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NUR 2063 / NUR2063 EXAM 1 KEY CONCEPTS WEEKS 1-3 ACTUAL EXAM 2026/2027 | Essentials of Pathophysiology | Rasmussen | Verified Q&A | Pass Guaranteed - A+ Graded

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Prepare for NUR 2063 Exam 1 Key Concepts Weeks 1-3 with this 2026/2027 updated resource for Rasmussen University. This A+ Graded guide contains verified questions and answers with detailed rationales covering pathophysiology foundations, cellular adaptation, injury and death, homeostasis, stress response, and fluid/electrolyte balance. Key topics include etiology, pathogenesis, signs vs symptoms, primary/secondary/tertiary prevention, hypertrophy, atrophy, dysplasia, apoptosis, necrosis, and General Adaptation Syndrome stages. Each answer is verified for accuracy to reinforce clinical judgment and pathophysiologic reasoning. With our Pass Guarantee, you can study with confidence. Download your complete NUR 2063 Exam 1 Weeks 1-3 guide instantly!

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NUR 2063 / NUR2063 Exam 1
Key Concepts - Weeks 1 - 3
Latest - Rasmussen University

Essentials of Pathophysiology - 120 Questions with Detailed Rationales



Total Questions 120

Sections 8

Cognitive Mix 30% Recall / 50% Application / 20% Analysis

Format Multiple Choice (4 options, 1 correct)

Coverage Weeks 1-3 pathophysiologic concepts




Section Topic Questions

1 Cellular Function, Adaptation, and Injury Q1-Q18

2 Genetics and Congenital Disorders Q19-Q32

3 Fluid and Electrolyte Imbalances Q33-Q50

4 Acid-Base Balance Q51-Q66

5 Inflammation and Wound Healing Q67-Q82

6 Immunity, Hypersensitivity, and Immunodeficiency Q83-Q98

7 Infection and Stress Response Q99-Q110

8 Key Concept Integration and Clinical Application Q111-Q120




NUR 2063 Exam 1 Key Concepts Weeks 1-3 - Rasmussen University - 2026/2027 Page 1

, This exam preparation package emphasizes pathophysiologic mechanism understanding rather than memorization. Each
rationale explains causal reasoning, clinical correlations, and key concept notes to support targeted review for the NUR
2063 Exam 1 at Rasmussen University. Questions span cell injury, genetics, fluid/electrolyte, acid-base, inflammation,
immunity, infection, and integrated case-based reasoning.




NUR 2063 Exam 1 Key Concepts Weeks 1-3 - Rasmussen University - 2026/2027 Page 2

, SECTION 1: Cellular Function, Adaptation, and Injury (Q1-Q18)
Q1: A 65-year-old patient with chronic heart failure has an enlarged heart on echocardiogram. The cardiomyocytes
have increased in size to compensate for increased workload. Which cellular adaptation does this represent?
A. Hyperplasia
B. Hypertrophy [CORRECT]
C. Metaplasia
D. Dysplasia
Correct Answer: B
Rationale: Hypertrophy is an increase in cell SIZE (not number) in response to increased workload or hormonal
stimulation—common in cardiac and skeletal muscle (non-dividing cells). Hyperplasia (A) is an increase in cell NUMBER
(glandular, epithelial tissue). Metaplasia (C) is reversible replacement of one adult cell type with another (smoking: columnar to
squamous). Dysplasia (D) is disordered growth (precancerous). Key concept: cardiac muscle cannot undergo hyperplasia because
cardiomyocytes are terminally differentiated—hypertrophy is the only option.

Q2: A chronic smoker undergoes bronchial biopsy. The normal ciliated pseudostratified columnar epithelium has
been replaced by stratified squamous epithelium. Which cellular adaptation is this, and what is its significance?
A. Hypertrophy—protective response
B. Metaplasia—reversible but may progress to malignancy if stimulus continues [CORRECT]
C. Dysplasia—already malignant
D. Anaplasia—loss of cell differentiation
Correct Answer: B
Rationale: Metaplasia is the reversible replacement of one adult cell type with another more able to withstand stress. Squamous
metaplasia in bronchi (from smoking) replaces ciliated columnar cells with squamous cells (loss of cilia → impaired mucus
clearance → infection risk). It is adaptive but if the stimulus persists, may progress to dysplasia and malignancy. Dysplasia (C) is
disordered atypical growth (precursor to cancer). Anaplasia (D) is lack of differentiation (malignant). Key concept: metaplasia is
reversible when the stimulus is removed.

