"Complete Student Q&A Guide to
Pathophysiology: 8th Edition by McCance
& Huether"
Ultimate Pathophysiology Test Bank:
Aligned with McCance & Huether’s 8th
Edition"
,
,Table of Contents
1. Cellular Biology
2. Altered Cellular and Tissue Biology: Environmental Agents
3. The Cellular Environment: Fluids and Electrolytes, Acids and Bases
4. Genes and Genetic Diseases
5. Genes, Environment-Lifestyle, and Common Diseases
6. Epigenetics and Disease
7. Innate Immunity: Inflammation
8. Adaptive Immunity
9. Alterations in Immunity and Inflammation
10. Infection
11. Stress and Disease
12. Cancer Biology
13. Cancer Epidemiology
14. Cancer in Children
15. Structure and Function of the Neurologic System
16. Pain, Temperature Regulation, Sleep, and Sensory Function
17. Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor Function
18. Disorders of the Central and Peripheral Nervous Systems and the Neuromuscular Junction
19. Neurobiology of Schizophrenia, Mood Disorders, and Anxiety Disorders
20. Alterations of Neurologic Function in Children
21. Mechanisms of Hormonal Regulation
22. Alterations of Hormonal Regulation
23. Obesity and Disorders of Nutrition
24. Structure and Function of the Reproductive Systems
25. Alterations of the Female Reproductive System
26. Alterations of the Male Reproductive System
27. Reproductive Function in Children
,28. Structure and Function of the Hematologic System
29. Alterations of Erythrocyte, Platelet, and Hemostatic Function
30. Alterations of Leukocyte and Lymphoid Function
31. Alterations of Hematologic Function in Children
32. Structure and Function of the Cardiovascular and Lymphatic Systems
33. Alterations of Cardiovascular Function
34. Alterations of Cardiovascular Function in Children
35. Structure and Function of the Pulmonary System
36. Alterations of Pulmonary Function
37. Alterations of Pulmonary Function in Children
38. Structure and Function of the Renal and Urologic Systems
39. Alterations of Renal and Urinary Tract Function
40. Alterations of Renal and Urinary Tract Function in Children
41. Structure and Function of the Digestive System
42. Alterations of Digestive Function
43. Alterations of Digestive Function in Children
44. Structure and Function of the Musculoskeletal System
45. Alterations of Musculoskeletal Function
46. Alterations of Musculoskeletal Function in Children
47. Structure and Function of the Integumentary System
48. Alterations of the Integument in Children
49. Shock, Multiple Organ Dysfunction Syndrome, and Burns in Adults
50. Shock, Multiple Organ Dysfunction Syndrome, and Burns in Children
1. A toxin causes lipid peroxidation of the plasma membrane,
leading to increased permeability and cell swelling. Which
of the following is the most likely mechanism by which this
toxin exerts its effect?
A. Inhibition of Na⁺/K⁺-ATPase
B. Generation of reactive oxygen species (ROS)
, C. Activation of caspases
D. Blockage of mitochondrial electron transport chain
Correct Answer: B
Rationale:
B. Generation of reactive oxygen species (ROS): ROS
initiate lipid peroxidation by abstracting hydrogen atoms
from membrane lipids, causing structural damage,
increased permeability, and cell swelling. This describes
the direct effect of ROS on membranes and is consistent
with the toxin’s action.
A. Inhibition of Na⁺/K⁺-ATPase: Although inhibition of
the Na⁺/K⁺-ATPase can lead to cell swelling by disrupting
ion gradients, it does not specifically cause lipid
peroxidation.
C. Activation of caspases: Caspase activation is associated
with apoptosis, which involves DNA fragmentation and
cell shrinkage, not plasma membrane lipid peroxidation and
swelling.
D. Blockage of mitochondrial electron transport chain:
While blocking the electron transport chain can lead to
ATP depletion and secondary ROS production, the direct
mechanism for membrane lipid peroxidation is generation
of ROS.
