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NSG 5140 Advanced Pathophysiology Midterm Exam South College: 200 Practice Questions on Cellular Adaptation, Genetics, Immunology, & Multi-System Disorders | pdf

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NSG 5140 Advanced Pathophysiology Midterm Exam South College: 200 Practice Questions on Cellular Adaptation, Genetics, Immunology, & Multi-System Disorders | pdf

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NSG 5140 Advanced Pathophysiology Midterm Exam
South College: 200 Practice Questions on Cellular
Adaptation, Genetics, Immunology, & Multi-System
Disorders | pdf


Feature Details
Course NSG 5140 – Advanced Pathophysiology
Institution South College
Program MSN / DNP
Credits 4
Focus Cellular pathophysiology, genetic mechanisms, immune
function, multi-system disease processes across the lifespan
Exam Multiple-choice, scenario-based
Format
Question 200
Count
Passing 80% (typical for graduate-level exams)
Score

SECTION 1: CELLULAR ADAPTATION & INJURY (Questions 1-35)

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 (hyperplasia)
 B) Increased myocyte size due to increased workload (hypertrophy)
 C) Replacement of cardiac cells with fibrous tissue
 D) Transformation of cardiac cells into smooth muscle

, Answer: B. Cardiac myocytes are terminally differentiated and respond to increased
workload by hypertrophy (increased cell size), not hyperplasia. Hypertrophy is an adaptive
response to increased demand .

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. ATP depletion causes failure of the Na⁺/K⁺ ATPase pump, leading to
intracellular sodium accumulation, water influx, and cellular swelling. This is the hallmark of
reversible cell injury .

3. A chronic smoker develops persistent cough and mucus hypersecretion due to an
increased number of mucus-secreting cells. This cellular change is best described
as:

 A) Atrophy
 B) Hyperplasia
 C) Metaplasia
 D) Dysplasia

Answer: C. Metaplasia is a reversible replacement of one differentiated cell type by
another. In chronic smokers, ciliated columnar epithelium is replaced by squamous mucus-
secreting cells in the airways .

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. Metaplasia results from reprogramming of tissue-resident stem cells in
response to chronic stress, involving changes in transcription factors (e.g., Sox2, p63) .

5. 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. Cellular swelling with mitochondrial and ER changes is characteristic of
reversible injury, primarily due to ATP depletion causing failure of Na⁺/K⁺ ATPase .

6. 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. Steatosis (fatty change) is an abnormal intracellular accumulation of
triglycerides, resulting from imbalances in lipid metabolism such as increased influx or
decreased oxidation .

7. A newborn presents with syndactyly (fused fingers). Which developmental
mechanism failed?

 A) Cell proliferation
 B) Apoptosis
 C) Cell migration
 D) Differentiation

Answer: B. Syndactyly results from failure of apoptosis during embryonic development.
Normally, apoptosis separates the digits during hand development .

8. Free radical injury causes cellular damage primarily through which mechanism?

 A) ATP depletion
 B) Lipid peroxidation
 C) Protein synthesis inhibition
 D) DNA repair enhancement

Answer: B. Free radicals cause cellular damage primarily through lipid peroxidation of cell
membranes, leading to membrane damage, protein oxidation, and DNA damage .

9. Which organelle is the primary source of free radicals during normal metabolism?

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