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Sem 2 - Pathological Processes > Regeneration And Repair > Flashcards

Regeneration And Repair Flashcards

1
Q

What is the underlying principle of would healing?

A
  1. Close the gap
  2. Repair it with a scar
  3. The smaller the scar the better
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2
Q

What processes are involved in wound healing?

A

Haemostasis - as vessels are open

Inflammation - as there has been tissue injury

Regeneration (resolution, restitution) and/or fibrous repair (organisation) - as structures have been injured or destroyed

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3
Q

What is regeneration?

A

Restitution with no or minimal evidence that there was 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

Abrasion - damage is superficial and tissue can repair itself completely.

Ulcer - Greater amount of damage, Not repair fully.

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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

What are stem cells?

A
  • Prolonged proliferation activity
  • Show asymmetric replication
  • Internal repair system to replace lost or damaged cells in tissues.
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7
Q

Whereabouts in the tissues are the stem cells?

A

Varies between tissues..

  • Epidermis - Basal layer adjacent to the basement membrane
  • Intestinal mucosa - bottoms of crypts
  • Liver - between hepatocyte and bile ducts.
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8
Q

What are the classifications of stem cells?

A
  • Unipotent
  • Multipotent
  • Totipotent
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9
Q

What are unipotent stem cells?

A

Most adult stem cells.

They only produce one type of differentiated cell eg epithelia

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10
Q

What are multipotent stem cells?

A

Produce several types of differentiated cell e.g. Haematopoietic stem cells.

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11
Q

What are totipotent stem cells?

A
  • Embryonic stem cells.
  • They can produce any type of cell and therefore any tissue in the body.
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12
Q

Can all tissues regenerate?

A

No! It depends on whether the tissues are:

—Labile tissues e.g. surface epithelia, haematopoietic tissues.

  • These contain short-lived cells that are replaced from cells derived from stem cells.

—Stable tissues e.g. liver parenchyma, bone, fibrous tissue, endothelium.

  • They normally undergo low levels of replication but, if necessary, can undergo rapid proliferation. Both stem cells and mature cells proliferate.

—Permanent tissues e.g. neural tissue, skeletal muscle, cardiac muscle.

  • Mature cells can’t undergo mitosis and no or only a few stem cells are present.
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13
Q

Where abouts on the cell cycle are the three types of cell depending on proliferative activity?

A

Labile cells are continuously going around the cell cycle.

Stable tissues are in G0 so they are not currently undergoing mitosis but can join if needed.

Permanent tissues are not in the cell cycle.

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14
Q

In what circumstances can regeneration take place?

A

If damage occurs in a Labile or stable tissue.

If the tissue damage is not extensive as regeneration requires an intact connective tissue scaffold.

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15
Q

What is fibrous repair (organisation) and when does it occur?

A

Healing with the formation of fibrous connective tissue - scar

  • Specialised tissue is lost
  • Healing by secondary intention

Occurs with: -

  • Significant tissue loss
  • If permanent or complex tissue is injured
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16
Q

Will the cell undergo regeneration or fibrous repair?

A
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17
Q

How does a scar form?

A

Haemostasis (seconds- minutes)

Acute inflammation (minutes-hours)

Chronic inflammation (1-2 days)

Granulation tissue then forms (3 days)

Early scar (7-10 days)

Scar maturation (weeks - 2 years)

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18
Q

What is granulation tissue?

A

Has a granular appearance and texture

Consists of:

  • Developing capillaries
  • Fibroblasts and myofibroblasts
  • Chronic inflammatory cells

Functions:

  • FIll the gap
  • Capillaries supply oxygen, nutrients and cells
  • Contracts and closes the hole
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19
Q

How does fibrous repair occur?

A
  1. Blood clots
  2. Neutrophils infiltrate and digest clot
  3. Macrophages and lymphocytes are recruited
  4. Vessels sprout and Moyo/fibroblasts make glycoproteins
  5. Vascular network, collagen synthesised, macrophages reduced.
  6. Maturity, cells much reduced, collagen matures, contracts and remodels.
20
Q

What cells are involved in fibrous repair?

