Test Bank for Robbins, Cotran & Kumar Pathologic
Basis of Disease | 11th Edition | A+ Graded
,Table of Contents
Chapter 1: The Cell as a Unit of Health and Disease.......................................................................... 3
Chapter 2: Cell Injury, Cell Death, and Adaptations ........................................................................ 21
Chapter 3: Inflammation and Repair .............................................................................................. 39
Chapter 4. Hemodynamic Disorders, Thromboembolic Disease, and Shock .................................... 56
Chapter 5. Genes and Human Diseases (1–25) ............................................................................... 72
Chapter 6: Diseases of the Immune System ................................................................................... 87
Chapter 7: Neoplasia.................................................................................................................... 103
Chapter 8. Infectious Diseases ..................................................................................................... 118
Chapter 9. Environmental and Nutritional Diseases ..................................................................... 135
Chapter 10. Diseases of Infancy and Childhood ............................................................................ 153
Chapter 11. Blood Vessels ............................................................................................................ 171
Chapter 12. The Heart.................................................................................................................. 189
Chapter 13. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus ........................... 207
Chapter 14. Red Blood Cell and Bleeding Disorders ...................................................................... 225
Chapter 15. The Lung ................................................................................................................... 243
Chapter 16. Head and Neck.......................................................................................................... 261
Chapter 17. The Gastrointestinal Tract ......................................................................................... 279
Chapter 18. Liver and Gallbladder ................................................................................................ 297
Chapter 19. The Pancreas ............................................................................................................ 315
Chapter 20. The Kidney ................................................................................................................ 333
Chapter 21. The Lower Urinary Tract and Male Genital System .................................................... 351
Chapter 22. The Female Genital Tract .......................................................................................... 368
Chapter 23. The Breast ................................................................................................................ 387
Chapter 24. The Endocrine System ............................................................................................... 405
Chapter 25. The Skin .................................................................................................................... 424
Chapter 26. Bones, Joints, and Soft Tissue Tumors ....................................................................... 442
Chapter 27. Peripheral Nerves and Skeletal Muscles .................................................................... 460
Chapter 28. The Central Nervous System ..................................................................................... 478
Chapter 29. The Eye ..................................................................................................................... 496
,Chapter 1: The Cell as a Unit of Health and Disease
1
A 62-year-old man presents with acute chest pain and is diagnosed with an ST-elevation myocardial
infarction. After 40 minutes of ischemia, cardiomyocytes begin to show mitochondrial swelling and loss
of membrane potential. Which cellular event most directly explains the progression to irreversible
injury?
A. Increased glycolytic activity
B. Opening of mitochondrial permeability transition pores
C. Activation of autophagy
D. Increased synthesis of heat shock proteins
ANS: B
Rationale:
Prolonged ischemia leads to ATP depletion and calcium influx, causing opening of mitochondrial
permeability transition pores. This results in loss of mitochondrial membrane potential, cessation of
oxidative phosphorylation, and failure of ATP production, which marks irreversible cell injury. Glycolysis
(A) is a temporary adaptive response. Autophagy (C) is protective. Heat shock proteins (D) help stabilize
proteins and do not cause irreversible injury.
2
A 45-year-old woman with septic shock develops acute kidney injury. Renal tubular cells show
cytoplasmic vacuolization and membrane blebbing. These findings most likely represent which type of
cellular response?
A. Apoptosis
B. Coagulative necrosis
C. Reversible cell injury
D. Liquefactive necrosis
ANS: C
Rationale:
Cellular swelling, cytoplasmic vacuolization, and membrane blebbing are classic features of reversible
injury due to ATP depletion and ion pump failure. Apoptosis involves cell shrinkage. Coagulative and
liquefactive necrosis represent irreversible injury with membrane rupture.
3
A neonate is born with severe lactic acidosis and muscle weakness. Genetic testing reveals a mutation in
mitochondrial DNA affecting cytochrome oxidase. Which consequence is most likely?
, A. Increased fatty acid oxidation
B. Impaired oxidative phosphorylation
C. Increased lysosomal degradation
D. Enhanced protein synthesis
ANS: B
Rationale:
Cytochrome oxidase is part of the electron transport chain. Defects impair oxidative phosphorylation,
reducing ATP production. This leads to energy failure and lactic acidosis. Fatty acid oxidation and protein
synthesis require functional mitochondria. Lysosomal activity is unrelated.
4
A patient undergoing chemotherapy develops neutropenia. Bone marrow biopsy shows increased
apoptosis of hematopoietic cells. Which mechanism most directly mediates chemotherapy-induced
apoptosis?
A. Activation of death receptors
B. Increased intracellular calcium
C. DNA damage activating p53
D. Depletion of lysosomal enzymes
ANS: C
Rationale:
Chemotherapeutic agents cause DNA damage, activating p53. This leads to transcription of pro-
apoptotic proteins such as Bax and PUMA, triggering mitochondrial apoptosis. Death receptors (A) are
extrinsic. Calcium (B) causes necrosis. Lysosomal depletion (D) is unrelated.
5
A 70-year-old man with chronic alcoholism develops fatty change in hepatocytes. Which mechanism is
primarily responsible for this finding?
A. Increased triglyceride synthesis
B. Decreased lipoprotein export
C. Increased ketone body production
D. Enhanced autophagy
ANS: B
Rationale:
Alcohol metabolism increases NADH, impairing fatty acid oxidation and lipoprotein synthesis. Decreased
export of triglycerides causes intracellular fat accumulation. Increased synthesis is secondary. Ketone
bodies and autophagy are not primary causes.
