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Healing And Repair Flashcards

(51 cards)

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1
Q

What does healing depend on

A

The type of tissue that is injured
The nature of the injury
Sufficient blood supply (angiogenesis)

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2
Q

Healing required

A

The regrowth of cells and ECM

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3
Q

ECM and cells composition in tissues

A

Differs between organs

E.g. Skin cells on the epidermis and the ECM basement membrane below

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4
Q

Types of tissue injury

A 
Toxins
Ischaemia
Burns
Trauma 
infection 
Surgical 
Inflammation - autoimmune
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5
Q

Tissue injury of all tissues causes

A

Inflammation

Which then promotes healing which is either resolution or repair

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6
Q

Example 1 - skin

Structure of normal skin

A

Epidermis - contains stem cells in constant cell cycle
Dermo-epidermal junction - connects the epidermis to the dermis via hemidesmosomes, basement membrane and collagens
Dermis - comprises fibroblasts, blood vessels and abundant extracellular matrix

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7
Q

The ECM in the dermis

A

Collagen fibres - provide structural support
Proteoglycans - form a hydrated gel which resists compressive forces whilst permitting rapid diffusion of nutrients, metabolites and hormones
Basement membrane - connect via hemidesomosomes
Elastic fibres- provide resilience by stretch and recoils functions

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8
Q

What is the basement membrane made out of

A 
Laminin
Type IV collagen fibres 
Plasma membrane 
Nidogen 
Perlecan 
Integrin --> main receptor type by which cells bind to the ECM
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9
Q

Types of wound healing in the skin

A

Primary intention

Secondary intention

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10
Q

What is primary intention healing

A

Primary intention wounds have the following characteristics

  • clean and uninfected
  • surgically incised
  • without much loss of cells and tissue
  • edges of wound are approximated by surgical sutures
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11
Q

What is secondary intention healing

A

The wound has the following characteristics

  • open with large tissue defect
  • having extensive loss of cells and tissues
  • the wound is not approximated by surgical sutures but is left open
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12
Q

Wound healing phases

A 
Clotting phase - fibrin clot providing rapid structural support 
Granulation tissue 'provisional ECM'
Angiogenesis 
Fibroplasia
Reepithelialisation
Wound contraction
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13
Q

Granulation tissue

A

Provisional ECM
Network of inflammatory cells, blood vessels, fibroblasts, loose fibrous tissue
Stimulates healing but it is loose and friable and would not support epithelia
Inflammatory cells mainly neutrophils
Blood vessels provide nutrients for the repair
Fibroblasts provide the support
Fibrous tissue is early collagen

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14
Q

Angiogenesis

A

New blood vessels to provide the nutrients which are needed to supply the healing tissue
Proteolysis of ECM to make way for new endothelium
Chemotaxis following the growth signals migrates into the surrounding space
Proliferation of the cells
Once formed and matured inhibition of growth

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15
Q

Fibroplasia

A

Is fibroblast proliferation and migration

Production of collagen, proteoglycans and elastin to reform the ECM to repair the damage

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16
Q

Reepithelialisation

A

Regeneration of damaged endothelium
1) transformation - become less differentiated more stem cell like
2) cells at the edge of the wound undergo mitosis
3) migration: newly formed cells migrate along the basal lamina using pseudopodia
Cell to cell and basal to cell lamina junctions are continually for,ed and broken during this process so the cells remain anchored as they migrate.
Healing ceases when there is contact inhibition - no gaps between the cells are present

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17
Q

Wound contraction and scarring

A

Complete reepithelialisation and dermal scarring
Not like normal skin there are no sweat ducts or hair and in normal dermis the collagen is randomly arranged and the dermis is more dense with cells
Fibroblasts develop properties of smooth muscle (myofibroblasts) allowing contraction of the wound

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18
Q

Regulation of wound healing in skin

A 
Macrophages, fibroblasts and endothelial cells produce GROWTH FACTORS which stimulate healing in the epidermis and dermis 
Integrins are major receptors for ECM and initiate growth factor signalling pathways 
Matrix metalloproteases (MMPs) are upregulated leading to the remodelling of the ECM. MMPs are inhibited by TIMPs (tissue inhibition of matrix metalloproteinases
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19
Q

