PATHOPHYSIOLOGY OF DISEASE: AN
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1
Reference
Ch. 1 — Introduction
Clinical stem
A 58-year-old man with long-standing hypertension presents
after an episode of syncope. BP on arrival is 90/60 mmHg with
cool, clammy skin and lactic acid 6.1 mmol/L. Cardiac troponins
are mildly elevated. The team suspects acute pump failure from
myocardial ischemia. Which cellular process most directly
explains the early (reversible) myocardial dysfunction in this
setting?
,Options
A. Mitochondrial permeability transition causing release of
cytochrome c and apoptosis
B. ATP depletion causing failure of the Na⁺/K⁺ ATPase with
intracellular sodium and water accumulation
C. Lysosomal membrane rupture producing autodigestion of the
myocardium
D. Activation of caspases leading to organized cell
fragmentation
Correct answer
B
Rationales
• Correct (B): Early ischemia causes ATP depletion, which
impairs energy-dependent pumps (especially Na⁺/K⁺
ATPase). Sodium accumulates intracellularly, osmotically
drawing water into cells and producing cellular swelling
and reversible dysfunction — a core mechanism described
in the Introduction.
• Incorrect (A): Mitochondrial permeability transition and
cytochrome c release promote apoptosis and are features
of irreversible injury, not the earliest reversible pump-
failure stage.
• Incorrect (C): Lysosomal rupture and autodigestion are
associated with later, irreversible necrotic processes rather
than the initial reversible ionic pump failure.
, • Incorrect (D): Caspase activation is central to apoptosis, a
regulated cell-death pathway, which differs mechanistically
and morphologically from the early reversible changes in
ischemia.
Teaching point
ATP-dependent pump failure -> ionic imbalance and reversible
cell swelling.
Citation (Simplified APA)
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction
Clinical stem
A 35-year-old woman presents with fatigue and pallor. CBC
shows microcytic anemia (MCV 72 fL). She reports heavy
menses. Bone marrow biopsy shows increased erythroid
precursors but small, hypochromic red cells. Which adaptive
cellular response best explains the marrow findings?
Options
A. Dysplasia resulting from chronic iron toxicity
B. Hyperplasia due to increased physiologic demand for red
cells
, C. Metaplasia of marrow stromal cells to erythroid lineage
D. Atrophy of erythroid lineage due to decreased trophic signals
Correct answer
B
Rationales
• Correct (B): Chronic blood loss increases erythropoietic
demand and stimulates compensatory hyperplasia of
erythroid precursors in marrow; key adaptive responses
are described in the Introduction as mechanisms to meet
increased functional demand.
• Incorrect (A): Dysplasia implies disordered maturation
often precancerous, not a regulated increase in precursor
number in response to demand.
• Incorrect (C): Metaplasia is a reversible change from one
differentiated cell type to another in epithelial or stromal
tissues; marrow erythroid expansion represents lineage
hyperplasia rather than metaplasia.
• Incorrect (D): Atrophy denotes decreased size/function
from reduced use or trophic signals; marrow shows
expansion, not atrophy.
Teaching point
Hyperplasia increases cell number to meet sustained functional
demand (e.g., erythropoiesis).
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1
Reference
Ch. 1 — Introduction
Clinical stem
A 58-year-old man with long-standing hypertension presents
after an episode of syncope. BP on arrival is 90/60 mmHg with
cool, clammy skin and lactic acid 6.1 mmol/L. Cardiac troponins
are mildly elevated. The team suspects acute pump failure from
myocardial ischemia. Which cellular process most directly
explains the early (reversible) myocardial dysfunction in this
setting?
,Options
A. Mitochondrial permeability transition causing release of
cytochrome c and apoptosis
B. ATP depletion causing failure of the Na⁺/K⁺ ATPase with
intracellular sodium and water accumulation
C. Lysosomal membrane rupture producing autodigestion of the
myocardium
D. Activation of caspases leading to organized cell
fragmentation
Correct answer
B
Rationales
• Correct (B): Early ischemia causes ATP depletion, which
impairs energy-dependent pumps (especially Na⁺/K⁺
ATPase). Sodium accumulates intracellularly, osmotically
drawing water into cells and producing cellular swelling
and reversible dysfunction — a core mechanism described
in the Introduction.
• Incorrect (A): Mitochondrial permeability transition and
cytochrome c release promote apoptosis and are features
of irreversible injury, not the earliest reversible pump-
failure stage.
• Incorrect (C): Lysosomal rupture and autodigestion are
associated with later, irreversible necrotic processes rather
than the initial reversible ionic pump failure.
, • Incorrect (D): Caspase activation is central to apoptosis, a
regulated cell-death pathway, which differs mechanistically
and morphologically from the early reversible changes in
ischemia.
Teaching point
ATP-dependent pump failure -> ionic imbalance and reversible
cell swelling.
Citation (Simplified APA)
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction
Clinical stem
A 35-year-old woman presents with fatigue and pallor. CBC
shows microcytic anemia (MCV 72 fL). She reports heavy
menses. Bone marrow biopsy shows increased erythroid
precursors but small, hypochromic red cells. Which adaptive
cellular response best explains the marrow findings?
Options
A. Dysplasia resulting from chronic iron toxicity
B. Hyperplasia due to increased physiologic demand for red
cells
, C. Metaplasia of marrow stromal cells to erythroid lineage
D. Atrophy of erythroid lineage due to decreased trophic signals
Correct answer
B
Rationales
• Correct (B): Chronic blood loss increases erythropoietic
demand and stimulates compensatory hyperplasia of
erythroid precursors in marrow; key adaptive responses
are described in the Introduction as mechanisms to meet
increased functional demand.
• Incorrect (A): Dysplasia implies disordered maturation
often precancerous, not a regulated increase in precursor
number in response to demand.
• Incorrect (C): Metaplasia is a reversible change from one
differentiated cell type to another in epithelial or stromal
tissues; marrow erythroid expansion represents lineage
hyperplasia rather than metaplasia.
• Incorrect (D): Atrophy denotes decreased size/function
from reduced use or trophic signals; marrow shows
expansion, not atrophy.
Teaching point
Hyperplasia increases cell number to meet sustained functional
demand (e.g., erythropoiesis).
