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Pathology > Chronic Inflammation and Wound Healing 1 > Flashcards

Chronic Inflammation and Wound Healing 1 Flashcards

1
Q

what are the functions of the skin?

A
  • protection
  • temperature regulation
  • Immunity
  • Sensory receptors
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2
Q

what is the superficial outer layer of the skin?

A

Epidermis

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3
Q

what is the structure of the epidermis?

A

5 layers/strata of keratinocytes

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4
Q

what cells are found in the epidermis?

A

Melanocytes

Langerhans cells

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5
Q

what is the dermis?

A

deeper ‘true’ skin

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6
Q

what is the structure of the dermis?

A

Papillary and reticular layers

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7
Q

what cell types are found in the dermis?

A

fibroblasts, collagen, elastic and reticular fibres

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8
Q

what are found in the dermis?

A

Nerve endings, hair follicles, glands, lymphatics, blood vessels

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9
Q

what is found in the hypodermis?

A

adipose tissue, macrophages

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10
Q

what is the main cell in the epidermis?

A

keratinocyte

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11
Q

what separates the epidermis from the dermis?

A

a basement membrane

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12
Q

what is the function of melanocytes in the basal layer?

A

transfer pigment into keratinocytes

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13
Q

when do the cells of the epidermis become differentiated?

A

Cells become terminally differentiated as they move to surface [takes 2-4 weeks]

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14
Q

what sort of tissue is the dermis?

A

Dense irregular connective tissue

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15
Q

what affects skin integrity?

A 
Age
Nutrition
Circulation
Hormonal status
hydration
Environment
Mobility
Assault
Disease processes
Sensation
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16
Q

what is a wound?

A

Alteration in skin’s integrity

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17
Q

what can cause a wound?

A

Injury
Disease
Environmental assault
Surgery

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18
Q

what does wound healing consist of?

A 
Highly regulated & synchronised process of cell:
Proliferation
Differentiation
Migration
Angiogenesis 
Production of granulation tissue
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19
Q

what granulation tissues are produced in wound healing?

A

fibroblasts, epithelial, endothelial, inflammatory cells

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20
Q

what happens during wound healing?

A

Co-ordinated breakdown, synthesis & remodelling of ECM

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21
Q

what are the phases of cutaneous wound healing?

A

Inflammatory Phase
Proliferative Phase
Remodelling Phase

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22
Q

what happens in the inflammatory phase of wound healing?

A

Following injury, damage to local blood vessels leads to platelet aggregation & clot formation. This phase also sees recruitment of neutrophils & macrophages

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23
Q

what happens in the proliferative phase of cutaneous wound healing?

A

During this phase granulation tissue is formed as fibroblasts proliferate & secrete collagen. Re-epithelialisation over new granulation tissue also occurs

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24
Q

what happens in the remodelling phase of cutaneous wound healing?

A

This phase occurs over weeks to months as granulation tissue is replaced by a mature connective tissue scar

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25
Q

how does an acute wound heal?

A

An acute wound progresses through hemostasis, inflammation, repair and remodeling to replace provisional wound matrix with mature scar tissue

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26
Q

what regulates acute wound healing?

A

Cytokines, proteases and growth factors regulate these phases

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27
Q

what happens to cause a chronic wound?

A

sequential healing is interrupted

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28
Q

what happens during hemostasis?

A 
Initial injury or trauma
Clot formation
Platelet activation 
Platelet release of factors
Fibrin matrix
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29
Q

when does inflammation occur?

A

3-7 days after injury

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30
Q

what are the features of inflammation?

A

Rubor [redness]
Calor [heat]
Tumor [swelling]
Dolor [pain]

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31
Q

why does vasodilation occur during inflammation?

A

Neutrophil and macrophage influx

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32
Q

what is the first process in wound healing?

A

inflammation

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33
Q

what are the cells involved in inflammation?

A 
leukocytes
Neutrophils
Monocytes
Macrophages
Lymphocytes
Mast cells
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34
Q

what are the inflammatory mediators?

