ANATOMICAL CHART COMPANY ATLAS
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Ch. Part I — Cellular Injury — Reversible vs.
Irreversible Injury (membrane integrity, ATP depletion)
Stem: A 68-year-old man with longstanding type 2 diabetes
reports progressive fatigue, reduced exercise tolerance, and
recent ankle swelling. On exam he has bilateral pitting edema
and pale, cool skin. Lab shows lactate mildly elevated and
serum albumin normal. You suspect chronic tissue hypoxia at
the cellular level due to microvascular disease. Which
pathophysiologic process best explains the early reversible
cellular changes in tissues with chronic hypoxia?
,A. Mitochondrial permeability transition leading to necrosis
B. Decreased ATP production causing sodium–potassium pump
failure and cellular swelling
C. Activation of caspases causing programmed apoptosis and
cell shrinkage
D. Lysosomal membrane rupture with autodigestion of
cytoplasm
Correct Answer: B
Rationale — Correct (B): Chronic hypoxia reduces oxidative
phosphorylation, lowering ATP. ATP-dependent Na⁺/K⁺ pump
failure causes intracellular Na⁺ and water accumulation →
cellular swelling, a reversible injury. This explains pale, cool
tissue and early dysfunction without structural loss.
Rationale — Incorrect:
A. Mitochondrial permeability transition is characteristic of
irreversible injury and necrosis; histologic rupture and cell
death would follow, not early reversible swelling.
C. Caspase-mediated apoptosis produces cell shrinkage and
organized removal without inflammation; it is not the classic
response to ATP depletion from hypoxia.
D. Lysosomal rupture and autodigestion occur in irreversible
injury/necrosis, not the initial reversible stage.
Teaching Point: ATP depletion → Na⁺/K⁺ pump failure → cellular
swelling is an early reversible sign of hypoxic injury.
,Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. Part I.
2
Reference: Ch. Part I — Cellular Adaptation — Hypertrophy and
Atrophy
Stem: A 55-year-old woman with long-standing hypertension
reports increasing exertional dyspnea. Echocardiogram shows
concentric left ventricular hypertrophy. Which cellular
adaptation and mechanism best account for the increased
myocardial wall thickness?
A. Hyperplasia from increased cardiomyocyte proliferation due
to growth factors
B. Hypertrophy due to increased synthesis of contractile
proteins triggered by mechanical stress
C. Metaplasia with replacement of myocytes by fibroblasts
D. Atrophy from decreased workload and proteasome activation
Correct Answer: B
Rationale — Correct (B): Cardiomyocytes are terminally
differentiated; they respond to pressure overload with
hypertrophy — increased cell size via upregulated synthesis of
contractile proteins driven by mechanical stress and
neurohormonal growth signals (e.g., angiotensin II, endothelin).
, Rationale — Incorrect:
A. Hyperplasia involves cell number increase; cardiac myocytes
rarely proliferate postnatally, so hyperplasia is not the
mechanism.
C. Metaplasia is reversible change from one adult cell type to
another (e.g., Barrett esophagus), not replacement of myocytes
by fibroblasts.
D. Atrophy implies decreased cell size from reduced workload;
the patient shows increased, not decreased, workload
adaptation.
Teaching Point: Pressure overload → cardiomyocyte
hypertrophy via increased contractile protein synthesis.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. Part I.
3
Reference: Ch. Part I — Cellular Adaptation — Metaplasia and
Risk of Malignant Transformation
Stem: A 52-year-old male chronic smoker has chronic cough and
bronchoscopy shows replacement of normal pseudostratified
ciliated epithelium in his bronchi with stratified squamous
epithelium. What is the primary adaptive mechanism and its
clinical significance?
A. Dysplasia resulting from irreversible DNA damage and
immediate carcinoma risk
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Ch. Part I — Cellular Injury — Reversible vs.
Irreversible Injury (membrane integrity, ATP depletion)
Stem: A 68-year-old man with longstanding type 2 diabetes
reports progressive fatigue, reduced exercise tolerance, and
recent ankle swelling. On exam he has bilateral pitting edema
and pale, cool skin. Lab shows lactate mildly elevated and
serum albumin normal. You suspect chronic tissue hypoxia at
the cellular level due to microvascular disease. Which
pathophysiologic process best explains the early reversible
cellular changes in tissues with chronic hypoxia?
,A. Mitochondrial permeability transition leading to necrosis
B. Decreased ATP production causing sodium–potassium pump
failure and cellular swelling
C. Activation of caspases causing programmed apoptosis and
cell shrinkage
D. Lysosomal membrane rupture with autodigestion of
cytoplasm
Correct Answer: B
Rationale — Correct (B): Chronic hypoxia reduces oxidative
phosphorylation, lowering ATP. ATP-dependent Na⁺/K⁺ pump
failure causes intracellular Na⁺ and water accumulation →
cellular swelling, a reversible injury. This explains pale, cool
tissue and early dysfunction without structural loss.
Rationale — Incorrect:
A. Mitochondrial permeability transition is characteristic of
irreversible injury and necrosis; histologic rupture and cell
death would follow, not early reversible swelling.
C. Caspase-mediated apoptosis produces cell shrinkage and
organized removal without inflammation; it is not the classic
response to ATP depletion from hypoxia.
D. Lysosomal rupture and autodigestion occur in irreversible
injury/necrosis, not the initial reversible stage.
Teaching Point: ATP depletion → Na⁺/K⁺ pump failure → cellular
swelling is an early reversible sign of hypoxic injury.
,Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. Part I.
2
Reference: Ch. Part I — Cellular Adaptation — Hypertrophy and
Atrophy
Stem: A 55-year-old woman with long-standing hypertension
reports increasing exertional dyspnea. Echocardiogram shows
concentric left ventricular hypertrophy. Which cellular
adaptation and mechanism best account for the increased
myocardial wall thickness?
A. Hyperplasia from increased cardiomyocyte proliferation due
to growth factors
B. Hypertrophy due to increased synthesis of contractile
proteins triggered by mechanical stress
C. Metaplasia with replacement of myocytes by fibroblasts
D. Atrophy from decreased workload and proteasome activation
Correct Answer: B
Rationale — Correct (B): Cardiomyocytes are terminally
differentiated; they respond to pressure overload with
hypertrophy — increased cell size via upregulated synthesis of
contractile proteins driven by mechanical stress and
neurohormonal growth signals (e.g., angiotensin II, endothelin).
, Rationale — Incorrect:
A. Hyperplasia involves cell number increase; cardiac myocytes
rarely proliferate postnatally, so hyperplasia is not the
mechanism.
C. Metaplasia is reversible change from one adult cell type to
another (e.g., Barrett esophagus), not replacement of myocytes
by fibroblasts.
D. Atrophy implies decreased cell size from reduced workload;
the patient shows increased, not decreased, workload
adaptation.
Teaching Point: Pressure overload → cardiomyocyte
hypertrophy via increased contractile protein synthesis.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. Part I.
3
Reference: Ch. Part I — Cellular Adaptation — Metaplasia and
Risk of Malignant Transformation
Stem: A 52-year-old male chronic smoker has chronic cough and
bronchoscopy shows replacement of normal pseudostratified
ciliated epithelium in his bronchi with stratified squamous
epithelium. What is the primary adaptive mechanism and its
clinical significance?
A. Dysplasia resulting from irreversible DNA damage and
immediate carcinoma risk
