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BPT > Immunology > Flashcards

Immunology Flashcards

1
Q

Autoimmune pancreatitis - check for?

A

IgG4 levels

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2
Q

IgG4 disease vs PSC

A

Both can have cholestatic LFT’s and biliary strictures

IgG4 likely to also have pancreatic involvement

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3
Q

When does T cell development occur in thymus?

A

In utero - have naive T cells (CD4/CD8) at birth

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4
Q

Process that occurs in thymus cortex?

A

Positive selection
- Addition of T cell receptor (random through rearrangement
- Ensuring T cell can bind MHC
- Tagging with CD4 or CD8 depending on which MHC it binds

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5
Q

Process in thymus medulla
- Deficiency of AIRE?

A

Negative selection
- TEst T cells to ensure no autoreactivity and appropriate activity against foreign
- Transcription genese make self antigens
- AIRE makes insulin, cascin - deficiency = autoimmune polyendocrine syndromes

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6
Q

Signal 1

A

Naive T cell receptor binds antigen/MHC
Binding proteins and STOP signal

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7
Q

Signal 2 -

A

Costimulation

Initial activation - CD80/86 on APC binding to CD28. Then APC produces CD40 to bind to CD40ligand

Suppression - subsequent production on T cells of CTLA4, PD-1
- CTLA4 binds CD80/86 with higher affinity

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8
Q

CD40ligand deficiency - disease?

A

Hyper IgM syndrome

No CD40ligand on T cells, so ineffective class swiitching on B cells

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9
Q

FK506?

A

Tacrolimus

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10
Q

Signal 3

A

IL-2 binding to CD25 receptor causing T cell
- differentiation (subsets)
- entering cell cycle and proliferation

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11
Q

Role of calcineurin

A

Dephosphorylates NFAT, which is a transcription factor that stimulates IL-2 production

Blocks release of NFAT, so IL-2 cannot be released

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12
Q

MoA of mTOR inhibitors

A

Bind FK binding protein
Inhibit IL-2 action including CDK and cyclin production

Induce cell cycle arrest in G1/S

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13
Q

TH1
- target
- cytokines

A

Intracellular (virus), autoimmunity

TNFa, IFNy, IL-2

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14
Q

TH2
- target
- cytokines

A

Parasites + allergy

IL-4, IL-5, IL-13

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15
Q

TH17
- target
- cytokines

A

Extracellular bacteria/fungi. Recruits neutrophils

IL-17A, IL-17F

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16
Q

Treg
- Target
- Cytokines

A

Suppressess immune system

TGFb, IL-10

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17
Q

How are CD8 cells stimulated to proliferate?

A

Binding antigen on MHC1

TH1 cells producing IL-2, IL-12 and IFNy to stimulated CD8 proliferation

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18
Q

Mechanism of CD8 cells causing cell death

A

Stimulate to form perforins, targeted cell killing by inducing apoptosis

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19
Q

Functions of antibodies

A

Stimulate complement via classical pathway (IgM and IgG)

Recruit immune cells - opsonisation + phagocytosis, antibody dependant cellular cytotoxicity

Neutralise pathogens

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20
Q

Class of antibody determined by?

A

Heavy chain type

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21
Q

Which antibodies form B cell receptors

A

IgM
IgD

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22
Q

Chromosome for heavy chain?

A

Chromosome 14

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23
Q

Antibody diversity
- When does it happen
- How

A

Occurs in antigen independant in bone marrow

VDJ recombination until functional antibody formed

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24
Q

Allelic exclusion

A

After VDJ recombination, once functional Ab produced, DNA locked so B cell can ony make one Ab

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25
Q

Immature B cell leaving BM characterised by?

A

IgM and IgD

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26
Q

Which antibody crosses placenta?

A

IgG

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27
Q

Which antibodies activate complement

A

IgM
IgG

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28
Q

Which IgG subclass does not bind complement

A

IgG4

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29
Q

Function of IgA

A

Ab found in secretions - first point of defence in areas exposes to outside world

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30
Q

Function of IgE

A

Embed in mast cells (sensitising event)

Can then be stimulated by re-exposure to antigen to cause mast cel degranulation

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31
Q

B2 cells - antigen dependant class switching process

A

B cell receptor binds antigen, displays on MHC 2

Co-stimulates CD4 cells, matures an forms subsets

T cell subset produces different cytokines for class switching
- TH1 –> IgG
- TH2 –> IgE and IgA

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32
Q

B2 Somatic hypermutation

A

B cell receptor binds atigen, DNA uncocked, random mutations to produce higher affinity B cell receptor

Highest affinity receptor selected, proliferates. Becomes:
- Plasma cell
- Memory cell - skips this process next time for faster immune response

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33
Q

B1 cells (t cell independant)

A

Can bind lipopolysaccharide antigens. Lie in marginal zones of spleen.

