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Immunology/Rheumatology > Immunology > Flashcards

Immunology Flashcards

1
Q

What complement deficiencies lead to an SLE-like condition and how does this occur?

A

C1, C4 and C2 Inability to clear self antigens

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2
Q

What complement deficiencies lead to increased risk of Neisseria?

A

Lytic phase complements - C5-C9 Alternative pathway - Factor D and properdin

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3
Q

What are the phagocytic immunodeficiencies?

A

Chronic granulomatous disease Cyclic neutropenia Neutrophil G6PD deficiency Leukocyte adhesion deficiency Myeloperoxidase deficiency

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4
Q

What are the features of phagocytic immunodeficiencies?

A

Deep seated infections Bacterial and fungal infections Delayed separation of cord

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5
Q

What are the clinical features of antibody/humoral immunodeficiency?

A

Mucosal infections S. pneumoniae and haemophilus Chronic diarrhoea esp due to giardia and gut infections Autoimmune cytopenias

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6
Q

What are the common antibody immunodeficiencies?

A

Common variable immunodeficiency

X-linked agammaglobulinaemia

Combined immunodeficiency

Good syndrome

Specific antibody deficiencies

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7
Q

What are the steps for the migration of leuokocytes?

A

Rolling adhesion

Tight binding

Diapedesis

Migrations

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8
Q

What are the complement activation pathways?

A

Classic

MBLECTIN

Alternative (via pathogens)

All come together at C3

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9
Q

Which cells express MHC1, which express MHC2?

A

MHC 1 - found on all nulceated cells. Recognised by CD8+ cells

MHC II - found on professional antigen presenting cells. Recognised by CD4+ cells

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10
Q

What are the T helper subsets and what are their roles?

A

Th1 - activates macrophages, induces B cells

Th2 - activates B cells, various effects on macrophages, promotes IgE

Th17 - protects against intracellular pathogens

Treg - secretes anti-inflammatory cytokines eg IL-10 and TGFb

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11
Q

What is the role of each of the immunoglobulin classes?

A

IgM - complement activation

IgG - opsonisation, complement activation. Switch triggered by INF-y

IgE - immunity against helminths, mast cell degranulation. Switch triggered by IL-4

IgA - mucosal immunity

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12
Q

What are the types of hypersensitivity reactions?

A

Type I - immediate (classic allergy)

Type II - cytotoxic reaction - antibody dependant (haemolytic anaemia, goodpastures)

Type III - immune complex reaction (vasculitis)

Type IV - delayed - cell mediated (contact dermatitis, asthma)

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13
Q

What are the disease associations with C-ANCA? What is its other name?

A

PR3-ANCA

Granulomatosis with polyangiitis >90%

Microscopic polyangiitis 30%

Associated with more frequent relapses

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14
Q

What are the disease associations with P-ANCA? What is its other name?

A

MPO-ANCA

Microscopic polyangiitis

Eosinophilic granulomatosis with polyangiitis

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15
Q

What is the treatment for ANCA associated vasculitis?

A

Induction with steroids + cyclophosphamide (some switch to AZA)

Maintanence with AZA or MTX

Maintaince therapy for 2-3 years

Bactrim prophylaxis

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16
Q

What drugs can cause an ANCA associated vasculitis?

A

Propythiouracil

Hydralazine

Allopurinol

Sulphasalazine

Minocycline

Cefotaxime

Ciprofloxacin

Clozapine

17
Q

Which ANCA type is associated with frequent relapses?

A

PR3-ANCA (c-ANCA)

18
Q

What is the classic renal picture with microscopic polyangiitis?

A

Primary pauciimmune necrotising GN

19
Q

What is the treatment for temporal arteriitis?

A

Steroids tappered over 1-2 years

Methotrexate can be used as a steroid sparing agent

Tocilizumab (anti-IL6) can be used for refractory cases

Disease activity monitored clinically and with ESR/CRP

20
Q

What is the HLA association with Behcets disease?

A

HLA-B51

21
Q

What is the management with Behcets?

A

Topical steroids

PO prednisone if refractory

Colchicine useful for arthitis

Can use immunosuppression if refractory - AZA, anti-TNF, cyclosporin

22
Q

What is the pathophysiology of X-linked severe combined immunodeficiency?

A

There is a mutation in the common y-chain of the cytokine receptors found on lymphocytes. The lack of activity of teh cytokines notably IL-7 means there is no T-cell development. While B cells can still develop the lack of T-cells causes a lack of stinumation and therefore lack of antibody synthesis. IL-15 is required for NK cell maturation so they are also lacking

23
Q

What are the clinical findings of severe combined immunodeficiency? What is the treatment?

A

Often males as majority is x-linked SCIDs but can be autosomal recessive

Presentation within 1st year of life

Widespead severe infections eg PJP, HSV, candida, pseudomonas. Can get GVHD from maternal T cells which cross the placenta. Small thymus, hypoplastic lymphoid tissue

Treatment is AlloSCT within 1 year of life or gene therapy for X-linked

24
Q

What is the mutation which causes x-linked agammaglobulinaemia?

A

A mutation in Bruton tyrosine kinase

25
Q

What is DiGeorge syndrome?

A

Caused by 22q11 deletion leading to failure of development of the 3rd and 4th pharyngeal pouches. This causes:

Abscent thymus and lack of T cell development (normal or reduced antibody levels) - fungal and viral infections

Abscent parathyroids - tetany

Defects of heart and great vessels

Abnormal appearance of facial features

26
Q

What are the clinical features of X linked agammaglobulinaemia?

A

Recurrent respiratory/mucosal infections after 6 months of age

Notably S. aureus, haemophilus, and s. pneumonia

Giardia (needs IgA for opsonization)

Enteroviruses

**all other viral, fungal and protezoal infections can be managed

27
Q

What infections are seen with each deficiency? (T cell, B cell, granulocyte, complement)

A
28
Q

What are the 6 HLA subclasses?

A

MHC I - HLA A, HLA B, HLA C

MHC II - HLA DP, HLA DQ, HLA DR

29
Q

Where are the HLA (MHC) genes located?

A

On chromosome 6

30
Q

What is the physiology of CTLA-4

A

Found on T cells

It has a significantly higher affinity for CD80/86(APC) than CD28(T cell) therefore preventing the second signal for T cell activation.

Repeated activation upregulates CTLA-4

31
Q

Which checkpoint inhibitor is most associated with thyroid disease?

A

PD-1

32
Q

Which checkpoint inhibitor is most associated with colitis?

A

CTLA-4

Immunology/Rheumatology (2 decks)

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