WESTERN GOVERNORS UNIVERSITY | ADVANCED PATHOPHYSIOLOGY
D115 OA PREP TEST BANK
Comprehensive objective assessment preparation covering cellular biology, fluid and electrolyte balance, immune
and inflammatory disorders, cardiovascular and respiratory pathophysiology, renal and endocrine dysfunction,
neurologic and musculoskeletal disorders, and gastrointestinal and reproductive pathophysiology aligned with
WGU D115 course competencies for 2026-2027.
150 Questions | 7 Sections | Verified Correct Answers with Rationales
Graded A+ | Newest Version 2026/2027
, D115 OA / WGU D115 OA PREP TEST BANK 2026/2027
WITH REAL EXAM QUESTIONS AND CORRECT ANSWERS WITH RATIONALES | WGU D115 ADVANCED PATHOPHYSIOLOGY OA PREP
SECTION 1: CELLULAR BIOLOGY AND ADAPTATION (Cell Injury, Adaptation, Death, Neoplasia,
Genetics)
Q1:
A 68-year-old patient has been immobilized in a long leg cast for 6 weeks following a femoral fracture. The orthopedic surgeon
notes significant decrease in muscle mass of the affected leg. Which cellular adaptation best describes this finding?
A. Hypertrophy
B. Hyperplasia
C. Atrophy **[CORRECT]**
D. Metaplasia
Correct Answer: C
Rationale: Atrophy is a decrease in cell size and/or number due to reduced workload, disuse, or inadequate blood supply. Immobilization leads to
disuse atrophy of skeletal muscle as cells reduce protein synthesis and increase proteolysis. Hypertrophy is an increase in cell size (not decrease),
hyperplasia is an increase in cell number, and metaplasia is a reversible change from one mature cell type to another (McCance & Huether).
Q2:
A 55-year-old man with long-standing, poorly controlled hypertension presents with shortness of breath. An echocardiogram
reveals thickening of the left ventricular wall without chamber dilation. Which cellular adaptation has occurred in the
myocardium?
A. Physiologic hypertrophy
B. Pathologic hypertrophy **[CORRECT]**
C. Hyperplasia
D. Atrophy
Correct Answer: B
Rationale: The left ventricular wall thickening (concentric hypertrophy) in response to chronic pressure overload from hypertension is pathologic
hypertrophy. Unlike physiologic hypertrophy (e.g., in an athlete's heart from increased demand), pathologic hypertrophy results from abnormal
stressors and can progress to heart failure. Hyperplasia is an increase in cell number, not relevant to cardiac myocytes which have limited
capacity to divide. Atrophy would be a decrease in cell size (McCance & Huether).
Q3:
Which statement correctly distinguishes hyperplasia from hypertrophy?
A. Hyperplasia increases cell size; hypertrophy increases cell number
B. Hyperplasia increases cell number; hypertrophy increases cell size **[CORRECT]**
C. Both hyperplasia and hypertrophy require cells capable of mitosis
D. Hypertrophy only occurs in response to hormonal stimulation
Correct Answer: B
Rationale: Hyperplasia is an increase in the number of cells, while hypertrophy is an increase in the size of individual cells. Both can occur
together (e.g., breast tissue during pregnancy). Importantly, hypertrophy can occur in tissues with limited or no mitotic capacity (e.g., cardiac
muscle, skeletal muscle), whereas hyperplasia requires cells capable of mitosis (e.g., glandular epithelium, skin). Option C is wrong because
hypertrophy does not require mitotic capability. Option D is wrong because hypertrophy occurs in response to various stimuli, not just hormonal
(McCance & Huether).
Q4:
A 52-year-old woman with a 30-pack-year smoking history has a bronchoscopy that reveals replacement of the normal ciliated
columnar epithelium in the large airways by stratified squamous epithelium. This cellular change is best described as:
A. Dysplasia
B. Anaplasia
C. Metaplasia **[CORRECT]**
D. Hyperplasia
Correct Answer: C
Rationale: Metaplasia is the reversible replacement of one mature cell type by another, often as an adaptive response to chronic irritation.
