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WGU D115 Advanced Pathophysiology OA Readiness Test Bank Version A & B Actual Exam 2026/2027 | Questions with Verified Answers | 100% Correct | Pass Guaranteed

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WGU D115 ADVANCED PATHOPHYSIOLOGY OA READINESS TEST BANK VERSION A & B ACTUAL EXAM 2026/2027 | PASS GUARANTEED Prepare with the actual WGU D115 OA Readiness Test Bank Versions A & B - Pass Guaranteed! This resource contains actual exam questions and verified answers for the 2026/2027 WGU D115 Advanced Pathophysiology Objective Assessment Readiness Test Bank Versions A & B. Guaranteed to help you pass or your money back. WHAT'S INCLUDED: • Actual OA Readiness Questions from D115 Versions A & B • 100% Verified Answers with pathophysiology rationales • Complete Test Bank Content tested on the actual assessment • Both Versions A & B with comprehensive coverage • Pathophysiology Standards from the real test • Professional PDF – Instant digital download • PASS GUARANTEED – Confidence in your success KEY FEATURES: • Actual Exam Content – Real WGU D115 pathophysiology questions • Both Versions A & B – Complete preparation coverage • Pass Guarantee – Your success assured • OA Readiness – Objective assessment standards preparation • Updated for 2026/2027 – Current WGU curriculum ACTUAL EXAM TOPICS: Advanced Disease Mechanisms – Actual exam questions System Pathophysiology – Real test scenarios Clinical Correlations – Pathophysiology content Case Study Analysis – Practice questions DETAILS: Course: D115 Advanced Pathophysiology University: Western Governors University (WGU) Format: OA Readiness Test Bank Versions: A & B Year: 2026/2027 Delivery: Instant Download Guarantee: Pass Guaranteed

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WGU D115 Advanced Pathophysiology OA
Readiness Test Bank Version A & B Actual
Exam 2026/2027 | Questions with Verified
Answers | 100% Correct | Pass Guaranteed
VERSION A
OA Readiness Practice Exam Test Bank – 80 Questions
Unit 1 Pathophysiology Focus Guide: Foundational Concepts
Key Mechanisms: Cellular adaptation (atrophy, hypertrophy), Genetic
expression in disease, Principles of inflammation and tissue repair
Q1 (Unit 1): A patient with long-standing hypertension presents with left
ventricular enlargement on echocardiogram but no evidence of valve
dysfunction. The nurse correlates this change to which primary cellular adaptive
process?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Dysplasia
**Correct Answer: B
Expert-Verified Rationale: Hypertrophy is the enlargement of individual
myocytes in response to chronic pressure overload without an increase in cell
number.
Q2 (Unit 1): A 68-year-old with COPD shows diaphragm muscle mass loss on
CT. Which intracellular signaling pathway is most responsible for this atrophy?
A. mTOR up-regulation
B. Ubiquitin-proteasome activation
C. Akt phosphorylation
D. Heat-shock protein induction
**Correct Answer: B
Expert-Verified Rationale: The ubiquitin-proteasome system is the dominant
catabolic pathway degrading contractile proteins in disuse atrophy.
Q3 (Unit 1): A researcher deletes the p53 tumor-suppressor gene in knockout
mice; subsequent exposure to UV-B produces melanomas within 4 weeks. This
best demonstrates which principle of genetic disease expression?

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A. Genomic imprinting
B. Loss-of-heterozygosity unmasking recessive oncogenesis
C. Trinucleotide repeat expansion
D. Epigenetic methylation silencing
**Correct Answer: B
Expert-Verified Rationale: Loss of the remaining functional p53 allele unmasks
the recessive oncogenic phenotype, illustrating loss-of-heterozygosity.
Q4 (Unit 1): After total knee replacement, a patient’s incision site shows orderly
collagen cross-linking and capillary regression over 3 weeks. Which TGF-β–
mediated event supports this transition?
A. Neutrophil extravasation
B. Fibroblast apoptosis
C. Endothelial VEGF up -regulation
D. Macrophage iNOS expression
**Correct Answer: B
Expert-Verified Rationale: TGF-β drives fibroblast apoptosis, halting collagen
deposition and permitting scar maturation during remodeling.
Q5 (Unit 1): A neonate with cystic fibrosis displays viscous airway secretions.
The primary cellular dysfunction involves which class of proteins?
A. Sodium channel conductance (ENaC)
B. Chloride channel regulation (CFTR)
C. Potassium channel gating (KvLQT1)
D. Aquaporin water transport (AQP5)
**Correct Answer: B
Expert-Verified Rationale: CFTR chloride channel malfunction creates
defective airway surface liquid hydration, producing thick mucus.
Q6 (Unit 1): A marathon runner’s gastrocnemius biopsy shows central nuclei
and increased cross-sectional area without fiber splitting. This represents:
A. Physiologic hypertrophy
B. Pathologic hyperplasia
C. Denervation atrophy
D. Metaplasia
**Correct Answer: A
Expert-Verified Rationale: Repetitive workload induces adaptive physiologic
hypertrophy characterized by increased fiber size with preserved architecture.
Q7 (Unit 1): A 45-year-old woman with BRCA1 mutation undergoes
prophylactic oophorectomy. The surgeon notes foci of ciliated columnar
epithelium within the ovarian cortex. This finding is best termed:
A. Dysplasia
B. Metaplasia
C. Anaplasia

