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IIH > Allergic Disease and Immunology > Flashcards

Allergic Disease and Immunology Flashcards

1
Q

Define hypersensitivity reaction.

A

A reaction of the immune system that is detrimental to the host, which is either:

  • A normal immune response triggered and persistent in the absence of a true pathogen.
  • An inappropriately exaggerated immune response.
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2
Q

Describe the 4 types of hypersensitivity reactions.

A

Type 1 - Type I IgE mediated mast cell degranulation and activated eosinophils and basophils.

Type 2 - Self IgG antibodies bind antigens on the patient’s own cell surfaces and cause damage directly.

Type 3 - Immune complexes formed of circulating antigen and IgG.

Type 4 - Cellular immune responses mediated by T cells.

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3
Q

Which of the 4 types of hypersensitivity reactions is known as allergy?

A

Type I.

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4
Q

List 6 examples of type 1 hypersensitivity reactions (allergies) in order of severity.

A

1 - Hay fever.

2 - Allergic asthma.

3 - Atopic dermatitis.

4 - Food allergy.

5 - Drug allergy.

6 - Latex allergy.

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5
Q

Give an example of a type II hypersensitivity reaction.

A

Autoimmune haemolytic anaemia.

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6
Q

List 2 examples of type III hypersensitivity reactions.

A

1 - Arthus reactions.

2 - Immune complex disease.

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7
Q

List 2 complications of type III hypersensitivity reactions.

A

1 - Glomerulonephritis.

2 - Vasculitis.

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8
Q

What are type IV hypersensitivity reactions otherwise known as?

A

Delayed hypersensitivity reactions.

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9
Q

List 2 examples of type IV hypersensitivity reactions.

A

1 - Contact dermatitis.

2 - Mantoux test (tuberculin reaction).

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10
Q

Which 2 types of hypersensitivity reaction are most common clinically?

A

Type 1 and 4.

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11
Q

How do type 1 and type 4 hypersensitivity reactions differ in time between exposure and onset?

A
  • Type 1 hypersensitivity reactions occur immediately after exposure.
  • Type 4 hypersensitivity reactions occur >4 hours after exposure.
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12
Q

How do type 1 and type 4 hypersensitivity reactions differ with regards to severity?

A
  • Type 1 hypersensitivity reactions are often life threatening.
  • Type 4 hypersensitivity reactions are often severe but not life threatening.
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13
Q

How do type 1 and type 4 hypersensitivity reactions differ with regards to the allergen that causes them?

A

The allergen is usually more difficult to identify with type 4 hypersensitivity reactions.

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14
Q

What is patch testing?

When is it used?

A
  • A method used to determine whether a substance causes allergic inflammation of a patient’s skin.
  • Used in the diagnosis of contact dermatitis.
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15
Q

Define sensitisation.

A

A phenomenon where the immune system recognises an allergen but doesn’t necessarily induce systemic symptoms.

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16
Q

Define atopy.

A

Predisposition to allergic disease.

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17
Q

Define anaphylaxis.

A

A severe, life threatening IgE mediated type 1 hypersensitivity (allergic) systemic or generalised reaction characterised by a dramatic fall in blood pressure and severe airway constriction.

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18
Q

Define anaphylactoid.

A

A severe, life threatening non-IgE mediated systemic reaction that mirrors anaphylaxis in clinical presentation.

19
Q

List the steps involved in type 1 hypersensitivity reactions.

A

1 - Allergen exposure.

2 - Sensitisation.

3 - Specific IgE production.

4 - Re-exposure to allergen and allergic response.

20
Q

What is the relative (qualitative) concentration of IgE in the blood compared with other immunoglobulin classes?

A

Very low.

21
Q

List 2 reasons for why IgE concentration might increase during type I hypersensitivity reactions.

A

1 - Increased production.

2 - Increased class switching to IgE.

22
Q

List 2 cytokines required for IgE class switching.

A

1 - IL-4.

and / or

2 - IL-13.

23
Q

Via which receptors does the IgE constant region bind to allergy effector cells?

A

FceR1.

24
Q

List the allergy effector cells.

