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NR 507 Final Exam (2023/2024) – Chamberlain Advanced Pathophysiology | Verified Questions with 100% Correct Answers

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This document provides verified exam questions and answers for the NR 507: Advanced Pathophysiology Final Exam (Chamberlain, 2023/2024). It follows the most recent course content and exam format, giving nurse practitioner students a trusted and accurate preparation resource. Each question is paired with the correct answer, reinforcing advanced pathophysiology knowledge and clinical application skills. This guide is ideal for Chamberlain nursing students preparing for success in the NR 507 Advanced Pathophysiology Final Exam.

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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).

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