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MedEd Path > MedEd Immuno 2 > Flashcards

MedEd Immuno 2 Flashcards

1
Q

what is oral allergy syndrome

A

allergy sx limited to mouth

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2
Q

when does the allergy not happen in oral allergy syndrome

A

cooked !
allergens are heat labile

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3
Q

in oral allergy syndrome, why can you be allergic to things other than allergen

A

cross reactive IgE to foods eg pollen –> stone fruit

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4
Q

2 examples of mixed IgE and cell mediated type 1 reaction

A

atopic dermatitis
eosinophilic oesophagitis

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5
Q

example of non IgE mediated allergic disease

A

coeliac
(lymphocytic destruction)

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6
Q

Ix for allergy

A

skin prick test
IgE bloods
oral challenge

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7
Q

benefits of skin prick test

A

easy to do
cheap
high negative predictive value

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8
Q

cons of skin prick test

A

need to stop antihistamines before
poor positive predictive value
affected by severe derm diseases (eg rlly bad eczema)
risk of anaphylaxis

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9
Q

what is IgE blood test aka

A

RAST

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10
Q

benefits of IgE blood test

A

prediction of allergy RISK

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11
Q

when is IgE blood test good

A

if skin prick test not possible

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12
Q

what is gold standard allergy test

A

oral food challenge

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13
Q

cons of oral food challenge

A

high risk of anaphylaxis
time consuming
difficult in little kids to see if they get sx
close supervision

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14
Q

what is the prerequisite for type 2 reactions

A

breakdown in self selection

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15
Q

examples of type 2 reaction

A

goodpastures
pemphigus vulgaris
graves
myasthenia gravis

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16
Q

how is type 2 and type 3 different

A

type 3 is a soluble Ag, type 2 is on your cells

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17
Q

example of type 3 reaction

A

SLE
polyarteritis nodosa

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18
Q

what type of damage is done in type 3 reactions

A

fibrinoid necrosis

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19
Q

effects of cd4 response

A

reactive oxygen species generation
lysozymes
inflam

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20
Q

effects of cd8 response

A

apoptosis from
- perforin
- granzyme

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21
Q

4 examples of type 4 reactions

A

contact dermatitis
tuberculin skin test
T1DM
Hashimoto’s

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22
Q

important determinants of transplant rejection

A

HLA / MHC
ABO blood group

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23
Q

what chr is HLA encoded on

A

6

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24
Q

types of HLA 1

A

A B C

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25
Q

types of HLA 2

A

DR DQ DP

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26
Q

which cells have HLA 1 or 2

A

all have 1
APCs have 2

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27
Q

which groups are most important to match

A

DR > B > A

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28
Q

what is the chance your sibling is your perfect HLA match

A

1/4

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29
Q

3 pathways by which t cells recognise transplant –> rejection

A

direct - donor APC present’s donor MHC to recipient t cells
indirect - recipient APC present’s donor peptides to recipient’s t cells
semi direct - recipient APC presents parts of MHC to recipient t cells

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30
Q

in what scenarios are anti HLA ABs made

A

not naturally occurring
pre formed - transplant, transfusion, pregnancy
post-formed - graft damage

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31
Q

which ABs involved in B cell mediated rejection occur naturally

A

anti A / B (blood group)

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32
Q

where do the ABs bind to transplant to cause rejection

A

endothelium of BV of graft

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33
Q

mx of transplant rejection

A

screen for it
- ABs - before / during / after
- T cell - biopsy

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34
Q

definitive diagnosis of transplant rejection

A

biopsy - inflammation

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35
Q

name induction immunosuppressants (pre op)

A

anti thymosite globulin (ATG)
anti CD52
anti CD25

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36
Q

name baseline immunosuppressants

A

calcineurin inhibitor
azothioprine or MMF
steroids

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37
Q

tx of t cell rejection

A

methylprednisolone IV then oral

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38
Q

tx of b cell rejection

A

plasma exchange
IVIG
anti CD5 / 20 (stops B cells producing ABs)

