TEST BANK
RUBIN'S PATHOLOGY: CLINICOPATHOLOGIC FOUNDATIONS OF
MEDICINE 7TH EDITION
DAVID S. STRAYER, EMANUEL RUBIN
,Test Bank Rubin's Pathology: Clinicopathologic Foundations of Medicine 7th Edition
Table of Contents:
Chapter 1: Cell Adaptation, Injury and Death
Chapter 2: Inflammation
Chapter 3: Repair, Regeneration and Fibrosis
Chapter 4: Immunopathology
Chapter 5: Neoplasia
Chapter 6: Developmental and Genetic Diseases
Chapter 7: Hemodynamic Disorders
Chapter 8: Environmental and Nutritional Pathology
Chapter 9: Infectious and Parasitic Diseases
Section II: Pathogenesis of Systemic Conditions Expandable section
Chapter 10: Aging
Chapter 11: Systemic Autoimmune Diseases
Chapter 12: Sepsis
Chapter 13: Obesity and Diabetes Mellitus
Chapter 14: The Pathology of Pregnancy
Chapter 15: The Amyloidoses
Section III: Diseases of Individual Organ SystemsExpandable section
Chapter 16: Blood Vessels
Chapter 17: The Heart
Chapter 18: The Respiratory System
Chapter 19: The Gastrointestinal Tract
Chapter 20: The Liver and Biliary System
Chapter 21: The Pancreas
Chapter 22: The Kidney
Chapter 23: The Lower Urinary Tract and Male Reproductive System
Chapter 24: The Female Reproductive System and Peritoneum
Chapter 25: The Breast
Chapter 26: Hematopathology
Chapter 27: The Endocrine System
Chapter 28: The Skin
Chapter 29: The Head and Neck
Chapter 30: Bones, Joints and Soft Tissue
Chapter 31: Skeletal Muscle and Peripheral Nervous System
Chapter 32: The Central Nervous System
Chapter 33: The Eye
Chapter 34: Forensic Pathology
,Rubin's Pathology: Clinicopathologic Foundations of
MedicineChapter 1: Cell Adaptation, Injury and Death
Ischemia and other toxic injuries increase the accumulation of intracellular calcium as a result
1. of:
A) release of stored calcium from the mitochondria.
B) improved intracellular volume regulation.
C) decreased influx across the cell membrane.
D) attraction of calcium to fatty infiltrates.
The patient is found to have liver disease, resulting in the removal of a lobe of his liver.
2. Adaptation to the reduced size of the liver leads to _ of the remaining liver cells.
A) metaplasia
B) organ atrophy
C) compensatory hyperplasia
D) physiologic hypertrophy
A person eating peanuts starts choking and collapses. His airway obstruction is partially
cleared, but he remains hypoxic until he reaches the hospital. The prolonged cell hypoxia
3. caused a cerebral infarction and resulting _ in the brain.
A) caspase activation
B) coagulation necrosis
C) rapid phagocytosis
D) protein p53 deficiency
Bacteria and viruses cause cell damage by , which is unique from the intracellular
4. damage caused by other injurious agents.
A) disrupting the sodium/potassium ATPase pump
B) interrupting oxidative metabolism processes
C) replicating and producing continued injury
D) decreasing protein synthesis and function
The patient has a prolonged interruption in arterial blood flow to his left kidney, causing
5. hypoxic cell injury and the release of free radicals. Free radicals damage cells by:
A) destroying phospholipids in the cell membrane.
B) altering the immune response of the cell.
C) disrupting calcium storage in the cell.
D) inactivation of enzymes and mitochondria.
, 6. Injured scells shave simpaired sflow sof ssubstances sthrough sthe scell smembrane sas sa sresult sof:
A) increased sfat sload.
B) altered spermeability.
C) altered sglucose sutilization.
D) increased ssurface sreceptors.
7. Reversible sadaptive sintracellular sresponses sare sinitiated sby:
A) stimulus soverload.
B) genetic smutations.
C) chemical smessengers.
D) mitochondrial sDNA.
8. Injured scells sbecome svery sswollen sas sa sresult sof:
A) increased scell sprotein ssynthesis.
B) altered scell svolume sregulation.
C) passive sentry sof spotassium sinto sthe scell.
D) bleb sformation sin sthe splasma smembrane.
A sdiabetic spatient shas simpaired ssensation, scirculation, sand soxygenation sof shis sfeet. sHe
ssteps son sa spiece sof sglass, sthe swound sdoes snot sheal, sand sthe sarea stissue sbecomes
snecrotic. sThe snecrotic
9. cell sdeath sis scharacterized sby:
A) rapid sapoptosis.
B) cellular srupture.
C) shrinkage sand scollapse.
D) chronic sinflammation.
A s99-year-old swoman shas sexperienced sthe sdecline sof scell sfunction sassociated swith sage. sA
10. group sof stheories sof scellular saging sfocus son sprogrammed:
A) changes swith sgenetic sinfluences.
B) elimination sof scell sreceptor ssites.
C) insufficient stelomerase senzyme.
D) DNA smutation sor sfaulty srepair.
An s89-year-old sfemale spatient shas sexperienced ssignificant sdecreases sin sher smobility sand
sstamina sduring sa s3-week shospital sstay sfor sthe streatment sof sa sfemoral shead sfracture.
sWhich sof sthe sfollowing sphenomena smost slikely saccounts sfor sthe spatients sdecrease sin
smuscle sfunction
11. that sunderlies sher sreduced smobility?
