Regeneration and Repair Flashcards

1
Q

What is regeneration?

A

(re) growth of cells and tissue to replace lost structure

- only possible with minor injuries as it requires an intact connective tissue scaffold

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2
Q

What are the three types of stem cells?

A
  • Totipotent = produce all cell types e.g. embryonic
  • Multiopotent = produce several cell types e.g. haemotopoietic
  • Unipotent = produce one cell type e.g. epithelial stem cells
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3
Q

What are the tissue classifications (regeneration ability)?

A
  • Labile tissue = continuously dividing e.g. epithelium
  • Stable tissue = low level of replication but can undergo rapid proliferation in response to stimuli e.g. liver
  • Permanent tissue = cells do not replicate e.g. cardiac, neurons
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4
Q

What is fibrous repair?

A

Replacement of a functioning tissue with a scar

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5
Q

Describe the process of scar formation

A

1) Bleeding and haemostasis -prevention of blood loss
2) Inflammation - acute then chronic, digest blood clot

3) Proliferation - angiogenesis, fibroblast, myofibroblasts and ECM
- granulation tissue fills the gap, capillaries supply O2 and nutrients

4) Remodelling - maturation of scar (reduced cell population (leukocytes), increased collagen, myofibroblasts contract)

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6
Q

Describe fibroblasts and their function

A
  • Spindle shaped nucleus with cytoplasmic extensions

- Secrete collagen and elastin to form ECM

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7
Q

Describe myofibroblasts and their function

A
  • Structure is between a fibroblast (spindle shaped nucleus) and smooth muscle
  • Express cellular actin = wound contraction
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8
Q

Describe briefly how collagen is synthesised

A

Pre-procollagen hydroxylase de to procollagen (cross linked to form triple helix)

Procollagen cleaved C+N terminals outside cells to cross link with each other

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9
Q

Describe scurvy

A

A collagen associated disease caused by vitamin C deficiency (essential for hydroxylation) which leads to defective triple helix structure of procollagen
Patients are unable to heal wounds, tendency to bleed and teeth loss

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10
Q

Describe Ehlers-Danlos syndrome

A

Diseased associated with collagen where collagen fibres lack adequate tensile strength

  • skin is hyper flexible, fragile, susceptible to injury and joints are hyper mobile
  • patients can suffer from rupture of colon or large arteries
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11
Q

Describe osteogenesis imperfecta

A

Disease where there is too little bone tissue these skeletal fragility presents
-patients usually present with blue sclera, hearing impairment and dental abnormalities

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12
Q

Describe Alport syndrome

A

X-linked (usually) disease that causes abnormal type IV collagen
-dysfunction of glomerular basement membrane, cochlea and lens of the eye

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13
Q

How do cells communicate to control scar formation?

A
  • local mediators (can be autocrine, paraffine or endocrine) such as growth factors that stimulate proliferation by transcription of genes that regulate entry of cell to cell cycle
  • cell to cell contact = contact inhibition (replication until they touch each other) detected by adhesion molecules
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14
Q

When does healing of primary intention take place?

A

For wounds that are incisional, closed, non-infected and sutured
-disruption of epithelial basement but death of only a limited no. of epithelia

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15
Q

When does healing by secondary intention take place?

A

For wounds with significant tissue loss and unopposed edges (infection, ulcer, abscess)
-considerable wound contraction required

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16
Q

List some local factors influencing regeneration and repair

A
  • size of wound
  • location of wound
  • blood supply
  • denervation
  • local inflammation
  • foreign bodies
  • necrotic tissue
  • mechanical stress
17
Q

List some systemic factors influencing regeneration and repair

A
  • age
  • anaemia, hypoxia, hypovolaemia
  • obesity
  • malignancy
  • diabetes
  • drugs e.g. steroids
  • vitamin deficiency
  • malnutrition
18
Q

What are some complications of fibrous repair?

A
  • formation of fibrous adhesions = blocking tubes and compromise organ function
  • loss of function = replacement of specialised cells to scar tissue
  • disruption of complex architecture
  • overproduction of scar tissue = keloid scar
  • excessive scar contraction = obstruction of tubes