5.2 Adaptation and injury Flashcards

1
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2
Q

What are the two types of adaptation to injury?

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  • Physiological adaptation-cellular response to normal stimulation
    • Hormones
    • Endogenous chemicals
  • Pathological adaptation-cellular response to stimulation secondary to underlying disease/ to avoid injury
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3
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4
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5
Q

What happens in hypertrophy?

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  • Increased work load (physiological and pathological stimuli)
  • Increased size of cells resulting in increased size of organ
  • No new cells, just larger cells
  • Non-dividing cells increase in size (myocytes, skeletal muscle)
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6
Q

What are two examples of things which lead to hypertrophy?

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7
Q

What is hyperplasia?

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  • Increase in number of cells in an organ or tissue
  • Only in cell populations capable of dividing
  • Physiological and pathological response
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8
Q

What are examples of physiological and pathological cause of hyperplasia?

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  • Physiological
    • Hormonal (puberty)
    • Compensatory (liver resection)
    • Increased demand (Low atmospheric O2 leads to increased erythrocytes)
  • Pathological
    • Hormonal (endometriosis)
    • Viral infection (skin warts)
    • Chronic stress (callous)
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9
Q

What is atrophy?

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  • Reduced size of organ resulting from decrease in cell size and number.
  • Physiological atrophy is common during normal development (embryonic structures, uterus following pregnancy)
  • Pathologic atrophy depends of the underlying cause.
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10
Q

What can cause atrophy?

A
  • Decreased work load
  • Immobilization
  • Loss of innervation
  • Loss of blood supply
  • Inadequate nutrition
  • Loss of endocrine stimulation
  • Pressure
  • Aging
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11
Q

What is metaplasia?

A
  • Replacement of one differentiated cell type with another
  • Cells sensitive to stress replaced by a cell type better able to withstand stress
  • Stem cell reprogramming
  • For example cigaratte smoking turns ciliated columnar to stratified squamous.
  • Chronic gastric reflux turns stratified squamous to gastric columnar epithelial
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12
Q

What is the difference between adaptation and reversible and irreversible injury?

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  • Adaptation: A response to stress or increased demand that maintains the steady state of the cell without compromising cellular function.
  • Reversible/ sublethal injury: A response to stress/ stimuli that compromises cellular function.
  • Irreversible injury: A response to stress/ stimuli that compromises cellular function to the point that it cannot recover
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13
Q

What happens in reversible injury?

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  • Cell function compromised
  • Recovery if injury is removed
  • May compromise organ function
  • Eg. Reversibly injured myocytes (transient ischemia) may be transiently non- contractile which will affect function of the heart
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14
Q

What happens in irreversible injury and cell death?

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  • When the cell cannot recover and it dies
  • Two types of cell death which differ in morphology, cause and roles in disease
  • Necrosis
  • Apoptosis
  • May have occurred before morphological changes become apparent
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15
Q

When does injury cause irreversible damage? What cell and injury factors

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16
Q

How is sequential development of changes seen in cell injury?

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  • Cells may be non- functional but viable
  • Cells may undergo biochemical changes and be non-viable (dead) before the appearance of ultrastructural, microscopic and macroscopic changes are apparent.
17
Q

What is the haemotoxylin stain?

A
  • It is used to stain acidic (or basophilic) structures a purplish blue.
  • Stains nucleic acids (DNA in nucleus, RNA in ribosomes and RER)
18
Q

What is the eosin stain?

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  • It stains basic (or acidophilic) structures red or pink (also sometimes termed ‘eosinophilic’)
  • Most proteins
19
Q

What morpholigcal features of injury can be seen with a light microscope?

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20
Q

What morphological features of reversible injury can be seen in the ultrastructure?

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21
Q

When does irreversible injury occur?

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  • Occurs when mitochondrial dysfunction can’t be reversed and when membranes lose their structural integrity
22
Q

What membrane changes are seen in irreversible injury?

A
  • Lysosomal membranes
    • Contents leak into cell
    • Nuclear and cytoplasmic components degraded
  • Plasma membrane
    • Loss of osmotic balance
    • Cellular contents leak into extracellular space (inflammation)
  • Mitochondrial membrane
23
Q

What are the six mechanisms of cell injury?

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24
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A
25
Q

How does a loss of ATP bring about other changes for cell injury?

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26
Q

How does damage to mitochondria bring about other cellular changes for cell injury?

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27
Q

What cellular changes does an influx of calcium cause during cell injury?

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28
Q

What are free radicals?

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  • Chemical species with unpaired electron in outer orbital
  • Unstable and reactive
  • Attack nucleic acid, protein and lipids
29
Q

What are reactive oxygen species?

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  • Oxygen derived free radical
  • Byproduct of respiration
  • Produced by phagocytic leukocytes
  • Removed by scavengers

Increase in reactive oxygen species or decrease in scavengers causes oxidative stress

30
Q

What leads to membrane damage during cell injury?

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31
Q

How does hypoxia affect respiration?

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32
Q

How does hypoxia affect ATP dependent transport?

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33
Q

How does hypoxia affect the synthesis of macromolecules?

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34
Q

What are the effects of cell membrane damage due to hypoxia?

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35
Q

What changes in morphology are seen when there is hypoxia of the heart?

A
  • Increased staining with eosin
  • Proteins now denatured so bind to eosin more strongly (eosinophilia)
  • Loss of basophilic RNA
  • Reduced nuclei (less haematoxylin staining)
  • Edema
  • Inflammatory cells
36
Q

What happens to proteins in hypoxia of the heart?

A
  • Intracellular proteins leak through damaged cell membrane
  • Cardiac specific enzymes
    • Cardiac isoform of creatine kinase
    • Contractile protein troponin
  • Serum levels reflect tissue injury
    • Myocardial infarction (irreversible injury, plasma membrane integrity lost)
    • Angina (reversible injury, plasma membrane intact)