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 — Fundamental concepts:
homeostasis, disease as disordered physiology
Stem: A 62-year-old man develops progressive fatigue, mild
orthostatic lightheadedness, and peripheral edema after several
episodes of an acute inflammatory illness. Vital signs show
resting tachycardia and a blood pressure that falls with
standing. Laboratory testing shows mild hypoalbuminemia but
normal serum sodium. Which pathophysiologic principle best
explains his combination of orthostatic symptoms and edema?
A. Failure of local autoregulation producing regional
hypoperfusion
B. Loss of effective circulating volume secondary to decreased
,plasma oncotic pressure
C. Increased capillary hydrostatic pressure due to renal sodium
retention alone
D. Systemic vasodilation caused by persistent inflammatory
mediator release
Correct answer: B
Rationale — Correct (B): Hypoalbuminemia reduces plasma
oncotic (colloid) osmotic pressure, lowering effective
intravascular volume despite normal total body sodium. This
causes transcapillary fluid shift producing peripheral edema and
decreases venous return leading to orthostatic intolerance and
reflex tachycardia. Chapter 1 frames disease manifestations as
consequences of disrupted fluid homeostasis and Starling
forces. AccessMedicine
Rationale — Incorrect:
A: Autoregulation explains regional perfusion control, not
generalized edema with hypoalbuminemia.
C: Renal sodium retention can raise hydrostatic pressure, but
the vignette emphasizes hypoalbuminemia and normal sodium.
D: Systemic vasodilation can cause orthostasis but would not
explain dependent edema absent capillary oncotic changes.
Teaching point: Low plasma oncotic pressure causes edema
while reducing effective circulating volume.
,Citation (APA): Hammer, G. D., & McPhee, S. J. (2025).
Pathophysiology of Disease (8th ed.). Chapter 1.
AccessMedicine
2)
Reference: Ch. 1 — Introduction — Acute vs. chronic disease
and compensatory responses
Stem: A 45-year-old woman reports new exertional dyspnea
over six months. Echocardiography shows concentric left
ventricular hypertrophy with preserved ejection fraction.
Laboratory studies show elevated B-type natriuretic peptide
(BNP). Which mechanism most plausibly links chronic increased
afterload to her symptoms?
A. Chronic increased afterload leads to myocyte hyperplasia,
reducing chamber stiffness and improving diastolic filling
B. Myocyte hypertrophy increases myocardial oxygen demand
and impairs relaxation, causing diastolic dysfunction and
elevated filling pressures
C. Afterload reduction causes eccentric remodeling and systolic
failure, raising BNP
D. Increased afterload causes microvascular dilation that
decreases perfusion pressure and limits contractility
Correct answer: B
Rationale — Correct (B): Chapter 1 emphasizes that chronic
hemodynamic stress provokes adaptive myocyte hypertrophy.
, While initially compensatory, hypertrophy increases oxygen
demand and stiffens the ventricle, impairing diastolic filling and
raising left-sided filling pressures and BNP—explaining
exertional dyspnea with preserved EF. AccessMedicine
Rationale — Incorrect:
A: Myocyte hyperplasia is not the dominant response in adult
heart; hypertrophy increases stiffness, not reduces it.
C: Afterload reduction would improve symptoms; eccentric
remodeling and systolic failure occur with volume overload or
later maladaptation, not initial concentric hypertrophy.
D: Microvascular dilation does not follow increased afterload
and would not account for concentric hypertrophy with
diastolic dysfunction.
Teaching point: Chronic pressure overload → myocyte
hypertrophy → diastolic dysfunction and raised filling pressures.
Citation (APA): Hammer, G. D., & McPhee, S. J. (2025).
Pathophysiology of Disease (8th ed.). Chapter 1.