Smoking causes columnar epithelium to transform to stratified squamous epithelium, which is more resistant to injury but lacks mucociliary
function. Dysplasia refers to abnormal maturation and shape of cells (a pre-neoplastic change). Anaplasia refers to undifferentiated, pleomorphic
cells seen in malignancy. Hyperplasia is an increase in cell number (McCance & Huether).
Q5:
A 38-year-old woman undergoes a routine Pap smear, which reveals cells with nuclear enlargement, hyperchromasia, and
irregular nuclear membranes. Biopsy confirms cervical intraepithelial neoplasia (CIN) III. The pathologist notes this is still a
reversible change if the causative agent is removed. Which cellular adaptation is this?
A. Metaplasia
B. Dysplasia **[CORRECT]**
C. Anaplasia
D. Atrophy
D115 OA Prep 2026/2027 | Page 2
,Correct Answer: B
Rationale: Dysplasia is characterized by deranged cell growth of a specific tissue, resulting in cells that vary in size, shape, and organization. It is
considered a pre-neoplastic change but can be reversible if the inciting stimulus (e.g., HPV infection) is removed. CIN III represents severe
dysplasia. Anaplasia refers to the loss of cellular differentiation seen in malignant neoplasms and is not reversible. Metaplasia is a change in cell
type, not the disordered growth seen here (McCance & Huether).
Q6:
A 45-year-old man presents with severe crushing chest pain. Coronary angiography reveals complete occlusion of the left anterior
descending artery. During the first 20 minutes of ischemia, myocardial cells experience decreased ATP production but maintain
plasma membrane integrity. Which phase of cell injury is this?
A. Irreversible injury, because coronary occlusion always causes necrosis
B. Reversible injury, because membrane integrity is maintained **[CORRECT]**
C. Apoptosis, because caspase enzymes are being activated
D. Necrosis, because the cell has lost the ability to generate ATP
Correct Answer: B
Rationale: In reversible cell injury, cells can recover if the injurious stimulus is removed. The key hallmarks are reduced ATP, cellular swelling,
and blebbing, but the plasma membrane remains intact. Membrane integrity is the critical dividing line: once the membrane is irreversibly
damaged, the injury becomes irreversible. Apoptosis is an active, programmed process, not the passive consequence of ischemia. While ATP is
depleted, the cell has not yet crossed the point of no return (McCance & Huether).
Q7:
Which of the following is the most characteristic ultrastructural finding of reversible cell injury?
A. Nuclear pyknosis and karyorrhexis
B. Mitochondrial swelling and plasma membrane blebbing **[CORRECT]**
C. Extensive calcium influx into the cytoplasm
D. DNA fragmentation into ladder-like bands
Correct Answer: B
Rationale: Mitochondrial swelling and plasma membrane blebbing are classic features of reversible cell injury. The mitochondria swell because of
impaired oxidative phosphorylation and calcium accumulation, while the cell membrane develops blebs from cytoskeletal damage. Nuclear
pyknosis and karyorrhexis are features of necrosis (irreversible injury). Extensive calcium influx is a mechanism that pushes cells from reversible
to irreversible injury. DNA ladder formation is characteristic of apoptosis (McCance & Huether).
Q8:
A 60-year-old woman has been on high-dose acetaminophen for chronic pain. She develops acute liver failure. Hepatocyte death
in this patient is characterized by loss of plasma membrane integrity, cellular swelling, and nuclear dissolution. Which type of
cell death has occurred?
A. Apoptosis
B. Necrosis **[CORRECT]**
C. Autophagy
D. Necroptosis
Correct Answer: B
Rationale: Necrosis is characterized by loss of plasma membrane integrity, cellular swelling (oncosis), and nuclear changes including pyknosis,
karyorrhexis, and karyolysis (nuclear dissolution). Acetaminophen overdose causes centrilobular hepatic necrosis through its toxic metabolite
NAPQI. Apoptosis, in contrast, involves cell shrinkage, membrane blebbing without loss of integrity, and chromatin condensation. Autophagy is a
survival mechanism. Necroptosis is a regulated form of necrosis but the clinical description here points to classic necrosis (McCance & Huether).