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39
Q

autologous vs allogenic SCT

A

autologous = patients own stem cells
allogenic = HLA matched donor SCs

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40
Q

when is autologous vs allogenic SCT used

A

autologous = MM, lymphoma, solid tumours
allogenic = leukaemia, myelodysplasia

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41
Q

which type of SCT has higher relapse rate

A

autologous

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42
Q

which type of SCT is more tolerable

A

autologous

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43
Q

which type of SCT has GVHD risk

A

allogenic

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44
Q

is GVHD reversible

A

NO

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45
Q

what is GVHD

A

donor lymphocytes attack recipient’s tissues
- GI / skin / bone Sx

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46
Q

which type of SCT needs immunosuppression

A

allogenic

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47
Q

how can the immune system be boosted (4)

A

vaccination
replacement of missing components
cytokines
checkpoint inhibition

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48
Q

3 requirements of a vaccination

A

generates immunological memory
no adverse reactions
practical

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49
Q

how can vaccines be enhanced

A

adjuvants
- boost response without affecting specificity
- more persistent Ag or assisted activation

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50
Q

example of vaccine adjuvant

A

aluminium salts

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51
Q

what is a depot adjuvant of vaccines

A

more persistent Ag

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52
Q

what is a stimulant adjuvant of vaccines

A

assisted activation

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53
Q

examples of live attenuated vaccine

A

MMR
VZV
BCG
oral polio (Sabin)
typhoid
yellow fever

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54
Q

pros of live attenuated vaccines

A

lifelong immunity possible (no boosters)
multi strain protection
all phases of immune system activated

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55
Q

cons of live attenuated vaccines

A

reversion to virulence possible
risk if immunocompromised
complex storage - refrigeration etc

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56
Q

examples of inactivated vaccines

A

influenza
polio - salk
cholera
plague
hep A
rabies
pertussis

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57
Q

examples of component vaccines

A

hep B
HPV
influenza recombinant

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58
Q

examples of toxoid vaccines

A

diptheria
tetanus

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59
Q

pros of inactivated / component vaccines

A

no reversion to virulence
safe if immunocompromised
easier storage
cheap

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60
Q

cons of inactivated / component vaccines

A

poor immunogenicity
repeated boosters needed
do not follow natural infection route eg SC for flu

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61
Q

examples of conjugate vaccines

A

meningitis
influenza
strep pneumonia
tetanus

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62
Q

pros of conjugate vaccines

A

effective against encapsulated bacteria
good for kids

63
Q

cons of conjugate vaccines

A

poor immunogenicity
repeated boosters
do not follow normal route of infection

64
Q

examples of DNA / RNA vaccines

A

covid pfizer
covid AZ

65
Q

pros of DNA / RNA vaccines

A

non infectious and non integrating

66
Q

cons of DNA / RNA vaccines

A

possible autoimmunity response
need target that envokes a good immune response

67
Q

what is a live attenuated vaccine

A

live pathogen modified to limit pathogenesis

68
Q

what is an inactivated / component vaccine

A

inactivated = destroyed pathogen
component = isolated Ag protein

69
Q

what is a conjugate vaccine

A

polysaccharide + Ag protein carrier

70
Q

what are DNA / RNA vaccines

A

pathogen’s DNA/RNA delivered to host via viral vector / lipids

71
Q

which vaccines are good against encapsulated bacteria

A

conjugate vaccines

72
Q

which vaccines can’t immuncompromised people have

A

live attenuated

73
Q

which vaccines are completely safe for immunocompromised people

A

inactivated / component

74
Q

pneumonic for encapsulated bacteria (and for examples of conjugate vaccines)

A

NHS
n. meningitis
h. influenza
strep pneumonia

75
Q

3 types of replacement of missing components for immune boosting

A

haematopoeitic stem cell transplant
ABs
T cell transfer

76
Q

what type of ABs can be given to boost immune system

A

normal Ig
specific Ig

77
Q

who gets normal Ig replacement

A

AB deficiencies eg alpha gamma globulinaemia, hyper IgM, CVID (all primary) or cancer / BMT (secondary)

