NURS 231 Pathophysiology Final Exam 2026/2027 – Portage
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Verified Answers | Comprehensive Pathophysiology
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1. A 68-year-old man with a 40 pack-year smoking history develops persistent
hypercapnia during an acute COPD exacerbation. Arterial blood gas shows pH
7.28, PaCO₂ 72 mmHg, HCO₃⁻ 34 mEq/L. Which cellular mechanism best
explains the concurrent increase in intracellular pH of neurons that contributes to
his somnolence?
A. Hypercapnia stimulates carbonic-anhydrase-mediated formation of
extracellular H₂CO₃, which rapidly crosses the neuronal membrane and
dissociates, buffering intracellular acid.
B. CO₂ diffuses freely into neurons; carbonic anhydrase forms H₂CO₃ → H⁺ +
HCO₃⁻; H⁺ is extruded via the Na⁺/H⁺ exchanger, leaving intracellular pH relatively
alkalemic.
C. Elevated CO₂ directly inhibits H⁺-ATPase pumps, preventing acid
accumulation.
D. Hypercapnia activates neuronal lactate transporters, removing lactic acid and
raising pH.
Correct Answer: B
Rationale: CO₂ crosses membranes freely; intracellular carbonic anhydrase rapidly
forms H⁺ and HCO₃⁻. The Na⁺/H⁺ exchanger exports H⁺, partially correcting intracellular
acidosis and producing a relative intracellular alkalinization that depresses neuronal
excitability, producing somnolence. The other options either misstate the direction of
pump activity or invoke nonexistent mechanisms.
, 2. A 54-year-old woman with congestive heart failure (EF 30%) and poorly controlled
diabetes presents with fatigue and muscle cramps. Laboratory results: Na⁺ 129
mEq/L, K⁺ 3.2 mEq/L, osmolality 260 mOsm/kg. Which pathophysiologic process
is the primary driver of her hyponatremia?
A. Osmotic diuresis from glycosuria causing isotonic fluid loss
B. Non-osmotic vasopressin release due to decreased effective circulating
volume
C. Aldosterone escape leading to renal sodium wasting
D. Syndrome of inappropriate antidiuretic hormone (SIADH) from cardiac
cachexia
Correct Answer: B
Rationale: Low EF reduces cardiac output, triggering arterial baroreceptor-mediated
ADH release despite hypo-osmolality. The resulting water retention dilutes serum
sodium. While SIADH can coexist, the dominant mechanism in hypotonic hyponatremia
with low osmolality is baroreceptor-mediated vasopressin release (a
"volume-appropriate" response). Glycosuria causes hypertonic losses and does not
lower osmolality.
3. A 26-year-old man with Crohn disease develops numbness and tingling in his
hands. Laboratory findings: Ca²⁺ 7.8 mg/dL, albumin 2.8 g/dL, Mg²⁺ 1.1 mg/dL,
iPTH 95 pg/mL (nl 10–65). Which intracellular signaling disruption best explains
his neurologic symptoms?
A. Hypomagnesemia impairs Ca²⁺-sensing receptor activation, suppressing PTH
secretion.
B. Low ionized calcium increases neuronal membrane sodium permeability,
lowering the threshold for action potentials.
C. Hypocalcemia prolongs voltage-gated Na⁺ channel inactivation, increasing
excitability.
D. Decreased serum Mg²⁺ blocks voltage-gated Ca²⁺ channels, preventing
neurotransmitter release.
Correct Answer: C
,Rationale: Hypocalcemia (ionized) stabilizes Na⁺ channels, delaying inactivation and
causing spontaneous repetitive firing (paresthesias, tetany). Hypomagnesemia
aggravates this by inhibiting PTH end-organ response, but the primary defect is
Ca²⁺-mediated membrane irritability.
4. A 72-hour-old neonate born at 28 weeks’ gestation develops respiratory distress,
frothy secretions, and cyanosis. Chest X-ray shows a ground-glass appearance
with air bronchograms. Which cellular event underlies the pathologic changes in
the lungs?
A. Apoptosis of type II pneumocytes leading to surfactant depletion
B. Necrosis of bronchial epithelium causing protein-rich exudate
C. Accumulation of neutrophil extracellular traps (NETs) in small airways
D. Fibrin deposition along alveolar basement membranes
Correct Answer: A
Rationale: In respiratory distress syndrome, immature type II cells cannot synthesize
adequate surfactant; resultant alveolar collapse and transudation of plasma proteins
produce the ground-glass pattern. Surfactant deficiency, not necrosis or NETs, is
primary.
