Allergy Flashcards

1
Q

What are the common names for hypersensitivity I, II, III, IV

A
I= Anaphylactic
II= Cytotoxic
III= Immune complex
IV= Delayed type
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2
Q

Describe type-II hypersensitivity

A
  • Antibody = IgG, IgM against combined self/foreign antigen
  • Antigen= cell surface
  • Response time= minutes/hours
  • Appearance= lysis & necrosis
  • Innocuous antigen= penicillin
  • Histology= Antibody & complement
  • Associated diseases= Erythroblastosis fettles, Goodpasture’s nephritis
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3
Q

Describe type-III hypersensitivity

A
  • Antibody= IgG, IgM
  • Antigen= Soluble
  • Response time= 3-8hours
  • Appearance= Erythema, oedema, necrosis, vasculitis
  • Innocuous antigen= mouldy hay-farmer’s lung
  • Histology= Complement & neutrophils
  • Associated diseases=SLE
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4
Q

Describe type-I hypersensitivity

A
  • Antibody= IgE
  • Antigen= Exogenous
  • Response time= 15-30mins
  • Appearance= Weal & flare
  • Histology= Basophils & eosinophils
  • Innocuous antigen= pollen-hay fever
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5
Q

Describe type-IV hypersensitivity

A
  • Antibody= None
  • Antigen= Tissue & organ specific T-cell mediated cytotoxicity
  • Response time= 48-72 hours
  • Appearance= erythema induration
  • Histology= monocytes & lymphocytes
  • Innocuous antigen= Poison ivy, tuberculin test, metals-nickel
  • Associated diseases= contact dermatitis
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6
Q

How does an allergy develop?

A
  • Environmental &/or genetic stimuli
  • Barrier dysfunction
  • All of above leads to sensitisation
  • Leads to changes in T cell sub-sets dominated by Th2
  • Causes IgE production
  • Forming an allergy
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7
Q

Why do we get allergies?

A
  • Components of immune system involved in responses to parasitic infection also involved in allergic response
  • System developed to produce rapid tissue-based response
  • Lack of infectious drive is a contributory factor in allergic disease
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8
Q

Describe the immune response to parasitic disease

A
  • Increase levels of IgE specific to pathogen-cross reactive
  • Tissue inflammation with basophil infiltration, eosinophilia & mastocytosis
  • Presence of CD4+ T cells secreting IL4, IL5, IL13
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9
Q

What is the hygiene hypothesis?

A
  • Stimulation by microbes is protective
  • Prevention of autoimmunity by infections
  • Pro-biotics in pregnant women
  • Mechanism Th1, Th2 deviation
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10
Q

What are genetic influences on the ‘allergic’ immune response?

A
  • Polygenic diseases
  • Cytokine gene cluster IL3,5,9,13
  • IL12R, IL4R
  • FCεRI
  • IFNγ, TNF
  • Not sufficient for disease only susceptibility
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11
Q

Define allergen

A

Antigens that initiate an IgE-mediated response, first encounter results in innate & IgM response

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12
Q

What is the conventional immune response?

A
  • Allergen requires processing
  • Presentation to T cells & cytokine release
  • Resukts in delineation of T-helper subsets into different types
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13
Q

How is IgE produced?

A
  • Th2 cell stimulated by IL4 and interaction with B cell

- B cell proliferation producing IgE

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14
Q

What are the roles of the Th2 T cell?

A
  • Multiple cytokine release
  • Innate inflammatory response
  • Drive for immunoglobulin production
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15
Q

What diseases are included in the atopic triad?

A
  • Asthma
  • Eczema
  • Rhinitis
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16
Q

Describe rhinitis

A
  • Allergic/non-allergic
  • Allergic-perennial/seasonal
  • Blocked nose, runny nose, with eye symptoms
  • House dust mite, animal danders, pollens
  • Treatment- antihistamines & nasal steroids
17
Q

Describe asthma

A
  • Inflammation & hyper-reactivity of small airways
  • In childhood aero-allergic stimuli-house dust mite key pathogenic importance
  • Immedite symptoms are IgE mediated
  • Damage to airways due tolerate phase response
  • Damaged airways hyper-reactive to non-allergic stimuli-fumes
18
Q

Describe atopic dermatitis

A
  • Many different types
  • Contact- allergic/non-allergic
  • Clinically-intense itching, blistering/weeping cracking skin
  • House dust mite major trigger
  • Topical steroids & moisturisers
19
Q

What is anaphylaxis?

A

Acute potentially life-threatening IgG mediated systemic hypersensitivity reaction

20
Q

How is an allergy diagnosed?

A
  • History
  • Specific IgE
  • Skin prick test
  • Intra-dermal test
  • Oral challenge test- gold standard
  • Basophil activation test
  • Component resolved diagnostics
21
Q

What are the advantages & disadvantages of Specific IgE?

A
  • A=safe

- D= False negatives/positives

22
Q

What are the advantages & disadvantages of the skin prick test

A
  • A= Quick, pateint satisfaction

- D= False positives/negatives, slight risk, antihistamines

23
Q

What are indications of treatment for allergy?

A
  • Life threatening reactions to wasp & bee sting
  • Severe hay fever
  • Animal dander allergy
24
Q

What is symptomatic and specific treatment for allergies?

A

Sym=Antihistamines, Steroids, Adrenaline

Spec= Immunotherapy (submit or sublingual)

25
Q

What are clinical manifestations of food allergies?

A
  • Gastrointestinal: vomiting, diarrhoea, oral symptoms
  • Respiratory: rhinitis, bronchospasm
  • Cutaneous: urticaria, angioedema, atopic dermititis
  • Anaphylaxis