Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BDS stage 2 > IAH theme 4 > Flashcards

IAH theme 4 Flashcards

1
Q

What are the aims of tissue and organ transplantation ?

A

transplants have to be physiologically fucntioning
process should not harm the recipient
Should not be rejected by the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is immunosupression selective ?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of reaction is hyperacute rejection ?

A

type II hypesensitivity- antibodies to the cell surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What happens in hyperacute rejection ?

A

pre existing antibodies IgG against MHC in vascular endothelium in grAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes a hyperacute rejection ?

A

mediated by MHC class I or ABO mismatch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why might a person have antibodies to MHC on hyperacute rejection ?

A

pregnancy
multiple blood transfusion
previsous transplants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens in hyperacute rejection when antibodies bind to vascular endothelium ?

A

complement activation- endothelial damage
graft haemorrhage
blood clotting- vascular blockage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How can we avoid hyperacute rejection ?

A

MHC antigen cross matching

serological testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What type of reactions are graft v host and transplant rejection

A

alloreaction- type IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is type IV hypersensitivity ?

A

T cell mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are alloantigens ?

A

antigens that vary between individuals of the same species- eg. MHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are alloreactions ?

A

Immune response by one individual to the alloantigen of another causes by alloreactive T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens in transplant rejection ?

A

Kidney is transplanted

recipients T cells attack transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens in graft v host disease ?

A

haemoatopoietic stem cell infusions
stem cells transplanted
T cells in the transplant attack recipients tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the preparations for transplantations ?

A 
limit ischaemia 
limit MHC class i/class II mismatch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is ischaemia and what does it lead to ?

A

inadequate blood supply

leads to tissue damage and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens if there is an MHC class I/class II mismatch ?

A 
alloreactive CD4 cells to class II
alloreactive CD8 cells to class I
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What happens if alloreactive T cells are produced ?

A

organ is attacked

acute rejection - type IV hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the gross appearance of an acutely rejected kidney ?

A

read areas of haemorrhage

grey areas of necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When are immunosuppression drugs given for transplantation ?

A

before and after surgery

increases likelihood if infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What can acute rejection progress to ?

A

chronic rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What type of reaction is chronic rejection ?

A

type III hypersensitivity - deposition of immune complexes of antibody/MHC molecules on vascular endothelium of graft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does immune complex deposition lead to in chronic rejection ?

A

monocytes and neutrophils activated

Allograft specific T cells develop leading to chronic allograft vasculopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What happens in chronic allograft vasculopathy ?

A

arteriosclerosis of graft- hypotension, fibrosis and atrophy
loss of fucntion
fibrotic tissue deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the other causes of chronic rejection ?

A

ischaemic injury
viral infection - due to immunosupression
relapse of original disorder - leukaemia eg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the structure of MHC class I ?

A

alpha 1 2 and 3
B2 microglobulin subunit
present to CD8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the structure of MHC class II ?

A

alpha 1 and 2
beta 1 and 2
present to CD4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is significant about MHC ?

A

lots of polymorphisms distributed differnetly within population
across different regions of the MHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does MHC relate to survival of transplanted organs ?

A

More MHC mismatches and the percentage of graft survival decreases
Half life diminshes with increasing mismatches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is graft half life ?

A

time taken for the amount of viable graft tissue to be reduced in half

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the order of MHC sensitivity of different organs ?

A

cornea is MHC neutral - easy to transplant
liver
Heart
Kidney
Bone marrow - require strict MHC matching - expresses a lot of MHC class II that can eb attacked by antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does a bone marrow transplant work ?

A

chemotherapy and irradiation to remove host bone marrow and kill cancer cells and stop immune response
infuse new haemoatopoietic stem cells that are matcheed
remake bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the conventional immumosupressive drugs ?

A

corticosteroids

cyclosporin and tacrolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What do corticosteroids do ?

A

inhibit inflammation by inhibting cyotkine production by macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does cyclosporin do #/

A

blocks IL-2 production by T cells and stops T cell proliferation as IL-2 is T cell growth factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the side effects of cyclosporin ?

A

lead to gingival overgrowth
kidney damage
hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What does the unique specifictity of antibodies allow ?

A

detection of proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the constant region ?

A 
amino acid similarity between antibodies of the same class
different classes have different constant regions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the variable region ?