A) Impaired smuscle scell smetabolism sresulting sfrom smetaplasia
B) Dysplasia sas sa sconsequence sof sinflammation sduring sbone sremodeling
C) Disuse satrophy sof smuscle scells sduring sa sprolonged speriod sof simmobility
RUBIN'S PATHOLOGY: CLINICOPATHOLOGIC FOUNDATIONS OF
MEDICINE 7TH EDITION
DAVID S. STRAYER, EMANUEL RUBIN
,Test Bank Rubin's Pathology: Clinicopathologic Foundations of Medicine 7th Edition
Table of Contents:
Chapter 1: Cell Adaptation, Injury and Death
Chapter 2: Inflammation
Chapter 3: Repair, Regeneration and Fibrosis
Chapter 4: Immunopathology
Chapter 5: Neoplasia
Chapter 6: Developmental and Genetic Diseases
Chapter 7: Hemodynamic Disorders
Chapter 8: Environmental and Nutritional Pathology
Chapter 9: Infectious and Parasitic Diseases
Section II: Pathogenesis of Systemic Conditions Expandable section
Chapter 10: Aging
Chapter 11: Systemic Autoimmune Diseases
Chapter 12: Sepsis
Chapter 13: Obesity and Diabetes Mellitus
Chapter 14: The Pathology of Pregnancy
Chapter 15: The Amyloidoses
Section III: Diseases of Individual Organ SystemsExpandable section
Chapter 16: Blood Vessels
Chapter 17: The Heart
Chapter 18: The Respiratory System
Chapter 19: The Gastrointestinal Tract
Chapter 20: The Liver and Biliary System
Chapter 21: The Pancreas
Chapter 22: The Kidney
Chapter 23: The Lower Urinary Tract and Male Reproductive System
Chapter 24: The Female Reproductive System and Peritoneum
Chapter 25: The Breast
Chapter 26: Hematopathology
Chapter 27: The Endocrine System
Chapter 28: The Skin
Chapter 29: The Head and Neck
Chapter 30: Bones, Joints and Soft Tissue
Chapter 31: Skeletal Muscle and Peripheral Nervous System
Chapter 32: The Central Nervous System
Chapter 33: The Eye
Chapter 34: Forensic Pathology
,Rubin's Pathology: Clinicopathologic Foundations of
MedicineChapter 1: Cell Adaptation, Injury and Death
Ischemia and other toxic injuries increase the accumulation of intracellular calcium as a result
1. of:
A) release of stored calcium from the mitochondria.
B) improved intracellular volume regulation.
C) decreased influx across the cell membrane.
D) attraction of calcium to fatty infiltrates.
The patient is found to have liver disease, resulting in the removal of a lobe of his liver.
2. Adaptation to the reduced size of the liver leads to _ of the remaining liver cells.
A) metaplasia
B) organ atrophy
C) compensatory hyperplasia
D) physiologic hypertrophy
A person eating peanuts starts choking and collapses. His airway obstruction is partially
cleared, but he remains hypoxic until he reaches the hospital. The prolonged cell hypoxia
3. caused a cerebral infarction and resulting _ in the brain.
A) caspase activation
B) coagulation necrosis
C) rapid phagocytosis
D) protein p53 deficiency
Bacteria and viruses cause cell damage by , which is unique from the intracellular
4. damage caused by other injurious agents.
A) disrupting the sodium/potassium ATPase pump
B) interrupting oxidative metabolism processes
C) replicating and producing continued injury
D) decreasing protein synthesis and function
The patient has a prolonged interruption in arterial blood flow to his left kidney, causing
5. hypoxic cell injury and the release of free radicals. Free radicals damage cells by:
A) destroying phospholipids in the cell membrane.
B) altering the immune response of the cell.
C) disrupting calcium storage in the cell.
D) inactivation of enzymes and mitochondria.
, 6. Injured scells shave simpaired sflow sof ssubstances sthrough sthe scell smembrane sas sa sresult sof:
A) increased sfat sload.
B) altered spermeability.
C) altered sglucose sutilization.
D) increased ssurface sreceptors.
7. Reversible sadaptive sintracellular sresponses sare sinitiated sby:
A) stimulus soverload.
B) genetic smutations.
C) chemical smessengers.
D) mitochondrial sDNA.
8. Injured scells sbecome svery sswollen sas sa sresult sof:
A) increased scell sprotein ssynthesis.
B) altered scell svolume sregulation.
C) passive sentry sof spotassium sinto sthe scell.
D) bleb sformation sin sthe splasma smembrane.
A sdiabetic spatient shas simpaired ssensation, scirculation, sand soxygenation sof shis sfeet. sHe
ssteps son sa spiece sof sglass, sthe swound sdoes snot sheal, sand sthe sarea stissue sbecomes
snecrotic. sThe snecrotic
9. cell sdeath sis scharacterized sby:
A) rapid sapoptosis.
B) cellular srupture.
C) shrinkage sand scollapse.
D) chronic sinflammation.
A s99-year-old swoman shas sexperienced sthe sdecline sof scell sfunction sassociated swith sage. sA
10. group sof stheories sof scellular saging sfocus son sprogrammed:
A) changes swith sgenetic sinfluences.
B) elimination sof scell sreceptor ssites.
C) insufficient stelomerase senzyme.
D) DNA smutation sor sfaulty srepair.
An s89-year-old sfemale spatient shas sexperienced ssignificant sdecreases sin sher smobility sand
sstamina sduring sa s3-week shospital sstay sfor sthe streatment sof sa sfemoral shead sfracture.
sWhich sof sthe sfollowing sphenomena smost slikely saccounts sfor sthe spatients sdecrease sin
smuscle sfunction
11. that sunderlies sher sreduced smobility?
A) Impaired smuscle scell smetabolism sresulting sfrom smetaplasia
B) Dysplasia sas sa sconsequence sof sinflammation sduring sbone sremodeling
C) Disuse satrophy sof smuscle scells sduring sa sprolonged speriod sof simmobility
