Theme 2 Lecture 6: Allergic Diseases Flashcards

1
Q

What is rhinitis commonly known as?

A

hay fever

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2
Q

What are the symptoms of rhinitis?

A

blocked/runny/itchy nose, sneezing

eye symptoms - itching, burning, watery eyes, redness

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3
Q

What is the treatment for rhinitis?

A

antihistamines or intranasal steroids

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4
Q

What type of hypersensitivity is allergic rhinitis?

A

type 1 - IgE mediated

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5
Q

What conditions are in the atopic triad?

A

rhinitis, asthma, eczema

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6
Q

What are the different types of rhinitis?

A
  1. allergic
    - seasonal: pollen, moulds
    - perennial: house dust mite, animal dander
  2. non-allergic
    - vasomotor
    - infective
    - structural
    - drugs
    - hormonal
    - polyps
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7
Q

What is asthma?

A

disease of inflammation and hyper-reactivity of the small airway

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8
Q

In childhood, which pathogen is of pathogenic importance as an allergic stimuli?

A

house dust mite

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9
Q

Explain how an allergen presented to a patient can result in allergic asthma

A
  1. allergen presented to antigen presenting cell
  2. antigen interacts with Th2 cell to encourage proliferation
  3. Th2 cells secrete cytokines which cause B cells/plasma to secrete IgE antibodies
  4. mast cell, basophil and eosinophil secrete histamine, leukotriene etc
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10
Q

What are the symptoms of dermatitis/eczema?

A

intense itching, blistering/weeping, cracking of skin

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11
Q

Explain the process of sensitization and memory induction

A
  1. first, sensitization to allergens and development of specific B and T cell memory
  2. differentiation and clonal expansion of allergen-specific Th2 leads to production of cytokines
  3. Class switching to IgE
  4. IgE+ memory
  5. B cell clonal expansion
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12
Q

Explain the immediate phase of the allergic reaction

A

cross-linking and degranulation of mast-cell and basophil causes release of vasoactive amines, lipid mediators, chemokines, cytokines
-immediate symptoms of allergic disease

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13
Q

Give a summary of the late phase inflammation response

A
  • allergen specific T cells are reactivated and clonally expand
  • local IgE-facilitated antigen presentation by dendritic cells increases T cell activation
  • Th1 cells produce IFN and TNF contribute to the activation and apoptosis of keratinocytes (in the skin), bronchial epithelial cells and pulmonary smooth-muscle cells
  • activation of mast cells and basophils which release histamine
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14
Q

Explain the actions of T cells in allergic rhinitis and asthma

A
  • Th2-cytokine-mediated induction of increased mucus production
  • local production of IgE
  • Th1-cell-mediated induction of bronchial epithelial-cell apoptosis
  • eosinophils one of the main inflammatory cells
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15
Q

What are the actions of T cells in atopic dermatitis?

A
  • Th1 cell mediated induction of keratinocyte apoptosis

- Th1 cell-mediated epithelial cell activation, and release of chemokines and pro-inflammatory cytokines

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16
Q

What does a specific IgE test measure?

A

the levels of different IgE antibodies

17
Q

What are the methods of analysing raw allergen material?

A
  • extraction –> extract immunoCAP
  • recombinant technology –> component immunoCAP
  • purification –> component immunoCAP
18
Q

What are the two skin tests for allergies?

A

skin prick test and intra-dermal test

19
Q

What size does the lesion in a skin prick test have to be for it to produce a positive result?

A

> 2mm wheal

20
Q

What happens when there is crosslinking of membrane bound IgE and a basophil?

A
  • basophils upregulate the expression of specific activation markers such as CD63, CD300a
  • they become activated
21
Q

What are the disadvantages to common allergy tests?

A

false positives and negatives

22
Q

How does allergen specific immunotherapy work?

A
  • decreases size of and number of cells in immediate phase and late phase allergic inflammation
  • prevents the development of new allergic sensitizations and reduces progression of allergic rhinitis to asthma
  • Th1:Th2 increases
  • production of IL-10, TGF
  • reduces number of mast cells and the ability of mast cells to release mediators
  • improves quality of life of treated individuals
23
Q

Name 6 major food allergens?

A
cows milk
eggs
legumes- peanut, soybean, tree nuts
-fish
-crustaceans/molluscs
-cereal grains
24
Q

What are the two ways a patient can experience food intolerance?

A
  • food characteristics - pharmacologic, toxin

- host characteristics - metabolic e.g lactase deficiency, psychological

25
Q

What are examples of IgE-mediated food allergies?

A
  • anaphylaxis
  • urticaria
  • angioedema
  • oral allergy syndrome
  • acute rhinitis
  • acute asthma
26
Q

What are examples of non-IgE mediated food allergies?

A
  • contact dermatitis
  • dermatitis herpetiformis
  • proctocolitis
  • FPIES
  • coeliac disease
  • heiner’s syndrome
27
Q

What are the clinical manifestations of allergic reactions?

A
  • vomiting
  • diarrhoea
  • oral symptoms
  • rhinitis
  • bronchospasm
  • urticaria
  • angioedema
  • anaphylaxis
28
Q

Is atopic dermatis IgE mediated or not?

A

its both

29
Q

What would you ask a patient who has recently had an allergic reaction?

A
  • detailed description of reaction
  • time between drug intake and onset of symptoms
  • number of doses taken before onset
  • aware of pharmacological effects and non-immunological ADR
30
Q

How can you manage allergies?

A
  • intradermal testing
  • graded challenge
  • desensitisation
31
Q

What type of hypersensitivity causes anaphylaxis?

A

type 1

32
Q

What type of hypersensitvity is caused by IgG antibodies?

A

type 2 and 3

33
Q

How does IgE antibody cause allergic reaction?

A

mast cell activation

34
Q

Which cells secerete IgE?

A

Plasma cells

35
Q

What is the gold standard test for allergies?

A

graded challenge - exposing a patient to allergen in controlled environment