Only produce IgM, provide limited immune response to encapsulated organisms

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34
Q

MAC components

A

C5b - C9

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35
Q

Common complement pathway componentns

A

All 3 pathways end in C3 convertase
- converts C3 to c3a and c3b

C3b can then also form C5 convertase
- converts C5 to c5a and c5b

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36
Q

General principles of a and b in complement

A

A - inflammation (anaphylotoxin

B - binds - opsonin or initiates mac

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37
Q

Classical pathway complement
- Recognises?
- Componenets

A

Immune complexes and damaged cells

C1q, C1r, C1s
C2 and C4 (C2 a and b)

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38
Q

Role of CRP

A

Activation of complmenet system

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39
Q

Lectin pathway
- good at recognising?

A

MASPS

Mannin (mannose binding lectin) - found on fungi
Lectin - found on carbohydrate residues, encapsulate bacteria

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40
Q

Regulator of MAC

A

CD55 and CD59

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41
Q

Disease with lack of CD55 and CD59
- Features
- Rx

A

PNH

Haemolysis, VTE and organ ischaemia

Eculizumab

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42
Q

Inhibition of factor C3b and C3 convertase

A

Factor I - C3b
Factor H - C3 convertase

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43
Q

aHUS pathophys and ttraetment

A

Factor H and I deficiency, dysregulated alternative complement pathway

Rx - Eculizumab

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44
Q

Pathophys and tests for C1 esterase deficienc

A

Lack of inhibition of bradykinin formation –> angio-oedema

Tests - low C4, low C1 esterase, high C1

Rx - C1 esterase concentrate, bradykinin receptor antagonist

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45
Q

Antibody most potent activator of complement

A

IgM

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46
Q

IgA forms

A

Monomer plasma
DImer external body surface

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47
Q

Complmenet responsible for opsonisation/opsonins

48
Q

REgulators of alternative pathway

A

Factor H
Factor I
Properdin

49
Q

Normal TOtal IG’s
Abnormal vaccination response

A

Specific antibody deficiency

50
Q

Most common manifestation of 2nd immunodeficiency cause by chronic systemic steroid use

A

Bacterial bronchopneumonia

51
Q

CVID malignancy highest risk

52
Q

Recurrent infection with catalse positive bacteria

A

Staph, Burhilderia, Serratia, fungal

Phagocyte deficiency –> Chronic granulomatous disease

53
Q

Recurrent infections

Bowel obstructions

Early childhood

A

Chronic granulomatous disease

54
Q

Test for CGD

A

Oxidative burst test - Dihydro rhodamine assay

55
Q

Recurrent infections
Food allergies
Severe eczema

A

Hyper IgE syndrome

56
Q

Hereditary angiooedema cf histamine mediated
- timing
-

A

Bradykinin - 48-96 hours

No urticaria

Non responsive to antihistamines, steroids, adrenaline

57
Q

CR3/CR4 deficiency

A

Leukocyte adhesion deficiency

Umbilical cord takes long time to fall off

58
Q

CR3/CR4 deficiency

A

Leukocyte adhesion deficiency

Umbilical cord takes long time to fall off

59
Q

IL-5

A

Mepoluzimab

60
Q

IL-5R

A

Benralizumab

61
Q

IL4- Ra

62
Q

IgE

A

Omalizumab

63
Q

Indications for desensitisation

A

Antibiotic - done in hospital

Aeroallergin - allergic rhinitis, asthma

64
Q

Contraindications for desensitisation

A

Type 3 or 4

SJS/TENS/AGEP

65
Q

Cause of thunderstorm asthma

66
Q

Contraindications to skin prick testing for IgE

A

Recent antihistamine use

Dermatographism or serious skin condition

67
Q

When to use allergen specific IgE

A

High risk anaphylaxis

Specific allergen

Recent antihistamines

68
Q

Type 3 drug reactions
- Cause
- Presentations

A

Immune complex

Serum sickness
Vasculitis
Lupus Nephritis

69
Q

Type 2 drug reactions
- Cause
- Presentations

A

Antibody

Low cell counts due to multiple drugs
- AIHA
- ITP
- Agranulocytosis

Also Anti-GBM

70
Q

Strongest associated with fatal food anaphylaxis?

A

Poorly controlled asthma - bronchocosntriction greatest cause of mortality

71
Q

Atopy vs sensitisation vs allerg

A

Atopy - genetic tendency to produce specific IgE for allergens

Sensitisation - IgE production following allergen exposure

Allergy - allergen specific IgE and symptoms following exposure

72
Q

Persistent hypotension on Beta blocker

A

Give glucagon

73
Q

Manageement of aspirin induced respiratory disease

A

Due to COX1 inhibition

Avoid COX1 inhibitors
Intranasal corticosteroids
Oral monteleukast

74
Q

Synthetic TLR7 agonist

75
Q

Most common presentation of IgG deficiency

A

Normal phenotype

76
Q

Low C4 - which cryoglobulinaemia?