A

antigen specificty

Fab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the antibodies like that are produced from conventional immunisation ?

A 
mixed specificity
mixed isotypes
variability in batches
limited amounts as drawn from the blood 
polyclonal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the monoclonal antibodies like ?

A

single specificity
single isotype made
no variabiltiy between batches- good quality
limitless production quality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are recombinant antibodies like ?

A 
single specificity
single isotype
no variability between batches
limitless production quality 
genetically altered to be human like- no immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How do we produce monoclonal antibodies ?

A

Take B cell from mouse immunised with antigen
combine with myeloma cells- B cell cancer cells
kill non hybridomas
select for antigen specific hybridoma
clone hybridoma- make limtless antibodies - monoclonal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How can we diagnose immunodeficiencies ?

A

IgG, IgM , IgE, IgA levels
whole blood cell count
lymohocyte count
flow cytometry- chracterise deficiecy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does flow cytometry work ?

A

label a mixture of cells with fluorescent antibodies to specific cell surface molecules - distingusih cells by cell surface expression
laser picks up the cells with a particular antibody
numerate them in a plot- see which deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is CD3 ?

A

cell surface molecule on CD4 and CD8 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is CD19 ?

A

On B cells only -

plot shows none present in XLA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How are autoimmune diseases analysed ?

A

physiological function- see if it is reduced, eg. hyperthyroidism in Graves disease

look for presence of autoantibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How do we detect serum autoantibodies ?

A

with ELISA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe the presence of ELISA for autoantibody detection ?

A

antigen in plate
serum added- might contain autoantibody
second antibody added which is enzyme linked
binds to Fc tail of autoantibody if present
enzyme added- colour chamge if binds to secodnary antibody
Quantification of colour change- spectrophometer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How can we use immunofluoresence for antigen detection ?

A

Direct immunoflupresence- antibody added that has F on it - binds to antigen

Indirect immunofluoresence- second antibody that bidns to a primary antibody, Second antibody only has F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which diseases can indirect immunofluoresence be used for ?

A

bullous pemphigoid- autoantigen in basement membrane, can use direct immunofluoresence to detect

Pemphigus vulgaris- more antigens in epithelial cells connections- immunofluoresence with second antibody

Good pastures syndrome- in glomerulus, immune complexes- detect complexes with antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How can we diagnose allergies ?

A

intradermal skin test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe the intradermal skin test ?

A

injection with saline- see if injection causes any response- shouldnt
inject with Histamine- see a normal allergic response
inject with suspected allergen- could be positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are some agents used to manipulate the immune response ?

A

adjuvants in vaccines

molecules that inhibit cytokine signalling pathways- Tofacitinib- for rheumatoid arthritis - reduce joint inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What do monoclonal antibodies end in ?

A

mab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the the types of monoclonal amtibodies ?

A

murine
chimeric
humanised
human

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the problems with human monoclonal antibodies ?

A

need to be injected in large amounts
cant be eliminated in glomeruli
Fc receptors- bind to other cells- increase retention
high production costs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How does omalizumab work ?

A

antibody against IgE- anti-IgE
stops IgE in circulation binding to Fc receptors on mast cells upon allergen exposure- no degranulation
used in chronic asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is an example of a biologic ?

A

infliximab in rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How does infliximab work ?

A

anti-TNF alpha
inhivits TNF alpha induced inflamamtion in rheumatoid arthritis
dampens joint inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the proven effects of infliximab ?

A

reduced pain and swollen joints

also reducd CRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What does CRP indicate ?

A

systemic inflamamtion- acute phase protein sin liver- higher CRp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is an adenoma ?

A

benign tumour
contained within a site
even when in an important area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is adenocarcinoma ?

A

malignant tumour
invasive
spreads

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Where can you find adenomas and adenocarcinomas ?

A

in glandular/secretory tissuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the key features of cancer ?

A

proliferation and invasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are cancer cells immunologically similar to ?

A

self cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Do cancer cells grow slowly or fast ?

A

slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How do we know the immune system can recognise ad reject tumours ?

A

immunodeficient animals- have higher incidence of cancer
immunosupressive therapy- increased cancer rates
cancer incidence increases with age due to immunosunescence
MHC differences can influence tumour survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the genetic changes and immune recognition that can happen in tumours ?

