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ESA 2 > MOD 4.1 - Healing and Repair > Flashcards

MOD 4.1 - Healing and Repair Flashcards

1
Q

What is the definition of regeneration?

A

The replacement of dead or damaged cells with functional/differentiated cells from stem cells

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2
Q

What is the definition of repair?

A

The response to injury with both regeneration and scar formation therefore permanently changing the normal structure

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3
Q

How does regeneration differ from repair?

A
  • Normal tissue structure is restored

Provided that damage isn’t extensive and the collagen framework is still in tact

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4
Q

What is a stem cell?

A

An undifferentiated cell that can differentiate indefinitely to more cells of the same type/other types

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5
Q

What are the features of a unipotent stem cell? Give an example

A
  • Produces ONE type of differentiated cell (for constant regeneration)
  • Crypts of Lieberkuhn
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6
Q

What are the features of a multipotent stem cell? Give an example

A
  • Produces several types of the same cell

- Haematopoietic cells

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7
Q

What are the features of totipotent stem cells? Give an example

A
  • Can produce any type of cell

- Embryonic stem cells

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8
Q

What are the functions of stem cells? (3)

A
  • 1 becomes a new stem cell
  • 1 becomes a specific cell for a specialised function
  • Derivatives replace lost cells that were terminally differentiated
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9
Q

What are the three tissue types for regeneration?

A
  • Labile
  • Stable/Quiescent
  • Permanent
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10
Q

What are the features of labile cells?

A
  • Divide continuously

- Rapidly reproduce throughout life

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11
Q

Why are labile cells significant?

A

Ensure that destroyed cells are constantly replaced

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12
Q

What are the features of stable cells?

A
  • Low/no rate of division

- Can proliferate rapidly if exposed to the right stimulus

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13
Q

Why are quiescent cells significant?

A
  • Response to a stimulus prevents premature differentiation

- Then maintains a constant supply of undifferentiated adult stem cells

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14
Q

What are the features of permanent cells?

A
  • No mitotic division

- No regeneration

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15
Q

Give examples of:

i) Labile tissues
ii) Quiescent tissues
iii) Permanent tissues

A

i) Epithelial cells, haematopoietic cells
ii) Hepatocytes
iii) Neurones, cardiac myocytes

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16
Q

In which stage of the cell cycle are:

i) Labile tissues
ii) Quiescent tissues
iii) Permanent tissues ?

A
  • Every stage as are in the cell cycle
  • G0 (but can enter cell cycle)
  • G0 (can’t enter cell cycle again)
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17
Q

What are the three mechanisms of control of regeneration and repair?

A
  • Cell signalling
  • Local mediators (growth factors)
  • Contact inhibition
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18
Q

What are the three main mechanisms for cell signalling?

A
  • Autocrine
  • Paracrine
  • Endocrine
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19
Q

What is autocrine signalling?

A

Cell makes and responds to its own signalling molecules

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20
Q

What is paracrine signalling?

A

A molecule is produced by ONE cell and acts upon adjacent cells with the appropriate receptors

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21
Q

What is endocrine signalling?

A

A hormone is synthesised by an endocrine gland and travels in the circulation to a distant site where it acts

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22
Q

Give examples of 4 growth factors and their functions

A
  • Epidermal Growth Factor (EGF) - Mitogenic for keratinocytes and fibroblasts
  • Platelet Derived Growth Factor (PDGF) - Promotes cells for inflammation and healing
  • Vascular Endothelial Growth Factor (VegF) - Promotes blood vessel formation
  • Tumour Necrosis Factor - Migration and proliferation of fibroblasts and secretion of collagenase
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23
Q

What is contact inhibition?

A

The inhibition of cell proliferation when cells come into contact with other cells

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24
Q

What are adhesion molecules and what is their function?

A
  • Proteins on the cell surface membrane that enable contact inhibition
  • Cell-cell = Cadherins
  • Cell-Extra Cellular Matrix = Integrins
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25
Q

What happens if there is a lack of adhesion molecules?

