GOULD'S PATHOPHYSIOLOGY FOR THE
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1
Reference
Ch. 1 — What Is Pathophysiology and Why Study It? —
Homeostasis and Disease
Stem
A 72-year-old patient experiences lightheadedness and
transient syncope when rising from bed. Vital signs show a rapid
drop in systolic blood pressure on standing. Considering
homeostatic mechanisms, which pathophysiologic explanation
best links the etiology to the patient’s manifestation?
Options
A. Decreased plasma oncotic pressure causes third-spacing and
,orthostatic hypotension.
B. Impaired baroreceptor reflex decreases sympathetic
vasoconstrictor response on standing.
C. Increased antidiuretic hormone release causes volume
overload and orthostatic intolerance.
D. Enhanced parasympathetic tone raises heart rate, producing
syncope.
Correct Answer
B
Rationales
Correct (B): Age-related impairment of baroreceptor sensitivity
reduces rapid sympathetic-mediated vasoconstriction upon
standing, causing an acute drop in arterial pressure and cerebral
perfusion; this mechanism links physiologic control failure to
orthostatic syncope. It reflects a failure in homeostatic reflexes
described in introductory pathophysiology.
Incorrect (A): Low oncotic pressure causes edema from fluid
shifts, not the rapid positional blood pressure change typical of
orthostatic reflex failure.
Incorrect (C): ADH-mediated water retention leads to volume
expansion rather than acute hypotension on standing; it would
not produce immediate syncope.
Incorrect (D): Increased parasympathetic tone would lower
heart rate (bradycardia), not raise it; bradycardia could cause
syncope, but the option is internally inconsistent and does not
explain postural blood pressure drop.
,Teaching Point
Baroreceptor failure impairs rapid sympathetic compensation
for postural changes, causing orthostatic hypotension.
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 Cellular Changes — Cellular Adaptation:
Atrophy and Hypertrophy
Stem
A 45-year-old construction worker develops progressive muscle
enlargement in one forearm after switching to a new tool
requiring stronger grip and repetitive contraction. Which
cellular adaptation best explains the sustained increase in
muscle fiber size?
Options
A. Hyperplasia of myofibers through increased cell division.
B. Hypertrophy due to increased synthesis of contractile
proteins within existing myofibers.
C. Metaplasia with transformation of fibroblasts to myocytes.
D. Dysplasia from disordered muscle cell arrangement.
Correct Answer
B
, Rationales
Correct (B): Skeletal muscle fibers are terminally differentiated;
increased functional demand leads to hypertrophy via
upregulated protein synthesis and enlargement of individual
myocytes, matching the mechanism for adaptive hypertrophy
outlined in the chapter.
Incorrect (A): Skeletal myofibers are not capable of significant
mitotic hyperplasia; hyperplasia applies to cell types with
proliferative capacity (e.g., epithelium).
Incorrect (C): Metaplasia is a reversible replacement of one
differentiated cell type by another (often epithelial), not
conversion of fibroblasts into contractile muscle fibers.
Incorrect (D): Dysplasia refers to disordered growth and atypia,
typically pre-neoplastic, and does not describe physiologic
enlargement from increased workload.
Teaching Point
Hypertrophy enlarges nondividing cells via increased protein
synthesis in response to increased functional demand.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
3
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1
Reference
Ch. 1 — What Is Pathophysiology and Why Study It? —
Homeostasis and Disease
Stem
A 72-year-old patient experiences lightheadedness and
transient syncope when rising from bed. Vital signs show a rapid
drop in systolic blood pressure on standing. Considering
homeostatic mechanisms, which pathophysiologic explanation
best links the etiology to the patient’s manifestation?
Options
A. Decreased plasma oncotic pressure causes third-spacing and
,orthostatic hypotension.
B. Impaired baroreceptor reflex decreases sympathetic
vasoconstrictor response on standing.
C. Increased antidiuretic hormone release causes volume
overload and orthostatic intolerance.
D. Enhanced parasympathetic tone raises heart rate, producing
syncope.
Correct Answer
B
Rationales
Correct (B): Age-related impairment of baroreceptor sensitivity
reduces rapid sympathetic-mediated vasoconstriction upon
standing, causing an acute drop in arterial pressure and cerebral
perfusion; this mechanism links physiologic control failure to
orthostatic syncope. It reflects a failure in homeostatic reflexes
described in introductory pathophysiology.
Incorrect (A): Low oncotic pressure causes edema from fluid
shifts, not the rapid positional blood pressure change typical of
orthostatic reflex failure.
Incorrect (C): ADH-mediated water retention leads to volume
expansion rather than acute hypotension on standing; it would
not produce immediate syncope.
Incorrect (D): Increased parasympathetic tone would lower
heart rate (bradycardia), not raise it; bradycardia could cause
syncope, but the option is internally inconsistent and does not
explain postural blood pressure drop.
,Teaching Point
Baroreceptor failure impairs rapid sympathetic compensation
for postural changes, causing orthostatic hypotension.
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 Cellular Changes — Cellular Adaptation:
Atrophy and Hypertrophy
Stem
A 45-year-old construction worker develops progressive muscle
enlargement in one forearm after switching to a new tool
requiring stronger grip and repetitive contraction. Which
cellular adaptation best explains the sustained increase in
muscle fiber size?
Options
A. Hyperplasia of myofibers through increased cell division.
B. Hypertrophy due to increased synthesis of contractile
proteins within existing myofibers.
C. Metaplasia with transformation of fibroblasts to myocytes.
D. Dysplasia from disordered muscle cell arrangement.
Correct Answer
B
, Rationales
Correct (B): Skeletal muscle fibers are terminally differentiated;
increased functional demand leads to hypertrophy via
upregulated protein synthesis and enlargement of individual
myocytes, matching the mechanism for adaptive hypertrophy
outlined in the chapter.
Incorrect (A): Skeletal myofibers are not capable of significant
mitotic hyperplasia; hyperplasia applies to cell types with
proliferative capacity (e.g., epithelium).
Incorrect (C): Metaplasia is a reversible replacement of one
differentiated cell type by another (often epithelial), not
conversion of fibroblasts into contractile muscle fibers.
Incorrect (D): Dysplasia refers to disordered growth and atypia,
typically pre-neoplastic, and does not describe physiologic
enlargement from increased workload.
Teaching Point
Hypertrophy enlarges nondividing cells via increased protein
synthesis in response to increased functional demand.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
3