Basis of Disease | 11th Edition | A+ Graded
,Table of Contents
Chapter 1: The Cell as a Unit of Health and Disease.......................................................................... 3
Chapter 2: Cell Injury, Cell Death, and Adaptations ........................................................................ 21
Chapter 3: Inflammation and Repair .............................................................................................. 39
Chapter 4. Hemodynamic Disorders, Thromboembolic Disease, and Shock .................................... 56
Chapter 5. Genes and Human Diseases (1–25) ............................................................................... 72
Chapter 6: Diseases of the Immune System ................................................................................... 87
Chapter 7: Neoplasia.................................................................................................................... 103
Chapter 8. Infectious Diseases ..................................................................................................... 118
Chapter 9. Environmental and Nutritional Diseases ..................................................................... 135
Chapter 10. Diseases of Infancy and Childhood ............................................................................ 153
Chapter 11. Blood Vessels ............................................................................................................ 171
Chapter 12. The Heart.................................................................................................................. 189
Chapter 13. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus ........................... 207
Chapter 14. Red Blood Cell and Bleeding Disorders ...................................................................... 225
Chapter 15. The Lung ................................................................................................................... 243
Chapter 16. Head and Neck.......................................................................................................... 261
Chapter 17. The Gastrointestinal Tract ......................................................................................... 279
Chapter 18. Liver and Gallbladder ................................................................................................ 297
Chapter 19. The Pancreas ............................................................................................................ 315
Chapter 20. The Kidney ................................................................................................................ 333
Chapter 21. The Lower Urinary Tract and Male Genital System .................................................... 351
Chapter 22. The Female Genital Tract .......................................................................................... 368
Chapter 23. The Breast ................................................................................................................ 387
Chapter 24. The Endocrine System ............................................................................................... 405
Chapter 25. The Skin .................................................................................................................... 424
Chapter 26. Bones, Joints, and Soft Tissue Tumors ....................................................................... 442
Chapter 27. Peripheral Nerves and Skeletal Muscles .................................................................... 460
Chapter 28. The Central Nervous System ..................................................................................... 478
Chapter 29. The Eye ..................................................................................................................... 496
,Chapter 1: The Cell as a Unit of Health and Disease
1
A 62-year-old man presents with acute chest pain and is diagnosed with an ST-elevation myocardial
infarction. After 40 minutes of ischemia, cardiomyocytes begin to show mitochondrial swelling and loss
of membrane potential. Which cellular event most directly explains the progression to irreversible
injury?
A. Increased glycolytic activity
B. Opening of mitochondrial permeability transition pores
C. Activation of autophagy
D. Increased synthesis of heat shock proteins
ANS: B
Rationale:
Prolonged ischemia leads to ATP depletion and calcium influx, causing opening of mitochondrial
permeability transition pores. This results in loss of mitochondrial membrane potential, cessation of
oxidative phosphorylation, and failure of ATP production, which marks irreversible cell injury. Glycolysis
(A) is a temporary adaptive response. Autophagy (C) is protective. Heat shock proteins (D) help stabilize
proteins and do not cause irreversible injury.
2
A 45-year-old woman with septic shock develops acute kidney injury. Renal tubular cells show
cytoplasmic vacuolization and membrane blebbing. These findings most likely represent which type of
cellular response?
A. Apoptosis
B. Coagulative necrosis
C. Reversible cell injury
D. Liquefactive necrosis
ANS: C
Rationale:
Cellular swelling, cytoplasmic vacuolization, and membrane blebbing are classic features of reversible
injury due to ATP depletion and ion pump failure. Apoptosis involves cell shrinkage. Coagulative and
liquefactive necrosis represent irreversible injury with membrane rupture.
3
A neonate is born with severe lactic acidosis and muscle weakness. Genetic testing reveals a mutation in
mitochondrial DNA affecting cytochrome oxidase. Which consequence is most likely?
, A. Increased fatty acid oxidation
B. Impaired oxidative phosphorylation
C. Increased lysosomal degradation
D. Enhanced protein synthesis
ANS: B
Rationale:
Cytochrome oxidase is part of the electron transport chain. Defects impair oxidative phosphorylation,
reducing ATP production. This leads to energy failure and lactic acidosis. Fatty acid oxidation and protein
synthesis require functional mitochondria. Lysosomal activity is unrelated.
4
A patient undergoing chemotherapy develops neutropenia. Bone marrow biopsy shows increased
apoptosis of hematopoietic cells. Which mechanism most directly mediates chemotherapy-induced
apoptosis?
A. Activation of death receptors
B. Increased intracellular calcium
C. DNA damage activating p53
D. Depletion of lysosomal enzymes
ANS: C
Rationale:
Chemotherapeutic agents cause DNA damage, activating p53. This leads to transcription of pro-
apoptotic proteins such as Bax and PUMA, triggering mitochondrial apoptosis. Death receptors (A) are
extrinsic. Calcium (B) causes necrosis. Lysosomal depletion (D) is unrelated.
5
A 70-year-old man with chronic alcoholism develops fatty change in hepatocytes. Which mechanism is
primarily responsible for this finding?
A. Increased triglyceride synthesis
B. Decreased lipoprotein export
C. Increased ketone body production
D. Enhanced autophagy
ANS: B
Rationale:
Alcohol metabolism increases NADH, impairing fatty acid oxidation and lipoprotein synthesis. Decreased
export of triglycerides causes intracellular fat accumulation. Increased synthesis is secondary. Ketone
bodies and autophagy are not primary causes.