78
Q

when is specific Ig replacement done

A

post exposure eg hep B, rabies, VZV

79
Q

3 examples of T cell transfer use

A

virus specific
tumour infiltrating
CART

80
Q

when is IL2 replacement given

A

renal cancer

81
Q

2 effects of IFN alpha replacement

A

antiviral
anti cancer

82
Q

examples of antiviral IFN alpha replacement

A

Hep B / C

83
Q

examples of anticancer IFN alpha replacement

A

kaposi’s sarcoma
hairy cell leukaemia
CML
melanoma

84
Q

when can IFN g replacement be given

A

chronic granulomatous disease
- increase macrophage function

85
Q

when can IFN b replacement be given

A

relapsing remitting MS
- this is reducing the immune system tho

86
Q

what is the point of giving checkpoint inhibitors

A

anti cancer
- immunosuppressive signals upregulated by cancer - removing the immune brakes = boosted immune response

87
Q

name 2 checkpoint inhibitors and their method of action

A

ipilimumab (CTLA4) - allows t cell activation
nivolumab (PD1) - prevents t cell death

88
Q

2 examples of when checkpoint inhibitors can be used

A

advanced melanoma
metastatic renal cell carcinoma

89
Q

how do steroids suppress the immune system

A

affect transcription

90
Q

2 descriptors of the effect of steroids

A

widespread
not immediate

91
Q

how do steroids affect prostaglandins

A

inhibit phospholipase a2 –> reduces prostaglandins –>
less inflammation

92
Q

3 effects of steroids on phagocytes

A

reduced trafficking –> neutrophil count RISES
reduced phagocytosis
reduced enzyme release

93
Q

4 effects of steroids on lymphocytes

A

lymphopenia
cytokine gene expression blocked
reduced AB production
pro-opportunistic

