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NR 507 Advanced Pathophysiology Week 8 Final Exam Actual Exam 2026/2027 | Questions with Verified Answers | 100% Correct | Pass Guaranteed

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NR 507 Advanced Pathophysiology Week 8 Final Exam Actual Exam 2026/2027 | Questions with Verified Answers | 100% Correct | Pass Guaranteed

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NR 507 Advanced Pathophysiology
Course
NR 507 Advanced Pathophysiology

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NR 507 Advanced Pathophysiology Week 8 Final Exam
Actual Exam 2026/2027 | Questions with Verified
Answers | 100% Correct | Pass Guaranteed



SECTION 1: Cellular Foundations & Genetic Disorders (15 Questions)

Q1: A 45-year-old alcoholic has ballooned hepatocytes on biopsy. Electron microscopy
shows a proliferated smooth endoplasmic reticulum. This adaptation is:

A. Atrophy

B. Hypertrophy

C. Hyperplasia

D. Metaplasia

Correct Answer: C

Rationale: Chronic ethanol → CYP2E1 induction → SER hyperplasia (↑ organelle number
= ↑ cell number). Clinical: Tolerance to anesthetic agents; guides peri-operative dosing.
Distractors: hypertrophy = ↑ cell size; atrophy = ↓ size; metaplasia = phenotype switch.



Q2: Which disorder shows autosomal-dominant, 100 % penetrance?

A. Cystic fibrosis

B. Sickle-cell disease

,C. Huntington disease

D. Phenylketonuria

Correct Answer: C

Rationale: HD = CAG-repeat expansion; every individual with ≥ 40 repeats manifests
chorea. NP role: 50 % offspring risk; genetic counseling mandatory. CF & PKU are AR;
sickle-cell AR with variable expression.



Q3: A BRCA1 mutation carrier asks why her cancer risk is high. The primary molecular
mechanism is:

A. Defective DNA mismatch repair

B. Impaired homologous recombination double-strand break repair

C. Activated RAS oncogene

D. Telomerase over-expression

Correct Answer: B

Rationale: BRCA1 repairs DNA double-strand breaks via HR; loss → genomic instability
→ triple-negative breast/ovarian cancers. Therapy: PARP inhibitors exploit synthetic
lethality. Mismatch repair (A) causes Lynch syndrome; RAS (C) drives proliferation;
telomerase (D) immortalizes but doesn’t initiate.



Q4: The earliest reversible change in acute hypoxic cell injury is:

A. Lysosomal rupture

B. Ribosomal detachment

,C. Decreased ATP → Na⁺/K⁺ pump failure → cellular swelling

D. Nuclear pyknosis

Correct Answer: C

Rationale: O₂ lack → oxidative phosphorylation stops → ATP ↓ → pump fails → Na⁺ &
water influx → hydropic change (reversible). Clinical correlate: AST/ALT rise before
irreversible necrosis. Lysosomal rupture & pyknosis signal irreversible damage.



Q5: A smoker’s bronchial biopsy shows stratified squamous epithelium replacing
pseudostratified columnar. This is:

A. Dysplasia

B. Metaplasia

C. Hyperplasia

D. Anaplasia

Correct Answer: B

Rationale: Chronic irritation (cigarette smoke) → protective switch to more durable
squamous phenotype. Risk: precursor to dysplasia/cancer; smoking cessation can
reverse. Dysplasia = disordered growth; anaplasia = malignant undifferentiation.



Q6: Which proto-oncogene conversion creates the Philadelphia chromosome in CML?

A. BCL2

B. ABL1

, C. MYC

D. RAS

Correct Answer: B

Rationale: t(9;22) BCR-ABL → constitutive tyrosine-kinase activity → uncontrolled
granulocyte proliferation. Targeted therapy: Imatinib inhibits kinase ATP pocket. MYC
(Burkitt), RAS (many solid tumors), BCL2 (follicular lymphoma).



Q7: A child with xeroderma pigmentosum cannot:

A. Repair UV-induced thymine dimers

B. Synthesize melanin

C. Undergo meiosis

D. Perform nucleotide-excision repair

Correct Answer: D

Rationale: NER pathway defect → thymine dimers persist → basal-cell & squamous-cell
cancers by age 10. NP advice: strict sun avoidance, dermatology q3-6 mo. Melanin
synthesis (B) normal; meiosis (C) unaffected.



Q8: The Warburg effect in cancer cells describes:

A. Increased oxidative phosphorylation

B. Aerobic glycolysis with lactate production

C. Gluconeogenesis activation

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