Cell Injury Flashcards

1
Q

How does stress affect cells?

A

Cell attempts to adapt
Failure to adapt can lead to cell death

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2
Q

What is hyperplasia?

A

Increase in cell number in response to external stimulus

Can be physiological or pathological

Reversed on withdrawal of stimulus
- Exception: Cancer keeps growing on absence of stimulus
- Hyperplastic tissue = risk site for development of cancer

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3
Q

Physiological and Pathological hyperplasia:

A

Physiological: E.g. breast tissue in puberty

Pathological: Hormonally induced e.g. excess oestrogen

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4
Q

What is Hypertrophy, when does it occur, and what can it cause?

A

Increase in cell size

Often occurs:
- In conjunction with hyperplasia
- In isolation in non-dividing cells (e.g. skeletal muscle)
- In response to mechanical stress

Becomes pathological when heart/muscle can no longer function leading to heart failure.

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5
Q

What is hypoxia and how is it caused?

A

Interferes with aerobic oxidative respiration

Caused by
•Ischaemia (restricted blood flow)
•Reduction in oxygen carrying capacity of the blood
•Inadequate blood oxygenation

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6
Q

What is hypoxic injury and what can it cause?

A

Reduction in intracellular generation of ATP:

  • Reduces sodium pump activity causing sodium to accumulate in cell resulting in gain of water causing cellular swelling
  • Depletion of glycolysis stores due to increase in anaerobic glycolysis
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7
Q

What is atrophy?

A

Reduction in cell size

Can be physiological or pathological:
- Physiological (e.g. embryological structures)
- Pathological (e.g. blocked blood supply)

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8
Q

5 types of necrosis:

A

COAGULATIVE NECROSIS
•Tissue with connective tissue, basic arrangement preserved

COLLIQUATIVE NECROSIS
•Tissue with minimal connective tissue ‘liquifies’

CASEOUS NECROSIS
•‘Cheese’-like necrotic debris

GRANGRENOUS NECROSIS
•DRY – sterile coagulative necrosis e.g. distal limb
•WET – coagulative necrosis with superimposed infection

FAT NECROSIS
•Focal necrosis in fat due to action of lipases (also trauma)

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9
Q

Autolysis

A

‘Rotting’ of tissue

Lysis of tissue by their own enzymes following death

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10
Q

Physiological importance of apoptosis:

A

Embryogenesis

Menstrual cycle

Immune system:
•Death of post-inflammatory neutrophils
•Removal of self-reactive lymphocytes
•Death of virally infected cells

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11
Q

Primary and secondary healing

A

Primary healing:
•Restitution with no – or minimal – residual defect

Secondary healing:
•Organisation and repair where there is tissue loss

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12
Q

Metaplasia

A

Reversible change in which one adult cell type is replaced by another adult cell type

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13
Q

How does ionising radiation damage cells?

A

Damages DNA

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14
Q

3 types of cell regeneration:

A

Labile : good capacity to regenerate (eg surface epithelial cells)

Stable : divide at a slow rate, but can regenerate if needed (eg hepatocytes in liver)

Permanent: eg nerve cells, striated muscle cells – no means of effective regeneration

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15
Q

What can happen if hypoxic injury persists?

A

Cytoskeleton can break down
Cell death

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