2. Which of the following adaptations is characterized by an
increase in cell size without an increase in cell number?
A. Hyperplasia
B. Metaplasia
, C. Hypertrophy
D. Dysplasia
Correct Answer: C
Rationale:
C. Hypertrophy: Hypertrophy is an adaptive increase in
the size of cells, resulting in increased tissue or organ size,
without producing additional cells.
A. Hyperplasia: Hyperplasia is an increase in cell number,
not size; it often occurs together with hypertrophy in some
tissues but is distinct.
B. Metaplasia: Metaplasia is a reversible change wherein
one differentiated cell type is replaced by another, not an
increase in size.
D. Dysplasia: Dysplasia refers to abnormal cell growth and
morphology; it is neither an increase in cell size alone nor a
controlled adaptation.
3. Carbon monoxide (CO) poisoning leads to tissue hypoxia
primarily because CO:
A. Blocks oxygen diffusion in alveoli
B. Binds irreversibly to hemoglobin and prevents oxygen
release
C. Binds to cytochrome oxidase in mitochondria
D. Has a higher affinity for myoglobin than hemoglobin
Correct Answer: B
Rationale:
, B. Binds irreversibly to hemoglobin and prevents
oxygen release: CO forms carboxyhemoglobin by binding
to the heme iron with much higher affinity than oxygen,
thus preventing oxygen binding and release to tissues.
A. Blocks oxygen diffusion in alveoli: CO does not
physically block diffusion; inhaled CO is absorbed into
blood but does not obstruct alveolar gas exchange.
C. Binds to cytochrome oxidase in mitochondria:
Cyanide, not CO, primarily binds to cytochrome oxidase.
CO’s main effect is hemoglobin binding.
D. Has a higher affinity for myoglobin than
hemoglobin: CO does bind myoglobin but its critical effect
is on hemoglobin; its affinity for myoglobin is not the key
event causing systemic hypoxia.
4. Which of the following cell injury mechanisms involves an
increase in intracellular calcium levels?
A. DNA strand breaks
B. Activation of phospholipases
C. Lipid peroxidation
D. Protein carbonylation
Correct Answer: B
Rationale:
B. Activation of phospholipases: Increased intracellular
Ca²⁺ activates phospholipases, which degrade membrane
phospholipids, contributing to membrane damage during
injury.
, A. DNA strand breaks: DNA strand breaks result from
direct genotoxic stress or free radicals but are not a direct
consequence of calcium influx.
C. Lipid peroxidation: Lipid peroxidation is driven by
free radicals, not directly by calcium.
D. Protein carbonylation: Protein carbonylation is a result
of oxidative modification by ROS, not by Ca²⁺.
5. A patient presents with acute lead poisoning. Which of the
following findings is characteristic of lead’s effect on cells?
A. Increased activity of δ-aminolevulinic acid dehydratase
(ALAD)
B. Formation of reactive oxygen species in mitochondria
C. Inhibition of ferrochelatase and ALAD
D. Direct alkylation of DNA
Correct Answer: C
Rationale:
C. Inhibition of ferrochelatase and ALAD: Lead inhibits
ferrochelatase and ALAD, enzymes in the heme
biosynthesis pathway, causing accumulation of
protoporphyrin and δ-aminolevulinic acid, leading to
anemia and neurologic toxicity.
A. Increased activity of δ-aminolevulinic acid
dehydratase (ALAD): In lead poisoning, ALAD activity is
decreased, not increased.
B. Formation of reactive oxygen species in
mitochondria: While oxidative stress can occur, the
, hallmark of lead toxicity is enzyme inhibition in heme
synthesis, not primary mitochondrial ROS generation.
D. Direct alkylation of DNA: Lead does not directly
alkylate DNA; alkylating agents (e.g., certain
chemotherapy drugs) cause that effect.
