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NURS 6501 – Advanced Pathophysiology: Week 6 Midterm actual Exam Questionsand Answers | pdf Fomart Level: Graduate

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NURS 6501 – Advanced Pathophysiology: Week 6 Midterm actual Exam Questionsand Answers | pdf Fomart Level: Graduate

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NURS 6501 – Advanced Pathophysiology: Week 6 Midterm
actual Exam Questionsand Answers | pdf Fomart Level:
Graduate

1. A 58-year-old man with chronic gastroesophageal reflux disease has been using proton
pump inhibitors for years. A esophageal biopsy shows columnar epithelium with goblet cells
replacing the normal squamous epithelium. This change is best classified as which type of
cellular adaptation?
A. Metaplasia, a reversible change in cell type in response to chronic injury
B. Dysplasia, a preneoplastic change characterized by disordered cell growth
C. Hyperplasia, an increase in cell number due to chronic irritation
D. Hypertrophy, an increase in cell size due to increased functional demand
Answer: A. Metaplasia, a reversible change in cell type in response to chronic injury

2. A 45-year-old woman with type 2 diabetes presents with a foot ulcer that has failed to heal.
Biopsy shows necrotic tissue with nuclear pyknosis, karyorrhexis, and karyolysis, as well as an
acute inflammatory infiltrate. This pattern of cell death is most consistent with which of the
following?
A. Coagulative necrosis, which preserves tissue architecture for days and is characteristic of ischemic injury
B. Liquefactive necrosis, which results from enzymatic digestion and is typical of abscess formation
C. Caseous necrosis, which has a cheese-like appearance and is associated with tuberculosis
D. Apoptosis, which is a regulated form of cell death that does not elicit inflammation
Answer: A. Coagulative necrosis, which preserves tissue architecture for days and is
characteristic of ischemic injury

3. A 30-year-old woman presents with fatigue and jaundice. Laboratory tests show an elevated
unconjugated bilirubin and decreased haptoglobin. A peripheral smear reveals spherocytes.
The spherocytes are most likely the result of which cellular injury mechanism?
A. Immune-mediated lysis of red blood cells leading to membrane damage and spherocyte formation
B. Oxidative stress causing lipid peroxidation and membrane blebbing
C. Genetic mutation in spectrin causing membrane instability and spherocyte formation
D. Hypoxic injury leading to ATP depletion and ion pump failure
Answer: C. Genetic mutation in spectrin causing membrane instability and spherocyte
formation

4. A 72-year-old man with pneumonia develops hypotension, tachycardia, and warm
extremities. Blood cultures are positive for gram-negative rods. Which of the following best
explains the systemic inflammatory response in this patient?
A. Lipopolysaccharide binding to toll-like receptor 4 on macrophages triggers release of TNF-± and IL-1
B. Gram-positive peptidoglycan activates the alternative complement pathway and causes mast cell
degranulation
C. Exotoxin A acts as a superantigen, polyclonally activating T cells and causing cytokine storm
D. Immune complex deposition in small vessels activates neutrophils and causes tissue damage
Answer: A. Lipopolysaccharide binding to toll-like receptor 4 on macrophages triggers release
of TNF-± and IL-1

, 5. A 25-year-old man with recurrent skin abscesses and a family history of similar problems has
a complete blood count showing eosinophilia and elevated IgE. He has a history of eczema and
recurrent respiratory infections. Which leukocyte function is most likely defective in this
patient?
A. Neutrophil oxidative burst, leading to recurrent pyogenic infections
B. Natural killer cell cytotoxicity, leading to viral infections
C. Complement opsonization, leading to encapsulated organism infections
D. T cell receptor signaling, leading to combined immunodeficiency
Answer: A. Neutrophil oxidative burst, leading to recurrent pyogenic infections

6. A 50-year-old woman with rheumatoid arthritis is prescribed a tumor necrosis factor (TNF)
inhibitor. Which of the following best describes the mechanism of action of this therapy in
reducing inflammation?
A. It neutralizes TNF-±, preventing its binding to TNF receptors and blocking downstream proinflammatory
signaling
B. It inhibits cyclooxygenase-2, reducing prostaglandin synthesis and pain
C. It blocks IL-6 receptor, decreasing acute phase protein production
D. It depletes B cells, reducing autoantibody production
Answer: A. It neutralizes TNF-±, preventing its binding to TNF receptors and blocking
downstream proinflammatory signaling

7. A 34-year-old woman who recently traveled to the southeastern United States has a fever,
headache, and a rash. She is diagnosed with a rickettsial infection. Which of the following best
describes the pathogenesis of this infection?
A. The organism is an obligate intracellular bacterium that replicates within endothelial cells, causing vasculitis
B. The organism produces a toxin that causes massive cytokine release and shock
C. The organism stimulates a strong granulomatous response leading to caseous necrosis
D. The organism adheres to mucosal surfaces and invades underlying tissue, causing abscess formation
Answer: A. The organism is an obligate intracellular bacterium that replicates within endothelial
cells, causing vasculitis

8. A 60-year-old male smoker presents with hemoptysis and weight loss. Chest X-ray shows a
mass in the right upper lobe. Biopsy reveals small cells with scant cytoplasm and high mitotic
rate. Which of the following genetic changes is most likely involved in the pathogenesis of this
tumor?
A. Activating mutation in the EGFR gene
B. Translocation involving the ALK gene
C. Inactivation of both RB1 and TP53 tumor suppressor genes
D. Amplification of the MYC oncogene
Answer: C. Inactivation of both RB1 and TP53 tumor suppressor genes

9. A 45-year-old woman with a BRCA1 mutation is concerned about her risk of developing
cancer. Which of the following best explains why BRCA1 mutations increase cancer risk?
A. Loss of BRCA1 impairs DNA double-strand break repair, leading to genomic instability
B. BRCA1 mutation causes overexpression of growth factors that stimulate cell proliferation
C. BRCA1 mutation inactivates the p53 pathway, allowing damaged cells to survive
D. BRCA1 mutation results in a defective mismatch repair system, increasing point mutations

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