WGU D115 Advanced Pathophysiology OA Exam
with Test Bank ACTUAL EXAM 2026/2027 | WGU
D115 Pathophysiology | Verified Q&A | Pass
Guaranteed - A+ Graded
SECTION 1: CELLULAR ADAPTATION, INJURY & NEOPLASIA (8 questions)
Q1: A 68-year-old male with a 40-pack-year smoking history presents with a chronic cough. Bronchial
biopsy reveals stratified squamous epithelium replacing the normal pseudostratified ciliated columnar
epithelium. Which cellular adaptation has occurred?
A. Hyperplasia, representing an increase in cell number due to chronic irritation
B. Hypertrophy, representing an increase in cell size in response to increased workload
C. Metaplasia, representing the reversible replacement of one differentiated cell type with another
better suited to withstand stress [CORRECT]
D. Dysplasia, representing disordered, neoplastic epithelial maturation
Correct Answer: C
Rationale: Metaplasia is the reversible replacement of one differentiated cell type by another mature
cell type better able to tolerate a particular stressor. In this case, chronic tobacco exposure causes the
normal respiratory pseudostratified ciliated columnar epithelium to be replaced by stratified squamous
epithelium, which is more resistant to chemical irritation but loses mucociliary clearance function. A is
wrong because hyperplasia involves increased cell number, not a change in cell type. B is wrong because
hypertrophy involves increased cell size, not epithelial transformation. D is wrong because dysplasia
represents disordered, pre-neoplastic maturation with nuclear atypia and loss of polarity, not a
reversible adaptive change to a different mature cell type.
Q2: A 45-year-old woman with chronic hypertension has left ventricular wall thickness of 14 mm
(normal <11 mm) on echocardiogram. The cardiomyocytes demonstrate increased organelle content
and protein synthesis. This represents which cellular adaptation?
A. Hyperplasia due to increased cardiomyocyte division in response to pressure overload
B. Hypertrophy due to increased synthesis of structural proteins and organelles [CORRECT]
,C. Atrophy due to decreased workload and reduced protein synthesis
D. Metaplasia due to replacement of cardiac muscle with fibrous tissue
Correct Answer: B
Rationale: Cardiac hypertrophy in response to chronic pressure overload (hypertension) occurs via
increased synthesis of contractile proteins (actin, myosin), mitochondria, and sarcoplasmic reticulum
within existing cardiomyocytes. Cardiac muscle cells are terminally differentiated and cannot undergo
hyperplasia. A is wrong because adult cardiomyocytes are terminally differentiated and cannot divide;
cardiac enlargement is never due to hyperplasia. C is wrong because atrophy involves decreased cell size
and protein synthesis, the opposite of what occurs in pressure overload. D is wrong because metaplasia
involves replacement of one differentiated cell type with another, not enlargement of existing muscle
cells.
Q3: A 55-year-old man presents with acute myocardial infarction. Histology of the infarcted tissue shows
cell swelling, loss of plasma membrane integrity, karyolysis, and intense inflammatory infiltration. Which
type of cell death is occurring?
A. Apoptosis, characterized by cell shrinkage, chromatin condensation, and formation of apoptotic
bodies without inflammation
B. Necrosis, characterized by ATP depletion, cell swelling, membrane rupture, and enzymatic digestion
with inflammation [CORRECT]
C. Autophagy, characterized by lysosomal degradation of cellular components for energy recycling
D. Pyroptosis, characterized by caspase-1 activation and pore formation in the plasma membrane
Correct Answer: B
Rationale: Myocardial infarction causes ischemic necrosis (coagulative necrosis) characterized by ATP
depletion, failure of ion pumps causing cell swelling, loss of plasma membrane integrity, karyolysis
(dissolution of nuclear chromatin), and intense neutrophilic infiltration due to release of intracellular
contents that trigger inflammation. A is wrong because apoptosis is energy-dependent, does not cause
inflammation, and shows cell shrinkage and chromatin condensation—not the swelling and karyolysis
described. C is wrong because autophagy is a regulated process of self-digestion for cellular
maintenance and does not produce the acute inflammatory response seen here. D is wrong because
pyroptosis is a programmed inflammatory cell death mediated by inflammasomes and gasdermin D pore
formation, typically in response to infection, not ischemic injury.
