ANATOMICAL CHART COMPANY ATLAS
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Part I — Cellular Energy Failure / Hypoxic Cell Injury
Stem
A 68-year-old man with long-standing COPD presents with
increasing dyspnea and SpO₂ 82% on room air. He is confused,
has a respiratory rate of 30/min, and a lactic acid of 4.2 mmol/L.
Which pathophysiologic process most likely explains his
confusion and rising lactate?
,A. Impaired oxidative phosphorylation from tissue hypoxia
leading to increased anaerobic glycolysis.
B. Excess aerobic metabolism causing hypercapnic cerebral
vasoconstriction.
C. Mitochondrial apoptosis triggered by cytokine release
causing immediate neuronal death.
D. Decreased hepatic clearance of lactate due to right-sided
heart failure.
Correct answer: A
Rationale — Correct (A)
Tissue hypoxia from low arterial oxygen reduces oxidative
phosphorylation in mitochondria, forcing cells into anaerobic
glycolysis and producing lactic acid. CNS neurons are highly
dependent on aerobic ATP; decreased ATP impairs ion pumps,
producing neuronal dysfunction and confusion. Elevated lactate
thus reflects systemic hypoxic metabolism.
Rationale — Incorrect
B. Hypercapnia causes cerebral vasodilation, not
vasoconstriction; it does not explain lactic acidosis.
C. Apoptosis is a programmed process that is slower and would
not primarily raise lactate; anaerobic metabolism explains acute
lactate rise.
D. Hepatic clearance contributes to lactate levels, but primary
driver here is global hypoxia from COPD causing anaerobic
metabolism.
,Teaching point:
Hypoxia → loss of oxidative phosphorylation → anaerobic
glycolysis and lactic acidosis; watch for mental status change.
Citation:
Stewart, J. (4th ed.). Anatomical Chart Company Atlas of
Pathophysiology. Part I.
2
Reference
Part I — Ischemia–Reperfusion Injury / Reactive Oxygen Species
Stem
A 54-year-old woman undergoes percutaneous coronary
intervention for an acute STEMI. Within hours of reperfusion
she develops ventricular arrhythmias and rising troponin
beyond expected levels. What mechanism best explains
reperfusion-related myocardial worsening?
A. Calcium overload and sudden generation of reactive oxygen
species causing membrane and mitochondrial damage.
B. Exaggerated bacterial infection of ischemic myocardium
causing septic myocardial necrosis.
C. Autoimmune-mediated delayed hypersensitivity destroying
viable cardiomyocytes.
D. Restoration of flow causing immediate normalization of ATP
and complete recovery of stunned myocardium.
Correct answer: A
, Rationale — Correct (A)
Reperfusion restores oxygen but also triggers a burst of reactive
oxygen species (ROS) and calcium influx, damaging membranes
and mitochondria; this leads to further cell death and
arrhythmias. Calcium overload opens mitochondrial
permeability transition pores, worsening injury beyond initial
ischemia.
Rationale — Incorrect
B. Infection is not an acute reperfusion phenomenon.
C. Autoimmune processes are delayed and would not explain
immediate arrhythmias.
D. Reperfusion can salvage tissue but may also cause
reperfusion injury; immediate complete recovery is not
guaranteed.
Teaching point:
Reperfusion can cause ROS- and calcium-mediated damage;
anticipate arrhythmias and oxidative injury after reperfusion.
Citation:
Stewart, J. (4th ed.). Anatomical Chart Company Atlas of
Pathophysiology. Part I.
3
Reference
Part I — Cell Death: Apoptosis versus Necrosis
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Part I — Cellular Energy Failure / Hypoxic Cell Injury
Stem
A 68-year-old man with long-standing COPD presents with
increasing dyspnea and SpO₂ 82% on room air. He is confused,
has a respiratory rate of 30/min, and a lactic acid of 4.2 mmol/L.
Which pathophysiologic process most likely explains his
confusion and rising lactate?
,A. Impaired oxidative phosphorylation from tissue hypoxia
leading to increased anaerobic glycolysis.
B. Excess aerobic metabolism causing hypercapnic cerebral
vasoconstriction.
C. Mitochondrial apoptosis triggered by cytokine release
causing immediate neuronal death.
D. Decreased hepatic clearance of lactate due to right-sided
heart failure.
Correct answer: A
Rationale — Correct (A)
Tissue hypoxia from low arterial oxygen reduces oxidative
phosphorylation in mitochondria, forcing cells into anaerobic
glycolysis and producing lactic acid. CNS neurons are highly
dependent on aerobic ATP; decreased ATP impairs ion pumps,
producing neuronal dysfunction and confusion. Elevated lactate
thus reflects systemic hypoxic metabolism.
Rationale — Incorrect
B. Hypercapnia causes cerebral vasodilation, not
vasoconstriction; it does not explain lactic acidosis.
C. Apoptosis is a programmed process that is slower and would
not primarily raise lactate; anaerobic metabolism explains acute
lactate rise.
D. Hepatic clearance contributes to lactate levels, but primary
driver here is global hypoxia from COPD causing anaerobic
metabolism.
,Teaching point:
Hypoxia → loss of oxidative phosphorylation → anaerobic
glycolysis and lactic acidosis; watch for mental status change.
Citation:
Stewart, J. (4th ed.). Anatomical Chart Company Atlas of
Pathophysiology. Part I.
2
Reference
Part I — Ischemia–Reperfusion Injury / Reactive Oxygen Species
Stem
A 54-year-old woman undergoes percutaneous coronary
intervention for an acute STEMI. Within hours of reperfusion
she develops ventricular arrhythmias and rising troponin
beyond expected levels. What mechanism best explains
reperfusion-related myocardial worsening?
A. Calcium overload and sudden generation of reactive oxygen
species causing membrane and mitochondrial damage.
B. Exaggerated bacterial infection of ischemic myocardium
causing septic myocardial necrosis.
C. Autoimmune-mediated delayed hypersensitivity destroying
viable cardiomyocytes.
D. Restoration of flow causing immediate normalization of ATP
and complete recovery of stunned myocardium.
Correct answer: A
, Rationale — Correct (A)
Reperfusion restores oxygen but also triggers a burst of reactive
oxygen species (ROS) and calcium influx, damaging membranes
and mitochondria; this leads to further cell death and
arrhythmias. Calcium overload opens mitochondrial
permeability transition pores, worsening injury beyond initial
ischemia.
Rationale — Incorrect
B. Infection is not an acute reperfusion phenomenon.
C. Autoimmune processes are delayed and would not explain
immediate arrhythmias.
D. Reperfusion can salvage tissue but may also cause
reperfusion injury; immediate complete recovery is not
guaranteed.
Teaching point:
Reperfusion can cause ROS- and calcium-mediated damage;
anticipate arrhythmias and oxidative injury after reperfusion.
Citation:
Stewart, J. (4th ed.). Anatomical Chart Company Atlas of
Pathophysiology. Part I.
3
Reference
Part I — Cell Death: Apoptosis versus Necrosis
