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
Question Stem
A 68-year-old patient has multiple chronic diseases and now
develops acute organ dysfunction after a minor infection. Which
pathophysiologic principle best explains why this patient
decompensated with only a mild infectious insult?
Options
A. Genetic mutations accumulated with age cause acute organ
failure.
,B. Reduced physiologic reserve and impaired homeostatic
mechanisms.
C. Acute infection always progresses to multiorgan failure in
older adults.
D. Increased baseline inflammatory mediator production
protects against decompensation.
Correct Answer
B
Rationales
Correct: Older patients often have decreased physiologic
reserve and impaired capacity to maintain homeostasis, so even
minor stressors can precipitate organ dysfunction.
A: Aging-related decompensation is not primarily from newly
acquired genetic mutations.
C: Acute infection does not always lead to multiorgan failure —
the outcome depends on reserve and response.
D: Chronic low-grade inflammation may exist with aging, but it
does not protect from decompensation.
Teaching Point
Diminished physiological reserve increases vulnerability to small
physiologic stresses.
Citation (Simplified APA)
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
,2
Reference
Ch. 1 — Introduction
Question Stem
You are designing a quality-improvement protocol to reduce
hospital-acquired complications. Which systems-level
pathophysiology concept should you prioritize to most directly
reduce patient harm?
Options
A. Genetic predisposition screening for all hospitalized patients.
B. Identification and interruption of common pathways leading
to tissue injury.
C. Increasing patient bedrest to limit metabolic demands.
D. Routinely testing for rare metabolic disorders.
Correct Answer
B
Rationales
Correct: Preventing hospital-acquired injury focuses on
interrupting common injury pathways (e.g., ischemia, infection,
pressure) to reduce harm.
A: Universal genetic screening is not a practical immediate
strategy for preventing hospital-acquired complications.
C: Prolonged bedrest increases risk (e.g., deconditioning,
pressure injury).
, D: Routine testing for rare disorders has low yield for reducing
common hospital harms.
Teaching Point
Targeting common injury pathways yields the greatest impact
on preventable harm.
Citation (Simplified APA)
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3
Reference
Ch. 1 — Introduction
Question Stem
A patient has persistent fatigue and weight loss. Lab tests show
elevated inflammatory markers but no clear infection. Using
pathophysiologic reasoning, which process best explains
systemic symptoms in chronic inflammation?
Options
A. Cytokine-mediated changes in metabolism and hypothalamic
regulation.
B. Direct organ invasion by bacteria without fever.
C. Loss of all endocrine function causing anorexia.
D. Rapid depletion of neutrophils causing malaise.
Clinical Medicine
8th Edition
Author(s)Gary D. Hammer; Stephen J. McPhee
TEST BANK
1
Reference
Ch. 1 — Introduction
Question Stem
A 68-year-old patient has multiple chronic diseases and now
develops acute organ dysfunction after a minor infection. Which
pathophysiologic principle best explains why this patient
decompensated with only a mild infectious insult?
Options
A. Genetic mutations accumulated with age cause acute organ
failure.
,B. Reduced physiologic reserve and impaired homeostatic
mechanisms.
C. Acute infection always progresses to multiorgan failure in
older adults.
D. Increased baseline inflammatory mediator production
protects against decompensation.
Correct Answer
B
Rationales
Correct: Older patients often have decreased physiologic
reserve and impaired capacity to maintain homeostasis, so even
minor stressors can precipitate organ dysfunction.
A: Aging-related decompensation is not primarily from newly
acquired genetic mutations.
C: Acute infection does not always lead to multiorgan failure —
the outcome depends on reserve and response.
D: Chronic low-grade inflammation may exist with aging, but it
does not protect from decompensation.
Teaching Point
Diminished physiological reserve increases vulnerability to small
physiologic stresses.
Citation (Simplified APA)
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
,2
Reference
Ch. 1 — Introduction
Question Stem
You are designing a quality-improvement protocol to reduce
hospital-acquired complications. Which systems-level
pathophysiology concept should you prioritize to most directly
reduce patient harm?
Options
A. Genetic predisposition screening for all hospitalized patients.
B. Identification and interruption of common pathways leading
to tissue injury.
C. Increasing patient bedrest to limit metabolic demands.
D. Routinely testing for rare metabolic disorders.
Correct Answer
B
Rationales
Correct: Preventing hospital-acquired injury focuses on
interrupting common injury pathways (e.g., ischemia, infection,
pressure) to reduce harm.
A: Universal genetic screening is not a practical immediate
strategy for preventing hospital-acquired complications.
C: Prolonged bedrest increases risk (e.g., deconditioning,
pressure injury).
, D: Routine testing for rare disorders has low yield for reducing
common hospital harms.
Teaching Point
Targeting common injury pathways yields the greatest impact
on preventable harm.
Citation (Simplified APA)
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3
Reference
Ch. 1 — Introduction
Question Stem
A patient has persistent fatigue and weight loss. Lab tests show
elevated inflammatory markers but no clear infection. Using
pathophysiologic reasoning, which process best explains
systemic symptoms in chronic inflammation?
Options
A. Cytokine-mediated changes in metabolism and hypothalamic
regulation.
B. Direct organ invasion by bacteria without fever.
C. Loss of all endocrine function causing anorexia.
D. Rapid depletion of neutrophils causing malaise.
