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Clinical pathology > Allergic diseases > Flashcards

Allergic diseases Flashcards

1
Q

Allergy and hypersensitivity

A

Damaging and sometimes fatal reactions produced by the normal immune system directed against non-toxic antigens

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2
Q

Type 2 hypersensitivity - cytotoxic

A

IgG/IgM Ab response against an antigen at the cell surface attached to the tissue - common antigen is penicilin

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3
Q

Type 2 hypersensitivity- cytotoxic associated diseases

A
  • Erythroblastosis fetalis - mum antigens attack child
  • Goodpasture’s nephritis
  • Penicillin mediated autoimmune haemolytic anamia
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4
Q

How does Type 3 hypersensitivity - immune complex work

A
  • IgG/IgM Ab’s vs soluble agent
  • Form an immune complex deposited in organs
  • Triggers complement pathway
  • Causes self-damage
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5
Q

What does an activated complement pathway do?

A

Activation of complement factors and macrophages, attacks neutrophils causing self damage

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6
Q

Type 3 hypersensitivity- immune complex clinical features

A

onset 3-8 hours

  • vasculitis
  • disease = SLE
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7
Q

How does Type 4 hypersensitivity- delayed work

A
  • Antigen specific T-cell
    mediated cytotoxicity
  • Antigen is recognised by antigen-presenting cells and presented to T cells in lymph nodes
    -T cells activate and cause cell damage to cytokines
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8
Q

Type 4 hypersensitivity- delayed clinical features

A

Delayed onset 48-72 hours

  • Erythema induration
  • Contact dermatitis
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9
Q

Why do we get allergies

A
  • Combination of genetic and environmental factors

- Lack of infectious drive is a contributory factor in allergic disease

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10
Q

Immune responses to parasitic disease

A
  • Increased levels of IgE
  • Tissue inflammation - Eosinophilia, mastocytosis and Basophil infiltration
  • Presence of CD4+ T cells - secrete cytokines (IL4, IL13)
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11
Q

What is the hygiene hypothesis

A

Immune stimulation by microbes protects against allergies so if microbes decrease allergies will increase

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12
Q

What is the mechanism behind the Hygiene Hypothesis

A

Antigenic competition - infections compete with immune system against allergens - T helper 1/2 balance

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13
Q

Genetic influences on the allergic immune response

A
  • Polygenic disease
  • FcERI receptor
  • IL4R + IL12R
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14
Q

How is IgE produced

A
  • Antigen is recognised by helper 2 and B cell
  • TH2 uses IL-4 to signal the B cell
  • B cell drives to produce IgE for mast cells
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15
Q

Role of the TH2 cell

A
  • Multiple cytokine release

- Activator for IgE production

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16
Q

Type 1 hypersensitivity- IgE mediated allergic response

A
  • IgE is produced in mast cells + basophils
  • Allergen binds to IgE
  • Bridging of 2 IgE by allergen causes release of mediators causing response
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17
Q

Type 1 hypersensitivity clinical features

A

Fast onset

  • Wheal and flare - potentially anaphylaxis
  • Late phase response involved in asthma
18
Q

Criteria for anaphylaxis

A
  • Sudden onset of illness with involvement of skin/mucosal tissue and sudden respiratory symptoms /reduced bp
  • Symptoms of end-organ dysfunction
19
Q

Treatment of anaphylaxis

A

Mild reaction = antihistamines

Systemic symptoms - adrenaline pen

20
Q

What is the Atopic triad

A

Asthma, rhinitis, eczema

21
Q

Rhinitis

A

Allergic - perennial or seasonal
Causes:
- House dust mite, pollens

22
Q

Rhinitis symptoms and treatment

A
  • Blocked nose, sneezing - with eye symptoms

- Treated with antihistamines and nasal steroids

23
Q

Asthma

A
  • Inflammation and hyper-reactivity of small airways

Stimulated by aero-allergic, house dust mite

24
Q

Asthma symptoms

A

Immediate symptoms are IgE mediated - also damage to airways due to late phase response by eosinophils

25
Q

Atopic dermatitis (eczema)

A

House dust mite is a major trigger - Atopic is more of an autoimmune type

26
Q

Atopic dermatitis symptoms and treatment

A

Intense itching, blistering and cracking of skin

- Treated with topical steroids and moisturisers

27
Q

Pathogenesis of asthma

A
  • Allergen is detected by APC and antigen is presented to TH2 cell
  • TH2 activates B cell + Eosinophil by cytokines
  • B cell causes IgE production in mast cells
  • Eosinophils contribute to late phase response
28
Q

What tests can be used to diagnose hypersensitivity

A
  • Specific IgE
  • Skin prick test
  • Intra dermal test
  • Graded challenge test
  • Basophil activation test
29
Q

Specific IgE test

A
  • Safe as it is a blood sample

- Produces false negatives and positives

30
Q

Skin prick test

A

Quick and high patient satisfaction

- Antihistamines are a slight risk - false +/-

31
Q

Intra-dermal test

A

Inject agent - done in context of rug allergies

32
Q

Graded challenge test

A

Gold standard

- Keep doubling agent until symptom shown or negative results shown

33
Q

Basophil activation test

A

Upon cross-linking of membrane-bound IgE, basophils up-regulate the expression of activation markers

34
Q

What are the symptomatic treatments for allergic reactions

A
  • Antihistamines
  • Steroids (nasal)
  • Adrenaline
35
Q

Mechanism of immunotherapy

A
  • Aim is to divert the immune system or alter it
  • Ratio of TH1/TH2 increased
  • Production of IL-10 increased
  • Reduced number of mast cells
36
Q

Major food allergens - water soluble glycoproteins 10-60 kd

A 
Cow's milk
egg
legumes
peanut
soybean
tree nuts
37
Q

What symptoms would an allergy in the GI show

A

Vomiting, diarrhoea, oral symptoms

38
Q

What symptoms would an allergy in the respiratory system show

A

Rhinitis and bronchospasm

39
Q

What symptoms would an allergy in the cutaneous layer show

A

Urticaria and angioedema

40
Q

How are drug allergies managed

A

Intradermal testing

Dermal graded challenge

Clinical pathology (69 decks)

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