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
Question Stem
A 68-year-old man with progressive dyspnea undergoes
evaluation and you suspect chronic hypoxia. Which cellular
adaptation most likely reflects chronic hypoxic stress in his
pulmonary tissue?
Options
A. Apoptosis of alveolar epithelial cells
B. Hyperplasia of Type II pneumocytes
,C. Metaplasia of bronchial epithelium from columnar to
squamous
D. Oncotic necrosis of alveolar macrophages
Correct Answer
C
Rationales
• Correct (C): Metaplasia (typical columnar → squamous) is
an adaptive replacement of one differentiated cell type
with another better suited to chronic stress (e.g., chronic
irritation or hypoxia in airways). It’s a reversible adaptive
response described in the introductory mechanisms of
disease.
• Incorrect (A): Apoptosis is programmed cell death and can
occur but is not the classic adaptive structural change to
chronic hypoxia.
• Incorrect (B): Hyperplasia of Type II pneumocytes can
follow alveolar injury to aid repair, but diffuse hyperplasia
is not the typical adaptation to chronic hypoxic airway
stress.
• Incorrect (D): Oncotic necrosis is a form of accidental cell
death due to severe injury and is not an adaptive,
organized response to chronic hypoxia.
Teaching Point
Metaplasia is an adaptive, reversible change to chronic stress in
epithelial tissues.
,Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
2
Reference
Ch. 1 — Introduction
Question Stem
A patient presents with fever after a bacterial infection. Which
mediator most directly resets the hypothalamic thermostat to
produce fever?
Options
A. Interleukin-10 (IL-10)
B. Prostaglandin E₂ (PGE₂)
C. Transforming growth factor-β (TGF-β)
D. Nitric oxide (NO)
Correct Answer
B
Rationales
• Correct (B): PGE₂ acts on the hypothalamus to raise the
thermoregulatory set point; it is the final mediator through
which pyrogenic cytokines induce fever.
, • Incorrect (A): IL-10 is an anti-inflammatory cytokine that
tends to down-regulate immune responses, not directly
causing fever.
• Incorrect (C): TGF-β regulates growth and repair and is not
the principal mediator of hypothalamic thermoregulation.
• Incorrect (D): NO is a vasodilator and has roles in septic
shock and inflammation but does not directly reset the
hypothalamic thermostat like PGE₂.
Teaching Point
PGE₂ produced in response to cytokines mediates fever by
acting on hypothalamic neurons.
Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3
Reference
Ch. 1 — Introduction
Question Stem
During clinical reasoning you need to differentiate reversible
from irreversible cell injury. Which feature best indicates
irreversibility at the cellular level?
Options
A. Cellular swelling with intact plasma membrane
Clinical Medicine
8th Edition
Author(s)Gary D. Hammer; Stephen J. McPhee
TEST BANK
1
Reference
Ch. 1 — Introduction
Question Stem
A 68-year-old man with progressive dyspnea undergoes
evaluation and you suspect chronic hypoxia. Which cellular
adaptation most likely reflects chronic hypoxic stress in his
pulmonary tissue?
Options
A. Apoptosis of alveolar epithelial cells
B. Hyperplasia of Type II pneumocytes
,C. Metaplasia of bronchial epithelium from columnar to
squamous
D. Oncotic necrosis of alveolar macrophages
Correct Answer
C
Rationales
• Correct (C): Metaplasia (typical columnar → squamous) is
an adaptive replacement of one differentiated cell type
with another better suited to chronic stress (e.g., chronic
irritation or hypoxia in airways). It’s a reversible adaptive
response described in the introductory mechanisms of
disease.
• Incorrect (A): Apoptosis is programmed cell death and can
occur but is not the classic adaptive structural change to
chronic hypoxia.
• Incorrect (B): Hyperplasia of Type II pneumocytes can
follow alveolar injury to aid repair, but diffuse hyperplasia
is not the typical adaptation to chronic hypoxic airway
stress.
• Incorrect (D): Oncotic necrosis is a form of accidental cell
death due to severe injury and is not an adaptive,
organized response to chronic hypoxia.
Teaching Point
Metaplasia is an adaptive, reversible change to chronic stress in
epithelial tissues.
,Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
2
Reference
Ch. 1 — Introduction
Question Stem
A patient presents with fever after a bacterial infection. Which
mediator most directly resets the hypothalamic thermostat to
produce fever?
Options
A. Interleukin-10 (IL-10)
B. Prostaglandin E₂ (PGE₂)
C. Transforming growth factor-β (TGF-β)
D. Nitric oxide (NO)
Correct Answer
B
Rationales
• Correct (B): PGE₂ acts on the hypothalamus to raise the
thermoregulatory set point; it is the final mediator through
which pyrogenic cytokines induce fever.
, • Incorrect (A): IL-10 is an anti-inflammatory cytokine that
tends to down-regulate immune responses, not directly
causing fever.
• Incorrect (C): TGF-β regulates growth and repair and is not
the principal mediator of hypothalamic thermoregulation.
• Incorrect (D): NO is a vasodilator and has roles in septic
shock and inflammation but does not directly reset the
hypothalamic thermostat like PGE₂.
Teaching Point
PGE₂ produced in response to cytokines mediates fever by
acting on hypothalamic neurons.
Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3
Reference
Ch. 1 — Introduction
Question Stem
During clinical reasoning you need to differentiate reversible
from irreversible cell injury. Which feature best indicates
irreversibility at the cellular level?
Options
A. Cellular swelling with intact plasma membrane
