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 Pathogenesis
Clinical stem
A 68-year-old man presents after a large gastrointestinal bleed.
His blood pressure is 86/54 mm Hg and heart rate 124/min.
Over the next hour his urine output falls to 10 mL/hr despite IV
crystalloids. Which physiological mechanism most directly
explains the acute tachycardia and reduced urine output in the
setting of hemorrhagic hypovolemia?
,A. Increased atrial natriuretic peptide causing natriuresis and
diuresis
B. Activation of sympathetic nervous system and renin–
angiotensin–aldosterone system (RAAS) causing
vasoconstriction and renal sodium retention
C. Cytokine-mediated vasodilation causing decreased effective
circulating volume
D. Increased pulmonary baroreceptor firing causing
parasympathetic predominance and bradycardia
Correct answer
B
Rationale — Correct (B)
Acute hemorrhage lowers arterial pressure and effective
arterial blood volume, triggering baroreceptor-mediated
sympathetic activation and RAAS release. Sympathetic tone
increases heart rate and peripheral vasoconstriction; RAAS
promotes sodium and water retention, reducing urine output.
These are classic compensatory homeostatic responses
described in Ch. 1.
Rationales — Incorrect
A. ANP causes natriuresis/diuresis and would oppose the
observed oliguria and tachycardia; it is not the primary acute
compensatory response to hypovolemia.
C. Cytokine-mediated vasodilation is seen in sepsis; in
hemorrhage the dominant response is vasoconstriction and
sympathetic activation.
,D. Pulmonary baroreceptors do not cause parasympathetic-
mediated bradycardia in hypovolemia; the opposite
(sympathetic response) occurs.
Teaching point
Acute hypovolemia → baroreceptor + SNS + RAAS activation →
tachycardia, renal sodium/water retention.
Citation (Simplified APA)
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
accessphysiotherapy.mhmedical.com+1
2
Reference
Ch. 1 — Introduction — Etiology vs Pathogenesis
Clinical stem
A 29-year-old woman presents with progressive muscle
weakness and ptosis that fluctuates during the day. Family
history is negative. Electrophysiology suggests a neuromuscular
junction transmission defect. Which statement best
distinguishes “etiology” from “pathogenesis” in this
presentation?
A. Etiology refers to the acetylcholine receptor defect;
pathogenesis is the genetic mutation causing it.
B. Etiology is the underlying cause (autoimmune antibodies);
pathogenesis describes how antibodies impair neuromuscular
, transmission.
C. Etiology and pathogenesis are synonymous and
interchangeable in this disorder.
D. Pathogenesis refers to epidemiologic risk factors; etiology
describes clinical manifestations.
Correct answer
B
Rationale — Correct (B)
Etiology denotes the cause (here, autoantibodies against
acetylcholine receptors). Pathogenesis describes the sequence
of molecular and cellular events by which those antibodies
reduce receptor availability and impair neuromuscular
transmission, producing fatigue and ptosis. Ch. 1 emphasizes
this etiologic vs mechanistic distinction.
Rationales — Incorrect
A. Reverses the terms: the receptor defect is a mechanism,
while autoimmune antibodies are the etiologic cause.
C. The textbook distinguishes etiology (cause) from
pathogenesis (mechanism); they are not synonymous.
D. Pathogenesis is about mechanisms, not epidemiologic risk
factors; etiology is the cause.
Teaching point
Etiology = cause; pathogenesis = mechanistic sequence from
cause to clinical effect.
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANKS
1
Reference
Ch. 1 — Introduction — Homeostasis and Pathogenesis
Clinical stem
A 68-year-old man presents after a large gastrointestinal bleed.
His blood pressure is 86/54 mm Hg and heart rate 124/min.
Over the next hour his urine output falls to 10 mL/hr despite IV
crystalloids. Which physiological mechanism most directly
explains the acute tachycardia and reduced urine output in the
setting of hemorrhagic hypovolemia?
,A. Increased atrial natriuretic peptide causing natriuresis and
diuresis
B. Activation of sympathetic nervous system and renin–
angiotensin–aldosterone system (RAAS) causing
vasoconstriction and renal sodium retention
C. Cytokine-mediated vasodilation causing decreased effective
circulating volume
D. Increased pulmonary baroreceptor firing causing
parasympathetic predominance and bradycardia
Correct answer
B
Rationale — Correct (B)
Acute hemorrhage lowers arterial pressure and effective
arterial blood volume, triggering baroreceptor-mediated
sympathetic activation and RAAS release. Sympathetic tone
increases heart rate and peripheral vasoconstriction; RAAS
promotes sodium and water retention, reducing urine output.
These are classic compensatory homeostatic responses
described in Ch. 1.
Rationales — Incorrect
A. ANP causes natriuresis/diuresis and would oppose the
observed oliguria and tachycardia; it is not the primary acute
compensatory response to hypovolemia.
C. Cytokine-mediated vasodilation is seen in sepsis; in
hemorrhage the dominant response is vasoconstriction and
sympathetic activation.
,D. Pulmonary baroreceptors do not cause parasympathetic-
mediated bradycardia in hypovolemia; the opposite
(sympathetic response) occurs.
Teaching point
Acute hypovolemia → baroreceptor + SNS + RAAS activation →
tachycardia, renal sodium/water retention.
Citation (Simplified APA)
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
accessphysiotherapy.mhmedical.com+1
2
Reference
Ch. 1 — Introduction — Etiology vs Pathogenesis
Clinical stem
A 29-year-old woman presents with progressive muscle
weakness and ptosis that fluctuates during the day. Family
history is negative. Electrophysiology suggests a neuromuscular
junction transmission defect. Which statement best
distinguishes “etiology” from “pathogenesis” in this
presentation?
A. Etiology refers to the acetylcholine receptor defect;
pathogenesis is the genetic mutation causing it.
B. Etiology is the underlying cause (autoimmune antibodies);
pathogenesis describes how antibodies impair neuromuscular
, transmission.
C. Etiology and pathogenesis are synonymous and
interchangeable in this disorder.
D. Pathogenesis refers to epidemiologic risk factors; etiology
describes clinical manifestations.
Correct answer
B
Rationale — Correct (B)
Etiology denotes the cause (here, autoantibodies against
acetylcholine receptors). Pathogenesis describes the sequence
of molecular and cellular events by which those antibodies
reduce receptor availability and impair neuromuscular
transmission, producing fatigue and ptosis. Ch. 1 emphasizes
this etiologic vs mechanistic distinction.
Rationales — Incorrect
A. Reverses the terms: the receptor defect is a mechanism,
while autoimmune antibodies are the etiologic cause.
C. The textbook distinguishes etiology (cause) from
pathogenesis (mechanism); they are not synonymous.
D. Pathogenesis is about mechanisms, not epidemiologic risk
factors; etiology is the cause.
Teaching point
Etiology = cause; pathogenesis = mechanistic sequence from
cause to clinical effect.
