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 1 — Stem:
A 68-year-old man develops sudden chest pain while shoveling
snow. Coronary artery occlusion causes myocardial ischemia.
Which cellular event best explains the immediate loss of ATP
during ischemia?
A. Increased mitochondrial oxidative phosphorylation due to
excess calcium
B. Reduced electron transport chain activity because of
decreased oxygen as terminal electron acceptor
C. Enhanced Na⁺/K⁺-ATPase activity driven by anaerobic
,glycolysis
D. Increased synthesis of high-energy phosphate bonds by
anaerobic respiration
Correct Answer: B
Rationales:
Correct: Ischemia decreases oxygen delivery so the electron
transport chain cannot use O₂ as the terminal electron acceptor,
halting oxidative phosphorylation and rapidly depleting ATP.
A: Excess calcium worsens injury but does not increase
oxidative phosphorylation without oxygen.
C: Na⁺/K⁺-ATPase activity falls as ATP falls; anaerobic glycolysis is
insufficient to sustain it.
D: Anaerobic glycolysis produces far fewer high-energy
phosphates than oxidative phosphorylation and cannot
compensate for lost ATP.
Teaching Point:
Ischemia halts oxidative phosphorylation by removing oxygen
as the electron acceptor.
Citation:
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
Reference: Ch. 1 — Introduction
Question 2 — Stem:
A febrile oncology patient has neutropenia and a low-grade
,fever. Which statement best describes why fever is often
beneficial during infection?
A. Fever reduces leukocyte mobility, protecting tissues from
damage.
B. Elevated temperature directly denatures bacterial toxins,
preventing sepsis.
C. Fever enhances immune efficiency by increasing leukocyte
activity and inhibiting some pathogens.
D. Fever suppresses acute-phase protein synthesis to conserve
energy.
Correct Answer: C
Rationales:
Correct: Fever is a regulated rise in hypothalamic set point
mediated by cytokines and PGE₂; it enhances leukocyte function
and can inhibit pathogen replication.
A: Fever increases leukocyte trafficking and function, not
reduces mobility.
B: Temperature elevations rarely denature toxins at physiologic
fevers; the immune-modulatory effects are more important.
D: Fever typically accompanies increased acute-phase protein
production, not suppression.
Teaching Point:
Fever is an adaptive host response that augments immune
function and pathogen control.
, Citation:
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
Reference: Ch. 1 — Introduction
Question 3 — Stem:
A long-term smoker develops columnar, mucin-secreting
epithelium in the distal esophagus. This metaplastic change
increases cancer risk. Which mechanism best explains how
metaplasia predisposes to malignancy?
A. Metaplasia causes irreversible DNA mutations in stem cells
immediately.
B. Reprogramming of stem/progenitor cells creates tissue better
suited to injury but more susceptible to carcinogens.
C. Metaplasia increases local blood flow causing genomic
instability.
D. Metaplastic tissue resists oxidative stress and thereby
accumulates mutations.
Correct Answer: B
Rationales:
Correct: Chronic injury drives reprogramming of
stem/progenitor cells to produce a different, more injury-
resistant cell type; these new cells can be less well adapted to
the microenvironment and more vulnerable to carcinogenic
transformation.
Clinical Medicine
8th Edition
Author(s)Gary D. Hammer; Stephen J. McPhee
TEST BANK
Reference: Ch. 1 — Introduction
Question 1 — Stem:
A 68-year-old man develops sudden chest pain while shoveling
snow. Coronary artery occlusion causes myocardial ischemia.
Which cellular event best explains the immediate loss of ATP
during ischemia?
A. Increased mitochondrial oxidative phosphorylation due to
excess calcium
B. Reduced electron transport chain activity because of
decreased oxygen as terminal electron acceptor
C. Enhanced Na⁺/K⁺-ATPase activity driven by anaerobic
,glycolysis
D. Increased synthesis of high-energy phosphate bonds by
anaerobic respiration
Correct Answer: B
Rationales:
Correct: Ischemia decreases oxygen delivery so the electron
transport chain cannot use O₂ as the terminal electron acceptor,
halting oxidative phosphorylation and rapidly depleting ATP.
A: Excess calcium worsens injury but does not increase
oxidative phosphorylation without oxygen.
C: Na⁺/K⁺-ATPase activity falls as ATP falls; anaerobic glycolysis is
insufficient to sustain it.
D: Anaerobic glycolysis produces far fewer high-energy
phosphates than oxidative phosphorylation and cannot
compensate for lost ATP.
Teaching Point:
Ischemia halts oxidative phosphorylation by removing oxygen
as the electron acceptor.
Citation:
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
Reference: Ch. 1 — Introduction
Question 2 — Stem:
A febrile oncology patient has neutropenia and a low-grade
,fever. Which statement best describes why fever is often
beneficial during infection?
A. Fever reduces leukocyte mobility, protecting tissues from
damage.
B. Elevated temperature directly denatures bacterial toxins,
preventing sepsis.
C. Fever enhances immune efficiency by increasing leukocyte
activity and inhibiting some pathogens.
D. Fever suppresses acute-phase protein synthesis to conserve
energy.
Correct Answer: C
Rationales:
Correct: Fever is a regulated rise in hypothalamic set point
mediated by cytokines and PGE₂; it enhances leukocyte function
and can inhibit pathogen replication.
A: Fever increases leukocyte trafficking and function, not
reduces mobility.
B: Temperature elevations rarely denature toxins at physiologic
fevers; the immune-modulatory effects are more important.
D: Fever typically accompanies increased acute-phase protein
production, not suppression.
Teaching Point:
Fever is an adaptive host response that augments immune
function and pathogen control.
, Citation:
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
Reference: Ch. 1 — Introduction
Question 3 — Stem:
A long-term smoker develops columnar, mucin-secreting
epithelium in the distal esophagus. This metaplastic change
increases cancer risk. Which mechanism best explains how
metaplasia predisposes to malignancy?
A. Metaplasia causes irreversible DNA mutations in stem cells
immediately.
B. Reprogramming of stem/progenitor cells creates tissue better
suited to injury but more susceptible to carcinogens.
C. Metaplasia increases local blood flow causing genomic
instability.
D. Metaplastic tissue resists oxidative stress and thereby
accumulates mutations.
Correct Answer: B
Rationales:
Correct: Chronic injury drives reprogramming of
stem/progenitor cells to produce a different, more injury-
resistant cell type; these new cells can be less well adapted to
the microenvironment and more vulnerable to carcinogenic
transformation.
