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
2
Q
what are altered self cells
A
host cells that are damaged and undergoing apoptosis, or cells that are malignant
3
Q
what is the key incitive for acute inflammation
A
microbial infection
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
4
Q
what does de novo mean
A
spontaneous - occurs without reason
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
6
Q
what are chronic inflammatory diseases often associated with
A
no resolution of disease and therefore tissue damage
7
Q
what are the three main processes involved in acute inflammation
A
vascular dilation
increased vascular permeability
neutrophil activation and migration
8
Q
what initiates innate immunity
A
acute inflammation
9
Q
which form of inflammation involves t cells and b cells
A
chronic inflammation
10
Q
what are the four main causes of acute inflammation
A
microbial infection
physical agents
irritant and corrosive chemicals
tissue necrosis
11
Q
describe microbial infection
A
this is a response resulting from microbial recognition
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
12
Q
what are irritants and corrosive chemicals that can lead to acute inflammation
A
acids alkali and oxidising agents
microbial virulence factors
13
Q
how can tissue necrosis lead to acute inflammation
A
lack of oxygen or nutrients due to inadequate blood flow
14
Q
what is infarction
A
inadequate blood flow
15
Q
what are the cardinal signs of inflammation
A
rubor
calor
tumor
dolor
loss of function
16
Q
who derived the five cardinal signs of inflammation
A
celsus
17
Q
describe rubor
A
this is redness, and is caused by the dilation of small blood vessels
18
Q
describe calor
A
this is heat, and is caused by increased blood flow
19
Q
what is hyperaemia
A
increased blood flow increasing the heat of the skin
20
Q
describe tumour
A
this is swelling and is caused by an accumulation of fluid in the extravascular space
20
Q
describe dolor
A
this is stretching and distortion of the tissues due to oedema
chemical mediators induce pain
21
Q
what are the stages of inflammation
A
initiation
progression
amplification
resolution
no resolution
22
describe initiation of inflammation
microbes in the dental plaque are recognised by gingival epithelial cells via pattern recognition receptors
23
describe progression of inflammation
containment of microbes by innate immune cells and antimicrobial compounds
24
describe amplification of inflammation
recruitment and activation of innate immune cells via chemokine activity and vascular dilation
24
describe resolution of inflammation
this is healing and repair and only occurs in acute inflammation
25
how does amplification of inflammation occur
via chemokine and cytokine activity, and through vasodilation
26
describe the process of how inflammation is amplified
- 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
27
explain the vascular response to inflammation
small blood vessels adjacent to the site of infection become dilated
endothelial cells will swell and tract
exudation
28
what is exudation
the vessels become leaky and allow passage of water, salts and some proteins
29
how does permeability of blood vessels change during inflammation
the endothelial cells swell and retract to get larger and more porous
30
what is provided to tissue from the inflammatory exudate
- fluids and salt
- glucose and oxygen
- complement proteins and antibodies
- fibrin
31
what is fibrin
long insoluble filamentous protein
32
what is the function of the fluid and salt in inflammatory tissue oedema
they dilate any toxins from the microbes
33
why are glucose and oxygen in the inflammatory oedema
they are there to support the immune cells and the inflammatory response
34
what are the soluble mediators that are released into inflammatory oedema
proteins and cytokines
antibodies for chronic inflammation
35
what is the main component of blood clots
fibrin
36
what are some chemical mediators
histamine
bradykinin
prostaglandins
37
what are some protein mediators
cytokines and chemokines
38
which chemical mediators lead to vascular dilation
histamine
prostaglandins
VIP
nitric oxide
PAF
39
what does histamine do
vascular dilation and the transient phase of vascular permeability
40
what does upregulation of adhesion molecules on the endothelium allow for
the adhesion of leukocytes to the endothelium
41
which mediators causes neutrophil polymorph chemotaxis
leucotrienes B4 and Il8
42
what regulates the process of inflammation
chemical and protein mediators
43
what produces histamine
the breakdown of histidine
44
where is histamine stored
granules of immune cells such as mast cells
45
describe the roles of histamine
neurotransmitter for itching
vascular dilation
46
do many immune cells express histmine receptors
yes
47
which cells produces prostaglandins
