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Flashcards in Hypersensitivity Deck (55)
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1

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

2

who determined the four stages and classifications of hypersensitivity?

Coombs and Gell in 1963 types I-IV

3

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

4

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

5

what are the clinical features of type I?

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

6

what is the primary response of type I?

degranulation and release of histamine, proteases and chemotactic factors

7

what is the secondary response of type I?

release of leukotrienes, prostaglandins, eosinophils

8

what cell has a central role in the type I?

there is a central role for the Th2 t helper cell

9

how is the mast cell adapted for this?

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

10

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

11

what do cytokines do?

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

12

what are signs of inflammation?

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

13

how can this be treated?

antihistamines, and nasal spray

14

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

15

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

16

what are the hallmarks of anaphylaxis?

diffuse urticaria and angiodema

17

what are the symptoms of anaphylaxis?

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

18

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.

19

which cell identifies the allergen?

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

20

The T cell differentiated into Th2 cells and secrete what?

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

21

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

22

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

they continue to produce ABs for further exposure

23

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.

24

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

25

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.

26

what if the atopic march saying?

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

27

how would you diagnose an allergy?

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

28

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

29

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

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

30

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

into the dermis - lower layer of the skin