, NUR 6220 PATHO FINAL EXAM AND PRACTICE EXAM
NEWEST 2026 TEST BANK| COMPLETE 300 REAL EXAM
QUESTIONS AND CORRECT VERIFIED ANSWERS/
ALREADY GRADED A+| NUR 6220 PATHO FINAL EXAM
PREP (MOST RECENT!!) — 300 Questions
Section 1: Cellular Adaptation and Injury (Questions 1-30)
1 A researcher investigates a novel compound that inhibits the mammalian target of rapamycin (mTOR) complex
1. In a mouse model of cardiac pressure overload, the compound prevents the expected increase in
cardiomyocyte size and reduces the expression of atrial natriuretic peptide (ANP). Which cellular adaptation is
being prevented?
A) Hyperplasia
B) Hypertrophy
C) Metaplasia
D) Dysplasia
Answer: B
Rationale: Cardiac pressure overload typically induces cardiomyocyte hypertrophy (increase in cell size), which is
mediated by mTORC1 signaling. The observed decrease in cell size and ANP expression confirms that hypertrophy
is blocked. Hyperplasia (increase in cell number) does not occur in adult cardiomyocytes. Metaplasia and dysplasia
involve changes in cell type or atypical growth, not size increase.
2 A biopsy from a patient with chronic gastroesophageal reflux disease shows replacement of stratified squamous
epithelium with columnar epithelium. This change is best described as:
A) Anaplasia
B) Dysplasia
C) Metaplasia
D) Hyperplasia
Answer: C
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with another, often in response to
chronic irritation. Here, squamous epithelium is replaced by columnar (Barrett esophagus). Anaplasia refers to loss
of differentiation in malignancy; dysplasia is disordered growth; hyperplasia is increased cell number.
3 In a cell undergoing ischemic injury, which of the following events occurs earliest and is most directly linked to
the failure of the Na+/K+ ATPase?
A) Swelling of the endoplasmic reticulum
B) Formation of blebs on the plasma membrane
C) Loss of microvilli
D) Cellular swelling
Answer: D
Rationale: Ischemia rapidly depletes ATP, impairing the Na+/K+ ATPase. Sodium and water accumulate
intracellularly, causing cellular swelling (hydropic change), the earliest manifestation of reversible injury. ER
swelling and bleb formation occur later. Loss of microvilli is also a later change.
,4 A drug induces mitochondrial permeability transition pore (MPTP) opening. This event is most likely to lead to:
A) Apoptosis via the extrinsic pathway
B) Necrosis due to ATP depletion
C) Autophagy
D) Ferroptosis
Answer: B
Rationale: Sustained MPTP opening collapses the mitochondrial membrane potential, halting oxidative
phosphorylation and causing ATP depletion. If ATP falls below critical levels, necrosis ensues due to failure of ion
pumps and membrane integrity. Apoptosis requires ATP; MPTP opening can trigger apoptosis if limited, but with
full opening, necrosis dominates. Autophagy is a survival mechanism; ferroptosis is iron-dependent and not
directly linked to MPTP.
5 A pathologist notes that cells in a tissue section have shrunken cytoplasm, condensed chromatin, and intact
organelles without inflammation. Which type of cell death is most likely?
A) Necrosis
B) Necroptosis
C) Apoptosis
D) Autophagy
Answer: C
Rationale: Apoptosis is characterized by cell shrinkage, chromatin condensation (pyknosis), and preservation of
organelle structure, with no inflammatory response due to rapid phagocytosis. Necrosis involves cell swelling,
membrane rupture, and inflammation. Necroptosis is a regulated form of necrosis that also causes inflammation.
Autophagy involves cytoplasmic vacuolization and digestion of organelles.
6 Which of the following best explains why cells in the center of a solid tumor often undergo necrosis despite
adequate blood supply?
