NR 507 Final Exam (2023/2024) – Chamberlain
Advanced Pathophysiology | Verified Questions
with 100% Correct Answers
Student Name: _________________________
Date: _______________
Time Limit: 90 minutes
Total Questions: 26
Cardiovascular Pathophysiology (5 Questions)
1. MCQ: What is the primary pathophysiological mechanism of left-sided heart
failure?
a. Increased pulmonary artery pressure
b. Increased left ventricular end-diastolic pressure
c. Decreased systemic vascular resistance
d. Reduced pulmonary edema
Rationale: Left-sided heart failure causes blood to back up into the left atrium and
pulmonary veins, increasing left ventricular end-diastolic pressure and leading to
pulmonary edema, per McCance & Huether (2023).
2. MCQ: A client with myocardial infarction develops cardiogenic shock. What is the
primary cause?
a. Increased preload
b. Decreased cardiac output
c. Elevated afterload
d. Increased contractility
Rationale: Cardiogenic shock results from the heart’s inability to pump effectively,
reducing cardiac output and causing systemic hypoperfusion, per McCance &
Huether (2023).
3. MCQ: Which electrolyte imbalance is most likely to cause ventricular arrhythmias
in a client with heart failure?
a. Hypernatremia
b. Hypokalemia
c. Hypercalcemia
d. Hypomagnesemia
Rationale: Hypokalemia disrupts cardiac membrane potential, increasing the risk
of ventricular arrhythmias, per cardiovascular pathophysiology (2023).
4. MCQ: In atherosclerosis, what is the primary component of plaque formation?
a. Calcium deposits
b. Lipid-laden macrophages
, 2
c. Red blood cells
d. Collagen fibers
Rationale: Lipid-laden macrophages (foam cells) form the core of atherosclerotic
plaques, initiating vessel narrowing, per McCance & Huether (2023).
5. MCQ: A client with hypertension develops left ventricular hypertrophy. What is
the underlying mechanism?
a. Decreased preload
b. Increased afterload
c. Reduced cardiac output
d. Decreased contractility
Rationale: Chronic hypertension increases afterload, causing the left ventricle to
hypertrophy to compensate for increased resistance, per cardiovascular
pathophysiology (2023).
Pulmonary Pathophysiology (5 Questions)
6. MCQ: What is the primary pathophysiological feature of acute respiratory distress
syndrome (ARDS)?
a. Bronchial constriction
b. Diffuse alveolar damage
c. Increased surfactant production
d. Airway obstruction
Rationale: ARDS is characterized by diffuse alveolar damage, leading to
impaired gas exchange and pulmonary edema, per McCance & Huether (2023).
7. MCQ: A client with COPD presents with hypercapnia. What is the primary cause?
a. Increased alveolar ventilation
b. Alveolar hypoventilation
c. Decreased carbon dioxide production
d. Enhanced diffusion capacity
Rationale: COPD causes airflow obstruction, leading to alveolar hypoventilation
and retention of CO2, per pulmonary pathophysiology (2023).
8. MCQ: In asthma, what triggers bronchoconstriction?
a. Decreased histamine release
b. Inflammatory mediator release
c. Increased surfactant levels
d. Reduced airway inflammation
Rationale: Inflammatory mediators (e.g., histamine, leukotrienes) cause
bronchoconstriction in asthma, per McCance & Huether (2023).
9. MCQ: A client with pulmonary embolism develops hypoxemia. What is the
primary mechanism?
a. Increased alveolar ventilation
b. Ventilation-perfusion mismatch
c. Enhanced oxygen diffusion
d. Decreased pulmonary edema
Rationale: Pulmonary embolism blocks pulmonary blood flow, causing a
ventilation-perfusion mismatch and hypoxemia, per McCance & Huether (2023).