6. During adaptive responses to chronic low oxygen tension,
cells increase the expression of hypoxia-inducible factor-1
(HIF-1). HIF-1 is a transcription factor that:
A. Suppresses VEGF expression
B. Promotes anaerobic glycolysis
C. Inhibits erythropoietin production
D. Degrades under hypoxic conditions
Correct Answer: B
Rationale:
B. Promotes anaerobic glycolysis: HIF-1 upregulates
genes encoding glycolytic enzymes, shifting metabolism
toward anaerobic glycolysis when oxygen is limited.
A. Suppresses VEGF expression: HIF-1 actually
enhances VEGF (vascular endothelial growth factor)
expression to promote angiogenesis.
C. Inhibits erythropoietin production: HIF-1 promotes
erythropoietin (EPO) production to increase red blood cell
formation.
D. Degrades under hypoxic conditions: HIF-1α is
normally degraded under normoxic conditions; under
hypoxia, it stabilizes and accumulates.
, 7. An environmental agent causes cross-linking of DNA,
leading to impaired replication and cell death. Which agent
is most likely responsible?
A. Carbon tetrachloride
B. Ultraviolet (UV) light
C. Benzene
D. Cisplatin
Correct Answer: D
Rationale:
D. Cisplatin: Cisplatin forms intrastrand and interstrand
DNA cross-links, preventing replication and transcription,
resulting in cell death.
A. Carbon tetrachloride: CCl₄ causes free radical–
mediated lipid peroxidation, not DNA cross-linking.
B. Ultraviolet (UV) light: UV light causes thymine dimers,
leading to DNA distortion but not classic interstrand cross-
links.
C. Benzene: Benzene’s toxicity is through bone marrow
suppression and oxidative metabolites, not DNA cross-
linking.
8. A cell exposed to sublethal injury shows increased
endoplasmic reticulum (ER) stress and accumulation of
unfolded proteins. Which adaptive response is activated?
A. Unfolded protein response (UPR)
B. Mitochondrial biogenesis
Pathophysiology: 8th Edition by McCance
& Huether"
Ultimate Pathophysiology Test Bank:
Aligned with McCance & Huether’s 8th
Edition"
,
,Table of Contents
1. Cellular Biology
2. Altered Cellular and Tissue Biology: Environmental Agents
3. The Cellular Environment: Fluids and Electrolytes, Acids and Bases
4. Genes and Genetic Diseases
5. Genes, Environment-Lifestyle, and Common Diseases
6. Epigenetics and Disease
7. Innate Immunity: Inflammation
8. Adaptive Immunity
9. Alterations in Immunity and Inflammation
10. Infection
11. Stress and Disease
12. Cancer Biology
13. Cancer Epidemiology
14. Cancer in Children
15. Structure and Function of the Neurologic System
16. Pain, Temperature Regulation, Sleep, and Sensory Function
17. Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor Function
18. Disorders of the Central and Peripheral Nervous Systems and the Neuromuscular Junction
19. Neurobiology of Schizophrenia, Mood Disorders, and Anxiety Disorders
20. Alterations of Neurologic Function in Children
21. Mechanisms of Hormonal Regulation
22. Alterations of Hormonal Regulation
23. Obesity and Disorders of Nutrition
24. Structure and Function of the Reproductive Systems
25. Alterations of the Female Reproductive System
26. Alterations of the Male Reproductive System
27. Reproductive Function in Children
,28. Structure and Function of the Hematologic System
29. Alterations of Erythrocyte, Platelet, and Hemostatic Function
30. Alterations of Leukocyte and Lymphoid Function
31. Alterations of Hematologic Function in Children
32. Structure and Function of the Cardiovascular and Lymphatic Systems
33. Alterations of Cardiovascular Function
34. Alterations of Cardiovascular Function in Children
35. Structure and Function of the Pulmonary System
36. Alterations of Pulmonary Function
37. Alterations of Pulmonary Function in Children
38. Structure and Function of the Renal and Urologic Systems
39. Alterations of Renal and Urinary Tract Function
40. Alterations of Renal and Urinary Tract Function in Children
41. Structure and Function of the Digestive System
42. Alterations of Digestive Function
43. Alterations of Digestive Function in Children
44. Structure and Function of the Musculoskeletal System
45. Alterations of Musculoskeletal Function
46. Alterations of Musculoskeletal Function in Children
47. Structure and Function of the Integumentary System
48. Alterations of the Integument in Children
49. Shock, Multiple Organ Dysfunction Syndrome, and Burns in Adults
50. Shock, Multiple Organ Dysfunction Syndrome, and Burns in Children
1. A toxin causes lipid peroxidation of the plasma membrane,
leading to increased permeability and cell swelling. Which
of the following is the most likely mechanism by which this
toxin exerts its effect?