A) High levels of lactate inhibit glycolytic enzymes
B) Activation of the unfolded protein response (UPR) triggers apoptosis
C ) H y p o x i a - i n d u c i b l e f a c t o r 1 ± ( H I F - 1 ± ) p r
D) Oncogene-induced senescence prevents cell division
Answer: B
Rationale: Tumor cells experience ER stress due to hypoxia and nutrient deprivation, leading to UPR activation.
Prolonged UPR shifts from survival to apoptosis, causing cell death. Lactate accumulation does not directly cause
n e c r o s i s ; H I F - 1 ± p r o m o t e s a n g i o g e n e s i s a n d
necrosis.
7 A patient with acetaminophen overdose develops centrilobular hepatic necrosis. The primary mechanism of
injury is:
A) Direct binding of acetaminophen to cytochrome P450 enzymes
B) Formation of a reactive metabolite that depletes glutathione
C) Inhibition of mitochondrial complex I
D) Activation of caspase-8
Answer: B
Rationale: Acetaminophen is metabolized by CYP2E1 to NAPQI, a reactive metabolite that depletes glutathione.
When glutathione is exhausted, NAPQI binds to cellular proteins, causing oxidative stress and necrosis. Direct
enzyme binding is not the primary mechanism; mitochondrial inhibition is secondary. Caspase-8 is involved in
extrinsic apoptosis, not the primary injury here.
, 8 A genetic mutation causes defective autophagy in neurons. Which of the following is the most likely
consequence?
A) Increased susceptibility to viral infections
B) Accumulation of ubiquitinated protein aggregates
C) Enhanced clearance of damaged mitochondria
D) Reduced apoptosis
Answer: B
Rationale: Autophagy degrades damaged organelles and protein aggregates. Defective autophagy leads to
accumulation of ubiquitinated proteins and p62-positive inclusions, as seen in neurodegenerative diseases like
Alzheimer's. Autophagy also contributes to pathogen clearance, but the primary neuronal consequence is protein
aggregate accumulation. Enhanced mitophagy would require functional autophagy; reduced apoptosis is not a
direct effect.
9 A researcher treats cultured hepatocytes with a high dose of iron and a glutathione synthesis inhibitor. Cell
death occurs that is prevented by ferrostatin-1 but not by Z-VAD-FMK (a pan-caspase inhibitor). This cell death
is most consistent with:
A) Apoptosis
B) Necroptosis
C) Ferroptosis
D) Pyroptosis
Answer: C
Rationale: Ferroptosis is an iron-dependent, non-apoptotic cell death characterized by lipid peroxidation. It is
inhibited by ferrostatin-1 (a lipophilic antioxidant) and not by caspase inhibitors. Apoptosis is caspase-dependent;
necroptosis requires RIPK1/RIPK3 and is not iron-dependent; pyroptosis involves caspase-1 and inflammasomes.
10 In a patient with chronic kidney disease, tubular epithelial cells show flattened morphology and decreased
metabolic activity. This adaptation is best classified as:
A) Atrophy
B) Hypoplasia
C) Metaplasia
D) Dysplasia
Answer: A
Rationale: Atrophy is a decrease in cell size and function due to reduced workload, blood supply, or nutrition. In
chronic kidney disease, tubular cells atrophy due to sustained ischemia and uremic toxins. Hypoplasia refers to
reduced cell number during development, not acquired. Metaplasia and dysplasia involve changes in cell type or
atypical growth, not simply reduced size/activity.
11 A researcher is studying the effects of chronic hypoxia on cardiac myocytes. Which adaptive cellular change is
most likely to be observed in the myocytes under sustained low oxygen tension?
A) Hyperplasia with increased cell number
B) Atrophy due to decreased workload
C) Metaplasia from cardiac to skeletal muscle phenotype
D) Hypertrophy with increased cell size and protein synthesis
Answer: D
Rationale: Chronic hypoxia imposes increased workload on cardiac myocytes to maintain cardiac output, leading to
compensatory hypertrophy (increase in cell size) rather than hyperplasia (cells are terminally differentiated).