Q9:
A researcher is studying a pathway of programmed cell death that requires ATP, involves cytochrome c release from
mitochondria, and produces cells that shrink and fragment into apoptotic bodies phagocytosed by macrophages. Which process
is being studied?
A. Necrosis
B. Apoptosis **[CORRECT]**
C. Coagulative necrosis
D. Liquefactive necrosis
Correct Answer: B
Rationale: Apoptosis is an energy (ATP)-dependent, tightly regulated process of programmed cell death. Key features include cytochrome c release
from mitochondria, activation of caspases, cell shrinkage, chromatin condensation, formation of apoptotic bodies, and phagocytosis by
macrophages without eliciting inflammation. Necrosis is a passive, energy-independent process that causes inflammation. Coagulative and
liquefactive necrosis are morphologic patterns of necrosis, not distinct death pathways (McCance & Huether).
Q10:
A patient suffers prolonged intestinal ischemia. Biopsy of the affected bowel reveals cells with severely swollen endoplasmic
reticulum, detached ribosomes, large mitochondrial amorphous densities, and numerous membrane blebs that have ruptured.
What does the presence of ruptured membrane blebs indicate?
A. The cell injury is still reversible
B. The cell injury has progressed to the irreversible stage **[CORRECT]**
C. Apoptosis has been initiated
D. The cell is undergoing autophagy as a protective response
D115 OA Prep 2026/2027 | Page 3
, Correct Answer: B
Rationale: Ruptured membrane blebs indicate that the plasma membrane integrity has been lost, marking the transition from reversible to
irreversible cell injury. While bleb formation occurs in reversible injury, bleb rupture is a critical event that allows uncontrolled calcium influx,
activation of degradative enzymes, and ultimately cell death. Severe mitochondrial damage with amorphous densities is also a hallmark of
irreversible injury. Once membrane integrity is lost, the cell cannot recover (McCance & Huether).
Q11:
Which of the following correctly differentiates necrosis from apoptosis?
A. Necrosis is energy-dependent and apoptosis is energy-independent
B. Necrosis requires ATP and apoptosis does not
C. Apoptosis is energy-dependent and does not elicit inflammation; necrosis is energy-independent and elicits inflammation
**[CORRECT]**
D. Both necrosis and apoptosis are energy-dependent processes
Correct Answer: C
Rationale: Apoptosis is an active, energy (ATP)-dependent process that does not elicit an inflammatory response because apoptotic cells are
phagocytosed before releasing intracellular contents. Necrosis is a passive, energy-independent process caused by overwhelming injury that leads
to membrane rupture, release of cellular contents, and subsequent inflammation. This distinction is fundamental: active/programmed (apoptosis)
vs. passive/accidental (necrosis) (McCance & Huether).
Q12:
A 62-year-old man dies of an acute myocardial infarction. Autopsy of the heart reveals a well-demarcated area in the left ventricle
that is firm, pale yellow, and shows coagulative necrosis microscopically with preserved cell outlines. Which type of necrosis is
this?
A. Liquefactive necrosis
B. Caseous necrosis
C. Coagulative necrosis **[CORRECT]**
D. Fat necrosis
Correct Answer: C
Rationale: Coagulative necrosis is the most common pattern of necrosis and is typically seen in hypoxic/ischemic injury to all tissues except the
brain. The architecture of dead tissue is preserved because protein denaturation (coagulation) occurs before enzymatic lysis. The heart is a classic
site. Liquefactive necrosis is seen in brain infarcts and bacterial infections. Caseous necrosis is characteristic of tuberculosis. Fat necrosis occurs
in pancreatic disease (McCance & Huether).
Q13:
A 70-year-old man presents with sudden onset right-sided weakness. CT scan shows an infarct in the left middle cerebral artery
territory. If a biopsy were obtained, which type of necrosis would most likely be found in the affected brain tissue?