A

1 - Mast cells.

2 - Basophils.

25
Q

Give an example of an enzyme that is used to diagnose anaphylaxis.

Why is it useful in diagnosing anaphylaxis?

What is the function of this enzyme?

A
  • Tryptase.
  • Because it is long-lasting (about 8 hours after the onset of anaphylaxis).
  • Tryptase is a mast cell mediator that is released by activated mast cells which has a role in inflammation.
26
Q

List 4 early phase mast cell mediators.

A

1 - Histamine.

2 - Kallikrein.

3 - Serotonin.

4 - Proteases.

27
Q

List 4 late phase mast cell mediators.

A

1 - Tryptase.

2 - Leukotrienes.

3 - Prostaglandins.

4 - Cytokines.

28
Q

What is the function of kallikrein?

A

Kallikrein activates bradykinin which causes increased vascular permeability.

29
Q

What is the general function of late phase mast cell mediators?

A

To promote cellular upregulation and secretion.

30
Q

List 7 effects of mast cell mediators.

A

1 - Vasodilation.

2 - Bronchoconstriction.

3 - Increase heart rate.

4 - Increase heart contractility.

5 - Increase glandular secretion.

6 - Increase vascular permeability.

7 - Irritation of nerve endings.

31
Q

List 3 treatments of anaphylaxis.

A

1 - Intramuscular adrenaline.

2 - Steroids.

3 - Antihistamines.

32
Q

Give an example of a visual feature of allergy effector cells.

A

They are highly granular.

33
Q

List 3 secretions of mast cells and basophils.

A

1 - Histamine.

2 - IL-4.

3 - IL-13.

34
Q

Where are mast cells, basophils and eosinophils located?

A
  • Mast cells are concentrated in tissues.
  • Basophils circulate in the blood and migrate to lymph nodes and prime for allergic responses (by undergoing IgE class switching)
  • Eosinophils circulate in the blood and migrate to tissues.
35
Q

Which molecule promotes haematopoiesis in the bone marrow to produce eosinophils?

Which cells release this molecule?

A
  • IL-5.

- CD4+ Th2 cells.

36
Q

Which molecules promote chemotaxis of eosinophils?

A

Eotaxins.

37
Q

List 2 roles of eosinophils.

A

1 - Control of anti-helminth immunity.

2 - Control of allergic disease.

38
Q

List 4 type 1 hypersensitivity reactions (allergies) in order of age of onset.

A

1 - Allergic dermatitis.

2 - Food allergies.

3 - Asthma.

4 - Rhinitis.

39
Q

List 3 genetic and 3 environmental causes of allergic disease.

A

Genetic:

Epistasis between genes such as:

1 - IL4R gene.

2 - FceR1 gene.

3 - Filaggrin gene.

Environmental:

1 - Early life exposure.

2 - Infections.

3 - Hygiene.

40
Q

What is the hygiene hypothesis of allergic disease?

A
  • The lack of exposure to germs in early life skew the immune system away from a Th1 phenotype to a Th2 phenotype.
  • Th2 cells release interleukins 3, 4, 5, 9 and 13, which cause:

1 - Mast cell activation.

2 - IgE class switching.

3 - Eosinophil activation and recruitment.

41
Q

What is the primary purpose of IgE-mediated immune responses?

A

To promote killing of parasites:

  • Helminths are recognised by mast cells as the first line of defence.
  • This occurs near body surfaces, where mast cells are abundant.
  • The response increases lymph and blood flow, causing angioedema.
  • The response involves mast cells recruiting other effectors.
42
Q

Describe the process of parasite killing.

A

1 - IgE binds to the parasite.

2 - Eosinophils bind to IgE via the FceR1 receptor.

3 - Eosinophils release toxic lysosomal granules containing major basic protein, ribonucleases, peroxidases, ROS and nitrogen radicals.

43
Q

Describe the process of parasite eradication.

A

Il-13 released from effector cells causes:

1 - Goblet cell hyperplasia.

2 - Increased mucus production.

3 - Increased smooth muscle contraction in the GIT.

IIH (26 decks)

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