A

Inflammatory cells -

Phagocytosis of debris - neutrophil, macrophages

-Production of chemical mediators - lymphocytes, macrophages

Endothelial cells

-Proliferation results in angiogenesis

Fibroblasts and myofibroblasts

  • Produce extracellular matrix proteins e.g. collagen
  • Responsible for wound contraction - Contraction of fibrils within myofibroblasts.
21
Q

What is collagen?

A
  • It is the most abundant protein in animals and there are 27 different types.
  • They account for almost 1/3 of mammalian body proteins
  • They provide an extracellular framework for all multicellular organisms
  • They are composed of triple helices of various polypeptide a-chains, rope-like appearance
  • Fibrillar collagens: I-III responsible for tissue strength
  • Amorphous collagens: IV-VI eg basement membrane
22
Q

What is type I collagen?

A

Type I is most common.

It is found in hard and soft tissue including: bones, tendons, ligaments, skin, sclera cornea, blood vessels, hollow organs.

23
Q

What is type IV collagen?

A

Makes up basement membranes -Secreted by epithelial cells

24
Q

How are fibrillar collagens made?

A
  • The whole process takes about 1-2 hours.
  • Polypeptide a chains are synthesised in ER of fibroblasts and myofibroblasts.
  • Enzymatic modification steps inc. Vit C dependant hydroxylation
  • A-chains align and cross-link to form procollagen triple helix
  • Soluble procollagen is secreted.
25
Q

What happens after the secretion of procollagen?

A
  • After secretion, procollagen is cleaved to give tropocollagen.
  • Tropocollagen polymerises to form microfibrils and then fibrils.
  • Bundles of fibrils form fibres
  • Cross-linking between molecules produce tensile strength
  • Slow remodelling by specific collagenases.
26
Q

What diseases are the result of defective collagen synthesis?

A

Acquired:

  • Scurvy

Inherited:

  • Ehlers-Danilo’s syndrome
  • Osteogenesis Imperfecta
  • Alport syndrome
27
Q

What is scurvy?

A
  • Vitamin C deficiency
  • Inadequate vitamin C dependant hydroxylation of procollagen a-chain leads to reduced cross-linking and defective helix formation.
  • Lacks strength, vulnerable to enzymatic degradation.
  • Particularly affects collagens supporting blood vessels.
28
Q

What are the consequences of scurvy?

A
  • Unable to heal wounds, tendency to bleed
  • Tooth loss
    • Collage 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 scars remains high long after healing process appears clinically complete.
29
Q

What is Ehlers Danilo’s syndrome?

A
  • Defective conversion of pro collagen to tropocollagen
  • Collagen fibres lack adequate tensile strength
  • Wound healing poor
  • Skin - hyperextensible, thin, fragile and susceptible to injury.
  • (Skin can still recoil because the elastic fibres are normal, it is just missing the tethering effect of normal collagen fibres.)
  • It causes: Hypermobile joints that have a predisposition to dislocation.
  • Sometimes: Rupture of colon, large arteries or cornea Retinal detachment.
30
Q

What is osteogenesis Imperfecta?

A
  • Brittle bone disease
  • Too little bone tissue and therefore extreme skeletal fragility.
    • Affected people have to try and avoid mechanical stress
    • Some develop severe, progressive deformation of long bones.
  • Blue sclerae- too little collagen within then and they are translucent.
  • Hearing impairment and dental abnormalities.
31
Q

What is Alport syndrome?

A
  • X-linked so patient is normally male.
  • Abnormal type IV collagen
  • Dysfunction of glomerular basement membrane, cochlea of ear and lens of eye
  • Presents with haematuria in children / adolescents and progresses to renal failure.
  • Also neural deafness and eye disorders.
32
Q

How are regeneration and repair triggered and controlled?

A

It is complex and poorly understood

Cells communicate with each other to produce a proliferative response.

Cell to cell signalling can be via:

  • Hormones
  • Local mediators (e.g. growth factors)
  • Direct cell-cell or cell-Stroma contact.
33
Q

What are growth factors?

