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Pathology and Immunity > Inflammation > Flashcards

Inflammation Flashcards

1
Q

what are particulate materials

A

these are any materials in the body that should not be there
this includes denture material

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2
Q

what are altered self cells

A

host cells that are damaged and undergoing apoptosis, or cells that are malignant

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3
Q

what is the key incitive for acute inflammation

A

microbial infection

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3
Q

describe the onset of acute inflammation

A

it is rapid and localised to specific tissues
involves the innate immune system only and the tissue is repaired afterward

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4
Q

what does de novo mean

A

spontaneous - occurs without reason

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5
Q

describe the onset of chronic inflammation

A

they are long term and are characterised by persistent bouts of inflammation.
involves the adaptive immune cells, and can impact many areas in the body
no tissue repair

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6
Q

what are chronic inflammatory diseases often associated with

A

no resolution of disease and therefore tissue damage

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7
Q

what are the three main processes involved in acute inflammation

A

vascular dilation
increased vascular permeability
neutrophil activation and migration

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8
Q

what initiates innate immunity

A

acute inflammation

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9
Q

which form of inflammation involves t cells and b cells

A

chronic inflammation

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10
Q

what are the four main causes of acute inflammation

A

microbial infection
physical agents
irritant and corrosive chemicals
tissue necrosis

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11
Q

describe microbial infection

A

this is a response resulting from microbial recognition

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11
Q

what are physical agents that can lead to acute inflammation

A

physical trauma
ultraviolent or other ionising radiation
heat from burns
cold from frostbite

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12
Q

what are irritants and corrosive chemicals that can lead to acute inflammation

A

acids alkali and oxidising agents
microbial virulence factors

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13
Q

how can tissue necrosis lead to acute inflammation

A

lack of oxygen or nutrients due to inadequate blood flow

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14
Q

what is infarction

A

inadequate blood flow

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15
Q

what are the cardinal signs of inflammation

A

rubor
calor
tumor
dolor
loss of function

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16
Q

who derived the five cardinal signs of inflammation

A

celsus

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17
Q

describe rubor

A

this is redness, and is caused by the dilation of small blood vessels

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18
Q

describe calor

A

this is heat, and is caused by increased blood flow

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19
Q

what is hyperaemia

A

increased blood flow increasing the heat of the skin

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20
Q

describe tumour

A

this is swelling and is caused by an accumulation of fluid in the extravascular space

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20
Q

describe dolor

A

this is stretching and distortion of the tissues due to oedema
chemical mediators induce pain

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21
Q

what are the stages of inflammation

A

initiation
progression
amplification
resolution
no resolution

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22
Q

describe initiation of inflammation

A

microbes in the dental plaque are recognised by gingival epithelial cells via pattern recognition receptors

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23
Q

describe progression of inflammation

A

containment of microbes by innate immune cells and antimicrobial compounds

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24
Q

describe amplification of inflammation

A

recruitment and activation of innate immune cells via chemokine activity and vascular dilation

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24
Q

describe resolution of inflammation

A

this is healing and repair and only occurs in acute inflammation

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25
Q

how does amplification of inflammation occur

A

via chemokine and cytokine activity, and through vasodilation

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26
Q

describe the process of how inflammation is amplified

A
  • cytokines and chemokines are produced by macrophages
  • in response to microbes
  • vasodilation allows an increase in passage of fluid and cells
  • cells and fluid will resolve inflammation
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27
Q

explain the vascular response to inflammation

A

small blood vessels adjacent to the site of infection become dilated
endothelial cells will swell and tract
exudation

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28
Q

what is exudation

A

the vessels become leaky and allow passage of water, salts and some proteins

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29
Q

how does permeability of blood vessels change during inflammation

A

the endothelial cells swell and retract to get larger and more porous

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30
Q

what is provided to tissue from the inflammatory exudate

A
  • fluids and salt
  • glucose and oxygen
  • complement proteins and antibodies
  • fibrin
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31
Q

what is fibrin

A

long insoluble filamentous protein

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32
Q

what is the function of the fluid and salt in inflammatory tissue oedema

A

they dilate any toxins from the microbes

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33
Q

why are glucose and oxygen in the inflammatory oedema

A

they are there to support the immune cells and the inflammatory response

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34
Q

what are the soluble mediators that are released into inflammatory oedema

A

proteins and cytokines
antibodies for chronic inflammation

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35
Q

what is the main component of blood clots

A

fibrin

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36
Q

what are some chemical mediators

A

histamine
bradykinin
prostaglandins

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37
Q

what are some protein mediators

A

cytokines and chemokines

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38
Q

which chemical mediators lead to vascular dilation

A

histamine
prostaglandins
VIP
nitric oxide
PAF

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39
Q

what does histamine do

A

vascular dilation and the transient phase of vascular permeability

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40
Q

what does upregulation of adhesion molecules on the endothelium allow for

A

the adhesion of leukocytes to the endothelium

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41
Q

which mediators causes neutrophil polymorph chemotaxis

A

leucotrienes B4 and Il8

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42
Q

what regulates the process of inflammation

A

chemical and protein mediators

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43
Q

what produces histamine

A

the breakdown of histidine

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44
Q

where is histamine stored

A

granules of immune cells such as mast cells

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45
Q

describe the roles of histamine

A

neurotransmitter for itching
vascular dilation

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46
Q

do many immune cells express histmine receptors

A

yes

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47
Q

which cells produces prostaglandins

A

macrophages and neutrophils with leukotrienes
fatty acid metabolism

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48
Q

what do prostaglandins do

A

cause vascular dilation
regulate cytokine production
regulate cell recruitment
act on nerve fibres
involved in tissue remodelling

