Lecture 18: Repair and regeneration Flashcards

1
Q

What is regeneration?

A

Cells can regrow
Restoration of normal structure and function

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2
Q

What is repair?

A

Cells cannot regrow
Scar formation
Loss of function

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3
Q

After injury and acute inflammation, what pathways can be taken?

A

Regeneration
Repair
Chronic inflammation

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4
Q

Two most important factors determining outcome of injury?

A
  1. ability of the cells to replicate
  2. ability to rebuild complex architectural structures
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5
Q

What different cell types in the repair / regeneration of cells cycle?

A
  1. Continuously cycling labile cells
    2 Permanent Cells
  2. Quiescent stable cells
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6
Q

What different cell types in the repair / regeneration of cells cycle?

A
  1. Continuously cycling labile cells
    2 Permanent Cells
  2. Quiescent stable cells
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7
Q

What is the labile cell population and characteristics?

A

High normal turnover
Active stem cell population
Excellent regenerative capacity

Example: Epithelia

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8
Q

What is the stable quiescent cell population and characteristics?

A

Low turnover
(physiological)
Turnover can massively increase
(if needed)
Good regenerative capacity

Example: liver, renal tubules

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9
Q

What is the permanent cell population and characteristics?

A

No turnover
(physiological)
Long life cells
No regenerative capacity

Example: neurons, striated muscle cells

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10
Q

Stem cell characteristics?

A

Prolonged self-renewal
Asymmetric replication
Reservoirs in many adult tissues

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11
Q

How do Stem cells form?

A
  1. Terminal
    differentiation
    2.Differentiating
    compartment
    3.Amplifying cell
    compartment
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12
Q

What is the population of Stem cells?

A

Present in many labile and stable cell populations
Located in specific areas (basal)
Survival = crucial to regeneration

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13
Q

Give an example of the rebuild of complex architectures which is limited?

A

Glomeruli, lung

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14
Q

An example of when survival of connective tissue is essential?

A

Cirrhosis

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15
Q

How does complete restitution occur?

A

Loss of labile cell population can be completely restored
e.g minor skin abrasion
Cells at edge of defect multiply to cover defect

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16
Q

What is contact inhibition?

A

when cells cover defect proliferation stops

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17
Q

What is complex regeneration controlled by?

A

growth factors
cell-cell interactions
cell-matrix interactions

These mechanisms are lost in neoplasia

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18
Q

What does regeneration depend on?

A

tissue cell kinetics
architecture
stem cell survival

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19
Q

how does healing by regeneration affect specialised function?

A

Restitution of
specialised function

20
Q

How does healing by repair affect specialised function?

A

Loss of specialised
function

21
Q

What happens during repair of cells/tissues?

A

Normal structure cannot be replaced
Healing by non-specialised fibrous tissue (‘Scar’)
Functional consequences

22
Q

What is Organisation?

A

the repair of specialised tissue by formation of a fibrous scar

23
Q

What is an example of organisation?

A

Example = common consequence of pneumonia and infarction

24
Q

Organisation characteristics?

A

Basic stereotyped pathological process
Production of granulation tissue (often on scaffold of fibrin)
Removal of dead tissue by phagocytosis
Granulation tissue contracts and accumulates collagen
Scar forms
Organised area = firm and puckered

25
What is Granulation tissue?
New capillary loops Phagocytic cell (Neutrophils and Macrophages) (Myo)fibroblasts
26
What does Endothelial cell proliferation include?
Buds Canalisation New vessels
27
What do phagocytes do?
Remove dead / Damaged tissue
28
What is included in Proliferation and migration of myofibroblasts?
Synthesise collagen and ECM Acquire myofibrils and contractile ability
29
What decreases in maturation of granulation tissue?
1. Vascularity 2. Cellularity
30
What increases in Maturation of Granulation tissue?
Collagen, ECM wound strength.
31
What is involved in healing by first intention?
Clean, uninfected surgical wound Good haemostasis Edges apposed
32
What is involved by healing by second intention?
Extensive loss of tissue Wound edges not apposed Apposition not physically possible Large haematoma Infection Foreign body More florid granulation tissue reaction More extensive scarring
33
Wound strength after a week?
10%
34
Wound strength after week 4- week 12?
70 - 80%
35
Local factors inhibiting healing?
Infection Haematoma Blood supply Foreign bodies Mechanical stress
36
Systemic factors inhibiting healing?
Age Drugs (eg steroids) Anaemia Diabetes Malnutrition Catabolic states Vitamin C deficiency Trace metal deficiency
37
What is a haematoma?
Haemorrhage around and within the bone - haematoma
38
Is haematoma organised?
Yes - removal of necrotic fragments
39
Fracture healing pathway?
Osteoblasts lay down disorganised woven bone (callus) Remodelling according to mechanical stress Replacement by more orderly lamellar bone
40
Non- union of fractures?
Misalignment Movement Infection Interposed soft tissue Pre-existing bone pathology ‘pathological fracture’
41
How are neurons organised in the brain?
Terminally differentiated
42
Support tissue in the brain?
Glial cells
43
What do you get in the brain when damage tissues are removed?
Cysts
44
What happens in the brain rather than scarring?
Gliosis
45
For growth factor and function for control of healing:
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