allergies Flashcards
what is an allergy or hypersensitive reaction
immune response against innocuous antigen in a pre-sensitised host
describe type 2 hypersensitive and its clinical features
cytotoxic
IgG and IgM response to antigen at cell surface attached to tissue
minutes to hours onset - cell lysis and necrosis
what are common antigens and associated disease of type 2 hypersensitivity
penicllin
erythroblast fetalis - Rh- mother and Rh+ foetus - antibodies made - if another Rh + baby its attacked
good pastures nephritis
penecillin mediated autoimmune haemolytic anaemia
describe type 3 hypersensitivity and its clinical features
immune complex
IgG and iGM against solum antigen - forms complex in organs which triggers complement pathway and self damage
commonly damages kidneys joints and extremities
onset 3-8 hours, vasculitis
what are the traditional cause of type 3 hypersensitive and what are the associated disease
serum sickens due to tetanus
SLE
describe type 4 hypersensitivity and the cancel features
delayed
antigen specific T cell mediated cytoxicity
antigen recognised by APC for primary exposure
subsequent exposure activates T cells causing cell damage due to cytokines
48-72 hours - erythema induration - patch test
what are common antigens of type 4 hypersensitivity and what are he associated conditions
metals such as nickel - tuberculin reaction
contact dermatitis - patch testing
what is an allergy a combination of
genetics and the environment
what are the three immune response to parasitic disease
increased levels of IgE
tissue inflammation with basophil infiltration and eosinophilia/mastocytosis
presence of CD4+ t helper cells secreting cytokines
what is the hygiene hypothesis
immune stimulation by microbes protects against allergies - so if microbes decrease then allergies increase
how do infections protect you against allergies
TH1/TH2 balance deviation - antigenic competition
immune regulation
what are some examples of genetic influence on the allergic immune response
polygenic disease
cytokine gene cluster Il3,5,9,13
FcERI
IFN / TNF
describe IgE production
antigen is recognised by TH2 and B cell (APC) - TH2 uses IL-4 to signal B cells which drives B cell production of IgE for mast cells and offers support for proliferation
what is an early priming event and what does it cause
decrease in barrier function allows allergen to access immune system - likely to increase risk of allergy developing
how do T helper cells differentiate
begin as naive T CD4 t cell then detects antigen presenting cell and pathogen which then change into TH1/2/17 or Treg
what is the primary cell mediator in type 1 Hypersensitivity and what is its role
TH2
multiple cytokine release - attracts innate inflammatory response but can cause tissue damage
drive for immunoglobulin production - B cell makes IgE which activates innate and adaptive reponse
what are the clinical features of a type 1 hyper reaction
fast onset 15- 30 minutes
wheal and flare - anaphylaxis
what is the late phase response of type 1 hypersesn
eosinophils
arachonidonic acid metabolised
mainly involved in asthma a
what are the physiological changes of anaphylaxis
sudden onset, skin mucosal tissue or both
sudden respiratory symptoms or reduced BP or end organ dysfunction
what is the difference in blood pressure reduction in a type 1 hypersesiivtiy reaction for children and adults
children - low systolic or greater than 30% decrease in SBP
adults - systolic BP less than 90 mmHg or greater than 30% decrease from baseline
how would you treat a mild vs severe anaphylaxis
mild - antihistamines
severe - adrenaline pen
what is the atopic triad
rhinitis
asthma
eczema (atopic dermatitis)
what is rhinitis and how do you treat it
allergic - all year (perineal) or seasonal
blocked nose, runny, itchy - eye symps
animal dander, pollens
anti-histamines and nasal steroids
what is asthma and what is the risk with damaged airways
inflammation and hyperactivity of small airways
IgE mediated and late response eosinophils
damaged airways = hyper-reactive to non-allergic stimulus such as cold air or smoke
what is atopic dermatitis and how do you treat it
no local IgE
more autoimune type response - itching and cracking of skin - house dust mite
topical steroids and moisturisers
describe the pathogenesis of asthma
allergen to apc
app to TH2
TH2 releases cytokines IL4/13 - B plasma cell and release IgE which targets mast cells
TH2 releases IL5 which activates eosinophils
what are the tests for hypersensitivity
specific IgE in the blood - can provide false neg and pos
skin prick test - false neg and pos
intra dermal test
graded challenge test
basophil activation test - IgE binding means basophils unregulated expression of activation markers
for most hypersensitivity reactions what is the general treatment
to treat symptoms - antihistamines steroids and adrenaline
specific - immunotherapy
what is the mechanism in terms of cells changes in allergen specific immunotherapy
increases in TH2 and TH2 cytokines such as IL-10
reduced numbers of mast cells and their ability to release mediators
less eosinophils and neutrophils at site of allergen
what specifically are major food allergens
water soluble glycoproteins 10-60kDa
what are the clinical manifestations of food allergies
vomiting, diarrhoea, oral symps
rhinitis and bronchospasm
urticaria and angioodeema
anaphylaxis
what do you need to ask about with the history of a drug allergy
indication of the drug
detailed description of the reaction
time between drug and onset
number of doses taken before onset
what is the management of drug allergies
intradermal testing as skin isn’t sensitive enough
dermal graded challenge
desensitisation - keep living does to exhaust mast cells
