Unit 9 - Cell death and adaptation Flashcards

1
Q

What causes different levels of tissue recovery?

A

Cellular injury - tissue function dependent on number of cells affected
Cell death - tissue with regenerative capacity and ECM undamaged, recovery to normal
Tissue regenerative capacity, but ECM damaged = permanent damage

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2
Q

What are the common causes of cellular injury?

A

-Lack of factors needed for normal cell function: blood, oxygen, nutrients, neural stimulation
- Physical: trauma, heat/cold
- Chemical: drug injury
- Inflammation: Autoimmune inflam
- Metabolic and genetic disorders: diabetes mellitus, obesity, glycogen storage disease

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3
Q

What determines the cell’s susceptibility to ischaemia or hypoxia?

A

Cell metabolic rate and anatomical position to arterial supply

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4
Q

How may cell injury or death present clinically?

A

Deranged tissue/organ function
Leaked intracellular contents in blood detected

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5
Q

How may cell injury/death present pathologically?

A

Morphological changes in tissue
Gross changes in surgical specimens
Light microscopic changes

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6
Q

How may cell morphology change in sublethal (reversible) cell injury?

A

Cell swelling:
Na/K+ pump failure = water influx
Membrane and organelle changes seen under EM
Fatty changes:
Deranged metabolism -> lipid accumulation intracellularly

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7
Q

What are the two main types of cell death?

A

Apoptosis:
Physiological process, specific enzymes break down cells, neat, normally single cells
Necrosis:
Not physiological, uncontrolled cell breakdown, non-specific enzyme activation, messy, large groups of cells

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8
Q

Name the two main patterns of necrosis

A

Coagulative
Liquifactive

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9
Q

Coagulative necrosis process

A

Most common
Leakage of cell contents from membrane breakdown
Inflammatory cell response
Leukocyte lysosomal enzymes are major factor in cell digestion
Macrophages are attracted and phagocytose and initiates granulation tissue

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10
Q

What is the gross appearance of coagulative necrosis?

A

Pale yellow from acute inflam cells
If blood flowing to tissue:
Haemorrhage
Acute inflammation
Infarction if dual blood supply

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11
Q

What does liquefactive necrosis arise from?

A

Focal bacteria and fungal infections

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12
Q

What are the features of liquefactive necrosis?

A

Abscess
No normal structures apparent
Soft disintegrating tissue

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13
Q

What are the possible outcomes of necrosis in different tissue types?

A

Tissues able to regenerate:
ECM intact -> return to normal
ECM damaged -> repair and scar
Tissues no regenerative capacity:
-> repair and fibrous scarring

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14
Q

Apoptosis

A

Cell death occurring normally through life
Elimination of unwanted cells/cells damaged beyond self repair
Cell death without host reaction
Programmed and controlled cell death

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15
Q

What does the morphology of apoptosis look like under a light microscope?

A

Darker staining small round bodies
Small black/very black shrunken fragments of nucleus

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16
Q

When may apoptosis occur under physiological situations? (removing unwanted cells)

A

Embryogenesis
Death of neutrophils and lymphocytes at end of inflammatory response
Involution (shrinking) of hormone dependent tissues

17
Q

When may apoptosis occur under pathological situations? (eliminating damaged cells)

A

DNA damage
Accumulation of misfolded proteins in the ER
Atrophy in organs

18
Q

Necrosis summary

A

Most common type of cell death
Usually coagulative
Micro: no nuclei
Macro: pale/haemorrhagic
Stimulate inflammatory response
Scar formation or replacement of cells by progenitor cells

19
Q

Gangrenous necrosis

A

When coagulative necrosis involves multiple layers
Massive inflammatory response with circulatory failure
‘Wet gangrene’ when infection of bacteria ontop

20
Q

Fat necrosis

A

Areas of fat destruction
Macrophages around the spaces
Due to physical trauma e.g. breast trauma, chemical damage e.g. lipases from pancreas inflammatory injury