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
Stem
A 68-year-old patient develops persistent polyuria and
polydipsia after a stroke that impaired hypothalamic regulation.
Explain how loss of homeostatic set-point control can produce
signs before structural damage appears, and which cellular-level
concept best explains early dysfunction.
Options
A. Cellular degeneration due to irreversible necrosis.
,B. Disruption of homeostatic control leading to functional
imbalance without immediate structural cell death.
C. Immediate activation of apoptosis in all affected neurons.
D. Compensatory hyperplasia of endocrine organs causing
symptoms.
Correct Answer
B
Rationale — Correct (3–4 sentences)
Loss of homeostatic regulation produces functional
disturbances (e.g., altered fluid balance) before irreversible cell
injury. Chapter 1 emphasizes that pathophysiology links altered
physiologic control mechanisms to clinical signs; dysfunction
can be present with intact cells. This explains
polyuria/polydipsia from neuroendocrine dysregulation without
initial structural cell death.
Rationale — Incorrect
A. Necrosis implies irreversible structural cell death, not an
early functional imbalance.
C. Apoptosis is programmed cell death, not an immediate
universal response to loss of set-point.
D. Hyperplasia is a structural adaptive change; it does not
explain acute dysregulation from hypothalamic injury.
Teaching Point (≤20 words)
Homeostatic failure causes functional disease before
irreversible cellular structural damage occurs.
,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
A middle-aged manual laborer develops skeletal muscle
enlargement after starting heavy resistance training. Which
cellular adaptation best describes increased cell size due to
heightened workload, and what is the main mechanism?
Options
A. Hyperplasia via increased cell number through mitosis.
B. Atrophy via decreased protein synthesis.
C. Hypertrophy via increased synthesis of structural proteins
and organelles.
D. Metaplasia via change in cell type to better withstand stress.
Correct Answer
C
Rationale — Correct (3–4 sentences)
Hypertrophy is increased cell size—common in skeletal and
cardiac muscle exposed to increased workload—driven by
augmented synthesis of contractile proteins and organelles.
Chapter 1 describes hypertrophy as an adaptive mechanism
, where cells enlarge to meet functional demand without
increasing cell number. This explains the laborer’s muscle
enlargement.
Rationale — Incorrect
A. Hyperplasia increases cell number and is typical of tissues
capable of mitosis, not post-mitotic skeletal muscle.
B. Atrophy is decreased cell size from reduced synthesis or
increased proteolysis—opposite of what occurs.
D. Metaplasia is a change in cell type, not simple enlargement
in response to workload.
Teaching Point
Hypertrophy: increased cell size from enhanced
protein/organelle synthesis in response to greater workload.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
3.
Reference
Ch. 1 — Introduction to Pathophysiology — Reversible vs.
Irreversible Cell Injury
Stem
A patient experiences a brief episode of limb ischemia that is
rapidly reperfused. At the cellular level, which finding most
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1.
Reference
Ch. 1 — Introduction to Pathophysiology — Homeostasis and
Disease
Stem
A 68-year-old patient develops persistent polyuria and
polydipsia after a stroke that impaired hypothalamic regulation.
Explain how loss of homeostatic set-point control can produce
signs before structural damage appears, and which cellular-level
concept best explains early dysfunction.
Options
A. Cellular degeneration due to irreversible necrosis.
,B. Disruption of homeostatic control leading to functional
imbalance without immediate structural cell death.
C. Immediate activation of apoptosis in all affected neurons.
D. Compensatory hyperplasia of endocrine organs causing
symptoms.
Correct Answer
B
Rationale — Correct (3–4 sentences)
Loss of homeostatic regulation produces functional
disturbances (e.g., altered fluid balance) before irreversible cell
injury. Chapter 1 emphasizes that pathophysiology links altered
physiologic control mechanisms to clinical signs; dysfunction
can be present with intact cells. This explains
polyuria/polydipsia from neuroendocrine dysregulation without
initial structural cell death.
Rationale — Incorrect
A. Necrosis implies irreversible structural cell death, not an
early functional imbalance.
C. Apoptosis is programmed cell death, not an immediate
universal response to loss of set-point.
D. Hyperplasia is a structural adaptive change; it does not
explain acute dysregulation from hypothalamic injury.
Teaching Point (≤20 words)
Homeostatic failure causes functional disease before
irreversible cellular structural damage occurs.
,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
A middle-aged manual laborer develops skeletal muscle
enlargement after starting heavy resistance training. Which
cellular adaptation best describes increased cell size due to
heightened workload, and what is the main mechanism?
Options
A. Hyperplasia via increased cell number through mitosis.
B. Atrophy via decreased protein synthesis.
C. Hypertrophy via increased synthesis of structural proteins
and organelles.
D. Metaplasia via change in cell type to better withstand stress.
Correct Answer
C
Rationale — Correct (3–4 sentences)
Hypertrophy is increased cell size—common in skeletal and
cardiac muscle exposed to increased workload—driven by
augmented synthesis of contractile proteins and organelles.
Chapter 1 describes hypertrophy as an adaptive mechanism
, where cells enlarge to meet functional demand without
increasing cell number. This explains the laborer’s muscle
enlargement.
Rationale — Incorrect
A. Hyperplasia increases cell number and is typical of tissues
capable of mitosis, not post-mitotic skeletal muscle.
B. Atrophy is decreased cell size from reduced synthesis or
increased proteolysis—opposite of what occurs.
D. Metaplasia is a change in cell type, not simple enlargement
in response to workload.
Teaching Point
Hypertrophy: increased cell size from enhanced
protein/organelle synthesis in response to greater workload.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
3.
Reference
Ch. 1 — Introduction to Pathophysiology — Reversible vs.
Irreversible Cell Injury
Stem
A patient experiences a brief episode of limb ischemia that is
rapidly reperfused. At the cellular level, which finding most
