PATHOPHYSIOLOGY OF DISEASE: AN
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANKS
1
Reference
Ch. 1 — Introduction — Homeostasis and Fever Mechanisms
Stem
A 28-year-old woman presents with acute onset of fever
(39.5°C), rigors, and diffuse myalgias. Laboratory testing shows
elevated plasma interleukin-1 and C-reactive protein. Which
mechanism best explains the increased core temperature in this
patient?
,A. Direct thermal stimulation of peripheral nociceptors causing
hypothalamic heat production.
B. Cytokine-induced prostaglandin E₂ synthesis in the
hypothalamus raising the thermoregulatory set point.
C. Systemic vasodilation increasing heat retention through
decreased core–shell gradient.
D. Increased skeletal muscle oxidative phosphorylation
producing excess heat independent of central control.
Correct answer: B
Rationale — Correct (B)
Elevated cytokines such as interleukin-1 stimulate prostaglandin
E₂ (PGE₂) production in the hypothalamus, which raises the
thermoregulatory set point, producing fever and rigors. This
mechanism, described in Hammer & McPhee’s introduction to
host responses, links inflammatory signaling to altered central
homeostasis.
Rationale — Incorrect
A. Peripheral nociceptor activation produces pain but does not
centrally reset hypothalamic temperature set point.
C. Vasodilation promotes heat loss rather than retention; fever
typically involves vasoconstriction initially.
D. Increased muscle heat contributes minimally and does not
explain coordinated set-point elevation driven by cytokines.
Teaching point:
Fever reflects cytokine-driven hypothalamic PGE₂ production
and an elevated temperature set point.
,Citation:
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction — Cellular Adaptation: Hypertrophy vs.
Hyperplasia
Stem
A 55-year-old man with longstanding systemic hypertension
develops concentric left ventricular hypertrophy on
echocardiography. Histology shows enlarged cardiomyocytes
without increased mitotic figures. Which cellular adaptation
and mechanism best account for this finding?
A. Hyperplasia from increased cardiomyocyte progenitor
proliferation mediated by growth factors.
B. Hypertrophy from increased synthesis of contractile proteins
driven by mechanical stress signaling.
C. Metaplasia with phenotypic shift of fibroblasts into myocytes
due to ischemia.
D. Atrophy due to decreased workload and proteasomal
degradation of contractile proteins.
Correct answer: B
Rationale — Correct (B)
Concentric ventricular thickening from pressure overload is
, classical hypertrophy: cardiomyocytes enlarge via increased
synthesis of contractile proteins in response to mechanical
stress and growth factor signaling. Hammer & McPhee
emphasize that hypertrophy increases cell size without new cell
division.
Rationale — Incorrect
A. Hyperplasia implies increased cell number with mitoses;
cardiomyocytes in adults rarely proliferate.
C. Metaplasia denotes epithelial phenotypic change, not
fibroblast-to-myocyte conversion.
D. Atrophy involves cell shrinkage and decreased protein
synthesis, opposite to hypertrophy.
Teaching point:
Pressure overload causes hypertrophy via increased contractile
protein synthesis, not hyperplasia.
Citation:
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
3
Reference
Ch. 1 — Introduction — Mechanisms of Ischemia–Reperfusion
Injury
Stem
A 67-year-old man undergoes successful reperfusion of an
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANKS
1
Reference
Ch. 1 — Introduction — Homeostasis and Fever Mechanisms
Stem
A 28-year-old woman presents with acute onset of fever
(39.5°C), rigors, and diffuse myalgias. Laboratory testing shows
elevated plasma interleukin-1 and C-reactive protein. Which
mechanism best explains the increased core temperature in this
patient?
,A. Direct thermal stimulation of peripheral nociceptors causing
hypothalamic heat production.
B. Cytokine-induced prostaglandin E₂ synthesis in the
hypothalamus raising the thermoregulatory set point.
C. Systemic vasodilation increasing heat retention through
decreased core–shell gradient.
D. Increased skeletal muscle oxidative phosphorylation
producing excess heat independent of central control.
Correct answer: B
Rationale — Correct (B)
Elevated cytokines such as interleukin-1 stimulate prostaglandin
E₂ (PGE₂) production in the hypothalamus, which raises the
thermoregulatory set point, producing fever and rigors. This
mechanism, described in Hammer & McPhee’s introduction to
host responses, links inflammatory signaling to altered central
homeostasis.
Rationale — Incorrect
A. Peripheral nociceptor activation produces pain but does not
centrally reset hypothalamic temperature set point.
C. Vasodilation promotes heat loss rather than retention; fever
typically involves vasoconstriction initially.
D. Increased muscle heat contributes minimally and does not
explain coordinated set-point elevation driven by cytokines.
Teaching point:
Fever reflects cytokine-driven hypothalamic PGE₂ production
and an elevated temperature set point.
,Citation:
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2
Reference
Ch. 1 — Introduction — Cellular Adaptation: Hypertrophy vs.
Hyperplasia
Stem
A 55-year-old man with longstanding systemic hypertension
develops concentric left ventricular hypertrophy on
echocardiography. Histology shows enlarged cardiomyocytes
without increased mitotic figures. Which cellular adaptation
and mechanism best account for this finding?
A. Hyperplasia from increased cardiomyocyte progenitor
proliferation mediated by growth factors.
B. Hypertrophy from increased synthesis of contractile proteins
driven by mechanical stress signaling.
C. Metaplasia with phenotypic shift of fibroblasts into myocytes
due to ischemia.
D. Atrophy due to decreased workload and proteasomal
degradation of contractile proteins.
Correct answer: B
Rationale — Correct (B)
Concentric ventricular thickening from pressure overload is
, classical hypertrophy: cardiomyocytes enlarge via increased
synthesis of contractile proteins in response to mechanical
stress and growth factor signaling. Hammer & McPhee
emphasize that hypertrophy increases cell size without new cell
division.
Rationale — Incorrect
A. Hyperplasia implies increased cell number with mitoses;
cardiomyocytes in adults rarely proliferate.
C. Metaplasia denotes epithelial phenotypic change, not
fibroblast-to-myocyte conversion.
D. Atrophy involves cell shrinkage and decreased protein
synthesis, opposite to hypertrophy.
Teaching point:
Pressure overload causes hypertrophy via increased contractile
protein synthesis, not hyperplasia.
Citation:
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
3
Reference
Ch. 1 — Introduction — Mechanisms of Ischemia–Reperfusion
Injury
Stem
A 67-year-old man undergoes successful reperfusion of an
