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Semester 2 Pathological Processes > L8: Regeneration and Repair > Flashcards

L8: Regeneration and Repair Flashcards

1
Q

When in the inflammatory response is repair necessary?

A

Acute phase–> fibrosis–> substantial damage/ tissue destruction
Chronic phase–> Prolonged inflammation

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2
Q

What processes are involved in wound healing?

A

Injury–> haemostasis (blood clots)–> inflammation–> regeneration or repair

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3
Q

What is regeneration?

A

Regrowth of cells–> no evidence/ minimal evidence of injury–> no scar formation

Physiological–> production of new cells–> haematopoesis (RBC, WBC) etc

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4
Q

When can regeneration take place?

A

Minor injuries–> superficial skin damage

  • Incision wound
  • Abrasion
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5
Q

Where do the new cells come from?

A

Stem cells –> differentiate into other cell types

  • -> self renew
  • -> replace damaged/ dead cells
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6
Q

What are the different types of stem cells?

A

Totipotent–> potential to differentiate into any cell type
Multipotent–> several cell types
Unipotent–> one cell type

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7
Q

Where are stem cells found?

A 
Scattered throughout (not totipotent stem cells)
e.g. skin/epidermis (stratum basale), intestinal mucosa (bottom of crypts), liver (between hepatocytes) etc...
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8
Q

Which tissue types are able to regenerate?

A

Labile tissue–> continuous replication of cells
e.g. epithelium, haematopoietic tissue
Stable tissue–> Normally low level of replication–> can undergo rapid proliferation–> response to stimuli
–> Go Quiescent cells
e.g. liver, kidneys, pancreas, bone, endothelium, smooth muscle
Permanent tissue–> cells do not replicate once left cell cycle
e.g. neurons, skeletal muscle, cardiac muscle

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9
Q

What is a requirement for tissue regeneration?

A

Intact architecture

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10
Q

What is the difference between regeneration and repair?

A

Regeneration–> replace damaged cells with new cells (regrowth of cells)
Repair–> Replacement of tissue with scar

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11
Q

After tissue injury how do cells know whether to undergo regeneration or repair?

A

Necrosis of liable or stable tissues
–> Collagen framework intact–> regeneration
–> Not intact or on-going chronic inflammation–> Fibrosis repair
Necrosis of permanent tissue
–> Firbous repair (scar tissue)

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12
Q

How does a scar form?

A

Bleeding and haemostasis
Inflammation
Proliferation
Remodelling

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13
Q

Describe each stage of scar formation?

A

1- Bleeding and haemostasis

  • -> Within seconds to minutes
  • -> Prevent blood loss

2- Inflammation

  • -> Acute then chronic
  • -> Digestion of blood clot, removal of dead tissue
  • -> Minutes- days

3- Proliferation

  • -> Capillaries (angiogenesis)
  • -> Fibroblasts–> produce and lay down collagen and elastin
  • -> Myofibroblasts
  • -> Extracellular matrix (ECM)
  • -> Formation of granulation tissue–> new collagen laid down
  • -> Days- weeks

4- Remodelling

  • -> Maturation of scar
  • -> Reduced cell population
  • -> Increased collagen
  • -> Myofibroblast contract–> seals gap
  • -> Scar formation
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14
Q

What is the function of proliferation?

A

Fill in the gaps
Capillaries supply O2 and nutrients
Contracts and closes the defect/ gap

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15
Q

What are the cells involved in fibrous repair? What is their function?

A 
Neutrophils and macrophages 
--> Phagocytosis
--> Release of chemical mediators
Lymphocytes
--> Eliminate pathogens 
--> Co-ordinate other cells 
Endothelial cells 
--> Proliferation 
--> Angiogenesis
Fibroblasts
--> secrete collagen and elastin
Myofibroblasts
--> Intracellular actin--> wound contraction
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16
Q

What is the difference between fibroblasts and myofibroblast?

A

Fibroblasts–> spindle shaped nucleus, cytoplasmic extensions–> secrete collagen and elastin to form ECM

Myofibroblasts–> between and smooth muscle and a fibroblast–> similar appearance to fibroblasts
–> intracellular actin–> contracts–> wound contraction

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17
Q

What is collagen?

