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Y2 Immuno (MCD) > Hypersensitivity and Allergy > Flashcards

Hypersensitivity and Allergy Flashcards

1
Q

What are hypersensitivity reactions usually mounted against?

A

Harmless foreign antigens Autoantigens Alloantigens

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2
Q

What are the four type of hypersensitivity reaction?

A

Type 1 – immediate hypersensitivity Type 2 – antibody-mediated cytotoxicity Type 3 – immune complex mediated Type 4 – delayed cell mediated

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3
Q

Describe the mechanism of type 1 hypersensitivity?

A

On 1st exposure you get sensitisation – IgE is produced, which binds to mast cells and basophils On subsequent exposure, antigen cross-links the IgE on the mast cells causing degranulation and release of inflammatory mediators

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4
Q

What types of diseases are examples of type 2 hypersensitivity?

A

Organ specific autoimmune diseases: e.g. myasthenia gravis, glomerulonephritis, pemphigus vulgaris, pernicious anaemia Autoimmune cytopenias (Ab mediated blood cell destruction) e.g. autoimmune haemolytic anaemia, thrombocytopenia, neutropenia

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5
Q

What are the consequences of immune complex formation in type 3 hypersensitivity?

A

Immune complexes deposit in blood vessels and tissues Activate complement and cause cell recruitment Can also activate other cascades such as clotting This can cause tissue damage and vasculitis

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6
Q

Give some examples of diseases caused by delayed type hypersensitivity.

A

Chronic graft rejections Graft-versus-host disease Coeliac disease Contact hypersensitivity

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7
Q

Describe the mechanism of delayed type hypersensitivity.

A

The transient/persistent antigen is presented to TH1 cells by APCs. Th1 then releases IFN-gamma which activates macrophages. Activated macrophages produce TNF-alpha, which is responsible for much of the tissue damage Th1 also releases IL-2 to activate cytotoxic T lymphocytes (CTLs) to release perforin Th1 also release fibroblast growth factor (FGF), stimulating fibroblasts to promote fibrosis and angiogenesis

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8
Q

What are three important cytokines released by Th2?

A

IL-4 IL-5 IL-13

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9
Q

What is the difference between the antigens involved in type 2 and type 3 hypersensitivity?

A

Type 2 – insoluble antigens (cell surface or matrix bound antigens) Type 3 – soluble antigens

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10
Q

What is atopy?

A

A form of allergy in which there is a hereditary or constitutional tendency to develop hypersensitivity reactions in response to allergens

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11
Q

How common is atopy?

A

Very common – about 50% of young adults in the UK

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12
Q

List some genetic risk factors of atopy.

A

About 80% of atopics have a family history The genetic component is polygenic but genes of the IL-4 cluster on chromosome 5 and genes for the IgE receptor on chromosome 11q have been linked to atopy

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13
Q

Among which age group is atopy most common?

A

Teens

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14
Q

Describe the gender difference in asthma

A

Males – asthma in childhood is more common Females – asthma in adulthood is more common

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15
Q

What other environmental factors affect atopy?

A

Family size - more common in small families Infections - early life exposure to infections is protective Animals - more exposure is protective Diet - breast feeding, anti-oxidants, fatty acids protect

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16
Q

What type of hypersensitivity and which antibody is responsible for anaphylaxis, urticaria and angioedema?

A

Type 1 hypersensitivity - IgE mediated

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17
Q

What type of hypersensitivity and which antibody is responsible for chronic urticaria?

A

Type 2 hypersensitivity - IgG mediated

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18
Q

What type of hypersensitivity is responsible for asthma, rhinitis and eczema?

A

Type 1 - IgE mediated and type 4 hypersensitivity

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19
Q

Describe sensitisation in atopic airway disease.

A
  • Dendritic cells capture allergens from the airway and present them to naive CD4+ T cells
  • Once the T cells are exposed to the antigen by APCs, they can become: Th1 cells or T regs or Th2 memory cells
  • Th1 cells secrete IFN-gamma which inhibts Th2 proliferation
  • Treg cells produce IL-10 which inhibits the development of CD4+ T cells into Th2 cells
  • Th2 cells lead to the activation of B cells via IL-4 and IL-13
  • The B cells produce IgE antibodies
20
Q

Describe what happens in second exposure to the allergen in the atopic airway.

