Tissue Repair & Chronic Inflammation Flashcards

0
Q

What type of injury does a scar become produced from

A

Prolonged and severe injury

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1
Q

Briefly explain scarring

A

Damage to connective tissue & intra cellular matrix which holds the tissue together and comes from a more prolonged and severe injury

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2
Q

What is normal homeostasis

A

A balance of proliferation and apoptosis

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3
Q

When an injury occurs, which two routes can a cell take

A
  • regeneration
    Or
  • repair
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4
Q

Which further two routes can a cell take other than regeneration

A
  • renewing tissues
    Or
  • stable tissues
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5
Q

What happens to renewing tissues

A

Complete regeneration:

Epidermis, GI tract epithelium, hematopoletic system

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6
Q

What happens to stable tissues

A

Compensatory growth of eg liver and kidney

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7
Q

Which further two routes can a cell take other than repair

A
  • wound
    Or
  • chronic inflammation
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8
Q

What happens to a tissue which forms a wound

A

Wound healing and scar formation (cannot compensate for injury)

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9
Q

What happens to a tissue during chronic inflammation

A

Fibrosis

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10
Q

Why would a tissue be unable to repair

A

If the injury persists and has to do with the type of injury, how severe it is and the time course of the injury

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11
Q

What happens to the tissue if the injury is mild

A

Tissue can heal without scarring as the scaffolding and connective tissue of cells remains intact

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12
Q

What happens to a cells which are unable to regenerate fully

A

Scarring

if injury persists eg from liver damage due to drinking

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13
Q

What type of cells are labile cells

A

Cells which divide and proliferate throughout life

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14
Q

What are labile cells derived from

A

Adult stem cells

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15
Q

What type of cells have a set life span

A

Labile cells

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16
Q

Give examples of labile cells

A
  1. Gut epithelium
  2. Corneal epithelium
  3. Blood cells
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17
Q

What example of cell is able to regrow and replenish at a mitotic rate

A

Epithelial cells

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18
Q

What is the name of corneal stem cells

A

Palisades of Vogt

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19
Q

What do palisades of Vogt do

A

Power our corneal stem cells and produce continual supply of corneal epithelial cells

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20
Q

Where are labile cells found within the cornea

A

Around the limbus

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21
Q

What do stable cells do

A

Usually divide slowly but if damaged can increase rate of cell division so can get tissue repair

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22
Q

Name examples of stable cells (can heal and grow but don’t usually turn over)

A
Hepatocytes eg liver
Fibroblasts
Vascular endothelial cells
Smooth muscle cells
Osteoblasts eg when bones break
Renal tubular epithelial cells eg kidney
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23
Q

Where can pockets of stem cells which have the same effect of epithelial stem cells (to replenish) be found within the body

A

Gut & skin

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24
Q

What are permanent cells

A

Cells that cannot divide but may be capable of some cellular repair if the nucleus and Golgi are not impaired

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25
Q

Name examples of permanent cells

A

Neurons in retina (cannot get new cells to grow so if they’re gone they’re gone)
&
Cardiac myocytes

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26
Q

What needs to be initiated in order for cell growth and replenishment

A

The growth cycle

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27
Q

What is the growth cycle

A

To switch the cell on to divide and multiply

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28
Q

What can the growth cycle be done by

A

Particular signalling molecules eg growth factors
Or
Integrin signalling pathways
Can switch on mitotic pathway to replenish cells which have been killed

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29
Q

What do growth factors/chemical switches regulate

A

Cell proliferation

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30
Q

What are the three types of growth factors

A

Autocrine
Paracrine
Hormones

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31
Q

Explain the autocrine growth factor

A

Self signalling

Comes from the cell and binds to the receptor which initiates cell division

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32
Q

Explain the paracrine growth factor

A

Comes from damaged cell

Sends signals to adjacent cell telling them to divide and replace them

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33
Q

Explain the hormone growth factor

A

Signals to distant tissue to repair parts of the body such as muscle or bone peripheral tissue
Eg growth hormone

