INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANKS
1
Reference
Ch. 1 — Introduction — Cellular Injury: Reversible vs.
Irreversible
Stem
A 62-year-old man presents with chest pain for 18 hours. ECG
shows evolving ST-segment changes. Troponin is markedly
elevated. A cardiac MRI performed 3 days later demonstrates a
transmural region of late gadolinium enhancement. Which
cellular process best explains the MRI appearance indicating
permanent loss of myocardial tissue?
,A. Reversible mitochondrial swelling with preserved cell
membrane integrity
B. Irreversible loss of plasma membrane integrity with
enzymatic digestion of cellular constituents
C. Accumulation of intracellular glycogen without cell death
D. Adaptive hypertrophy of surviving cardiomyocytes without
cell loss
Correct answer
B
Rationale — Correct
Transmural late gadolinium enhancement indicates fibrosis
from necrotic cell death. Hammer & McPhee describe
irreversible injury as characterized by loss of plasma membrane
integrity and enzymatic digestion of cell components leading to
inflammation and replacement by fibrous tissue. This
mechanism explains permanent MRI signal changes.
Rationale — Incorrect
A. Mitochondrial swelling with intact membranes is a feature of
reversible injury and would not produce permanent scar.
C. Glycogen accumulation is a reversible metabolic change and
does not explain tissue loss or fibrosis.
D. Hypertrophy is an adaptive response of surviving cells; it
does not produce the transmural scar pattern seen here.
Teaching point
Irreversible injury = membrane rupture → enzymatic digestion
→ fibrosis.
,Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction — Mechanisms of Ischemic Cell Injury
Stem
A middle-aged woman with prolonged hypotension following
major trauma develops acute kidney injury with muddy brown
granular casts. Which pathophysiologic mechanism most
directly produced the observed tubular epithelial cell necrosis?
A. Chronic adaptive increase in renal blood flow
B. ATP depletion leading to loss of ion pump function and cell
swelling
C. Autoimmune attack on tubular basement membrane
D. Hypersensitivity-mediated microvascular thrombosis
Correct answer
B
Rationale — Correct
Ischemia causes rapid ATP depletion, impairing Na⁺/K⁺-ATPase
and Ca²⁺ pumps, leading to ionic imbalance, cell swelling, and
necrosis — classic in acute tubular necrosis producing muddy
brown casts. Hammer & McPhee emphasize ATP depletion as
the proximate cause of ischemic cell injury.
, Rationale — Incorrect
A. Chronic adaptive increased flow is not present in acute
ischemia and would not cause necrosis.
C. Autoimmune attack is not the primary mechanism in
ischemic tubular injury.
D. Hypersensitivity with thrombosis is less characteristic;
ischemia due to hypotension is primarily ATP depletion.
Teaching point
Ischemic ATP depletion → pump failure → ionic imbalance →
necrosis.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
3
Reference
Ch. 1 — Introduction — Oxidative Stress and Free Radical Injury
Stem
A patient undergoes reperfusion of a limb after 6 hours of
ischemia. Within hours, tissue swelling and progressive cellular
damage occur disproportionate to the period of ischemia.
Which mechanism best accounts for reperfusion-associated
injury?
A. Restoration of aerobic ATP production preventing further
damage