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
Pathophysiology-Focused Question Stem
A 58-year-old patient develops fainting spells after taking a new
antihypertensive that causes abrupt vasodilation. Explain how
disruption of homeostatic control of blood pressure can
produce syncope and which compensatory mechanism is most
immediately invoked. Use cellular/tissue-level reasoning to
predict the earliest physiologic response.
Options
A. Increased ADH release to expand intravascular volume.
,B. Baroreceptor-mediated sympathetic activation causing
tachycardia and vasoconstriction.
C. Renin–angiotensin–aldosterone system (RAAS) activation
causing sodium retention over hours.
D. Peripheral chemoreceptor stimulation causing increased
respiratory rate.
Correct Answer
B
Rationale — Correct (3–4 sentences)
Baroreceptors detect the sudden drop in arterial pressure and
trigger rapid sympathetic outflow, producing tachycardia and
peripheral vasoconstriction to restore perfusion. This is the
immediate neural compensatory response operating within
seconds and is driven by mechanosensitive afferents rather
than slower endocrine systems. The cellular effect includes
increased myocardial contractility and arteriolar smooth-muscle
constriction via catecholamine signaling.
Rationale — Incorrect
A. ADH release contributes to volume retention but is a slower
hormonal response and does not rapidly reverse acute
vasodilation.
C. RAAS increases blood volume and peripheral resistance but
acts over minutes to hours, not seconds.
D. Peripheral chemoreceptors respond primarily to
hypoxemia/hypercapnia and do not directly correct acute
hypotension.
,Teaching Point (≤20 words)
Baroreceptor-sympathetic response is the immediate neural
compensation for sudden blood pressure drops.
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:
Atrophy, Hypertrophy
Pathophysi-Focused Question Stem
A patient has chronic unilateral renal artery stenosis; the
contralateral kidney enlarges over months. Which cellular
process best explains compensatory enlargement, and which
intracellular change is essential to support increased functional
demand?
Options
A. Hyperplasia with increased cell number via mitotic division
and cyclin upregulation.
B. Hypertrophy with increased cellular protein synthesis and
organelle biogenesis.
C. Metaplasia with phenotypic transformation of tubular
epithelium.
, D. Dysplasia with disordered growth and increased nuclear
atypia.
Correct Answer
B
Rationale — Correct (3–4 sentences)
Compensatory enlargement of the contralateral kidney is classic
hypertrophy: surviving cells increase in size and functional
capacity through upregulated protein synthesis and organelle
proliferation (mitochondria, ER) to meet higher workload.
Hypertrophy is driven by growth factor and mechanical-stress
signaling pathways that increase synthesis of contractile and
metabolic proteins rather than increasing cell number. These
intracellular alterations improve single-cell output without
necessitating mitosis.
Rationale — Incorrect
A. Hyperplasia increases cell number and occurs in tissues
capable of mitosis (e.g., liver), but compensatory renal
enlargement here is primarily hypertrophy of nephrons.
C. Metaplasia refers to change in cell type and is not a
compensatory enlargement mechanism.
D. Dysplasia denotes disordered growth often preceding
neoplasia, not adaptive functional enlargement.
Teaching Point (≤20 words)
Hypertrophy increases individual cell protein and organelle
content to meet increased functional demand.
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1.
Reference
Ch. 1 — Introduction to Pathophysiology — Homeostasis and
Disease
Pathophysiology-Focused Question Stem
A 58-year-old patient develops fainting spells after taking a new
antihypertensive that causes abrupt vasodilation. Explain how
disruption of homeostatic control of blood pressure can
produce syncope and which compensatory mechanism is most
immediately invoked. Use cellular/tissue-level reasoning to
predict the earliest physiologic response.
Options
A. Increased ADH release to expand intravascular volume.
,B. Baroreceptor-mediated sympathetic activation causing
tachycardia and vasoconstriction.
C. Renin–angiotensin–aldosterone system (RAAS) activation
causing sodium retention over hours.
D. Peripheral chemoreceptor stimulation causing increased
respiratory rate.
Correct Answer
B
Rationale — Correct (3–4 sentences)
Baroreceptors detect the sudden drop in arterial pressure and
trigger rapid sympathetic outflow, producing tachycardia and
peripheral vasoconstriction to restore perfusion. This is the
immediate neural compensatory response operating within
seconds and is driven by mechanosensitive afferents rather
than slower endocrine systems. The cellular effect includes
increased myocardial contractility and arteriolar smooth-muscle
constriction via catecholamine signaling.
Rationale — Incorrect
A. ADH release contributes to volume retention but is a slower
hormonal response and does not rapidly reverse acute
vasodilation.
C. RAAS increases blood volume and peripheral resistance but
acts over minutes to hours, not seconds.
D. Peripheral chemoreceptors respond primarily to
hypoxemia/hypercapnia and do not directly correct acute
hypotension.
,Teaching Point (≤20 words)
Baroreceptor-sympathetic response is the immediate neural
compensation for sudden blood pressure drops.
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:
Atrophy, Hypertrophy
Pathophysi-Focused Question Stem
A patient has chronic unilateral renal artery stenosis; the
contralateral kidney enlarges over months. Which cellular
process best explains compensatory enlargement, and which
intracellular change is essential to support increased functional
demand?
Options
A. Hyperplasia with increased cell number via mitotic division
and cyclin upregulation.
B. Hypertrophy with increased cellular protein synthesis and
organelle biogenesis.
C. Metaplasia with phenotypic transformation of tubular
epithelium.
, D. Dysplasia with disordered growth and increased nuclear
atypia.
Correct Answer
B
Rationale — Correct (3–4 sentences)
Compensatory enlargement of the contralateral kidney is classic
hypertrophy: surviving cells increase in size and functional
capacity through upregulated protein synthesis and organelle
proliferation (mitochondria, ER) to meet higher workload.
Hypertrophy is driven by growth factor and mechanical-stress
signaling pathways that increase synthesis of contractile and
metabolic proteins rather than increasing cell number. These
intracellular alterations improve single-cell output without
necessitating mitosis.
Rationale — Incorrect
A. Hyperplasia increases cell number and occurs in tissues
capable of mitosis (e.g., liver), but compensatory renal
enlargement here is primarily hypertrophy of nephrons.
C. Metaplasia refers to change in cell type and is not a
compensatory enlargement mechanism.
D. Dysplasia denotes disordered growth often preceding
neoplasia, not adaptive functional enlargement.
Teaching Point (≤20 words)
Hypertrophy increases individual cell protein and organelle
content to meet increased functional demand.