A 
Prostaglandins
Histamine 
Interleukins
TNF alpha
Matrixmetalloproteases [MMPs]
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35
Q

what is the first cell to arrive at the site of inflammation?

A

neutrophils

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36
Q

what are the specialised functions of neutrophils?

A

phagocytosis and destruction of invading microorganisms particularly bacteria

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37
Q

what do the factors released by neutrophils in a clot do?

A

amplify aggregation response
initiate coagulation cascade
act as chemoattractants for cells

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38
Q

what activates the transmigration of neutrophils?

A

Activated by pro-inflammatory cytokines e.g. IL-1b TNF-a, IFN-g

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39
Q

where do neutrophils migrate to?

A

Neutrophils transmigrate across endothelium

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40
Q

what happens when Neutrophils transmigrate across endothelium?

A

Increased expression of adhesion molecules e.g. P-& E-selectins, ICAMs

41
Q

what are macrophages?

A

professional phagocytes

42
Q

what do macrophages do?

A

Remove senescent, dead and damaged cells

Remove large microorganisms

43
Q

how are macrophages formed?

A

Macrophages mature in the tissue from circulating monocytes

44
Q

when do monocytes and macrophages appear?

A

within 2 days of injury

45
Q

how is monocyte and macrophage infiltration regulated?

A

regulated by gradient of chemotactic GFs & pro-inflammatory cytokines secreted by platelets, keratinocytes, fibroblasts & leukocytes

46
Q

what is the importance of GFs –TGF-b, TGF-a, bFGF, PDGF & VEGF ?

A

promote cell proliferation and ECM synthesis

47
Q

what is the function of lymphocytes?

A

to enable adaptive or acquired immunity

48
Q

what is the role of B-lymphocytes?

A

B lymphocytes remain in the bone marrow & secrete antibodies

49
Q

what is the function of T lymphocytes?

A

T lymphocytes kill virus infected cells & regulate the activities of other white blood cells

50
Q

what is the most frequent leukocyte in the remodelling phase?

A

T cells

51
Q

what are chemokines important for?

A

lymphocyte chemotaxis & function

52
Q

what is the role of mast cells in inflammation?

A

source of pro-inflammatory mediators and cytokines that promote inflammation and vascular changes important in tissue repair

Important cell in secretion of histamine

53
Q

where are mast cells found?

A

within the connective tissue

54
Q

what do mast cells rely on?

A

heavily on degranulation

55
Q

what is degranulation?

A

secretion of stored vesicles/granules into the extracellular space

56
Q

what is the purpose of degranulation?

A

Immune cells use this process to release signaling or effector molecules critical in wound healing

57
Q

what cells are involved in proliferation?

A

fibroblasts

58
Q

what do chemoattractants do?

A

Secrete EMC
Collagen
Elastin
Fibronectin

59
Q

what is the role of the matrix scaffold?

A

Communication between fibroblasts & ECM

60
Q

what happens in proliferation - angiogenesis?

A 
Fragmentation of basement membrane
Migration of endothelial cells
Proliferation
Capillary tube formation
Granulation tissue
61
Q

what happens in epithelialisation?

A 
Detachment of basal keratinocytes
Migration
Proliferation
Differentiation
New epithelium has fewer basal cells, lacks rete pegs and more susceptible to malignant transformation
62
Q

when does maturation and remodelling start?

A

commences when the wound is closed

63
Q

when does maturation and remodelling end?

A

when scar is remodelled

64
Q

how long can the maturation and remodelling phase last?

A

up to 2 years

65
Q

what decreases after the remodelling phase?

A

cellularity

vascularity

66
Q

how much of the original tensile strength is left after remodelling?

A

80%

67
Q

what happens during maturation and remodelling?

A

Collagen synthesis-lysis balance
Collagenases, proteolytic enzymes, metalloproteases [MMPs]
Maturation of collagen fibers by cross-linking
Increased tensile strength

68
Q

what is granulation tissue replaced by during remodelling?

