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 — What Is
Pathophysiology and Why Study It?
Stem: A 56-year-old patient presents with fatigue, pallor, and
microcytic anemia. As part of a pathophysiologic analysis, you
are asked to explain why manifestations such as pallor occur
before organ-level failure. Which explanation best links
pathophysiology concepts from cellular change to clinical signs?
A. Clinical signs reflect random cellular damage and therefore
have little predictable relationship to organ dysfunction.
B. Early clinical signs occur because altered cellular function
(e.g., decreased hemoglobin synthesis) disrupts tissue
,homeostasis before structural organ damage is evident.
C. Organ-level failure must occur before any clinical signs are
present because cells compensate indefinitely.
D. Pallor arises from psychosomatic responses and is not
addressed by cellular pathophysiology.
Correct answer: B
Rationale — Correct: Early clinical signs reflect altered cell
function that disturbs homeostasis (for example, decreased
hemoglobin production reduces oxygen delivery and produces
pallor and fatigue) before gross structural damage to the organ
is apparent. This mechanistic chain—etiology → cellular
dysfunction → tissue/organ manifestation—is central to
pathophysiology.
Rationale — Incorrect:
A. Incorrect — clinical signs are not random; they often follow
predictable mechanisms tied to cellular dysfunction.
C. Incorrect — cells and tissues have limited compensatory
capacity; dysfunction commonly precedes frank organ failure.
D. Incorrect — pallor in anemia is physiological, not
psychosomatic, and is explained by cellular-level decreases in
erythrocyte/hemoglobin function.
Teaching point: Clinical signs often reflect functional cellular
disruption before structural organ failure.
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 —
Homeostasis and Stressors
Stem: A patient exposed to sustained loud noise develops
tinnitus and diminished hearing thresholds over months. From
a pathophysiologic perspective, which statement best describes
the relationship between stressor, homeostasis, and cellular
adaptation?
A. Homeostasis implies cells cannot change; any change
indicates irreversible injury.
B. Sustained stressors prompt adaptive cellular responses that
preserve function; maladaptation occurs when the stressor
overwhelms adaptive capacity.
C. Cellular adaptation only occurs in congenital conditions and
not from environmental stressors.
D. Homeostatic imbalance always leads directly to necrosis
without intermediate adaptation.
Correct answer: B
Rationale — Correct: Homeostasis is dynamic; sustained
stressors (e.g., noise) induce adaptive responses (structural or
functional) to preserve function. When the stress exceeds
adaptive capacity, maladaptive changes and injury follow. This
progression—stress → adaptation → decompensation—is a
core pathophysiologic principle.
, Rationale — Incorrect:
A. Incorrect — cells can and do change (adapt) in response to
stress.
C. Incorrect — adaptation occurs in response to many
environmental and physiologic stressors, not only congenital
factors.
D. Incorrect — imbalance often leads first to adaptation or
reversible injury rather than immediate necrosis.
Teaching point: Adaptation preserves function; injury occurs
when stress exceeds adaptive capacity.
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 — Cellular
Adaptation: Atrophy
Stem: An elderly patient with chronic malnutrition shows
muscle wasting and decreased organ mass. Which cellular
mechanism best explains atrophy in this context?
A. Increased cellular protein synthesis driven by growth factors.
B. Reduced metabolic demand with decreased protein synthesis
and increased proteasomal degradation (ubiquitin–proteasome
pathway).
C. Uncontrolled cell proliferation leading to smaller cells.
D. Metaplasia of muscle cells into adipose tissue.
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1)
Reference: Ch. 1 — Introduction to Pathophysiology — What Is
Pathophysiology and Why Study It?
Stem: A 56-year-old patient presents with fatigue, pallor, and
microcytic anemia. As part of a pathophysiologic analysis, you
are asked to explain why manifestations such as pallor occur
before organ-level failure. Which explanation best links
pathophysiology concepts from cellular change to clinical signs?
A. Clinical signs reflect random cellular damage and therefore
have little predictable relationship to organ dysfunction.
B. Early clinical signs occur because altered cellular function
(e.g., decreased hemoglobin synthesis) disrupts tissue
,homeostasis before structural organ damage is evident.
C. Organ-level failure must occur before any clinical signs are
present because cells compensate indefinitely.
D. Pallor arises from psychosomatic responses and is not
addressed by cellular pathophysiology.
Correct answer: B
Rationale — Correct: Early clinical signs reflect altered cell
function that disturbs homeostasis (for example, decreased
hemoglobin production reduces oxygen delivery and produces
pallor and fatigue) before gross structural damage to the organ
is apparent. This mechanistic chain—etiology → cellular
dysfunction → tissue/organ manifestation—is central to
pathophysiology.
Rationale — Incorrect:
A. Incorrect — clinical signs are not random; they often follow
predictable mechanisms tied to cellular dysfunction.
C. Incorrect — cells and tissues have limited compensatory
capacity; dysfunction commonly precedes frank organ failure.
D. Incorrect — pallor in anemia is physiological, not
psychosomatic, and is explained by cellular-level decreases in
erythrocyte/hemoglobin function.
Teaching point: Clinical signs often reflect functional cellular
disruption before structural organ failure.
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 —
Homeostasis and Stressors
Stem: A patient exposed to sustained loud noise develops
tinnitus and diminished hearing thresholds over months. From
a pathophysiologic perspective, which statement best describes
the relationship between stressor, homeostasis, and cellular
adaptation?
A. Homeostasis implies cells cannot change; any change
indicates irreversible injury.
B. Sustained stressors prompt adaptive cellular responses that
preserve function; maladaptation occurs when the stressor
overwhelms adaptive capacity.
C. Cellular adaptation only occurs in congenital conditions and
not from environmental stressors.
D. Homeostatic imbalance always leads directly to necrosis
without intermediate adaptation.
Correct answer: B
Rationale — Correct: Homeostasis is dynamic; sustained
stressors (e.g., noise) induce adaptive responses (structural or
functional) to preserve function. When the stress exceeds
adaptive capacity, maladaptive changes and injury follow. This
progression—stress → adaptation → decompensation—is a
core pathophysiologic principle.
, Rationale — Incorrect:
A. Incorrect — cells can and do change (adapt) in response to
stress.
C. Incorrect — adaptation occurs in response to many
environmental and physiologic stressors, not only congenital
factors.
D. Incorrect — imbalance often leads first to adaptation or
reversible injury rather than immediate necrosis.
Teaching point: Adaptation preserves function; injury occurs
when stress exceeds adaptive capacity.
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 — Cellular
Adaptation: Atrophy
Stem: An elderly patient with chronic malnutrition shows
muscle wasting and decreased organ mass. Which cellular
mechanism best explains atrophy in this context?
A. Increased cellular protein synthesis driven by growth factors.
B. Reduced metabolic demand with decreased protein synthesis
and increased proteasomal degradation (ubiquitin–proteasome
pathway).
C. Uncontrolled cell proliferation leading to smaller cells.
D. Metaplasia of muscle cells into adipose tissue.