A. Coagulative necrosis
B. Liquefactive necrosis **[CORRECT]**
C. Caseous necrosis
D. Gangrenous necrosis
Correct Answer: B
Rationale: The brain is the major exception to coagulative necrosis in ischemic injury. Brain infarcts undergo liquefactive necrosis because the
brain is rich in lipids and has limited connective tissue scaffolding. Enzymatic lysis of the dead tissue transforms it into a soft, liquid mass that is
eventually phagocytosed and forms a cystic cavity. Coagulative necrosis occurs in most other solid organs (heart, kidney, spleen). Caseous necrosis
is seen in tuberculosis, and gangrene involves necrosis with bacterial putrefaction (McCance & Huether).
Q14:
A pathologist examines a tissue specimen and notes that the dead cells have been completely digested, creating a soft, viscus
mass. No preserved cell outlines are visible. Surrounding the area is a prominent inflammatory infiltrate. Which type of necrosis
is most consistent with these findings?
A. Coagulative necrosis
B. Liquefactive necrosis **[CORRECT]**
C. Fat necrosis
D. Fibrinoid necrosis
Correct Answer: B
Rationale: Liquefactive necrosis is characterized by complete digestion of dead cells, resulting in a soft, liquid mass with no preserved tissue
architecture. It is typically caused by bacterial infections (where neutrophils release hydrolytic enzymes) or occurs in brain infarcts. The
prominent inflammatory infiltrate is consistent with enzymatic tissue digestion. Coagulative necrosis preserves cell outlines. Fat necrosis shows
saponification of fat into chalky deposits. Fibrinoid necrosis involves deposition of fibrin-like material in vessel walls (McCance & Huether).
Q15:
During ischemia-reperfusion injury, the return of blood flow paradoxically causes additional tissue damage. Which mechanism
best explains this phenomenon?
A. Sudden increase in ATP production overwhelms the cell
B. Reoxygenation generates a burst of reactive oxygen species that damage cell membranes **[CORRECT]**
C. Reperfusion causes immediate apoptosis through caspase-independent pathways
D. Sudden restoration of oxygen causes vasoconstriction and worsens ischemia
Correct Answer: B
D115 OA Prep 2026/2027 | Page 4
D115 OA PREP TEST BANK
Comprehensive objective assessment preparation covering cellular biology, fluid and electrolyte balance, immune
and inflammatory disorders, cardiovascular and respiratory pathophysiology, renal and endocrine dysfunction,
neurologic and musculoskeletal disorders, and gastrointestinal and reproductive pathophysiology aligned with
WGU D115 course competencies for 2026-2027.
150 Questions | 7 Sections | Verified Correct Answers with Rationales
Graded A+ | Newest Version 2026/2027
, D115 OA / WGU D115 OA PREP TEST BANK 2026/2027
WITH REAL EXAM QUESTIONS AND CORRECT ANSWERS WITH RATIONALES | WGU D115 ADVANCED PATHOPHYSIOLOGY OA PREP
SECTION 1: CELLULAR BIOLOGY AND ADAPTATION (Cell Injury, Adaptation, Death, Neoplasia,
Genetics)
Q1:
A 68-year-old patient has been immobilized in a long leg cast for 6 weeks following a femoral fracture. The orthopedic surgeon
notes significant decrease in muscle mass of the affected leg. Which cellular adaptation best describes this finding?
A. Hypertrophy
B. Hyperplasia
C. Atrophy **[CORRECT]**
D. Metaplasia
Correct Answer: C
Rationale: Atrophy is a decrease in cell size and/or number due to reduced workload, disuse, or inadequate blood supply. Immobilization leads to
disuse atrophy of skeletal muscle as cells reduce protein synthesis and increase proteolysis. Hypertrophy is an increase in cell size (not decrease),
hyperplasia is an increase in cell number, and metaplasia is a reversible change from one mature cell type to another (McCance & Huether).
Q2:
A 55-year-old man with long-standing, poorly controlled hypertension presents with shortness of breath. An echocardiogram
reveals thickening of the left ventricular wall without chamber dilation. Which cellular adaptation has occurred in the
myocardium?
