NR 283 FINAL EXAM QUESTIONS AND ANSWERS 2026/2027
| Already Graded A+ | Chamberlain College of Nursing
Pathophysiology | Pass Guaranteed
UNIT 1: CELLULAR FUNCTION & ADAPTATION (12 Questions)
Q1
A 68-year-old patient presents with progressive fatigue, weight loss, and a persistent
cough. Chest CT reveals a 3 cm spiculated mass in the right upper lobe. Biopsy
confirms non-small cell lung carcinoma. The patient has a 40 pack-year smoking history
and worked in asbestos insulation for 15 years.
Which cellular adaptation process best explains the initial metaplastic changes in the
bronchial epithelium that preceded malignant transformation?
A. Hyperplasia resulting from chronic inflammation and cellular regeneration
B. Dysplasia characterized by loss of cellular uniformity and nuclear pleomorphism
[CORRECT]
C. Hypertrophy of ciliated columnar cells to increase mucociliary clearance
D. Anaplasia with complete loss of cellular differentiation and function
,Correct Answer: B
Rationale:
This question assesses understanding of cellular adaptations and the progression to
malignancy, a core NR 283 competency.
Pathophysiological Progression:
1. Metaplasia: Reversible change from normal pseudostratified ciliated columnar
epithelium to stratified squamous epithelium (smoker's epithelium) due to
chronic irritation from smoking and asbestos
2. Dysplasia: Disordered, dysfunctional metaplasia with nuclear pleomorphism,
hyperchromatism, loss of polarity—this is the premalignant stage
3. Carcinoma in situ: Full-thickness dysplasia without basement membrane
invasion
4. Invasive carcinoma: Malignant cells breach basement membrane
Analysis of Options:
A. Hyperplasia: Incorrect. While inflammation causes hyperplasia (increased cell
number), this is not the specific adaptation to chronic chemical irritation. Hyperplasia
alone doesn't explain the histological transformation seen in smoking-related changes.
B. Dysplasia [CORRECT]: Correct. Dysplasia represents the disordered, dysfunctional
stage of metaplasia that precedes malignancy. Key features include:
● Loss of cellular uniformity
● Nuclear pleomorphism (variation in size and shape)
● Hyperchromatic nuclei
● Increased nuclear-to-cytoplasmic ratio
,Loss of normal tissue architecture
● This is the premalignant cellular adaptation that creates the fertile ground for
malignant transformation when combined with carcinogen exposure (tobacco +
asbestos = synergistic effect).
C. Hypertrophy: Incorrect. Hypertrophy (increased cell size) does not occur in bronchial
epithelium in response to smoking. The ciliated cells are actually damaged and
destroyed, not enlarged. This represents a fundamental misunderstanding of smoking
pathophysiology.
D. Anaplasia: Incorrect. Anaplasia (complete loss of differentiation) is a feature of
established malignancy, not the precursor adaptation. The question asks about changes
that "preceded malignant transformation," making anaplasia too advanced in the
sequence.
Clinical Integration: Understanding this progression is essential for nursing implications
in cancer screening, smoking cessation education, and recognizing that dysplastic
changes may be reversible if irritant exposure ceases.
Q2
A 45-year-old female presents with severe cellular injury following ischemic insult during
a myocardial infarction. Laboratory studies reveal elevated cardiac troponins and
lactate dehydrogenase.
, Which intracellular event represents the irreversible stage of cellular injury that commits
the cell to death?
A. Depletion of ATP stores and failure of the sodium-potassium pump
B. Influx of calcium ions and activation of phospholipases
C. Mitochondrial swelling with loss of oxidative phosphorylation
D. Severe damage to cell membranes with massive calcium influx and lysosomal
enzyme release [CORRECT]
Correct Answer: D
Rationale:
This question distinguishes reversible vs. irreversible cellular injury, critical for
understanding myocardial infarction pathophysiology.
