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Pathological Processes > Regeneration and Repair > Flashcards

Regeneration and Repair Flashcards

1
Q

What are the processes involved in wound healing?

A
  1. Haemostasis
    • stopping the flow of the blood as vessel are open
  2. Inflammation
    • injury to the tissue triggers the inflammatory response
  3. Regeneration and/or Repair
    • structures have been injured or destroyed and need to be repaired
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2
Q

What is regeneration?

A

The resolution or restitution of an injury to replace structures that have been lost or damaged. There should be little or no evidence of previous injury. Examples include healing by primary intention (the closing of a wound) or the regeneration of a superficial abrasion.

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3
Q

What is the difference between an abrasion and an ulcer?

A

In an abrasion the damage is very superficial and does not damage the skin further than the mucosa. The tissue is able to undergo complete restitutionwithout any intervention

The tissue damage in an ulcer extends into the submucosa and an area of scarring will occur.

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4
Q

Which cells replicate in regeneration?

A

Newly differentiated cells are mainly derived from stem cells as many termically differentiated cells cannot divided.

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5
Q

What are stem cells?

A

Cells with prolonged proliferative activity which show asymmetric replication (one daughter cell remains a stem cell while the other mature).

They express an internal repair system to replace lost or damage cells in tissue (self-renewal).

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6
Q

What is the difference between embryonic stem cells (eSCs) and adult stem cells?

A

eSCs are pluripotent and can differentiate into any cell of the body where as adult stem cells can normally only give rise to one type of cell (unipotent) of a specific lineage.

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7
Q

Where in the tissue are adult stem cells found?

A

Varies dependant on tissue:

  • Epidermis - basal layer adjacent to the basement membrane
    • except from the lens of the eye and renal podocytes
  • Intestinal mucosa - bottom of intestinal crypts
  • Liver - inbetween hepatocytes and bile ducts
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8
Q

What are the examples of unipotent, multipotent and totipotent stem cells?

A

Unipotent:

  • most adult stem cells that can only produce one type of differentiated cell e.g. epithelia

Multipotent:

  • produce several different type of differentiated cell e.g. haemtopoeitic stem cells

Totipotent:

  • embryonic stem cells
  • can produce any type of cell/tissue in the body
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9
Q

Can all tissues regenerate?

A

No, only labile and stable tissue. Permenant tissues cannot regenerate.

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10
Q

What are labile tissues?

A

Continuously dividing tissues that proliferate throughout life, replacing cells that are destroyed.

Examples:

  • surface epithelia
  • mucosal lining of secretory ducts
  • columnar epithelial in GI and uterus
  • tranistional epithelial in urinary tract
  • bone marrow cells and haematopoetic tissues
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11
Q

What are stable tissues?

A

‘Quiescent tissues’ - dormant/inactive

Low levels of replication but can undergo rapid division in response to stimuli to reconstruct the tissue of origin.

Examples:

  • parenchymal cells of the liver, kidneys and pancreas
  • mesenchymal cells
    • fibroblasts
    • bone osteoclasts
    • smooth muscle cells
    • vascular endothelial cells
    • resting lymphocytes
    • other WBC
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12
Q

What are permanent tissues?

A

Non-dividing mature cells that cannot undergo mitoses in postnatal life and there are no or only a few stem cells present.

Examples:

  • neurones
  • skeletal muscle cells
  • cardiac muscle cells
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13
Q

In what circumstances can regeneration take place?

A
  • when the damage occurs in labile or stable tissue
  • the damage in not extensive; there is still an intact connective tissue scaffold
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14
Q

What is fibrous repair?

A

Healing with formation of fibrous connective tissue froming a scar.

  • the specalised tissue is lost
  • secondary intention healing (wound is extensive and involves considerable tissue loss
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15
Q

When does fibrous repair/organisation occur?

A
  • when significant tissue is lost
  • when permenant of complex tissue is injured
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16
Q

Outline the pathways to regeneration and fibrous repair

A
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17
Q

How does a scar form? Give timeframe

A
  1. Haemostasis (seconds - minutes)
  2. Acute inflammation (minutes - hours)
  3. Chronic inflammation (1 - 2 days)
  4. Granulation tissue forms (3 days)
  5. Early scar (7 - 10 days)
  6. Scar maturation (weeks - 2 years)
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18
Q

What is granulation tissue?

A

Tissues that consists of:

  • developing capilleries
    • very vascular and red
  • fibroblasts and myofibroblasts
  • chronic inflammatory cells

It has a granular appearance and texture. New connective tissue that contains microscopic blood vessels as part of the healing process. Grows from the base of the wound and can fill any size.

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19
Q

What is the function of granulation tissue?

A
  • fills the wound gap
  • capillaries supply oxygen, nutrients and cells
  • contracts and closes the hole
    • orchestrated by myofibroblasts
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20
Q

What are the stages of fibrous repair?

A
  1. Blood clots
  2. Neutrophils infiltrate and digest clot
  3. Macrophages and lymphocytes are recruited
  4. Vessels sprout. Myofibroblasts and fibroblasts make glycoproteins
  5. Vascular network formed, collagen is synthesised and macrophages reduce
  6. Maturation of the wound, cells are reduced, collagen matures and contracts and remodels
    • can occur 1-2 years after the injury.
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21
Q

Which cells are involved in fibrous repair?

