shift depletes the circulating volume
while total body water remains unchanged, producing hypotension and reflex tachycardia. Renal sodium retention
and ADH secretion would expand rather than deplete the plasma volume, and movement of intracellular fluid into
vessels would increase, not decrease, intravascular volume.
Q6. A postoperative patient receiving hypotonic IV fluids develops nausea, headache, and lethargy. Laboratory
results show a serum sodium of 121 mEq/L. Which mechanism most likely contributed to this electrolyte
disturbance?
A. Excessive loss of sodium-rich fluid through perspiration
B. Excess aldosterone secretion retaining sodium and water equally
C. Excess antidiuretic hormone promoting renal free water retention and dilution of serum sodium
[CORRECT]
D. Osmotic diuresis from hyperglycemia pulling water out of the body
Correct Answer: C
Rationale: Surgery, pain, nausea, and medications stimulate nonosmotic ADH release; when hypotonic fluids are
simultaneously administered, the retained free water dilutes serum sodium, producing hypotonic (dilutional)
hyponatremia. The resulting hypo-osmolality moves water into brain cells, causing headache, nausea, confusion, and,
if severe, seizures. Isolated sodium loss tends to produce hypovolemic hyponatremia but is not the dominant
postoperative mechanism, aldosterone excess expands volume without this degree of dilution, and osmotic diuresis
causes water loss with a trend toward hypernatremia.
Q7. An older adult with an impaired thirst response and limited access to water develops restlessness, weakness,
dry mucous membranes, and a serum sodium of 158 mEq/L. What is the primary underlying mechanism?
A. A water deficit exceeding the sodium deficit, raising extracellular osmolarity [CORRECT]
B. Excessive sodium intake with proportional water retention
C. A shift of water from the extracellular compartment into the cells
D. Excess ADH causing dilution of extracellular sodium
Correct Answer: A
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Rationale: Hypernatremia almost always represents a relative water deficit: free water loss or inadequate intake
makes the extracellular fluid hypertonic, and the hyperosmolar ECF then pulls water out of cells, including brain
cells, producing restlessness, weakness, and altered mentation. Pure sodium excess with proportionate water
retention is uncommon and would not generate cellular dehydration, a water shift into cells is the physiology of
hyponatremia, and ADH excess dilutes serum sodium, producing hyponatremia rather than hypernatremia.
Q8. A patient with acute kidney injury has a serum potassium of 7.1 mEq/L. Which electrocardiographic change
reflects the electrophysiologic effect of this electrolyte level?
A. Flattened T waves with prominent U waves
B. ST-segment depression with inverted T waves
C. Shortened PR interval with narrow, peaked P waves
D. Tall, peaked (tented) T waves with progressive QRS widening [CORRECT]
Correct Answer: D
Rationale: Hyperkalemia raises the resting membrane potential toward threshold, which first exaggerates
repolarization, producing tall peaked T waves; as severity increases, conduction slows, causing PR prolongation,
QRS widening, and ultimately a sine-wave pattern leading to ventricular fibrillation or asystole. Flattened T waves
with U waves are classic for hypokalemia, ST depression with T-wave inversion suggests myocardial ischemia, and
narrow peaked P waves do not describe potassium-related conduction changes.
Q9. A patient taking furosemide for heart failure develops muscle weakness, abdominal distention, and leg
cramping. Laboratory results show a potassium of 2.8 mEq/L. Which mechanism explains the potassium loss?
A. Increased potassium reabsorption in the collecting ducts
B. Increased distal nephron sodium delivery with aldosterone-mediated potassium secretion
[CORRECT]
C. Decreased aldosterone secretion reducing potassium excretion
D. A shift of potassium from the extracellular fluid into cells caused by acidosis
Correct Answer: B
Rationale: Loop diuretics block the sodium-potassium-chloride cotransporter in the loop of Henle, dramatically
increasing sodium delivery to the distal nephron, where aldosterone stimulates principal cells to secrete potassium
into the urine; the resulting hypokalemia hyperpolarizes cell membranes, producing skeletal muscle weakness,
decreased gastrointestinal motility, and cramps. Increased reabsorption or reduced aldosterone would raise serum
potassium, and acidosis shifts potassium out of cells toward hyperkalemia, the opposite of the alkalosis that loop
diuretics typically create.
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