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Pathology > Inflammation and wound healing (year 2) > Flashcards

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

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2
Q

what injuries may causes inflammation?

A

infectious agents, mechanical trauma, heat, radiation, cancer, necrotic cells

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3
Q

what are the classic signs of inflammation?

A 
heat
redness
swelling
pain
loss of function
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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

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5
Q

what accumulates in the extravascular system during inflammation?

A

leukocytes (white blood cells) and fluid

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6
Q

is inflammation always good?

A

no it can be harmful

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7
Q

the fluid involved in inflammation is plasma which includes proteins, name some of these proteins

A

clotting factors, fibrinogen, bradykinin, complement components

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8
Q

name the leukocytes that may be present during inflammation

A 
neutrophils
eosinophils
basophils
monocytes
lymphocytes
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9
Q

what are the polymorphonuclear leukocytes?

A

neutrophils, eosinophils and basophils

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10
Q

what colour do neutrophils stain in H&E?

A

neither blue or pink (neutral)

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11
Q

what colour do eosinophils stain in H&E?

A

pink

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12
Q

what shape are the nuclei of mononuclear cells?

A

round

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13
Q

name the mononuclear cells

A

lymphocytes

monocyte (in circulation) and macrophage (in tissue)

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14
Q

what are the 4 important components/cells of inflammation?

A

plasma, circulating cells, endothelial cells, cells and extracellular matrix

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15
Q

what are the cells in the extracellular matrix?

A

mast cells, fibroblasts, resident macrophages and lymphocytes

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16
Q

what are the components of the extracellular matrix?

A

structural fibres - collagen
adhesive glycoproteins
proteoglycans

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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

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18
Q

define acute inflammation with its main characteristics

A

short durations characterised by oedema and neutrophils

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19
Q

define chronic inflammation and its main characteristics

A

longer duration characterised by macrophages, lymphocytes, fibrosis, proliferation of blood vessels and necrosis

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20
Q

define exudation

A

escape of fluid, proteins and blood cells from the vascular system into interstitial tissues or body cavities

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21
Q

define transudation

A

escape of just fluid from the vascular system into the interstitial tissues or body cavity

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22
Q

how do transudates and exudates appear?

A

transudate - clear or lightly coloured

exudate - turbid to opaque with variable colour

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23
Q

what is oedema?

A

excess of fluid in interstitial tissue or in serous cavities

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24
Q

what is pus?

A

inflammatory exudate rich in leukocytes (neutrophils) and cell debris

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25
Q

acute inflammation is dominated by vascular changes, what are these?

A

alterations in vascular flow (increased blood flow)
structural changes in the microvasculature (leakage of plasma and proteins)
emigration of leukocytes from microcirculation

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26
Q

what specific vascular changes occur during acute inflammation?

A

vasodilation

stasis - slowing of flow

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27
Q

why does stasis occur during acute inflammation?

A

loss of fluid and increased blood viscosity

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28
Q

what are the three causes of increased vascular permeability?

A

endothelium-mediated vascular leakage
protein leakage from venules
increased hydrostatic pressure in capillary beds

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29
Q

what causes endothelium mediated vascular leakage?

A

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

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30
Q

what happens to leukocytes in normal laminar blood flow?

A

circulating leukocytes can roll on endothelial cells but won’t attach

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31
Q

what happens to leukocytes during stasis and vasodilation?

A

come into contact with the endothelial cells more so more chance to attach and send signals

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32
Q

what are the 5 stages of extravasation?

A 
rolling
activation
adherence
transmigration
migration
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33
Q

what is the rolling stage of extravasation?

A

leukocytes role along the endothelium

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34
Q

what is the activation stage of extravasation?

A

leukocytes are activated

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35
Q

what is the adherence stage of extravasation?

A

leukocytes stably adhere to endothelium

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36
Q

what is the transmigration stage of extravasation?

A

leukocytes moves through the vessel wall

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37
Q

what is the migration stage of extravasation?

A

leukocytes migrate in interstitial fluid towards chemotactic stimuli

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38
Q

what are the two components that facilitate the interaction between white blood cells and endothelial cells?

A

selectins and integrins

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39
Q

what does the type of emigrating leukocyte depend on?

A

age of inflammatory lesion and type of injury/stimuli

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40
Q

usually in the first 6-24 hours what leukocyte is predominantly filtered?

A

neutrophils

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41
Q

usually in the 24-48 hour period after the stimuli of inflammation what leukocyte is predominantly filtered?

