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Pathological Processes > Regenertaion And Repair > Flashcards

Regenertaion And Repair Flashcards

1
Q

What processes are involved in wound healing?

A
  1. Haemostasis – as vessels are open (blood leaks out into EC spaces, clot forms)
  2. Inflammation – as there has been tissue injury
  3. Regeneration (resolution, restitution) and/or repair (organisation) – as structures have, been injured or destroyed
    Or fibrous repair - structures may have been lost
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2
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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3
Q

What is the difference between abrasion and an ulcer

A

Abrasion superficially - effects mucosa - can repair completely
• if submucosa is affected - some scarring will occur - greater tissue damage
Ulcer =

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4
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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5
Q

How do stem cells replicate?

A
  • Prolonged proliferative activity
  • Show asymmetric replication - 1 stem cell 1 differentiated cell
  • ‘Internal repair system’ to replace lost or damaged cells in tissues
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6
Q

Whereabouts in teh tissues are stem cells?

A

• Varies between tissues
– Epidermis
– basal layer adjacent to the basement membrane
– Intestinal mucosa
– bottom of crypts (In the crypts the cell transitions from the base up and die at the top by apoptosis - Stem cells at the bottom of the crypt )
– Liver
– between hepatocytes and bile ducts

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7
Q

What are 3 types of stem cells?

A

• Unipotent:
– Most adult stem cells
– Only produce one type of differentiated cell, e.g. epithelia

• Multipotent:
– Produce several types of differentiated cell, e.g.

• Totipotent:
– Embryonic stem cells
– Can produce any type of cell and therefore any tissues of haematopoietic stem cells the body

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8
Q

Can all tissues regenerate?

A

• No, it depends on whether the tissues are:

– Labile tissues, e.g. surface epithelia, haematopoietic tissues
(Labile are constantly dividing - differ entiated cells that are constantly used up)
– Contain short-lived cells that are replaced from cells derived
from stem cells

– Stable tissues, e.g. liver parenchyma, bone, fibrous tissue,
endothelium
– Normally low level of replication but if necessary can undergo rapid proliferation, both stem cells and mature cells proliferate cells present
• Not activile diving tht amuch normally - but can increase rate of proliferation to replace lost cells in injury

– Permanent tissues, e.g. neural tissue, skeletal muscle, cardiac muscle
– Mature cells can’t undergo mitoses and no or only a few stem

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9
Q

In which 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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10
Q

What is fibrous repair and when does it occur?

A

• Healing with 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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11
Q

In which situation does regeneration/fibrous repair occur?

A

Regeneration only is collagen framework is intact in necrosis or labile or stable tissues only

In necrosis of permanant tissues or when collagen destroyed/ongoing chronic inflammation - fibrous repair scar

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12
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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13
Q

What is granulation tissue?

A 
• Has a granular appearance and texture 
• Consists of:
– Developing capillaries 
– Fibroblasts and myofibroblasts 
– Chronic inflammatory cells - lymphocytes and macrophages 
- ECM proteins 
• Functions:
– Fills the gap 
– Capillaries supply oxygen, nutrients and cells 
– Contracts and closes the hole
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14
Q

What is fibrous repair?

A
  1. Blood clots
  2. Neutrophils infiltrate and digest clot - acute inflammation
  3. Macrophages and lymphocytes are recruited - chronic inflammation - angiogenesis = production of new blood vessels
  4. Vessels sprout, mayo/fibroblasts make glycoproteins, granulation tissue forms
  5. Vascular network of collagen synthesises, macrophages reduced, fibroblasts produce collagen and vascularity decreases
  6. Maturity, nflammatory cells move out, cells much reduced, collagen matures, contracts and remodels - leaving firm fibrous scar
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15
Q

Which cella are involves in fibrous repair?

A

• Inflammatory cells
– Phagocytosis of debris – neutrophils, macrophages - these digest the clot and release mediators for repair
– 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

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16
Q

What is collagen?

A

• Most abundant protein in animals, 27 different types known numbered in order of discovery
• !ccounts for almost a third of mammalian body’s proteins
• Provides extracellular framework for all multicellular organisms, i.e., responsible for holding body together, including the skeleton
• Composed of triple helices of various polypeptide alpha
chains, rope-like appearance
• Fibrillar collagens: I – III, responsible for tissue strength
• Amorphous collagens: IV-VI, e.g. basement membrane

17
Q

What diseases are the result of defective collagen synthesis?

A

• Acquired
– Scurvy

• Inherited
– Ehlers-Danlos syndrome
– Osteogenesis imperfecta
– Alport syndrome

18
Q

What is scurvy?

A

• Vitamin C Deficiency
• Historically seen in long sea voyages and malnourished armies in WW1
• Inadequate vitamin C dependent hydroxylation of procollagen alpha chains leads to reduced cross- linking and defective helix formation
• Lacks strength, vulnerable to enzymatic degradation
• Particularly affects collagens supporting blood vessels
• Unable to heal wounds, tendency to bleed
• Tooth loss
– Collagen in periodontal ligament has 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

19
Q

What is Ehlers-Danlos syndrome?