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34
Q

Where are receptors for signal transduction found

A

On the cell

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35
Q

Name three types of receptors for signalling transduction

A
  1. Intrinsic kinase activity
  2. G-protein coupled receptors
  3. Receptors lacking intrinsic kinase activity
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36
Q

What is intrinsic kinase activity

A

Growth factors which bind to the receptor and activate kinases

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37
Q

Give examples of intrinsic kinase activity growth factors

A

PI3-kinase
Mitogenic activated protein kinase (MAP)
PLC-y

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38
Q

What do kinases do

A

Activate transcription factors that regulate the cell cycle

ie phosphorelation & dephosphorelation coupling switches receptors on & off

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39
Q

Give examples of G protein coupled receptors

A
Serotonin 
Vasopressin 
Histamine (activated by G protein & increases vasodilation) 
Glucagon 
Corticotrophin
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40
Q

As part of the G protein coupled receptors, what is cAMP and calcium important for

A

Tight junction formation
Ion channels
Transcription factors

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41
Q

Give examples of receptors lacking intrinsic kinase activity

A

Interleukins
Interferons
Growth hormones
Prolactin

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42
Q

What do receptors lacking intrinsic kinase activity activate

A

JAK (Janus kinase family) activate transcription factors that shuttle to the nucleus

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43
Q

Receptors lacking intrinsic kinase activity don’t rely on…

A

Phosphorylation and dephosphorylation coupling eg MAP kinase

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44
Q

What does mitogenic protein activated kinase use to activate mitosis

A

Phosphorylation

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45
Q

What happens in the IP3 pathway

A

IP3 binds to the IP3 receptor in the endoplasmic reticulum
Which increases intracellular calcium
Intracellular calcium effects transcription and translation as well as fluid transport
And activates calcium getting chloride channels
Cells under stress are swollen so it gets rid of fluid

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46
Q

What does the MAP kinase pathway activate

A

Transcription and translation

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47
Q

What does the JAK/STAT pathway regulate

A

Growth initiation

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48
Q

What are cyclic amp and what do they affect

A

Families of G proteins

Which also affect transcription and translation

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49
Q

What are G protein coupled receptors found in

A

Rod outer segments eg rhodopsin and cyclic Gmp

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50
Q

List the properties of extra cellular matrix & cell matrix interactions

A
  • mechanical support & anchorage for cell migration (needs collagen or fibrin to hold on to to move along)
  • control cell growth through intergrin cellular receptors
  • maintain cell differentiation via intergrin receptors
  • scaffold for tissue renewal which requires as basement membrane if BM damaged results in a scar
  • establishes tissue micro environment (barrier)
  • storage & regulation of growth factors for rapid deployment is EGF, FGF
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51
Q

What is the extra cellular matrix important for

A

Cell stability and vitality

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52
Q

What do we get if the extra cellular matrix breaks

A

Scarring

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53
Q

What does the integrin cellular receptors integrate between

A

Cell membrane and its basement membrane of its partner

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54
Q

What does the maintenance of cell differentiation via intergrin receptors go into

A

Another cell type
If you take a cell away from its environment it will differentiate into some other cell type eg fibroblasts or immature cells

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55
Q

What happens to the cell without scaffolding

A

No tissue repair or renewal

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56
Q

If JAKs doesn’t rely on phosphorylation, what do they respond to

A

Cytokines
Which regulates growth differentiation and cell movement where all the receptors help to increase cell tight junctions, divide and become motile which increases fluid permeability etc

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57
Q

What happens to cells which are moved away from their micro environment eg removed from their basement membrane

