Immuno Flashcards
Atypical granulomatous infection in previously healthy patient
IFN gamma, IFNgamma receptor deficiency, IL-12, IL-12 receptor
Salmonella, atypical
Mycobacteria, TB and BCG.
Patients are unable to form granulomata
6 days every 3 weeks; give G-CSF
Cyclic neutropenia
X linked tyrosine kinase - BTK gene
Failed production of mature B cells, no antibodies, symptoms 3-6 months
Brutons agammaglobulinaemia
congenital neutropenia=NO NEUTROPHILS
Kostmann
Rheumatoid arthritis patient with mycobacterial infections
Iatrogenic - TNF antagonists
Recurrent infections with negative NBT and dihidrorhodamine tests
Chronic granulomatous disease
Young girl with normal B cells, normal CD8+ but absence of CD4+ (jaundice and hepatosplenomegaly). kid unwell by 3 months of age:
Bare Lymphocyte Syndrome BLS. IgG would be low
(Answer type 1 and 2 exist, but more common to have type 2 with absent CD4 compared to type 1 with absent CD8).
Young boy with normal B cells and absence of CD8+ and CD4+
Di George
Immune deficiency that has improved with age but not mum is concerned about delayed speaking and language
Di George
Normal B and T cells, high IgM but absence of IgA, IgE and IgG– Pneumocystis Cariini and failure to thrive.
Answer – CD40L deficiency – this is hyper-IgM. Presents in first years of life with recurrent bacterial infections. X-linked; can’t class switch so no IgA and IgG
Patient with recurrent pneumococcal infections and meningitisforming membrane attack complex) can predispose to infection from encapsulated organisms.
C5-C9 Deficiency
A 6-month old boy with severe failure to thrive and recurrent infections, early infant death…etc… his T cells were undetectable and B cells were NORMAL even if you think they should be lower
(Answer – X-linked SCID) Failure to thrive, and deficiency in IL-2.
SLE. Membraneous lymphogromelulonephritis
C1q deficieny.
Marker of antibody mediated rejection
C4d
Most important to match for rejection
HLA: DR>B>A
Hyper-acute rejection (ABO incompatibility)
Preformed Ab activates complement
Thrombosis and necrosis, prevented by cross matching properly
Can lead to development of post transplantation lymphoproliferative disease. PTLD is a proliferation (rapid increase) of lymphoid (immune) cells. It can develop in people who are taking immunosuppressive drugs to prevent rejection of an organ or an allogeneic (donor) bone marrow or stem cell transplant
calceurin inhibitors
Causes progressive multifocal leukoencephalopathy
mycophenolaTe myofetil T cells
Mechanism behind GVHD Graft versus host disease (GvHD)
○ Donor cells attacking host
○ Days-weeks, rash, N+V, bloody diarrhoea, abdo pain, jaundice
○ Prophylaxis: methotrexate/cyclosporine
○ Treat with steroids
Mechanism behind antibody mediated rejection
○ Antibodies attack vessels
○ Exposure -> proliferation + maturation of B cells ->
○ Effector phase - antibodies bind to graft endothelium
(->vasculitis), two weeks after the actual transplant
Mechanism behind cellular rejection
○ T cells, type IV reaction
○ TReat with T cell suppressors
○ Donor APC presenting antibodies to recipient
○ Cellular infiltrate
Diffuse systemic scleroderma
scl-70 topoisomerase
Limited cutaneous scleroderma
anti-centromere
Anti phospholipid syndrome
anti-cardiolipin
epistaxis and haematuria
Wegener’s granulomatosis c-ANCA
Serum sickness - Type X reaction?
III reaction, following antibiotics, symptoms take 7-12h to develop
dry eyes and mouth antibodies
anti-Ro, anti-La
weight loss, anti TTG antibodies, anti-endomysial antibodies, steatorrhoea
Coeliac
CREST
Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly, Telangiectasia
SLE
anti ds DNA
Pernicious anaemia
anti parietal cell > anti intrinsic factor