Atrophy occurs with decreased workload, not increased. Metaplasia is a reversible change from one differentiated
NEWEST 2026 TEST BANK| COMPLETE 300 REAL EXAM
QUESTIONS AND CORRECT VERIFIED ANSWERS/
ALREADY GRADED A+| NUR 6220 PATHO FINAL EXAM
PREP (MOST RECENT!!) — 300 Questions
Section 1: Cellular Adaptation and Injury (Questions 1-30)
1 A researcher investigates a novel compound that inhibits the mammalian target of rapamycin (mTOR) complex
1. In a mouse model of cardiac pressure overload, the compound prevents the expected increase in
cardiomyocyte size and reduces the expression of atrial natriuretic peptide (ANP). Which cellular adaptation is
being prevented?
A) Hyperplasia
B) Hypertrophy
C) Metaplasia
D) Dysplasia
Answer: B
Rationale: Cardiac pressure overload typically induces cardiomyocyte hypertrophy (increase in cell size), which is
mediated by mTORC1 signaling. The observed decrease in cell size and ANP expression confirms that hypertrophy
is blocked. Hyperplasia (increase in cell number) does not occur in adult cardiomyocytes. Metaplasia and dysplasia
involve changes in cell type or atypical growth, not size increase.
2 A biopsy from a patient with chronic gastroesophageal reflux disease shows replacement of stratified squamous
epithelium with columnar epithelium. This change is best described as:
A) Anaplasia
B) Dysplasia
C) Metaplasia
D) Hyperplasia
Answer: C
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with another, often in response to
chronic irritation. Here, squamous epithelium is replaced by columnar (Barrett esophagus). Anaplasia refers to loss
of differentiation in malignancy; dysplasia is disordered growth; hyperplasia is increased cell number.
3 In a cell undergoing ischemic injury, which of the following events occurs earliest and is most directly linked to
the failure of the Na+/K+ ATPase?
A) Swelling of the endoplasmic reticulum
B) Formation of blebs on the plasma membrane
C) Loss of microvilli
D) Cellular swelling
Answer: D
Rationale: Ischemia rapidly depletes ATP, impairing the Na+/K+ ATPase. Sodium and water accumulate
intracellularly, causing cellular swelling (hydropic change), the earliest manifestation of reversible injury. ER
swelling and bleb formation occur later. Loss of microvilli is also a later change.
,4 A drug induces mitochondrial permeability transition pore (MPTP) opening. This event is most likely to lead to:
A) Apoptosis via the extrinsic pathway
B) Necrosis due to ATP depletion
C) Autophagy
D) Ferroptosis
Answer: B
Rationale: Sustained MPTP opening collapses the mitochondrial membrane potential, halting oxidative
phosphorylation and causing ATP depletion. If ATP falls below critical levels, necrosis ensues due to failure of ion
pumps and membrane integrity. Apoptosis requires ATP; MPTP opening can trigger apoptosis if limited, but with
full opening, necrosis dominates. Autophagy is a survival mechanism; ferroptosis is iron-dependent and not
directly linked to MPTP.
5 A pathologist notes that cells in a tissue section have shrunken cytoplasm, condensed chromatin, and intact
organelles without inflammation. Which type of cell death is most likely?
A) Necrosis
B) Necroptosis
C) Apoptosis
D) Autophagy
Answer: C
Rationale: Apoptosis is characterized by cell shrinkage, chromatin condensation (pyknosis), and preservation of
organelle structure, with no inflammatory response due to rapid phagocytosis. Necrosis involves cell swelling,
membrane rupture, and inflammation. Necroptosis is a regulated form of necrosis that also causes inflammation.
Autophagy involves cytoplasmic vacuolization and digestion of organelles.
6 Which of the following best explains why cells in the center of a solid tumor often undergo necrosis despite
adequate blood supply?