Q4: A 35-year-old woman develops fat necrosis in her breast after trauma. Histology reveals shadowy
outlines of dead adipocytes with basophilic calcium deposits. What is the underlying mechanism?
,A. Lipolysis by pancreatic lipases released into systemic circulation
B. Enzymatic digestion of triglycerides by tissue lipases with saponification and calcium deposition
[CORRECT]
C. Coagulative necrosis with preservation of tissue architecture followed by dystrophic calcification
D. Liquefactive necrosis with complete digestion of tissue by neutrophilic enzymes
Correct Answer: B
Rationale: Traumatic fat necrosis occurs when tissue lipases hydrolyze triglycerides in adipocytes into
fatty acids, which then combine with calcium to form insoluble calcium soaps (saponification), producing
the characteristic basophilic deposits and shadowy cell outlines. A is wrong because pancreatic lipase
release causes fat necrosis in acute pancreatitis (enzymatic fat necrosis), not traumatic breast injury. C is
wrong because coagulative necrosis preserves tissue architecture in solid organs (heart, kidney, spleen)
and does not involve saponification. D is wrong because liquefactive necrosis occurs in the brain or
abscesses due to enzymatic digestion by neutrophils, not lipase-mediated fat breakdown.
Q5: A patient with Lynch syndrome (hereditary nonpolyposis colorectal cancer, HNPCC) develops
colorectal cancer at age 42. Which genetic mechanism is primarily responsible?
A. Activation of proto-oncogenes through chromosomal translocation
B. Loss of function in DNA mismatch repair (MMR) genes (MLH1, MSH2, MSH6, PMS2) leading to
microsatellite instability [CORRECT]
C. Germline mutation in the APC tumor suppressor gene causing chromosomal instability
D. Amplification of HER2/neu receptor leading to increased cell proliferation signaling
Correct Answer: B
Rationale: Lynch syndrome is caused by autosomal dominant mutations in DNA mismatch repair (MMR)
genes (MLH1, MSH2, MSH6, PMS2). Loss of MMR function results in failure to correct replication errors,
leading to microsatellite instability (MSI) and accumulation of mutations in oncogenes and tumor
suppressor genes. A is wrong because proto-oncogene activation through translocation is characteristic
of hematologic malignancies (e.g., Philadelphia chromosome in CML), not Lynch syndrome. C is wrong
because APC mutations cause familial adenomatous polyposis (FAP), a different hereditary colorectal
cancer syndrome with chromosomal instability. D is wrong because HER2 amplification is seen in breast
and gastric cancers, not in the MMR-deficient pathway of Lynch syndrome.
Q6: A tumor biopsy demonstrates cells with marked nuclear pleomorphism, hyperchromasia, high
nuclear-to-cytoplasmic ratio, and numerous mitotic figures including abnormal forms. These findings are
most consistent with:
, A. Benign neoplasm with well-differentiated cells resembling normal tissue
B. Low-grade malignancy with minimal nuclear atypia and rare mitoses
C. High-grade malignancy with poor differentiation and anaplastic features [CORRECT]
D. Reactive hyperplasia with increased cell proliferation but normal maturation
Correct Answer: C
Rationale: The described features—marked nuclear pleomorphism (variation in size and shape),
hyperchromasia (dark-staining nuclei), high nuclear-to-cytoplasmic ratio, and atypical mitotic figures—
are hallmarks of anaplasia, which indicates high-grade, poorly differentiated malignancy. These features
reflect genomic instability and loss of normal cellular regulatory mechanisms. A is wrong because benign
neoplasms show well-differentiated cells that closely resemble normal tissue with minimal atypia. B is
wrong because low-grade malignancies show only mild to moderate nuclear atypia with rare mitotic
figures. D is wrong because reactive hyperplasia maintains normal maturation patterns and does not
show the marked pleomorphism, hyperchromasia, or atypical mitoses characteristic of malignancy.
