NSG 5140 ADVANCED PATHOPHYSIOLOGY
FINAL TEST CHAPTER 1-14 COMPLETE
2026/2027 STUDY QUESTIONS WITH A+
Section I: Cellular Injury, Adaptation, and Death
1. A 68-year-old male with chronic hypertension develops left ventricular wall
thickening. Which cellular adaptation best explains this finding?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Dysplasia
Rationale: Hypertrophy is an increase in individual cell size in response to
increased workload. Cardiac myocytes are permanent cells and cannot undergo
hyperplasia; chronic pressure overload therefore produces hypertrophic
enlargement.
2. Which organelle contains the genetic code necessary for oxidative
phosphorylation?
A. Lysosome
B. Mitochondria
C. Nucleus
D. Golgi apparatus
Rationale: Mitochondria possess their own circular DNA encoding components
of the electron transport chain required for oxidative phosphorylation.
3. A biopsy from a chronic smoker's bronchus shows replacement of ciliated
columnar epithelium by stratified squamous epithelium. This is best described
as:
A. Hyperplasia
B. Dysplasia
, C. Metaplasia
D. Anaplasia
Rationale: Metaplasia is the reversible replacement of one mature differentiated
cell type with another better suited to withstand chronic irritation.
4. SATA: Which findings are characteristic of reversible cellular injury?
Select all that apply.
A. Cellular swelling
B. Hydropic degeneration
C. Nuclear pyknosis
D. Karyorrhexis
E. Ribosomal detachment
Rationale: Cellular swelling and hydropic degeneration reflect Na⁺/K⁺-ATPase
failure and are reversible. Ribosomal detachment reduces protein synthesis but is
recoverable. Pyknosis and karyorrhexis are nuclear changes of irreversible
injury/cell death.
5. Reperfusion injury following myocardial ischemia is primarily mediated
by:
A. ATP depletion
B. Reactive oxygen species
C. Calcium deficiency
D. Decreased intracellular pH
Rationale: Restoration of blood flow reintroduces oxygen, generating reactive
oxygen species that peroxidize membrane lipids and trigger mitochondrial
permeability transition.
6. The "two-hit hypothesis" is most directly applicable to which class of
genes?
A. Proto-oncogenes
B. Tumor suppressor genes
, C. DNA repair genes
D. Oncogenes
Rationale: The two-hit hypothesis states that both alleles of a tumor suppressor
gene must be inactivated for loss of growth restraint and neoplastic
transformation.
7. Which type of necrosis is characteristic of ischemic injury in the brain?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Fat necrosis
Rationale: Brain tissue is rich in enzymes and lacks firm structural support;
ischemic death leads to enzymatic digestion and liquefactive necrosis.
8. A tuberculous lymph node biopsy shows a cheese-like, yellow-white necrotic
center. This is:
A. Coagulative necrosis
B. Fat necrosis
C. Caseous necrosis
D. Fibrinoid necrosis
Rationale: Caseous necrosis is the hallmark of tuberculosis and appears grossly
as friable, cheese-like material.
9. SATA: Which are features of apoptosis? Select all that apply.
A. Cell shrinkage
B. Chromatin condensation
C. Absence of inflammation
D. Cell membrane rupture
E. Neutrophil infiltration
Rationale: Apoptosis is programmed, non-inflammatory cell death characterized
by shrinkage and nuclear fragmentation; membrane integrity is maintained until
late phagocytic uptake.
, 10. A 72-year-old male with Alzheimer disease shows accumulation of
lipofuscin in neurons. Lipofuscin represents:
A. Iron overload
B. Wear-and-tear pigment
C. Melanin accumulation
D. Bilirubin deposition
Rationale: Lipofuscin is an indigestible lipid–protein polymer that accumulates
with aging and oxidative stress ("wear-and-tear" pigment).
11. A patient with severe acute pancreatitis develops fat necrosis in
peripancreatic tissue. This is caused by:
A. Bacterial endotoxin
B. Pancreatic lipase release
C. Ischemic coagulative death
D. Immune complex deposition
Rationale: Released pancreatic lipases saponify peripancreatic fat, producing
chalky-white fat necrosis.
12. Which molecular event is the critical threshold between reversible and
irreversible cell injury?
A. ATP depletion to 50% of normal
B. Loss of cell membrane integrity
C. Ribosomal detachment
D. Cellular swelling
Rationale: Irreversible injury is defined by loss of membrane integrity,
permitting influx of extracellular calcium and leakage of intracellular enzymes.