5. A 48-year-old woman with asthma on inhaled fluticasone develops dyspnea and
wheezing after stopping her inhaler abruptly. Bronchoscopy fluid shows elevated
IL-5 and eosinophils. Which adaptive immune process is most responsible for
this exacerbation?
A. Th1-mediated macrophage activation releasing IFN-γ
B. Th2 skewing with IgE-coated mast cell degranulation
C. Th17 neutrophilic inflammation driven by IL-23
D. T-regulatory cell suppression of eosinophil apoptosis
Correct Answer: B
, Rationale: Withdrawal of inhaled corticosteroid removes suppression of Th2 cytokines
(IL-4, IL-5, IL-13), promoting IgE synthesis and eosinophilic inflammation—the hallmark
of allergic asthma.
6. A 62-year-old man with a history of rheumatic fever presents with fatigue and
lower-extremity edema. Echocardiography reveals thickened mitral valve leaflets
with doming and a mean gradient of 8 mmHg. Which hemodynamic
consequence best explains his systemic findings?
A. Diastolic dysfunction from impaired left ventricular filling
B. Systolic dysfunction due to pressure overload
C. Right ventricular volume overload from pulmonary regurgitation
D. Reduced systemic vascular resistance from inflammatory cytokines
Correct Answer: A
Rationale: Mitral stenosis impedes left atrial emptying, elevating left atrial pressure and
reducing ventricular preload. The ventricle is intrinsically normal; symptoms stem from
diastolic dysfunction and secondary pulmonary hypertension, not systolic failure.
7. A 34-year-old woman with systemic lupus erythematosus develops sudden-onset
dyspnea and pleuritic chest pain. D-dimer is markedly elevated, and CT
angiography shows bilateral segmental filling defects. Which endothelial
perturbation underlies her pulmonary embolism?
A. Antiphospholipid antibody-mediated platelet activation and thrombin
generation
B. Deficiency of protein C leading to unchecked factor Va activity
C. Endothelial damage from immune-complex deposition activating factor XII
D. High-titer anti-dsDNA promoting fibrinolysis inhibition
Correct Answer: A
Rationale: Antiphospholipid antibodies (anticardiolipin, β2-glycoprotein-I) activate
endothelium and platelets, up-regulate tissue factor, and impair protein S, creating a
Learning Complete Final Examination | Actual Questions &
Verified Answers | Comprehensive Pathophysiology
Assessment | Pass Guarantee
1. A 68-year-old man with a 40 pack-year smoking history develops persistent
hypercapnia during an acute COPD exacerbation. Arterial blood gas shows pH
7.28, PaCO₂ 72 mmHg, HCO₃⁻ 34 mEq/L. Which cellular mechanism best
explains the concurrent increase in intracellular pH of neurons that contributes to
his somnolence?
A. Hypercapnia stimulates carbonic-anhydrase-mediated formation of
extracellular H₂CO₃, which rapidly crosses the neuronal membrane and
dissociates, buffering intracellular acid.
B. CO₂ diffuses freely into neurons; carbonic anhydrase forms H₂CO₃ → H⁺ +
HCO₃⁻; H⁺ is extruded via the Na⁺/H⁺ exchanger, leaving intracellular pH relatively
alkalemic.
C. Elevated CO₂ directly inhibits H⁺-ATPase pumps, preventing acid
accumulation.
D. Hypercapnia activates neuronal lactate transporters, removing lactic acid and
raising pH.
Correct Answer: B
Rationale: CO₂ crosses membranes freely; intracellular carbonic anhydrase rapidly
forms H⁺ and HCO₃⁻. The Na⁺/H⁺ exchanger exports H⁺, partially correcting intracellular
acidosis and producing a relative intracellular alkalinization that depresses neuronal
excitability, producing somnolence. The other options either misstate the direction of
pump activity or invoke nonexistent mechanisms.
, 2. A 54-year-old woman with congestive heart failure (EF 30%) and poorly controlled
diabetes presents with fatigue and muscle cramps. Laboratory results: Na⁺ 129
mEq/L, K⁺ 3.2 mEq/L, osmolality 260 mOsm/kg. Which pathophysiologic process
is the primary driver of her hyponatremia?
A. Osmotic diuresis from glycosuria causing isotonic fluid loss
B. Non-osmotic vasopressin release due to decreased effective circulating
volume
C. Aldosterone escape leading to renal sodium wasting
D. Syndrome of inappropriate antidiuretic hormone (SIADH) from cardiac
cachexia
Correct Answer: B
Rationale: Low EF reduces cardiac output, triggering arterial baroreceptor-mediated
ADH release despite hypo-osmolality. The resulting water retention dilutes serum
sodium. While SIADH can coexist, the dominant mechanism in hypotonic hyponatremia
with low osmolality is baroreceptor-mediated vasopressin release (a
"volume-appropriate" response). Glycosuria causes hypertonic losses and does not
lower osmolality.
