Pathophysiology of Disease: An Introduction to
Clinical Medicine
8th Edition
Author(s)Gary D. Hammer; Stephen J. McPhee
TEST BANK
Reference
Ch. 1 — Introduction
Question Stem
A 68-year-old patient has progressive dyspnea and bilateral
crackles. You suspect heart failure secondary to chronic
ischemic injury. Which pathophysiologic principle best explains
how repeated ischemic episodes produced decreased cardiac
output?
Options
A. Reversible cellular swelling increases muscle contractility.
B. Persistent ischemia causes myocyte necrosis and loss of
contractile units.
C. Ischemia always produces purely electrical conduction
,defects without structural change.
D. Ischemia triggers hyperplasia of cardiomyocytes to preserve
output.
Correct Answer
B
Rationales
Correct: Recurrent ischemia causes irreversible myocyte
necrosis and loss of functioning contractile units, reducing
effective stroke volume and cardiac output. This mechanism
links cellular injury to organ-level pump failure.
A (incorrect): Reversible cellular swelling is an early, transient
change and does not increase contractility; it impairs function.
C (incorrect): Ischemia causes both structural (necrosis,
remodeling) and electrical changes — not solely conduction
defects.
D (incorrect): Mature cardiomyocytes undergo hypertrophy (not
hyperplasia) in response to chronic stress; hyperplasia is not the
primary response.
Teaching Point
Irreversible myocyte necrosis reduces contractile mass, causing
heart failure.
Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
,2
Reference
Ch. 1 — Introduction
Question Stem
A patient with severe sepsis develops hypotension and lactic
acidosis despite fluid resuscitation. Which mechanism most
directly explains the progressive cellular dysfunction in this
setting?
Options
A. Enhanced oxidative phosphorylation due to increased oxygen
delivery.
B. Mitochondrial dysfunction leading to impaired ATP
generation.
C. Increased activity of the Na⁺/K⁺-ATPase pump.
D. Upregulation of aerobic glycolysis restoring ATP stores.
Correct Answer
B
Rationales
Correct: In severe sepsis, mitochondrial injury from
inflammatory mediators and hypoperfusion impairs oxidative
phosphorylation, decreasing ATP and causing cellular
dysfunction and lactic acidosis.
A (incorrect): Oxidative phosphorylation is impaired—not
enhanced—during sepsis despite attempts to increase delivery.
C (incorrect): Na⁺/K⁺-ATPase activity falls when ATP is depleted,
, contributing to ion imbalance and swelling.
D (incorrect): Cells shift toward anaerobic glycolysis but this is
insufficient to restore ATP and produces lactate.
Teaching Point
Sepsis causes mitochondrial failure and ATP depletion, driving
organ dysfunction.
Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3
Reference
Ch. 1 — Introduction
Question Stem
You are reviewing a lab report showing markedly elevated
plasma troponin in a patient with chest pain. Which statement
best links a biomarker rise to pathophysiology?
Options
A. Troponin increases only when reversible ischemia without
necrosis occurs.
B. Troponin rise reflects necrosis of cardiomyocytes with loss of
membrane integrity.
C. Elevated troponin always indicates renal failure rather than
myocardial injury.
Clinical Medicine
8th Edition
Author(s)Gary D. Hammer; Stephen J. McPhee
TEST BANK
Reference
Ch. 1 — Introduction
Question Stem
A 68-year-old patient has progressive dyspnea and bilateral
crackles. You suspect heart failure secondary to chronic
ischemic injury. Which pathophysiologic principle best explains
how repeated ischemic episodes produced decreased cardiac
output?
Options
A. Reversible cellular swelling increases muscle contractility.
B. Persistent ischemia causes myocyte necrosis and loss of
contractile units.
C. Ischemia always produces purely electrical conduction
,defects without structural change.
D. Ischemia triggers hyperplasia of cardiomyocytes to preserve
output.
Correct Answer
B
Rationales
Correct: Recurrent ischemia causes irreversible myocyte
necrosis and loss of functioning contractile units, reducing
effective stroke volume and cardiac output. This mechanism
links cellular injury to organ-level pump failure.
A (incorrect): Reversible cellular swelling is an early, transient
change and does not increase contractility; it impairs function.
C (incorrect): Ischemia causes both structural (necrosis,
remodeling) and electrical changes — not solely conduction
defects.
D (incorrect): Mature cardiomyocytes undergo hypertrophy (not
hyperplasia) in response to chronic stress; hyperplasia is not the
primary response.
Teaching Point
Irreversible myocyte necrosis reduces contractile mass, causing
heart failure.
Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
,2
Reference
Ch. 1 — Introduction
Question Stem
A patient with severe sepsis develops hypotension and lactic
acidosis despite fluid resuscitation. Which mechanism most
directly explains the progressive cellular dysfunction in this
setting?
Options
A. Enhanced oxidative phosphorylation due to increased oxygen
delivery.
B. Mitochondrial dysfunction leading to impaired ATP
generation.
C. Increased activity of the Na⁺/K⁺-ATPase pump.
D. Upregulation of aerobic glycolysis restoring ATP stores.
Correct Answer
B
Rationales
Correct: In severe sepsis, mitochondrial injury from
inflammatory mediators and hypoperfusion impairs oxidative
phosphorylation, decreasing ATP and causing cellular
dysfunction and lactic acidosis.
A (incorrect): Oxidative phosphorylation is impaired—not
enhanced—during sepsis despite attempts to increase delivery.
C (incorrect): Na⁺/K⁺-ATPase activity falls when ATP is depleted,
, contributing to ion imbalance and swelling.
D (incorrect): Cells shift toward anaerobic glycolysis but this is
insufficient to restore ATP and produces lactate.
Teaching Point
Sepsis causes mitochondrial failure and ATP depletion, driving
organ dysfunction.
Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3
Reference
Ch. 1 — Introduction
Question Stem
You are reviewing a lab report showing markedly elevated
plasma troponin in a patient with chest pain. Which statement
best links a biomarker rise to pathophysiology?
Options
A. Troponin increases only when reversible ischemia without
necrosis occurs.
B. Troponin rise reflects necrosis of cardiomyocytes with loss of
membrane integrity.
C. Elevated troponin always indicates renal failure rather than
myocardial injury.