A 
normal peptide presentation by class I
mutation and becomes cancerous 
presentation of mutant peptide from a mutated cellular protein 
reactivated embryonic genes
overexpression of normal self protein
72
Q

Which viruses are associated with human cancers?

A

HIV
HPV
EBV
HepB and Hep C

73
Q

Which type of viral infection leads to cancers ?

A

chronic viral infections

74
Q

How is HPV associated with cancer ?

A

certain strains - cause warts

warts are benign that cause cellualr transformation

75
Q

WHich cancers is HPV associated with ?

A

oral cancer
cervical cancer
cancers of the UGT
head and neck

76
Q

What does Hep B virus do in cancer ?

A

transforms liver cells into hepatocellular carcinoma

77
Q

What does EBV do in cancer ?

A

lead to lymphomas

78
Q

What are lymphomas ?

A

cancer of mature lymphocytes

79
Q

Which cancers does HIV lead to ?

A

karposis sarcoma

skin cancer- HHV8

80
Q

How do viruses cause cancer ?

A

viruses set up chronic infections
interfere with normal division mechanisms leading to hyperplasia
increased cell proliferation and transformation into cancer

81
Q

Which bacterial infections can lead to cancer ?

A

helicobacter pylori
stomach ulcers
stomach cancer

82
Q

Describe the progression of HPV associated cancer ?

A

increasingly displastic cells
no longer stratified squamous
invasion into connective tissue- cancerous lesions
dysplasia - cancer transformation

83
Q

What is CIN ?

A

cervical intraepithelial neoplasia

84
Q

Can HPV related cancer regress ?

A

yes the cancer can regress

85
Q

Which strains of HPV are associated with cancer ?

A

HPV 16 and 18

cancerous transformation

86
Q

What is the cause of 99% of cervical cancer cases ?

A

HPV

87
Q

What is the immune response like against HPV ?

A

lesions are cleared within 2 years
good immune response to HPV
immune supression is effective in the majority

88
Q

Why do not all people clear HPV infection ?

A

the HPV antigen is not recognised

viruses escape epithelial cells

89
Q

How does HPV cause cancer ?

A

infect epithelial cells

inhibit tumour supresssor mechanisms like p53 so cells proliferate above the normal regulatory mechanisms

90
Q

How do tumour supressor mechanisms work ?

A

p53 delays the cell cycle so

cells can be repaired and then replicated

91
Q

What does inhibiting p53 lead to ?

A

mutated cells still proliferate

92
Q

What happens to p53 in cancer ?

A

inhibited/mutated

93
Q

How many types of HPV are there and what doe sit mean ?

A

30-40 types

many multivalent oncognenic vaccines needed

94
Q

What type of cancer due to HPV is increasing ?

A

head and neck

95
Q

What is suspected to reduce and eliminate cervical cancer rates ?

A

screening programmes
availability of invasive surgery
vaccination for boys

96
Q

What is preventing us deciding if HPV vaccine elimianates cervical cancer ?

A

latency period

97
Q

What is predicitve modelling ?

A

modelling technique that HPV associated cervical cancer will decrease due to spread of vaccine line n australia- also used for boys

98
Q

What are the downsides of predictive modelling ?

A

some high grade cancers are not caused by HPV
not sure of effectiveness against CIN3 cancers
infections may just regress and the cancers regress randomly

99
Q

How do HPV and HCV spread ?

A

contaminated blood
blood contaminated instruments
sex
mother to child in childbirth

100
Q

What do HBV and HCV cause ?

A

hepatitis
liver cirrhosis- scarring, fibrosis and loss of tissue function
hepatocellular carcinoma
both have a long incubation period

101
Q

What is acute hepatitis associated with ?

A

clearance by the immune system

sets up chronic infections in immunosupressed patients

102
Q

What does HCV do ?

A

inhibits activation of dendritic cells
no specific T cells
impaired viral clearance

103
Q

What does Hepatitis C do ?

A

mutates rapidly

causes chronic hepatitis

104
Q

Which Hep has an effective vaccine ?

A

hepatitis B

105
Q

What do Hep B and Hep C do with Tregs ?

A

promote Tregs

promote viral infection through supression of antiviral responses

106
Q

Which immunotherapy techniques are used to target specific antigens ?

A

monoclonal antibodies

107
Q

How can monoclonal antibodies be used in the treatment of cancers ?