Stages of Ischemic Cell Injury:
Reversible Injury (early ischemia):
● ATP depletion (anaerobic glycolysis fails)
● Sodium-potassium pump failure (cellular edema)
● Mitochondrial swelling (loss of cristae)
● Ribosomal detachment (protein synthesis stops)
● Key point: If blood flow restored, cell can recover
| Already Graded A+ | Chamberlain College of Nursing
Pathophysiology | Pass Guaranteed
UNIT 1: CELLULAR FUNCTION & ADAPTATION (12 Questions)
Q1
A 68-year-old patient presents with progressive fatigue, weight loss, and a persistent
cough. Chest CT reveals a 3 cm spiculated mass in the right upper lobe. Biopsy
confirms non-small cell lung carcinoma. The patient has a 40 pack-year smoking history
and worked in asbestos insulation for 15 years.
Which cellular adaptation process best explains the initial metaplastic changes in the
bronchial epithelium that preceded malignant transformation?
A. Hyperplasia resulting from chronic inflammation and cellular regeneration
B. Dysplasia characterized by loss of cellular uniformity and nuclear pleomorphism
[CORRECT]
C. Hypertrophy of ciliated columnar cells to increase mucociliary clearance
D. Anaplasia with complete loss of cellular differentiation and function
,Correct Answer: B
Rationale:
This question assesses understanding of cellular adaptations and the progression to
malignancy, a core NR 283 competency.
Pathophysiological Progression:
1. Metaplasia: Reversible change from normal pseudostratified ciliated columnar
epithelium to stratified squamous epithelium (smoker's epithelium) due to
chronic irritation from smoking and asbestos
2. Dysplasia: Disordered, dysfunctional metaplasia with nuclear pleomorphism,
hyperchromatism, loss of polarity—this is the premalignant stage
3. Carcinoma in situ: Full-thickness dysplasia without basement membrane
invasion
4. Invasive carcinoma: Malignant cells breach basement membrane
Analysis of Options:
A. Hyperplasia: Incorrect. While inflammation causes hyperplasia (increased cell
number), this is not the specific adaptation to chronic chemical irritation. Hyperplasia
alone doesn't explain the histological transformation seen in smoking-related changes.
B. Dysplasia [CORRECT]: Correct. Dysplasia represents the disordered, dysfunctional
stage of metaplasia that precedes malignancy. Key features include:
● Loss of cellular uniformity
● Nuclear pleomorphism (variation in size and shape)
● Hyperchromatic nuclei
● Increased nuclear-to-cytoplasmic ratio
,Loss of normal tissue architecture
● This is the premalignant cellular adaptation that creates the fertile ground for
malignant transformation when combined with carcinogen exposure (tobacco +
asbestos = synergistic effect).
C. Hypertrophy: Incorrect. Hypertrophy (increased cell size) does not occur in bronchial
epithelium in response to smoking. The ciliated cells are actually damaged and
destroyed, not enlarged. This represents a fundamental misunderstanding of smoking
pathophysiology.
D. Anaplasia: Incorrect. Anaplasia (complete loss of differentiation) is a feature of
established malignancy, not the precursor adaptation. The question asks about changes
that "preceded malignant transformation," making anaplasia too advanced in the
sequence.
Clinical Integration: Understanding this progression is essential for nursing implications
in cancer screening, smoking cessation education, and recognizing that dysplastic
changes may be reversible if irritant exposure ceases.
Q2
A 45-year-old female presents with severe cellular injury following ischemic insult during
a myocardial infarction. Laboratory studies reveal elevated cardiac troponins and
lactate dehydrogenase.
, Which intracellular event represents the irreversible stage of cellular injury that commits
the cell to death?
A. Depletion of ATP stores and failure of the sodium-potassium pump
B. Influx of calcium ions and activation of phospholipases
C. Mitochondrial swelling with loss of oxidative phosphorylation
D. Severe damage to cell membranes with massive calcium influx and lysosomal
enzyme release [CORRECT]
Correct Answer: D
Rationale:
This question distinguishes reversible vs. irreversible cellular injury, critical for
understanding myocardial infarction pathophysiology.
Stages of Ischemic Cell Injury:
Reversible Injury (early ischemia):
● ATP depletion (anaerobic glycolysis fails)
● Sodium-potassium pump failure (cellular edema)
● Mitochondrial swelling (loss of cristae)
● Ribosomal detachment (protein synthesis stops)
● Key point: If blood flow restored, cell can recover
