Inflammation and wound healing (year 2) Flashcards
1
Q
what is inflammation?
A
response to injury as part of the immune response causing swelling and a leukocyte response
2
Q
what injuries may causes inflammation?
A
infectious agents, mechanical trauma, heat, radiation, cancer, necrotic cells
3
Q
what are the classic signs of inflammation?
A
heat redness swelling pain loss of function
4
Q
why does the inflammatory response occur?
A
it is a protective response to try and eliminate the initial cause and consequences of cell injury
5
Q
what accumulates in the extravascular system during inflammation?
A
leukocytes (white blood cells) and fluid
6
Q
is inflammation always good?
A
no it can be harmful
7
Q
the fluid involved in inflammation is plasma which includes proteins, name some of these proteins
A
clotting factors, fibrinogen, bradykinin, complement components
8
Q
name the leukocytes that may be present during inflammation
A
neutrophils eosinophils basophils monocytes lymphocytes
9
Q
what are the polymorphonuclear leukocytes?
A
neutrophils, eosinophils and basophils
10
Q
what colour do neutrophils stain in H&E?
A
neither blue or pink (neutral)
11
Q
what colour do eosinophils stain in H&E?
A
pink
12
Q
what shape are the nuclei of mononuclear cells?
A
round
13
Q
name the mononuclear cells
A
lymphocytes
monocyte (in circulation) and macrophage (in tissue)
14
Q
what are the 4 important components/cells of inflammation?
A
plasma, circulating cells, endothelial cells, cells and extracellular matrix
15
Q
what are the cells in the extracellular matrix?
A
mast cells, fibroblasts, resident macrophages and lymphocytes
16
Q
what are the components of the extracellular matrix?
A
structural fibres - collagen
adhesive glycoproteins
proteoglycans
17
Q
what are the functions of the extracellular matrix?
A
sequestration of water
reservoir for growth factors
substratum for cells to adhere to, grow and proliferate within
18
Q
define acute inflammation with its main characteristics
A
short durations characterised by oedema and neutrophils
19
Q
define chronic inflammation and its main characteristics
A
longer duration characterised by macrophages, lymphocytes, fibrosis, proliferation of blood vessels and necrosis
20
Q
define exudation
A
escape of fluid, proteins and blood cells from the vascular system into interstitial tissues or body cavities
21
Q
define transudation
A
escape of just fluid from the vascular system into the interstitial tissues or body cavity
22
Q
how do transudates and exudates appear?
A
transudate - clear or lightly coloured
exudate - turbid to opaque with variable colour
23
Q
what is oedema?
A
excess of fluid in interstitial tissue or in serous cavities
24
Q
what is pus?
A
inflammatory exudate rich in leukocytes (neutrophils) and cell debris
25
acute inflammation is dominated by vascular changes, what are these?
alterations in vascular flow (increased blood flow)
structural changes in the microvasculature (leakage of plasma and proteins)
emigration of leukocytes from microcirculation
26
what specific vascular changes occur during acute inflammation?
vasodilation
| stasis - slowing of flow
27
why does stasis occur during acute inflammation?
loss of fluid and increased blood viscosity
28
what are the three causes of increased vascular permeability?
endothelium-mediated vascular leakage
protein leakage from venules
increased hydrostatic pressure in capillary beds
29
what causes endothelium mediated vascular leakage?
chemical mediators such as histamines causing endothelial contraction
cytokines and hypoxia causing endothelial retraction
severe burns of lytic bacterial infections causing necrosis
activation of adherent leukocytes releasing toxic oxygen species and enzymes
30
what happens to leukocytes in normal laminar blood flow?
circulating leukocytes can roll on endothelial cells but won't attach
31
what happens to leukocytes during stasis and vasodilation?
come into contact with the endothelial cells more so more chance to attach and send signals
32
what are the 5 stages of extravasation?