A

Dedifferentiate and can’t maintain their identity

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58
Q

What happens to an RPE cell which has been moved from its micro environment

A

Lacks micro villi
Lacks differentiation
No regularity
No hexagonal shape

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59
Q

What are proteoglycans important for

A

Signalling proteins for cell differentiation

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60
Q

Name some examples of basement membranes

A

Type 4 collagen
Laminin
Proteoglycan

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61
Q

What do integrin receptors do

A

Anchor the cell down to eg collagen fibres to maintain cell communication and differentiation

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62
Q

What do integrins interconnect with in generic tissues

A

The basement membrane
Also
With the cellular matrix and fibroblasts

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63
Q

What do proteoglycans form

A

Extracellular matrix

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64
Q

What are proteoglycans attached by to connect with fibroblasts

A

Integrins

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65
Q

What is the interstitial matrix composed of

A

Fibrillar collagens
Elastin
Proteoglycan and
Hyaluronan

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66
Q

Describe the connection between integrin receptors to a cell nucleus

A

Direct lines like spiders webs with cytoskeletal attachments to the cell nucleus

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67
Q

What is the significance of intergrin receptors connecting to the cell nucleus via cytoskeletal attachments

A

If there’s disruption to intergrin receptors, the signal will go to the cytoskeletal attachments

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68
Q

Why do integrin receptors attach to the cytoskeletal attachments

A

So there’s a physical communication between the extra cellular environment and integrin receptors to the cell nucleus, which maintains differentiation and protein attachment, migration and form of the cell

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69
Q

What does damage to the extracellular matrix release

A

bFGF

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70
Q

Which two things do heparin sulfate bind together

A

Fibroblast growth factor to FGF receptor

71
Q

Name one thing the extra cellular matrix contains which is readily accessible incase of damage

A

Growth factors

72
Q

Describe what happens if there has been damage to the extracellular matrix

A

We get free fibroblast growth factors floating around which signals to the cell that the extracellular matrix has been damaged, so it needs to create more fibroblasts (which locks things down with heparin sulfate complex bFGF) so when it’s smashed FGF is exposed and without heparin sulfate can signal to the cell nucleus to say the extracellular matrix has been damaged

73
Q

Which two responses occur after an injury

A

Cellular and vascular

74
Q

What two things can happen following a cellular and vascular response from and injury

A

Acute injury (stimulus removed)
Or
Persistent tissue damage

75
Q

Which two routes can a cell take following acute injury (stimulus removed)

A

Either

  1. Parenchymal cell death - intact tissue framework ie superficial wounds and some inflammatory processes
  2. Parenchymal cell death - damaged tissue framework ie deep wounds to proteoglycans and collagen
76
Q

What happens as a result of parenchymal cell death - intact tissue framework

A

Regeneration (restitution of normal structure)
if matrix is intact (labile/stable tissue) eg liver regeneration after partial hepatectomy, superficial skin wounds, resorption of exudate in lobar pneumonia

77
Q

What happens as a result of parenchymal cell death - damaged tissue framework

A

Repair ie scar formation

Eg deep excisional wounds, myocardial infarction

78
Q

What is persistent tissue damage

A

An ongoing infection or auto immune change or ongoing ingestion of toxic particles ie chronic inflammation = fibrosis tissue scar

79
Q

What happens as a result of persistent tissue damage

A

Fibrosis ie tissue scar eg chronic inflammatory diseases (cirrhosis, chronic pancreatitis, pulmonary fibrosis)

80
Q

List the actions of a macrophage

A
  1. Debridement removal of injured tissue & debris
  2. Anti microbial activity
  3. Chemotaxis and proliferation of fibroblasts and keratinocytes
  4. Angiogenesis
  5. Deposition and remodelling of ECM
81
Q

Give examples of debridement removal of injured tissue and debris

A
  • phagocytosis of dead/necrotic tissue
  • collagenase
  • elastin (both help to break down & mush up area)
82
Q

Give examples of antimicrobial activity

A
  • nitric acid

- ROS (generate reactive oxygen species & o3)

