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Pathological Processes > Healing: Regeneration and Repair > Flashcards

Healing: Regeneration and Repair Flashcards

1
Q

What is the underlying principal of wound healing?

A
  • Close the gap
  • Repair it with a scar
  • The smaller the scar the better
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2
Q

What processes are involved in wound healing?

A
  • Haemostasis (vessels are open)
  • Inflammation (there has been tissue injury)
  • Regeneration (resolution, restitution and/or repair)
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3
Q

What is regeneration?

A

Restitution with no, or minimal, evidence that there was a previous injury.

  • Healing by primary intention
  • Superficial abrasion
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4
Q

What is the difference between an abrasion and an ulcer?

A

An ulcer is a more severe version of abrasion as it goes below the level of the muscularis mucosae

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5
Q

Which cells replicate in regeneration?

A

New differentiated cells are mainly derived from stem cells (many terminally differentiated cells can’t divide)

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6
Q

Whereabouts in the tissues are the stem cells?

A

Epidermis - basal layer adjacent to the basement membrane
Intestinal mucosa - bottom of crypts
Liver - between hepatocytes and bile ducts

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7
Q

What are unipotent stem cells?

A

Only one type of differentiated cell e.g. epithelia (most adult stem cells)

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8
Q

What are multipotent stem cells?

A

Stem cells that produce several types of differentiated cells e.g. haematopoietic stem cells

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9
Q

What are totipotent stem cells?

A

Embryonic stem cells that can produce any type of cell and therefore any tissues of the body

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10
Q

Where are blood cells derived from?

A

Multipotent stem cells in bone marrow

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11
Q

What are labile tissues?

A

Tissues that contain short-lived cells that are replaced from the cells derived from stem cells e.g. surface epithelia, haematopoietic tissues

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12
Q

What are stable tissues?

A

Tissues with a low level of replication but if necessary can undergo rapid proliferation, both stem cells and mature cells proliferate e.g. liver parenchyma, bone, fibrous tissue, endothelium. Cells are in G0 but can enter G1 when needed.

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13
Q

What are permanent tissues?

A

Tissues in which mature cells cannot undergo mitoses and no or only a few stem cells are present e.g. neural tissue, skeletal muscle and cardiac muscle.

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14
Q

In what circumstances can regeneration take place?

A
  • If the damage occurs in a labile or stable tissue
  • If the tissue damage is not extensive
  • Regeneration requires an intact connective tissue scaffold
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15
Q

What is fibrous repair (organisation)?

A

Healing with formation of fibrous connective tissue = scar

  • specialised tissue is lost
  • healing by secondary intention
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16
Q

When does fibrous repair occur?

A

With significant tissue loss and if permanent or complex tissue is injured e.g. a whole glomerulus.

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17
Q

How does a scar form?

A 
Seconds - minutes: haemostasis 
Minutes - hours: acute inflammation 
1-2 days: chronic inflammation 
3 days: granulation tissue forms
7-10 days: early scar 
Weeks - 2 years: scar maturation
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18
Q

What is granulation tissue?

A

It has a granular appearance and texture. It consists of developing capillaries, fibroblasts and myofibroblasts and chronic inflammatory cells

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19
Q

What is the function of granulation tissue?

A

Fills the gap, capillaries supply oxygen, nutrients and cells and contracts and closes the hole.

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20
Q

Describe 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 make glycoproteins
  5. Vascular network, collagen synthesised, macrophages reduced
  6. Maturity, cells much reduced, collagen matures, contracts and remodels
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21
Q

Which cells are involved in fibrous repair?

A
  • Inflammatory cells
  • Endothelial cells
  • Fibroblasts and myofibroblasts
22
Q

Describe the role of inflammatory cells in fibrous repair

A
  • Phagocytosis of debris (neutrophils and macrophages)

- Production of chemical mediators (lymphocytes and macrophages)

23
Q

Describe the role of endothelial cells in fibrous repair

A

Proliferation of endothelial cells results in angiogenesis

24
Q

Describe the role of fibroblasts and myofibroblasts in fibrous repair

A
  • Produce extracellular matrix proteins e.g. collagen

- Responsible for wound contraction - contraction of fibrils with myofibroblasts

25
Q

What is collagen?

A
  • Most abundant protein in animals
  • Provides extracellular framework for all multicellular organisms
  • Composed of triple helices
26
Q

What are the different types of collagen?

A

Fibrilar collagens: I-III, responsible for tissue strength

Amorphous collagens IV-VI e.g. basement membrane

27
Q

What is type I collagen?

A

Most common, found in hard and soft tissues

- Bones, tendons, ligaments, skin, sclera, cornea, blood vessels, hollow organs

28
Q

What is type IV collagen?

A

Makes up the basement membrane

- Secreted by epithelial cells

29
Q

How are fibrillar collagens made?

A
  • Polypeptide alpha chains synthesised in ER of fibroblasts and myofibroblasts
  • Enzymatic modification steps including vitamin C dependant hydroxylation
  • Alpha chains align and cross-link to form pro collagen triple helix
  • Soluble pro collagen is secreted
  • Cleaved to tropocollagen
  • Polymerises to form microfibrils and then fibrils
  • Bundles of fibrils form fibres
  • Cross-linking between molecules produces tensile strength
  • Slow remodelling by specific collagenases
30
Q

What diseases are the result of defective collagen synthesis?

A

Acquired - scurvy

Inherited - EDS, osteogenesis imperfecta, alport syndrome

31
Q

What is scurvy?