```
rolling
activation
adherence
transmigration
migration
```
33
what is the rolling stage of extravasation?
leukocytes role along the endothelium
34
what is the activation stage of extravasation?
leukocytes are activated
35
what is the adherence stage of extravasation?
leukocytes stably adhere to endothelium
36
what is the transmigration stage of extravasation?
leukocytes moves through the vessel wall
37
what is the migration stage of extravasation?
leukocytes migrate in interstitial fluid towards chemotactic stimuli
38
what are the two components that facilitate the interaction between white blood cells and endothelial cells?
selectins and integrins
39
what does the type of emigrating leukocyte depend on?
age of inflammatory lesion and type of injury/stimuli
40
usually in the first 6-24 hours what leukocyte is predominantly filtered?
neutrophils
41
usually in the 24-48 hour period after the stimuli of inflammation what leukocyte is predominantly filtered?
macrophages
42
what is the change of leukocyte secretion during inflammation due to?
changes to adhesion molecules and chemokine patterns
| short life of neutrophils
43
define chemotaxis
movement of cells directed by a chemical gradient, move towards area of greatest concentration
44
what are chemokines?
small proteins produced by almost all cells
45
what are the effects of chemokines?
chemotaxis, angiogenesis, collagen production
46
when leukocytes arrive at their destination what is their role?
phagocytosis
47
what are the three steps of phagocytosis?
recognition and attachment
engulfment
killing/degredation
48
what happens during engulfment during phagocytosis?
foreign body is enclosed within a phagosome their is then fusion of the lysosome forming a phagolysosome and finally degranulation of lysosomal granules
49
what are some things that may go wrong during killing/degradation that could cause further tissue injury?
regurgitation during feeding
frustrated phagocytosis
exocytosis of granules
50
what are chemical mediators of inflammation?
substances that initiate and regulate the inflammatory response
51
where can chemical mediators of inflammation derive from?
plasma or cells
52
what are the features of chemical mediators of inflammation?
usually bind specifically to receptors
| have direct enzymatic activity or mediate oxidative damage
53
name some chemical mediators of inflammation
histamine, serotonin, prostaglandins, cytokines, kinins, complement
54
where is arachidonic acid found?
cell membrane phospholipids
55
what is the function of arachidonic acid metabolites?
short lived hormones that mediate all the steps of inflammation
56
what are the systemic effects of acute inflammation?
```
pyrexia
lethargy
increased BP
shivering
redirecting blood
```
57
what causes the systemic effects of acute inflammation?
acute phase proteins
58
what are the four possibilities for the outcome of inflammation?
complete resolution
progression to chronic inflammation
healing by fibrosis
abscess formation
59
what is the best outcome of acute inflammation?
complete resolution meaning return to normal function
60
what must occur for complete resolution of acute inflammation?
```
return to normal vascular permeability
drainage of fluid/proteins
drainage of macrophages
phagocytosis of degenerate neutrophils
phagocytosis of necrotic debris by macrophages
disposal of macrophages
```
61
under what specific circumstances may chronic inflammation develop from acute?
persistant infection - parasites and mycobacterium
prolonged irritation - foreign bodies and toxins
cellular immune response - autoimmunity or viral infection
62
several process occur during chronic inflammation, what are these?
active inflammation
tissue destruction
regeneration or repair
63
what cells dominate during active inflammation?
mononuclear - macrophages, leukocyte, plasma cells
64
what happens during regeneration/repair during chronic inflammation?
connective tissue replaces damaged tissue
angiogenesis
fibrosis
65
what are the cells of chronic inflammation?
macrophages
66
what roles do macrophages have during chronic inflammation?
```
phagocytosis
antigen presentation (MHC II)
secretes proinflammatories, procoagulants, enzymes
wound healing
regulates ,monocytes and granulocytes
```
67
are neutrophils and macrophages undergo cell division?
neutrophils - no
| macrophages - mitotically active
68
other than macrophages, what cells are seen during chronic inflammation?
lymphocytes, plasma cells, mast cells/eosinophils (parasitic infection)
69
what is a plasma cell?
a B lymphocyte that has been triggered by an antigen to produce antibody
70
tissue destruction occurs in chronic inflammation induced by leukocytes, what ways does this cause damage?
lysosomal enzymes
oxygen-derived active metabolites
products of arachidonic acid metabolism
71
when does regeneration and repair occur in chronic inflammation?
regeneration - mild superficial injury
| repair - severe injury repaired to a scar
72
what is the aim of regeneration/repair?
restore anatomical and functional integrity
73
what is the key deciding factor for whether you get regeneration or repair?
regeneration - leaves tissue framework intact
| repair - damage to tissue framework
74
what factor plays a role in deciding if regeneration or repair occurs?
