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FRACP Exam > Immunology > Flashcards

Immunology Flashcards

1
Q

What IL does anakinra block?

A

IL-1

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2
Q

What IL does Sekukinumab block?

A

IL17

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3
Q

How do toll like receptors induce an immune response?

A

Act via NF-kappa-B which causes release of cytokines/chemokines and expression of costimulatory molecules

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4
Q

What are intracellular TLR?

A

TLR3,7-9 (recognise DNA/RNA of engulfed pathogens)

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5
Q

What is TLR4s role in sepsis?

A

in Gram - bacteraemia there is widespread lipopolysaccaride that activates TLR4 to stimulate cytokine release throughout the body leading to shock.
TLRs are meant to only be a localised reaction but lead to shock in disseminated infeciton

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6
Q

What are the common pro-inflammatory cytokines?

A

IL-1, IL-6, TNF

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7
Q

What does Tocilizumab block?

A

IL-6

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8
Q

What is one of the main role sof PAMPs and PRR?

A

Upregulation of costimulation receptors (B7-CD28)

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9
Q

Deficiency of MAC part of complement makes pts more susceptible to what?

A

Neisseria infections

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10
Q

What do the C1-3 complement component deficiencies lead to?

A

Immune complex disease - SLE, GN, Vasculitis

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11
Q

What is deficient in angioedema?

A

C1esterase inhibitor

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12
Q

What is the major mediator in C1esterase inhibitor deficiency?

A

Bradykinin (hereditary angioedema)

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13
Q

What is the pattern of inheritance of hereditary angioedema?

A

AD

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14
Q

What test is used to differentiate heredutary from acquired C1 inhibitor deficiency?

A

C1q levels - depleted in acquired (where complement is consumed by another deisorder e.g MGUS or lymphoma)

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15
Q

What is icatibant?

A

Bradykinin-2 receptor antagonist - used in hereditary angioedema

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16
Q

What is chronic granulomatous disease?

A

Deficiency of subunit of NADPH oxidase - leading to recurrent infections. - Test with NBT test ( to check for oxygen metabolism)

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17
Q

What is seen on mature B-cell surface compared to immature?

A

IgM AND IgD (only IgM on immature)

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18
Q

Recurrent sinupulmonary and gut infections (sinusitis, bronchtis, tonsilitis, otitis media) are signs of what?

A

Lack of antibody response - as in CVID

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19
Q

What are needed for diagnosis of CVID

A

Marked decreased IgG +/- low IgA +/- Low IgM
- on 2 occasions
AND one of
- Poor antibody response to vaccination
IgG <2 and delay to proviginf Ig replacement
Low switched memory B cells
Absent isohaemagglutinins AND be >4y/o

20
Q

What are non-infection features of CVID?

A

Autoimmunity (ITP, AIHA), vitiligo, Cancers - gastric, lympohoma

21
Q

How do you treat CVID?

A

IgG regularly, prompt treatment of infection, no live vaccines

22
Q

X-linked Agammaglubulinaemi is secondary to what?

A

BTK mutation - Brutons TYR kinase

23
Q

What are clinical features of X-linked agammablobulinaemia

A

Recurrent infections from age ~6 months

24
Q

B cell levels are ~0 in what ?

A

X-linked agammaglobulinaemia

25
Q

What is eculizumab?

A

Anticomplement MAB - used in PNH

26
Q

What E.coli subtype is implicated in HUS?

A

E.coli 0157:H7 + shiga toxin producing E.coli

27
Q

How doe Shiga toxin cause HUS?

A

Binds to glucophingolipid receptor activating endothlin 1 -> vasoconstriction -> acure renal failure
Also causes neutrophil activation which damaged glomululaer cells and form thrombus

28
Q

What is

A
29
Q

What is anatercept?

A

Anti B-7

30
Q

What is polyglandular syndrome 1?

A

AIRE gene - Autoimmune Regulator gene.
AIRE mutated in this leading to recurrent candida and hypoparathyroid and adrenal insufficiency

31
Q

What is polyglandular syndrome 2?

A

Common phenotype of autoimmune thyroid involvement, addisons disease as well as T1DM and coeliac disease in 20% of cases.
Polygenic association with HLADR3 and 4

32
Q

Ustekinumab?

A

IL12, IL23 inhibitor

33
Q

What protein is overactive in familial mediterranean fever?

A

Pyrin

34
Q

What are high risk HLA for T1DM?

A

HLA DR4-DQ8 and/or DR3-DQ2

35
Q

What is the mechanism of GVHD?

A

Graft T cell sensitisation against host MHC antigens

36
Q

What goes ani-GBM antibody attack?

A

alpha-3 subunit of type IV collagen in the GBM

37
Q

What meds cause Jak-kinase inhibiotion?

A

Tofacitinib, baricitinib

38
Q

How does natalizumab work??

A

Anti-alpha 4 interrin

39
Q

What infections are more common with proteasone inhibitor use? (bortezumib)

A

HSV, resp tract, influ complications

40
Q

What is the MoA of Abatercept?

A

Costimulation blockade of CD28

41
Q

What cell has CD14?

A

Macrophage-monocyte lineage

42
Q

What cells have MHC I?

A

ALL cells (except RBC and some neurons)

43
Q

What are the features of bechets¿

A

Turkish people
Autoimflammatory vasculitis
Apthous ulcers recurrent,
Occular inflammation, genital ulcers, erythema nodosum, pustules
VTE
Tx with colcicine + steroids

44
Q

What are the features of PAN?

A

Arteritis
Ishchaemia with infarct
No GN, lung haemorrhage, No ANCA
Ass Hep B
Steroids
Subacute over weeks-months
Tx with steroids
Doens’t relapse/uncommonly

45
Q

What results in HyperIgM?

A

Mutation in CD40-CD40L costimulatory pathway
- reults in no T cell activation og B cells => they can only make IgM

46
Q

What is caused by mutation in britons tyrosine kinase?

A

X-linked Agammaglobulinaemia

47
Q

What are the features of Haemophagocytic lymphohistiocytosis:

A

Defectve NK cells and CD8 T cells.
Can be triggered by viruses eg EBV, CMV, malignancy,
Fevers, hepatosplenomegaly, high ferritin, cytopenia, high LDL, TGL, Bili
Hamophagocytosis (phagocytosis of BM)

FRACP Exam (15 decks)

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