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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

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2
Q

Is immunosupression selective ?

A

no

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3
Q

What type of reaction is hyperacute rejection ?

A

type II hypesensitivity- antibodies to the cell surface

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4
Q

What happens in hyperacute rejection ?

A

pre existing antibodies IgG against MHC in vascular endothelium in grAT

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5
Q

What causes a hyperacute rejection ?

A

mediated by MHC class I or ABO mismatch

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6
Q

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

A

pregnancy
multiple blood transfusion
previsous transplants

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7
Q

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

A

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

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8
Q

How can we avoid hyperacute rejection ?

A

MHC antigen cross matching

serological testing

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9
Q

What type of reactions are graft v host and transplant rejection

A

alloreaction- type IV

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10
Q

What is type IV hypersensitivity ?

A

T cell mediated

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11
Q

What are alloantigens ?

A

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

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12
Q

What are alloreactions ?

A

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

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13
Q

What happens in transplant rejection ?

A

Kidney is transplanted

recipients T cells attack transplant

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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

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15
Q

What are the preparations for transplantations ?

A 
limit ischaemia 
limit MHC class i/class II mismatch
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16
Q

What is ischaemia and what does it lead to ?

A

inadequate blood supply

leads to tissue damage and inflammation

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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
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18
Q

What happens if alloreactive T cells are produced ?

A

organ is attacked

acute rejection - type IV hypersensitivity

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19
Q

What is the gross appearance of an acutely rejected kidney ?

A

read areas of haemorrhage

grey areas of necrosis

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20
Q

When are immunosuppression drugs given for transplantation ?

A

before and after surgery

increases likelihood if infections

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21
Q

What can acute rejection progress to ?

A

chronic rejection

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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

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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

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24
Q

What happens in chronic allograft vasculopathy ?

A

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

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25
Q

What are the other causes of chronic rejection ?

A

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

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26
Q

What is the structure of MHC class I ?

A

alpha 1 2 and 3
B2 microglobulin subunit
present to CD8

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27
Q

What is the structure of MHC class II ?

A

alpha 1 and 2
beta 1 and 2
present to CD4

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28
Q

What is significant about MHC ?

A

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

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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

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30
Q

What is graft half life ?

A

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

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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

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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

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33
Q

What are the conventional immumosupressive drugs ?

A

corticosteroids

cyclosporin and tacrolimus

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34
Q

What do corticosteroids do ?

A

inhibit inflammation by inhibting cyotkine production by macrophages

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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

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36
Q

What are the side effects of cyclosporin ?

A

lead to gingival overgrowth
kidney damage
hypertension

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37
Q

What does the unique specifictity of antibodies allow ?

A

detection of proteins

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38
Q

What is the constant region ?

A 
amino acid similarity between antibodies of the same class
different classes have different constant regions
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39
Q

What is the variable region ?

A

antigen specificty

Fab

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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
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41
Q

What are the monoclonal antibodies like ?

A

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

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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
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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

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44
Q

How can we diagnose immunodeficiencies ?

A

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

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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

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46
Q

What is CD3 ?

A

cell surface molecule on CD4 and CD8 cells

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47
Q

What is CD19 ?

A

On B cells only -

plot shows none present in XLA

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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

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49
Q

How do we detect serum autoantibodies ?

A

with ELISA

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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

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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

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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

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53
Q

How can we diagnose allergies ?

A

intradermal skin test

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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

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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

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56
Q

What do monoclonal antibodies end in ?

A

mab

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57
Q

What are the the types of monoclonal amtibodies ?

A

murine
chimeric
humanised
human

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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

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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

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60
Q

What is an example of a biologic ?

A

infliximab in rheumatoid arthritis

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61
Q

How does infliximab work ?

A

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

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62
Q

What are the proven effects of infliximab ?

A

reduced pain and swollen joints

also reducd CRP

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63
Q

What does CRP indicate ?

A

systemic inflamamtion- acute phase protein sin liver- higher CRp

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64
Q

What is an adenoma ?

A

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

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65
Q

What is adenocarcinoma ?

A

malignant tumour
invasive
spreads

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66
Q

Where can you find adenomas and adenocarcinomas ?

A

in glandular/secretory tissuse

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67
Q

What are the key features of cancer ?

A

proliferation and invasion

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68
Q

What are cancer cells immunologically similar to ?

A

self cells

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69
Q

Do cancer cells grow slowly or fast ?

A

slowly

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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

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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 ?

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 ?

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 ?

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 ?

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 ?

176
Q

What is doxycycline ?

A

doxyxline

inhibit MMP

BDS stage 2 (28 decks)

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