PATHOPHYSIOLOGY OF DISEASE: AN
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
Q1
Reference
Ch. 1 — Introduction — Concepts: Homeostasis, Stress, and
Cellular Adaptation
Stem
A 67-year-old man with chronic tobacco use reports progressive
exertional dyspnea and a chronic productive cough. Chest CT
shows diffuse centrilobular emphysematous changes.
Pulmonary function tests reveal increased total lung capacity
and decreased DLCO. Which cellular adaptation and primary
,pathophysiologic mechanism best explain his decreased gas
transfer?
A. Hyperplasia of alveolar type II cells causing surfactant
dysfunction.
B. Squamous metaplasia of bronchioles reducing alveolar
surface area.
C. Loss of alveolar septal elastic tissue from protease-
antiprotease imbalance.
D. Apoptosis of pulmonary macrophages resulting in surfactant
accumulation.
Correct answer
C
Rationales
Correct (C): Chapter 1 emphasizes that chronic stressors
(smoking) lead to protease-antiprotease imbalance and
oxidative injury causing destruction of alveolar septa and loss of
elastic recoil, reducing diffusing capacity (DLCO) and increasing
TLC — classic emphysema pathophysiology. AccessMedicine
(A): Hyperplasia of type II pneumocytes occurs in some injuries
but would not explain loss of alveolar septa or decreased DLCO
and increased TLC.
(B): Squamous metaplasia affects conducting airways and
predisposes to carcinoma but does not account for widespread
loss of gas-exchange surface.
(D): Loss of macrophages would impair clearance, not produce
emphysematous septal destruction; apoptosis of macrophages
,causing surfactant accumulation is not a primary mechanism
here.
Teaching point
Protease–antiprotease imbalance and oxidative injury destroy
alveolar septa, reducing DLCO.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1. AccessMedicine
Q2
Reference
Ch. 1 — Introduction — Concepts: Reversible vs Irreversible Cell
Injury; Hypoxia
Stem
A 42-year-old woman presents after hours of severe
hypotension from septic shock. Her serum lactate is 9 mmol/L
and liver enzymes are mildly elevated. On biopsy, hepatocytes
show cellular swelling and clumping of nuclear chromatin
without membrane rupture. Which statement best links the
observed microscopic findings to the underlying mechanism?
A. Persistent ATP depletion impaired Na⁺/K⁺ ATPase causing
cellular swelling; changes are potentially reversible.
B. Activation of caspases produced nuclear fragmentation,
indicating irreversible apoptosis.
C. Lysosomal membrane rupture released hydrolases causing
, immediate cell membrane dissolution.
D. Excessive ROS caused cross-linking of membrane proteins
producing irreversible necrosis.
Correct answer
A
Rationales
Correct (A): Chapter 1 outlines that hypoxic/ischemic injury
leads to ATP depletion, failure of ion pumps (Na⁺/K⁺ ATPase),
intracellular Na⁺ and water accumulation (cellular swelling) and
clumped chromatin — classic reversible injury. AccessMedicine
(B): Caspase-mediated apoptosis yields cell shrinkage and DNA
laddering, not diffuse swelling with chromatin clumping.
(C): Lysosomal rupture and hydrolase release cause irreversible
necrosis with membrane disruption; early swelling without
rupture implies reversibility.
(D): ROS can cause irreversible damage, but the presence of
swelling and chromatin clumping without membrane loss points
to reversible ATP-depletion mechanisms.
Teaching point
ATP depletion → ion-pump failure → cellular swelling; early
changes are often reversible.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1. AccessMedicine
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
Q1
Reference
Ch. 1 — Introduction — Concepts: Homeostasis, Stress, and
Cellular Adaptation
Stem
A 67-year-old man with chronic tobacco use reports progressive
exertional dyspnea and a chronic productive cough. Chest CT
shows diffuse centrilobular emphysematous changes.
Pulmonary function tests reveal increased total lung capacity
and decreased DLCO. Which cellular adaptation and primary
,pathophysiologic mechanism best explain his decreased gas
transfer?
A. Hyperplasia of alveolar type II cells causing surfactant
dysfunction.
B. Squamous metaplasia of bronchioles reducing alveolar
surface area.
C. Loss of alveolar septal elastic tissue from protease-
antiprotease imbalance.
D. Apoptosis of pulmonary macrophages resulting in surfactant
accumulation.
Correct answer
C
Rationales
Correct (C): Chapter 1 emphasizes that chronic stressors
(smoking) lead to protease-antiprotease imbalance and
oxidative injury causing destruction of alveolar septa and loss of
elastic recoil, reducing diffusing capacity (DLCO) and increasing
TLC — classic emphysema pathophysiology. AccessMedicine
(A): Hyperplasia of type II pneumocytes occurs in some injuries
but would not explain loss of alveolar septa or decreased DLCO
and increased TLC.
(B): Squamous metaplasia affects conducting airways and
predisposes to carcinoma but does not account for widespread
loss of gas-exchange surface.
(D): Loss of macrophages would impair clearance, not produce
emphysematous septal destruction; apoptosis of macrophages
,causing surfactant accumulation is not a primary mechanism
here.
Teaching point
Protease–antiprotease imbalance and oxidative injury destroy
alveolar septa, reducing DLCO.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1. AccessMedicine
Q2
Reference
Ch. 1 — Introduction — Concepts: Reversible vs Irreversible Cell
Injury; Hypoxia
Stem
A 42-year-old woman presents after hours of severe
hypotension from septic shock. Her serum lactate is 9 mmol/L
and liver enzymes are mildly elevated. On biopsy, hepatocytes
show cellular swelling and clumping of nuclear chromatin
without membrane rupture. Which statement best links the
observed microscopic findings to the underlying mechanism?
A. Persistent ATP depletion impaired Na⁺/K⁺ ATPase causing
cellular swelling; changes are potentially reversible.
B. Activation of caspases produced nuclear fragmentation,
indicating irreversible apoptosis.
C. Lysosomal membrane rupture released hydrolases causing
, immediate cell membrane dissolution.
D. Excessive ROS caused cross-linking of membrane proteins
producing irreversible necrosis.
Correct answer
A
Rationales
Correct (A): Chapter 1 outlines that hypoxic/ischemic injury
leads to ATP depletion, failure of ion pumps (Na⁺/K⁺ ATPase),
intracellular Na⁺ and water accumulation (cellular swelling) and
clumped chromatin — classic reversible injury. AccessMedicine
(B): Caspase-mediated apoptosis yields cell shrinkage and DNA
laddering, not diffuse swelling with chromatin clumping.
(C): Lysosomal rupture and hydrolase release cause irreversible
necrosis with membrane disruption; early swelling without
rupture implies reversibility.
(D): ROS can cause irreversible damage, but the presence of
swelling and chromatin clumping without membrane loss points
to reversible ATP-depletion mechanisms.
Teaching point
ATP depletion → ion-pump failure → cellular swelling; early
changes are often reversible.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1. AccessMedicine
