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 Mechanisms and Clinical
Correlation
Clinical stem
A 54-year-old man presents with progressive fatigue and pallor
over 3 months. Lab testing shows normocytic anemia, low
reticulocyte count, and an elevated creatinine compared with
prior values. The clinician hypothesizes impaired erythropoietin
production as the primary driver. Which pathophysiologic
reasoning most strongly supports this hypothesis?
,A. Chronic blood loss causing iron deficiency leading to low
hemoglobin and low reticulocytes.
B. Primary bone-marrow aplasia causing decreased red cell
production and low reticulocyte count.
C. Reduced renal erythropoietin output due to chronic kidney
disease leading to decreased erythroid stimulation.
D. Hemolytic anemia with peripheral destruction causing low
haptoglobin and high reticulocyte count.
Correct answer
C
Rationales
Correct (C): Hammer & McPhee emphasize linking organ
dysfunction to systemic manifestations. Chronic kidney
dysfunction reduces renal erythropoietin synthesis, producing a
normocytic, low-reticulocyte anemia consistent with decreased
marrow stimulation. This mechanism best explains
simultaneous rising creatinine and low reticulocyte production.
Incorrect (A): Iron deficiency from chronic blood loss typically
causes microcytic anemia and would often show iron indices
abnormalities; reticulocyte responses depend on iron
availability but the normocytic picture and renal failure point
elsewhere.
Incorrect (B): Primary marrow aplasia would produce
pancytopenia or isolated marrow findings and generally
requires marrow confirmation; the concurrent renal
impairment favors decreased erythropoietin over intrinsic
,marrow failure.
Incorrect (D): Hemolysis produces an elevated reticulocyte
count and hemolytic markers (low haptoglobin, high LDH). The
low reticulocyte count observed here argues against hemolysis.
Teaching point
Renal failure → decreased erythropoietin → normocytic anemia
with low reticulocyte count.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction — Reversible versus Irreversible Cellular
Injury
Clinical stem
A 67-year-old woman experiences transient chest pain;
troponin is minimally elevated for 6 hours and returns toward
baseline. Cardiac MRI shows a brief region of myocardial edema
without persistent wall motion abnormality. Which statement
best applies to the cellular biology underlying this
presentation?
A. Reperfusion after brief ischemia causes irreversible necrosis
mediated by extensive membrane rupture.
B. Short ischemic episodes produce reversible cellular injury
, marked by loss of ATP, reversible membrane ion pump
dysfunction, and cytoplasmic swelling.
C. Apoptotic pathways are immediately activated after any
ischemia and always cause permanent loss of myocardial cells.
D. Persistent mitochondrial permeability transition pore
opening is absent in reversible injury and thus not relevant
here.
Correct answer
B
Rationales
Correct (B): Chapter 1 outlines that reversible ischemic injury
features ATP depletion, reversible ion-pump failure, sodium and
water influx, and cytoplasmic swelling; this mechanism aligns
with transient troponin leak and edema without permanent
dysfunction.
Incorrect (A): Irreversible necrosis with membrane rupture
typically follows prolonged ischemia; the MRI and functional
recovery argue against extensive necrosis.
Incorrect (C): While apoptosis can be induced by severe stress,
it is not uniformly immediate nor always leads to clinically
significant permanent cell loss after brief ischemia.
Incorrect (D): Mitochondrial permeability transition pore
opening can be involved in both reversible and irreversible
injury dynamics; stating it is absent in reversible injury is overly
absolute and inconsistent with the nuanced concept presented
in the chapter.
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1
Reference
Ch. 1 — Introduction — Disease Mechanisms and Clinical
Correlation
Clinical stem
A 54-year-old man presents with progressive fatigue and pallor
over 3 months. Lab testing shows normocytic anemia, low
reticulocyte count, and an elevated creatinine compared with
prior values. The clinician hypothesizes impaired erythropoietin
production as the primary driver. Which pathophysiologic
reasoning most strongly supports this hypothesis?
,A. Chronic blood loss causing iron deficiency leading to low
hemoglobin and low reticulocytes.
B. Primary bone-marrow aplasia causing decreased red cell
production and low reticulocyte count.
C. Reduced renal erythropoietin output due to chronic kidney
disease leading to decreased erythroid stimulation.
D. Hemolytic anemia with peripheral destruction causing low
haptoglobin and high reticulocyte count.
Correct answer
C
Rationales
Correct (C): Hammer & McPhee emphasize linking organ
dysfunction to systemic manifestations. Chronic kidney
dysfunction reduces renal erythropoietin synthesis, producing a
normocytic, low-reticulocyte anemia consistent with decreased
marrow stimulation. This mechanism best explains
simultaneous rising creatinine and low reticulocyte production.
Incorrect (A): Iron deficiency from chronic blood loss typically
causes microcytic anemia and would often show iron indices
abnormalities; reticulocyte responses depend on iron
availability but the normocytic picture and renal failure point
elsewhere.
Incorrect (B): Primary marrow aplasia would produce
pancytopenia or isolated marrow findings and generally
requires marrow confirmation; the concurrent renal
impairment favors decreased erythropoietin over intrinsic
,marrow failure.
Incorrect (D): Hemolysis produces an elevated reticulocyte
count and hemolytic markers (low haptoglobin, high LDH). The
low reticulocyte count observed here argues against hemolysis.
Teaching point
Renal failure → decreased erythropoietin → normocytic anemia
with low reticulocyte count.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction — Reversible versus Irreversible Cellular
Injury
Clinical stem
A 67-year-old woman experiences transient chest pain;
troponin is minimally elevated for 6 hours and returns toward
baseline. Cardiac MRI shows a brief region of myocardial edema
without persistent wall motion abnormality. Which statement
best applies to the cellular biology underlying this
presentation?
A. Reperfusion after brief ischemia causes irreversible necrosis
mediated by extensive membrane rupture.
B. Short ischemic episodes produce reversible cellular injury
, marked by loss of ATP, reversible membrane ion pump
dysfunction, and cytoplasmic swelling.
C. Apoptotic pathways are immediately activated after any
ischemia and always cause permanent loss of myocardial cells.
D. Persistent mitochondrial permeability transition pore
opening is absent in reversible injury and thus not relevant
here.
Correct answer
B
Rationales
Correct (B): Chapter 1 outlines that reversible ischemic injury
features ATP depletion, reversible ion-pump failure, sodium and
water influx, and cytoplasmic swelling; this mechanism aligns
with transient troponin leak and edema without permanent
dysfunction.
Incorrect (A): Irreversible necrosis with membrane rupture
typically follows prolonged ischemia; the MRI and functional
recovery argue against extensive necrosis.
Incorrect (C): While apoptosis can be induced by severe stress,
it is not uniformly immediate nor always leads to clinically
significant permanent cell loss after brief ischemia.
Incorrect (D): Mitochondrial permeability transition pore
opening can be involved in both reversible and irreversible
injury dynamics; stating it is absent in reversible injury is overly
absolute and inconsistent with the nuanced concept presented
in the chapter.
