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NSG 5140 Advanced Pathophysiology Midterm Exam Review Comprehensive Questions with Verified Answers and Rationales Already A+ [MOST RECENT]

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NSG 5140 Advanced Pathophysiology Midterm Exam Review Comprehensive Questions with Verified Answers and Rationales Already A+ [MOST RECENT]

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NSG 5140 Advanced
Pathophysiology Midterm Exam
Review Comprehensive Questions
with Verified Answers and
Rationales Already A+ [MOST
RECENT]
Question 1

A patient with chronic hypertension develops left ventricular wall
thickening. Which mechanism best explains this adaptation?

A. Increased myocyte number due to cell division
B. Increased myocyte size due to increased workload
C. Replacement of cardiac cells with fibrous tissue
D. Transformation of cardiac cells into smooth muscle

Correct Answer: B. Increased myocyte size due to increased
workload

Rationale: Cardiac myocytes are terminally differentiated cells that
cannot undergo mitosis. When faced with increased workload (afterload)
from chronic hypertension, they respond through hypertrophy—an
increase in individual cell size rather than cell number. This adaptation
increases contractile force to maintain cardiac output against elevated
resistance. The PI3K/Akt/mTOR pathway drives this protein synthesis
response. Fibrous tissue replacement would indicate pathological
remodelling rather than adaptive hypertrophy.

,Question 2

During ischemic injury, loss of ATP most directly leads to:

A. Increased oxidative phosphorylation
B. Failure of the sodium-potassium pump
C. Increased protein synthesis
D. Mitochondrial membrane stabilization

Correct Answer: B. Failure of the sodium-potassium pump

Rationale: ATP is the primary energy source for the Na⁺/K⁺ ATPase
pump. When hypoxia limits oxidative phosphorylation, ATP production
decreases. Without sufficient ATP, the pump fails to maintain the
electrochemical gradient, causing intracellular sodium accumulation,
water influx, and cellular swelling. This represents the hallmark of
reversible cellular injury. If the insult persists, irreversible injury with
mitochondrial damage and cell death follows .




Question 3

A pathologist examines a biopsy from the bronchial epithelium of a
chronic smoker. The normal pseudostratified ciliated columnar
epithelium is replaced by stratified squamous epithelium. Which
molecular event is most likely initiating this change?

A. Increased expression of anti-apoptotic Bcl-2 in basal cells
B. Reprogramming of stem cells due to chronic irritation and altered
transcription factor signaling
C. Somatic mutation in the p53 gene leading to loss of cell cycle control
D. Epigenetic silencing of E-cadherin promoting epithelial-mesenchymal
transition

,Correct Answer: B. Reprogramming of stem cells due to chronic
irritation and altered transcription factor signaling

Rationale: This describes metaplasia—the reversible replacement of one
differentiated cell type by another in response to chronic stress or
irritation. Metaplasia results from reprogramming of tissue-resident stem
cells, often involving changes in transcription factors such as Sox2 and
p63. While metaplasia itself is not malignant, it can predispose to
dysplasia and carcinoma if the irritant persists. p53 mutation and E-
cadherin silencing are associated with neoplastic transformation, not
metaplasia .




Question 4

Which of the following is the hallmark of reversible cellular injury?

A. Nuclear pyknosis
B. Cellular swelling
C. Karyorrhexis
D. Apoptosis

Correct Answer: B. Cellular swelling

Rationale: Reversible injury is characterized by cellular swelling (oncosis)
due to failure of ion pumps and water influx. This is caused by ATP
depletion leading to Na⁺/K⁺ pump failure. If the injurious stimulus is
removed, the cell can recover. Nuclear changes such as pyknosis (nuclear
shrinkage), karyorrhexis (nuclear fragmentation), and karyolysis (nuclear
dissolution) indicate irreversible injury. Apoptosis is a programmed cell
death process that is energy-dependent and does not cause
inflammation .

, Question 5

What type of necrosis is most often seen in hypoxic injury in the
brain?

A. Coagulative necrosis
B. Caseous necrosis
C. Liquefactive necrosis
D. Fat necrosis

Correct Answer: C. Liquefactive necrosis

Rationale: Ischemic injury in the brain leads to liquefactive necrosis,
where dead cells are enzymatically digested, creating a cystic space filled
with fluid. This occurs because the brain has high lipid content and
abundant hydrolytic enzymes released from inflammatory cells and
microglia. In contrast, the heart and kidneys typically exhibit coagulative
necrosis with hypoxic injury, preserving tissue architecture for several
days. Caseous necrosis is characteristic of tuberculosis, and fat necrosis
occurs in adipose tissue injury.




Question 6

A researcher studying pressure overload in cardiac myocytes
observes that sustained mechanical stretch leads to increased
protein synthesis and cell enlargement without cell division. Which
intracellular signalling pathway is most directly responsible for this
adaptive response?

A. Activation of the PI3K/Akt/mTOR pathway leading to increased
translation

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