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 — Concepts: Disease as disordered
physiology; levels of analysis (etiology → pathogenesis →
morphology → clinical significance)
Stem
A 45-year-old man presents with progressive dyspnea and ankle
swelling over 3 months. Echocardiography shows left ventricular
dilation with reduced ejection fraction. Laboratory testing
shows elevated BNP and mild hyponatremia. Which mechanistic
,chain best explains the patient's symptoms from a
pathophysiologic viewpoint?
A. Primary myocardial cell death → systemic inflammatory
cytokine release → peripheral vasodilation causing edema
B. Chronic myocardial pressure overload → concentric
hypertrophy → decreased chamber compliance causing
pulmonary congestion
C. Loss of cardiomyocyte contractile function and remodeling →
reduced forward cardiac output → neurohormonal activation
(RAAS, SNS) → sodium and water retention producing
peripheral edema and hyponatremia
D. Isolated renal tubular dysfunction → volume overload →
secondary cardiac dilation and reduced ejection fraction
Correct answer: C
Rationale — Correct (C)
Heart failure symptoms stem from decreased effective forward
output; that reduced perfusion triggers compensatory
neurohormonal systems (SNS, RAAS, ADH) which increase
sodium and water retention, expanding intravascular volume
and causing congestive symptoms (dyspnea, peripheral edema)
and dilutional hyponatremia. This links molecular/cellular loss
of contractility to systemic manifestations (Chapter 1 emphasis
on connecting mechanisms to clinical findings).
Rationale — Incorrect
A: Primary myocardial cell death alone does not primarily cause
peripheral vasodilation; inflammatory cytokines can contribute
,to cachexia and malaise but do not explain the classic
neurohormonal retention pattern.
B: Pressure overload typically produces concentric hypertrophy;
this patient has dilation and reduced EF consistent with systolic
dysfunction and remodeling, not isolated decreased compliance
from concentric hypertrophy.
D: Primary renal tubular disease could cause volume overload
but would not explain reduced ejection fraction and cardiac
remodeling as the initiating event.
Teaching point
Reduced cardiac output → neurohormonal activation → volume
retention links cellular dysfunction to congestion.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction — Cellular injury: reversible vs
irreversible; ischemia/hypoxia mechanisms
Stem
A 62-year-old woman with diabetes is found unresponsive after
prolonged hypotension from sepsis. Labs show lactic acidosis
and markedly elevated AST/ALT. Which cellular mechanism most
likely produced the hepatocellular injury pattern?
, A. ATP depletion leading to failure of ion pumps → cell swelling
and reversible injury only
B. Hypoxic injury causing mitochondrial permeability transition
→ loss of oxidative phosphorylation → necrosis with release of
intracellular enzymes
C. Autoimmune cytotoxic T-cell mediated apoptosis of
hepatocytes → minimal enzyme release
D. Chronic oxidative stress inducing accumulation of lipofuscin
without acute enzyme elevation
Correct answer: B
Rationale — Correct (B)
Prolonged hypoxia/ischemia causes mitochondrial dysfunction
(permeability transition) and failure of oxidative
phosphorylation, leading to necrotic cell death with membrane
rupture and release of intracellular enzymes (AST/ALT). Chapter
1 highlights mitochondrial failure as the pivot from reversible to
irreversible injury.
Rationale — Incorrect
A: ATP depletion and ion pump failure characterize early
reversible injury but prolonged mitochondrial failure progresses
to irreversible necrosis with enzyme release.
C: Immune-mediated apoptosis typically yields little enzyme
spill because membranes remain intact; pattern here is acute
necrosis.
D: Lipofuscin is a marker of chronic wear-and-tear, not acute
ischemic hepatocellular necrosis.
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1
Reference
Ch. 1 — Introduction — Concepts: Disease as disordered
physiology; levels of analysis (etiology → pathogenesis →
morphology → clinical significance)
Stem
A 45-year-old man presents with progressive dyspnea and ankle
swelling over 3 months. Echocardiography shows left ventricular
dilation with reduced ejection fraction. Laboratory testing
shows elevated BNP and mild hyponatremia. Which mechanistic
,chain best explains the patient's symptoms from a
pathophysiologic viewpoint?
A. Primary myocardial cell death → systemic inflammatory
cytokine release → peripheral vasodilation causing edema
B. Chronic myocardial pressure overload → concentric
hypertrophy → decreased chamber compliance causing
pulmonary congestion
C. Loss of cardiomyocyte contractile function and remodeling →
reduced forward cardiac output → neurohormonal activation
(RAAS, SNS) → sodium and water retention producing
peripheral edema and hyponatremia
D. Isolated renal tubular dysfunction → volume overload →
secondary cardiac dilation and reduced ejection fraction
Correct answer: C
Rationale — Correct (C)
Heart failure symptoms stem from decreased effective forward
output; that reduced perfusion triggers compensatory
neurohormonal systems (SNS, RAAS, ADH) which increase
sodium and water retention, expanding intravascular volume
and causing congestive symptoms (dyspnea, peripheral edema)
and dilutional hyponatremia. This links molecular/cellular loss
of contractility to systemic manifestations (Chapter 1 emphasis
on connecting mechanisms to clinical findings).
Rationale — Incorrect
A: Primary myocardial cell death alone does not primarily cause
peripheral vasodilation; inflammatory cytokines can contribute
,to cachexia and malaise but do not explain the classic
neurohormonal retention pattern.
B: Pressure overload typically produces concentric hypertrophy;
this patient has dilation and reduced EF consistent with systolic
dysfunction and remodeling, not isolated decreased compliance
from concentric hypertrophy.
D: Primary renal tubular disease could cause volume overload
but would not explain reduced ejection fraction and cardiac
remodeling as the initiating event.
Teaching point
Reduced cardiac output → neurohormonal activation → volume
retention links cellular dysfunction to congestion.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction — Cellular injury: reversible vs
irreversible; ischemia/hypoxia mechanisms
Stem
A 62-year-old woman with diabetes is found unresponsive after
prolonged hypotension from sepsis. Labs show lactic acidosis
and markedly elevated AST/ALT. Which cellular mechanism most
likely produced the hepatocellular injury pattern?
, A. ATP depletion leading to failure of ion pumps → cell swelling
and reversible injury only
B. Hypoxic injury causing mitochondrial permeability transition
→ loss of oxidative phosphorylation → necrosis with release of
intracellular enzymes
C. Autoimmune cytotoxic T-cell mediated apoptosis of
hepatocytes → minimal enzyme release
D. Chronic oxidative stress inducing accumulation of lipofuscin
without acute enzyme elevation
Correct answer: B
Rationale — Correct (B)
Prolonged hypoxia/ischemia causes mitochondrial dysfunction
(permeability transition) and failure of oxidative
phosphorylation, leading to necrotic cell death with membrane
rupture and release of intracellular enzymes (AST/ALT). Chapter
1 highlights mitochondrial failure as the pivot from reversible to
irreversible injury.
Rationale — Incorrect
A: ATP depletion and ion pump failure characterize early
reversible injury but prolonged mitochondrial failure progresses
to irreversible necrosis with enzyme release.
C: Immune-mediated apoptosis typically yields little enzyme
spill because membranes remain intact; pattern here is acute
necrosis.
D: Lipofuscin is a marker of chronic wear-and-tear, not acute
ischemic hepatocellular necrosis.