A

target cancer molecules like B cells in lymphoma - ritumixab

target host immune system to boost performance using checkpoint inhibitor drugs l

targeting cancer and using radiotherapy to kill isotypes

108
Q

Why do we get a GVH response in BMT ?

A

allogenic donor T cells circualte and activate causing tissue damage
interact with dendritic cells

109
Q

What is BMT use dfor ?

A

rescue haemoatopietic system after chemotherapy and irradiation for leukaemia

110
Q

As well as a GVHR what do you get ?

A

graft v leukameia response - donor T cells attack leuakaemia cells as well

111
Q

What happens in allogenic HLA matched non self transplantation ?

A

GVH

GVL as well

112
Q

What happens in autologous self donors ?

A

no GVHR
but no GVL effect
relapse

113
Q

What do new BMT regimens involve ?

A

therpauetic T cells to indice controlled GVL effect

114
Q

Give an example of adoptive T cell therapy ?

A

chimeric antigen receptors
expressed in T cells
confer anti tumour specificity in lymphocytes
target tumour

115
Q

What percentage of pathogens enter by the nose and mouth ?

A

70%

116
Q

What is the mucosa lined with ?

A

glandular epithelium

bathed in secretions

117
Q

What are some elements of the immune response in the mouth ?

A

enzymes- lysozyme break cell walla by osmosis and lysis
AMPs- lysis
lactoferrin-enzyme that complexes ion, prevents growth

118
Q

What is the main Ig in the mouth ?

A

IgA- in the mouth from saliva

119
Q

What is mucin ?

A

highly glycosylated protein
mixes with water- coagulates bacteria
so they can be swallowed

120
Q

Is the oral mucosa keratinised ?

A

no except for the masticatory mucosa

121
Q

What do epithelial cells make in defence ?

A

beta defensins

122
Q

What is the advantage of squamous epithelial cells ?

A

exfoliate as a defence

get rid of colonisers and prevent attachment

123
Q

What is the GCF ?

A

serum exudate
adaptive elemetns- IgM and IgG
cellular elements like neutrophils
AMPs

124
Q

When does GCF increase ?

A

in inflamamtion and pocket depth- increases

125
Q

What are the salivary glands in the mouth ?

A

minor- many and widely distributed

major- parotid, sublingual and submandibular

126
Q

What are flow characteristics ?

A

GCF pocket/ urine/saliva- flow dislodges bacteria

127
Q

What are the different solubilities of bacteria ?

A

soluble phase
mucosal phase
tooth surface
plaque biofilm

128
Q

What are AMPs and what do they do ?

A

defensins/statherin

disrupt bacterial membranes and enveloped viruses

129
Q

What are adhesive proteins ?

A

mucin, PRPs, Agglutinin

bacterial adhesion in fluid phase, promote adhesion to teeth

130
Q

What are metal ion chelators ?

A

lactoferrin

scavenge for zinc and iron respectively

131
Q

What are protease inhibitors ?

A

cystatin

prevent nutrient acquisition by bacteria

132
Q

What in the interface in the mouth with the systemic immune response ?

A

GCF

133
Q

Where does GCF originate ?

A

in the gingival crevice

134
Q

What are the defences of the oral mucosa ?

A

barrier fucntion- keratinocytes
desquamtion of oral epithelium
AMPs
mucus layer

135
Q

What is the role of the phase 1 natural host defence in the mouth ?

A

act to inactivate
clear
prevent attachment and prevent invasion

136
Q

What are the components of the host defence ?

A 
salivary components 
integrity of oral mucosa 
acquired enamel pellicle 
commensal flora - competition for nutrients 
vascualrity- host defences
137
Q

What are the components of the gingival epithelium ?

A

oral epithelium
junctional epithelium
sulcar epithelium

138
Q

What is the role of the junctional epithelium ?

A

attachment of the gingiva to enamel

139
Q

What are aspects of infection with periodontitis ?

A 
migration of JE 
loss off attachment 
bone loss
plaque development 
tissue loss and loss of fucntion
140
Q

What is the role of phase 2 in the mouth ?

A

innate immunity

containmet, prevention and spread and clearance

141
Q

What are the aspects of innate immunity in the mouth ?

A

GCF elements
macrophages- signalling and cytokines
neutrophils- phagocytosis
complement- opsinisation, chemotaxis and lyis

142
Q

Why do neutrophils move through the gingiva ?