A. Physiologic hypertrophy
B. Pathologic hypertrophy **[CORRECT]**
C. Hyperplasia
D. Atrophy
Correct Answer: B
Rationale: The left ventricular wall thickening (concentric hypertrophy) in response to chronic pressure overload from hypertension is pathologic
hypertrophy. Unlike physiologic hypertrophy (e.g., in an athlete's heart from increased demand), pathologic hypertrophy results from abnormal
stressors and can progress to heart failure. Hyperplasia is an increase in cell number, not relevant to cardiac myocytes which have limited
capacity to divide. Atrophy would be a decrease in cell size (McCance & Huether).
Q3:
Which statement correctly distinguishes hyperplasia from hypertrophy?
A. Hyperplasia increases cell size; hypertrophy increases cell number
B. Hyperplasia increases cell number; hypertrophy increases cell size **[CORRECT]**
C. Both hyperplasia and hypertrophy require cells capable of mitosis
D. Hypertrophy only occurs in response to hormonal stimulation
Correct Answer: B
Rationale: Hyperplasia is an increase in the number of cells, while hypertrophy is an increase in the size of individual cells. Both can occur
together (e.g., breast tissue during pregnancy). Importantly, hypertrophy can occur in tissues with limited or no mitotic capacity (e.g., cardiac
muscle, skeletal muscle), whereas hyperplasia requires cells capable of mitosis (e.g., glandular epithelium, skin). Option C is wrong because
hypertrophy does not require mitotic capability. Option D is wrong because hypertrophy occurs in response to various stimuli, not just hormonal
(McCance & Huether).
Q4:
A 52-year-old woman with a 30-pack-year smoking history has a bronchoscopy that reveals replacement of the normal ciliated
columnar epithelium in the large airways by stratified squamous epithelium. This cellular change is best described as:
A. Dysplasia
B. Anaplasia
C. Metaplasia **[CORRECT]**
D. Hyperplasia
Correct Answer: C
Rationale: Metaplasia is the reversible replacement of one mature cell type by another, often as an adaptive response to chronic irritation.
Smoking causes columnar epithelium to transform to stratified squamous epithelium, which is more resistant to injury but lacks mucociliary
function. Dysplasia refers to abnormal maturation and shape of cells (a pre-neoplastic change). Anaplasia refers to undifferentiated, pleomorphic
cells seen in malignancy. Hyperplasia is an increase in cell number (McCance & Huether).
Q5:
A 38-year-old woman undergoes a routine Pap smear, which reveals cells with nuclear enlargement, hyperchromasia, and
irregular nuclear membranes. Biopsy confirms cervical intraepithelial neoplasia (CIN) III. The pathologist notes this is still a
reversible change if the causative agent is removed. Which cellular adaptation is this?
A. Metaplasia
B. Dysplasia **[CORRECT]**
C. Anaplasia
D. Atrophy
D115 OA Prep 2026/2027 | Page 2
,Correct Answer: B
Rationale: Dysplasia is characterized by deranged cell growth of a specific tissue, resulting in cells that vary in size, shape, and organization. It is
considered a pre-neoplastic change but can be reversible if the inciting stimulus (e.g., HPV infection) is removed. CIN III represents severe
dysplasia. Anaplasia refers to the loss of cellular differentiation seen in malignant neoplasms and is not reversible. Metaplasia is a change in cell
type, not the disordered growth seen here (McCance & Huether).
Q6:
A 45-year-old man presents with severe crushing chest pain. Coronary angiography reveals complete occlusion of the left anterior
descending artery. During the first 20 minutes of ischemia, myocardial cells experience decreased ATP production but maintain
plasma membrane integrity. Which phase of cell injury is this?
A. Irreversible injury, because coronary occlusion always causes necrosis
B. Reversible injury, because membrane integrity is maintained **[CORRECT]**
C. Apoptosis, because caspase enzymes are being activated
D. Necrosis, because the cell has lost the ability to generate ATP
Correct Answer: B
Rationale: In reversible cell injury, cells can recover if the injurious stimulus is removed. The key hallmarks are reduced ATP, cellular swelling,
and blebbing, but the plasma membrane remains intact. Membrane integrity is the critical dividing line: once the membrane is irreversibly
damaged, the injury becomes irreversible. Apoptosis is an active, programmed process, not the passive consequence of ischemia. While ATP is
depleted, the cell has not yet crossed the point of no return (McCance & Huether).