A

macrophages

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42
Q

what is the change of leukocyte secretion during inflammation due to?

A

changes to adhesion molecules and chemokine patterns

short life of neutrophils

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43
Q

define chemotaxis

A

movement of cells directed by a chemical gradient, move towards area of greatest concentration

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44
Q

what are chemokines?

A

small proteins produced by almost all cells

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45
Q

what are the effects of chemokines?

A

chemotaxis, angiogenesis, collagen production

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46
Q

when leukocytes arrive at their destination what is their role?

A

phagocytosis

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47
Q

what are the three steps of phagocytosis?

A

recognition and attachment
engulfment
killing/degredation

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48
Q

what happens during engulfment during phagocytosis?

A

foreign body is enclosed within a phagosome their is then fusion of the lysosome forming a phagolysosome and finally degranulation of lysosomal granules

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49
Q

what are some things that may go wrong during killing/degradation that could cause further tissue injury?

A

regurgitation during feeding
frustrated phagocytosis
exocytosis of granules

50
Q

what are chemical mediators of inflammation?

A

substances that initiate and regulate the inflammatory response

51
Q

where can chemical mediators of inflammation derive from?

A

plasma or cells

52
Q

what are the features of chemical mediators of inflammation?

A

usually bind specifically to receptors

have direct enzymatic activity or mediate oxidative damage

53
Q

name some chemical mediators of inflammation

A

histamine, serotonin, prostaglandins, cytokines, kinins, complement

54
Q

where is arachidonic acid found?

A

cell membrane phospholipids

55
Q

what is the function of arachidonic acid metabolites?

A

short lived hormones that mediate all the steps of inflammation

56
Q

what are the systemic effects of acute inflammation?

A 
pyrexia
lethargy
increased BP
shivering
redirecting blood
57
Q

what causes the systemic effects of acute inflammation?

A

acute phase proteins

58
Q

what are the four possibilities for the outcome of inflammation?

A

complete resolution
progression to chronic inflammation
healing by fibrosis
abscess formation

59
Q

what is the best outcome of acute inflammation?

A

complete resolution meaning return to normal function

60
Q

what must occur for complete resolution of acute inflammation?

A 
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
Q

under what specific circumstances may chronic inflammation develop from acute?

A

persistant infection - parasites and mycobacterium
prolonged irritation - foreign bodies and toxins
cellular immune response - autoimmunity or viral infection

62
Q

several process occur during chronic inflammation, what are these?

A

active inflammation
tissue destruction
regeneration or repair

63
Q

what cells dominate during active inflammation?

A

mononuclear - macrophages, leukocyte, plasma cells

64
Q

what happens during regeneration/repair during chronic inflammation?

A

connective tissue replaces damaged tissue
angiogenesis
fibrosis

65
Q

what are the cells of chronic inflammation?

A

macrophages

66
Q

what roles do macrophages have during chronic inflammation?

A 
phagocytosis
antigen presentation (MHC II)
secretes proinflammatories, procoagulants, enzymes
wound healing
regulates ,monocytes and granulocytes
67
Q

are neutrophils and macrophages undergo cell division?

A

neutrophils - no

macrophages - mitotically active

68
Q

other than macrophages, what cells are seen during chronic inflammation?

A

lymphocytes, plasma cells, mast cells/eosinophils (parasitic infection)

69
Q

what is a plasma cell?

A

a B lymphocyte that has been triggered by an antigen to produce antibody

70
Q

tissue destruction occurs in chronic inflammation induced by leukocytes, what ways does this cause damage?

A

lysosomal enzymes
oxygen-derived active metabolites
products of arachidonic acid metabolism

71
Q

when does regeneration and repair occur in chronic inflammation?

A

regeneration - mild superficial injury

repair - severe injury repaired to a scar

72
Q

what is the aim of regeneration/repair?

A

restore anatomical and functional integrity

73
Q

what is the key deciding factor for whether you get regeneration or repair?

A

regeneration - leaves tissue framework intact

repair - damage to tissue framework

74
Q

what factor plays a role in deciding if regeneration or repair occurs?

A

the type of tissue

75
Q

what is a good example of a tissue that is good at regenerating?

A

skin - rapidly dividing active tissue

76
Q

what are continuously dividing cells known as?

A

labile cells such as epidermis

77
Q

what is regeneration induced by?

A

growth factors that initiate signalling pathways influencing the cell cycle

78
Q

what is fibrosis?

