Allergic diseases Flashcards
Allergy and hypersensitivity
Damaging and sometimes fatal reactions produced by the normal immune system directed against non-toxic antigens
Type 2 hypersensitivity - cytotoxic
IgG/IgM Ab response against an antigen at the cell surface attached to the tissue - common antigen is penicilin
Type 2 hypersensitivity- cytotoxic associated diseases
- Erythroblastosis fetalis - mum antigens attack child
- Goodpasture’s nephritis
- Penicillin mediated autoimmune haemolytic anamia
How does Type 3 hypersensitivity - immune complex work
- IgG/IgM Ab’s vs soluble agent
- Form an immune complex deposited in organs
- Triggers complement pathway
- Causes self-damage
What does an activated complement pathway do?
Activation of complement factors and macrophages, attacks neutrophils causing self damage
Type 3 hypersensitivity- immune complex clinical features
onset 3-8 hours
- vasculitis
- disease = SLE
How does Type 4 hypersensitivity- delayed work
- Antigen specific T-cell
mediated cytotoxicity - Antigen is recognised by antigen-presenting cells and presented to T cells in lymph nodes
-T cells activate and cause cell damage to cytokines
Type 4 hypersensitivity- delayed clinical features
Delayed onset 48-72 hours
- Erythema induration
- Contact dermatitis
Why do we get allergies
- Combination of genetic and environmental factors
- Lack of infectious drive is a contributory factor in allergic disease
Immune responses to parasitic disease
- Increased levels of IgE
- Tissue inflammation - Eosinophilia, mastocytosis and Basophil infiltration
- Presence of CD4+ T cells - secrete cytokines (IL4, IL13)
What is the hygiene hypothesis
Immune stimulation by microbes protects against allergies so if microbes decrease allergies will increase
What is the mechanism behind the Hygiene Hypothesis
Antigenic competition - infections compete with immune system against allergens - T helper 1/2 balance
Genetic influences on the allergic immune response
- Polygenic disease
- FcERI receptor
- IL4R + IL12R
How is IgE produced
- Antigen is recognised by helper 2 and B cell
- TH2 uses IL-4 to signal the B cell
- B cell drives to produce IgE for mast cells
Role of the TH2 cell
- Multiple cytokine release
- Activator for IgE production
Type 1 hypersensitivity- IgE mediated allergic response
- IgE is produced in mast cells + basophils
- Allergen binds to IgE
- Bridging of 2 IgE by allergen causes release of mediators causing response
Type 1 hypersensitivity clinical features
Fast onset
- Wheal and flare - potentially anaphylaxis
- Late phase response involved in asthma
Criteria for anaphylaxis
- Sudden onset of illness with involvement of skin/mucosal tissue and sudden respiratory symptoms /reduced bp
- Symptoms of end-organ dysfunction
Treatment of anaphylaxis
Mild reaction = antihistamines
Systemic symptoms - adrenaline pen
What is the Atopic triad
Asthma, rhinitis, eczema
Rhinitis
Allergic - perennial or seasonal
Causes:
- House dust mite, pollens
Rhinitis symptoms and treatment
- Blocked nose, sneezing - with eye symptoms
- Treated with antihistamines and nasal steroids
Asthma
- Inflammation and hyper-reactivity of small airways
Stimulated by aero-allergic, house dust mite
Asthma symptoms
Immediate symptoms are IgE mediated - also damage to airways due to late phase response by eosinophils