macrophages and neutrophils with leukotrienes
fatty acid metabolism
48
what do prostaglandins do
cause vascular dilation
regulate cytokine production
regulate cell recruitment
act on nerve fibres
involved in tissue remodelling
49
what is the most abundant prostalglandin
PGE2
50
what is the enzyme that regulates prostaglandin production
cyclo oxygenase II
51
what is tissue resolution
process that functions to provide tissue with necessary tools to eliminate inciting cause and repair any damage
52
how can all immune responses for inflammation be described as
proteolytic cascades
53
what are the four enzymatic cascades involved in acute inflammation
complement
kinin system
coagulation
fibrinolytic system
54
what are the three pathways for the complement system
classical
alternative
mannose binding lectin pathway
55
what is the initiating factor for classical pathways for complement
antibody attached to a microbe
56
what is the initiation for the alternative pathway of the complement system
microbial cell wall
57
what is the initiating factor for the mannose binding lectin pathway in the complement system
carbohydrates on the pathogen surface
58
which molecules are involved in the kinin system
plasma proteins and enzymes
59
what is coagulation factor XII
hageman factor
60
what is the role of kallikrein
convert kininogens to kinins
61
what is the most common kinin
bradykinin
62
what are the three pathways for the coagulation system
intrinsic
extrinsic
common
63
what is the intrinsic coagulation pathway
activated when blood comes into contact with sub endothelial connective tissues (outside blood vessel)
64
what is the extrinsic coagulation pathway
damaged blood vessel leads to human factor 7 leaving the vessel and encountering tissue factors in surrounding tissue
65
what is the common pathway for coagulation system
production of thrombin which in turn produces fibrin for clot formation
66
what does the fibrinolytic system activate
plasmin
67
what is the fibrinolytic systems role in vascular permeability
it is indirect as the products of fibrin degradation promote the permeability
68
what is an example of a thrombolytic drug
urokinase
69
what is haemostasis the balance between
the coagulation and the fibrinolytic system
haemostasis is stopping the flow of blood
70
what can bleeding to death result from
trauma
major surgery
hemophilia
71
what can clotting to death result from
stroke
thrombosis
MI
72
what are some congenital coagulation disorders
von willebrand disease
haemophilia A
haemophili B
73
what are some anticoagulant drugs
warfarin
heparin
74
what does the complement system lead to
membrane attack complex formation
anaphylatoxin production
75
what does the kinin system produce
bradykinins
76
what does coagulation produce
stable blood clots from fibrin
77
how does plasmin prevent excessive clotting
it degrades fibrin
78
what is suppuration
abscess formation, an outcome from acute inflammation which can lead to chronic inflammation
79
what is the transfer of acute to chronic inflammation dependent on
tissue involved
amount of tissue destruction
nature of the harmful agent
80
what are the three types of dental abscess
gingival
periodontal
periapical
81
what is a gingival abscess
an abscess formed due to infection or trauma to the surface of the gum tissue
82
what is a periodontal abscess
forms due to an infection that has moved deeper into the gum areas
83
what is a periapical abscess
abscess of a tooth due to infection of the pulp
84
what is a key factor for suppuration
neutrophil infiltration
85
what is pus
bacteria with dead and dying neutrophils
86
what surrounds accumulating pus
pyogenic membrane
87
why do abscesses form to prevent further infection
the bacteria within the abscess is fairly inaccessible so this prevents spreading of the infection
88
describe resolution in acute inflammation
this is the complete restoration of tissues after an episode of acute inflammation
89
what does tissue restoration after inflammation require
- 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
what is the most common outcome of acute inflammation
resolution
91
what are inflammatory reactions aimed for
eliminating the inciting cause
92
what are the inciting causes of inflammation
invading microorganisms
particulate materials
altered self cells
transformed malignant cells
93
what is acute inflammation a response to
infection or damage
94
how can chronic inflammation arise from acute inflammation
due to persistent exposure to the causes of acute inflammation
can also arise de novo
95
what is swelling defined as
an excess of watery fluid collecting in the tissues of the body
increased blood and lymph flow
96
which cardinal sign of infection involves mediator release
dolor, pain
97
histamine is released via what process
degranulation
98
another flashcard asking you to name the roles of histamine!!