A

Abundant mammalian protein
Provides extracellular framework
29 different types
Type 1–> bones, tendon, ligament, skin, sclera
Type 4–> basement membrane, lens, glomerular filtration

18
Q

How is collagen synthesised?

A
  1. Peptide of gly-x-y–> alpha chain preprocollagen –> in ER of (myo)fibroblasts
  2. Hydroxylation of Pro and Lys aa–> vitamin C dependent–> procollagen
  3. Release from ribosome
  4. Glycosylation
  5. Triple helix–> alpha chains crosslinked–> in cytoplasm
  6. Secreted from cell
  7. Cleave N and C terminal–> tropocollagen
  8. Tropocollagen crosslinked–> microfibrils–> fibrils and collagen fibres
19
Q

What are some of the diseases associated with defective collagen?

A

Acquired–> developed later in life
Scurvy

Inherited–> born with it
Ehlers- Danlos syndrome
Osteogensis Imperfecta
Alport Syndrome

20
Q

What is Scurvy?

A

Vit C deficiency
Inadequate hydroxylation of pre-pro collagen
Defective triple-helix= defective collagen
Unable to heal wounds properly, tendancy to bleed, tooth loss

21
Q

What is Ehlers-Danlos syndrome?

A

Heterogenous group of 6 inherited disorders
Collagen fibres lack adequate tensile stress and strength
Hyperextensible, fragile, susceptible to injury
Hypermobile joints

22
Q

What is osteogenesis imperfecta?

A

Brittle bone disease
Little bone tissue and extreme skeletal fragility
Blue Sclerae

23
Q

What is Alport Syndrome?

A

X-linked disease
Type IV collagen dysfunctional
Usually male
Haematuria in childhood–> chronic renal failure

24
Q

How are regeneration and repair controlled?

A

Cells communicate with each other to produce a proliferative response

25
Q

What are the mechanisms of communication between cells?

A

Direct cell-cell/ Cell-stromal contract
Local Mediators (Growth factors)
Hormones

26
Q

What are growth factors? What do they do? What are some examples?

A 
Polypeptide that act on cell surface 
Cause other cells to enter the cell cycle and proliferate 
--> reach M phase and divide
Helpful for healing 
Examples: 
Epidermal Growth Factors 
Vascular Endothelial Growth Factors 
Platelet Derived Growth Factors 
Tumour Necrosis Factors

defective in cancer

27
Q

What are the different types of cell communication for local mediators and hormones?

A

Autocrine–> respond to signalling molecules produced by self
Paracrine–> signals from cells in local area
Endocrine–> signals released into bloodstream act on target cells

28
Q

How does epidermal growth factor work?

A

Binds to EGF receptor (EGFR)
Produced by keratinocytes, inflammatory cells and macrophages
Mitogenic for epithelial cells, hepatocytes and fibroblasts

29
Q

How does VEG-F work?

A

Inducer of BV development (vasculogenesis)
Growth of new BV (angiogenesis)
In chronic inflammation, wound healing and tumours

30
Q

What does platelet derived GF do?

A

Stored in platelet alpha granules
Released upon activation
Produced by macrophages, endothelial cells, smooth muscle cells and tumour cells
Migration and proliferation of fibroblasts, SMC, and monocytes

31
Q

What does TNF do?

A

Induces fibroblast migration and proliferation and collagenase secretion

32
Q

Why is direct cell-cell contact important?

A

Important to stop cell proliferation–> contact inhibition
Cadherins (cell surface molecules) interact–> inhibit proliferation

defective in cancer

33
Q

What are the two classifications of wound healing?

A

Primary Intention
Secondary Intention
Determined by the size of the wound

34
Q

What is closing by primary intention? What are the different stages?

A

Incision, closed, non-infected and sutured wounds (apposed edges)
Disruption of epithelial BM but death of only an limited number of cells
Stages
1- haemostasis (seconds to minutes)
–> narrow space–> clotted blood–> dehydration of surface–> scab
2- inflammation (minutes to hours)
–> neutrophils appear at margin–> inhibit bacteria
3- Migration of cells (up to 48 hours)
–> macrophages –> scavenge dead neutrophils–> activated, secrete cytokines–> attract other cells (fibroblasts)
4- Regeneration (3 days) –> replace neutrophils–> granulation tissue invades (fibroblasts and new capillaries)–> produce collagen
5- Early scarring (7-10 days)–> filled with granulation tissue–> fibroblast proliferate, deposit collagen–> fibrous mass
6- Scar maturation (1 month- 2 years)–> mass of fibrous tissue many collagen fibres–> few cells and vessels–> appears white

35
Q

What is healing by secondary intention?