A

Type 2 and Type 3

77
Q

When is varicella infectious
What precautions

A

1-2 days before rash –> rash cursted over

Droplet

78
Q

VZV vaccine PPx
- When
- Who to give

A

Exposure < 5 days

Not immuncompromised, Not pregnant, > 12 months

79
Q

VZV Ig
- When
- Who to give

A

Exposure < 10 days

Pregnant or immunocompromised who have inadequate Ig levels (check Ig levels)

80
Q

Dysregulated response to EBV infection

A

X linked lymphproliferative disease

81
Q

Periodic fever syndrome

A

Inflammasomes

82
Q

STAT3?

A

Hyper IgE syndrome
- Prevents Th17 cell production

83
Q

Common cytokine receptor gamma chain deficiency

84
Q

Function of CRP

A

Bind phospholipi - recognise foreign pathogens and damaged cells

Activates complement system

85
Q

Benefit of conjugate vaccines

A

Elicites T cell response (polsaccharide bound to protein), elicits T cell response

86
Q

Storiform fibrosis

87
Q

Allergy symptoms
Recurrent pancreatitis or sclerosing cholangitis
Good response to steroids

A

IgG4 disease

88
Q

Only vaccine CI in egg allergy

A

Yellow fever

89
Q

Bone tumour epiphysis

A

Chondroblastoma

90
Q

Metaphysis bone cancers

A

Osteosarcoma

91
Q

When to stop IVIG in 2nd hypogammagobulinaemia

A

When Ig levels normalised

92
Q

MoA of fingolimod

A

Spingosine 1 phosphate receptor modulator

Prevents leukocyte migration

93
Q

A/E of fingolimod

A

Life threateing HSV

Bradycardia

94
Q

MoA of dupilumab

Indication

A

Blocks apha subunit of IL-4 (blocks both IL-4 and IL-13)

Eczema

95
Q

MoA of tofactinib

A

inhibits JAK1 and JAK3 (in contrast to ruxolitinib)

96
Q

Indications that can clear allergy status

A

> 10 years with unknown reaction
Childhood nonspecific exanthem
10 years ago delayed reaction

97
Q

Delayed anaphylaxis mammalian food

Sensitised event?

A

Tick bites

98
Q

Most common cancer immunodeficiencies?

99
Q

Management of chemotherapy induced diarrhoea
1st
2nd

A

1st - loperamide

2nd- SC octreotide

100
Q

Fluoropyrimidine chemotherapy -severe toxicity with 1st dose
- treatment
- test for?

A

Uridine triacetate

Check for polymorphisms in F DU metabolising enzymes

101
Q

Features separating angioodema syndrome vs anaphylaxis

A

Angiooedema
- No urticaria
- Asymmetrical
- Doesn’t involve dependant areas

102
Q

Clinical features of HAE

A

Young
Recurrent abdominal attacks

103
Q

Diagnostic HAE

A

Low C4
Normal C1q

C1 inh
-low - HAE 1
- normal but impaired function - HAE 2

104
Q

Clinical features and associates Acquired angiooedema

A

Age > 40

Malignancy - NHL
MGUS

104
Q

Clinical features and associates Acquired angiooedema

A

Age > 40

Malignancy - NHL
MGUS

105
Q

Clinical features and associates Acquired angiooedema

A

Age > 40

Malignancy - NHL
MGUS

106
Q

Diagnostic acquired angiooedema

A

Low C4
Low C1 Inh
Low C1q

107
Q

Super antigen
- Example
- How it works

A

Exotoxins from staph (TSS)

Can cross link MHC class II antigen presenting cell

AND

The adjacent T cell receptor

108
Q

Mab with x - composition?

A

x is cool like a chimera
chimeric

109
Q

Mab with z - composition?

A

Humans get z scored

humanised

110
Q

Mab with m

A

man = human

fully human

111
Q

Amplifies normal alternative complement pathway

A

Foreign or damaged cells

112
Q

B2 microglobulin - what structure?

113
Q

Where does class switching and somatic hypermutation take place?

A

Germinal centres - temporary structures formed in 2nd lymphoid organs

114
Q

What does innate immune system detect?

A

Pattern recognition

PAMP - microbes only
DAMPS - damage associated peptides

115
Q

HLH pathophys

A

Deficient CD8 and NK activity

Unsuppressed macrophage activation

BPT (18 decks)

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