Q7: A 60-year-old man with hepatitis C cirrhosis develops hepatocellular carcinoma. Analysis reveals a
mutation in the TP53 tumor suppressor gene. What is the normal function of p53 that is lost in this
cancer?
A. Promotion of cell cycle progression from G1 to S phase by activating cyclin-dependent kinases
B. Initiation of DNA repair, cell cycle arrest at G1/S checkpoint, and activation of apoptosis in response
to DNA damage [CORRECT]
C. Inhibition of apoptosis by blocking caspase activation and cytochrome c release
D. Promotion of angiogenesis by upregulating vascular endothelial growth factor (VEGF)
Correct Answer: B
Rationale: The p53 protein, encoded by TP53, functions as the "guardian of the genome." In response to
DNA damage, p53 activates transcription of p21, causing G1/S cell cycle arrest to allow DNA repair; if
damage is irreparable, p53 triggers apoptosis via Bax upregulation and mitochondrial cytochrome c
release. Loss of p53 function allows cells with damaged DNA to proliferate. A is wrong because p53
inhibits, not promotes, cell cycle progression—it induces cell cycle arrest, whereas cyclin-CDK complexes
drive progression. C is wrong because p53 promotes, not inhibits, apoptosis through transcriptional
upregulation of pro-apoptotic Bcl-2 family members. D is wrong because p53 actually inhibits
angiogenesis by downregulating VEGF and upregulating thrombospondin-1; loss of p53 promotes
angiogenesis indirectly.
Q8: A patient with chronic renal failure has serum calcium of 7.2 mg/dL and phosphate of 6.8 mg/dL.
Metastatic calcification is noted in the lungs and gastric mucosa. What is the primary pathophysiologic
mechanism?
with Test Bank ACTUAL EXAM 2026/2027 | WGU
D115 Pathophysiology | Verified Q&A | Pass
Guaranteed - A+ Graded
SECTION 1: CELLULAR ADAPTATION, INJURY & NEOPLASIA (8 questions)
Q1: A 68-year-old male with a 40-pack-year smoking history presents with a chronic cough. Bronchial
biopsy reveals stratified squamous epithelium replacing the normal pseudostratified ciliated columnar
epithelium. Which cellular adaptation has occurred?
A. Hyperplasia, representing an increase in cell number due to chronic irritation
B. Hypertrophy, representing an increase in cell size in response to increased workload
C. Metaplasia, representing the reversible replacement of one differentiated cell type with another
better suited to withstand stress [CORRECT]
D. Dysplasia, representing disordered, neoplastic epithelial maturation
Correct Answer: C
Rationale: Metaplasia is the reversible replacement of one differentiated cell type by another mature
cell type better able to tolerate a particular stressor. In this case, chronic tobacco exposure causes the
normal respiratory pseudostratified ciliated columnar epithelium to be replaced by stratified squamous
epithelium, which is more resistant to chemical irritation but loses mucociliary clearance function. A is
wrong because hyperplasia involves increased cell number, not a change in cell type. B is wrong because
hypertrophy involves increased cell size, not epithelial transformation. D is wrong because dysplasia
represents disordered, pre-neoplastic maturation with nuclear atypia and loss of polarity, not a
reversible adaptive change to a different mature cell type.
Q2: A 45-year-old woman with chronic hypertension has left ventricular wall thickness of 14 mm
(normal <11 mm) on echocardiogram. The cardiomyocytes demonstrate increased organelle content
and protein synthesis. This represents which cellular adaptation?
