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 presents after a minor urinary tract
infection with confusion and a temperature of 38.4°C. You note
an acute rise in heart rate and respiratory rate. Explain,
mechanistically, why loss of homeostatic balance produces
systemic clinical signs rather than isolated cellular
abnormalities.
,Options
A. Local cellular damage always releases hormones that act
systemically to produce generalized signs.
B. Homeostatic regulatory systems (neural, endocrine, immune)
respond to local insults causing systemic physiologic changes.
C. Systemic signs reflect genetic predisposition rather than
response to local stressors.
D. Isolated cellular abnormalities remain confined and never
produce systemic effects.
Correct Answer
B
Rationale — Correct (3–4 sentences)
Systemic clinical signs follow because homeostasis depends on
integrated neural, endocrine, and immune feedback. A local
infection activates innate immune mediators (cytokines),
neuroendocrine responses (fever via hypothalamic set-point),
and autonomic adjustments (tachycardia, tachypnea). Gould
emphasizes that pathophysiology links local cellular
derangements to organism-level compensatory responses.
Rationale — Incorrect
A. Hormone release is not the sole mechanism; immune
mediators and neural circuits also drive systemic responses.
C. Genetic predisposition may influence susceptibility but does
not explain acute systemic responses to infection.
D. Local cellular changes can and often do produce systemic
effects through signaling and compensatory systems.
,Teaching Point (≤20 words)
Homeostatic disruption triggers integrated neural-endocrine-
immune responses producing systemic 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 — Stressors and
Cellular Response
Stem
A nurse reviews a chart of a patient exposed to prolonged
hypoxia at high altitude. Which cellular responses should the
nurse expect when oxygen delivery is chronically reduced but
not absent, and why?
Options
A. Necrosis via immediate membrane rupture in all affected
cells.
B. Adaptive changes such as increased mitochondrial density
and altered gene expression promoting anaerobic metabolism.
C. Instant apoptosis mediated by caspases in every cell.
D. Unchanged cellular architecture because hypoxia only affects
organs with low metabolic demands.
, Correct Answer
B
Rationale — Correct (3–4 sentences)
Chronic, sublethal hypoxia elicits adaptive responses:
upregulation of glycolytic enzymes, HIF-mediated gene
expression, and sometimes mitochondrial biogenesis to sustain
ATP. Gould describes these as compensatory cellular
adaptations that preserve viability under persistent stress. Such
changes differ from immediate irreversible injury.
Rationale — Incorrect
A. Necrosis with membrane rupture is characteristic of severe,
acute energy failure, not chronic adaptation.
C. Apoptosis may occur selectively but is not the universal
immediate response to chronic hypoxia.
D. Hypoxia affects high-metabolic tissues and still induces
adaptive remodeling where possible.
Teaching Point (≤20 words)
Chronic sublethal stress triggers adaptive metabolic and
structural remodeling (HIF activation, glycolysis upregulation).
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 — Introduction to Pathophysiology — Homeostasis and
Disease
Stem
A 68-year-old patient presents after a minor urinary tract
infection with confusion and a temperature of 38.4°C. You note
an acute rise in heart rate and respiratory rate. Explain,
mechanistically, why loss of homeostatic balance produces
systemic clinical signs rather than isolated cellular
abnormalities.
,Options
A. Local cellular damage always releases hormones that act
systemically to produce generalized signs.
B. Homeostatic regulatory systems (neural, endocrine, immune)
respond to local insults causing systemic physiologic changes.
C. Systemic signs reflect genetic predisposition rather than
response to local stressors.
D. Isolated cellular abnormalities remain confined and never
produce systemic effects.
Correct Answer
B
Rationale — Correct (3–4 sentences)
Systemic clinical signs follow because homeostasis depends on
integrated neural, endocrine, and immune feedback. A local
infection activates innate immune mediators (cytokines),
neuroendocrine responses (fever via hypothalamic set-point),
and autonomic adjustments (tachycardia, tachypnea). Gould
emphasizes that pathophysiology links local cellular
derangements to organism-level compensatory responses.
Rationale — Incorrect
A. Hormone release is not the sole mechanism; immune
mediators and neural circuits also drive systemic responses.
C. Genetic predisposition may influence susceptibility but does
not explain acute systemic responses to infection.
D. Local cellular changes can and often do produce systemic
effects through signaling and compensatory systems.
,Teaching Point (≤20 words)
Homeostatic disruption triggers integrated neural-endocrine-
immune responses producing systemic 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 — Stressors and
Cellular Response
Stem
A nurse reviews a chart of a patient exposed to prolonged
hypoxia at high altitude. Which cellular responses should the
nurse expect when oxygen delivery is chronically reduced but
not absent, and why?
Options
A. Necrosis via immediate membrane rupture in all affected
cells.
B. Adaptive changes such as increased mitochondrial density
and altered gene expression promoting anaerobic metabolism.
C. Instant apoptosis mediated by caspases in every cell.
D. Unchanged cellular architecture because hypoxia only affects
organs with low metabolic demands.
, Correct Answer
B
Rationale — Correct (3–4 sentences)
Chronic, sublethal hypoxia elicits adaptive responses:
upregulation of glycolytic enzymes, HIF-mediated gene
expression, and sometimes mitochondrial biogenesis to sustain
ATP. Gould describes these as compensatory cellular
adaptations that preserve viability under persistent stress. Such
changes differ from immediate irreversible injury.
Rationale — Incorrect
A. Necrosis with membrane rupture is characteristic of severe,
acute energy failure, not chronic adaptation.
C. Apoptosis may occur selectively but is not the universal
immediate response to chronic hypoxia.
D. Hypoxia affects high-metabolic tissues and still induces
adaptive remodeling where possible.
Teaching Point (≤20 words)
Chronic sublethal stress triggers adaptive metabolic and
structural remodeling (HIF activation, glycolysis upregulation).
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
3)
