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 — Homeostasis and Allostasis
Question (Stem)
A 62-year-old man with long-standing hypertension presents
with episodic lightheadedness and orthostatic hypotension
after starting a new antihypertensive. His lab tests show normal
electrolytes. Which pathophysiologic principle best explains
why the patient experiences symptomatic instability when a
previously compensated physiologic control (blood pressure) is
abruptly altered?
,A. Loss of negative feedback set-point resetting (allostatic
overload) leading to failure to maintain homeostasis.
B. Irreversible cellular injury of baroreceptor neurons causing
permanent autonomic dysfunction.
C. Acute inflammatory-mediated endothelial injury causing
transient loss of vascular tone.
D. Autoimmune destruction of renal juxtaglomerular cells
leading to abrupt renin–angiotensin failure.
Correct Answer
A
Rationale — Correct Option
Abrupt changes in a chronic set-point (e.g., blood pressure) can
exceed compensatory mechanisms — termed allostatic
overload — producing symptomatic failure to maintain
homeostasis. The Introduction emphasizes regulatory set-point
adjustments and that sudden perturbations of long-standing
compensation (e.g., chronic hypertension treated aggressively)
produce symptoms due to transient mismatch between new
input and adapted control systems. This explains orthostatic
intolerance after rapid blood pressure lowering. (Hammer &
McPhee, Ch. 1).
Rationale — Incorrect Options
B. Baroreceptor neuronal irreversible injury would be unlikely
after starting an antihypertensive and would produce
persistent, not episodic, dysfunction.
C. Acute inflammatory endothelial injury would present with
,signs of inflammation (fever, edema) and is not the mechanism
after initiating antihypertensive therapy.
D. Autoimmune destruction of juxtaglomerular cells is rare and
would cause chronic renin deficiency rather than an acute
symptomatic response after medication change.
Teaching Point
Sudden reversal of chronic set-point adaptations causes
symptomatic allostatic failure.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2)
Reference
Ch. 1 — Introduction — Reversible versus Irreversible Cell Injury
Question (Stem)
A 45-year-old woman presents with acute chest pain. Cardiac
troponin I is mildly elevated; ECG shows transient ST-segment
depression that resolves on repeat testing. Which mechanistic
interpretation best accounts for transient troponin release with
reversible ischemia?
A. Short-lived membrane permeability increases allowing
limited cytosolic enzyme leakage without mitochondrial
permeability transition.
B. Complete loss of sarcolemmal integrity with necrotic cell
, death and secondary inflammation.
C. Apoptotic activation with internucleosomal DNA
fragmentation releasing intracellular proteins.
D. Autophagic cell death with lysosomal digestion of contractile
proteins and enzyme release.
Correct Answer
A
Rationale — Correct Option
Transient ischemia can cause reversible increases in plasma
membrane permeability and shedding of cytosolic enzymes
(small troponin release) without irreversible mitochondrial
permeability transition or necrosis. Chapter 1 distinguishes
reversible membrane alterations from irreversible injury; brief
ischemia produces reversible functional impairment and limited
cytosolic leakage.
Rationale — Incorrect Options
B. Complete sarcolemmal rupture and necrosis produce
sustained troponin elevation and inflammatory response,
inconsistent with transient ECG changes.
C. Apoptosis typically compartmentalizes cellular contents in
apoptotic bodies and is less likely to cause substantial troponin
release detected in circulation.
D. Autophagy is generally a survival mechanism; autophagic cell
death with enzyme release is not the main cause of transient
troponin elevations after brief ischemia.
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1)
Reference
Ch. 1 — Introduction — Homeostasis and Allostasis
Question (Stem)
A 62-year-old man with long-standing hypertension presents
with episodic lightheadedness and orthostatic hypotension
after starting a new antihypertensive. His lab tests show normal
electrolytes. Which pathophysiologic principle best explains
why the patient experiences symptomatic instability when a
previously compensated physiologic control (blood pressure) is
abruptly altered?
,A. Loss of negative feedback set-point resetting (allostatic
overload) leading to failure to maintain homeostasis.
B. Irreversible cellular injury of baroreceptor neurons causing
permanent autonomic dysfunction.
C. Acute inflammatory-mediated endothelial injury causing
transient loss of vascular tone.
D. Autoimmune destruction of renal juxtaglomerular cells
leading to abrupt renin–angiotensin failure.
Correct Answer
A
Rationale — Correct Option
Abrupt changes in a chronic set-point (e.g., blood pressure) can
exceed compensatory mechanisms — termed allostatic
overload — producing symptomatic failure to maintain
homeostasis. The Introduction emphasizes regulatory set-point
adjustments and that sudden perturbations of long-standing
compensation (e.g., chronic hypertension treated aggressively)
produce symptoms due to transient mismatch between new
input and adapted control systems. This explains orthostatic
intolerance after rapid blood pressure lowering. (Hammer &
McPhee, Ch. 1).
Rationale — Incorrect Options
B. Baroreceptor neuronal irreversible injury would be unlikely
after starting an antihypertensive and would produce
persistent, not episodic, dysfunction.
C. Acute inflammatory endothelial injury would present with
,signs of inflammation (fever, edema) and is not the mechanism
after initiating antihypertensive therapy.
D. Autoimmune destruction of juxtaglomerular cells is rare and
would cause chronic renin deficiency rather than an acute
symptomatic response after medication change.
Teaching Point
Sudden reversal of chronic set-point adaptations causes
symptomatic allostatic failure.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2)
Reference
Ch. 1 — Introduction — Reversible versus Irreversible Cell Injury
Question (Stem)
A 45-year-old woman presents with acute chest pain. Cardiac
troponin I is mildly elevated; ECG shows transient ST-segment
depression that resolves on repeat testing. Which mechanistic
interpretation best accounts for transient troponin release with
reversible ischemia?
A. Short-lived membrane permeability increases allowing
limited cytosolic enzyme leakage without mitochondrial
permeability transition.
B. Complete loss of sarcolemmal integrity with necrotic cell
, death and secondary inflammation.
C. Apoptotic activation with internucleosomal DNA
fragmentation releasing intracellular proteins.
D. Autophagic cell death with lysosomal digestion of contractile
proteins and enzyme release.
Correct Answer
A
Rationale — Correct Option
Transient ischemia can cause reversible increases in plasma
membrane permeability and shedding of cytosolic enzymes
(small troponin release) without irreversible mitochondrial
permeability transition or necrosis. Chapter 1 distinguishes
reversible membrane alterations from irreversible injury; brief
ischemia produces reversible functional impairment and limited
cytosolic leakage.
Rationale — Incorrect Options
B. Complete sarcolemmal rupture and necrosis produce
sustained troponin elevation and inflammatory response,
inconsistent with transient ECG changes.
C. Apoptosis typically compartmentalizes cellular contents in
apoptotic bodies and is less likely to cause substantial troponin
release detected in circulation.
D. Autophagy is generally a survival mechanism; autophagic cell
death with enzyme release is not the main cause of transient
troponin elevations after brief ischemia.
