Core Immunology - Allergic Diseases (11) Flashcards

(63 cards)

1
Q

Allergy

A

Undesirable, damaging and sometimes fatal reaction produced by immune system, directed against innocuous antigens in a pre-sensitised (immune host)

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2
Q

Immunopathological classification

A

Coombs and Gel 1963 - IV types, extended classification - type V

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3
Q

Type 2 allergy

A

Cytotoxic

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4
Q

Type 2 immunopathogenesis

A

IgG/IgM Ab response against self/foreign antigen at cell surface - complement activation/phagocytosis/ADCC

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5
Q

Type 2 clinical features

A

Onset minutes to hours, cell lysis and necrosis

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6
Q

Type 2 common antigens

A

Penicillin

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7
Q

Type 2 associated diseases

A

Erythroblastosis fetalis, Goodpasture’s nephritis

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8
Q

Type 3 allergy

A

Immune complex

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9
Q

Type 3 immunopathology

A

IgG/IgM Ab against soluble antigen (immune complex deposition)

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10
Q

Type 3 clinical features

A

Onset 3-8 hours, vasculitis

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11
Q

Type 3 cause

A

Serum sickness

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12
Q

Type 3 associated diseases

A

SLE

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13
Q

Inhaled >

A

Farmer’s lung, alveolar/capillary interface

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14
Q

Type IV allergy

A

Delayed

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15
Q

Type IV clinical features

A

Delayed onset 48-72 hours, erythema induration

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16
Q

Type IV common antigen

A

Metals - nickel (tuberculin reaction)

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17
Q

Type IV associated diseases

A

Contact dermatitis

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18
Q

Immune response to parasitic disease

A

Increased IgE, specific to pathogen (cross-reactive), tissue inflammation (eosinophilia, mastocytosis, basophil infiltration), presence of CD4+ T cells secreting (IL4, IL5, IL13)

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19
Q

Hygiene hypothesis

A

Microbes stimulation is protective, increase asthma after anti-parasitic treatment, prevention of autoimmunity, pro-biotics in pregnancy (Th1 Th2 deviation)

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20
Q

Genetic influence on allergic immune response - polygenic disease, cytokine gene cluster (IL3,5,9,13), IL12R, IL4R, FC3RI, IFNy, TNF, Not sufficient for disease, only suscepibility

A

??

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21
Q

4 groups of susceptibility genes for allergic disease

A
  1. Sensing the environment
  2. Barrier function
  3. Regulation of (atopic) inflammation
  4. Tissue response genes
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22
Q

Allergens

A

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

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23
Q

Conventional immune response

A

Allergen requires processing, presentation to T cells, cytokine release > delineation of T-helper subsets into different types

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24
Q

IgE production

A

Th2 cell stimulates B cell with IL-4, stimulates B cell proliferation > IgE release

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25
Type 1 allergy
Fc receptor for IgE on mast cell > degranulation > vasoactive amines > smooth muscle, blood vessel mucous gland, platelets, sensory nerve endings > eosinophil
26
Primary mediators released from degranulation (initial response)
Histamine, proteases, chemotactic factors
27
Secondary mediators (late-phase response)
Membrane phospholipid > Arachidonic acid > leukotrienes and prostaglandin
28
Role of Th2
Multiple cytokine release - innate inflammatory response (IL-4 and IL-13), drive for Ig production
29
Th1 cells produce
IFN and TNF
30
Role of Th1
Activation and apoptosis of keratinocytes, bronchial epithelial cells and pulmonary smooth muscle (activation of mast cells and basophils > histamine)
31
Atopic triad
Asthma, rhinitis, eczema
32
Allergic rhinitis
Nasal congestion (oedema, mucus, nasal polyps)
33
Asthma
Airway inflammation (oedema, mucus)
34
Rhinitis allergic
Perennial/seasonal (allergic/non-allergic)
35
Rhinitis symptoms
Blocked nose, runny nose (eye symptoms)
36
Antigens for Rhinitis
House dust mite, animal danders
37
Rhinitis treatment
Antihistamines and nasal steroids
38
Early phase response/acute allergic symptoms
Mucus hypersecretion, increase of vascular permeability (oedema), vasodilation, C-sensory nerve stimulation)
39
Late phase response/chronic allergic inflammation
Sneezing, nasal itching, rhinorrhea, nasal obstruction, occular symptoms, nasal hyperresponsiveness
40
What is asthma?
Disease of inflammation and hyper-reactivity of small airways
41
Asthma in childhood
Aero-allergic stimuli (house dust mite)
42
Asthma immediate symptoms are mediated by what
IgE
43
Asthma damage to airways due to
Late phase response (infiltration of eosniphil, lymphocyte, Th, basophil), hyper-reactive to non-allergic stimulis (fumes)
44
Pathogenesis of asthma
Allergen > APC > Th2 > IL-5/IL-4/13 > eosinophil/mast cell basophil > histamine, leukotrienes, prostaglandins, cytokines > allergic asthma
45
Contact dermatitis
Allergic/non-allergic
46
Atopic dermatitis clinically
Intense itching, blistering/weeping, cracking of skin
47
Major trigger in atopic dermatitis
House dust mite
48
Treatment for atopic dermatitis
Topical steroids and moisturisers
49
How do you get pruritus?
Th2 - IL-31 > pruritus/scratch
50
Anaphylaxis
Acute, life-threatening, IgE mediated systemic hypersensitivity reaction
51
Diagnosis of allergy
- Specific IgE (>0.35) - Skin prick test (>3mm) - Intra-dermal test - Oral challenge test (gold standard) - Basophil activation test - Component resolved diagnostics
52
Basophil activation test
When IgE, upregulate expression of markers (CD63, CD203c, CD300a) > activated
53
Advantages of specific IgE
Safe
54
Disadvantages of specific IgE
False negatives and positives
55
Advantages of skin prick test
Quick, patient satisfaction
56
Disadvantages of skin prick
False negatives and positives, antihistamines, slight risk
57
Treatment
Antihistamines, steroids, adrenaline, immunotherapy (subcutaneous/sublingual)
58
Indications for treatment
Life threatening reactions to wasp, bee sting, severe hay fever, animal dander allergy
59
Not helpful for treatment
Multiple allergies, food allergy, allergic rashes (eczema, urticaria)
60
Major food allergens
Cow's milk, egg, legumes (peanut, soybean, tree nuts), fish, crustaceans/molluscs, cereal grains
61
Adverse food reactions - GI clinical
Vomiting, diarrhoea, oral symptoms
62
Adverse food reactions - resp clinical
Rhinitis and bronchospasm (anaphylaxis)
63
Adverse food reactions - cutaneous
Urticaria, angioedema, role of food in atopic dermatitis unclear