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NSG 5140 ADVANCED PATHOPHYSIOLOGY – WEEK 10 FINAL EXAM 2026/2027 COMPLETE (140) CURRENT TESTING QUESTIONS AND CORRECT ANSWERS WITH DETAILED RATIONALES.

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Prepare effectively for the NSG 5140 Advanced Pathophysiology Week 10 Final Exam with this focused study resource. It supports review of disease processes, pathophysiological mechanisms, clinical manifestations, diagnostic concepts, and physiological responses relevant to advanced nursing practice. Use the material to reinforce your understanding, review key topics, and identify areas that may require additional study. This resource is suited for graduate nursing students, advanced practice nursing learners, and candidates preparing for the NSG 5140 Week 10 final examination

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NSG 5140 ADVANCED PATHOPHYSIOLOGY – WEEK 10
FINAL EXAM 2026/2027 COMPLETE (140) CURRENT
TESTING QUESTIONS AND CORRECT ANSWERS WITH
DETAILED RATIONALES.
PATHOPHYSIOLOGY
Prepare effectively for the NSG 5140 Advanced Pathophysiology Week 10 Final Exam
with this focused study resource. It supports review of disease processes,
pathophysiological mechanisms, clinical manifestations, diagnostic concepts, and
physiological responses relevant to advanced nursing practice. Use the material to
reinforce your understanding, review key topics, and identify areas that may require
additional study. This resource is suited for graduate nursing students, advanced
practice nursing learners, and candidates preparing for the NSG 5140 Week 10 final
examination.



MULTIPLE CHOICE.
DOMAIN 1 — Cellular Adaptation, Injury, and Death (Questions 1–14)
1. A chronic smoker develops a persistent cough and mucus
hypersecretion due to an increased number of mucus-secreting cells
replacing normal ciliated columnar epithelium in the airways. This
cellular change is BEST described as:
A. Atrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Answer: C. Metaplasia
Rationale: Metaplasia is a reversible replacement of one differentiated cell
type by another. In chronic smokers, the normal ciliated columnar epithelium
is replaced by squamous or mucus-secreting cells as an adaptive response to

, Page 2 of 60


chronic irritation. This differs from hyperplasia (increase in cell number),
atrophy (decrease in cell size), and dysplasia (disordered cellular growth).
2. A patient with a history of hypertension develops an increase in the size
of cardiac muscle cells. Which cellular adaptation is responsible?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Atrophy
Answer: B. Hypertrophy
Rationale: Hypertrophy is an increase in cell size in response to increased
workload or hormonal stimulation. Cardiac myocytes enlarge to handle
increased afterload from hypertension. This differs from hyperplasia, which is
an increase in cell number.
3. During ischemic injury to the heart muscle, which type of cell death will
occur?
A. Liquefactive necrosis
B. Coagulative necrosis
C. Caseous necrosis
D. Fat necrosis
Answer: B. Coagulative necrosis
Rationale: Coagulative necrosis is the hallmark of ischemic death in most
solid organs, including the heart. Tissue architecture is preserved for several
days because ischemia denatures structural proteins and inactivates
lysosomal enzymes. Liquefactive necrosis occurs in the brain, caseous
necrosis in tuberculosis, and fat necrosis in pancreatic or breast tissue.
4. A researcher studying pressure overload in cardiac myocytes observes
that sustained mechanical stretch leads to increased protein synthesis

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and cell enlargement without cell division. Which intracellular signaling
pathway is MOST directly responsible?
A. Activation of the PI3K/Akt/mTOR pathway
B. Induction of p53-mediated cell cycle arrest
C. Upregulation of caspases
D. Activation of the unfolded protein response
Answer: A. Activation of the PI3K/Akt/mTOR pathway
Rationale: Cardiac myocytes respond to increased workload by undergoing
hypertrophy, driven by the PI3K/Akt/mTOR pathway that enhances protein
synthesis. p53 activation promotes apoptosis or senescence, caspase
activation leads to apoptosis, and the unfolded protein response is triggered
by ER stress.
5. Which cellular change is characteristic of reversible injury?
A. Karyorrhexis
B. Pyknosis
C. Cellular swelling
D. Karyolysis
Answer: C. Cellular swelling
Rationale: Cellular swelling (hydropic change) is a hallmark of reversible
injury caused by failure of the sodium-potassium pump, leading to
intracellular water accumulation. Karyorrhexis, pyknosis, and karyolysis are
features of irreversible injury and cell death.
6. A patient's biopsy reveals an increase in the number of cells in the
breast tissue. This is BEST described as:
A. Hypertrophy
B. Hyperplasia
C. Metaplasia

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D. Dysplasia
Answer: B. Hyperplasia
Rationale: Hyperplasia is an increase in the number of cells in an organ or
tissue. It can be physiologic (hormonal, compensatory) or pathologic. This
differs from hypertrophy, which is an increase in cell size.
7. A 65-year-old patient with chronic heart failure presents with worsening
dyspnea, jugular venous distension, and peripheral edema. Which
compensatory mechanism is MOST directly responsible for the edema?
A. Decreased aldosterone secretion
B. Increased atrial natriuretic peptide release
C. Activation of the renin-angiotensin-aldosterone system
D. Suppression of antidiuretic hormone
Answer: C. Activation of the renin-angiotensin-aldosterone system
Rationale: In heart failure, reduced cardiac output activates the RAAS,
increasing aldosterone-mediated sodium and water retention, expanding
plasma volume, and worsening edema.
8. Which cellular adaptation is characterized by a decrease in cell size?
A. Hypertrophy
B. Hyperplasia
C. Atrophy
D. Metaplasia
Answer: C. Atrophy
Rationale: Atrophy is a decrease in cell size, often resulting from decreased
workload, loss of innervation, diminished blood supply, or aging. It can lead to
reduced organ size and function.
9. A patient has a biopsy showing cells with large, hyperchromatic nuclei
and abnormal tissue architecture. This finding is MOST consistent with:

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