A. Inhibition of Na⁺/K⁺-ATPase
B. Generation of reactive oxygen species (ROS)
, C. Activation of caspases
D. Blockage of mitochondrial electron transport chain
Correct Answer: B
Rationale:
B. Generation of reactive oxygen species (ROS): ROS
initiate lipid peroxidation by abstracting hydrogen atoms
from membrane lipids, causing structural damage,
increased permeability, and cell swelling. This describes
the direct effect of ROS on membranes and is consistent
with the toxin’s action.
A. Inhibition of Na⁺/K⁺-ATPase: Although inhibition of
the Na⁺/K⁺-ATPase can lead to cell swelling by disrupting
ion gradients, it does not specifically cause lipid
peroxidation.
C. Activation of caspases: Caspase activation is associated
with apoptosis, which involves DNA fragmentation and
cell shrinkage, not plasma membrane lipid peroxidation and
swelling.
D. Blockage of mitochondrial electron transport chain:
While blocking the electron transport chain can lead to
ATP depletion and secondary ROS production, the direct
mechanism for membrane lipid peroxidation is generation
of ROS.
2. Which of the following adaptations is characterized by an
increase in cell size without an increase in cell number?
A. Hyperplasia
B. Metaplasia
, C. Hypertrophy
D. Dysplasia
Correct Answer: C
Rationale:
C. Hypertrophy: Hypertrophy is an adaptive increase in
the size of cells, resulting in increased tissue or organ size,
without producing additional cells.
A. Hyperplasia: Hyperplasia is an increase in cell number,
not size; it often occurs together with hypertrophy in some
tissues but is distinct.
B. Metaplasia: Metaplasia is a reversible change wherein
one differentiated cell type is replaced by another, not an
increase in size.
D. Dysplasia: Dysplasia refers to abnormal cell growth and
morphology; it is neither an increase in cell size alone nor a
controlled adaptation.
3. Carbon monoxide (CO) poisoning leads to tissue hypoxia
primarily because CO:
A. Blocks oxygen diffusion in alveoli
B. Binds irreversibly to hemoglobin and prevents oxygen
release
C. Binds to cytochrome oxidase in mitochondria
D. Has a higher affinity for myoglobin than hemoglobin
Correct Answer: B
Rationale:
, B. Binds irreversibly to hemoglobin and prevents
oxygen release: CO forms carboxyhemoglobin by binding
to the heme iron with much higher affinity than oxygen,
thus preventing oxygen binding and release to tissues.
A. Blocks oxygen diffusion in alveoli: CO does not
physically block diffusion; inhaled CO is absorbed into
blood but does not obstruct alveolar gas exchange.
C. Binds to cytochrome oxidase in mitochondria:
Cyanide, not CO, primarily binds to cytochrome oxidase.
CO’s main effect is hemoglobin binding.
D. Has a higher affinity for myoglobin than
hemoglobin: CO does bind myoglobin but its critical effect
is on hemoglobin; its affinity for myoglobin is not the key
event causing systemic hypoxia.
