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 — Homeostasis and Disease
Mechanisms
Stem: A 58-year-old man presents with progressive fatigue,
orthostatic lightheadedness, and resting tachycardia.
Laboratory studies show a fall in daytime blood pressure,
hemoconcentration, and elevated plasma catecholamines. You
are asked to explain how chronic alterations in steady-state set
points produce these clinical signs. Which pathophysiologic
principle best accounts for this presentation?
,A. Failure of negative feedback leading to persistent
compensatory activation.
B. Loss of redundancy in parallel physiologic pathways
producing abrupt decompensation.
C. Resetting of the homeostatic set point with new steady state
and maladaptive compensation.
D. Autoimmune-mediated destruction of the baroreceptors.
Correct answer: C
Rationale — Correct (3–4 sentences): Resetting of the
homeostatic set point explains a new, maladaptive steady state
in which blood pressure regulation and autonomic tone operate
around an altered baseline. Chapter 1 emphasizes that disease
often reflects altered set points (not simply on/off failure)
where compensatory mechanisms become chronic and produce
new physiologic equilibria. The elevated catecholamines and
hemoconcentration reflect chronic compensatory shifts rather
than an acute loss of feedback alone.
Rationale — A (1–3 sentences): Failure of negative feedback can
cause persistent activation, but this option implies loss of
feedback rather than establishment of a new set point; it does
not fully explain the chronic steady-state changes described in
the vignette.
Rationale — B (1–3 sentences): Loss of redundancy typically
causes vulnerability to acute failure; it does not account for a
gradually established new baseline with chronic compensatory
markers.
Rationale — D (1–3 sentences): Autoimmune baroreceptor
,destruction is mechanistically unlikely and would be expected
to show different clinical and histologic evidence; Chapter 1
does not prioritize this mechanism in introductory homeostasis
discussion.
Teaching point (≤20 words): Disease often represents a shifted
homeostatic set point with chronic maladaptive compensation.
Citation: Hammer, G. D., & McPhee, S. J. (2025).
Pathophysiology of Disease (8th ed.). Chapter 1.
2.
Reference: Ch. 1 — Introduction — Cellular Adaptation to Stress
Stem: A 45-year-old woman with a long history of alcohol use is
found to have hepatomegaly and elevated liver enzymes. A
biopsy shows hepatocyte enlargement with increased smooth
endoplasmic reticulum and mitochondrial proliferation without
necrosis. Which adaptive response best explains these
histologic findings?
A. Hypertrophy due to increased functional demand.
B. Hyperplasia from increased cell proliferation.
C. Metaplasia with change in cell lineage.
D. Dysplasia from genomic instability.
Correct answer: A
Rationale — Correct (3–4 sentences): Hypertrophy is
characterized by increased cell size and organelle proliferation
(e.g., SER and mitochondria) in response to increased metabolic
load or toxin processing. Chapter 1 describes hypertrophy as an
, adaptive enlargement of existing cells to meet increased
functional demand, matching the biopsy findings without cell
number increase or malignant features. The presence of
enlarged hepatocytes with more organelles is classic for
hypertrophic adaptation to chronic toxin exposure.
Rationale — B (1–3 sentences): Hyperplasia implies increased
cell number and is not consistent with isolated enlargement
and organelle proliferation without mitotic activity.
Rationale — C (1–3 sentences): Metaplasia involves a reversible
change in cell type (e.g., columnar to squamous) and is not
represented by organelle proliferation within hepatocytes.
Rationale — D (1–3 sentences): Dysplasia implies disordered
growth and nuclear atypia; the vignette lacks features of
genomic instability or premalignant change.
Teaching point: Hypertrophy increases cell organelles and size
to meet chronic functional demands.
Citation: Hammer, G. D., & McPhee, S. J. (2025).
Pathophysiology of Disease (8th ed.). Chapter 1.
3.
Reference: Ch. 1 — Introduction — Reversible vs Irreversible
Cell Injury
Stem: A patient with prolonged limb ischemia becomes
reperfused after 6 hours. Muscle biopsy shows sarcolemmal
disruption, myofibrillar necrosis, and loss of nuclei. Troponin-I is
normal. Which interpretation best describes the biopsy in light
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1.