A

deposition of collagen fibres as an attempt to replace lost tissue by fibrosis

79
Q

when will fibrosis occur?

A

when there has been tissue damage to both parenchymal cells and stromal framework

80
Q

what is fibrosis also known as?

A

scaring

81
Q

what is the beginning stage of fibrosis?

A

formation of granulation tissue

82
Q

how long after injury does granulation tissue begin to form?

A

24 hours - initial fibrin framework

83
Q

what does granulation tissue contain?

A

new blood vessels and proliferating fibroblasts

84
Q

describe the process of angiogenesis

A

degradation of basement membrane
migration of endothelial cells
proliferation of endothelial cells
recruitment of periendothelial cells

85
Q

eventually tissue remodelling occurs, what is the granulation tissue replaced by and what does this involve?

A

scar

involves alteration to the composition of the extracellular matrix

86
Q

what is an abscess?

A

suppurative (neutrophil dominated) inflammation buried in a tissue or confined space, created by necrosis

87
Q

what can cause necrosis of tissue?

A

reduced perfusion or bacterial toxins

88
Q

what is the most common cause of abscesses?

A

bacteria

89
Q

why are abscesses difficult to treat with antibiotics?

A

poor blood supply

90
Q

what does wound healing involve?

A 
acute inflammation
regeneration
extracellular matrix synthesis
remodelling of connective tissue
collagenisation
91
Q

what stimulates wound healing?

A 
acute inflammation mediators
growth factors
cell-ECM interaction
angiogenesis
fibrosis
92
Q

what is healing by first intention?

A

wounds with opposed edges (surgical wound)

93
Q

what is healing by second intention?

A

when there is a deficit in the skin

94
Q

give examples of healing by second intention

A

infarction, abscess, ulceration

95
Q

what factors effect wound healing?

A

systemic - nutritional and hormonal

local - foreign material, poor perfusion, size and type of wound, infection, movement

96
Q

what are some abnormalities of wound healing?

A

wound dehiscence
ulceration
excessive formation of repair components (exuberant granulation tissue
contraction

97
Q

what is wound dehiscence?

A

the edges of the wound don’t meet

98
Q

what are the 5 parts of a morphological diagnosis of inflammation?

A 
degree
duration
distribution
type of inflammation
organ-itis
99
Q

what are the ways of classifying the degree of inflammation?

A

mild, moderate, severe

100
Q

what are the three ways of describing the duration of the lesion?

A

acute, subacute, chronic

101
Q

what are the four ways of describing the distribution of the lesion?

A

focal, multifocal, disseminated, diffuse

102
Q

how is a lesion with the duration of a few hours to days described?

A

acute

103
Q

how is a lesion with the duration of a few to many days described?

A

subacute

104
Q

what does a focal lesion mean?

A

just one area affected

105
Q

what does a diffuse lesion mean?

A

whole organ is affected

106
Q

what does a multifocal lesion mean?

A

multiple small lesions

107
Q

what does a locally extensive lesion mean?

A

one large area is affected

108
Q

what is a disseminate lesion?

A

whole organ affected but only by small lesions

109
Q

what words can be used to describe the type of inflammation?

A

this describes the exudate

serous, fibrinous, suppurative, haemorrhage, necrotising, necrohaemorrhagic

110
Q

what is a serous exudate?

A

think of serum
outpouring of thin fluid (transudate)
seen in blisters and other serous/mucosal surfaces

111
Q

what is a fibrinous exudate?

A

serum and proteins, this leads to a clotted exudate found on serosal and mucosal surfaces

112
Q

what is a suppurative/purulent exudate?

A

dominated by neutrophils

is a pus formed from necrotic tissue, neutrophils and fibrin

113
Q

what is the prefix used for accumulation of pus?

A

pyo-

114
Q

what is a pustule?

A

pus within the dermis/epidermis

115
Q

what is an empyema?

A

pus within a pre-existing space

116
Q

what is an abscess?

A

pus within a cavity which has developed due to tissue necrosis

117
Q

what is a haemorrhage exudate?

A

dominated by blood due to severe damage of blood vessels

118
Q

what is a necrotising inflammation?

A

exudation and severe tissue necrosis, often associated with ulcers

119
Q

what is chronic active inflammation?

A

low level inflammation that has acute flair ups

120
Q

what cells dominate granulomatous inflammation?

A

macrophages

121
Q

what is an ulcer?

A

focal full-thickness defect in the epithelium surface or an organ/tissue

Pathology (17 decks)

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