Allergy Flashcards
define hypersensitivity
immune response that causes collateral damage to self
what mediates type 1 hypersensitivity reactions
IgE
what mediates type 2 hypersensitivity reactions
IgG
what mediates type 3 hypersensitivity reactions
immune complex mediated
what mediates type 4 hypersensitivity reactions
cell mediated (TH1, TC cells)
name 2 other allergic disorders
eczema and rhinitis
when does a type 1 allergy occur after exposure to allergen
immediate- minutes and up to 2 hours after
what are the routes of contact of allergens
skin contact, inhalation, ingestion and injection
describe the pathophysiology of sensitisation to an allergen
antigen binds to dendritic cells which then activate T cells (TH2) which produce IL-4, IL-5, IL-13 which activate B cells to create allergen specific IgE which acitvate mast cells to produce histamines, leukotrienes, cytokines, prostaglandins
what is urticaria and its features
compressible dermal swelling, very itchy- lesions appear within 1 hour and last 2-6 hours (up to 24hrs)
what is angioedema and its features
localised swelling of subcutaneous tissue or mucous membranes-non pitting oedema- not itchy
what happens to respiratory function during an allergic reaction
lowered
what is anaphylaxis
severe life threatening generalised or systemic hypersensitivity reaction
what are the symptoms of anaphylaxis
rapidly developing, pharyngeal or laryngeal oedema, bronchospasm with tachypnoea, hypotension, tachycardia, associated skin and mucosal changes
what investigations can be made into allergies
history (most important), specific IgE (RAST- blood test for specific allergen), skin prick or prick prick test, challenge test, serum mast cell tryptase levels (during anaphylaxis)
what is more accurate specific IgE or skin prick test
skin prick
when do you do a challenge test
only if SPT negative
how are allergies managed
avoidance
1- antihistamines (prevent effects of mast cell activation)
2-corticosteroids (anti-inflammatory agents (oral prednisolone))
adrenaline autoinjector (for anaphlyaxis)
what dosage of adrenaline should adults get
300 micrograms
what dosage of adrenaline should children get
150 micrograms
how many pens should each patient be perscribed
2
how other the IgE can hypersensitivity reactions be mediated
direct mast cell degranulation (morphine, aspirin, NSAIDs)
metabolic (lactose intolerance)
toxic (scombroid fish toxin)
what type of reaction is allergic contact dermatitis
type 4, delayed hypersensitivity, (after 24-48hrs)
describe the pathophysiology of non IgE reactions
Sensitization phase (afferent phase). Haptens penetrate the epidermis (step 1) and are taken up by epidermal cells, including skin.
Dendritic cells (DCs) migrate to the draining lymph nodes (step 2), where they present haptenated peptides to both CD8+ effector T cells
and downregulatory CD4+ T cells (step 3). Specific T-cell precursors clonally expand in draining lymph nodes, recirculate via the blood,
and migrate to tissues, including the skin (step 4). (Right) Elicitation phase (challenge phase, efferent phase). When the same hapten is
applied to the skin, it is taken up by epidermal cells, including skin DCs and keratinocytes (step 5), which present haptenated peptides to
specific T cells. Activation of CD8+ cytotoxic T lymphocytes induces apoptosis of keratinocytes and production of cytokines and
chemokines by skin resident cells (step 6). This leads to the recruitment of leukocytes from the blood to the skin. CD4+ T cells may block
activation/expansion of CD8+ effectors in lymph nodes during sensitization and in the skin during the elicitation phase of contact hypersensitivity
