ANATOMICAL CHART COMPANY ATLAS
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
1)
Reference: Ch. 1 — Cellular Structure and Function — Plasma
Membrane Integrity
Stem: A 68-year-old man with a recent myocardial infarction
(MI) becomes hypotensive and hypoxic. A nurse notes rising
serum lactate and worsening metabolic acidosis. Which
pathophysiologic process at the cellular level best explains
impaired ATP production and lactic acidosis in the myocardium
after the MI?
A. Failure of mitochondrial oxidative phosphorylation due to
,loss of oxygen supply
B. Increased mitochondrial biogenesis to compensate for
ischemia
C. Activation of lysosomal enzymes causing intracellular
glycogen accumulation
D. Enhanced Na⁺/K⁺-ATPase activity preserving membrane
potential
Correct Answer: A
Rationale — Correct (A): Ischemia deprives mitochondria of
oxygen, halting oxidative phosphorylation and ATP generation.
Cells switch to anaerobic glycolysis, producing lactate and
causing metabolic acidosis. Myocardial cells' high energy
demand makes them particularly vulnerable to ATP depletion
after MI.
Rationale — Incorrect (B): Mitochondrial biogenesis is a longer-
term adaptive response and cannot restore immediate ATP in
acute ischemia.
Rationale — Incorrect (C): Lysosomal enzyme activation
degrades substrates; it does not explain decreased oxidative
phosphorylation or lactate rise.
Rationale — Incorrect (D): Na⁺/K⁺-ATPase requires ATP; ATP
depletion decreases its activity, leading to ionic imbalance
rather than preservation.
Teaching Point: Oxygen loss rapidly halts mitochondrial ATP
production → anaerobic glycolysis and lactate accumulation.
,Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. 1.
2)
Reference: Ch. 2 — Cellular Adaptation — Hypertrophy and
Atrophy
Stem: A 55-year-old male with long-standing hypertension has
concentric left ventricular hypertrophy on echocardiogram.
Which cellular mechanism most directly accounts for the
increased myocardial cell size?
A. Increased synthesis of contractile proteins due to persistent
biomechanical stress
B. Increased apoptosis reducing cell number and leaving larger
cells behind
C. Accumulation of intracellular lipids causing cell swelling
D. Conversion of cardiomyocytes into pluripotent stem cells
Correct Answer: A
Rationale — Correct (A): Chronic pressure overload induces
signaling pathways (e.g., MAPK, calcineurin) that upregulate
gene expression for contractile proteins, causing cardiomyocyte
hypertrophy and increased cell size to normalize wall stress.
Rationale — Incorrect (B): Apoptosis reduces cell number and
does not increase individual cell size; it often follows
maladaptation.
Rationale — Incorrect (C): Lipid accumulation causes
, intracellular inclusions, not organized increase in contractile
elements characteristic of hypertrophy.
Rationale — Incorrect (D): Cardiomyocyte transdifferentiation
into stem cells is not a recognized physiologic adaptation to
pressure overload.
Teaching Point: Chronic mechanical stress induces protein
synthesis → cardiomyocyte hypertrophy.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. 2.
3)
Reference: Ch. 2 — Cellular Injury — Reversible vs. Irreversible
Injury
Stem: A patient with prolonged limb ischemia shows pale,
noncontractile muscle tissue on exam. Microscopically, the
nurse learns there is karyolysis and membrane rupture. Which
process indicates the transition from reversible to irreversible
cell injury?
A. Loss of plasma membrane integrity and nuclear dissolution
B. Cellular swelling due to Na⁺/K⁺ pump dysfunction
C. Ribosomal detachment from rough endoplasmic reticulum
D. Glycogen depletion within the cytoplasm
Correct Answer: A
Rationale — Correct (A): Loss of membrane integrity and
nuclear breakdown (karyolysis) are hallmark signs of irreversible
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
1)
Reference: Ch. 1 — Cellular Structure and Function — Plasma
Membrane Integrity
Stem: A 68-year-old man with a recent myocardial infarction
(MI) becomes hypotensive and hypoxic. A nurse notes rising
serum lactate and worsening metabolic acidosis. Which
pathophysiologic process at the cellular level best explains
impaired ATP production and lactic acidosis in the myocardium
after the MI?
A. Failure of mitochondrial oxidative phosphorylation due to
,loss of oxygen supply
B. Increased mitochondrial biogenesis to compensate for
ischemia
C. Activation of lysosomal enzymes causing intracellular
glycogen accumulation
D. Enhanced Na⁺/K⁺-ATPase activity preserving membrane
potential
Correct Answer: A
Rationale — Correct (A): Ischemia deprives mitochondria of
oxygen, halting oxidative phosphorylation and ATP generation.
Cells switch to anaerobic glycolysis, producing lactate and
causing metabolic acidosis. Myocardial cells' high energy
demand makes them particularly vulnerable to ATP depletion
after MI.
Rationale — Incorrect (B): Mitochondrial biogenesis is a longer-
term adaptive response and cannot restore immediate ATP in
acute ischemia.
Rationale — Incorrect (C): Lysosomal enzyme activation
degrades substrates; it does not explain decreased oxidative
phosphorylation or lactate rise.
Rationale — Incorrect (D): Na⁺/K⁺-ATPase requires ATP; ATP
depletion decreases its activity, leading to ionic imbalance
rather than preservation.
Teaching Point: Oxygen loss rapidly halts mitochondrial ATP
production → anaerobic glycolysis and lactate accumulation.
,Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. 1.
2)
Reference: Ch. 2 — Cellular Adaptation — Hypertrophy and
Atrophy
Stem: A 55-year-old male with long-standing hypertension has
concentric left ventricular hypertrophy on echocardiogram.
Which cellular mechanism most directly accounts for the
increased myocardial cell size?
A. Increased synthesis of contractile proteins due to persistent
biomechanical stress
B. Increased apoptosis reducing cell number and leaving larger
cells behind
C. Accumulation of intracellular lipids causing cell swelling
D. Conversion of cardiomyocytes into pluripotent stem cells
Correct Answer: A
Rationale — Correct (A): Chronic pressure overload induces
signaling pathways (e.g., MAPK, calcineurin) that upregulate
gene expression for contractile proteins, causing cardiomyocyte
hypertrophy and increased cell size to normalize wall stress.
Rationale — Incorrect (B): Apoptosis reduces cell number and
does not increase individual cell size; it often follows
maladaptation.
Rationale — Incorrect (C): Lipid accumulation causes
, intracellular inclusions, not organized increase in contractile
elements characteristic of hypertrophy.
Rationale — Incorrect (D): Cardiomyocyte transdifferentiation
into stem cells is not a recognized physiologic adaptation to
pressure overload.
Teaching Point: Chronic mechanical stress induces protein
synthesis → cardiomyocyte hypertrophy.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. 2.
3)
Reference: Ch. 2 — Cellular Injury — Reversible vs. Irreversible
Injury
Stem: A patient with prolonged limb ischemia shows pale,
noncontractile muscle tissue on exam. Microscopically, the
nurse learns there is karyolysis and membrane rupture. Which
process indicates the transition from reversible to irreversible
cell injury?
A. Loss of plasma membrane integrity and nuclear dissolution
B. Cellular swelling due to Na⁺/K⁺ pump dysfunction
C. Ribosomal detachment from rough endoplasmic reticulum
D. Glycogen depletion within the cytoplasm
Correct Answer: A
Rationale — Correct (A): Loss of membrane integrity and
nuclear breakdown (karyolysis) are hallmark signs of irreversible
