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 — Disease as a disruption of homeostasis
Stem
A 56-year-old woman presents with progressive exertional
dyspnea and lower-extremity edema over months. Laboratory
testing shows hypoalbuminemia and elevated BNP. Which
pathophysiologic principle best explains why a focal injury in
the myocardium can lead to systemic edema and end-organ
hypoperfusion?
,A. Loss of cell membrane integrity in affected cardiomyocytes
leads to immediate systemic inflammatory cytokine storm.
B. Localized decrease in myocardial contractile mass reduces
effective forward cardiac output, producing compensatory fluid
retention and increased hydrostatic pressure.
C. Focal myocardial injury causes direct renal parenchymal
damage via circulating cardiotoxins, producing nephrotic
syndrome.
D. Myocardial injury increases oncotic pressure systemically by
increasing plasma proteins that sequester fluid interstitially.
Correct answer
B
Rationale — Correct (B)
A reduction in effective myocardial contractile mass lowers
forward output, activating neurohormonal compensatory
mechanisms (RAAS, sympathetic tone) that promote salt and
water retention and raise venous pressures. Increased
hydrostatic pressure in the systemic and pulmonary capillaries
favors transudation of fluid into interstitial spaces, causing
edema and organ hypoperfusion. This is the classic mechanism
linking focal cardiac dysfunction to systemic manifestations
(Hammer & McPhee, Ch. 1).
Rationale — Incorrect
A. A cytokine storm is not the usual immediate consequence of
focal cardiomyocyte loss; systemic inflammation may occur but
does not explain chronic volume retention.
,C. There is no primary mechanism whereby injured myocardium
directly causes nephrotic syndrome via circulating cardiotoxins.
D. Oncotic pressure is decreased (hypoalbuminemia) in many
edematous states; myocardial injury does not increase plasma
proteins to sequester fluid.
Teaching point
Reduced forward cardiac output triggers neurohormonal
retention and hydrostatic edema.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction — Etiology versus pathogenesis
Stem
A 28-year-old man with a family history of early-onset colon
cancer undergoes genetic testing and is found to carry a
pathogenic variant in a DNA mismatch-repair gene. He currently
has no lesions on colonoscopy. Which statement best
distinguishes etiology from pathogenesis in this context?
A. Etiology refers to the cellular changes caused by the gene
mutation; pathogenesis refers to the statistical risk conferred.
B. Etiology identifies the inherited mutation as the causal
factor; pathogenesis describes the sequence of molecular and
, cellular events that lead from that mutation to tumor
formation.
C. Etiology and pathogenesis are interchangeable; both mean
“cause” of disease.
D. Etiology predicts time to disease onset; pathogenesis
predicts severity only.
Correct answer
B
Rationale — Correct (B)
Etiology denotes the causal factor (the inherited mismatch-
repair gene mutation), while pathogenesis describes the
mechanistic sequence (accumulation of replication errors,
microsatellite instability, progression from dysplasia to
adenoma to carcinoma) by which the mutation produces
cancer. This distinction is core to clinical reasoning per Hammer
& McPhee, Chapter 1.
Rationale — Incorrect
A. Etiology is not the cellular changes themselves; it is the
cause.
C. They are distinct concepts; interchangeable use is imprecise.
D. Neither term solely predicts timing or severity; both relate to
cause and mechanism.
Teaching point
Etiology = cause; pathogenesis = mechanistic sequence linking
cause to disease.
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1
Reference
Ch. 1 — Introduction — Disease as a disruption of homeostasis
Stem
A 56-year-old woman presents with progressive exertional
dyspnea and lower-extremity edema over months. Laboratory
testing shows hypoalbuminemia and elevated BNP. Which
pathophysiologic principle best explains why a focal injury in
the myocardium can lead to systemic edema and end-organ
hypoperfusion?
,A. Loss of cell membrane integrity in affected cardiomyocytes
leads to immediate systemic inflammatory cytokine storm.
B. Localized decrease in myocardial contractile mass reduces
effective forward cardiac output, producing compensatory fluid
retention and increased hydrostatic pressure.
C. Focal myocardial injury causes direct renal parenchymal
damage via circulating cardiotoxins, producing nephrotic
syndrome.
D. Myocardial injury increases oncotic pressure systemically by
increasing plasma proteins that sequester fluid interstitially.
Correct answer
B
Rationale — Correct (B)
A reduction in effective myocardial contractile mass lowers
forward output, activating neurohormonal compensatory
mechanisms (RAAS, sympathetic tone) that promote salt and
water retention and raise venous pressures. Increased
hydrostatic pressure in the systemic and pulmonary capillaries
favors transudation of fluid into interstitial spaces, causing
edema and organ hypoperfusion. This is the classic mechanism
linking focal cardiac dysfunction to systemic manifestations
(Hammer & McPhee, Ch. 1).
Rationale — Incorrect
A. A cytokine storm is not the usual immediate consequence of
focal cardiomyocyte loss; systemic inflammation may occur but
does not explain chronic volume retention.
,C. There is no primary mechanism whereby injured myocardium
directly causes nephrotic syndrome via circulating cardiotoxins.
D. Oncotic pressure is decreased (hypoalbuminemia) in many
edematous states; myocardial injury does not increase plasma
proteins to sequester fluid.
Teaching point
Reduced forward cardiac output triggers neurohormonal
retention and hydrostatic edema.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction — Etiology versus pathogenesis
Stem
A 28-year-old man with a family history of early-onset colon
cancer undergoes genetic testing and is found to carry a
pathogenic variant in a DNA mismatch-repair gene. He currently
has no lesions on colonoscopy. Which statement best
distinguishes etiology from pathogenesis in this context?
A. Etiology refers to the cellular changes caused by the gene
mutation; pathogenesis refers to the statistical risk conferred.
B. Etiology identifies the inherited mutation as the causal
factor; pathogenesis describes the sequence of molecular and
, cellular events that lead from that mutation to tumor
formation.
C. Etiology and pathogenesis are interchangeable; both mean
“cause” of disease.
D. Etiology predicts time to disease onset; pathogenesis
predicts severity only.
Correct answer
B
Rationale — Correct (B)
Etiology denotes the causal factor (the inherited mismatch-
repair gene mutation), while pathogenesis describes the
mechanistic sequence (accumulation of replication errors,
microsatellite instability, progression from dysplasia to
adenoma to carcinoma) by which the mutation produces
cancer. This distinction is core to clinical reasoning per Hammer
& McPhee, Chapter 1.
Rationale — Incorrect
A. Etiology is not the cellular changes themselves; it is the
cause.
C. They are distinct concepts; interchangeable use is imprecise.
D. Neither term solely predicts timing or severity; both relate to
cause and mechanism.
Teaching point
Etiology = cause; pathogenesis = mechanistic sequence linking
cause to disease.
