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NR 507 Week 8 Final Exam Questions 1-100 NR-507 Advanced Pathophysiology NR 507 Week 8 Final Exam Examplify Online Proctored Questions and Answers Graded A+

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NR 507 Week 8 Final Exam Questions 1-100 NR-507 Advanced Pathophysiology NR 507 Week 8 Final Exam Examplify Online Proctored Questions and Answers Graded A+

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NR 507 Week 8 Final Exam Questions 1-100 NR-507 Advanced
Pathophysiology NR 507 Week 8 Final Exam Examplify Online
Proctored Questions and Answers Graded A+
SECTION 1: CELLULAR ADAPTATION, INJURY & NEOPLASIA (Questions 1–20)

1. Which cellular adaptation is characterized by a decrease in cell size resulting in reduced tissue
mass?

A. Hypertrophy
B. Hyperplasia
C. Atrophy
D. Metaplasia

Rationale: Atrophy is a decrease in cell size due to reduced workload, loss of innervation,
decreased blood supply, inadequate nutrition, or loss of hormonal stimulation. Hypertrophy is
increased cell size, hyperplasia is increased cell number, and metaplasia is replacement of one
cell type with another.



2. A 58-year-old male with long-standing uncontrolled hypertension develops left ventricular
hypertrophy. Which mechanism best explains this adaptation?

A. Hyperplasia of cardiac myocytes
B. Hypertrophy of cardiac myocytes
C. Metaplasia of cardiac tissue
D. Dysplasia of myocardial cells

Rationale: Cardiac myocytes are terminally differentiated and cannot divide. They respond
to chronic pressure overload by increasing in size (hypertrophy) through addition of structural
proteins. Hyperplasia is not possible in cardiac muscle.



3. A chronic smoker undergoes bronchoscopy, and biopsy reveals replacement of normal
ciliated columnar epithelium with stratified squamous epithelium. This is best described as:

A. Hyperplasia
B. Dysplasia
C. Metaplasia
D. Anaplasia

, Rationale: Metaplasia is the reversible replacement of one mature cell type with another,
often as an adaptive response to chronic irritation. In smokers, squamous metaplasia occurs
because squamous cells are better able to withstand the stress of smoke. This is not dysplasia,
which involves disordered growth.



4. A pathologist notes cells with marked variation in size and shape, enlarged hyperchromatic
nuclei, and loss of normal tissue organization, but the basement membrane remains intact. This
finding is most consistent with:

A. Metaplasia
B. Dysplasia
C. Carcinoma in situ
D. Anaplasia

Rationale: Dysplasia is characterized by disordered cellular growth with atypical cells and
loss of organization, but it does not invade through the basement membrane. Carcinoma in situ
would show similar changes but with full-thickness involvement. Anaplasia denotes lack of
differentiation seen in malignancy.



5. Which of the following best distinguishes apoptosis from necrosis?

A. Apoptosis causes cell swelling; necrosis causes cell shrinkage
B. Apoptosis is programmed and does not trigger inflammation; necrosis is uncontrolled and
triggers inflammation
C. Apoptosis is energy-independent; necrosis requires ATP
D. Apoptosis always occurs in pathological states

Rationale: Apoptosis is an energy-dependent, programmed cell death that results in cell
shrinkage, chromatin condensation, and apoptotic body formation without inflammation.
Necrosis is uncontrolled cell death with cell swelling, membrane rupture, and significant
inflammation.



6. A patient with myocardial infarction is found to have coagulative necrosis in the affected
heart muscle. Which microscopic feature is characteristic of this type of necrosis?

A. Complete liquefaction of tissue
B. Preservation of tissue architecture with loss of nuclei

,C. Cheesy white debris formation
D. Fat accumulation within cells

Rationale: Coagulative necrosis preserves the basic tissue outline for days due to protein
denaturation, but cells lose their nuclei. It is typical of ischemic injury in solid organs such as
heart, kidney, and spleen.



7. What is the most common cause of cellular injury?

A. Free radicals
B. Chemical agents
C. Hypoxia
D. Genetic mutations

Rationale: Hypoxia (lack of sufficient oxygen) is the single most common cause of cellular
injury. It leads to ATP depletion, failure of the sodium-potassium pump, cellular swelling, and
ultimately cell death if prolonged.



8. Which mechanism of cell injury is specifically associated with reperfusion of ischemic tissue?

A. Hypoxic injury
B. Oxidative stress from reactive oxygen species
C. Mechanical trauma
D. Genetic mutation

Rationale: Ischemia-reperfusion injury occurs when blood supply returns to previously
ischemic tissue, causing oxidative stress from reactive oxygen species (free radicals). The
reintroduction of oxygen leads to generation of ROS that damage cellular membranes, proteins,
and DNA.



9. A tumor suppressor gene that regulates cell cycle arrest and apoptosis in response to DNA
damage is:

A. RAS
B. MYC
C. p53
D. BCL-2

, Rationale: p53 is a critical tumor suppressor gene that induces cell cycle arrest to allow DNA
repair or triggers apoptosis if damage is irreparable. Mutation of p53 leads to uncontrolled cell
growth and is one of the most common genetic alterations in cancer.



10. Which term describes the degree of differentiation of a tumor?

A. Stage
B. Grade
C. Size
D. Metastatic potential

Rationale: Grade refers to how closely the tumor cells resemble normal tissue of origin.
Well-differentiated tumors are low grade; poorly differentiated or anaplastic tumors are high
grade. Stage refers to extent of spread.



11. A patient with alcohol abuse presents with jaundice and hepatomegaly. Biopsy reveals
accumulation of fat vacuoles within hepatocytes. This cellular change is best described as:

A. Hypertrophy
B. Hyperplasia
C. Fatty change (steatosis)
D. Metaplasia

Rationale: Fatty change (steatosis) is the accumulation of triglycerides within parenchymal
cells, commonly seen in the liver with alcohol abuse, obesity, and diabetes. It is a reversible
form of cell injury.



12. Which enzyme is most specific for myocardial injury and is used as a biomarker for
myocardial infarction?

A. Alanine aminotransferase (ALT)
B. Aspartate aminotransferase (AST)
C. Creatine kinase-MB (CK-MB)
D. Alkaline phosphatase (ALP)

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