Immuno Flashcards
EBV and amoxicillin/ampicillin/cephalosporin
Causes hypersensitivity reaction in presence of EBV - not true allergy
Ibrutinib can be used in which leukemia?
CLL
mAb Tx Psoriasis
Ustekinumab (anti IL-12/23)
Guselkumab (anti IL-23)
Sekukinumab (anti IL-17A for PA and ankalosing spondylitis)
Tx RA (not DDMARD/MTX)
Rituximab (anti CD20), anti-TNFa (etanercept or adalimumab), tocilizumab (anti-IL6)
Wegener’s with severe flare
Cyclophosphamide
Worsening Crohn’s, already on Azathioprine and Prednisolone, what tx?
Infliximab (Anti-TNFa)
Malignant melanoma medical treatment
Pembrolizumab
Explanation: Pembrolizumab is anti PD-1, just like Nivolmab.
Ipilimumab is an anti CTLA-4
Rituximab target and used in
anti-CD20
Used in Lymphoma, RA, SLE
Transplant drugs
Tacrolimus, Cyclosporin Azathioprine Mycophenolate Mofetil Antithymocyte globulin (ATG Prednisolone Basiliximab (anti-CD25/IL-2) (prophylactic)
typical regime is: CNI + AZA/MMF +/- steroids
Type I hypersensitivity
Allergy/Atopic eczema
Type II hypersensitivity
Auto-immune/auto-inflammatory e.g. Graves
Type III hypersensitivity
Complex mediated e.g. SLE
Type IV hypersensitivity
Delayed e.g. contact dermatitis, diabetes
CD40L associated
Hyper IgM
GPA’s other name
Wegener’s Granulomatosis
eGPA’s other name
Churg-Strauss Syndrome
Monitoring SLE (inactive, active, severe disease)
Inactive: C3 and C4 normal
Active: C3 normal, C4 low
Sever: C3 and C4 low
Immune condition with chest and renal involvement
Good-pasture’s classically but can be GPA/eGPA
Features of hyperacute rejection (transplant)
Minutes-hours Pre-formed Abs to HLA activate complement –> Thrombosis and necrosis Prevent by cross-match and HLA typing
Features of acute cellular rejection (transplant)
Weeks-months. Activated by direct APCs.
CD4 cells –> type IV hypersensitivity reaction –> cellular infiltrate
Tx: T-cell immunosuppression e.g. Steroids
Memory aid: T cell = T 4
Features of acute Ab-mediated rejection (transplant)
Weeks-months B-cells –> antibodies –> attack vessels and endothelial cells –> vasculitis Complement deposition (C4d - stains positive in Ab mediated rejection). Treat with B-cell immunosuppression & remove Abs
Features of chronic rejection (transplant)
Months-years Various immune+non-immune mechs –> fibrosis, GN, ischaemia –> Tx: minimise organ damage RF: multiple acute rejections, HTN, hyperlipidaemia
GvHD
Days-weeks (T cell mediated) Rash, bloody D&V, & jaundice Tx: Immunosuppress with steroids
Acute vascular rejection
4-6 days post transplant after xenograft - presents similarly to hyperacute
H1 vs H2 antagonisst
H1 = antihistamines H2 = reducing gastric acid
Itchy skin when running in cold for an hour
Acute urticarial –> H1 antagonist
Hereditary angioedema treatment
C1q esterase inhibitor (reduces swelling)
Measure of mast cell degranulation
Mast cell tryptase levels
Chemokine promoting eosinophil growth
IL-5
Tingly mouth after eating apples, melons etc.
OAS (Sxs limited to mouth)
Woman with flushed face, breathing problems (happened multiple times) and hepatomegaly
Hereditary angioedema Tx: C1 esterase inhibitor
Kid with rash on extensor surfaces, IgE mediated
Atopic dermatitis
Hypertensive and diabetic with angioedema - potential cause?
ACE inhibitor
Absent T cells and normal B cells
X-linked SCID
… can also be DiGeorge syndrome, but Q usually has more hints
1m baby, serious bacterial infections Normal CD8, no CD4 B cells present IgM present, IgG absent
Bare Lymphocyte Syndrome (Type 2) Absent expression of MHC Class II molecules
Jaundiced 4m baby, FTT, recurrent infections raised ALP, low CD4, defect protein regulates MHC class 2
Bare Lymphocyte Syndrome (Type 2) Associated with sclerosing cholangitis –> jaundice
Recurrent strep. pneumonia FHx of having it and dying young
Complement deficiency (Encapsulated organism)
Child with recurrent infections, improved with age, now delay in language and speech
DiGeorge Immune function improves with age Can be associated with lots of speech/language issues and LDs as well as rest of CATCH-22
Loss of the terminal complement pathway
Encapsulated organisms
Recurrent meningitis
Complement deficiency (C5-9) Encapsulated organism e.g. Hib or N. meningitidis
Recurrent infections, negative NBT test
Chronic Granulomatous disease
PID causing atypical granulomas
IFNy/IL12 or receptor deficiency Predisposed to mycobacterial infections Inability to form granulomas hence atypical
Recurrent infections negative NBT test negative dihydrorhodamine test
Chronic Granulomatous disease
6m boy, sevete FTT & recurrent infections No T cells, B cells normal
X linked SCID
Alternative complement pathway components
Factor B, I & P “BIP”
Alternative complement pathway components
Factor B, I & P “BIP”
Lady with spinal fracture due to TB
IFNy/IL12 or receptor deficiency Mycobacteria susceptible –> Pott’s disease
Felty’s syndrome (3 features)
RA, neutropenia/leukopenia and splenomegaly
Rheumatoid arthritis and splenomegaly
Felty’s
Monocytes in peripheral skin cells
Langerhands
Cells that express Foxp3 and CD25
Treg
Responsible for killing cancerous cells + inhibited by MHC-I
NK cells
PEP exists against (3)
Rabies, HIV, tetanus
Routine vaccine that is not given to immunocompromised patients
MMR
If oral steroids in past 3 months delay vaccine
Vaccine target HA
Influenza