A
  • Tumour
  • LAD-1 (leukocyte adhesion deficiency - deficiency of integrins, causes leukocytes to not be able to adhere to the vessel walls making fighting off infection difficult
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26
Q

What is fibrous repair? When does this occur?

A
  • Replacement of functional tissue by scar tissue
  • After the necrosis of permanent cells
  • If the collagen framework of the tissue is destroyed after necrosis of labile/stable cells
27
Q

What are the three stages of fibrosis repair?

A
  • Infiltration of inflammatory cells
  • Replacement of clot by granulation tissue
  • Maturation
28
Q

What happens prior to the infiltration of inflammatory cells during fibrous repair? Why is this significant?

A
  • Formation of a blood clot
  • Stops bleeding
  • Promotes an inflammatory response
29
Q

Which cells are involved in the inflammatory response during fibrous repair?

A
  • Macrophages and neutrophils (for phagocytosis of debris/necrotic tissue)
  • Lymphocytes and and macrophages (mediate chronic inflammation)
30
Q

When is the clot replaced with granulation tissue?

A

Approximately 24-72 hours after initial injury

31
Q

What are the two stages of replacement of the clot?

A
  • Angiogenesis

- Migration and differentiation of myoblasts and fibroblasts

32
Q

What is angiogenesis?

A

The formation of new blood vessels from pre-existing blood vessels

33
Q

Describe the process of angiogenesis

Very Deep Enemas Puncture My Rectum

A
  • Vasodilation of pre-existing vessels due to NO
  • Degradation of the basement membrane
  • Endothelial cells migrate towards the angiogenic stimulus (VegF)
  • Proliferation of endothelial cells
  • Maturation of cells and tubular remodelling
  • Recruitment of outer cells e.g. smooth muscle cells
34
Q

What is the significance of angiogenesis?

A
  • Provides access for inflammatory cells and fibroblasts

- Delivers oxygen and nutrients

35
Q

What is the significance of the migration and differentiation of myo/fibroblasts?

A

Necessary for the production of the extra cellular matrix

36
Q

What is the composition of the ECM? How is this significant to function?

A
  • Collagen and elastin fibres (tensile strength and recoil)
  • Proteoglycans (adhesion)
  • Adhesive proteins
37
Q

What are some of the functions of the extracellular matrix?

A
  • Mechanical support
  • Separation of tissues
  • Cell communication
38
Q

How is collagen synthesised?

CHADPOGRL

A
  • Cleavage of signal by signal peptidase to form preprocollagen
  • Hydroxylation of proline residues by prolyl hydrolase (Fe2+ and Vit C)
  • Addition of N-liked oligosaccharides
  • Disulphide bond formation by protein disulphide isomerase
  • Procollagen forms
  • O-linked glycosylation
  • Golgi packaging then exocytosis
  • Removal of N&C peptides with procollagen peptidases
  • Lateral aggregations and cross-linking by lysyl oxidase (Cu2+ and Vit B)
39
Q

Which types of collagen are used in the framework?

A
  • Fibrillar (1-3, dermis, bone and cartilage) - Uninterrupted alpha helices that form fibrils
  • Amorphous (4-6, basement membrane) - Interrupted helices that form sheets
40
Q

What happens to collagen production if a patient has scurvy?

A
  • Little or no hydroxylation of proline residues
  • Weak collagen that is vulnerable to enzymatic degradation
  • Blood vessel collagen is particularly vulnerable which can lead to haemorrhage
41
Q

What happens to collagen production if a patient suffers from Ehlers-Danlos syndrome?

A
  • Conversion of procollagen to tropocollagen is defective
  • If in types 1-3 gives no tensile strength of skin
  • Hyperextension of joints
42
Q

What happens in the maturation stage of fibrous repair?

A
  • High collagen deposition
  • Neutrophils are replaced by macrophages (unless infected)
  • Myofibroblasts contract which reduces the size of the wound
  • Differentiation and reduction of vessels
43
Q

When can a wound heal by primary intention? Why?

