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Advanced Pathophysiology (NURS 611) – Maryville University – Exam 1 Study Guide (2025/2026) | Comprehensive Notes and Key Concepts

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This document provides a complete Exam 1 Study Guide for NURS 611 – Advanced Pathophysiology at Maryville University, prepared for the 2023/2024 academic year. It covers foundational concepts in human pathophysiology, including cellular injury and adaptation, inflammation, genetic disorders, fluid and electrolyte balance, and acid-base regulation. Each section summarizes critical mechanisms, clinical correlations, and exam-focused details to support understanding and retention. Ideal for graduate nursing students, this guide aligns with Maryville’s MSN curriculum and helps strengthen preparation for advanced clinical courses.

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Uploaded on
October 17, 2025
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Written in
2025/2026
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Advanced Pathophysiology (NURS 611) –
Maryville University – Exam 1 Study
Guide (2025/2026) | Comprehensive Notes
and Key Concepts

This study guide for NURS 611 Exam 1 (2023/2024) at Maryville University covers key topics
from Weeks 1-4, focusing on cellular injury, inflammation, immune responses, genetics, and
neoplasia, based on the standard curriculum (e.g., McCance & Huether's Pathophysiology,
Chapters 1-10). It includes 80 multiple-choice and select-all-that-apply questions with verified
answers in red and concise rationales for clarity. Exam 1 typically includes 75-100 questions
(90 minutes, 70% pass rate). Use this guide to review foundational pathophysiology concepts,
cellular mechanisms, and clinical correlations. Cross-reference with course notes, McCance &
Huether, and Quizlet sets (“NURS 611 Exam 1 Maryville 2023”).




Section 1: Cellular Injury and Adaptation (20 Questions)
1. What is the primary cause of hypoxic cellular injury?
Inadequate oxygen delivery
Rationale: Hypoxia deprives cells of oxygen, impairing ATP production via oxidative
phosphorylation, leading to cell swelling and potential necrosis.



2. What is the hallmark of reversible cellular injury?
Cellular swelling
Rationale: Reversible injury causes Na+/K+ ATPase failure, leading to water influx and
swelling; recovery possible if insult is removed.



3. What type of cellular adaptation occurs in response to chronic mechanical stress?
Hypertrophy
Rationale: Hypertrophy increases cell size (e.g., cardiac muscle in hypertension) to meet
increased functional demand.

, 4. What is the mechanism of apoptosis?
Programmed cell death via caspase activation
Rationale: Apoptosis involves intrinsic (mitochondrial) or extrinsic (death receptor) pathways,
leading to orderly cell dismantling without inflammation.



5. What causes necrosis?
Severe, irreversible cellular injury
Rationale: Necrosis results from trauma, ischemia, or toxins, causing cell membrane rupture and
inflammation; types include coagulative and liquefactive.



6. What is a key feature of atrophy?
Decreased cell size
Rationale: Atrophy occurs due to reduced workload, denervation, or nutrient loss (e.g., muscle
wasting in immobility).



7. What is the primary source of free radical injury?
Reactive oxygen species (ROS)
Rationale: ROS from metabolism or inflammation damage DNA, proteins, and lipids;
antioxidants (e.g., vitamin C) mitigate injury.



8. What is the pathophysiology of ischemia-reperfusion injury?
ROS production upon oxygen restoration
Rationale: Reperfusion generates ROS, causing oxidative damage to cells; seen in myocardial
infarction post-revascularization.



9. What is metaplasia?
Reversible change in cell type
Rationale: Metaplasia (e.g., squamous metaplasia in smokers’ airways) adapts to stress but may
predispose to malignancy if persistent.



10. What is a common cause of cellular injury from chemical agents?
Direct toxicity or metabolite damage
Rationale: Chemicals (e.g., acetaminophen overdose) produce toxic metabolites, causing hepatic
necrosis; antidotes like N-acetylcysteine used.

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