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NSG 5140 | Midterm Exam: Advanced Pathophysiology- Questions with CORRECT Answers | Latest update 2026/2027 - South College

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NSG 5140 | Midterm Exam: Advanced Pathophysiology- Questions with CORRECT Answers | Latest update 2026/2027 - South College

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NSG 5140 | Midterm Exam: Advanced
Pathophysiology- Questions with CORRECT Answers |
Latest update 2026/2027 - South College

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

Answer: B
Rationale: Cardiac myocytes are terminally differentiated and respond to increased
workload by hypertrophy (increased cell size), not hyperplasia .



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

Answer: B
Rationale: ATP depletion causes failure of the Na⁺/K⁺ ATPase pump, leading to cellular
swelling and eventual cell death .



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

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

• B. Induction of p53-mediated cell cycle arrest and senescence

• C. Upregulation of caspases and initiation of apoptosis

• D. Activation of the unfolded protein response (UPR) due to ER stress

Answer: A
Rationale: Cardiac myocytes respond to increased workload by undergoing
hypertrophy driven by the PI3K/Akt/mTOR pathway that enhances protein synthesis .



4. 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

Answer: B
Rationale: Metaplasia results from reprogramming of tissue-resident stem cells or
undifferentiated cells in response to chronic stress, often involving changes in
transcription factors .



5. Which cellular adaptation is characterized by a decrease in cell size and function
due to decreased workload or loss of innervation?

• A. Hypertrophy

• B. Hyperplasia

• C. Atrophy

, • D. Metaplasia

Answer: C
Rationale: Atrophy is reduced cell size and function resulting from disuse, denervation,
ischemia, or other causes .



6. Apoptosis differs from necrosis because apoptosis:

• A. Causes inflammation

• B. Is always pathologic

• C. Requires ATP

• D. Results in cell membrane rupture

Answer: C
Rationale: Apoptosis is an energy-dependent, programmed process that does not
provoke inflammation .



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

• A. Apoptosis triggers intense inflammation; necrosis does not

• B. Apoptosis is programmed, controlled cell death; necrosis is uncontrolled and
often inflammatory

• C. Apoptosis affects large tissue areas; necrosis is always single cells

• D. Apoptosis occurs only in cancer; necrosis only in infection

Answer: B
Rationale: Apoptosis is a regulated, energy-dependent process of individual cell death
without inflammation, while necrosis is uncontrolled, often inflammatory cell death
affecting tissue areas .



8. In a patient with prolonged ischemia due to renal artery stenosis, proximal
tubular epithelial cells exhibit swelling of mitochondria and dilation of the

, endoplasmic reticulum on electron microscopy. Which phase of cell injury does
this morphology represent, and what is the primary underlying biochemical
defect?

• A. Irreversible injury; massive calcium influx into mitochondria

• B. Reversible injury; depletion of ATP leading to failure of ion pumps

• C. Necroptosis; activation of receptor-interacting protein kinases

• D. Apoptosis; cytochrome c release from mitochondria

Answer: B
Rationale: Cellular swelling with mitochondrial and ER changes is characteristic of
reversible injury due to ATP depletion causing failure of Na⁺/K⁺ ATPase .



9. A liver biopsy from a patient with nonalcoholic steatohepatitis (NASH) shows
hepatocytes with large fat vacuoles displacing the nucleus to the periphery. Which
cellular adaptation is most directly responsible for this histological finding?

• A. Hypertrophy due to increased metabolic demand

• B. Intracellular accumulation of triglycerides secondary to impaired fatty acid
oxidation

• C. Hyperplasia of hepatocytes following loss of neighboring cells

• D. Metaplasia of hepatocytes to adipose-like cells

Answer: B
Rationale: Steatosis (fatty change) is an abnormal intracellular accumulation of
triglycerides from imbalances in lipid metabolism .



10. A cell exposed to a sublethal dose of ionizing radiation undergoes growth
arrest and expresses senescence-associated β-galactosidase. Which molecular
pathway is most likely driving this response?

• A. Activation of telomerase to maintain telomere length

• B. Stabilization of p53 and upregulation of p21 leading to cell cycle arrest

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