A

Vitamin C deficiency. Inadequate vitamin C dependant hydroxylation of pro collagen alpha chains leads to reduced cross-linking and defective helix formation. Lacks strength, vulnerable to enzymatic degradation. Particularly affects collagens supporting blood vessels.

32
Q

What are the symptoms of scurvy?

A
  • Unable to heal wounds with a tendency to bleed
  • Tooth loss (collagen in periodontal ligament 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 wounds remains high long after the healing process)
33
Q

What is EDS?

A
  • Ehlers-Danlos Syndrome
  • Heterogenous group of 11 inherited disorders
  • Defective conversion of pro collagen to tropocollagen
  • Collagen fibres lack adequate tensile strength
34
Q

What are the symptoms of EDS?

A
  • Wound healing poor
  • Skin = hyper extensible, thin, fragile and susceptible to injury
  • Joints = hypermobile, predisposition to joint dislocation
  • In some forms: rupture of colon, large arteries or cornea, retinal detachment
35
Q

What is osteogenesis imperfecta?

A
  • Brittle bone disease

- Too little bone tissue and therefore extreme skeletal fragility

36
Q

What are the symptoms of osteogenesis imperfecta?

A
  • Affected people have to try and avoid mechanical stress
  • Some develop severe, progressive deformation of long bones
  • Blue sclerae (too little collagen)
  • Hearing impairment
  • Dental abnormalities
37
Q

What is Alport syndrome?

A
  • Usually X-linked disease = usually male
  • Type IV collagen abnormal
  • Dysfunction of glomerular basement membrane, cochlea of ear and lens of eye
  • Presents with haematuria in children/adolescents progressing to renal failure
  • Also neural deafness and eye disorders
38
Q

How are regeneration and repair triggered and controlled?

A

Complex and poorly understood processes. Cells communicate with each other to produce a proliferative response. Cell to cell signalling can be via hormones, local mediators and cell-cell/stroma contact.

39
Q

What are growth factors?

A
  • Polypeptides that act on cell surface receptors
  • Important in wound healing
  • Coded by proto-oncogenes
  • ‘Local hormones’
  • Bind to specific receptors, stimulate transcription of genes that regulate entry of cell into cell cycle and the cells passage through it.
40
Q

Apart from cell proliferation, what other effects can growth factors have?

A
  • Inhibition of division
  • Locomotion
  • Contractility
  • Differentiation
  • Viability
  • Activation
  • Angiogenesis
41
Q

What are growth factors produced by?

A

Cells such as platelets, macrophages and endothelial cells.

42
Q

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

A

Contact inhibition (signalling through adhesion molecules)

  • Cadherins bind cells to each other
  • Integrins bind cells to the extracellular matrix
  • Inhibits proliferation in intact tissue, promotes proliferation in damaged tissues (altered in malignant cells)
43
Q

What is meant by healing by primary intention and healing by secondary intention?

A

Descriptions of wound healing related to the size of the wound and the amount of lost tissue, most often used for skin wounds.

44
Q

What is healing by primary intention?

A
  • Incised, closed, non-infected and sutured wounds
  • Disruption of basement membrane continuity but death of only a small number of epithelial and connective tissue cells
  • Minimal clot and granulation tissue
45
Q

What occurs in healing by primary intention?

A
  • Epidermis regenerates (basal epidermal cells deposit basement membrane, fuse in the midline of beneath scab, undermine scab which falls off)
  • Dermis undergoes fibrous repair
  • Minimal contraction and scarring, good strength
46
Q

What is healing by secondary intention?

A
  • Excisional wound, wounds with tissue loss and separated edges, infected wounds, e.g. infarct, ulcer, abscess
  • Open wound filled by abundant granulation tissue - grows in form wound margins.
47
Q

What occurs in healing by secondary intention?

A
  • Same as with primary but more = longer time taken
  • Considerable wound contraction must take place to close wound (initially occurs as scab contracts when it dries and shrinks, after 1 week myofibroblasts appear and contract, contracts as if margins are drawn into the centre)
  • Substantial scar formation
48
Q

How does bone heal?

A
  • Haematoma: fills gap and surrounds injury
  • Granulation tissue forms: cytokines activate osteoprogenitor cells
  • Soft callus: at 1 week, fibrous tissue and cartilage within which woven bone forms
  • Hard callus: after several weeks, initially even bone = weaker and less organised than lamellar bone but can form quickly
  • Lamellar bone: replaces woven bone, remodelled to direction of mechanical stress, bone not stresses is resorbed and outline is re-established.
49
Q

Which local factors can influence wound healing?

A
  • Type, size, location of wound
  • Mechanical stress
  • Blood supply
  • Local infection
  • Foreign bodies
50
Q

Which general factors can influence wound healing?

A
  • Age
  • Anaemia, hypoxia and hypovolaemia
  • Obesity (pulls wound apart)
  • Diabetes
  • Genetic disorders
  • Drugs e.g. steroids
  • Vitamin deficiency
  • Malnutrition
51
Q

What are the complications fibrous repair?

A
  • Insufficient fibrosis (wound dehiscence, hernia, ulceration)
  • Formation of adhesions (compromise organ function/ block tubes)
  • Loss of function (due to replacement of specialised functional parenchymal cells by scar tissue)
  • Disruption of complex tissue relationships within an organ (distortion of architecture)
  • Overproduction of fibrous scar tissue (keloid)
  • Excessive scar contraction (obstruction of tubes, disfiguring scars etc)
52
Q

How can you predict the type of healing that will occur?

A
  • Type of tissue
  • Extent of injury
  • Presence of persistent infection

Pathological Processes (13 decks)

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