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TEST BANK FOR Rubin's Pathology: Clinicopathologic Foundations of Medicine 7th Edition by David S. Strayer& Emanuel Rubin , ISBN: 9781451183900 |LATEST EDITION| Guide A+

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TEST BANK FOR RUBIN'S PATHOLOGY- CLINICOPATHOLOGIC FOUNDATIONS OF MEDICINE 7TH EDITION BY DAVID S. STRAYER, EMANUEL RUBIN- 1. Ischemia and other toxic injuries increase the accumulation of intracellular calcium as a result 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. 2. The patient is found to have liver disease, resulting in the removal of a lobe of his liver. 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 3. 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 caused a cerebral infarction and resulting _ in the brain. A) caspase activation B) coagulation necrosis C) rapid phagocytosis D) protein p53 deficiency 4. Bacteria and viruses cause cell damage by , which is unique from the intracellular 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 5. The patient has a prolonged interruption in arterial blood flow to his left kidney, causing 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 cells have impaired flow of substances through the cell membrane as a result of: A) increased fat load. B) altered permeability. C) altered glucose utilization. D) increased surface receptors. 7. Reversible adaptive intracellular responses are initiated by: A) stimulus overload. B) genetic mutations. C) chemical messengers. D) mitochondrial DNA. 8. Injured cells become very swollen as a result of: A) increased cell protein synthesis. B) altered cell volume regulation. C) passive entry of potassium into the cell. D) bleb formation in the plasma membrane. 9. A diabetic patient has impaired sensation, circulation, and oxygenation of his feet. He steps on a piece of glass, the wound does not heal, and the area tissue becomes necrotic. The necrotic cell death is characterized by: A) rapid apoptosis. B) cellular rupture. C) shrinkage and collapse. D) chronic inflammation. 10. A 99-year-old woman has experienced the decline of cell function associated with age. A group of theories of cellular aging focus on programmed: A) changes with genetic influences. B) elimination of cell receptor sites. C) insufficient telomerase enzyme. D) DNA mutation or faulty repair. 11. An 89-year-old female patient has experienced significant decreases in her mobility and stamina during a 3-week hospital stay for the treatment of a femoral head fracture. Which of the following phenomena most likely accounts for the patients decrease in muscle function that underlies her reduced mobility? A) Impaired muscle cell metabolism resulting from metaplasia B) Dysplasia as a consequence of inflammation during bone remodeling C) Disuse atrophy of muscle cells during a prolonged period of immobility

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RUBIN\\\\\\\'S PATHOLOGY- CLINICOPATHOLOGIC FOUNDATIONS
Course
RUBIN\\\\\\\'S PATHOLOGY- CLINICOPATHOLOGIC FOUNDATIONS

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TEST BANK
RUBIN'S PATHOLOGY:
CLINICOPATHOLOGIC
FOUNDATIONS OF MEDICINE
PR
7th Edition by David S. Strayer, Emanuel Rubin
O
FD
O
C

,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
PR
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
O
Chapter 18: The Respiratory System
Chapter 19: The Gastrointestinal Tract
Chapter 20: The Liver and Biliary System
FD
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
O
Chapter 26: Hematopathology
Chapter 27: The Endocrine System
Chapter 28: The Skin
C
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
Medicine
(ANSWERS AT THE END OFEACH CHAPTER)

Chapter 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.
PR
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.
O
A) metaplasia
B) organ atrophy
FD
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.
O
A) caspase activation
B) coagulation necrosis
C
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 cells have impaired flow of substances through the cell membrane as a result of:
A) increased fat load.
B) altered permeability.
C) altered glucose utilization.
D) increased surface receptors.
7. Reversible adaptive intracellular responses are initiated by:
PR
A) stimulus overload.
B) genetic mutations.
C) chemical messengers.
D) mitochondrial DNA.
8. Injured cells become very swollen as a result of:
O
A) increased cell protein synthesis.
B) altered cell volume regulation.
FD
C) passive entry of potassium into the cell.
D) bleb formation in the plasma membrane.
A diabetic patient has impaired sensation, circulation, and oxygenation of his feet. He steps on
a piece of glass, the wound does not heal, and the area tissue becomes necrotic. The necrotic
O
9. cell death is characterized by:
A) rapid apoptosis.
B) cellular rupture.
C
C) shrinkage and collapse.
D) chronic inflammation.
A 99-year-old woman has experienced the decline of cell function associated with age. A
10. group of theories of cellular aging focus on programmed:
A) changes with genetic influences.
B) elimination of cell receptor sites.
C) insufficient telomerase enzyme.
D) DNA mutation or faulty repair.

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Institution
RUBIN\\\\\\\'S PATHOLOGY- CLINICOPATHOLOGIC FOUNDATIONS
Course
RUBIN\\\\\\\'S PATHOLOGY- CLINICOPATHOLOGIC FOUNDATIONS

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