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D. Desmoplasia
**Correct Answer: B
Expert-Verified Rationale: Metaplasia is the reversible substitution of one adult
epithelium for another, here serosa to ciliated columnar.
Q8 (Unit 1): A burn patient receives topical silver sulfadiazine to limit wound
colonization. The drug’s anti-inflammatory action is primarily mediated by
inhibition of which enzyme?
A. Cyclo-oxygenase-2
B. Lipoxygenase
C. Myeloperoxidase
D. Inducible nitric oxide synthase
**Correct Answer: A
Expert-Verified Rationale: Silver salts down-regulate COX-2, decreasing
prostaglandin synthesis and secondary inflammation.
Q9 (Unit 1): A 70-year-old man with alcoholic cirrhosis exhibits gynecomastia.
Which estrogen-metabolizing pathway is most impaired?
A. 17β-HSD oxidation in Leydig cells
B. Hepatic CYP3A4 clearance of estradiol
C. Aromatase conversion of testosterone
D. Sulfotransferase conjugation in gut epithelium
**Correct Answer: B
Expert-Verified Rationale: Hepatocyte dysfunction reduces CYP3A4-mediated
estradiol clearance, elevating circulating estrogens.
Q10 (Unit 1): A renal transplant biopsy shows acute cellular rejection with
CD8+ perforin granules. Perforin exerts cytotoxicity through which final
common pathway?
A. Caspase-3 activation via granzyme B
B. Fas-ligand trimerization
C. ROS generation via NADPH oxidase
D. Terminal complement C5b-9 insertion
**Correct Answer: A
Expert-Verified Rationale: Granzyme B delivered by perforin pores cleaves and
activates caspase-3, executing apoptosis.
Q11 (Unit 1): A 55-year-old with mesothelioma shows pleural plaques with
“asbestos bodies.” These ferruginous bodies represent which macrophage-
mediated process?
A. Phagocytosis with frustrated phagosome leakage
B. Efferocytosis of apoptotic mesothelial cells
C. Autophagic degradation of ferritin
D. NLRP3 inflammasome assembly
**Correct Answer: A

, 4


Expert-Verified Rationale: Macrophages engulf asbestos fibers but
incompletely digest them, leading to iron coating and frustrated phagosome
rupture.
Q12 (Unit 1): A 30-year-old woman with systemic lupus exhibits photosensitive
rash. Which UV-induced self-DNA modification triggers TLR-7 activation?
A. 8-oxoguanine formation
B. CpG hypomethylation
C. Thymidine dimer accumulation
D. Cytosine deamination
**Correct Answer: B
Expert-Verified Rationale: Hypomethylated CpG DNA from apoptotic
keratinocytes engages TLR-7, propagating autoimmunity.
Q13 (Unit 1): A child with Fanconi anemia develops bone-marrow failure.
Which DNA repair pathway is defective?
A. Base-excision repair
B. Homologous recombination cross-link repair
C. Mismatch repair
D. Non-homologous end joining
**Correct Answer: B
Expert-Verified Rationale: Fanconi proteins orchestrate homologous
recombination to resolve DNA inter-strand cross-links.
Q14 (Unit 1): A 60-year-old smoker’s bronchial biopsy shows goblet-cell
hyperplasia. This reversible change is driven chiefly by which transcription
factor?
A. STAT-3
B. NF-κB
C. HIF-1α
D. PPAR-γ
**Correct Answer: B
Expert-Verified Rationale: Cigarette smoke activates NF-κB, up-regulating
mucin genes and driving goblet-cell metaplasia.
Q15 (Unit 1): A 48-hour-old neonate develops physiologic jaundice. The
predominant mechanism is:
A. Hemolysis from G6PD deficiency
B. Immaturity of hepatic UGT1A1 conjugation
C. Crigler-Najjar type I mutation
D. Biliary atresia
**Correct Answer: B
Expert-Verified Rationale: Delayed expression of UGT1A1 glucuronyl-
transferase limits bilirubin conjugation in neonates.

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