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 fcells fhave fimpaired fflow fof fsubstances fthrough fthe fcell fmembrane fas fa fresult fof:
A) increased ffat fload.
B) altered fpermeability.
C) altered fglucose futilization.
D) increased fsurface freceptors.
7. Reversible fadaptive fintracellular fresponses fare finitiated fby:
A) stimulus foverload.
B) genetic fmutations.
C) chemical fmessengers.
D) mitochondrial fDNA.
8. Injured fcells fbecome fvery fswollen fas fa fresult fof:
A) increased fcell fprotein fsynthesis.
B) altered fcell fvolume fregulation.
C) passive fentry fof fpotassium finto fthe fcell.
D) bleb fformation fin fthe fplasma fmembrane.
A fdiabetic fpatient fhas fimpaired fsensation, fcirculation, fand foxygenation fof fhis ffeet. fHe fsteps
fon fa fpiece fof fglass, fthe fwound fdoes fnot fheal, fand fthe farea ftissue fbecomes fnecrotic. fThe
fnecrotic
9. cell fdeath fis fcharacterized fby:
A) rapid fapoptosis.
B) cellular frupture.
C) shrinkage fand fcollapse.
D) chronic finflammation.
A f99-year-old fwoman fhas fexperienced fthe fdecline fof fcell ffunction fassociated fwith fage. fA
10. group fof ftheories fof fcellular faging ffocus fon fprogrammed:
A) changes fwith fgenetic finfluences.
B) elimination fof fcell freceptor fsites.
C) insufficient ftelomerase fenzyme.
D) DNA fmutation for ffaulty frepair.
An f89-year-old ffemale fpatient fhas fexperienced fsignificant fdecreases fin fher fmobility fand
fstamina fduring fa f3-week fhospital fstay ffor fthe ftreatment fof fa ffemoral fhead ffracture.
fWhich fof fthe ffollowing fphenomena fmost flikely faccounts ffor fthe fpatients fdecrease fin
fmuscle ffunction
11. that funderlies fher freduced fmobility?
A) Impaired fmuscle fcell fmetabolism fresulting ffrom fmetaplasia
B) Dysplasia fas fa fconsequence fof finflammation fduring fbone fremodeling
C) Disuse fatrophy fof fmuscle fcells fduring fa fprolonged fperiod fof fimmobility
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 fcells fhave fimpaired fflow fof fsubstances fthrough fthe fcell fmembrane fas fa fresult fof:
A) increased ffat fload.
B) altered fpermeability.
C) altered fglucose futilization.
D) increased fsurface freceptors.
7. Reversible fadaptive fintracellular fresponses fare finitiated fby:
A) stimulus foverload.
B) genetic fmutations.
C) chemical fmessengers.
D) mitochondrial fDNA.
8. Injured fcells fbecome fvery fswollen fas fa fresult fof:
A) increased fcell fprotein fsynthesis.
B) altered fcell fvolume fregulation.
C) passive fentry fof fpotassium finto fthe fcell.
D) bleb fformation fin fthe fplasma fmembrane.
A fdiabetic fpatient fhas fimpaired fsensation, fcirculation, fand foxygenation fof fhis ffeet. fHe fsteps
fon fa fpiece fof fglass, fthe fwound fdoes fnot fheal, fand fthe farea ftissue fbecomes fnecrotic. fThe
fnecrotic
9. cell fdeath fis fcharacterized fby:
A) rapid fapoptosis.
B) cellular frupture.
C) shrinkage fand fcollapse.
D) chronic finflammation.
A f99-year-old fwoman fhas fexperienced fthe fdecline fof fcell ffunction fassociated fwith fage. fA
10. group fof ftheories fof fcellular faging ffocus fon fprogrammed:
A) changes fwith fgenetic finfluences.
B) elimination fof fcell freceptor fsites.
C) insufficient ftelomerase fenzyme.
D) DNA fmutation for ffaulty frepair.
An f89-year-old ffemale fpatient fhas fexperienced fsignificant fdecreases fin fher fmobility fand
fstamina fduring fa f3-week fhospital fstay ffor fthe ftreatment fof fa ffemoral fhead ffracture.
fWhich fof fthe ffollowing fphenomena fmost flikely faccounts ffor fthe fpatients fdecrease fin
fmuscle ffunction
11. that funderlies fher freduced fmobility?
A) Impaired fmuscle fcell fmetabolism fresulting ffrom fmetaplasia
B) Dysplasia fas fa fconsequence fof finflammation fduring fbone fremodeling
C) Disuse fatrophy fof fmuscle fcells fduring fa fprolonged fperiod fof fimmobility