A

In second exposure, the allergens are presented by dendritic APCs to memory Th2 cells, which then release IL-5, which causes eosinophil degranulation Th2 cells also release IL-4 and IL-13, which stimulate production of IgE by plasma cells The antigens crosslink the IgE on the surface of mast cells causing degranulation

21
Q

What percentage of blood leukocytes are eosinophils?

A

0-5%

22
Q

Describe the appearance of the nucleus of eosinophils.

A

Bi-lobed

23
Q

What receptors do mast cells have on their cell surface?

A

IgE receptors

24
Q

What mediators are released by mast cells?

A

Preformed: histamines, cytokines, toxic proteins Newly synthesised: leukotrienes, prostaglandins

25
Q

What percentage of blood leukocytes are neutrophils?

A

55-60%

26
Q

What three processes cause airway narrowing in an acute asthma attack?

A

Vascular leakage leading to airways wall oedema Mucus secretion fills up the lumen Smooth muscle contraction around the bronch

27
Q

Describe the changes seen in a patient with chronic asthma.

A
  • The lumen of the airway is narrowed and the airway wall is grossly thickened
  • There will be cellular infiltration by Th2 lymphocytes and eosinophils
  • There will be smooth muscle hypertrophy, mucus plugging, epithelial shedding and subepithelial fibrosis
28
Q

State some important clinical features of asthma.

A

Chronic episodic wheeze Bronchial hyperresponsiveness Cough Mucus production Breathlessness Reduced and variable peak expiratory flow (PEF)

29
Q

What can allergic eczema lead to sensitisation of?

A

House dust mites – their proteins can get through dry, cracked skin

30
Q

What type of hypersensitivity is food allergy?

A

Type 1 hypersensitivity (IgE)

31
Q

What are the symptoms of a mild reaction to a food allergy?

A

Itchy lips and mouth Angioedema Urticaria

32
Q

What are the symptoms of a severe reaction to a food allergy?

A

Nausea Abdominal pain Diarrhoea Anaphylaxis

33
Q

What is anaphylaxis?

A

Severe generalised allergic reaction

34
Q

What is anaphylaxis caused by?

A

Generalised degranulation of IgE sensitised mast cells

35
Q

State some symptoms of anaphylaxis.

A
  • Itchiness around mouth, pharynx and lips
  • Swelling of the lips and throat
  • Wheeze, chest tightness, dyspnoea
  • Faintness, collapse
  • Diarrhoea and vomiting
36
Q

How can you test for allergies?

A

Skin prick test

37
Q

What is the emergency treatment of anaphylaxis?

A

Adrenaline

38
Q

Describe the step-by-step treatment of asthma.

A
  • Step 1: short acting beta 2 agonist (e.g. salbutamol)
  • Step 2: low-moderate dose inhaled steroids (e.g. beclomethasone, budesonide, fluticasone)
  • Step 3: add long acting beta 2 agonist or a leukotriene receptor antagonist + high dose inhaled corticosteroids
  • Step 4: add courses of oral steroids
39
Q

What are the two types of immunotherapy that are used to develop tolerance in patients?

A

Subcutaneous immunotherapy (SCIT) Sublingual immunotherapy (SLIT)

40
Q

What is produced in appropriate immune tolerance?

A

Regulatory T cells and regulatory (blocking) antibody IgG4

41
Q

What types of diseases are examples of type 1 hypersensitivity?

A

Anaphylaxis Asthma Rhinitis - seasonal or perennial Food allergy

42
Q

What are the two types of allergic rhinitis?

A

Seasonal - hayfever from grass or tree pollens Perennial - house dust mite, pets

43
Q

What are the symptoms of allergic rhinitis?

A
  • Sneezing
  • rhinorrhoea
  • itchy nose and eyes
  • nasal blockage,
  • sinusitis,
  • loss of smell/taste
44
Q

What is allergic eczema?

A

Chronic itchy skin rash

45
Q

What is allergic aczema caused by?

A

House dust mite (HDM) sensitisation and dry cracked skin - enables HDM to enter the body more easily Complicated by bacterial and rarely viral infections

Y2 Immuno (MCD) (5 decks)

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