Q3: A patient with a fractured femur has a cast removed after 6 weeks. The affected leg has noticeable muscle
wasting. Which cellular adaptation explains this finding?
A. Atrophy due to decreased workload and disuse [CORRECT]
B. Hypertrophy due to inflammation
C. Hyperplasia due to tissue regeneration
D. Metaplasia due to chronic irritation
Correct Answer: A
Rationale: Atrophy is a decrease in cell SIZE due to decreased workload (disuse), decreased nutrition, decreased hormonal
stimulation, denervation, or ischemia. Disuse atrophy occurs in immobilized limbs (casts, bed rest). Mechanisms include
decreased protein synthesis and increased protein degradation (ubiquitin-proteasome pathway). Key concept: atrophy is
reversible with restored activity and nutrition; irreversible if the cell dies.




NUR 2063 Exam 1 Key Concepts Weeks 1-3 - Rasmussen University - 2026/2027 Page 3

, Q4: A patient who suffered a myocardial infarction has elevated cardiac troponin levels. Which cellular injury
mechanism BEST explains the release of these intracellular enzymes?
A. Reversible injury with mitochondrial swelling
B. Membrane damage and increased permeability allowing intracellular contents to leak [CORRECT]
C. Nuclear condensation and apoptosis
D. Hypertrophy of cardiac myocytes
Correct Answer: B
Rationale: Severe or sustained ischemia causes irreversible cell injury through ATP depletion, failure of Na+/K+ ATPase,
intracellular Na+ and Ca2+ accumulation, water influx, mitochondrial swelling, and ultimately membrane rupture. Once the
plasma membrane is damaged, intracellular enzymes (troponin, CPK-MB, LDH) leak into the bloodstream. These biomarkers are
diagnostic of MI. Reversible injury (A) does not cause enzyme leakage. Apoptosis (C) is controlled, not necrosis. Key concept:
membrane integrity is the critical threshold between reversible and irreversible injury.

Q5: A patient receives thrombolytic therapy (tPA) for an acute ischemic stroke. Upon reperfusion, the patient's
neurologic status worsens, and brain imaging shows increased edema. Which mechanism BEST explains this
phenomenon?
A. Continued ischemia despite treatment
B. Reperfusion injury due to free radical production and calcium overload [CORRECT]
C. Allergic reaction to alteplase
D. Apoptosis of neuronal cells
Correct Answer: B
Rationale: Reperfusion injury occurs when blood flow is restored to ischemic tissue. Mechanisms: (1) ROS/free radical
production (superoxide, hydrogen peroxide, hydroxyl radicals) causing lipid peroxidation, protein damage, DNA breaks; (2)
calcium overload from membrane damage; (3) inflammatory cell infiltration; (4) mitochondrial permeability transition pore
opening. Paradoxically, restoration of oxygen supply worsens damage. Treatment considerations: therapeutic hypothermia, free
radical scavengers. Key concept: time is brain—early reperfusion minimizes both ischemic and reperfusion injury.

Q6: A patient with severe anemia has tissue hypoxia despite normal blood pressure and perfusion. Which
mechanism distinguishes hypoxia from ischemia?
A. Hypoxia results from reduced blood flow; ischemia results from reduced oxygen content
B. Hypoxia is reduced oxygen content in blood; ischemia is reduced blood flow to tissue [CORRECT]
C. Both are identical processes
D. Hypoxia only affects the brain; ischemia affects all tissues
Correct Answer: B
Rationale: Ischemia = reduced blood FLOW (arterial occlusion, venous congestion, low perfusion)—deprives tissue of oxygen
AND metabolic substrates, and prevents waste removal. Hypoxia = inadequate oxygen DELIVERY to tissue despite adequate
blood flow—causes include anemia (low Hgb), CO poisoning (Hgb unable to carry O2), cyanide poisoning (histotoxic—cells
unable to use O2), high altitude (low PaO2). Ischemia is generally worse than hypoxia because metabolic substrates are also
lacking and waste accumulates. Key concept: ischemia causes hypoxia, but hypoxia can occur without ischemia.




NUR 2063 Exam 1 Key Concepts Weeks 1-3 - Rasmussen University - 2026/2027 Page 4

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