Reference: Ch. 1 — Introduction — Homeostasis and Disease
Mechanisms
Stem: A 58-year-old man presents with progressive fatigue,
orthostatic lightheadedness, and resting tachycardia.
Laboratory studies show a fall in daytime blood pressure,
hemoconcentration, and elevated plasma catecholamines. You
are asked to explain how chronic alterations in steady-state set
points produce these clinical signs. Which pathophysiologic
principle best accounts for this presentation?
,A. Failure of negative feedback leading to persistent
compensatory activation.
B. Loss of redundancy in parallel physiologic pathways
producing abrupt decompensation.
C. Resetting of the homeostatic set point with new steady state
and maladaptive compensation.
D. Autoimmune-mediated destruction of the baroreceptors.
Correct answer: C
Rationale — Correct (3–4 sentences): Resetting of the
homeostatic set point explains a new, maladaptive steady state
in which blood pressure regulation and autonomic tone operate
around an altered baseline. Chapter 1 emphasizes that disease
often reflects altered set points (not simply on/off failure)
where compensatory mechanisms become chronic and produce
new physiologic equilibria. The elevated catecholamines and
hemoconcentration reflect chronic compensatory shifts rather
than an acute loss of feedback alone.
Rationale — A (1–3 sentences): Failure of negative feedback can
cause persistent activation, but this option implies loss of
feedback rather than establishment of a new set point; it does
not fully explain the chronic steady-state changes described in
the vignette.
Rationale — B (1–3 sentences): Loss of redundancy typically
causes vulnerability to acute failure; it does not account for a
gradually established new baseline with chronic compensatory
markers.
Rationale — D (1–3 sentences): Autoimmune baroreceptor
,destruction is mechanistically unlikely and would be expected
to show different clinical and histologic evidence; Chapter 1
does not prioritize this mechanism in introductory homeostasis
discussion.
Teaching point (≤20 words): Disease often represents a shifted
homeostatic set point with chronic maladaptive compensation.
Citation: Hammer, G. D., & McPhee, S. J. (2025).
Pathophysiology of Disease (8th ed.). Chapter 1.
2.
Reference: Ch. 1 — Introduction — Cellular Adaptation to Stress
Stem: A 45-year-old woman with a long history of alcohol use is
found to have hepatomegaly and elevated liver enzymes. A
biopsy shows hepatocyte enlargement with increased smooth
endoplasmic reticulum and mitochondrial proliferation without
necrosis. Which adaptive response best explains these
histologic findings?
A. Hypertrophy due to increased functional demand.
B. Hyperplasia from increased cell proliferation.
C. Metaplasia with change in cell lineage.
D. Dysplasia from genomic instability.
Correct answer: A
Rationale — Correct (3–4 sentences): Hypertrophy is
characterized by increased cell size and organelle proliferation
(e.g., SER and mitochondria) in response to increased metabolic
load or toxin processing. Chapter 1 describes hypertrophy as an
, adaptive enlargement of existing cells to meet increased
functional demand, matching the biopsy findings without cell
number increase or malignant features. The presence of
enlarged hepatocytes with more organelles is classic for
hypertrophic adaptation to chronic toxin exposure.
Rationale — B (1–3 sentences): Hyperplasia implies increased
cell number and is not consistent with isolated enlargement
and organelle proliferation without mitotic activity.
Rationale — C (1–3 sentences): Metaplasia involves a reversible
change in cell type (e.g., columnar to squamous) and is not
represented by organelle proliferation within hepatocytes.
Rationale — D (1–3 sentences): Dysplasia implies disordered
growth and nuclear atypia; the vignette lacks features of
genomic instability or premalignant change.
Teaching point: Hypertrophy increases cell organelles and size
to meet chronic functional demands.
Citation: Hammer, G. D., & McPhee, S. J. (2025).
Pathophysiology of Disease (8th ed.). Chapter 1.
3.
Reference: Ch. 1 — Introduction — Reversible vs Irreversible
Cell Injury
Stem: A patient with prolonged limb ischemia becomes
reperfused after 6 hours. Muscle biopsy shows sarcolemmal
disruption, myofibrillar necrosis, and loss of nuclei. Troponin-I is
normal. Which interpretation best describes the biopsy in light