83
Q

Give examples of chemotaxis and proliferation of fibroblasts and keratinocytes

A
  • PDGF
  • TGF-b
  • TNF
  • IL-1
  • KGF-7
    (Release growth factors to bring fibroblasts to the area to help with wound healing especially TNF/tumour necrosis factor which is important for signalling to fibroblasts)
84
Q

Give examples of deposition and remodelling of ECM

A
  • TGF-b
  • PDGF
  • TNF
  • OPN
  • IL-1 (clearing away debris from basement membrane, so involved in remodelling & rebuilding the area & clearing it up)
  • collagenase
  • MMPs (rebuilding area)
85
Q

What occurs from 0-6 days after wounding

A

Inflammation (initial phase)

  • clot formation
  • chemotaxis (brings macrophages)
86
Q

What occurs from 6-12 days after wounding

A

Proliferation (macrophages go on to proliferation of fibroblasts)

  • re-epilelialisation (new blood vessels grow)
  • angiogenesis and granulation tissue
  • provisional matrix (extracellular)
87
Q

What occurs 12-16 days after wounding

A
Maturation (scar formation) 
- collagen deposition 
- collagen matrix 
- wound contraction
In maturation, overtime granulation dissolves which results in more permanent damage to tissue and healing leads to maturation
88
Q

What happens as inflammation and wound healing begin together

A
  1. Increased neutrophils- bacterial killing and clearing of damaged tissues
  2. Increased macrophages - wound healing - growth factors
    - EGF - epidermal growth factor (released for epithelial growth)
    - FGF - fibroblast growth factor (is increased)
    - TGF - transforming growth factor (helps differentiation, transforms cell type from one to the other)
89
Q

What happens during tissue repair

A
  1. Acute inflammation
  2. Angiogenesis
  3. Migration and proliferation of fibroblasts
  4. Scar formation
  5. Remodelling of connective tissue
90
Q

why does angiogenesis occur

A
  • the wound edge is ischaemic
    the usual vascular architecture is damaged
  • thus the healing process cannot proceed without a sufficient blood flow
  • macrophages secrete angiogenesis factor
    VEGF = vascular endothelial growth factor
91
Q

give example of eye diseases where VEGF is involved

A
  • ARMD - produces new blood vessels in wet form

- diabetic retinopathy

92
Q

when does angiogenesis being during tissue repair

A

in the first few days

93
Q

how does angiogenesis work

A
  • endothelial cells proliferate to form capillary buds at the wound surface
  • buds form loops which eventually fuse to form a new capillary bed
94
Q

when can angiogenesis be delayed

A

if there is vascular disease (e.g. diabetes), necrosis or steroid therapy

95
Q

what do macrophages form if you get a cut

A

new VEGF (angiogenesis from pre-existing vessels)

96
Q

what do new VEGFs cause

A

new blood vessels to grow, sprouting off the broken one

ie ischaemic signals to grow new blood vessels producing a mature network

97
Q

what are the blood vessels of the immature network like

A

leaky

98
Q

what do the leaky blood vessels form

A

a bruise

99
Q

why do the leaky blood vessels form a bruise

A

they are not well formed and are immature, pooling of blood from leaky vessels

100
Q

what are EPCs

A

endothelial precursor cells

flow around in the blood and circulate around the body

101
Q

what are EPCs derived from

A

stem cells of bone marrow

102
Q

what do EPCs do

A

find a leak, and will initiate angiogenesis, if they bump into an area of breakage or leakage, they will bud & form capillaries called angiogenesis

103
Q

what does fibroblast proliferation do

A

rebuilds scaffolding to enable epithelial cells and endothelial cells to migrate and regrow to new tissue

104
Q

what can fibroblast proliferation lay down

A

collagen, fibrin, fibronectin

and have actin myosin contractile components so acts as a glue to help repair our wound