94
Q

how do anti proliferative agents suppress the immune system

A

inhibit DNA synthesis

95
Q

3 examples of anti proliferative agents

A

azothioprine
cyclophosphamide
mycophenolate mofetil

96
Q

what type of cells do anti proliferative agents affect the most

A

cells with rapid turnover

97
Q

2 types of cell signalling inhibitors used to dampen immune system

A

calcineurin inhibitors
mTOR inhibitors

98
Q

how do calcineurin inhibitors dampen immune system

A

reduce IL2 expression –> reduce cell proliferation / function

99
Q

2 examples of calcineurin inhibitors

A

tacrolimus
cyclosporine

100
Q

what conditions are calcineurin inhibitors used in

A

transplant
psoriasis
SLE

101
Q

how do mTOR inhibitors dampen immune system

A

inhibit t cell proliferation and function

102
Q

2 examples of mTOR inhibitors

A

rapamycin
sirolimus

103
Q

when are mTOR inhibitors used

A

transplant

104
Q

2 drugs that target T cell surface Ags

A

basiliximab
abatacept

105
Q

how does basiliximab dampen immune system

A

inhibits t cell proliferation

106
Q

use of basiliximab

A

rejection prophylaxis

107
Q

how does abatacept dampen immune system

A

fusion protein that blocks T cell activation

108
Q

use of abatacept

A

RA

109
Q

example of b cell surface Ag targeting agents

A

rituximab

110
Q

how does rituximab dampen immune system

A

depletes mature b cells

111
Q

use of rituximab

A

NHL

112
Q

how does vedlizumab work

A

prevents leucocyte migration

113
Q

use of vedlizumab

A

IBD

114
Q

what does basiliximab bind to

A

cd25

115
Q

what does abatacept bind to

A

cd80 / 86

116
Q

what does rituximab bind to

A

cd20

117
Q

what does vedlizumab bind to

A

alpha 4 beta 7 integrin

118
Q

name 2 TNFa blockers and common indications for use

A

infliximab
adalimumab
RA / psoriatic arthritis

119
Q

what can infliximab be used for

A

RA
ank spon
psoriasis / psoriatic arthritis
IBD

120
Q

what does etanercept target and what is it used for

A

TNF alpha and beta
ank spon, JIA, RA, psoriatic arthritis

121
Q

what does ustekinumab target and what is it used for

A

p40 subunit of IL12/23
psoriasis, psoriatic arthritis, crohns

122
Q

what does secukinumab target and what is it used for

A

IL17A
psoriasis, psoriatic arthritis, ank spon

123
Q

what does natalizumab target and what is it used for

A

a4b1 integrin
MS

124
Q

what does denosumab target and what is it used for

A

RANK ligand
osteoporosis

125
Q

what does toculizumab target and what is it used for

A

IL6R
RA, castleman’s disease

126
Q

when is plasma exchange used and what is being removed

A

severe AB mediated disease
- goodpastures (anti GBM)
- MG (anti Ach R)
- humoural transplant rejection / ABO incompatability (anti HLA/AB)

127
Q

limitation of plasma exchange & solution

A

rebound AB production
- prescribe anti proliferative (MFM)

128
Q

generic SEs of immunosuppression

A

infection - atypicals and more severe
malignancy - EBV lymphoma, melanoma, non melanoma skin cancer
- AID

129
Q

SE of steroids

A

metabolic - DM, dyslipidaemia, osteoporosis, adrenal suppression
peptic ulcers
avascular necrosis
cataracts, glaucoma
pancreatitis

130
Q

important prescribing note with steroids & reason why

A

do not stop suddenly - adrenal suppression –> crisis **key one

131
Q

SEs of cyclophosphamide

A

haemorrhagic cystitis **key one
bladder cancer
non melanoma skin cancer
infertility M>F
PCJ pneumonia

132
Q

SEs of MMF

A

PML (JC virus reactivation) ** key one
herpes reactivation

133
Q

SE of azothioprine

A

BM suppression **key one

134
Q

SE of all cell surface Ag agents

A

infusion reactions

135
Q

Se of rituximab

A

worsening CVD
PML

136
Q

SE of abatacept

A

TB
Hep B/C

137
Q

SE of vedlizumab

A

hepatotoxic
PML

138
Q

SE of TNFa/b ABs

A

TB
Hep B/C
lupus like disease
demyelination

139
Q

SE of toclizumab

A

dyslipidaemia
hepatotoxicity

140
Q

SE of denosumab

A

avascular necrosis of jaw **key one

141
Q

what test should you do prior to starting AZ

A

TPMT

142
Q

how is HIV detected

A

ABs - serology
Ag = direct confirmation of viral particles
RNA / DNA = direct confirmation of viral genetic material

143
Q

when will HIV ABs be positive

A

after seroconversion 15-45 days

144
Q

in whom can’t you use AB test to detect HIV infection

A

neonates - passive transfer from mother

145
Q

describe HIV lifecycle

A

binding to host cell
fusion with host cell membrane
reverse transcription
integration
replication
assembly
budding

146
Q

which class of drugs inhibit HIV lifecycle at binding to host cell

A

CCR5 inhibitors

147
Q

which class of drugs inhibit HIV lifecycle at fusion with host cell membrane

A

fusion inhibitors

148
Q

which class of drugs inhibit HIV lifecycle at reverse transcription

A

NRTIs or NNRTIs

149
Q

example of NRTI and use

A

tenofovir - PrEP

150
Q

which class of drugs inhibit HIV lifecycle at integration

A

integrase inhibitors

151
Q

which class of drugs inhibit HIV lifecycle at budding

A

protease inhibitors

152
Q

when should HIV+ patients be given ART

A

immediately after Dx - no longer wait for low CD4 etc

153
Q

what types of drugs would a newly Dx HIV+ patient be given

A

2 NRTIs and a protease inhibitor

MedEd Path (10 decks)

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