AccessMedicine
3)
Reference: Ch. 1 — Introduction — Cellular adaptation:
atrophy, hypertrophy, hyperplasia, metaplasia
Stem: A 58-year-old lifelong smoker complains of chronic
cough. Bronchoscopy reveals columnar epithelial cells in the
trachea replaced by stratified squamous epithelium. Which
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1)
Reference: Ch. 1 — Introduction — Fundamental concepts:
homeostasis, disease as disordered physiology
Stem: A 62-year-old man develops progressive fatigue, mild
orthostatic lightheadedness, and peripheral edema after several
episodes of an acute inflammatory illness. Vital signs show
resting tachycardia and a blood pressure that falls with
standing. Laboratory testing shows mild hypoalbuminemia but
normal serum sodium. Which pathophysiologic principle best
explains his combination of orthostatic symptoms and edema?
A. Failure of local autoregulation producing regional
hypoperfusion
B. Loss of effective circulating volume secondary to decreased
,plasma oncotic pressure
C. Increased capillary hydrostatic pressure due to renal sodium
retention alone
D. Systemic vasodilation caused by persistent inflammatory
mediator release
Correct answer: B
Rationale — Correct (B): Hypoalbuminemia reduces plasma
oncotic (colloid) osmotic pressure, lowering effective
intravascular volume despite normal total body sodium. This
causes transcapillary fluid shift producing peripheral edema and
decreases venous return leading to orthostatic intolerance and
reflex tachycardia. Chapter 1 frames disease manifestations as
consequences of disrupted fluid homeostasis and Starling
forces. AccessMedicine
Rationale — Incorrect:
A: Autoregulation explains regional perfusion control, not
generalized edema with hypoalbuminemia.
C: Renal sodium retention can raise hydrostatic pressure, but
the vignette emphasizes hypoalbuminemia and normal sodium.
D: Systemic vasodilation can cause orthostasis but would not
explain dependent edema absent capillary oncotic changes.
Teaching point: Low plasma oncotic pressure causes edema
while reducing effective circulating volume.
,Citation (APA): Hammer, G. D., & McPhee, S. J. (2025).
Pathophysiology of Disease (8th ed.). Chapter 1.
AccessMedicine
2)
Reference: Ch. 1 — Introduction — Acute vs. chronic disease
and compensatory responses
Stem: A 45-year-old woman reports new exertional dyspnea
over six months. Echocardiography shows concentric left
ventricular hypertrophy with preserved ejection fraction.
Laboratory studies show elevated B-type natriuretic peptide
(BNP). Which mechanism most plausibly links chronic increased
afterload to her symptoms?
A. Chronic increased afterload leads to myocyte hyperplasia,
reducing chamber stiffness and improving diastolic filling
B. Myocyte hypertrophy increases myocardial oxygen demand
and impairs relaxation, causing diastolic dysfunction and
elevated filling pressures
C. Afterload reduction causes eccentric remodeling and systolic
failure, raising BNP
D. Increased afterload causes microvascular dilation that
decreases perfusion pressure and limits contractility
Correct answer: B
Rationale — Correct (B): Chapter 1 emphasizes that chronic
hemodynamic stress provokes adaptive myocyte hypertrophy.
, While initially compensatory, hypertrophy increases oxygen
demand and stiffens the ventricle, impairing diastolic filling and
raising left-sided filling pressures and BNP—explaining
exertional dyspnea with preserved EF. AccessMedicine
Rationale — Incorrect:
A: Myocyte hyperplasia is not the dominant response in adult
heart; hypertrophy increases stiffness, not reduces it.
C: Afterload reduction would improve symptoms; eccentric
remodeling and systolic failure occur with volume overload or
later maladaptation, not initial concentric hypertrophy.
D: Microvascular dilation does not follow increased afterload
and would not account for concentric hypertrophy with
diastolic dysfunction.
Teaching point: Chronic pressure overload → myocyte
hypertrophy → diastolic dysfunction and raised filling pressures.
Citation (APA): Hammer, G. D., & McPhee, S. J. (2025).
Pathophysiology of Disease (8th ed.). Chapter 1.
AccessMedicine
3)
Reference: Ch. 1 — Introduction — Cellular adaptation:
atrophy, hypertrophy, hyperplasia, metaplasia
Stem: A 58-year-old lifelong smoker complains of chronic
cough. Bronchoscopy reveals columnar epithelial cells in the
trachea replaced by stratified squamous epithelium. Which
