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TEST BANK RUBIN'S PATHOLOGY: CLINICOPATHOLOGIC FOUNDATIONS OF MEDICINE 7TH EDITION DAVID S. STRAYER, EMANUEL RUBIN

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TEST BANK RUBIN'S PATHOLOGY: CLINICOPATHOLOGIC FOUNDATIONS OF MEDICINE 7TH EDITION DAVID S. STRAYER, EMANUEL RUBIN 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

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Subido en
7 de octubre de 2025
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267
Escrito en
2025/2026
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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 dcells dhave dimpaired dflow dof dsubstances dthrough dthe dcell dmembrane das da dresult dof:
A) increased dfat dload.
B) altered dpermeability.
C) altered dglucose dutilization.
D) increased dsurface dreceptors.
7. Reversible dadaptive dintracellular dresponses dare dinitiated dby:
A) stimulus doverload.
B) genetic dmutations.
C) chemical dmessengers.
D) mitochondrial dDNA.
8. Injured dcells dbecome dvery dswollen das da dresult dof:
A) increased dcell dprotein dsynthesis.
B) altered dcell dvolume dregulation.
C) passive dentry dof dpotassium dinto dthe dcell.
D) bleb dformation din dthe dplasma dmembrane.
A ddiabetic dpatient dhas dimpaired dsensation, dcirculation, dand doxygenation dof dhis dfeet. dHe
dsteps don da dpiece dof dglass, dthe dwound ddoes dnot dheal, dand dthe darea dtissue dbecomes
dnecrotic. dThe dnecrotic
9. cell ddeath dis d characterized dby:
A) rapid dapoptosis.
B) cellular drupture.
C) shrinkage dand dcollapse.
D) chronic dinflammation.
A d99-year-old dwoman dhas dexperienced dthe ddecline dof dcell dfunction dassociated dwith dage. dA
10. group dof dtheories d of dcellular daging dfocus don dprogrammed:
A) changes dwith dgenetic dinfluences.
B) elimination dof dcell dreceptor dsites.
C) insufficient dtelomerase denzyme.
D) DNA dmutation dor dfaulty drepair.
An d89-year-old dfemale dpatient dhas dexperienced dsignificant ddecreases din dher dmobility
dand dstamina dduring da d3-week dhospital dstay dfor dthe dtreatment dof da dfemoral dhead
dfracture. dWhich dof dthe dfollowing dphenomena dmost dlikely daccounts dfor dthe dpatients
ddecrease din dmuscle dfunction
11. that dunderlies dher dreduced dmobility?
A) Impaired dmuscle dcell dmetabolism dresulting dfrom dmetaplasia
B) Dysplasia das da dconsequence dof dinflammation dduring dbone dremodeling
C) Disuse datrophy dof dmuscle d cells dduring da dprolonged dperiod dof dimmobility
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