A
  • inflammatory cells
    • neutrophils and macrophages
      • phagocytose debris
    • lymphocytes and macrophages
      • produce chemical mediators
  • endothelial cells
    • proliferation results in angiogenesis
  • fibroblasts and myofibroblasts
    • produce the extracellular matrix proteins e.g. collagen
    • responsible for wound contraction; contraction of fibrils within myofibroblasts
22
Q

What is collagen?

A
  • most abundant protein in the body
  • 27 different types
  • provides extracellular framework
  • made of triple helices of various polypeptide alpha chains
  • rope like appearance
  • fibrillar collagens I-III
    • responsible for tissue strength
  • amorphous collagens IV-VI
    • basement membrane
23
Q

What is the most common type of collagen?

A

type I

  • found in hard and soft tissue:
    • bones
    • tendons
    • liganments
    • skin
    • sclera
    • cornea
    • blood vessels
    • hollow organs
24
Q

How are fibrillar collagens made?

A
  1. Polypeptide alpha chains are synthesised in the ER of fibroblasts and myofibroblasts
  2. Enzymatic modification
    • vitamin C dependant hydroxylation
  3. Alpha chains align and cross link to form procollagen triple helix
  4. Soluble procollagen is secreted
  5. Procollagen is cleaved to tropocollagen
  6. Tropocollagen polymerises to form microfibrils and then fibrils
  7. Bundles of fibrils form fibres
  8. Cross linking of molceules produces tensile strength
  9. Slow remodelling by specific collagenases
25
Q

What diseases are the result of defective collagen synthesis?

A

Accquired:

  • scurvy (vitamin C deficiency)

Inherited:

  • Ehlers-Danlos syndrome
  • Osteogenesis imperfecta
  • Alport syndrome
26
Q

What is scurvy?

A

Disease cause by vitamin C deficiency.

  • inadequate vitamin C dependant hydroxylation of procollagen alpha chains leads to reduced cross linking and defective helix formation
  • lack of strength and tissues are vunerable to enzymatic degradation
  • particularly affects collagen supporting blood vessels
    • signs are increased bleeding especially from the gums.

Symptoms:

  • unable to heal wounds, tendancy to bleed
  • tooth loss
    • collagen in periodontal ligaments has a short half life and normal collagen is replaced by defective collagen
  • old scars break down and open up as fresh wounds
    • collagen turnover in scars remains high long after healing process appears clinically complete
27
Q

What is Ehlers-Danlos syndrome?

A

heterogenous group of 11 inherited disorders causing defective conversion of procollagen to tropocollagen therefore, collagen fibres lack adequate tensile strength

28
Q

What are the symptoms of Ehlers-Danlos syndrome?

A
  • poor wound healing
  • skin is hyperextensible, thin fragile and susceptible to injury
    • note: skin recoil is still normal because of normal elastic fibres
  • hypermobile joints and predisposition to joint dislocation

In some forms:

  • rupture of colon, large arteries or cornea
  • retinal detachment
29
Q

What is osteogenesis imperfecta?

A

Autosomal dominant congenital defect of bone formation from a defect in type I collagen synthesis. Also known as ‘brittle bone disease’ or Lobstein’s disease.

Clinical features:

  • blue sclera (from too little collagen)
  • multiple bone fractures
  • hearing impairment and dental abnormalities

Pts with OI need to avoid mechanical stress due to extreme skeletal fragility.

30
Q

What is Alport syndrome?

A

majority X-linked disease - normally affects males.

  • abnormality in type IV collagen

Dysfunction:

  • glomerular basement membrane (glomerulonephritis)
    • haematuria to eventual renal failure
    • proteinuria
  • cochlea of ear
    • inner ear problem (organ of corti) therefore neural deafness
  • lens of eye
    • myopia
    • lens opacity
31
Q

How is regeneration and repair triggered and controlled?

A

Cell to cell signalling via:

  • hormones
  • local mediators e.g growth factors)
  • direct cell-cell or cell-stroma contact

Producing a proliferative response

32
Q

What are growth factors?

A
  • coded by proto-oncogenes
  • polypeptides that act on cell surface receptors
  • bind to specific receptors on cells to stimulate transcription of genes that regulate entry of cell into cell cycle and the cell’s passage through it
  • examples:
    • epidermal growth factor (EGF)
    • fibroblast growth factor
33
Q

What features other than cell proliferation do growth factors have?

A
  • inhibition of division
  • locomotion (movement within cells)
  • contractility (myofibroblasts in wound repair)
  • differentiation
  • viability
  • activation
  • angiogenesis
34
Q

What are examples of growth factors?

A
  • epidermal growth factor
  • vascular endothelial growth factor
  • platelet-derived growth factor
    • a multitude of functions not just specific to platelets
  • tumour necrosis factor
35
Q

What produces growth factors?

A
  • Platelets
  • Macrophages
  • Endothelial cells
36
Q

What is the role of cell-cell and cell-stroma contact?