3. A 26-year-old man with Crohn disease develops numbness and tingling in his
hands. Laboratory findings: Ca²⁺ 7.8 mg/dL, albumin 2.8 g/dL, Mg²⁺ 1.1 mg/dL,
iPTH 95 pg/mL (nl 10–65). Which intracellular signaling disruption best explains
his neurologic symptoms?
A. Hypomagnesemia impairs Ca²⁺-sensing receptor activation, suppressing PTH
secretion.
B. Low ionized calcium increases neuronal membrane sodium permeability,
lowering the threshold for action potentials.
C. Hypocalcemia prolongs voltage-gated Na⁺ channel inactivation, increasing
excitability.
D. Decreased serum Mg²⁺ blocks voltage-gated Ca²⁺ channels, preventing
neurotransmitter release.
Correct Answer: C
,Rationale: Hypocalcemia (ionized) stabilizes Na⁺ channels, delaying inactivation and
causing spontaneous repetitive firing (paresthesias, tetany). Hypomagnesemia
aggravates this by inhibiting PTH end-organ response, but the primary defect is
Ca²⁺-mediated membrane irritability.
4. A 72-hour-old neonate born at 28 weeks’ gestation develops respiratory distress,
frothy secretions, and cyanosis. Chest X-ray shows a ground-glass appearance
with air bronchograms. Which cellular event underlies the pathologic changes in
the lungs?
A. Apoptosis of type II pneumocytes leading to surfactant depletion
B. Necrosis of bronchial epithelium causing protein-rich exudate
C. Accumulation of neutrophil extracellular traps (NETs) in small airways
D. Fibrin deposition along alveolar basement membranes
Correct Answer: A
Rationale: In respiratory distress syndrome, immature type II cells cannot synthesize
adequate surfactant; resultant alveolar collapse and transudation of plasma proteins
produce the ground-glass pattern. Surfactant deficiency, not necrosis or NETs, is
primary.
5. A 48-year-old woman with asthma on inhaled fluticasone develops dyspnea and
wheezing after stopping her inhaler abruptly. Bronchoscopy fluid shows elevated
IL-5 and eosinophils. Which adaptive immune process is most responsible for
this exacerbation?
A. Th1-mediated macrophage activation releasing IFN-γ
B. Th2 skewing with IgE-coated mast cell degranulation
C. Th17 neutrophilic inflammation driven by IL-23
D. T-regulatory cell suppression of eosinophil apoptosis
Correct Answer: B
, Rationale: Withdrawal of inhaled corticosteroid removes suppression of Th2 cytokines
(IL-4, IL-5, IL-13), promoting IgE synthesis and eosinophilic inflammation—the hallmark
of allergic asthma.
6. A 62-year-old man with a history of rheumatic fever presents with fatigue and
lower-extremity edema. Echocardiography reveals thickened mitral valve leaflets
with doming and a mean gradient of 8 mmHg. Which hemodynamic
consequence best explains his systemic findings?
A. Diastolic dysfunction from impaired left ventricular filling
B. Systolic dysfunction due to pressure overload
C. Right ventricular volume overload from pulmonary regurgitation
D. Reduced systemic vascular resistance from inflammatory cytokines
Correct Answer: A
Rationale: Mitral stenosis impedes left atrial emptying, elevating left atrial pressure and
reducing ventricular preload. The ventricle is intrinsically normal; symptoms stem from
diastolic dysfunction and secondary pulmonary hypertension, not systolic failure.
7. A 34-year-old woman with systemic lupus erythematosus develops sudden-onset
dyspnea and pleuritic chest pain. D-dimer is markedly elevated, and CT
angiography shows bilateral segmental filling defects. Which endothelial
perturbation underlies her pulmonary embolism?
A. Antiphospholipid antibody-mediated platelet activation and thrombin
generation
B. Deficiency of protein C leading to unchecked factor Va activity
C. Endothelial damage from immune-complex deposition activating factor XII
D. High-titer anti-dsDNA promoting fibrinolysis inhibition
Correct Answer: A
Rationale: Antiphospholipid antibodies (anticardiolipin, β2-glycoprotein-I) activate
endothelium and platelets, up-regulate tissue factor, and impair protein S, creating a