A

If it is:

  • Clean and uninfected
  • Made surgically
  • Has easily opposable edges
  • Limited cell death and basement membrane interruption
44
Q

Describe the healing process by primary intention. What does this lead to?

A
  • Contraction of myofibroblasts leads to decrease in size of clot
  • Decrease in amount of granulation tissue
  • Reepithelialisation from the top down
  • Fibrous repair of dermis
  • Results in a fine, thin scar
45
Q

What is a potential negative of healing by primary intention?

A

Can trap infection at the site of the wound which can result in an abscess

46
Q

When can a wound heal by secondary intention? Why?

A
  • When edges can’t be opposed easily/at all
  • Abscess
  • Ulceration
  • Large wound
  • There is an extensive loss of all cells
47
Q

Describe the healing process by secondary intention. What does this lead to?

A
  • Formation of a large clot that dries to form a scab
  • Large inflammatory response resulting in the formation of a lot of granulation tissue
  • Reepithelialisation from the base up with a high collagen deposition
  • Larger contraction of myofibroblasts to reduce volume eventually results in a large scar
48
Q

Describe the stages of bone fracture healing

A

1) Formation of a haemotoma
2) Soft tissue callus forms
3) Bony callus forms
4) Bone is remodelled in the direction of mechanical stress to allow for controlled weight bearing

49
Q

What is the purpose of the haemotoma?

A
  • To fill the gap left by the fracture

- To provide a fibrin mesh for: macrophages, endothelial cells, fibroblasts and osteoblasts

50
Q

Describe the formation of the soft tissue callus

A
  • Formation of granulation tissue
  • Ingrowth of vascular tissue
  • Inward migration of mesenchymal cells
  • Collagen matrix is laid down and osteoid is secreted by osteoblasts
  • Osteoid mineralises which leads to the soft callus
51
Q

What is the purpose of the bony callus?

A
  • Bridges gap between the two edges of bone
52
Q

What is a myofibroblast?

A

A cell that has features of both smooth muscle and fibroblasts which gives a contracting element to the wound

53
Q

What are the local factors that influence the efficacy of healing and repair?

A
  • Type, size and location of wound
  • Lack of movement
  • Blood supply
  • Infection
  • Foreign material
54
Q

What are the systemic factors that influence the efficacy of healing and repair?

A
  • Age
  • Drugs and hormones (steroids)
  • Deficiencies e.g. Vit C, amino acids
  • General health e.g. diabetes
55
Q

Describe the complications of insufficient fibrosis (2)

A
  • Wound dehiscence (bulging) - especially on abdomen due to pressure
  • Ulceration
56
Q

Describe the complications of excessive fibrosis (2)

A
  • Keloid scars (extend beyond boundaries of original wound and don’t fade)
  • Liver cirrhosis (chronic irritation by e.g. alcohol)
57
Q

Describe the complications of excessive contraction (2)

A
  • Strictures (obstruction of a tube or channel)

- Contractures (limitation of joint movement)

58
Q

Describe the regenerative capacity of cardiac muscle. When can cardiac muscle become damaged and what happens as a result?

A
  • Capacity is low, if any at all

- After MI - leads to scar formation which can compromise cardiac function

59
Q

Describe the regenerative capacity of the liver

A
  • Very, very good
  • Up to 60% can be removed and the liver will double in size within 1 month
  • Compensatory hyperplasia (increase in cell size)
60
Q

Describe the regenerative capacity of the PNS

A
  • Severing of nerve = Wallerian degeneration
  • Regeneration can happen by elongation of proximal nerve stumps
  • Schwann cells from distal degenerated axons guide end to tissue that was initially innervated
61
Q

What is the growth rate of axons?

A

1-3mm per day

62
Q

What is the regenerative capacity of connective tissue?

A
  • Poor

- Due to lack of blood supply, lymphatic drainage and nerve innervation

63
Q

What is the regenerative capacity of the CNS?

A
  • Poor as nerve tissue is permanent
  • Damaged cells are instead replaced by glial cells
  • Loss of function

ESA 2 (63 decks)

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