Q7:
Which of the following is the most characteristic ultrastructural finding of reversible cell injury?
A. Nuclear pyknosis and karyorrhexis
B. Mitochondrial swelling and plasma membrane blebbing **[CORRECT]**
C. Extensive calcium influx into the cytoplasm
D. DNA fragmentation into ladder-like bands
Correct Answer: B
Rationale: Mitochondrial swelling and plasma membrane blebbing are classic features of reversible cell injury. The mitochondria swell because of
impaired oxidative phosphorylation and calcium accumulation, while the cell membrane develops blebs from cytoskeletal damage. Nuclear
pyknosis and karyorrhexis are features of necrosis (irreversible injury). Extensive calcium influx is a mechanism that pushes cells from reversible
to irreversible injury. DNA ladder formation is characteristic of apoptosis (McCance & Huether).
Q8:
A 60-year-old woman has been on high-dose acetaminophen for chronic pain. She develops acute liver failure. Hepatocyte death
in this patient is characterized by loss of plasma membrane integrity, cellular swelling, and nuclear dissolution. Which type of
cell death has occurred?
A. Apoptosis
B. Necrosis **[CORRECT]**
C. Autophagy
D. Necroptosis
Correct Answer: B
Rationale: Necrosis is characterized by loss of plasma membrane integrity, cellular swelling (oncosis), and nuclear changes including pyknosis,
karyorrhexis, and karyolysis (nuclear dissolution). Acetaminophen overdose causes centrilobular hepatic necrosis through its toxic metabolite
NAPQI. Apoptosis, in contrast, involves cell shrinkage, membrane blebbing without loss of integrity, and chromatin condensation. Autophagy is a
survival mechanism. Necroptosis is a regulated form of necrosis but the clinical description here points to classic necrosis (McCance & Huether).
Q9:
A researcher is studying a pathway of programmed cell death that requires ATP, involves cytochrome c release from
mitochondria, and produces cells that shrink and fragment into apoptotic bodies phagocytosed by macrophages. Which process
is being studied?
A. Necrosis
B. Apoptosis **[CORRECT]**
C. Coagulative necrosis
D. Liquefactive necrosis
Correct Answer: B
Rationale: Apoptosis is an energy (ATP)-dependent, tightly regulated process of programmed cell death. Key features include cytochrome c release
from mitochondria, activation of caspases, cell shrinkage, chromatin condensation, formation of apoptotic bodies, and phagocytosis by
macrophages without eliciting inflammation. Necrosis is a passive, energy-independent process that causes inflammation. Coagulative and
liquefactive necrosis are morphologic patterns of necrosis, not distinct death pathways (McCance & Huether).
Q10:
A patient suffers prolonged intestinal ischemia. Biopsy of the affected bowel reveals cells with severely swollen endoplasmic
reticulum, detached ribosomes, large mitochondrial amorphous densities, and numerous membrane blebs that have ruptured.
What does the presence of ruptured membrane blebs indicate?
A. The cell injury is still reversible
B. The cell injury has progressed to the irreversible stage **[CORRECT]**
C. Apoptosis has been initiated
D. The cell is undergoing autophagy as a protective response
D115 OA Prep 2026/2027 | Page 3
, Correct Answer: B
Rationale: Ruptured membrane blebs indicate that the plasma membrane integrity has been lost, marking the transition from reversible to
irreversible cell injury. While bleb formation occurs in reversible injury, bleb rupture is a critical event that allows uncontrolled calcium influx,
activation of degradative enzymes, and ultimately cell death. Severe mitochondrial damage with amorphous densities is also a hallmark of
irreversible injury. Once membrane integrity is lost, the cell cannot recover (McCance & Huether).
Q11:
Which of the following correctly differentiates necrosis from apoptosis?