A

• Heterogeneous group of 11 inherited disorders
• Defective conversion of procollagen to tropocollagen
• Collagen fibres lack adequate tensile strength
• Wound healing poor
• Skin - hyperextensible, thin, fragile and susceptible to injury
– NB. Skin can recoil because elastic fibres are normal, it is
just missing the tethering effect of normal collagen
fibres
• Joints – hypermobile, predisposition to joint dislocation
• In some forms:
– Rupture of colon, large arteries or cornea – Retinal detachment
• ‘Rubber people’

20
Q

What is osteogenesis imperfecta?

A

• = brittle bone disease, Lobstein’s 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 them and they are translucent
• Hearing impairment and dental abnormalities

21
Q

What is Alport syndrome?

A

• Usually X-linked disease, therefore patients
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

22
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 (e.g., growth factors)
– Direct cell-cell or cell-stroma contact

23
Q

What are growth factors?

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

Signal transduction - message sent from cell membrane through cytoplasm to the nucleus where transcription factors are activated that promote the transcription of genes that push the cells through the cell cycle -
Epidermal growth actor - cascade - map kinase - enzymatic cascade o kinase enzy,Es that amplify the signal from the membrane
In the nucleus - e2f transcription factors - push the cell from g1 to s phase

24
Q

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

A

• Inhibition of division • Locomotion • Contractility • Differentiation • Viability • Activation • Angiogenesis

25
Q

Name some growth factors and where they are produced?

A
  • Epidermal growth factor
  • Vascular endothelial growth factor
  • Platelet derived growth factor
  • Tumour necrosis factor
  • Produced by cells such as platelets, macrophages, endothelial cells
  • NB: Names can be obsolete or misleading!
26
Q

What is the role of cell-cell and cell-stream 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

Cells in layer - anti proliferation signal
If cells pulled apart - contact signals lost - proproliferatove signals sent

Beta cadherin

27
Q

What is meant by healing by primary/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

28
Q

What is healing by primary intention?

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

Scalpel cut on the skin
Edges of the wound can be drawn back together eg sutured - closed off
Blood clot from in dermis - gives rise to granulation tissue
Contact inhibition lost in epidermis
Small amount of scarring

29
Q

What occurs in healing by primary intention

A

• Epidermis regenerates
– Basal epidermal cells at edge of cut creep over denuded cells, approximately 0.5mm/day, deposit basement membrane, fuse in midline beneath scab, undermine scab which falls off
• Dermis undergoes fibrous repair
• Sutures out at about 10 days - approximately 10% normal strength
• Minimal contraction & scarring, good strength

30
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 from wound margins
Cant suture the edges together -eg infacrtion, ulcer etc
Large amount of blood clot forming, large amount of granulation tissue
Surface of the blood clot forms a scab
Formation of granulation tissue in blood clot contraction where blood clot dries out - scab - also, myofibroblasts - contractile quality to opulent des of the wound togtehr - make large wound a bit smaller - longer to heal - increased risk of developing complications

31
Q

What occurs in healing by secondary intention?

A

• Same processes as in 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 1 week myofibroblasts appear and contract
– Contracts as if margins are drawn into the centre – final
shape of scar depends on original shape of wound
• Substantial scar formation, new epidermis often
thinner than usual
• Takes longer than healing by primary intention

32
Q

What are split thickness and full thickness skin grafts?

A

Split - halfway through the skin graft
Transfer skin to different site in the body - skin taken from a donor ste to injury site, both heal
Full thickness - transplanting skin from one area - use this - better cosmetic effect

33
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 woven bone, remodelled to
direction of mechanical stress, bone not stressed is resorbed
and outline is re-established

34
Q

What local factors can influence would healing?

A

Local factors:

  1. Type, size, location of wound
  2. Mechanical stress
  3. Blood supply
  4. Local infection
  5. Foreign bodies
35
Q

What general factors can influence wound healing

A

General Factors:

  1. Age
  2. Anaemia, hypoxia and hypovolaemia
  3. Obesity
  4. Diabetes
  5. Genetic disorders
  6. Drugs
  7. Vitamin deficiency
  8. Malnutrition
36
Q

What are the complications of fibrous repair?

A

• Insufficient fibrosis
– Wound dehiscence, hernia, ulceration
– For example obesity, elderly, malnutrition, steroids
• Formation of adhesions
– Compromising organ function or blocking tubes,
e.g., intestinal obstruction following abdominal surgery
• Loss of function
– Due to replacement of specialised functional
parenchymal cells by scar tissue, e.g., healed myocardial infarction with non-contracting area of myocardium
• Disruption of complex tissue relationships within an organ
– Distortion of architecture interfering with normal function, e.g., liver cirrhosis
• Overproduction of fibrous scar tissue
– Keloid scar
• Excessive scar contraction
– Can cause obstruction of tubes, disfiguring scars
following burns or joint contractures (fixed flexures)

37
Q

What does the type of healing that will occur depend on?

A

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

Pathological Processes (12 decks)

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