A
  • Particularly important in wound healing.
  • Polypeptides that act on cell surface receptors.
  • Coded by protooncogenes.
  • ‘Local hormones’
  • Bind to specific receptors, and stimulate the transcription of genes that regulate the entry of cells into the cell cycle and the cell’s passage through it.
34
Q

What types of growth factors are there?

A
  • Epidermal growth factor
  • Vascular growth factor
  • Platelet derived growth factor
  • Tumour necrosis factor.

They are produced by cells such as platelets, macrophages, endothelial cells BUT names can be misleading!

35
Q

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

A
  • Inhibition of division
  • Locomotion
  • Contractility
  • Differentiation
  • Viability
  • Activation
  • Angiogenesis
36
Q

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

A

Contact inhibition

  • Signalling through adhesion molecules
    • Cadherins bind cells to each other
    • Integrins bind cells to the extracellular maxtrix
  • Inhibits proliferation intact tissue, promotes proliferation in damaged tissues.
  • Altered in malignant cells.
37
Q

What is ‘healing my primary intention’ and ‘healing by secondary intention’?

A

Describing of wound healing related to the size of the wound and the amount of lost tissue. ‘Secodnary intention’ is a bigger wound with more tissue lost.

Most often used for skin wounds.

38
Q

What is healing by primary intention?

A

Incised, closed, non-infected and sutured wound. Eg cut in the skin by a scalpel.

Disruption of the basement membrane continuity but death of only small number of epithelial and connective tissue cells.

Minimal clot and granulation tissue.

39
Q

What occurs in healing by primary intention?

A
  • Epidermis regenerates
    • Basal epidermal cells at edge of cut creep over denude cells, appoximately 0.5mm/day, deposit basement membrane, fuse in midline beneath scap, indermine scab which falls off.
  • Dermis undergoes fibrous repair.
  • Sutures out at about 10 days - appox 10% normal strength
  • Minimal contraction and scarring, good strength
40
Q

What is healing by secondary intention?

A

Excisional wound, wounds with tissue loss and separated edges, infected wounds e.g. infarct, ulcer, abcess

Open wound filled by abundant granulation tissue - grows in from wound margins.

41
Q

What occurs in healing by secondary intention?

A
  • Same process as primary intention but more so:
  • Considerable wound contraction must take place to close wound.
    • Initially occurs as scab contracts when it dries and shrinks.
    • After a week myofibroblats appear and contract
    • Contracts as if margins are drawn into the centre - final shape of scar depends on orgional shape of wound
  • Longer to heal so increased risk of complications
  • Substantial scar formation, new epidermis often thinner than usual.
42
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 woven bone - weaker and less organised than lamellar bone but can form quickly.

Lamellar bone: replaces woveb bone, remodelled to direction of mechanican stress, bone not stressed is resorbed and outline is re-established.

43
Q

What local factors can influence would healing?

A
  • Type, size and location of wound
  • Mechanical stress
  • Blood supply
  • Local infection
  • Foreign bodies
44
Q

What general factors can influence wound healing?

A
  • Age
  • Anaemia, hypoxia and hypovolaemia (decreased blood volume)
  • Obesity
  • Diabetes
  • Genetic disorders
  • Drugs
  • Vitamin deficiency
  • Malnutrition
45
Q

What are the complications of fibrous repair?

A
  • Insufficient fibrosis
    • -Wound dishiscence, hernia, ulceration
    • -Eg obesity, elderly, malnutrition and steroids
  • Formations of adhesions
    • -Comprimising organ functions or blocking tubes.
  • Loss of function
    • -Due to replacement of specialised functional parenchyma cells by scar tissue
  • Disruption of complex tissue relationships within an organ
    • -distortion of architecture interfering with normal function
  • Overproduction of fibrous scar tissue
    • -keloid scar
  • Excessive scar contraction
    • -can cuase obstruction of tubes, disfiguring scars following bursn or joint contractures
46
Q

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

A

It will depend on:

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

Sem 2 - Pathological Processes (13 decks)

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