allergies Flashcards

1
Q

what is an allergy or hypersensitive reaction

A

immune response against innocuous antigen in a pre-sensitised host

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2
Q

describe type 2 hypersensitive and its clinical features

A

cytotoxic
IgG and IgM response to antigen at cell surface attached to tissue

minutes to hours onset - cell lysis and necrosis

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3
Q

what are common antigens and associated disease of type 2 hypersensitivity

A

penicllin

erythroblast fetalis - Rh- mother and Rh+ foetus - antibodies made - if another Rh + baby its attacked

good pastures nephritis

penecillin mediated autoimmune haemolytic anaemia

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4
Q

describe type 3 hypersensitivity and its clinical features

A

immune complex

IgG and iGM against solum antigen - forms complex in organs which triggers complement pathway and self damage
commonly damages kidneys joints and extremities

onset 3-8 hours, vasculitis

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5
Q

what are the traditional cause of type 3 hypersensitive and what are the associated disease

A

serum sickens due to tetanus

SLE

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6
Q

describe type 4 hypersensitivity and the cancel features

A

delayed

antigen specific T cell mediated cytoxicity
antigen recognised by APC for primary exposure
subsequent exposure activates T cells causing cell damage due to cytokines

48-72 hours - erythema induration - patch test

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7
Q

what are common antigens of type 4 hypersensitivity and what are he associated conditions

A

metals such as nickel - tuberculin reaction

contact dermatitis - patch testing

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8
Q

what is an allergy a combination of

A

genetics and the environment

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9
Q

what are the three immune response to parasitic disease

A

increased levels of IgE

tissue inflammation with basophil infiltration and eosinophilia/mastocytosis

presence of CD4+ t helper cells secreting cytokines

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10
Q

what is the hygiene hypothesis

A

immune stimulation by microbes protects against allergies - so if microbes decrease then allergies increase

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11
Q

how do infections protect you against allergies

A

TH1/TH2 balance deviation - antigenic competition

immune regulation

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12
Q

what are some examples of genetic influence on the allergic immune response

A

polygenic disease
cytokine gene cluster Il3,5,9,13
FcERI
IFN / TNF

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13
Q

describe IgE production

A

antigen is recognised by TH2 and B cell (APC) - TH2 uses IL-4 to signal B cells which drives B cell production of IgE for mast cells and offers support for proliferation

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14
Q

what is an early priming event and what does it cause

A

decrease in barrier function allows allergen to access immune system - likely to increase risk of allergy developing

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15
Q

how do T helper cells differentiate

A

begin as naive T CD4 t cell then detects antigen presenting cell and pathogen which then change into TH1/2/17 or Treg

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16
Q

what is the primary cell mediator in type 1 Hypersensitivity and what is its role

A

TH2
multiple cytokine release - attracts innate inflammatory response but can cause tissue damage

drive for immunoglobulin production - B cell makes IgE which activates innate and adaptive reponse

17
Q

what are the clinical features of a type 1 hyper reaction

A

fast onset 15- 30 minutes

wheal and flare - anaphylaxis

18
Q

what is the late phase response of type 1 hypersesn

A

eosinophils
arachonidonic acid metabolised
mainly involved in asthma a

19
Q

what are the physiological changes of anaphylaxis

A

sudden onset, skin mucosal tissue or both

sudden respiratory symptoms or reduced BP or end organ dysfunction

20
Q

what is the difference in blood pressure reduction in a type 1 hypersesiivtiy reaction for children and adults

A

children - low systolic or greater than 30% decrease in SBP

adults - systolic BP less than 90 mmHg or greater than 30% decrease from baseline

21
Q

how would you treat a mild vs severe anaphylaxis

A

mild - antihistamines

severe - adrenaline pen

22
Q

what is the atopic triad

A

rhinitis
asthma
eczema (atopic dermatitis)

23
Q

what is rhinitis and how do you treat it

A

allergic - all year (perineal) or seasonal
blocked nose, runny, itchy - eye symps
animal dander, pollens

anti-histamines and nasal steroids

24
Q

what is asthma and what is the risk with damaged airways

A

inflammation and hyperactivity of small airways
IgE mediated and late response eosinophils

damaged airways = hyper-reactive to non-allergic stimulus such as cold air or smoke

25
Q

what is atopic dermatitis and how do you treat it

A

no local IgE
more autoimune type response - itching and cracking of skin - house dust mite

topical steroids and moisturisers

26
Q

describe the pathogenesis of asthma

A

allergen to apc
app to TH2
TH2 releases cytokines IL4/13 - B plasma cell and release IgE which targets mast cells
TH2 releases IL5 which activates eosinophils

27
Q

what are the tests for hypersensitivity

A

specific IgE in the blood - can provide false neg and pos

skin prick test - false neg and pos

intra dermal test

graded challenge test

basophil activation test - IgE binding means basophils unregulated expression of activation markers

28
Q

for most hypersensitivity reactions what is the general treatment

A

to treat symptoms - antihistamines steroids and adrenaline

specific - immunotherapy

29
Q

what is the mechanism in terms of cells changes in allergen specific immunotherapy

A

increases in TH2 and TH2 cytokines such as IL-10

reduced numbers of mast cells and their ability to release mediators

less eosinophils and neutrophils at site of allergen

30
Q

what specifically are major food allergens

A

water soluble glycoproteins 10-60kDa

31
Q

what are the clinical manifestations of food allergies

A

vomiting, diarrhoea, oral symps

rhinitis and bronchospasm

urticaria and angioodeema

anaphylaxis

32
Q

what do you need to ask about with the history of a drug allergy

A

indication of the drug
detailed description of the reaction
time between drug and onset
number of doses taken before onset

33
Q

what is the management of drug allergies

A

intradermal testing as skin isn’t sensitive enough
dermal graded challenge
desensitisation - keep living does to exhaust mast cells