A. Hyperplasia due to increased cardiomyocyte division in response to pressure overload
B. Hypertrophy due to increased synthesis of structural proteins and organelles [CORRECT]
,C. Atrophy due to decreased workload and reduced protein synthesis
D. Metaplasia due to replacement of cardiac muscle with fibrous tissue
Correct Answer: B
Rationale: Cardiac hypertrophy in response to chronic pressure overload (hypertension) occurs via
increased synthesis of contractile proteins (actin, myosin), mitochondria, and sarcoplasmic reticulum
within existing cardiomyocytes. Cardiac muscle cells are terminally differentiated and cannot undergo
hyperplasia. A is wrong because adult cardiomyocytes are terminally differentiated and cannot divide;
cardiac enlargement is never due to hyperplasia. C is wrong because atrophy involves decreased cell size
and protein synthesis, the opposite of what occurs in pressure overload. D is wrong because metaplasia
involves replacement of one differentiated cell type with another, not enlargement of existing muscle
cells.
Q3: A 55-year-old man presents with acute myocardial infarction. Histology of the infarcted tissue shows
cell swelling, loss of plasma membrane integrity, karyolysis, and intense inflammatory infiltration. Which
type of cell death is occurring?
A. Apoptosis, characterized by cell shrinkage, chromatin condensation, and formation of apoptotic
bodies without inflammation
B. Necrosis, characterized by ATP depletion, cell swelling, membrane rupture, and enzymatic digestion
with inflammation [CORRECT]
C. Autophagy, characterized by lysosomal degradation of cellular components for energy recycling
D. Pyroptosis, characterized by caspase-1 activation and pore formation in the plasma membrane
Correct Answer: B
Rationale: Myocardial infarction causes ischemic necrosis (coagulative necrosis) characterized by ATP
depletion, failure of ion pumps causing cell swelling, loss of plasma membrane integrity, karyolysis
(dissolution of nuclear chromatin), and intense neutrophilic infiltration due to release of intracellular
contents that trigger inflammation. A is wrong because apoptosis is energy-dependent, does not cause
inflammation, and shows cell shrinkage and chromatin condensation—not the swelling and karyolysis
described. C is wrong because autophagy is a regulated process of self-digestion for cellular
maintenance and does not produce the acute inflammatory response seen here. D is wrong because
pyroptosis is a programmed inflammatory cell death mediated by inflammasomes and gasdermin D pore
formation, typically in response to infection, not ischemic injury.
Q4: A 35-year-old woman develops fat necrosis in her breast after trauma. Histology reveals shadowy
outlines of dead adipocytes with basophilic calcium deposits. What is the underlying mechanism?
,A. Lipolysis by pancreatic lipases released into systemic circulation
B. Enzymatic digestion of triglycerides by tissue lipases with saponification and calcium deposition
[CORRECT]
C. Coagulative necrosis with preservation of tissue architecture followed by dystrophic calcification
D. Liquefactive necrosis with complete digestion of tissue by neutrophilic enzymes
Correct Answer: B
Rationale: Traumatic fat necrosis occurs when tissue lipases hydrolyze triglycerides in adipocytes into
fatty acids, which then combine with calcium to form insoluble calcium soaps (saponification), producing
the characteristic basophilic deposits and shadowy cell outlines. A is wrong because pancreatic lipase
release causes fat necrosis in acute pancreatitis (enzymatic fat necrosis), not traumatic breast injury. C is
wrong because coagulative necrosis preserves tissue architecture in solid organs (heart, kidney, spleen)
and does not involve saponification. D is wrong because liquefactive necrosis occurs in the brain or
abscesses due to enzymatic digestion by neutrophils, not lipase-mediated fat breakdown.
Q5: A patient with Lynch syndrome (hereditary nonpolyposis colorectal cancer, HNPCC) develops
colorectal cancer at age 42. Which genetic mechanism is primarily responsible?
