Healing And Repair- muscle Flashcards

1
Q

What happens after injury occurs

A
Injury
   ⬇️
Inflammation 
   ⬇️
Repair : 

1) tissues capable of regeneration
* Regeneration process- replacing injured or dead cells functional identical cells

> limited injuries- regeneration of normal anatomy
Extensive injury- partial regeneration and scarring (repair by fibrous healing)

2) tissues not capable of regeneration
Repair and organisation process

> scarring only (repair by fibrous healing)

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2
Q

Cell types (classified by ability to regenerate)

A

Labile cells
stable cells
permanent cells

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3
Q

Labile cells

A

Epithelial cells in skin and digestive system

The cells undergo continuous proliferation have a short lifespan

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4
Q

Stable cells

A

Bone cells liver cells

Usually divide in frequently but can divide rapidly when stimulated by lost cells for example a fracture

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5
Q

Permanent cells

A

Neurons cardiac muscle

Divide only in the fetus and cannot be replaced with lost

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6
Q

Healing by first intention

A

Eg a cut or a bone fracture

loss of part of a labile or stable cell population can be completely restored

The result is indistinguishable from normal has minimal defect

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7
Q

Healing by second intention

A

Eg healing of open wound or 3rd° burn

Extensive tissue loss or damage requires a repair process

Involves the formation of fibrovascular connective tissue- fibreous scar tissue

Tissues not capable of regeneration

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8
Q

Tissue repair stages

A

Three overlapping processes:

Inflammation
Proliferation
Remodelling

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9
Q

End of inflammation/beginning of proliferation

A

1)Role of macrophages: leaked out of capillaries go to affect area

Neutrophils- degrade pathogens

Monocytes- release enzymes phagocytosis secrete cytokines which attract cells for proliferation

2)Angiogenesis: new capillary blood and blood vessels are formed from pre existing blood vessles

Endothelial stem cells from undamaged part of vessles migrate to the damaged area attracted to area by chemicals- fibronectin found on fibrin scab and other angiogenic factors released by cells such as macrophages and platelets.

Endothelial growth and proliferation are directly stimulated by hypoxia and lactic acid in the wound. New capillaries formed eventually forming a blood Flow through the region which supplies nutrients and get rid of metabolic waste

3)Migration of fibroblasts to the area of damage

At the same time there is an increase of fibroblasts that were on site numbers peak at 1 to 2 weeks after Injury occurred. Main cells. Fibroplasia ends 2/4 weeks after wounding.

Production of cells decrease indicators proliferation is beginning.

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10
Q

Healing and repair – proliferation

A

1)Roll fibroblasts-Form granulation tissue

•Migrate to the site of wound

2)Fibroblasts secrete the extracellular matrix and collagen e.g proteoglycans (look at inflammation)

  • Forms a new mesh work (scaffolding)
  • Haphazard arrangement of immature fibres immature type 3 collagen

3) More organised bundles of collagen are formed as more collagen is laid down and the repair is gradually strengthened near the end of proliferation intermolecular cross links are formed between collagen fibres and this strengthens repair but can reduce extensibility of tissue as they cannot slide over each other.
4) new tissue = granulation tissue and it contains new capillaries and cells called myofibroblasts
5) contraction of the repair begins the action of myofibroblasts which are specialised fibroblasts - collagen secreting but also contain muscle like contractile proteins
6) They attached to edges of the wound and each other and contract to pull the wound edges together- smaller wound scar develops

**Fibronectin is important because it acts as an anchor for myofibroblasts

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11
Q

Importance of fibronectin

A

** Fibronectin is important because it acts as an anchor for myofibroblasts

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12
Q

Duration of proliferation

A

3 weeks

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13
Q

Remodelling

A

1) Fibroblasts and myofibroblast start to leave the scare Tissue changes from a predominantly cellular to fibrous structure
2) Change of collagen type from the immature type 3 to mature type 1

3)Gradual realignment of collagen fibrrs along the lines of stress to attain the mechanical characteristics of the tissue prior to injury
more parallel than haphazard. Proteoglycans etc affected by direction and magnitude of stress.

4) fibroblasts are aligned parallel to lines of stress mechanical forces influence metabolism increasing production in extracellular matrix, fibronectin= parallel to lines of stress so if patient doesn’t move these processes won’t occur. Exercise v important movement =6 months
5) Vascularity of scars diminishes

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14
Q

Remodelling duration

A

6 months

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15
Q

Muscle healing and repair

How muscles are injured

A

Muscle tissues heal by regeneration and repair

1) Muscles injured by direct trauma - fracture or blow
2) mechanical strain- stretching forces eccentric
3) exercise or ischaemia - compression lack of O2:

  • Tearing/rupture of muscle
  • Intramuscular blood vessels torn
  • Torn muscle fibres retract and the gap between the stumps is filled with haematoma
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16
Q

Muscle healing and repair

Cell death of muscles

A

1) Necrosis cell death of muscles
2) Torn sarcolemma reseals stem cells which protects intact myofibrils and localises necrosis
3) Inflammatory response initiated

Macrophages remove dead tissue inner part of endomysium (basil laminar) left intact acts as scaffold and satilite cells begin formation of new muscle fibres

Angiogenesis starts near end of inflammation phase

Haematoma replaced by granulation tissue produces scaffold for fibroblasts- secrete collagen formation of extracellular matrix type 3 then type 1 and satilite cells

17
Q

How is muscle repaired

A

Regeneration of muscle fibres occur by satellite cells

Occurs in conjunction with fibre scar formation

18
Q

Satellite cells,progenitor cells:

A

Lie dormant unless stimulated and found between sarcolema and basal Lamelle

**regeneration process

  • Special myoblasts
  • residence stem cell population and muscles
  • join with each other for multinucleated myotubes

Some differentiate into myoblasts immediately after injury others undergo cell division before differentiation

19
Q

Myotubes

A

Mature to form new multinucleated muscle fibres or fuse with and repair damaged muscle fibres eventually muscle fibres will mature developing normal striations and proliferally locates nuclei

20
Q

Regenerating muscle

A

1) Regenerating muscle fibres extend towards and replace the connective tissue scar between the survived stumps of injured muscle fibres
2) Fuse with scar forming musculotendinous junctions
3) Regenerating fibrous cells replace fibrous tissue and the regeneration continues to myotube phase even in the abscenes of innovation but atrophy will occur if reininnovation is not accomplished eventually
4) Reinnovation- requires regrow the of axon sprout which penetrates the fibrous scar of central zone
5) Nerve fibres regenerate
6) Revascularisation new capillaries adequate O2 apply this allows aerobics metabolism for regenerating myofibres younger myotubes have fewer mitochondria rely on anaerobic metabolism

21
Q

Quality of muscle tissue

A
  • Extent of muscle tissue loss
  • Blood supply
  • Lack of further disruption
  • Excessive scar tissue can inhibit regeneration-varying levels of residual fibrosis can occur
  • capacity of stem cell division deceases with age decline of regeneration