NSG 3850 EXAM 3 — PATHOPHYSIOLOGY II exam with verified answers
1. A client with left-sided heart failure develops pulmonary crackles and severe
dyspnea. What is the primary pathophysiologic cause?
A. Increased pulmonary capillary hydrostatic pressure
B. Decreased systemic vascular resistance
C. Increased renal filtration
D. Decreased venous pressure
Answer: A
Rationale: Left ventricular failure causes blood to back up into the pulmonary circulation,
increasing pulmonary capillary hydrostatic pressure and promoting fluid movement into the
interstitial and alveolar spaces.
2. Which mechanism contributes most directly to edema in right-sided heart
failure?
A. Increased systemic venous pressure
B. Decreased capillary pressure
C. Increased arterial oxygenation
D. Decreased aldosterone secretion
Answer: A
Rationale: Right-sided heart failure causes systemic venous congestion, increasing hydrostatic
pressure and promoting fluid movement into peripheral tissues.
3. A client with chronic hypertension develops left ventricular hypertrophy.
What mechanism best explains this change?
A. Increased afterload
B. Decreased preload
C. Reduced blood viscosity
D. Increased venous drainage
Answer: A
Rationale: Chronic hypertension increases the resistance against which the left ventricle must
pump. The increased workload promotes myocardial hypertrophy.
,4. Which finding is most characteristic of cardiogenic shock?
A. Severe hypotension with evidence of poor tissue perfusion
B. Increased cardiac output
C. Warm skin with normal perfusion in every case
D. Increased urine production
Answer: A
Rationale: Cardiogenic shock occurs when the heart cannot generate adequate cardiac output,
resulting in hypotension and inadequate tissue perfusion.
5. A myocardial infarction causes necrosis of cardiac muscle primarily because
of:
A. Prolonged ischemia
B. Excessive oxygen delivery
C. Increased coronary blood flow
D. Increased cellular glucose uptake
Answer: A
Rationale: Prolonged interruption of coronary blood flow deprives myocardial cells of oxygen
and nutrients, leading to irreversible injury and necrosis.
6. Which pathophysiologic change is characteristic of atherosclerosis?
A. Lipid accumulation and inflammatory changes within arterial walls
B. Complete absence of endothelial injury
C. Decreased arterial plaque formation
D. Increased arterial elasticity
Answer: A
Rationale: Atherosclerosis involves endothelial dysfunction, lipid accumulation, inflammation,
and plaque development within arterial walls.
,7. A client with COPD develops chronic CO₂ retention. Which acid-base
disturbance is most likely?
A. Respiratory acidosis
B. Respiratory alkalosis
C. Metabolic alkalosis
D. Metabolic acidosis
Answer: A
Rationale: Hypoventilation and impaired CO₂ elimination cause carbon dioxide retention,
increasing carbonic acid and producing respiratory acidosis.
8. Which pathophysiologic change is characteristic of emphysema?
A. Destruction of alveolar walls
B. Increased alveolar surface area
C. Increased elastic recoil
D. Complete reversal of airflow obstruction
Answer: A
Rationale: Emphysema involves destruction of alveolar walls, loss of elastic recoil, and reduced
surface area available for gas exchange.
9. Asthma is primarily characterized by:
A. Reversible airway inflammation and bronchoconstriction
B. Permanent destruction of all alveoli
C. Complete absence of airway inflammation
D. Chronic pulmonary fibrosis in every patient
Answer: A
Rationale: Asthma involves airway inflammation, bronchial hyperresponsiveness, and variable
airflow obstruction that is often reversible.
10. A client develops pulmonary edema. Which mechanism causes impaired
oxygenation?
, A. Fluid accumulation in the alveoli interferes with gas exchange
B. Increased alveolar ventilation
C. Increased oxygen diffusion
D. Increased pulmonary surface area
Answer: A
Rationale: Alveolar fluid increases the diffusion distance for oxygen and interferes with normal
ventilation-perfusion matching.
11. Which finding is characteristic of acute respiratory distress syndrome
(ARDS)?
A. Severe hypoxemia that is difficult to correct
B. Increased lung compliance
C. Normal alveolar-capillary permeability
D. Increased oxygen diffusion
Answer: A
Rationale: ARDS involves diffuse inflammatory injury and increased alveolar-capillary
permeability, producing pulmonary edema and severe hypoxemia.
12. A pulmonary embolism primarily causes respiratory impairment by:
A. Blocking pulmonary blood flow
B. Increasing blood flow to obstructed areas
C. Increasing alveolar ventilation everywhere
D. Increasing hemoglobin production immediately
Answer: A
Rationale: A pulmonary embolus obstructs pulmonary circulation, creating areas that are
ventilated but inadequately perfused.