4. Which of the following cell injury mechanisms involves an
increase in intracellular calcium levels?
A. DNA strand breaks
B. Activation of phospholipases
C. Lipid peroxidation
D. Protein carbonylation
Correct Answer: B
Rationale:
B. Activation of phospholipases: Increased intracellular
Ca²⁺ activates phospholipases, which degrade membrane
phospholipids, contributing to membrane damage during
injury.
, A. DNA strand breaks: DNA strand breaks result from
direct genotoxic stress or free radicals but are not a direct
consequence of calcium influx.
C. Lipid peroxidation: Lipid peroxidation is driven by
free radicals, not directly by calcium.
D. Protein carbonylation: Protein carbonylation is a result
of oxidative modification by ROS, not by Ca²⁺.
5. A patient presents with acute lead poisoning. Which of the
following findings is characteristic of lead’s effect on cells?
A. Increased activity of δ-aminolevulinic acid dehydratase
(ALAD)
B. Formation of reactive oxygen species in mitochondria
C. Inhibition of ferrochelatase and ALAD
D. Direct alkylation of DNA
Correct Answer: C
Rationale:
C. Inhibition of ferrochelatase and ALAD: Lead inhibits
ferrochelatase and ALAD, enzymes in the heme
biosynthesis pathway, causing accumulation of
protoporphyrin and δ-aminolevulinic acid, leading to
anemia and neurologic toxicity.
A. Increased activity of δ-aminolevulinic acid
dehydratase (ALAD): In lead poisoning, ALAD activity is
decreased, not increased.
B. Formation of reactive oxygen species in
mitochondria: While oxidative stress can occur, the
, hallmark of lead toxicity is enzyme inhibition in heme
synthesis, not primary mitochondrial ROS generation.
D. Direct alkylation of DNA: Lead does not directly
alkylate DNA; alkylating agents (e.g., certain
chemotherapy drugs) cause that effect.
6. During adaptive responses to chronic low oxygen tension,
cells increase the expression of hypoxia-inducible factor-1
(HIF-1). HIF-1 is a transcription factor that:
A. Suppresses VEGF expression
B. Promotes anaerobic glycolysis
C. Inhibits erythropoietin production
D. Degrades under hypoxic conditions
Correct Answer: B
Rationale:
B. Promotes anaerobic glycolysis: HIF-1 upregulates
genes encoding glycolytic enzymes, shifting metabolism
toward anaerobic glycolysis when oxygen is limited.
A. Suppresses VEGF expression: HIF-1 actually
enhances VEGF (vascular endothelial growth factor)
expression to promote angiogenesis.
C. Inhibits erythropoietin production: HIF-1 promotes
erythropoietin (EPO) production to increase red blood cell
formation.
D. Degrades under hypoxic conditions: HIF-1α is
normally degraded under normoxic conditions; under
hypoxia, it stabilizes and accumulates.
, 7. An environmental agent causes cross-linking of DNA,
leading to impaired replication and cell death. Which agent
is most likely responsible?
A. Carbon tetrachloride
B. Ultraviolet (UV) light
C. Benzene
D. Cisplatin
Correct Answer: D
Rationale:
D. Cisplatin: Cisplatin forms intrastrand and interstrand
DNA cross-links, preventing replication and transcription,
resulting in cell death.
A. Carbon tetrachloride: CCl₄ causes free radical–
mediated lipid peroxidation, not DNA cross-linking.
B. Ultraviolet (UV) light: UV light causes thymine dimers,
leading to DNA distortion but not classic interstrand cross-
links.
C. Benzene: Benzene’s toxicity is through bone marrow
suppression and oxidative metabolites, not DNA cross-
linking.
8. A cell exposed to sublethal injury shows increased
endoplasmic reticulum (ER) stress and accumulation of
unfolded proteins. Which adaptive response is activated?
A. Unfolded protein response (UPR)
B. Mitochondrial biogenesis