A) High levels of lactate inhibit glycolytic enzymes
B) Activation of the unfolded protein response (UPR) triggers apoptosis
C ) H y p o x i a - i n d u c i b l e f a c t o r 1 ± ( H I F - 1 ± ) p r
D) Oncogene-induced senescence prevents cell division
Answer: B
Rationale: Tumor cells experience ER stress due to hypoxia and nutrient deprivation, leading to UPR activation.
Prolonged UPR shifts from survival to apoptosis, causing cell death. Lactate accumulation does not directly cause
n e c r o s i s ; H I F - 1 ± p r o m o t e s a n g i o g e n e s i s a n d
necrosis.
7 A patient with acetaminophen overdose develops centrilobular hepatic necrosis. The primary mechanism of
injury is:
A) Direct binding of acetaminophen to cytochrome P450 enzymes
B) Formation of a reactive metabolite that depletes glutathione
C) Inhibition of mitochondrial complex I
D) Activation of caspase-8
Answer: B
Rationale: Acetaminophen is metabolized by CYP2E1 to NAPQI, a reactive metabolite that depletes glutathione.
When glutathione is exhausted, NAPQI binds to cellular proteins, causing oxidative stress and necrosis. Direct
enzyme binding is not the primary mechanism; mitochondrial inhibition is secondary. Caspase-8 is involved in
extrinsic apoptosis, not the primary injury here.
, 8 A genetic mutation causes defective autophagy in neurons. Which of the following is the most likely
consequence?
A) Increased susceptibility to viral infections
B) Accumulation of ubiquitinated protein aggregates
C) Enhanced clearance of damaged mitochondria
D) Reduced apoptosis
Answer: B
Rationale: Autophagy degrades damaged organelles and protein aggregates. Defective autophagy leads to
accumulation of ubiquitinated proteins and p62-positive inclusions, as seen in neurodegenerative diseases like
Alzheimer's. Autophagy also contributes to pathogen clearance, but the primary neuronal consequence is protein
aggregate accumulation. Enhanced mitophagy would require functional autophagy; reduced apoptosis is not a
direct effect.
9 A researcher treats cultured hepatocytes with a high dose of iron and a glutathione synthesis inhibitor. Cell
death occurs that is prevented by ferrostatin-1 but not by Z-VAD-FMK (a pan-caspase inhibitor). This cell death
is most consistent with:
A) Apoptosis
B) Necroptosis
C) Ferroptosis
D) Pyroptosis
Answer: C
Rationale: Ferroptosis is an iron-dependent, non-apoptotic cell death characterized by lipid peroxidation. It is
inhibited by ferrostatin-1 (a lipophilic antioxidant) and not by caspase inhibitors. Apoptosis is caspase-dependent;
necroptosis requires RIPK1/RIPK3 and is not iron-dependent; pyroptosis involves caspase-1 and inflammasomes.
10 In a patient with chronic kidney disease, tubular epithelial cells show flattened morphology and decreased
metabolic activity. This adaptation is best classified as:
A) Atrophy
B) Hypoplasia
C) Metaplasia
D) Dysplasia
Answer: A
Rationale: Atrophy is a decrease in cell size and function due to reduced workload, blood supply, or nutrition. In
chronic kidney disease, tubular cells atrophy due to sustained ischemia and uremic toxins. Hypoplasia refers to
reduced cell number during development, not acquired. Metaplasia and dysplasia involve changes in cell type or
atypical growth, not simply reduced size/activity.
11 A researcher is studying the effects of chronic hypoxia on cardiac myocytes. Which adaptive cellular change is
most likely to be observed in the myocytes under sustained low oxygen tension?
A) Hyperplasia with increased cell number
B) Atrophy due to decreased workload
C) Metaplasia from cardiac to skeletal muscle phenotype
D) Hypertrophy with increased cell size and protein synthesis
Answer: D
Rationale: Chronic hypoxia imposes increased workload on cardiac myocytes to maintain cardiac output, leading to
compensatory hypertrophy (increase in cell size) rather than hyperplasia (cells are terminally differentiated).
Atrophy occurs with decreased workload, not increased. Metaplasia is a reversible change from one differentiated