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49
Q

what is the most abundant prostalglandin

A

PGE2

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50
Q

what is the enzyme that regulates prostaglandin production

A

cyclo oxygenase II

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51
Q

what is tissue resolution

A

process that functions to provide tissue with necessary tools to eliminate inciting cause and repair any damage

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52
Q

how can all immune responses for inflammation be described as

A

proteolytic cascades

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53
Q

what are the four enzymatic cascades involved in acute inflammation

A

complement
kinin system
coagulation
fibrinolytic system

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54
Q

what are the three pathways for the complement system

A

classical
alternative
mannose binding lectin pathway

55
Q

what is the initiating factor for classical pathways for complement

A

antibody attached to a microbe

56
Q

what is the initiation for the alternative pathway of the complement system

A

microbial cell wall

57
Q

what is the initiating factor for the mannose binding lectin pathway in the complement system

A

carbohydrates on the pathogen surface

58
Q

which molecules are involved in the kinin system

A

plasma proteins and enzymes

59
Q

what is coagulation factor XII

A

hageman factor

60
Q

what is the role of kallikrein

A

convert kininogens to kinins

61
Q

what is the most common kinin

A

bradykinin

62
Q

what are the three pathways for the coagulation system

A

intrinsic
extrinsic
common

63
Q

what is the intrinsic coagulation pathway

A

activated when blood comes into contact with sub endothelial connective tissues (outside blood vessel)

64
Q

what is the extrinsic coagulation pathway

A

damaged blood vessel leads to human factor 7 leaving the vessel and encountering tissue factors in surrounding tissue

65
Q

what is the common pathway for coagulation system

A

production of thrombin which in turn produces fibrin for clot formation

66
Q

what does the fibrinolytic system activate

A

plasmin

67
Q

what is the fibrinolytic systems role in vascular permeability

A

it is indirect as the products of fibrin degradation promote the permeability

68
Q

what is an example of a thrombolytic drug

A

urokinase

69
Q

what is haemostasis the balance between

A

the coagulation and the fibrinolytic system

haemostasis is stopping the flow of blood

70
Q

what can bleeding to death result from

A

trauma
major surgery
hemophilia

71
Q

what can clotting to death result from

A

stroke
thrombosis
MI

72
Q

what are some congenital coagulation disorders

A

von willebrand disease
haemophilia A
haemophili B

73
Q

what are some anticoagulant drugs

A

warfarin
heparin

74
Q

what does the complement system lead to

A

membrane attack complex formation
anaphylatoxin production

75
Q

what does the kinin system produce

A

bradykinins

76
Q

what does coagulation produce

A

stable blood clots from fibrin

77
Q

how does plasmin prevent excessive clotting

A

it degrades fibrin

78
Q

what is suppuration

A

abscess formation, an outcome from acute inflammation which can lead to chronic inflammation

79
Q

what is the transfer of acute to chronic inflammation dependent on

A

tissue involved
amount of tissue destruction
nature of the harmful agent

80
Q

what are the three types of dental abscess

A

gingival
periodontal
periapical

81
Q

what is a gingival abscess

A

an abscess formed due to infection or trauma to the surface of the gum tissue

82
Q

what is a periodontal abscess

A

forms due to an infection that has moved deeper into the gum areas

83
Q

what is a periapical abscess

A

abscess of a tooth due to infection of the pulp

84
Q

what is a key factor for suppuration

A

neutrophil infiltration

85
Q

what is pus

A

bacteria with dead and dying neutrophils

86
Q

what surrounds accumulating pus

A

pyogenic membrane

87
Q

why do abscesses form to prevent further infection

A

the bacteria within the abscess is fairly inaccessible so this prevents spreading of the infection

88
Q

describe resolution in acute inflammation

A

this is the complete restoration of tissues after an episode of acute inflammation

89
Q

what does tissue restoration after inflammation require

A
  • minimal cell death and tissue damage
  • occurrence in tissues with regenerative capacity (ie not teeth)
  • rapid elimination of causative agent
  • rapid removal of fluid and debris by vascular/lymphatic drainage
90
Q

what is the most common outcome of acute inflammation

A

resolution

91
Q

what are inflammatory reactions aimed for

A

eliminating the inciting cause

92
Q

what are the inciting causes of inflammation

A

invading microorganisms
particulate materials
altered self cells
transformed malignant cells

93
Q

what is acute inflammation a response to

A

infection or damage

94
Q

how can chronic inflammation arise from acute inflammation

A

due to persistent exposure to the causes of acute inflammation
can also arise de novo

95
Q

what is swelling defined as

A

an excess of watery fluid collecting in the tissues of the body
increased blood and lymph flow

96
Q

which cardinal sign of infection involves mediator release

A

dolor, pain

97
Q

histamine is released via what process

A

degranulation

98
Q

another flashcard asking you to name the roles of histamine!!

