Hypersensitivity + Role of Each Ig = important Flashcards
(43 cards)
What is hypersensitivity
Group of disorders
Immune system = exaggerated or inappropriate response to environmental antigens which do not usually cause damage
What are the types of hypersensitivity
Type 1 = allergy
Type 2 = cell / cytotoxic - IgG or IgM binding to antigen
Type 3 = immune complex
Type 4 = delayed / T helper travelling to antigen and relcruiting macrophages
Type 5 = Ab
What is type 1
Antigen binds to IgE bound to mast cell in blood which triggers release of histamine / other cytokines
Causes immediate allergic reaction or anaphylaxis
What causes type 1
Genetics - hypersensitive T cells releasing Th2
Environment
What is allergy
Clinical expression of atopy
Hypersensitivity to allergen that immune system recognises as foreign
Large proportion can be atopic without developing allergy
What is atopy / atopic triad
Genetic tendency to develop allergic diseases due to hypersensitivity Triad of - Asthma - Eczema - Hayfever Also food allergy / allergic rhinitis
What is pathophysiology behind sensitisation phase of type 1
APC picks up allergen
Goes to LN
CD4 predisposed to respond aggressively (atopy)
Release Th2 cytokine + IL
IgE produced by B cells
Bind to mast cell in blood = degranulation on repeat exposure
What happens in reaction phase early
Allergen binds to IgE
Mast cells immediate degranulate on 2nd exposure
Histamine released = inflammation
Leads to mucosal oedema / secretion / muscle contraction + vaasodilator + increased permeability
Leads to rash, swelling, wheeze, cough
What happens in late reaction phase
8-12 hours after allergy
Further differentiation of Cd4 and TH2
Other cells - eosinophil / basophil / leukotrienes
What are examples of diseases of type 1
Atopic dermatitis
Anaphylaxis
How do you investigate type 1
History - timing, exposure, symptoms, FH
Skin prick
Skin patch testing
Serum tryptase - rises after allergic response
Serum IgE
RAST
Food challenge = best way
What is skin prick useful for
Food + pollen allergy Inexpensive and easy to perform Diluted allergen pierced into skin Histamine = +ve Sterile water = control Wheel forms if allergic
When is skin patch testing used
Contact dermatitis (type IV)
What is RAST
Determines amount of IgE reacting to specific allergic Graded 0 (-ve) to 6 (+ve)
How do you treat type 1 hypersensitivity
Avoidance of allergy Anti-histamine Corticosteroid IM Adrenaline in anaphylaxis May need epipen if serious reaction Desensitisation immunotherapy = expensive
What is type 2 hypersensitivity
Ab mediated destruction of cells by activating complement
IgG or IgM
Antigen can be self or exogenous so blur between autoimmune + hypersensitive
How does Ab mediated desutrciton
MO / Neurtrophils = phagocytosis Complement activation via antigen / Ab complex MAC forms Opsonisation NK cells = apoptosis ADCC
What are clinical disorders of type 2 hypersensitivity
Haemolytic reaction - autoimmune to self or after blood Haemolytic disease of new born Hyperacute graft rejection Transfusion reaction Myasthenia graves Anti-GBM Pemphigus ITP
How do you treat / prevent
X-match
Tissue typing
Rhesus screening
Immune suppression if autoimmune / transplant rejection
What is type 3 hypersensitivity
Abnormal deposition antigen / antibody complex in tissue
Can be due to self or exogenous antigen
Physiological immune complex formation
Plasma cells release IgM to pathogen Picks up antigen Presents to T helper via MHC Creates bond Releases IL and B cell switching occurs Activates complement / opsonisation + phagocytosis
When does it become hypersensitive
If occurs with small molecules that are not normally picked up by MO e.g. DNA
Forms abnormal complex and tissue damage
Symptoms 4-10 hours after exposure
System illness if form in circulation
Localised if form in tissue
What is an example
SLE
RA
HSP
Failure of tolerance = auto reactive T and B circulate
Anti-dsDNA produced inappropriately
Complex land anywhere so systemic illness
What precipitates
Infection / sunburn
Damages cells and releases DAN which is detect as foreign