A. Activation of proto-oncogenes through chromosomal translocation
B. Loss of function in DNA mismatch repair (MMR) genes (MLH1, MSH2, MSH6, PMS2) leading to
microsatellite instability [CORRECT]
C. Germline mutation in the APC tumor suppressor gene causing chromosomal instability
D. Amplification of HER2/neu receptor leading to increased cell proliferation signaling
Correct Answer: B
Rationale: Lynch syndrome is caused by autosomal dominant mutations in DNA mismatch repair (MMR)
genes (MLH1, MSH2, MSH6, PMS2). Loss of MMR function results in failure to correct replication errors,
leading to microsatellite instability (MSI) and accumulation of mutations in oncogenes and tumor
suppressor genes. A is wrong because proto-oncogene activation through translocation is characteristic
of hematologic malignancies (e.g., Philadelphia chromosome in CML), not Lynch syndrome. C is wrong
because APC mutations cause familial adenomatous polyposis (FAP), a different hereditary colorectal
cancer syndrome with chromosomal instability. D is wrong because HER2 amplification is seen in breast
and gastric cancers, not in the MMR-deficient pathway of Lynch syndrome.
Q6: A tumor biopsy demonstrates cells with marked nuclear pleomorphism, hyperchromasia, high
nuclear-to-cytoplasmic ratio, and numerous mitotic figures including abnormal forms. These findings are
most consistent with:
, A. Benign neoplasm with well-differentiated cells resembling normal tissue
B. Low-grade malignancy with minimal nuclear atypia and rare mitoses
C. High-grade malignancy with poor differentiation and anaplastic features [CORRECT]
D. Reactive hyperplasia with increased cell proliferation but normal maturation
Correct Answer: C
Rationale: The described features—marked nuclear pleomorphism (variation in size and shape),
hyperchromasia (dark-staining nuclei), high nuclear-to-cytoplasmic ratio, and atypical mitotic figures—
are hallmarks of anaplasia, which indicates high-grade, poorly differentiated malignancy. These features
reflect genomic instability and loss of normal cellular regulatory mechanisms. A is wrong because benign
neoplasms show well-differentiated cells that closely resemble normal tissue with minimal atypia. B is
wrong because low-grade malignancies show only mild to moderate nuclear atypia with rare mitotic
figures. D is wrong because reactive hyperplasia maintains normal maturation patterns and does not
show the marked pleomorphism, hyperchromasia, or atypical mitoses characteristic of malignancy.
Q7: A 60-year-old man with hepatitis C cirrhosis develops hepatocellular carcinoma. Analysis reveals a
mutation in the TP53 tumor suppressor gene. What is the normal function of p53 that is lost in this
cancer?
A. Promotion of cell cycle progression from G1 to S phase by activating cyclin-dependent kinases
B. Initiation of DNA repair, cell cycle arrest at G1/S checkpoint, and activation of apoptosis in response
to DNA damage [CORRECT]
C. Inhibition of apoptosis by blocking caspase activation and cytochrome c release
D. Promotion of angiogenesis by upregulating vascular endothelial growth factor (VEGF)
Correct Answer: B
Rationale: The p53 protein, encoded by TP53, functions as the "guardian of the genome." In response to
DNA damage, p53 activates transcription of p21, causing G1/S cell cycle arrest to allow DNA repair; if
damage is irreparable, p53 triggers apoptosis via Bax upregulation and mitochondrial cytochrome c
release. Loss of p53 function allows cells with damaged DNA to proliferate. A is wrong because p53
inhibits, not promotes, cell cycle progression—it induces cell cycle arrest, whereas cyclin-CDK complexes
drive progression. C is wrong because p53 promotes, not inhibits, apoptosis through transcriptional
upregulation of pro-apoptotic Bcl-2 family members. D is wrong because p53 actually inhibits
angiogenesis by downregulating VEGF and upregulating thrombospondin-1; loss of p53 promotes
angiogenesis indirectly.
Q8: A patient with chronic renal failure has serum calcium of 7.2 mg/dL and phosphate of 6.8 mg/dL.
Metastatic calcification is noted in the lungs and gastric mucosa. What is the primary pathophysiologic
mechanism?