A

vasodilation
increased vascular permeability
smooth muscle contraction
bronchoconstriction
neurotransmission

99
Q

what does arachidonic acid produce

A

leukotrienes and prostaglandins

100
Q

how are the enzymatic cascades for acute inflammation linked together

A

they are all driven or stimulated by an enzyme that circulates in the blood called the hageman factor which activates systems in addition to the complement system

101
Q

what is hageman factor

A

a serine protease found circulating inactive in the blood
it can activate the classical complement pathway both directly and indirectly

102
Q

how does hageman factor directly activate the complement pathway

A

by promoting the formation of the antibody complex

103
Q

how can hageman factor indirectly activate the complement pathway

A

through the kinin and fibrinolytic systems

104
Q

what is the main plasma protein involved in the kinin system

A

kallikrein

105
Q

what are the two main molecules involved in the kinin system

A

kallikrein and neutrophils

106
Q

what does kallikrein do in the kinin system

A

it converts kininogens to kinins

107
Q

what is contacted in the intrinsic coagulation system

A

collagen

108
Q

what does the final coagulation pathway drive

A

the formation of the stable blood clot through the production of fibrin

109
Q

what do the intrinsic and extrinsic coagulation pathways converge to form

A

the common pathway to form the stable bloot clot through the action of thrombin

110
Q

what drives intrinsic coagulation

A

internatal trauma like non functioning endothelial cells
coagulation drives repair of the vessels

111
Q

what drives extrinsic coagulation

A

external trauma where there is a major change in the vasculature of the human body where there is excessive bleeding either out of or into a tissue

112
Q

which process activates plasmin

A

the fibrinolytic system

113
Q

how does the fibrinolytic system activate the complement system

A

plasmin cleaves C3 component protein

114
Q

what converts plasminogen into plasmin

A

kallikrein and hageman factor

115
Q

who are thrombolytic drugs given to

A

people who struggle to break down excessive clots on their own

116
Q

what does plasmin degrade

A

fibrin

117
Q

how do thrombolytic drugs work

A

they promote the activity of antithrombin which targets the thrombin enzyme which drives the formation of a stable clot

118
Q

what are some acute inflammatory diseases linked to dentistry

A

gingivitis
abscess formation
pericoronitis
angular cheilitis
ludwigs angina

119
Q

what are the two major acute inflammatory diseases in the oral environment

A

abscess formation and gingivitis

120
Q

what is a pyogenic membrane

A

this is a component of granulation tissue which is involved in tissue repair

121
Q

what are the two classes of chronic inflammation

A

non specific and specific

122
Q

what characterises non specific chronic inflammation

A

persistent acute inflammation and excessive suppuration

123
Q

what characterises specific chronic inflammation

A

arises de novo
persisent exposure to agent
can be granulomatous

124
Q

what infiltrates tissues during a non specific chronic inflammatory resopnse

A

tissue macrophages
t cells
b cells
more adaptive immune cells

125
Q

what does periodontitis lead from

A

persistent bouts of gingivitis

126
Q

what induces a specific chronic inflammatory response

A

non immunological or immunological agents

127
Q

what does granulomatous mean

A

involving the formation of granulomas

128
Q

which type of inflammation is characterisde by excessively activated tissue macrophages

A

specific chronic inflammation

129
Q

is there any warning for the manifestation of specific chronic inflammation

A

no

130
Q

what can cause a resistance of infective agent to phagocytes and intracellular killing leading to inflammation

A

tuberculosis
leprosy
viral infections

131
Q

what are some endogenonus materials that cause inflammation

A

nectrotic adipose tissue
bone
uric acid crystals

132
Q

what are some exogenous materials

A

silica
asbestos fibres
suture materials
implanted prosthetics

133
Q

what are some autoimmune diseases that cause inflammation

A

hashimotos
chronic gastritis
rheumatoid arthritis
hypersensitivity reactions

134
Q

what are some primary granulomatous diseases that cause inflammation

A

crohns disease
sarcoidosis

135
Q

describe rheumatiod arthritis pathogenesis

A

loss of tolerance to citrullinated proteins in synovial fluid

136
Q

describe sjogrens syndrome

A

host t and b cells attach the cells of the salivary and lacrimal glands

137
Q

explaoin peptide citrullination in rheumatoid arthritis

A

proteins and peptides within the host change from arginine to citrulline. this usually happens but sometimes PAD enzymes will accelerate it. because the b and t cells see them as a threat because citrulline is not found naturally in the body, and this leads to destruction of those cells

138
Q

describe orofacial granulomatosis

A

this is characterised by excessively activated tissue macrophages called epithelioid macrophages that fuse to form giant cells
they form in soft tissue

139
Q

why is there a rippled appearance in orofacial granulomatosis

A

lots of macrophages fuse together and cause ripples in a particular tissue

Pathology and Immunity (16 decks)

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