PATHOPHYSIOLOGY OF DISEASE: AN
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1)
Reference
Ch. 1 — Introduction — Homeostasis and Clinical Presentation
Stem
A 54-year-old man presents with lightheadedness and
orthostatic hypotension after starting a new antihypertensive
medication. Laboratory studies show normal hemoglobin and
electrolytes. Which pathophysiologic principle best explains
why a previously asymptomatic patient develops symptomatic
hypotension after a small pharmacologic perturbation?
,A. Loss of redundancy in physiologic control reduces
compensatory reserve.
B. A single-point mutation causing exaggerated drug sensitivity.
C. Acute tissue necrosis leading to sympathetic failure.
D. Primary endocrine failure unrelated to the drug.
Correct answer: A
Rationale — Correct (A):
Chapter 1 emphasizes homeostasis and the concept of
physiological reserve and redundancy. Small perturbations (e.g.,
a medication) can produce symptoms when compensatory
mechanisms are already operating near capacity; loss of
redundancy or reduced reserve manifests as symptomatic
failure despite minor insults. This explains orthostatic symptoms
without structural damage.
Rationale — Incorrect (B):
A single-point mutation causing exaggerated sensitivity would
be rare and is not the most parsimonious mechanism here;
Chapter 1 focuses on systems-level reserve rather than
uncommon genetic variants for typical iatrogenic reactions.
Rationale — Incorrect (C):
Acute tissue necrosis causing sympathetic failure would present
with additional signs (e.g., organ dysfunction); the vignette lacks
such evidence.
Rationale — Incorrect (D):
Primary endocrine failure would have biochemical
,abnormalities; labs are normal and the temporal relation to
drug initiation supports a homeostatic reserve explanation.
Teaching point:
Physiologic reserve limits determine symptom onset after minor
perturbations.
Citation:
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2)
Reference
Ch. 1 — Introduction — Cellular Adaptation vs. Injury
Stem
A 45-year-old habitual alcoholic develops hepatomegaly and
mild transaminase elevation. Liver biopsy shows hepatocyte
enlargement with increased smooth endoplasmic reticulum and
intracellular fat vacuoles but no widespread necrosis. Which
description best characterizes the hepatocyte response?
A. Reversible cellular adaptation involving altered organelle
content and metabolic stress.
B. Irreversible necrosis due to overwhelming ATP depletion.
C. Apoptosis mediated by caspase activation and inflammatory
cell infiltration.
D. Autoimmune-mediated cytotoxic T-lymphocyte injury.
, Correct answer: A
Rationale — Correct (A):
Chapter 1 differentiates adaptation from injury. Hepatocyte
enlargement with increased SER and steatosis represents
reversible adaptation to chronic toxin exposure and altered lipid
metabolism. Organellar proliferation reflects adaptive
upregulation rather than irreversible cell death.
Rationale — Incorrect (B):
Irreversible necrosis would show cell membrane rupture and
inflammatory response; biopsy lacks necrosis.
Rationale — Incorrect (C):
Apoptosis is programmed cell death with cell shrinkage and
apoptotic bodies; biopsy describes enlargement and steatosis,
not apoptotic morphology.
Rationale — Incorrect (D):
Autoimmune cytotoxicity would show lymphocytic infiltrates
and scattered apoptotic hepatocytes, not isolated adaptive
organellar changes.
Teaching point:
Adaptive organelle remodeling signals reversible cellular
response to chronic stress.
Citation:
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1)
Reference
Ch. 1 — Introduction — Homeostasis and Clinical Presentation
Stem
A 54-year-old man presents with lightheadedness and
orthostatic hypotension after starting a new antihypertensive
medication. Laboratory studies show normal hemoglobin and
electrolytes. Which pathophysiologic principle best explains
why a previously asymptomatic patient develops symptomatic
hypotension after a small pharmacologic perturbation?
,A. Loss of redundancy in physiologic control reduces
compensatory reserve.
B. A single-point mutation causing exaggerated drug sensitivity.
C. Acute tissue necrosis leading to sympathetic failure.
D. Primary endocrine failure unrelated to the drug.
Correct answer: A
Rationale — Correct (A):
Chapter 1 emphasizes homeostasis and the concept of
physiological reserve and redundancy. Small perturbations (e.g.,
a medication) can produce symptoms when compensatory
mechanisms are already operating near capacity; loss of
redundancy or reduced reserve manifests as symptomatic
failure despite minor insults. This explains orthostatic symptoms
without structural damage.
Rationale — Incorrect (B):
A single-point mutation causing exaggerated sensitivity would
be rare and is not the most parsimonious mechanism here;
Chapter 1 focuses on systems-level reserve rather than
uncommon genetic variants for typical iatrogenic reactions.
Rationale — Incorrect (C):
Acute tissue necrosis causing sympathetic failure would present
with additional signs (e.g., organ dysfunction); the vignette lacks
such evidence.
Rationale — Incorrect (D):
Primary endocrine failure would have biochemical
,abnormalities; labs are normal and the temporal relation to
drug initiation supports a homeostatic reserve explanation.
Teaching point:
Physiologic reserve limits determine symptom onset after minor
perturbations.
Citation:
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2)
Reference
Ch. 1 — Introduction — Cellular Adaptation vs. Injury
Stem
A 45-year-old habitual alcoholic develops hepatomegaly and
mild transaminase elevation. Liver biopsy shows hepatocyte
enlargement with increased smooth endoplasmic reticulum and
intracellular fat vacuoles but no widespread necrosis. Which
description best characterizes the hepatocyte response?
A. Reversible cellular adaptation involving altered organelle
content and metabolic stress.
B. Irreversible necrosis due to overwhelming ATP depletion.
C. Apoptosis mediated by caspase activation and inflammatory
cell infiltration.
D. Autoimmune-mediated cytotoxic T-lymphocyte injury.
, Correct answer: A
Rationale — Correct (A):
Chapter 1 differentiates adaptation from injury. Hepatocyte
enlargement with increased SER and steatosis represents
reversible adaptation to chronic toxin exposure and altered lipid
metabolism. Organellar proliferation reflects adaptive
upregulation rather than irreversible cell death.
Rationale — Incorrect (B):
Irreversible necrosis would show cell membrane rupture and
inflammatory response; biopsy lacks necrosis.
Rationale — Incorrect (C):
Apoptosis is programmed cell death with cell shrinkage and
apoptotic bodies; biopsy describes enlargement and steatosis,
not apoptotic morphology.
Rationale — Incorrect (D):
Autoimmune cytotoxicity would show lymphocytic infiltrates
and scattered apoptotic hepatocytes, not isolated adaptive
organellar changes.
Teaching point:
Adaptive organelle remodeling signals reversible cellular
response to chronic stress.
Citation:
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
