hypersensitivity and allergy Flashcards
what do hypersensitivity reactions occur against
against harmless foregin antigens, alloantigens (transfusion/graft rejection) and autoantigens (autoimmune disease)
types of hypersenstivity
type 1 (immediate)- type 2 (antibody dependent )- type 3 (immune complex mediated)- type 44 (delayed cell mediated)
what diseases have type 1
anaphylaxis, asthmas, rhinitis and food allergy
mechanism of type 1 hypersensitivty- initial and secondary
1- initial exposure where SENSITISATION (not tolerance) occurs: IgE antibodies produced and bind to IgE rceptors on mast cells/basophils. 2- second exposure where IgE CROSS LINK on mast cells/basophils, causing DEGRANULATION of these cells= release of mediators eg histamines/leukotrienes
what diseases have type 2
organ-specific autoimmune diseases eg glomerulonephritis AND autoimmune cytopenias (destrcution of blood cell eg haemolytic anemia)
how to test for type 11
immunofluorescence or ELISA for autoantibodies
mechanism of type 3 and example
antigen-antibody complexes form in blood vessels and tissues= complement activation= tissue and blood vessel damage eg kidney SLE
what diseases have type 4 and TH1 or TH2 mediated
chronic graft rejection, coeliac disease (TH1 mediated), and asthma, rhinitis and eczema (TH2 mediated)
mechanism in TH1 mediated type 4- difference cells and cytokines
TH1 cells produce IL2 to activate cytotoxic T cells, produce IFN gamma to activate macrophages which produce TNF, and activate FIBROBLASTS too= fibrosis
antibodies involved in type 2/3
IgG
genetic risk factors to allergies- important? poly or monogenic + example
important as most allergics have family history- but many genes involved eg of IL4
environmental risk factors
age (reduces as you age), gender, family size (more in small families), animals (protects you), diet and infections (protect you)
(GAFIDA)
types of inflammation and mediated by what type of hypersensitivty, and what mixed
anaphylaxis, urticaria (itchy rash) and angiodema type 1 mediated: chronic urticaria type 2 mediated, asthma/rhinitsi and eczema MIXED (type 1 and 4)
type 4 TH2 mediated- atopic airway disease- mechanism and how eonisophils recruited
sensitisation- TH2 cells cause B cell proliferation= IgE antibodies produced by mast cells. second exposure- TH2 cells cause more IgE production AND recruit eonisophils via IL5
importance of neutrophils- in what disease particularly
particularly in asthma
mechanism in asthma and how airway narrowed
mast cell activation and degranulation, as well as eonisophil recruitment= histamine/leukotriene release= airway narrowing (VCSM contraction+ mucus secretion)
DIAGRAM two phase response in asthma
if given allergen, there is early response (sudden drop in PEF- type 1), then a late response (gradual drop in PEF- type 4)
symptoms of asthma
cough, wheezing, mucus production and breathlessness
types of allergic rhinitis
seasonal or perennial (year round)
symptoms of allergic rhinitis
sneezing, itchy nose/eyes and nasal blockage
mild and severe symptoms of food allergy
mild- urticaria/angioedema: severe- diarrhoea, anaphylaxis
anaphylaxis- symptoms and corresponding parts of body
severe allergic reaction= swelling of lips (angioedema)ie affects skin, diarrhoea and vomiting ie affects GI, breathlessness, fainting ie affects resp and cardio system
diagnosis
skin prick tests (add allergen to skin), total IgE, RAST (add blood to allergen in lab and look at IgE response), and lung function for asthma
treatment of anaphylaxis
antihistamines and adrenaline (Epipen)