13. Which mechanism is central to acute kidney injury?
A. Sudden reduction in renal function
B. Permanent increase in glomerular filtration
1. A client with left-sided heart failure develops pulmonary crackles and severe
dyspnea. What is the primary pathophysiologic cause?
A. Increased pulmonary capillary hydrostatic pressure
B. Decreased systemic vascular resistance
C. Increased renal filtration
D. Decreased venous pressure
Answer: A
Rationale: Left ventricular failure causes blood to back up into the pulmonary circulation,
increasing pulmonary capillary hydrostatic pressure and promoting fluid movement into the
interstitial and alveolar spaces.
2. Which mechanism contributes most directly to edema in right-sided heart
failure?
A. Increased systemic venous pressure
B. Decreased capillary pressure
C. Increased arterial oxygenation
D. Decreased aldosterone secretion
Answer: A
Rationale: Right-sided heart failure causes systemic venous congestion, increasing hydrostatic
pressure and promoting fluid movement into peripheral tissues.
3. A client with chronic hypertension develops left ventricular hypertrophy.
What mechanism best explains this change?
A. Increased afterload
B. Decreased preload
C. Reduced blood viscosity
D. Increased venous drainage
Answer: A
Rationale: Chronic hypertension increases the resistance against which the left ventricle must
pump. The increased workload promotes myocardial hypertrophy.
,4. Which finding is most characteristic of cardiogenic shock?
A. Severe hypotension with evidence of poor tissue perfusion
B. Increased cardiac output
C. Warm skin with normal perfusion in every case
D. Increased urine production
Answer: A
Rationale: Cardiogenic shock occurs when the heart cannot generate adequate cardiac output,
resulting in hypotension and inadequate tissue perfusion.
5. A myocardial infarction causes necrosis of cardiac muscle primarily because
of:
A. Prolonged ischemia
B. Excessive oxygen delivery
C. Increased coronary blood flow
D. Increased cellular glucose uptake
Answer: A
Rationale: Prolonged interruption of coronary blood flow deprives myocardial cells of oxygen
and nutrients, leading to irreversible injury and necrosis.
6. Which pathophysiologic change is characteristic of atherosclerosis?
A. Lipid accumulation and inflammatory changes within arterial walls
B. Complete absence of endothelial injury
C. Decreased arterial plaque formation
D. Increased arterial elasticity
Answer: A
Rationale: Atherosclerosis involves endothelial dysfunction, lipid accumulation, inflammation,
and plaque development within arterial walls.
,7. A client with COPD develops chronic CO₂ retention. Which acid-base
disturbance is most likely?
A. Respiratory acidosis
B. Respiratory alkalosis
C. Metabolic alkalosis
D. Metabolic acidosis
Answer: A
Rationale: Hypoventilation and impaired CO₂ elimination cause carbon dioxide retention,
increasing carbonic acid and producing respiratory acidosis.
8. Which pathophysiologic change is characteristic of emphysema?
A. Destruction of alveolar walls
B. Increased alveolar surface area
C. Increased elastic recoil
D. Complete reversal of airflow obstruction
Answer: A
Rationale: Emphysema involves destruction of alveolar walls, loss of elastic recoil, and reduced
surface area available for gas exchange.
9. Asthma is primarily characterized by:
A. Reversible airway inflammation and bronchoconstriction
B. Permanent destruction of all alveoli
C. Complete absence of airway inflammation
D. Chronic pulmonary fibrosis in every patient
Answer: A
Rationale: Asthma involves airway inflammation, bronchial hyperresponsiveness, and variable
airflow obstruction that is often reversible.
10. A client develops pulmonary edema. Which mechanism causes impaired
oxygenation?
, A. Fluid accumulation in the alveoli interferes with gas exchange
B. Increased alveolar ventilation
C. Increased oxygen diffusion
D. Increased pulmonary surface area
Answer: A
Rationale: Alveolar fluid increases the diffusion distance for oxygen and interferes with normal
ventilation-perfusion matching.
11. Which finding is characteristic of acute respiratory distress syndrome
(ARDS)?
A. Severe hypoxemia that is difficult to correct
B. Increased lung compliance
C. Normal alveolar-capillary permeability
D. Increased oxygen diffusion
Answer: A
Rationale: ARDS involves diffuse inflammatory injury and increased alveolar-capillary
permeability, producing pulmonary edema and severe hypoxemia.
12. A pulmonary embolism primarily causes respiratory impairment by:
A. Blocking pulmonary blood flow
B. Increasing blood flow to obstructed areas
C. Increasing alveolar ventilation everywhere
D. Increasing hemoglobin production immediately
Answer: A
Rationale: A pulmonary embolus obstructs pulmonary circulation, creating areas that are
ventilated but inadequately perfused.
13. Which mechanism is central to acute kidney injury?
A. Sudden reduction in renal function
B. Permanent increase in glomerular filtration