105
Q

when does fibroblast proliferation begin after wound

A

2 days

106
Q

what do cells migrate from during fibroblast proliferation

A

from neighbouring connective tissue

107
Q

during fibroblast proliferation, what do growth factors from macrophages and platelets stimulate

A

collagen production by fibroblasts and proteoglycans

108
Q

what do fibroblasts form

A

granulation tissue

109
Q

what is granulation tissue the area of

A

area of scarring

with fibrosis and soft tissue made up of fibroblasts & macrophages & proteoglycans i.e. a spongy tissue

110
Q

what does fibroblast proliferation depend on

A

the vascular supply and having nutrients such as collagen, zinc, copper to that area to sustain proliferation and synthesis of basement membrane (e.g. need to produce their own membrane and scaffold)

111
Q

what do fibroblasts which have formed their granulation tissue consist of

A

new blood vessels and proliferating fibroblasts

112
Q

what does leaky, high permeable granulation tissue end up to be

A

scar tissue

113
Q

what do a lot more blood vessels =

A

angiogenesis packed full of arithrocytes

114
Q

what is the connective tissue formation the synthesis of

A

collagen by fibroblasts

115
Q

what does connective tissue formation require

A

nutrients - blood supply

116
Q

which nutrients does the connective tissue require during formation

A

amino acids
zinc copper iron
vitamin A & E

117
Q

what is the interstitial matrix synthesis produced by

A

fibroblasts

118
Q

what is the interstitial matrix made out of

A

granulation tissue

119
Q

what does the interstitial matrix affect

A

the architecture and strength of collagen fibres

120
Q

what is secreted during interstitial matrix synthesis

A

proteoglycans (GAGS + protein core)

121
Q

what do the secreted proteoglycans (GAGS & protein core) bind to during interstitial matrix synthesis

A

collagen fibres, to form a rigid scar as proteoglycan content decreases (ie amount of proteoglycans decrease with more collagen in the area)

122
Q

what happens when the amount of proteoglycans decreases with more collagen in the area

A

start to get contractions of fibres in the fibroblasts which pull the wound together

123
Q

during epithelialisation, what is in constant renewal

A

the squamous stratified epithelium

124
Q

what happens to the epithelial cells from adjacent basement membranes during epithelialisation

A

detach divide and migrate across the wound

125
Q

what won’t epithelial cells form without

A

a basement membrane

126
Q

what do the epithelial cells form when formed via adjacent membranes during epithelialisation

A

form a monolayer of epithelial cells

127
Q

what initiates the response of epithelialisation

A

epithelial growth factor (EGF), derived from macrophages platelets initiate the response

128
Q

what happens following epithelialisation

A

wound contraction

129
Q

what happens during wound contraction

A

movement of wound edges towards the centre

130
Q

what does wound contraction occur through

A

generation of forces in the contractile elements of the fibroblasts towards the centre of the wound

131
Q

what happens as the wound contracts during wound contraction

A

collagen and proteoglycans are secreted that lock the new tissue in place

132
Q

what aligns near the wound during wound contraction

A

fibroblasts

133
Q

what is wound remodelling also known as

A

scar maturation

134
Q

when does wound remodelling occur

A

> 3 weeks after injury

can persist for months to years

135
Q

what does increased collagen cross linking = during wound remodelling

A

increased strength

136
Q

what is wound remodelling a regression of

A

surface capillary network

137
Q

what is decreased during wound remodelling

A

proteoglycan content and thus water content

138
Q

briefly list the stages of wound healing e.g. form a burn

A
  • epithelium is removed from burn
  • bruised area = leaky blood vessels
  • which are replaced by proteoglycans and new blood vessels are grown
  • keratin on the skin forms a scar
139
Q

what is chronic inflammation

A

ongoing inflammation with attempts of wound healing or

unregulated injury/repair in a perpetual cycle

140
Q

list the outcomes of acute inflammation

A
  1. resolution
  2. healing by connective tissue replacement (is damaged)
  3. progression to chronic inflammation (ongoing healing)
141
Q