A

move through the gingiva in response to commensal flora to IL8

143
Q

What is IL8 ?

A

a chemokine

144
Q

What do neutrophils do in the gingiva ?

A

physiological inflamamtion state in the gut

145
Q

What happens to neutrophils in periodontitis ?

A

neutrophil migration upregulated in respose to pathogenic microflora
IL8 also increases

146
Q

What happens to people with neutrophil defects ?

A

they have increased susceptibiltiy to periodontitis

147
Q

What type of inflamamtion does HIV lead to ?

A

necrotising ulcertaive gingivitis

148
Q

Compare the intestinal burden in the intestine and sulcar/JE ?

A

high amount of flora in the intestine

variable amount of flora in the SE/JE

149
Q

What are the bacteria like in intestine and the sulcar/JE ?

A

bacteria in solution in gut

bacteria in biolfim in sulcar/JE

150
Q

What is the mucus layer like in the intestine and the JE ?

A

thick mucus in the gut

no mucin in the JE but in the mouth

151
Q

What are the antibodies in the gut/SE ?

A

gut- IgA

crevice- IgG

152
Q

What are the jucntions like in the gut/SE ?

A

gut- tight jucntions

JE- porous

153
Q

What are the inflammatory states in the gut/JE ?

A

gut- stbael physiologial inflamamtion

JE- difficult to prevent a damaging inflammation

154
Q

What type of Ig is IgA ?

A

mucosal

155
Q

What is the tole of phase 3 in the mouth ?

A

enchancement of innate immunity

long lasting specific immunity

156
Q

What are periodontal antibodies good for ?

A

enhancing the innate immunity

157
Q

What does phase 2 do to phase 3 ?

A

broadcast
amplify
enhancement

158
Q

What does phase 3 do to phase 2 ?

A

regulated by cytokines

mediated by T cells and antibodies

159
Q

What is salivary IgA secreted from ?

A

salivary glands

with S-IgM

160
Q

What does S-IgA do ?

A

inhibition of adherence and penetrance
neutraliation of viruses and virulence factors
form complexes with mucous - agglutinate and swallowed

161
Q

What are the different types of IgA ?

A

IgA1- against proteins

IgA2- agaisnr polysaccharides

162
Q

How is salivary IgA made ?

A

antigen uptake - phgocytosis and endocytosis
presented to dendritic cells
T cell acitvation and B cell activation
b cells make IgA
B cells migrate to over mucosal sites
IgA secreted via endocytosis acorss basolateral membrane

163
Q

What is the conformation of IgA ?

A

J chain

dimeric when secreted

164
Q

What are the characteristics of the sungingival microbiota ?

A 
streptococci 
actinomyces 
biofilm 
anerobic 
immune response is difficult
165
Q

What are some examples of PAMPs ?

A 
LPS
lipoteichoic acid (GP_
DNA 
fimbriae
Fatty acids like acetic acid
166
Q

What happens to PAMPs?

A

recognised by TLRs and intracellualr signalling pathway

167
Q

Which cells recognise PAMPs ?

A

dendritic cells
macrophages
epithelial cells
fibroblasts

168
Q

What is the end result of PAMP detection ?

A

cytokines- reinforce cells
chemokines
AMPs
prostanoids

169
Q

What is the tole of the primary phase?

A

recognition

170
Q

What is the role of the secondary phase ?

A

diversification
reinfrocement
amplification
braodcast

171
Q

What is IL-1 beta ?

A 
inflamamtroy cytokine
activates neutrophils 
activates macropahes - make more IL1 
activates capillary endothelium - more neutrophils and macrophages 
activate dendritic cells for APC
172
Q

What happens to IL-1 id plaque persists ?

A

chronic activation

173
Q

How can high levels of IL-1 be detected ?

A

BY ELISA in the GCF

174
Q

What happens in chronic activation of IL-1 ?

A

activation of osteoclasts- bone resorption
fibroblasts- MMPs= chew up collagen
fibroblasts- collagen in chew up in PDL
neutrophils over stimulated to make IL-1

175
Q

What is in ahigh level in GCF in periodontitis ?

A

MMP

176
Q

What is doxycycline ?

A

doxyxline

inhibit MMP

BDS stage 2 (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions