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REVISION > acute innate regeneration > Flashcards

acute innate regeneration Flashcards

1
Q

what is acute inflammation?

A

response of living tissue to infection or damage
develops quickly
initiates innate immunity

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2
Q

what are the 3 main processes if acute inflammation?

A

vascular dilation
increased vascular permeability
neutrophil activation and migration

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3
Q

what are the 4 main causes of acute inflammation?

A

microbial infection
physical trauma
irritant or corrosive chemicals
tissue necrosis

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4
Q

what are the 5 consequences of actor inflammation?

A

redness (rubor)
heat (calor)
swelling (tumor)
pain (dolor)
loss of function

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5
Q

what causes redness in acute inflammation?

A

dilation of small blood vessels

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6
Q

what causes heat in acute inflammation?

A

increased blood flow (hyperaemia)

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7
Q

what causes swelling in acute inflammation?

A

accumulation of fluid in extra vascular space (oedema)

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8
Q

what causes pain in actor inflammation?

A

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

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9
Q

what is an example of acute inflammation?

A

gingivitis

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10
Q

what are the stages of acute inflammation?

A

initiation
progression
amplification
resolution

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11
Q

at what stage does acute turn chronic inflammation?

A

no resolution of acute inflammation

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12
Q

what happens in the initiation stage of acute inflammation?

A

microbes recognised by epithelium via TLR

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13
Q

what happens in the progression stage of acute inflammation?

A

containment of microbes by innate immune cells and antimicrobial compounds (AMPs and IgA)

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14
Q

what happens in the amplification stage of acute inflammation?

A

recruit and activate innate immune cells
via
-chemokine and cytokine activity
-vascular dilation
-increased vascular permeability

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15
Q

what happens in the resolution phase of acute inflammation?

A

healing and repair

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16
Q

what is the vascular response to acute inflammation?

A
  • small blood vessels adjacent to damaged site become dilated
  • endothelial cells swell and retract (promotes immune cell passage)
  • exudation = vessels become leaky and water, salt, proteins pass
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17
Q

what does leaky blood vessels in acute inflammation lead to? what is it?

A

oedema formation
= excess of watery fluid collecting in cavities or tissues

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18
Q

increased lymph flow is oedema formation leads to what? what does this provide the tissue with?

A

inflammatory exudate forming
- fluids and salts
- glucose and o2
- complement proteins and antibodies
- fibrin
and immune cells

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19
Q

what chemical mediators does oedema contain?

A

bradykinin
histamine
prostaglandins

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20
Q

how is histamine made and where is it stored? what does it present as? what does it cause?

A
  • breakdown of histidine
  • stores in granules of mast cells
  • neurotranmitter = itching
  • vasodilation
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21
Q

what produces prostaglandins?
what is the most abundant?
what is the main function?

A
  • macrophages and neutrophils with leukotrienes
  • prostaglandin E2
  • vasodilation
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22
Q

what drives prostaglandin production?

A

cycle-oxygenase ii
(COX II)
from macrophages and neutrophils

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23
Q

what are the 4 proteolytic enzyme cascades?

A

complement system
kinin system
coagulation system
fibrinolytic system

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24
Q

what is formed during the activation of the plasma factors?

A

enzyme complexes
protein cleavage

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25
Q

how are the plasma factors interconnected?

A

proteins produced in some systems lead onto other systems

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26
Q

what systems does coagulation factor XII activate?

A

kinin system
fibrinolytic system
coagulation system

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27
Q

what is another name for coagulation factor 12?

A

hageman factor

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28
Q

what are the 3 complement pathways? how are they initiated?

A

classical pathway = Antibodies attached to microbes
alternative pathway = microbial cell wall
mannose binding lectin pathway = carbs on pathogen surface

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29
Q

what are the 2 main outcomes of the complement pathway?

A

anaphylatoxins produced
membrane attack complex formed

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30
Q

what do anaphylatoxins do?

A

activate immune cells
induce permeability of blood vessels for recruitment of immune cells

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31
Q

what does the membrane attack complex do?

A

drives degradation of microbial cells

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32
Q

what is the protein in kinin system generated by coagulation factor 12?

A

kalikrein

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33
Q

what does kallikrein do?

A

converts kininogens to kinins eg bradykinin

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34
Q

what does Bradykinin do?

A
  • increases permeability of blood vessels
  • activates complement proteins
  • induces immune cells to produce chemical and protein mediators
  • pain via NS
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35
Q

what are the 3 pathways of the coagulation system?

A

intrinsic
extrinsic
common

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36
Q

what is the outcome of the coagulation system?

A

production of thrombin for clot formation

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37
Q

what does the fibrinolytic system result in?

A

activation of plasmin

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38
Q

what 2 proteins play a role in the fibrinolytic system? where from?

A

kallikrein from kinin system
hageman factor

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39
Q

what is the main function of plasmin?

A

breakdown fibrin to prevent excess blood clotting

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40
Q

how does plasmin activate complement?

A

cleaves C3

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41
Q

what is the indirect role of plasmin?

A

produce fibrin degradation products
to promote vascular permeability

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42
Q

what else drives conversion of plasminogen to plasmin? where is it found?

A

tPA on endothelial cells

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43
Q

give an example of a thrombolytic drug that drives the degradation of plasmin?

A

urokinase

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44
Q

what is haemostasis?

A

balance between coagulation and fibrinolytic systems (clotting to death vs bleeding to death)

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45
Q

what does haemostasis mean?

A

stop of blood flow

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46
Q

what are the 2 types of coagulation disorders?

A

congenital = haemophilia a or b
acquired = warfarin or heparin

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47
Q

what is a congenital coagulation disorder?

A

disease

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48
Q

what is an acquired coagulation disorder?

A

caused by drugs

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49
Q

what is it important to consider patients with coagulation disorders in dental surgery?

A

for example on extraction of tooth
wounds may take longer to heal or have complications

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50
Q

which outcome of acute inflammation can lead to chronic inflammation?

A

abscess formation (suppration)

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51
Q

what does abscess formation depend on?

A

tissue involved
amount of tissue destruction
nature of harmful agent

52
Q

what type of inflammation leads to resolution and regeneration?

A

acute

53
Q

what type of inflammation leads to repair?

A

chronic

54
Q

what are the 3 types of dental abscesses?

A

gingival
periodontal
periapical

55
Q

what is suppuration?

A

puss formation

56
Q

what is pus?

A

bacteria with dead or dying neutrophils

57
Q

what surrounds pus?

A

pyogenic membrane

58
Q

what is the purpose of an abscess?

A

prevents spread of the bacteria or microbe

59
Q

what does resolution require in acute inflammation?

A
  • minimal cell death/tissue damage
  • tissues must have regenerative capacity
  • rapid elimination of causative agent
  • rapid removal of fluid and debris by vascular/lymphatic drainage
60
Q

what is innate immunity?

A

first ling of non specific response that responds to any microbial threat

61
Q

what is tissue homeostasis?

A

balance between protection and destruction as the immune system encounters microbes daily

62
Q

when does innate immunity occur?

A

hours to 4 days

63
Q

what is a disadvantage of the innate immune response?

A

it has no lasting protective immunity

64
Q

why is the innate immune system effective?

A

as it has regular contact with potential pathogens and destroys them quickly so they rarely cause disease

65
Q

what are the 3 components of innate immunity?

A

epithelium (structural and mechanical support)
innate immune subset and complement
chemokines and cytokines

66
Q

what do epithelial barriers and the oral cavity produce in saliva?

A

antimicrobial peptides
immunoglobulins IgA
lactoferrin
lysozyme
cystatins

67
Q

what are major families of antimicrobial peptides?

A

b defensives
humans neutrophil peptides

68
Q

name 2 roles of antimicrobial peptides?

A

modulate host immunity
directly kill microbes

69
Q

what does SIgA do?

A

secretory piece = absorb saliva forming protective layer
dimeric form = attaches to multiple microbes

70
Q

what does lactoferrin do?

A

transports ions

71
Q

what is lysozyme?

A

targets cell wall or bacteria

72
Q

what is crystatins?

A

antiprotenase activity and supports remineralisation of teeth

73
Q

what are the main receptors in innate immune cells?

A

Toll like receptors

74
Q

what are TLR primarily for?

A

bacterial and viral recognition

75
Q

name 3 other types of microbial recognition receptors in innate immune system?
what is each for?

A
  1. dectin and glucan = fungi
  2. NOD-Like = bacterial
  3. Protease-activated = microbial and allergen
76
Q

what do Pattern recognition receptors recognise?

A

pathogen associated molecular patterns

77
Q

what is the 3 signals in T cell differentiation?

A
  1. antigen recognition
  2. co-stimulatory receptors
  3. cytokine tells T cell what to do
78
Q

name 3 groups of cytokines? how is it decided?

A

interleukin family
TNF family
interferons
- depends on structure

79
Q

what is autocrine signalling?

A

cell acting on cell it was secreted from

80
Q

what is paracrine signalling?

A

cell acting on neighbouring cell

81
Q

what is endocrine signalling?

A

enter circulation and alter behaviour of distant cell

82
Q

what type of signalling can cytokines do?

A

autocrine
paracrine
endocrine

83
Q

where are cytokine receptors and what do they recognise?

A

on target cell and recognise different cytokines

84
Q

what happens if TLR or cytokine receptor recognises target?

A

downstream signalling cascade
different effector responses

85
Q

what are chemokines?

A

chemotactic cytokines the direct cells to site of infection

86
Q

what is chemotaxis?

A

move cell in direction corresponding to gradient of increasing or decreasing conc of particular substance

87
Q

what is the main role of chemokines?

A

immune cell recruitment

88
Q

what do chemokines and cytokines tell cell to do?

A

chemokine = where to go
cytokine = what to do

89
Q

name examples of chemokine receptors?

A

CXC
C
CC
CX3C

90
Q

how do we maintain tissue homeostasis?

A

pro inflammatory and anti inflammatory
chemokines/cytokines

91
Q

what happens with immune over reaction?

A

autoimmune
allergy

92
Q

what happens with immune under reaction?

A

infection
cancer

93
Q

what are cytokines?

A

signalling molecules that coordinate immune response

94
Q

what is the most abundant immune cell at the oral mucosa? what %

A

neutrophils 95%

95
Q

what are neutrophils attracted along?

A

CXCL8 gradient (IL8)

96
Q

how do neutrophils know where to go to get to infection?

A

cell adhesion molecules control attractions between immune cells and endothelial cells

97
Q

what are the 3 families of cell adhesion molecules?

A

selections
integrins
immunoglobulin superfamily
- on different types of immune cells

98
Q

what is the primary role of cell adhesion molecules?

A

immune cell trafficking and cell to cell interactions

99
Q

what is the primary function of neutrophils?

A

engulf
destroy
degrade pathogens

100
Q

how do neutrophils degranulate?

A

release granules once TLR have been activated

= release antimicrobial peptides and enzymes from vesicles

101
Q

how do neutrophils produce NETS?

A
  • once activated
  • releases proteins and genetic material (chromatin)
  • forms extra cellular fibril matrix
  • traps pathogens
102
Q

how are antimicrobials associated with NETs?

A

held whilst administered

103
Q

what forms NETs?

A

chromatin
proteins

104
Q

what are monocytes precursors for?

A

macrophages

105
Q

when do monocytes differentiate into macrophages?

A

when they migrate to tissue

106
Q

how do monocytes migrate to target tissue?

A

cell adhesion molecules

107
Q

what are the 2 subsets of macrophages?

A

M1 = pro inflammatory
M2 = anti-inflammatory

108
Q

what is the primary function of macrophage?

A

phagocytose and present antigen to adaptive immune cells

109
Q

what do granules of granulocytes contain?

A

proteinases
antimicrobials
chemical mediators

110
Q

what induced cells to degranulate?

A

M(P)AMPs
complement proteins
cytokines other inflammatory mediators

111
Q

which cells phagocytose?

A

macrophages
neutrophils
dendritic cells

112
Q

what is the 3 parts to phagocytosis?

A

degradation and removal of threat
antigen presentation
apoptosis

113
Q

what are the 2 types of APC with examples?

A

nonprofessional = epithelial, endothelial, fibroblasts

professional = macrophage, dendritic cell

114
Q

what is the steps of phagocytosis?

A
  1. microbe ingested by phagocyte
  2. formation of a phagosome
  3. fusion of phagosome with lysosome = phagolysosome
  4. digestion of ingested microbe by enzymes
  5. residual body formed w indigestible materials
  6. discharge of the waste material
115
Q

what is antigen presentation?

A

interaction between MHC I or MHCII and the antigen then this complex is presented to T cell

116
Q

what links the innate and adaptive immune system?

A

phagocytosis and antigen presentation

117
Q

how much of blood does plasma make up?

A

55%

118
Q

what kind of response is plasma factors?

A

humoral

119
Q

what is complement?

A

soluble proteins in circulation that drives inflammation or opsonisation

120
Q

what is opsonisation?

A

coating of pathogens by antibodies or complement proteins

121
Q

if an antibody is attached to a microbe what complement pathway is activated?

A

classical

122
Q

if complement proteins recognise the microbial cell wall what kind of complement is activated?

A

alternative

123
Q

if carbs on pathogen surface are recognised by complement proteins which complement pathway is activated?

A

mannitose binding lectin

124
Q

what 2 enzymes are produced in complement?

A

C3 and C5 convertase

125
Q

what is the function of C3 and C5 convertase?

A

degradation of C3 and C5 proteins producing anaphylatoxins

126
Q

what do anaphylaxis lead to?

A

SM contraction and capillary leakage therefor increased infiltration of immune cells to site of infection

127
Q

how do anaphylatoxins promote immune cell recruitment?

A
  • increases adhesion of cells to vessel wall
  • induce granulation
  • cytokine production
  • antigen presentation
  • regulate adaptive immune response

REVISION (12 decks)

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