how long can chronic inflammation go on for

A

weeks, months, years

142
Q

what steps does the tissue go through with chronic inflammation

A
  • repair
  • inflammation
  • injury (ongoing)
    all co-exist
143
Q

what are the causes of chronic inflammation

A
  • persistent infections
  • immune mediated
  • prolonged exposure to toxin
144
Q

give examples of persistent infections which cause chronic inflammation

A

viral

fungal

145
Q

give examples of immune mediated causes of chronic inflammation

A
  • autoimmune disease e.g. MS, RA, SLE

- unregulated immune response to antigen e.g. environmental (asthma), bacterial (IBS)

146
Q

what is IBS caused from

A

bugs in the gut of chronic inflammation & scarring

147
Q

give examples of prolonged exposure to toxin as causes of chronic inflammation

A
  • exogenous - silica, asbestosis

- endogenous - atherosclerosis/lipids

148
Q

what is atherosclerosis

A

hypertension - chronic inflammation of arterial walls

149
Q

list the morphologic features of chronic inflammation

A
  • infiltration
  • tissue destruction
  • attempts at healing
150
Q

what are the morphologic features of infiltration during chronic inflammation

A

macrophages/lymphocytes (T-B)/plasma cells (Ab)

151
Q

what is tissue destruction induced by of morphological features during chronic inflammation

A

persistent offending agent or by the inflammatory cells

152
Q

what are the attempts at healing of morphological features during chronic inflammation

A
  • connective tissue replacement
  • angiogenesis
  • fibrosis
153
Q

what does chronic =

A

changes to tissues which causes damage

154
Q

what are chronic inflammatory cells

A
  • macrophages/lymphocytes/plasma cells
155
Q

what forms constellation to tissues

A

T & B cells

156
Q

what are the names of macrophages which have formed from stem cells in the bone marrow

A

monoblasts

157
Q

what are the name of macrophages in the blood

A

monocyte

158
Q

what are the name of macrophages in the tissues

A

macrophage

159
Q

what is the name of macrophages in the CNS

A

microglia

160
Q

what is the name of macrophages in the liver

A

kupffer cells

161
Q

what are the name of macrophages in the lungs

A

alveolar macrophages

162
Q

what are the name of macrophages in the bone

A

osteoclasts

163
Q

what role does M1 macrophages have

A

a destructive role which releases cytokines and interleukins to damage the tissue and cause inflammation, M1 cells are associated with

  • reactive oxygen and nitrogen species
  • proteases
  • cytokines, including cheekiness
  • coagulation factors
  • AA metabolites
164
Q

what are M1 cells inhibited by

A

interleukin 4 & 13

165
Q

what is a pale macrophage

A

an activated macrophage where the DNA is coiled

166
Q

what are M2 macrophages involved in

A
reduce inflammatory cytokines 
involved in repair and 
making epithelial cells grow 
- growth factors (PDGF, FGF, TGFbeta)
- fibrogenic cytokines
- angiogenic factors (FGF)
- remodelling collagenases
167
Q

what is the two varieties of macrophages M1 and M2 for

A

balancing wound healing

168
Q

what are macrophages activated by

A

T-cells

169
Q

what are activated via macrophages

A

cytokines (IL-40

170
Q

what do macrophages persist in

A

chronic inflammation

171
Q

what do macrophages continue through tissue repair

A

tissue injury and fibrosis

172
Q

what are the other cells apart from macrophages, in chronic inflammation

A

lymphocytes: T & B cells

173
Q

what do macrophages attract

A

lymphocytes (IL 12 or present antigen)

174
Q

what do T-cells recruit

A

monocytes/macrophages (TNF-IL17)

175
Q

what happens to the reaction when T cells are involved

A

reaction becomes chronic/severe

176
Q

why does the reaction become more severe when T cells are involved

A

as T cells and macrophages co-stimulate each other