PATHOPHYSIOLOGY OF DISEASE: AN
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1
1. Reference
Ch. 1 — Introduction — Homeostasis and Disease
Mechanisms
Clinical stem
A 58-year-old man presents with gradual exertional dyspnea
and orthopnea over 3 months. Physical exam shows displaced
PMI and bibasilar crackles. Laboratory studies show elevated B-
type natriuretic peptide (BNP) and modest hyponatremia.
,Considering homeostatic principles, which pathogenic process
best explains his progressive symptoms?
A. Failure of negative feedback resulting in maladaptive volume
retention.
B. Primary intrinsic myocardial infection causing cellular
necrosis.
C. Autoimmune-mediated destruction of cardiomyocytes.
D. Sporadic degenerative loss of conduction tissue causing
bradycardia.
Correct answer
A
Rationales
Correct (A): Heart failure exemplifies disrupted homeostasis
where compensatory neurohormonal negative-feedback
systems (RAAS, sympathetic activity) become maladaptive,
promoting volume retention and worsening pulmonary
congestion—consistent with elevated BNP and hyponatremia.
This links system-level compensation to clinical decompensation
(Hammer & McPhee, Ch.1).
Incorrect (B): Acute infectious necrosis would present more
abruptly with fever, high troponin, and focal wall motion
abnormalities rather than a chronic progressive volume-
overload picture.
Incorrect (C): Autoimmune myocarditis is possible but usually
has subacute onset with inflammatory markers and younger
age spectra; mechanism not the prototypical chronic
,homeostatic failure described.
Incorrect (D): Conduction tissue degeneration causing
bradycardia would produce syncope or presyncope, not volume
overload with elevated BNP.
Teaching point
Chronic failure of homeostatic negative feedback often drives
progressive organ dysfunction.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2. Reference
Ch. 1 — Introduction — Acute vs Chronic Disease
Processes
Clinical stem
A 35-year-old woman reports sudden onset of high fever,
pleuritic chest pain, and shortness of breath over 48 hours.
Chest radiograph shows a focal lobar consolidation. Which
pathophysiologic distinction most aligns with her presentation
compared with chronic lung disease?
A. Predominantly reversible cellular dysfunction with rapid
onset.
B. Progressive accumulation of extracellular matrix causing fixed
airflow limitation.
C. Longstanding maladaptive remodeling with insidious
, symptom escalation.
D. Genetic predisposition without inflammatory cell influx.
Correct answer
A
Rationales
Correct (A): Acute infectious pneumonia causes rapid,
predominantly reversible cellular and tissue dysfunction with
inflammatory exudate; this contrasts with chronic fibrotic
remodeling. This differentiates acute versus chronic temporal
pathogenesis (Ch.1).
Incorrect (B): ECM accumulation and fixed airflow limitation
characterize chronic obstructive or fibrotic processes, not an
acute lobar consolidation.
Incorrect (C): Insidious remodeling describes chronic disease;
the vignette’s 48-hour onset supports acute pathology.
Incorrect (D): Genetic predisposition alone wouldn’t explain
acute febrile consolidation with inflammatory signs.
Teaching point
Acute disease: rapid, often reversible cellular injury; chronic
disease: remodeling and fixed dysfunction.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1
1. Reference
Ch. 1 — Introduction — Homeostasis and Disease
Mechanisms
Clinical stem
A 58-year-old man presents with gradual exertional dyspnea
and orthopnea over 3 months. Physical exam shows displaced
PMI and bibasilar crackles. Laboratory studies show elevated B-
type natriuretic peptide (BNP) and modest hyponatremia.
,Considering homeostatic principles, which pathogenic process
best explains his progressive symptoms?
A. Failure of negative feedback resulting in maladaptive volume
retention.
B. Primary intrinsic myocardial infection causing cellular
necrosis.
C. Autoimmune-mediated destruction of cardiomyocytes.
D. Sporadic degenerative loss of conduction tissue causing
bradycardia.
Correct answer
A
Rationales
Correct (A): Heart failure exemplifies disrupted homeostasis
where compensatory neurohormonal negative-feedback
systems (RAAS, sympathetic activity) become maladaptive,
promoting volume retention and worsening pulmonary
congestion—consistent with elevated BNP and hyponatremia.
This links system-level compensation to clinical decompensation
(Hammer & McPhee, Ch.1).
Incorrect (B): Acute infectious necrosis would present more
abruptly with fever, high troponin, and focal wall motion
abnormalities rather than a chronic progressive volume-
overload picture.
Incorrect (C): Autoimmune myocarditis is possible but usually
has subacute onset with inflammatory markers and younger
age spectra; mechanism not the prototypical chronic
,homeostatic failure described.
Incorrect (D): Conduction tissue degeneration causing
bradycardia would produce syncope or presyncope, not volume
overload with elevated BNP.
Teaching point
Chronic failure of homeostatic negative feedback often drives
progressive organ dysfunction.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2. Reference
Ch. 1 — Introduction — Acute vs Chronic Disease
Processes
Clinical stem
A 35-year-old woman reports sudden onset of high fever,
pleuritic chest pain, and shortness of breath over 48 hours.
Chest radiograph shows a focal lobar consolidation. Which
pathophysiologic distinction most aligns with her presentation
compared with chronic lung disease?
A. Predominantly reversible cellular dysfunction with rapid
onset.
B. Progressive accumulation of extracellular matrix causing fixed
airflow limitation.
C. Longstanding maladaptive remodeling with insidious
, symptom escalation.
D. Genetic predisposition without inflammatory cell influx.
Correct answer
A
Rationales
Correct (A): Acute infectious pneumonia causes rapid,
predominantly reversible cellular and tissue dysfunction with
inflammatory exudate; this contrasts with chronic fibrotic
remodeling. This differentiates acute versus chronic temporal
pathogenesis (Ch.1).
Incorrect (B): ECM accumulation and fixed airflow limitation
characterize chronic obstructive or fibrotic processes, not an
acute lobar consolidation.
Incorrect (C): Insidious remodeling describes chronic disease;
the vignette’s 48-hour onset supports acute pathology.
Incorrect (D): Genetic predisposition alone wouldn’t explain
acute febrile consolidation with inflammatory signs.
Teaching point
Acute disease: rapid, often reversible cellular injury; chronic
disease: remodeling and fixed dysfunction.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
