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what is a hypersensitivity reaction?

reaction that is produced by the normal immune system that is directed against innocuous antigens in a pre-sensitised host


who determined the four stages and classifications of hypersensitivity?

Coombs and Gell in 1963 types I-IV


which cells are involved in hypersensitivity?

dendritic cells - circulate and sample environment and present to T and B cells
antibodies - specific to particular protein sequences
macrophages - clear out rubbish in immune system
T and B cells - produce cytokines for communication in immune system


what is a Type I hypersensitivity?

it is an IgE mediated mast cell and basophil degranulation
it is the release of preformed and de novo synthesised inflammatory mediators


what are the clinical features of type I?

fast onset, weal and flare, mild, moderate or severe


what is the primary response of type I?

degranulation and release of histamine, proteases and chemotactic factors


what is the secondary response of type I?

release of leukotrienes, prostaglandins, eosinophils


what cell has a central role in the type I?

there is a central role for the Th2 t helper cell


how is the mast cell adapted for this?

it has preformed mediators such as histamine and IgE receptors on it's surface


what happens once the antibodies and antigens connect?

the antibodies on the mass cells will connect to antigen with at least two antibodies, and cross link. This signals mast cells to throw out granules and releases histamine


what do cytokines do?

cytokines will cause the B cells to proliferate into IgE plasma cells


what are signs of inflammation?

flushing, urticaria, cutaneous and oral pruritus (itching), abdo pain/nausea/vomiting, runny nose and sneezing


how can this be treated?

antihistamines, and nasal spray


what are the effects of histamine?

swelling, inflammation, higher HR and blood clots, gastric acid secretion, dilation of blood vessels, bronchoconstriction, increased permeability of capillaries and adrenaline release


what is moderate to severe hypersensitivity reaction?

it is anaphylaxis. It is a medical emergency and is an acute, potentially life threatening, IgE mediated systemic hypersensitivity reaction


what are the hallmarks of anaphylaxis?

diffuse urticaria and angiodema


what are the symptoms of anaphylaxis?

hoarseness, cough, shortness of breath, wheezing and cyanosis (respiratory arrest), severe abdo pain, diarrhoea, nausea and vomiting, hypotension


why do we get allergies?

components of the immune system respond to parasitic infection are also involved in allergic response. The system has developed to produce a rapid tissue based response to re-infection. Lack of infectious drive is a contributory factor in allergic disease. It is a combination of genetic (genetic predisposition) and environmental factors.


which cell identifies the allergen?

dendritic cell and presents it to naive T cell which has a specific receptor recognising the antigen


The T cell differentiated into Th2 cells and secrete what?

cytokines IL-4 and IL-3 - act as signals to naive B cells


what do naive B cells become and how are they adapted?

memory B cells and they have specific IgEs recognising the allergen on further exposure


these memory B cells remain in the system for what reason?

they continue to produce ABs for further exposure


what is the dual allergen exposure hypothesis?

we have early cutaneous exposure to food protein through disrupted skin barriers which leads to allergen sensitisation. Oral exposure leads to tolerance. There are additional theories that relate to environmental factors such as vitamin D for the immunological mechanisms important in preventing food allergens and establishing oral tolerance.


what did the LEAP study show?

that allergies can still develop despite early primary and secondary prevention strategies and that oral exposure can also increase sensitisation


why does genetics influence allergies?

can have a tendency to have an allergy if family also have it but not always the case. There are polygenic diseases, cytoline gene cluster for interleukins etc and therefore this is for susceptibility and not sufficient for the disease alone.


what if the atopic march saying?

eczema and food allergies tend to decrease over age - there is a general connection between allergies.


how would you diagnose an allergy?

you would use histroy, a specific antibody test (IgE), an intradermal test, oral challenge test


what do you need to make sure of before conducting a skin prick test?

that the patient has not been on antihistamines recently, and wait 15 minutes for result - over 3mm


why do you use a control in the skin prick test?

to make sure they have no reacted to the skin prick itself


which layer of the skin does the intradermal tesing injection go into?

into the dermis - lower layer of the skin