Allergy
·
= Immunologic reaction to common
substances which are harmless to most people
·
Previous exposure ®
antibodies or specific lymphocytes against these substances
·
Types:
o Atopy:
·
Predisposition to produce IgE
antibodies to common environmental substances (also called immediate or Type 1
hypersensitivity).
·
Order of incidence:
§ Adults aged 20 – 44 in New Zealand: Asthma 15%, hay-fever 35%, Maori
more symptomatic
§ Mediators lead to vasodilation, vascular leakage (swelling), smooth
muscle spasm (eg respiratory).
§ Similar symptoms can occur from non-allergic hypersensitivity =>
non-atopic
o Contact Allergies: direct skin contact with nickel, chrome, rubber. Due
to lymphocyte (delayed-type hypersensitivity, type IV) not IgE antibodies
o Allergic Alveolitis ® lung inflammation. Eg farmer‟s lung, pigeon fancier‟s lung. Due to
lymphocytes and IgG (not IgE)
·
Risk factors:
o Allergy predominates in young adults and children: while non-specific
hypersensitivity is more common later in life
o Genetic Factors: One parent ® doubled risk of child having
atopic disease. Both parents ® 4 times risk
o Early childhood factors important in subsequent development of allergic
disease:
§ High house dust mite/cat/pollen exposure in early months ® risk
§ Exposure to tobacco smoke in utero/infancy ® risk
§ Early life infections ® ¯risk: ?improved shift from TH2 environment of uterus to non-allergic TH1 immune responses which dominate in most infections (especially intracellular pathogens)
§ First born children at greater risk
o The workplace is a major source of allergen exposure
·
Bee sting allergy:
o Don‟t have to have atopic history
o If anaphylaxis as a child, 1 in 6 chance next time. For adult, 60% chance next time
o Carry adrenaline until desensitisation (serial antigen shots ® 95% effective)
o Anaphylaxis: give 0.5 m of 1:1000 adrenaline IM if in community setting (iv in hospital if you can give slow
infusion). IM gives good diffusion, safer, effective and fewer problems with
cardiac vasoconstriction cf bolus
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