A

Significant tissue loss
Unapposed edges (infection, ulcer, abcess)
Abundant clot, inflammation and granulation tissue
Considerable wound contraction required (myofibroblasts)
Dermis requires significant repair
Epidermis regenerates from edges

36
Q

How does bone fracture healing take place?

A
  1. Haemotoma formation
    - -> BV in bone and periosteum break
    - -> Mass of clotted blood forms
    - -> Bone cells at edge of trabecular die
    - -> Swelling and inflammation occur–> cytokines released
    - -> Phagocytic cells and osteoclast begin to remove dead and damaged tissue
    - -> Macrophages will eventually remove the clot
  2. Soft callus
    - -> New BV infiltrate the periosteum
    - -> Procallus (soft callus) of granulation tissue forms
    - -> Fibroblast produce collagen fibres that span trabeculae
    - -> Other fibroblast produce cartilage
    - -> Osteoblast in periosteum and endosteum start laying down bone
  3. Hard callus
    - -> New bone trabeculae being to appear
    - -> Trabeculae develop become hard (bony) callus
    - -> Endochondrial Ossification replaces cartilage with bone
    - -> Intranmembraneous ossification produce bone in gaps
  4. Remodelling
    - -> Cancellous bone remodelled to compact bone
    - -> Material bulging out and in removed by osteoclasts
    - -> Final step–> remodelling–> original bone shape
37
Q

What are the local factors affect wound healing?

A

Local and systemic factors
Local:
–> Size, location and type of wound–> primary or secondary intention, regeneration or scarring
–> Mechanical stress–> weight-bearing/ loading will take longer
–> Blood supply–> O2 and nutritens, myofribroblast and fibroblast supplied–> takes longer if no blood supply
–> Infection–> produces peristant tissue injury and inflammation
–> Foreign bodies–> inflammation and injury
–> Haematoma–> large can slow healing
–> Necrotic tissue–> needs clearing
–> Protection–> help to keep the wound clean and free
–> Surgical techniques –> bad techniques slows healing

38
Q

What are the systemic factors that affect healing?

A

Age–> elderly heal more slowly
Anaemia, hypoxia and hypovolaemia–> poor O2 delivery to healing tissue
Obesity–> increased tension on wounds
Diabetes–> impairs blood supply
Malignancy–> Wasting of body (caused by it)
Genetic disorders
Drugs–> steroids, cytotoxics, antibiotics
Vitamin deficiency–> Vit C deficiency inhibits collagen synthesis
Malnutrition or proteins loss–> lack of essential substances

39
Q

What are some of the complications associated with fibrous repair?

A
  1. Insufficient fibrosis–> wound dehiscence (edges of wound don’t meet)–> obesity, elderly, malnutrition and steroid used (skin thinner less for suture to hold to)
  2. Excessive fibrosis–> Keloid scar–> over production of collagen, exceeds borders of scar
  3. Adhesion–> fibrous bands, cause obstruction of tubes (if around organ or tube)
  4. Loss of function–> replacement of specialised tissue by fibrous tissue –> heart- myocardium can’t contract
  5. Disruption of architecture–> liver cirrhosis
  6. Excessive scar contraction–> constriction of tubes, fixed flexion deformaties (contractures)
40
Q

How does healing affect certain tissues?

A
  • Cardiac muscle–> regenerative capacity limited–> scar formation–> compromised function
  • Liver–> can regenerate, architecture damaged–> cirrhosis
  • Peripheral nerves–> axons degenerate–> proximal stumps sprout and elongate–> Schwann cells guide back to tissue they innervate–> 1-3mm/day
  • Cartilage–> no blood supply–> doesn’t heal well
  • CNS–> permanent tissue–> replaced by CNS support elements

Semester 2 Pathological Processes (16 decks)

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