po p o Rubin's p o Pathology: Clinicopathologic Foundations of
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Edition
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Table of Contents:
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Chapter 1: Cell Adaptation, Injury and Death
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Chapter 2: Inflammation
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Chapter 3: Repair, Regeneration and Fibrosis
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Chapter 4: Immunopathology
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Chapter 5: Neoplasia
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Chapter 6: Developmental and Genetic Diseases
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Chapter 7: Hemodynamic Disorders
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Chapter 8: Environmental and Nutritional Pathology
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Chapter 9: Infectious and Parasitic Diseases
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Section II: Pathogenesis of Systemic Conditions Expandable section
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Chapter 10: Agingp o p o
Chapter 11: Systemic Autoimmune Diseases
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Chapter 12: Sepsis
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Chapter 13: Obesity and Diabetes Mellitus
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Chapter 14: The Pathology of Pregnancy
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Chapter 15: The Amyloidoses
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Section III: Diseases of Individual Organ SystemsExpandable section
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Chapter 16: Blood Vessels
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Chapter 17: The Heart
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Chapter 18: The Respiratory System
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Chapter 19: The Gastrointestinal Tract
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Chapter 20: The Liver and Biliary System
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Chapter 21: The Pancreas
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Chapter 22: The Kidney
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Chapter 23: The Lower Urinary Tract and Male Reproductive System
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Chapter 24: The Female Reproductive System and Peritoneum
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Chapter 25: The Breast
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Chapter 26: Hematopathology
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Chapter 27: The Endocrine System
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Chapter 28: The Skin
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Chapter 29: The Head and Neck
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Chapter 30: Bones, Joints and Soft Tissue
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Chapter 31: Skeletal Muscle and Peripheral Nervous System
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Chapter 32: The Central Nervous System
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Chapter 33: The Eye
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Chapter 34: Forensic Pathology
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,Rubin's Pathology: Clinicopathologic Foundations of Medicine
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Chapter 1: Cell Adaptation, Injury and Death
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Ischemia and other toxic injuries increase the accumulation of intracellular
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1. pocalcium as a result of: po po po p o
A) release of stored calcium from the mitochondria.
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B) improved intracellular volume regulation. po po po
C) decreased influx across the cell membrane. p o p o po po po
D) attraction of calcium to fatty infiltrates.
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The patient is found to have liver disease, resulting in the removal of a
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2. lobe of his liver. Adaptation to the reduced size of the liver leads to
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_ of the remaining liver cells.
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A) metaplasia
B) organ atrophy po
C) compensatory hyperplasia po
D) physiologic hypertrophy po
A person eating peanuts starts choking and collapses. His airway
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obstruction is partially cleared, but he remains hypoxic until he
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3. reaches the hospital. The prolonged cell hypoxia caused a cerebral
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infarction and resulting
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brain.
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A) caspase activation po
B) coagulation necrosis po
C) rapid phagocytosis po
D) protein p53 deficiency po p o
Bacteria and viruses cause cell damage by
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4. from the intracellular damage caused by other injurious agents.
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A) disrupting the sodium/potassium ATPase pumppo p o p o po
B) interrupting oxidative metabolism processes p o po po
C) replicating and producing continued po po po p o injury
D) decreasing protein synthesis and function po po p o po
The patient has a prolonged interruption in arterial blood flow to his left kidney,
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5. pocausing hypoxic cell injury and the release of free radicals. Free radicals
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damage cells by:
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A) destroying phospholipids in the cell membrane. po p o po po po
, B) altering the immune response of the cell.
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C) disrupting calcium storage in the cell.
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D) inactivation of enzymes and mitochondria. p o po p o po
6. Injured cells have impaired flow of substances through the cell membrane as a
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result of:
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A) increased fat load. po po
B) altered permeability.
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C) altered glucose utilization.
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D) increased surface receptors.
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7. Reversible adaptive intracellular responses are initiated by:
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A) stimulus overload. p o
B) genetic mutations.
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C) chemical messengers. po
D) mitochondrial DNA. po
8. Injured cells become very swollen as a result
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A) increased cell protein synthesis.
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B) altered cell volume regulation.
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C) passive entry of potassium
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D) bleb formation in the plasma membrane.
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A diabetic patient has impaired sensation, circulation, and oxygenation of his
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feet. He steps on a piece of glass, the wound does not heal, and the
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9. area tissue becomes necrotic. The necrotic cell death is characterized by:
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A) rapid apoptosis.
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B) cellular rupture. po
C) shrinkage and collapse. po po
D) chronic inflammation.
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A 99-year-old woman has experienced the decline of cell function associated with
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10. age. A group of theories of cellular aging focus on programmed:
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A) changes with genetic influences.
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B) elimination of cell receptor sites. p o po po po
C) insufficient telomerase enzyme. po po
D) DNA mutation or faulty repair.
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