vasodilation
increased vascular permeability
smooth muscle contraction
bronchoconstriction
neurotransmission
99
what does arachidonic acid produce
leukotrienes and prostaglandins
100
how are the enzymatic cascades for acute inflammation linked together
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
what is hageman factor
a serine protease found circulating inactive in the blood
it can activate the classical complement pathway both directly and indirectly
102
how does hageman factor directly activate the complement pathway
by promoting the formation of the antibody complex
103
how can hageman factor indirectly activate the complement pathway
through the kinin and fibrinolytic systems
104
what is the main plasma protein involved in the kinin system
kallikrein
105
what are the two main molecules involved in the kinin system
kallikrein and neutrophils
106
what does kallikrein do in the kinin system
it converts kininogens to kinins
107
what is contacted in the intrinsic coagulation system
collagen
108
what does the final coagulation pathway drive
the formation of the stable blood clot through the production of fibrin
109
what do the intrinsic and extrinsic coagulation pathways converge to form
the common pathway to form the stable bloot clot through the action of thrombin
110
what drives intrinsic coagulation
internatal trauma like non functioning endothelial cells
coagulation drives repair of the vessels
111
what drives extrinsic coagulation
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
which process activates plasmin
the fibrinolytic system
113
how does the fibrinolytic system activate the complement system
plasmin cleaves C3 component protein
114
what converts plasminogen into plasmin
kallikrein and hageman factor
115
who are thrombolytic drugs given to
people who struggle to break down excessive clots on their own
116
what does plasmin degrade
fibrin
117
how do thrombolytic drugs work
they promote the activity of antithrombin which targets the thrombin enzyme which drives the formation of a stable clot
118
what are some acute inflammatory diseases linked to dentistry
gingivitis
abscess formation
pericoronitis
angular cheilitis
ludwigs angina
119
what are the two major acute inflammatory diseases in the oral environment
abscess formation and gingivitis
120
what is a pyogenic membrane
this is a component of granulation tissue which is involved in tissue repair
121
what are the two classes of chronic inflammation
non specific and specific
122
what characterises non specific chronic inflammation
persistent acute inflammation and excessive suppuration
123
what characterises specific chronic inflammation
arises de novo
persisent exposure to agent
can be granulomatous
124
what infiltrates tissues during a non specific chronic inflammatory resopnse
tissue macrophages
t cells
b cells
more adaptive immune cells
125
what does periodontitis lead from
persistent bouts of gingivitis
126
what induces a specific chronic inflammatory response
non immunological or immunological agents
127
what does granulomatous mean
involving the formation of granulomas
128
which type of inflammation is characterisde by excessively activated tissue macrophages
specific chronic inflammation
129
is there any warning for the manifestation of specific chronic inflammation
no
130
what can cause a resistance of infective agent to phagocytes and intracellular killing leading to inflammation
tuberculosis
leprosy
viral infections
131
what are some endogenonus materials that cause inflammation
nectrotic adipose tissue
bone
uric acid crystals
132
what are some exogenous materials
silica
asbestos fibres
suture materials
implanted prosthetics
133
what are some autoimmune diseases that cause inflammation
hashimotos
chronic gastritis
rheumatoid arthritis
hypersensitivity reactions
134
what are some primary granulomatous diseases that cause inflammation
crohns disease
sarcoidosis
135
describe rheumatiod arthritis pathogenesis
loss of tolerance to citrullinated proteins in synovial fluid
136
describe sjogrens syndrome
host t and b cells attach the cells of the salivary and lacrimal glands
137
explaoin peptide citrullination in rheumatoid arthritis
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
describe orofacial granulomatosis
this is characterised by excessively activated tissue macrophages called epithelioid macrophages that fuse to form giant cells
they form in soft tissue
139
why is there a rippled appearance in orofacial granulomatosis
lots of macrophages fuse together and cause ripples in a particular tissue
