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
what are the sensitisation cells of the skin
langerhan cells (dendritic cells)
what type of reaction is irritant contact dermatitis
non immunological, doesnt reqcuire prior sensitisation, contact with agents that abrade irritate and traumatise the skin
name 2 endogenous skin reactions
atopic eczema, psoriasis
what are the managements for contact dermatitis
avoidance, emollients, topical steroids, UV phototherapy, immunosuppresants
what mediates type 2 hypersensitivity reactions
IgG and IgM antibodies and complement
describe the initial sensitisation phase of type 4 delayed reactions
dendritic antigen presenting cells langerhans in skin) (antigens binds to MHC-2) migrates to regional lymph nodes, activates Y cells to produce pool of memory T cells in lymph nodes
specific memory T cells released and distributed throughout circulation to encounter antigen in future
describe what happens in a type 4 reactions when there is subsequent challenge with antigen
antigen on dendritic (langerhan) cell migrates to dermis and encounters and activates specific T cells
release of cytokines from T cells leading to further cell recruitment
name 4 types of cutaneous type 4 hypersensitivity
allergic contact dermatitis
photo allergy
skin response to bacteria, fungus, viruses
abnormal delayed response in atopic eczema
describe contact dermatitis
small blisters and erosions due to delayed hypersensitivity to irritant
name three types of cutaneous type 1 reactions and what causes them
urticaria- red wheals, caused by dilated blood vessels and leakage o fluid into surrounding tissue
angio-oedema- deeper cutaneous reaction than urticaria, causing swelling of sub-cutaneous tissues including mucous membranes
anaphylaxis- w/ urticaria +/- angio-oedema, laryngeal swelling, bronchospasm, hypotension