Growth factor and its effect

EGF

A

Fibronectin secretion

Reepithelialisation

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20
Q

FGF1,2

A

Fibroblasts growth and reepithelialisation

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21
Q

IGF

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A

Cell proliferation

22
Q

KGF/FGF7

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A

Reepithelialisation

23
Q

PDGF

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A

Fibroblasts chemotaxis

24
Q

TGF- alpha

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A

Fibronectin secretion

Repepithelialisation

25
TGFbeta
Fibroblast chemotaxis Angiogenesis Extracellular matrix deposition Inhibits cell proliferation
26
Factors influencing wound healing
``` Systemic - nutrition - malnourished - metabolic status - diabetic - circulatory status - PVD - hormones - Cushings Local - local blood supply - infection - foreign body - mechanical factors - wound reopening after surgery ```
27
Wound strength
1 week back to 10% strength Collagen levels inc would strength Inc Plateau at 70/80% which is at 3 months Ever return to 100%
28
Pathological healing
Keloid scar in pigmented skin Contracture after burns collagen contraction prevents hands from moving Chronic leg ulcer- healing doesn't happen due to inadequate blood supply - insufficient nutrients
29
Liver organisation
Little ECM Hepatocytes are packed closely together forming sinusoids ECM is confined to the portal tracts with only a thin layer in contact with the heptocytes, composed mainly of collagen - line the edge of the sinusoids
30
Regeneration of the liver following injury
Hepatocytes are stimulated out of 'quiescent' G0 phase back into the cell cycle New ECM is deposited between the hepatocytes Angiogenesis establishes new sinusoids
31
Resolution vs repair
Resolution is where the same tissue is replaced so the proliferation of hepatocytes replaces old tissue Repair is damaging in this case it is where the regenerating nodules are surrounded by fibrous tissue causing cirrhosis Pathological repair- regenerating cells cause a damaging structure due to the surrounding cells
32
What cells regulate the liver healing process
Stellate and kupffer cells Produce growth factors and cytokines which regulates healing Key role in stimulating the hepatocytes to enter the cell cycle
33
What does HGF do
Hepatocytes growth factor | Hepatocyte replication
34
EGF
Endothelial cell growth factor | Hepatocyte replication and angiogenesis
35
PDGF
Platelet derived GF Stellate cell proliferation and chemotaxis Also angiogenesis
36
TNF
Tumour necrosis factor Hepatocyte replication Stellate cell activation and myofibroblastic differentiation
37
TGF-beta
Deposition of ECM Inhibition of hepatocyte replication It is one of the key regulators of fibrosis As in the skin the collagen remodelled is mediated by MMPs a TIMPs
38
VEGF
Angiogenesis
39
IL-6
Hepatocyte replication
40
Factors effecting the development of cirrhosis
Time course of liver injury - paracetamol overdose causes severe liver one point in time - does not lead to cirrhosis - alcohol generally causes much less severe injury but over a longer time period - can cause cirrhosis Anatomic site of injury - damage to the parenchyma by alcohol causes classical cirrhosis with fibrosis mediated largely by stellate cells in the sinusoids - damage to the portal tracts in Primary biliary cirrhosis causes biliary pattern of fibrosis mainly affecting the portal structures
41
Clinical consequences of cirrhosis
``` Jaundice Spider naevi Palmar erythema Gynaecomastia Splenimegaly Flapping tremour Loss of parenchyma function: impaired protein synthesis, processing drugs and hormones and production of clotting factors Portal hypertension Infection - spontaneous bacterial peritonitis Hepatocellular carcinoma ```
42
What happens after an MI
Influx of inflammatory cells | Fibrous scar left behind
43
Regulation of fibrosis in the heart
Fibroblasts and myofibroblasts produce matrix proteins in response to inflammatory mediators released by macrophages and inflammatory cells Mediators include inflammatory cytokines - TNF-alpha, IL1, IL6,and fibrogenic factors such as TGF-beta, PDGF and angiotensin2
44
Consequence of myocardial fibrosis
``` Contractile dysfunction Arrhythmia Myocardial rupture Pericarditis Ventricular aneurysm Papillary muscle dysfunction ```
45
What does healing depend on
Type of tissue that is injured The nature of the injury Sufficient blood supply - angiogenesis
46
What does a tissue need to do in order to heal
Regrowth of cells and ECM
47
Types of cells which and the levels of healing they permit
Labile cells - constant cells cycle repair often repairing with some tissue formation different than before - skin scarring Stable cells - inflammation produces a stimulus to cause repair and growth in which damage doesn't usually happen - but it can Permanent cell - little to no capacity to regenerate
48
Types of labile cells
Squamous epithelium Columnar epithelium Urothelium Haematopoietic cells
49
Type of stable cells
``` Hepatocytes Pancreatic acinar cells Fibroblasts Smooth muscle Endothelium ```
50
Types of permanent cells
Cardiac myocytes Neurone Skeletal muscle
51
ECM regrowth requires
``` Cell mediators - fibroblasts - macrophages - inflammatory cells Molecular mediators - TGF-beta - growth factors PDGF, EGF, HGF, FGF - inflammatory cytokines - TNF alpha, IL1, IL6 - MMPs, and TIMPs ```

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