the type of tissue
75
what is a good example of a tissue that is good at regenerating?
skin - rapidly dividing active tissue
76
what are continuously dividing cells known as?
labile cells such as epidermis
77
what is regeneration induced by?
growth factors that initiate signalling pathways influencing the cell cycle
78
what is fibrosis?
deposition of collagen fibres as an attempt to replace lost tissue by fibrosis
79
when will fibrosis occur?
when there has been tissue damage to both parenchymal cells and stromal framework
80
what is fibrosis also known as?
scaring
81
what is the beginning stage of fibrosis?
formation of granulation tissue
82
how long after injury does granulation tissue begin to form?
24 hours - initial fibrin framework
83
what does granulation tissue contain?
new blood vessels and proliferating fibroblasts
84
describe the process of angiogenesis
degradation of basement membrane
migration of endothelial cells
proliferation of endothelial cells
recruitment of periendothelial cells
85
eventually tissue remodelling occurs, what is the granulation tissue replaced by and what does this involve?
scar
| involves alteration to the composition of the extracellular matrix
86
what is an abscess?
suppurative (neutrophil dominated) inflammation buried in a tissue or confined space, created by necrosis
87
what can cause necrosis of tissue?
reduced perfusion or bacterial toxins
88
what is the most common cause of abscesses?
bacteria
89
why are abscesses difficult to treat with antibiotics?
poor blood supply
90
what does wound healing involve?
```
acute inflammation
regeneration
extracellular matrix synthesis
remodelling of connective tissue
collagenisation
```
91
what stimulates wound healing?
```
acute inflammation mediators
growth factors
cell-ECM interaction
angiogenesis
fibrosis
```
92
what is healing by first intention?
wounds with opposed edges (surgical wound)
93
what is healing by second intention?
when there is a deficit in the skin
94
give examples of healing by second intention
infarction, abscess, ulceration
95
what factors effect wound healing?
systemic - nutritional and hormonal
| local - foreign material, poor perfusion, size and type of wound, infection, movement
96
what are some abnormalities of wound healing?
wound dehiscence
ulceration
excessive formation of repair components (exuberant granulation tissue
contraction
97
what is wound dehiscence?
the edges of the wound don't meet
98
what are the 5 parts of a morphological diagnosis of inflammation?
```
degree
duration
distribution
type of inflammation
organ-itis
```
99
what are the ways of classifying the degree of inflammation?
mild, moderate, severe
100
what are the three ways of describing the duration of the lesion?
acute, subacute, chronic
101
what are the four ways of describing the distribution of the lesion?
focal, multifocal, disseminated, diffuse
102
how is a lesion with the duration of a few hours to days described?
acute
103
how is a lesion with the duration of a few to many days described?
subacute
104
what does a focal lesion mean?
just one area affected
105
what does a diffuse lesion mean?
whole organ is affected
106
what does a multifocal lesion mean?
multiple small lesions
107
what does a locally extensive lesion mean?
one large area is affected
108
what is a disseminate lesion?
whole organ affected but only by small lesions
109
what words can be used to describe the type of inflammation?
this describes the exudate
| serous, fibrinous, suppurative, haemorrhage, necrotising, necrohaemorrhagic
110
what is a serous exudate?
think of serum
outpouring of thin fluid (transudate)
seen in blisters and other serous/mucosal surfaces
111
what is a fibrinous exudate?
serum and proteins, this leads to a clotted exudate found on serosal and mucosal surfaces
112
what is a suppurative/purulent exudate?
dominated by neutrophils
| is a pus formed from necrotic tissue, neutrophils and fibrin
113
what is the prefix used for accumulation of pus?
pyo-
114
what is a pustule?
pus within the dermis/epidermis
115
what is an empyema?
pus within a pre-existing space
116
what is an abscess?
pus within a cavity which has developed due to tissue necrosis
117
what is a haemorrhage exudate?
dominated by blood due to severe damage of blood vessels
118
what is a necrotising inflammation?
exudation and severe tissue necrosis, often associated with ulcers
119
what is chronic active inflammation?
low level inflammation that has acute flair ups
120
what cells dominate granulomatous inflammation?
macrophages
121
what is an ulcer?
focal full-thickness defect in the epithelium surface or an organ/tissue