A

CONTACT INHIBITION

  1. Adhesion molecule signalling altered
    • cadherins for cell-cell
    • integrins for cell-ECM
  2. Inhibits the proliferation of intact tissue, promotes proliferation of damaged tissue
  3. Altered in oncogenic/malignant cells
37
Q

What is does the ‘intention’ of wound healing describe?

A

Size of the wound and the amount of tissue loss. Terms are often used for skin wounds.

38
Q

What is healing by primary intention?

A
  • Incised, closed, non-infected and sutured wounds
  • disruption of the basement membrane continuity
  • a small number of epithelial and connective tissue loss
  • minimal clot and granulation tissue
39
Q

What are the stages of healing by primary intention?

A
  1. Haemostasis - platelets and cytokines for a haematoma
  2. Inflammation - removal of cell debris and pathogens present
  3. Proliferation - cytokines cause proliferation of fibroblasts producing collagen to close the wound. VEGF promotes angiogenesis
  4. Remodelling - devascularisation of the region and apoptosis of fibroblasts

General:

  1. Epidermis regenerates
  2. Dermis undergoes fibrous repair

Sutures can be removed ~10 days

Minimal contraction & scarring, good strength

40
Q

How does the epidermis regenerate in primary intention healing?

A

Basal cells are the edge of the cut creep over denude cells (rate = 0.5mm/day):

  • depositing basement membrane
  • fuse midline beneath the scab
  • undermine the scab which falls off
41
Q

What is healing by secondary intention?

A
  • Larger wounds and edges cannot be sutured together e.g.
    • excisional wounds
    • wounds with tissue loss and separated edges
    • infected wounds
      • infarct, ulcer, abscess
  • Open wound filled with abundant granulation tissue that grows in from wound margins
42
Q

What are the stages of secondary intention healing?

A
  1. Haemostasis
    • large fibrin mesh fills the wound
    • scab contracts when drying and shrinking
  2. Inflammation
    • removes cell debris and pathogens present
  3. Proliferation
    • granulation tissue forms at the bottom of the wound to fill to the level of epithelium
    • epithelium then proliferates to cover the wound
  4. Remodelling
    • resolving of the inflammatory response
    • wound contraction

Myofibroblasts appear after one week. Substantial scar formation and new epidermis is thinner than usual

Takes longer than healing by secondary intention

43
Q

How does the donor site heal in split-thickness skin grafts?

A

Split-thickness skin grafts contain the epidermis and part of the dermis, leaving structures behind (hair follicle, sweat gland etc.) to regenerate. High chance of graft survival. Poor cosmetic appearance and greater chance of distortion or contraction.

Full-thickness skin grafts have a better cosmetic appearance but are more likely to be rejected.

44
Q

How do bones heal?

A
  1. Haematoma
    • fills the gap and surrounds the injury
  2. Granulation tissue forms
    • cytokines activate osteoprogenitor cells
  3. Soft callus
    • at 1 week
    • fibrous tissue and cartilage within which woven bone forms
  4. Hard callus
    • after several weeks
    • initially woven bone which is weaker and less organised that lamellar bone but can form quickly
  5. Lamellar bone
    • replaces woven bone
    • remodels to the direction of mechanical stress
      • bone that is not stressed is reabsorbed and outline is reestablished
45
Q

What local factors influence wound healing?

A
  • type, size and location of the wound
  • mechanical stress
  • blood supply
  • local infections
  • foreign bodies
46
Q

What general factors influence wound healing?

A
  • age
  • anaemia, hypoxia and hypovolaemia
  • obesity
  • diabetes
  • genetic disorders
  • drugs
  • vitamin deficiency and malnutrition
47
Q

What are the complications of fibrous repair?

A
  • Insufficient fibrosis (in obese, elderly, malnutrition or steroids)
    • wound dehiscence
    • hernia
    • ulceration
  • Formation of adhesions
    • compromised organ function or blocks tubes
  • Loss of function
    • due to the replacement of specialised functional cells (parenchymal cells)
      • example: MI area healed with non contracting area
    • due to distorting the architecture
      • liver cirrhosis
  • Overproduction of fibrous scar tissue
    • keloid scar
  • Excessive scar contraction
    • obstruction of tubes or disfiguring flexors (burns)
48
Q

What are myofibroblasts and what is their function?

A

Contractile cells that produce collagen. elastin and GAGs. Responsible for wound contraction.

49
Q

What is Wallerian degeneration?

A

Axon distal to the injury degrades. Proximal degradation occurs to the previous node of Ranvier.

50
Q

What is a traumatic neuroma?

A

Reactive proliferative of Schwann cells and axons

  • usually occurs post-surgically or due to trauma to a nerve
  • firm painful nodules form on the skin
51
Q

What are hypertrophic scars?

A

Raised fibrotic scar at the site of injury. Can spontaneously resolve and the response is related to the injury

52
Q

What is proud flesh?

A

Excess growth of granulation tissue which sticks out of the wound and prevents epithelial from growing over it. Can be removed with silver nitrate sticks or surgery.

Pathological Processes (9 decks)

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