13. A 55-year-old female with chronic GERD has Barrett esophagus. The
mechanism underlying this change is:
A. Increase in cell number
B. Metaplasia from squamous to columnar epithelium
FINAL TEST CHAPTER 1-14 COMPLETE
2026/2027 STUDY QUESTIONS WITH A+
Section I: Cellular Injury, Adaptation, and Death
1. A 68-year-old male with chronic hypertension develops left ventricular wall
thickening. Which cellular adaptation best explains this finding?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Dysplasia
Rationale: Hypertrophy is an increase in individual cell size in response to
increased workload. Cardiac myocytes are permanent cells and cannot undergo
hyperplasia; chronic pressure overload therefore produces hypertrophic
enlargement.
2. Which organelle contains the genetic code necessary for oxidative
phosphorylation?
A. Lysosome
B. Mitochondria
C. Nucleus
D. Golgi apparatus
Rationale: Mitochondria possess their own circular DNA encoding components
of the electron transport chain required for oxidative phosphorylation.
3. A biopsy from a chronic smoker's bronchus shows replacement of ciliated
columnar epithelium by stratified squamous epithelium. This is best described
as:
A. Hyperplasia
B. Dysplasia
, C. Metaplasia
D. Anaplasia
Rationale: Metaplasia is the reversible replacement of one mature differentiated
cell type with another better suited to withstand chronic irritation.
4. SATA: Which findings are characteristic of reversible cellular injury?
Select all that apply.
A. Cellular swelling
B. Hydropic degeneration
C. Nuclear pyknosis
D. Karyorrhexis
E. Ribosomal detachment
Rationale: Cellular swelling and hydropic degeneration reflect Na⁺/K⁺-ATPase
failure and are reversible. Ribosomal detachment reduces protein synthesis but is
recoverable. Pyknosis and karyorrhexis are nuclear changes of irreversible
injury/cell death.
5. Reperfusion injury following myocardial ischemia is primarily mediated
by:
A. ATP depletion
B. Reactive oxygen species
C. Calcium deficiency
D. Decreased intracellular pH
Rationale: Restoration of blood flow reintroduces oxygen, generating reactive
oxygen species that peroxidize membrane lipids and trigger mitochondrial
permeability transition.
6. The "two-hit hypothesis" is most directly applicable to which class of
genes?
A. Proto-oncogenes
B. Tumor suppressor genes
, C. DNA repair genes
D. Oncogenes
Rationale: The two-hit hypothesis states that both alleles of a tumor suppressor
gene must be inactivated for loss of growth restraint and neoplastic
transformation.
7. Which type of necrosis is characteristic of ischemic injury in the brain?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Fat necrosis
Rationale: Brain tissue is rich in enzymes and lacks firm structural support;
ischemic death leads to enzymatic digestion and liquefactive necrosis.
8. A tuberculous lymph node biopsy shows a cheese-like, yellow-white necrotic
center. This is:
A. Coagulative necrosis
B. Fat necrosis
C. Caseous necrosis
D. Fibrinoid necrosis
Rationale: Caseous necrosis is the hallmark of tuberculosis and appears grossly
as friable, cheese-like material.
9. SATA: Which are features of apoptosis? Select all that apply.
A. Cell shrinkage
B. Chromatin condensation
C. Absence of inflammation
D. Cell membrane rupture
E. Neutrophil infiltration
Rationale: Apoptosis is programmed, non-inflammatory cell death characterized
by shrinkage and nuclear fragmentation; membrane integrity is maintained until
late phagocytic uptake.
, 10. A 72-year-old male with Alzheimer disease shows accumulation of
lipofuscin in neurons. Lipofuscin represents:
A. Iron overload
B. Wear-and-tear pigment
C. Melanin accumulation
D. Bilirubin deposition
Rationale: Lipofuscin is an indigestible lipid–protein polymer that accumulates
with aging and oxidative stress ("wear-and-tear" pigment).
11. A patient with severe acute pancreatitis develops fat necrosis in
peripancreatic tissue. This is caused by:
A. Bacterial endotoxin
B. Pancreatic lipase release
C. Ischemic coagulative death
D. Immune complex deposition
Rationale: Released pancreatic lipases saponify peripancreatic fat, producing
chalky-white fat necrosis.
12. Which molecular event is the critical threshold between reversible and
irreversible cell injury?
A. ATP depletion to 50% of normal
B. Loss of cell membrane integrity
C. Ribosomal detachment
D. Cellular swelling
Rationale: Irreversible injury is defined by loss of membrane integrity,
permitting influx of extracellular calcium and leakage of intracellular enzymes.
13. A 55-year-old female with chronic GERD has Barrett esophagus. The
mechanism underlying this change is:
A. Increase in cell number
B. Metaplasia from squamous to columnar epithelium