A

mature connective tissue

69
Q

what is fibronectin and type 3 collagen replaced by during remodelling?

A

type 1 collagen

70
Q

why do embryos heal without scarring?

A

high levels of TGF-b-3

71
Q

what is the difference between an embryonic wound and an adult wound?

A

Adult wounds have low levels of TGF-b-3 and high levels of TGF-b-1 & TGF-b-2
whereas embryos have high levels of TGF-b-3

72
Q

what are examples of excess degradation of ECM?

A 
Chronic wounds
Dermal photoaging
Atherosclerosis
Rheumatoid arthritis
Cancer invasion
Metastasis
73
Q

why does inflammation continue in chronic wounds?

A
  • neutrophils remain overactive

- proteases break down new tissue and destroy growth factors

74
Q

what leads to chronic, non-healing wounds?

A

loss of regulation of Co-ordinated breakdown, synthesis & remodelling of ECM

75
Q

why might ulcers fail remain in chronic inflammatory phase?

A

tissue hypoxia
bacterial components
foreign bodies
necrotic tissue

76
Q

which MMPs are high in chronic dermal wounds?

A

MMP-2, MMP-9

77
Q

what is the link between diabetes and TGF-b?

A

Plasma glucose concentrations modulate TGF-b

78
Q

what is the relationship between chronic wounds and proteases?

A

Unbalanced proteolytic activity

79
Q

what are MMPs?

A
  • matrix metalloproteases

Zinc-dependent endopeptidases

80
Q

what are the 4 subdivisions of MMPs?

A

Collagenases (collagen)
Stromelysin (b.mem, laminin, fibronectin)
Gelatinases (elastin)
Membrane-type (MT-MMP)

81
Q

what happens to the concentrations of MMP in normal tissues?

A

they are expressed at low levels

82
Q

when is production of MMPs increased?

A

Production & activation increased when tissue remodelling required

83
Q

which MMPs are collagenases?

A

MMP-1

MMP-8

84
Q

which MMPs are gelatinises?

A

MMP-2

MMP-9

85
Q

which MMPs are stromelysins?

A

MMP-3
MMP-10
MMP-11

86
Q

what are TIMPs?

A

tissue inhibitors of metalloproteinases

87
Q

how are TIMPs controlled?

A

down regulated by proinflammatory cytokines

88
Q

when are TIMPs produced?

A

excess of MMP activity

89
Q

what happens when TIMPs are produced?

A

Mediators crucial for repair are degraded & inactivated by wound proteases
Fibronectin
PDGF
VEGF

90
Q

what are a source of ROS in chronic wounds?

A

Neutrophils & senescent fibroblasts

91
Q

what are the impacts of ROS’?

A

Damage cell membranes & structural proteins (ECM)

Affect signalling pathways - activation of transcription factors control:
proinflammatory cytokines (IL-1,-6, TFN-a)
Proteolytic enzymes (MMPs)
92
Q

what is a consequence of ROS?

A

Disturbed oxidant/antioxidant balance – amplifies persistent inflammatory state of chronic wounds

93
Q

what are biofilms?

A

bacterial communities surrounded by polysaccharide matrix

94
Q

why are chronic wounds an ideal environment for biofilms?

A

Wound remains open for a prolonged period of time - increasing odds of bacterial infection
Wound bed provides surface for growth
Poor blood flow & hypoxia discourage native defences
Wounds inoculated with bacteria form biofilms

95
Q

what are some characteristics of biofilms?

A

Often polymicrobial and resistant to antimicrobials

96
Q

true or false - chronic wounds are a risk for neoplastic progression

A

true

97
Q

when is the incidence of squamous cell carcinoma increased?

A

in chronic leg ulcers

98
Q

what are malignant progressions in chronic wounds associated with?

A

changes in MMPs
Increase in MMPs 7, 12 & 13
Decrease in MMP 19

Pathology (17 decks)

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