GOULD'S PATHOPHYSIOLOGY FOR THE
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1
Reference
Ch. 1 — Introduction to Pathophysiology — Homeostasis and
Disease Concepts
Stem (2–4 sentences)
A 68-year-old man presents with progressive fatigue and weight
loss. Laboratory tests show loss of muscle mass and low-grade
fever. Considering pathophysiologic principles, which concept
best explains how persistent disruption of internal steady states
leads to clinical disease manifestations in this patient?
Options
A. Allostasis — frequent resetting of physiologic set points
,protects against disease.
B. Homeostatic failure — inability to maintain internal stability
resulting in organ dysfunction.
C. Redundancy — multiple organs compensate so clinical
manifestations remain absent.
D. Reserve capacity — excess functional capacity prevents any
manifestations until late disease.
Correct answer
B
Rationale — Correct (3–4 sentences)
Homeostatic failure describes the loss of mechanisms that
maintain internal stability; when compensatory systems are
overwhelmed or exhausted, cellular and organ dysfunction
produce clinical manifestations such as muscle wasting and
constitutional symptoms. Gould emphasizes that disease often
reflects the breakdown of homeostatic control rather than a
single abnormality. This explains progressive symptoms when
adaptation and reserve are no longer sufficient.
Rationale — Incorrect
A. Allostasis refers to adaptive change in set points but is not
the mechanism producing progressive organ dysfunction when
compensatory mechanisms fail.
C. Redundancy can delay manifestations but does not account
for progressive symptoms once redundant systems are
overwhelmed.
D. Reserve capacity delays manifestations but eventual failure
,produces disease; it does not explain the current symptomatic
state.
Teaching point (≤20 words)
Disease often reflects failed homeostasis — compensatory
mechanisms exhausted, producing organ dysfunction and
clinical signs.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
2
Reference
Ch. 1 — Introduction to Pathophysiology — Cellular Adaptation
Stem (2–4 sentences)
A middle-aged woman with long-standing hypertension has left
ventricular hypertrophy on echocardiogram. Explain the
primary cellular adaptation that accounts for increased
myocardial wall thickness and how it initially preserves cardiac
output.
Options
A. Hyperplasia — increased cardiomyocyte number to augment
contractility.
B. Hypertrophy — increased cardiomyocyte size due to
enhanced protein synthesis.
C. Metaplasia — transformation of cardiomyocytes into
, fibroblasts improving force generation.
D. Dysplasia — disordered cardiomyocyte maturation increasing
work capacity.
Correct answer
B
Rationale — Correct (3–4 sentences)
Hypertrophy is growth of existing cells (not cell number) with
increased synthesis of contractile proteins and organelles,
producing thicker myocardial walls that initially improve
contractile force and maintain cardiac output under increased
afterload. Gould outlines hypertrophy as a common adaptive
response to increased mechanical load such as hypertension.
Over time, maladaptive changes (fibrosis, ischemia) may reduce
function.
Rationale — Incorrect
A. Hyperplasia is increased cell number and is not a feature of
adult cardiomyocytes, which are terminally differentiated.
C. Metaplasia is a change in cell type and does not occur as an
adaptive increase in contractile tissue.
D. Dysplasia is disordered growth associated with neoplastic
risk, not physiologic adaptation to load.
Teaching point (≤20 words)
Hypertrophy increases cell size and contractile proteins to meet
increased workload; cell number usually does not change in
myocardium.
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1
Reference
Ch. 1 — Introduction to Pathophysiology — Homeostasis and
Disease Concepts
Stem (2–4 sentences)
A 68-year-old man presents with progressive fatigue and weight
loss. Laboratory tests show loss of muscle mass and low-grade
fever. Considering pathophysiologic principles, which concept
best explains how persistent disruption of internal steady states
leads to clinical disease manifestations in this patient?
Options
A. Allostasis — frequent resetting of physiologic set points
,protects against disease.
B. Homeostatic failure — inability to maintain internal stability
resulting in organ dysfunction.
C. Redundancy — multiple organs compensate so clinical
manifestations remain absent.
D. Reserve capacity — excess functional capacity prevents any
manifestations until late disease.
Correct answer
B
Rationale — Correct (3–4 sentences)
Homeostatic failure describes the loss of mechanisms that
maintain internal stability; when compensatory systems are
overwhelmed or exhausted, cellular and organ dysfunction
produce clinical manifestations such as muscle wasting and
constitutional symptoms. Gould emphasizes that disease often
reflects the breakdown of homeostatic control rather than a
single abnormality. This explains progressive symptoms when
adaptation and reserve are no longer sufficient.
Rationale — Incorrect
A. Allostasis refers to adaptive change in set points but is not
the mechanism producing progressive organ dysfunction when
compensatory mechanisms fail.
C. Redundancy can delay manifestations but does not account
for progressive symptoms once redundant systems are
overwhelmed.
D. Reserve capacity delays manifestations but eventual failure
,produces disease; it does not explain the current symptomatic
state.
Teaching point (≤20 words)
Disease often reflects failed homeostasis — compensatory
mechanisms exhausted, producing organ dysfunction and
clinical signs.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
2
Reference
Ch. 1 — Introduction to Pathophysiology — Cellular Adaptation
Stem (2–4 sentences)
A middle-aged woman with long-standing hypertension has left
ventricular hypertrophy on echocardiogram. Explain the
primary cellular adaptation that accounts for increased
myocardial wall thickness and how it initially preserves cardiac
output.
Options
A. Hyperplasia — increased cardiomyocyte number to augment
contractility.
B. Hypertrophy — increased cardiomyocyte size due to
enhanced protein synthesis.
C. Metaplasia — transformation of cardiomyocytes into
, fibroblasts improving force generation.
D. Dysplasia — disordered cardiomyocyte maturation increasing
work capacity.
Correct answer
B
Rationale — Correct (3–4 sentences)
Hypertrophy is growth of existing cells (not cell number) with
increased synthesis of contractile proteins and organelles,
producing thicker myocardial walls that initially improve
contractile force and maintain cardiac output under increased
afterload. Gould outlines hypertrophy as a common adaptive
response to increased mechanical load such as hypertension.
Over time, maladaptive changes (fibrosis, ischemia) may reduce
function.
Rationale — Incorrect
A. Hyperplasia is increased cell number and is not a feature of
adult cardiomyocytes, which are terminally differentiated.
C. Metaplasia is a change in cell type and does not occur as an
adaptive increase in contractile tissue.
D. Dysplasia is disordered growth associated with neoplastic
risk, not physiologic adaptation to load.
Teaching point (≤20 words)
Hypertrophy increases cell size and contractile proteins to meet
increased workload; cell number usually does not change in
myocardium.