A. Necrosis is energy-dependent and apoptosis is energy-independent
B. Necrosis requires ATP and apoptosis does not
C. Apoptosis is energy-dependent and does not elicit inflammation; necrosis is energy-independent and elicits inflammation
**[CORRECT]**
D. Both necrosis and apoptosis are energy-dependent processes
Correct Answer: C
Rationale: Apoptosis is an active, energy (ATP)-dependent process that does not elicit an inflammatory response because apoptotic cells are
phagocytosed before releasing intracellular contents. Necrosis is a passive, energy-independent process caused by overwhelming injury that leads
to membrane rupture, release of cellular contents, and subsequent inflammation. This distinction is fundamental: active/programmed (apoptosis)
vs. passive/accidental (necrosis) (McCance & Huether).
Q12:
A 62-year-old man dies of an acute myocardial infarction. Autopsy of the heart reveals a well-demarcated area in the left ventricle
that is firm, pale yellow, and shows coagulative necrosis microscopically with preserved cell outlines. Which type of necrosis is
this?
A. Liquefactive necrosis
B. Caseous necrosis
C. Coagulative necrosis **[CORRECT]**
D. Fat necrosis
Correct Answer: C
Rationale: Coagulative necrosis is the most common pattern of necrosis and is typically seen in hypoxic/ischemic injury to all tissues except the
brain. The architecture of dead tissue is preserved because protein denaturation (coagulation) occurs before enzymatic lysis. The heart is a classic
site. Liquefactive necrosis is seen in brain infarcts and bacterial infections. Caseous necrosis is characteristic of tuberculosis. Fat necrosis occurs
in pancreatic disease (McCance & Huether).
Q13:
A 70-year-old man presents with sudden onset right-sided weakness. CT scan shows an infarct in the left middle cerebral artery
territory. If a biopsy were obtained, which type of necrosis would most likely be found in the affected brain tissue?
A. Coagulative necrosis
B. Liquefactive necrosis **[CORRECT]**
C. Caseous necrosis
D. Gangrenous necrosis
Correct Answer: B
Rationale: The brain is the major exception to coagulative necrosis in ischemic injury. Brain infarcts undergo liquefactive necrosis because the
brain is rich in lipids and has limited connective tissue scaffolding. Enzymatic lysis of the dead tissue transforms it into a soft, liquid mass that is
eventually phagocytosed and forms a cystic cavity. Coagulative necrosis occurs in most other solid organs (heart, kidney, spleen). Caseous necrosis
is seen in tuberculosis, and gangrene involves necrosis with bacterial putrefaction (McCance & Huether).
Q14:
A pathologist examines a tissue specimen and notes that the dead cells have been completely digested, creating a soft, viscus
mass. No preserved cell outlines are visible. Surrounding the area is a prominent inflammatory infiltrate. Which type of necrosis
is most consistent with these findings?
A. Coagulative necrosis
B. Liquefactive necrosis **[CORRECT]**
C. Fat necrosis
D. Fibrinoid necrosis
Correct Answer: B
Rationale: Liquefactive necrosis is characterized by complete digestion of dead cells, resulting in a soft, liquid mass with no preserved tissue
architecture. It is typically caused by bacterial infections (where neutrophils release hydrolytic enzymes) or occurs in brain infarcts. The
prominent inflammatory infiltrate is consistent with enzymatic tissue digestion. Coagulative necrosis preserves cell outlines. Fat necrosis shows
saponification of fat into chalky deposits. Fibrinoid necrosis involves deposition of fibrin-like material in vessel walls (McCance & Huether).
Q15:
During ischemia-reperfusion injury, the return of blood flow paradoxically causes additional tissue damage. Which mechanism
best explains this phenomenon?
A. Sudden increase in ATP production overwhelms the cell
B. Reoxygenation generates a burst of reactive oxygen species that damage cell membranes **[CORRECT]**
C. Reperfusion causes immediate apoptosis through caspase-independent pathways
D. Sudden restoration of oxygen causes vasoconstriction and worsens ischemia
Correct Answer: B
D115 OA Prep 2026/2027 | Page 4
